Intern Handbook 1998 вЂ“ 2000 References Available from Medical Education What follows is a compilation of various references, which may be useful, educational or amusing. ***************************************** INTERN'S CREDO There's no admission like no admission. Anonymous ***************************************** 2 THE HOUSE OFFICER'S 15 LAWS OF HOSPITAL PRACTICE...........................................................................11 THE HOUSE OFFICER'S 10 LAWS OF OUTPATIENT PRACTICE ......................................................................11 THE HOUSE OFFICER'S FIVE RULES FOR LAB TESTS ....................................................................................11 SIX MEDICAL TRUISMS .........................................................................................................................................11 10 MEDICAL CLICHES ...........................................................................................................................................11 OCCUPATIONAL HAZARDS FOR PHYSICIANS PRACTICING IN THE UNITED STATES................................12 THE LECTURER (POEM)........................................................................................................................................12 WHAT IS THE SINGLE MOST IMPORTANT SKILL TO LEARN EARLY IN YOUR RESIDENCY? .....................12 CARDIAC ARREST -- VF & PULSELESS VT* .......................................................................................................13 CARDIAC ARREST -- PULSELESS ELECTRICAL ACTIVITY..............................................................................13 CARDIAC ARREST -- ASYSTOLE .........................................................................................................................14 CARDIAC DYSRHYTHMIAS ...................................................................................................................................18 SINUS BRADYCARDIA...........................................................................................................................................18 SINUS TACHYCARDIA ...........................................................................................................................................18 SUPRAVENTRICULAR EXTRASYSTOLE .............................................................................................................18 ATRIAL FLUTTER, ATRIAL FIBRILLATION .........................................................................................................18 CODE DRUGS ACLS ..............................................................................................................................................19 ANTI-ARRHYTHMICS .............................................................................................................................................20 VASODILATOR DRUGS .........................................................................................................................................21 DOPAMINE INFUSION ............................................................................................................................................21 ATRIOVENTRICULAR (AV) HEART BLOCK DURING ANESTHESIA .................................................................22 SUPRAVENTRICULAR (SV) TACHYCARDIA .......................................................................................................22 SV-TACHYCARDIA WITH PREEXCITATION-SYNDROME (WPW, LGL) ............................................................22 BRADYCARDIA DYSRHYTHMIA AND AV-BLOCK ..............................................................................................22 BRADYCARDIA AND HYPOTENSION IN THE PRESENCE OF BETA-BLOCKADE ..........................................22 VENTRICULAR DYSRHYTHMIA ............................................................................................................................22 PROLONGED QT-INTERVAL .................................................................................................................................22 3 VENTRICULAR EXTRASYSTOLES CAUSED BY DIGITALIS INTOXICATION ...................................................22 VENTRICULAR FIBRILLATION..............................................................................................................................23 DIGITALIZATION.....................................................................................................................................................23 DIGITALIS INTOXICATION .....................................................................................................................................23 LOWN CLASSIFICATION .......................................................................................................................................23 SWAN GANZ CATHETER.......................................................................................................................................23 '7-3' - RULE FOR FLUID MONITORING.................................................................................................................24 MEDICAL HISTORY-TAKING IN THE MODERN ERA ..........................................................................................24 HISTORY, PHYSICAL, & NOTES ...........................................................................................................................25 MEDICAL HISTORY (ALTERNATIVE) ...................................................................................................................27 PHYSICALEXAMINATION ......................................................................................................................................28 CARDIAC PHYSICAL EXAM SIGNS ......................................................................................................................31 MINI-MENTAL STATUS EXAM ...............................................................................................................................32 PROGRESS/SOAP NOTE (NON-ICU) ....................................................................................................................33 PROGRESS NOTE (ICU).........................................................................................................................................33 OPERATIVE NOTE..................................................................................................................................................34 PROCEDURE NOTE................................................................................................................................................34 DISCHARGE SUMMARY ........................................................................................................................................34 LABOR AND DELIVERY H&P ................................................................................................................................34 DELIVERY NOTE (EXAMPLE)................................................................................................................................35 INCOMPLETE ABORTION ADMIT ORDERS.........................................................................................................35 PREGNANCY AND DRUGS TO BE AVOIDED-.....................................................................................................35 APGAR SCORE.......................................................................................................................................................35 NEONATAL/BIRTH H&P .........................................................................................................................................36 PRIMITIVE REFLEXES OF INFANCY ....................................................................................................................36 PEDIATRIC H&P......................................................................................................................................................36 ESTIMATING BODY SURFACE AREA IN CHILDREN..........................................................................................37 4 ABBREVIATED PSYCH HISTORY .........................................................................................................................37 MENTAL STATUS EXAM:.......................................................................................................................................37 ABBREVIATED NEUROLOGICAL EXAM..............................................................................................................38 GLASGOW COMA SCALE .....................................................................................................................................38 DERMATOMES, ANTERIOR VIEW ........................................................................................................................39 DERMATOMES, POSTERIOR VIEW ......................................................................................................................40 EKG LEADS.............................................................................................................................................................42 MEDICAL ORDERS.................................................................................................................................................42 SIGN-OUT NOTE .....................................................................................................................................................43 DISCHARGE ORDERS............................................................................................................................................43 PRESENTING PATIENTS .......................................................................................................................................43 ACUTE PAIN MANAGEMENT ................................................................................................................................44 EVIDENCE BASED..................................................................................................................................................47 CENTRAL LINES: PLACEMENT AND PROBLEMS..............................................................................................49 DRAIN MANAGEMENT ...........................................................................................................................................50 NASOGASTRIC TUBE MANAGEMENT.................................................................................................................52 NEEDLE STICKS AND OTHER EXPOSURES TO BLOOD AND BODY FLUIDS ................................................52 WOUND COMPLICATIONS ....................................................................................................................................52 PROCEDURES ........................................................................................................................................................53 GRAM STAIN ...........................................................................................................................................................54 FLUIDS & ELECTROLYTES ...................................................................................................................................55 NORMAL PHYSIOLOGIC VALUES ........................................................................................................................55 ACID-BASE DISORDERS .......................................................................................................................................57 NORMAL LAB VALUES..........................................................................................................................................58 ACID-BASE..............................................................................................................................................................62 APPROACH TO INTERPRETING ACID-BASE STATUS ......................................................................................62 ARTERIAL BLOOD GAS LECTURE SLIDES ABGS.............................................................................................63 5 ACUTE RESPIRATORY FAILURE LECTURE SLIDES ARF.................................................................................82 HYPERCALCEMIA ..................................................................................................................................................96 HYPERKALEMIA.....................................................................................................................................................98 HYPERNATREMIA ..................................................................................................................................................99 HYPOKALEMIA .................................................................................................................................................... 100 HYPOMAGNESEMIA............................................................................................................................................ 101 HYPONATREMIA ................................................................................................................................................. 102 HYPOPHOSPHATEMIA ....................................................................................................................................... 103 MAGNESIUM TOXICITY....................................................................................................................................... 103 CONVERSIONS EQUATIONS ............................................................................................................................. 104 RENAL FUNCTION............................................................................................................................................... 104 ACUTE RENAL FAILURE .................................................................................................................................... 104 OLIGURIA (SUDDEN)- ......................................................................................................................................... 107 ACUTE TUBULAR NECROSIS (ATN) ................................................................................................................. 108 CHRONIC RENAL FAILURE................................................................................................................................ 109 MYOCARDIAL ISCHEMIA.................................................................................................................................... 111 MYOCARDIAL INFARCTION (MI) ....................................................................................................................... 115 THE USE OF BETA-BLOCKERS FOR ACUTE MYOCARDIAL INFARCTION ................................................. 117 RECOMMENDED IV DOSAGE OF BETA-BLOCKERS FOR PATIENTS WITH ACUTE MYOCARDIAL INFARCTION ON ADMISSION ............................................................................................................................ 117 THROMBOLYTIC AGENTS IN ACUTE MYOCARDIAL INFARCTION .............................................................. 117 CONTRAINDICATIONS TO THROMBOLYSIS ................................................................................................... 118 CONGESTIVE HEART FAILURE (CHF) .............................................................................................................. 118 DIASTOLIC HEART FAILURE (DHF) .................................................................................................................. 122 TORSADES DES POINTES (POLYMORPHIC VT) ............................................................................................. 123 PULMONARY ARTERY CATHETERIZATION .................................................................................................... 123 HEMODYNAMIC EXAMPLES .............................................................................................................................. 126 SWAN GANZ CATHETER WAVE FORMS.......................................................................................................... 127 6 GOLDMAN MULTIFACTORIAL CARDIAC RISK INDEX (MCRI)....................................................................... 128 HYPERTENSIVE CRISIS-..................................................................................................................................... 128 HYPERTENSIVE CRISIS AND SPECIFIC DRUG THERAPY- ............................................................................ 129 AORTIC DISSECTION:......................................................................................................................................... 130 SUBARACHNOID HEMORRHAGE: .................................................................................................................... 130 ISCHEMIC STROKE:............................................................................................................................................ 130 ISCHEMIC HEART DISEASE OR MYOCARDIAL INFARCTION: ..................................................................... 130 LEFT VENTRICULAR FAILURE:....................................................................................................................... 130 HYPERADRENERGIC STATES........................................................................................................................... 130 ECLAMPSIA: ........................................................................................................................................................ 130 POST-OPERATIVE HYPERTENSION: ............................................................................................................... 130 ACUTE RENAL INSUFFICIENCY:....................................................................................................................... 130 PERICARDITIS- .................................................................................................................................................... 133 CARDIAC TAMPONADE- .................................................................................................................................... 134 CAUSES OF ORTHOSTATIC HYPOTENSION:................................................................................................. 137 CHRONIC OBSTRUCTIVE PULMONARY DISEASE.......................................................................................... 140 DIFFERENTIAL DIAGNOSES OF PULMONARY ABNORMALITIES ................................................................ 146 PULMONARY FUNCTION TESTING PFT ........................................................................................................... 148 PULMONARY EMBOLISM LECTURE SLIDES(DR. GOFF) .............................................................................. 152 TB MYCOBACTERIUM TUBERCULOSIS........................................................................................................... 164 TEN RULES FOR READING CHEST X-RAYS.................................................................................................... 165 CHEST RADIOGRAPHY LECTURE BY DR. GOFF............................................................................................ 166 RULES ON OXYGEN THERAPY -- WHAT EVERY HOUSE OFFICER.............................................................. 182 SIGNS OF OBVIOUS BREATHING (WOB) ......................................................................................................... 183 THE FOUR MOST IMPORTANT EQUATIONS IN CLINICAL PRACTICE.......................................................... 183 NORMAL RANGES FOR VENTILATORY VALUES ........................................................................................... 189 PLEURAL EFFUSIONS ........................................................................................................................................ 190 7 ABDOMINAL PAIN ............................................................................................................................................... 196 CHARACTERISTIC PHYSICAL FINDINGS IN THE ACUTE ABDOMEN........................................................... 196 GASTROINTESTINAL BLEEDING (ACUTE UPPER)-........................................................................................ 197 ALCOHOLISM ...................................................................................................................................................... 199 ALCOHOLIC WITHDRAWAL-.............................................................................................................................. 201 ALCOHOL-............................................................................................................................................................ 201 VIOLENT PATIENTS- ........................................................................................................................................... 202 RANSON'S CRITERIA: FOR DETERMINING PROGNOSIS OF ACUTE PANCREATITIS ............................... 203 MODIFIED CHILD'S INDEX FOR GRADING SEVERITY OF LIVER DZ ........................................................... 203 ACUTE BLINDNESS ............................................................................................................................................ 203 ACUTE DYSTONIC REACTION........................................................................................................................... 204 SEIZURES............................................................................................................................................................. 205 STATUS EPILEPTICUS........................................................................................................................................ 208 LUMBAR PUNCTURE TESTS ............................................................................................................................. 208 CSF ANALYSIS .................................................................................................................................................... 209 STROKE RISK FACTORS AND PREVENTION THERAPY................................................................................ 209 COMA (COMMON CAUSES)- .............................................................................................................................. 210 ANTIBIOTICS & INFECTIOUS DISEASE ............................................................................................................ 210 HIV & AIDS STATS, ETC ..................................................................................................................................... 211 DIARRHEA............................................................................................................................................................ 214 ANTIRETROVIRAL (AIDS) AGENTS, DAILY DOSAGE AND MAJOR TOXICITIES -....................................... 214 PROPHYLAXIS OF OPPORTUNISTIC INFECTIONS AIDS ............................................................................... 215 CDC RECOMMENDATIONS FOR REDUCING PERINATAL HIV TRANSMISSION ......................................... 216 FEVER CLUES- DIAGNOSTIC SIGNIFICANCE BY MAGNITUDE OF THE TEMPERATURE: ..................... 217 FEVER OF UNKNOWN ORIGIN- FUO................................................................................................................ 218 HEAT STROKE..................................................................................................................................................... 219 NEUROLEPTIC MALIGNANT SYNDROME- ....................................................................................................... 220 8 MENINGITIS- COMMON CAUSES OF MENINGITIS BY AGE: ...................................................................... 221 DIABETIC KETOACIDOSIS DKA ........................................................................................................................ 225 DIFFERENTIAL DIAGNOSIS DKA HNKC ........................................................................................................... 225 HEMOGLOBIN A1C [GLYCOHEMOGLOBIN] AND BLOOD GLUCOSE ......................................................... 228 THYROID DISEASE INTRODUCTION................................................................................................................. 229 THYROTOXIC CRISIS-......................................................................................................................................... 231 THYROID STORM ................................................................................................................................................ 231 ADRENAL INSUFFICIENCY- ............................................................................................................................... 231 ANTICOAGULATION TREATMENT .................................................................................................................... 232 ANTICOAGULANT INR RECOMMENDATIONS FOR VARIOUS SITUATIONS-............................................... 233 BLEEDING DISORDERS- .................................................................................................................................... 234 BLOOD TRANSFUSION COMPLICATIONS-...................................................................................................... 234 MEDICAL EVALUATION OF SURGICAL RISK .................................................................................................. 236 THROMBOEMBOLISM PROPHYLAXIS IN SURGICAL PROCEDURES .......................................................... 239 ANTIBIOTICS FOR ENDOCARDITIS PROPHYLAXIS ....................................................................................... 240 POISONING .......................................................................................................................................................... 241 ACETAMINOPHEN TOXICITY- ............................................................................................................................ 241 CARBON MONOXIDE POISONING- ................................................................................................................... 242 CIGUATERA FISH POISONING- ......................................................................................................................... 244 ANAPHYLAXIS..................................................................................................................................................... 244 SCABIES-.............................................................................................................................................................. 245 ACUTE ARTHRITIS .............................................................................................................................................. 246 PRESSURE ULCERS IN ADULTS: ..................................................................................................................... 247 PULMONARY BEDSIDE REFERENCE ............................................................................................................... 251 ENDOTRACHEAL TUBE PLACEMENT .............................................................................................................. 253 MASSIVE HEMOPTYSIS (ANY OF THE BELOW) .............................................................................................. 253 GUIDELINES FOR FLUID CHALLENGES BY CVP OR PCWP ......................................................................... 255 9 EVIDENCE BASED MEDICINE LECTURES ....................................................................................................... 256 WORKSHEET FOR USING AN ARTICLE ABOUT THERAPY OR PREVENTION........................................... 274 WORKSHEET FOR USING AN ARTICLE ABOUT ASSESSING DIAGNOSTIC TESTS................................... 291 WORKSHEET FOR USING AN ARTICLE ABOUT PROGNOSIS ...................................................................... 293 WORKSHEET FOR USING AN ARTICLE ABOUT CAUSATION OF HARM..................................................... 294 WORKSHEET FOR USING AN ARTICLE ABOUT AN ECONOMIC ANALYSIS............................................... 298 WORKSHEET FOR USING AN ARTICLE REPORTING VARIATIONS IN THE OUTCOMES OF HEALTH SERVICES............................................................................................................................................................. 300 INDEX.................................................................................................................................................................... 302 10 THE HOUSE OFFICER'S 15 LAWS OF HOSPITAL PRACTICE (http://www.mtsinai.org/pulmonary/books/house/rules-a.html) 1. (Wherever you are . . .) if it happens here it happens everywhere. 2. Money not spent on the terminally ill will not go to feed hungry children. (This law is a corollary of: money not spent on military hardware . . .) 3. There is always family. When a patient is admitted with "no family" you just haven't found them yet. 4. When a consensus is needed for DNR status, there's always a key family member who is out of town. 5. If you order a CAT scan and a weight measurement on the same patient at the same time, the former will be done and charted before a scale is found. 6. Hospitalized patients can invariably be divided into two distinct groups. One group wants to go home as soon as possible and the other group never wants to leave. 7. The medical literature deals with patients who have only one disease. Most of your patients have more than one disease. 8. The number of layers of clothing through which the chest is auscultated directly correlates with the house officer's level of training. 9. After a patient is in the hospital for three days no one will know the patient's complete list of medications. 10. Any chart note worth writing is worth being legible; if a peer canвЂ™t quickly and easily read it, it might as well not have been written. 11. If God wanted us to have plastic tubes we'd be born with them: use it or remove it. 12. Dyspnea in a hospitalized patient is never due to anxiety. If a physician attributes dyspnea to anxiety the physician is either a fool or has completed an exhaustive workup for causes of dyspnea. Most of the time the physician is a fool. 13. The top three causes of fever in a hospitalized patient are: infection, infection, and infection. 14. When you assume another cause of fever remember the previous law. 15. In 1920 about 90% percent of all diagnoses were made with just a thorough medical history; in the 1990s the percentage is the same. Ditto for the next century. THE HOUSE OFFICER'S 10 LAWS OF OUTPATIENT PRACTICE 1. A drug proven effective after multi-center trials costing millions of dollars doesn't work very well if patients don't take it. 2. No study has ever shown that an outpatient can reliably ingest more than three drugs for more than three weeks. 3. No study has even shown the efficacy of more than three drugs taken simultaneously. 4. The drugs you think your patient is taking are never exactly the same as what your patient is taking. 5. Drugs for which blood monitoring is necessary should be avoided unless unequivocally needed - they all have a narrow therapeutic window. Examples: theophylline, digoxin, coumadin, procainamide. 6. The more complicated your patient, the more likely your patient is seeing other physicians for the same or related problems. 7. Outpatients can invariably be divided into two groups: those with no questions, and those who always have one more question. 8. An appointment every three months for a patient with two or more diseases taking two or more medications is about as helpful as no appointment at all. 9. Often the best treatment for a patient with chronic disease is the doctor's phone number. 10. You will be retired before your hospital's outpatient department implements a really useful record keeping system. THE HOUSE OFFICER'S FIVE RULES FOR LAB TESTS (NOTE: chest x-rays have their own set of rules) 1. Don't order a test if the outcome will have no effect on the management of your patient. 2. If the ordering of a lab test is equivocal, pretend you are the one paying for it. Then make your decision. 3. If a test result surprises you because it is abnormal, consider repeating it or obtaining a complementary test (e.g., CRP for ESR). If the test is abnormal a second time believe it. 4. Only people can lie. Lab tests are not people. Lab tests don't lie. 5. A hundred things can screw up a lab test result, from improper labeling to improper data transcription. The better you know your patient the better you will recognize a screw up. SIX MEDICAL TRUISMS 1. Not all asthmatics wheeze. However, finding a dyspneic asthmatic "without wheezing" usually means the patient was not auscultated during forced expiration (I question this. / Dr.Goff.). 2. Daily weights are seldom accurate because no one pays for them. A "weight service" that could charge per patient would maintain the scales and provide accurate daily weights. 3. Chronic complainers, hypochondriacs and Munchausen patients can contract the same diseases as everyone else. 4. The most underrated piece of medical equipment is the fax machine. 5. American hospitals have 19th century record keeping systems because they spend 19th century dollars on the problem. 6. An on-time patient deserves an on-time doctor. 10 MEDICAL CLICHES (Some of which are true some of the time) 11 10. Not charted not done. 9. Doctors make the worst patients. 8. Doctors' relatives have the most complications. 7. Doctors are lousy investors. 6. Only nice people get cancer. 5. Nasty people don't get bad diseases. 4. See one, do one, teach one. 3. Doctors bury their mistakes. 2. The patient is the one with the disease. 1. If something can go wrong, it will. Occupational Hazards for Physicians Practicing in the United States (Other countries may present different infectious disease risks; hazards are listed alphabetically) AIDS - Rare, but AIDS transmission from a patient's blood has been documented Assault- including murder - particularly at risk are ED physicians and psychiatrists who see patients with psychosis or a character disorder Asthma - mainly from formaldehyde, among pathologists Infectious hepatitis - particularly among surgeons Non-infectious hepatitis - mainly from halothane, among anesthesiologists Sclerotherapist's conjunctivitis - endoscopists occasionally squirt their eyes with sclerotherapy chemical Stress and burnout - all physicians at risk, and of course the problem is not unique to the medical profession Substance abuse - risk increased because of easy access to drugs Suicide - rate is definitely higher in some medical specialties (e.g., psychiatry) than in the general population Tuberculosis - particularly among physicians who work with multi-drug resistant TB THE LECTURER (poem) Tell us what we need to know. Please don't bore us with your show. Your slides, dear sir, put one to sleep. The words you use are way too deep. The problem, alas, is clear to see, You address a special fraternity. Who know the line, arcane reference; But none of them in this audience. Solution? None, I fear. You're too insensitive to hear What all of us show so well. You've simply lost us, truth to tell. Polite we'll be and clap the end. And hide the message we wish to send. Applause is for one reason, true Thank God, dear sir, you are through! 1. Determine the question 2. Establish urgency (emergent, urgent, elective) 3. Look for yourself (not everything is in the chart) 4. Be brief (short notes, <= 5 recommendations) 5. Be specific (spec drugs, mode of admin, duration,) 6. Provide contingency plans 7. Honor thy turf (discuss with surgeon before patient) 8. Teach...with tact 9. Talk is cheap...and effective (call requesting MD and discuss the findings) 10. Follow-up (if needed) What is the Single Most Important Skill to Learn Early in Your Residency? "How to take a history," "How to talk to patients," "How to write orders," "How to obtain DNR," or " How to Interpret a Chest x-ray/EKG/blood smear, etc." 12 My answer is: How to perform Advanced Cardiac Life Support or "ACLS." If you don't know ACLS, basically what to do in a life-threatening cardiac emergency, and how to do it, the patient can die within minutes. All other skills mentioned are obviously important, and in the career of most physicians will no doubt be much more useful than knowing ACLS. ACLS, taught in an intensive one or two day course, is now a requirement of virtually all hospital residents (it is also required of all ICU and CCU nurses). ACLS certification is good for two years, at which time the course is taken again. While the various cardiac treatment algorithms change somewhat over time, the basics do not. You need to know how to quickly insert a peripheral intravenous line and ventilate an apneic patient with a bag-valve mask device (AMBU bag). You need to know how to intubate, should that become necessary. (In many hospitals an always-available, in-house anesthesiologist intubates chest team patients. If your hospital is set up this way, fine.) You need to know where the defibrillator is kept, how to use it, what drugs to use for which arrhythmias and, not least important, when to stop. You need to feel comfortable when a chest team is called. You need to know enough so that if the patient doesn't survive, it is not because you didn't know something, but because there was nothing else to do. Cardiac Arrest -- VF & Pulseless VT* ABCs Initiate basic CPR Attach defibrillator Defibrillate at 200 Joules Defibrillate at 300 Joules Defibrillate at 360 Joules Continue CPR Intubate IV Access Epinephrine 1 mg IV push may repeat 3-5 min; may use higher doses Defibrillate 360 J after every dose Lidocaine 1.5 mg/kg IV push may repeat 3-5 min, up to 3 mg/kg Defibrillate 360 J after every dose Bretylium 5 mg/kg IV push may repeat 5 min at 10 mg/kg Defibrillate 360 J after every dose Continue: Drug-Shock-Drug-Shock, etc. ________ Cardiac Arrest -- Pulseless Electrical Activity ABCs Initiate Basic CPR Intubate IV Access Consider Possible Causes while checking for blood flow with Doppler Ultrasound HYPOVOLEMIA HYPOXIA CARDIAC TAMPONADE TENSION PNEUMOTHORAX HYPOTHERMIA PULMONARY EMBOLISM DRUG OVERDOSE HYPERKALEMIA ACIDOSIS MYOCARDIAL INFARCTION Epinephrine 1 mg IV push Atropine 1 mg IV push 13 Cardiac Arrest -- Asystole ABCs Initiate CPR Intubate IV access Confirm asystole in more than one monitor lead Consider possible causes: HYPOXIA HYPERKALEMIA HYPOKALEMIA ACIDOSIS DRUG OVERDOSE HYPOTHERMIA Consider transcutaneous pacing (available on some defibrillator models) Epinephrine 1 mg IV push Atropine 1 mg IV push Anti-Arrhythmic Drugs: Beta-Blockers: Calcium Antagonists: 14 15 16 17 Cardiac Dysrhythmias _______________________ Sinus Bradycardia Atropine Isoprenaline Pacemaker Sinus Tachycardia Rectify cause Beta Blocker (in the presence of Coronary Heart Disease (CHD)) Digitalis (Heart failure) Supraventricular Extrasystole Digitalis (in the presence of CHD with hemodynamic disturbances) Beta-Blocker (Attention: Heart Failure) Quinidine Atrial Flutter, Atrial Fibrillation Verapamil (Isoptin) 2.5mg iv as a Bolus, max. 7.5mg for awake patients (see below) Beta-Blocker (Attention: Do not combine with Verapamil) Propafenone Cardioversion / Defibrillation in the presence of hemodynamic disturbances Chronic: Digoxin, Quinidine 18 Code Drugs ACLS 19 Anti-Arrhythmics 20 Vasodilator Drugs Dopamine Infusion 21 Atrioventricular (AV) Heart Block during Anesthesia Reduce frequency: Adrenaline 5mcg IV repeat Bolus Increase frequency: Phenylephrine 50-100mcg IV if hypotensive Esmolol 100 - 200 mg iv if normotensive Supraventricular (SV) Tachycardia Propranolol: 1 - 10 mg i.v., in 0.5 - 1 mg increments Verapamil: 2.5 mg iv as a Bolus, max. 7.5 mg for awake patients. Attention: Volatile agents can cause Myocardial depression Propafenone Cardioversion / Defibrillation SV-Tachycardia with Preexcitation-Syndrome (WPW, LGL) Valsalva Maneuver, Aortic pressure / Carotid pressure Procainamide: 1.5mg/kg IV (in the presence of VHF and WPW: Cardioversion) Propafenone: 1mg/kg iv Verapamil (see above) Propranolol: 1-10mg i.v., in 0.5 - 1mg increments Attention: No Digitalis, Do note combine Beta-Blockers and Verapamil! Bradycardia Dysrhythmia and AV-Block Atropine: 0.5-1mg i.v. Isoprenaline: Start with 0.5 - 5mcg/min i.v. Pacemaker Bradycardia and Hypotension in the presence of Beta-Blockade Atropine: 0.5-1mg IV Isoprenaline: Start with 0.5 - 5mcg/min IV Pacemaker Calcium (as Inotrope) Aminophylline: 4 - 6mg/kg i.v. Glucagon: (5 - 10mg) Ventricular Dysrhythmia Hypoxemia ?, Hypercapnia ?, Myocardial Ischaemia ?, Central Catheter ?, Hypokalemia ?, Digitalis Intoxication ? Lidocaine Bolus: (1 mg/kg) i.v., Infusion 1 вЂ“ 4 mg/min, Procaine Propafenone: 35 mg i.v. or Propranolol: 0.5 mg i.v. repeated Potassium (Aim: > 4mmol/l) Magnesium Prolonged QT-Interval Attention: No Succinylcholine - it lengthens QT! Possibly aforementioned Beta block, possibly aforementioned left Stellate (ganglion) block Thiopental for induction Avoid: Lidocaine, Procainamide, Quinidine Ventricular Extrasystoles caused by Digitalis Intoxication 22 Lidocaine 1mg/kg iv Beta-blocker Magnesium Alternative : Phenytoin (Epanutin) 3.5 - 5mg/kg IV (max. 50mg/min) Ventricular Fibrillation See: Resuscitation (REA) Figure DIGITALIZATION Quick saturation: 0.25 - 0.5 (-1.0) mg slowly iv, then in 4 - 6 hourly intervals 0.25 - 0.5 mg iv Medium saturation: 1.0 to 1.5 mg po, then every 6 hours 0.25 mg po until compensation Slow saturation: 0.5 - 1.5 mg po daily, divided into a number of single doses Maintenance: 0.125 - 0.75 mg po/ day Therapeutic plasma concentration: 0.5 - 2.0 ng/ml Reduce dosage in the presence of : Kidney insufficiency, liver insufficiency, pulmonary heart disease, CHD, Hypothyroidism, Medicines (Erythromycin, Tetracycline, Quinidine, Verapamil, Spironolactone, Amiodarone), Acidosis, Hypoxia. Rule: Reduce digoxin dose by same % as reduction in clearance! Contra-indications: AV-Block 2. В° Or 3. В°, Sinus Bradycardia, Sinus-Arrest, Hypokalemia, WPW-Syndrome DIGITALIS INTOXICATION Indications: AV - Blocks, Ventricular Extrasystoles (VES), Sinus Tachycardia (ST) decreasing Plasma level: toxic > 3 ng/ml Laboratory: Potassium, Magnesium, Calcium, Creatinine-Clearance, ABGA Therapy: Remedy Hypokalemia / Hypoxia Lidocaine Atropine Phenytoin (Epanutin) 3.5 - 5 mg/kg iv (max. 50 mg / min) Digitalis anti-bodies (FAB-Fragments) Digitalis antidote BM (Attention: Extremely expensive); use your knowledge of approximate glycoside levels in the body to decide dose: 80 mg Digitalis (Digibind) antibodies bind 1 mg Digoxin. If glycoside levels unknown, administer ca. 6 injection bottles (Demand 24-hour duty from clinical pharmacology !) Beta-blocker LOWN Classification I II III IVa IVb V < 30 PVC/h > 30 Multifocal PVCs PVCs in runs Ventricular tachycardia R-on-T phenomenon SWAN GANZ Catheter Possible Indications: Unstable angina pectoris 23 Left trunk stenosis (> 90%) or equivalent (prox. RIVA + prox. Circumflex.) Acute myocardial infarction Complications from a MI (VSD, Mitral insuff.) Poor LV Function (EF < 30%) Two-valve surgery Replacement of the mitral valve Apparent cardiac insufficiency Severe pulmonary arterial hypertension (at rest) Repeat heart operation Major vascular surgery '7-3' - Rule for fluid monitoring Initial PCWP Fluid < 10 mmHg 200 ml in 10 minutes 10-15 mmHg 100 ml in 10 minutes > 15 mmHg 50 ml in 10 minutes Reaction Therapy PCWP increases > 7 mmHg Stop PCWP increases 3 - 7 mmHg Wait 10 minutes Always > 3 mmHg Stop PCWP increases < 3 mmHg more fluid MEDICAL HISTORY-TAKING IN THE MODERN ERA The "art" of history taking means getting the story in as complete a fashion as possible, so that you learn what is worth knowing. What is worth knowing includes: 1) the sequence of events that culminated in placing the patient before you; 2) an understanding of the patient's complaint, and 3) an appreciation of the patient as a human being. It does no good to learn every detail of the HPI if you are clueless about the patient's anxieties, fears, and perceptions. Similarly, you may be the most empathic, perceptive doctor around, but if you don't know who treated the patient last week and for what, or don't know the medications your patient is taking and why, you won't be very effective. SUMMARY: The history should be logical, complete, and answer all questions the reasonable reviewer might ask. To learn what is bothering the patient, you must care about, and listen to, the patient. Unfortunately, the house officer's response in many situations is all too often, "The patient is a poor historian," a response that suggests it is the patient's obligation to render a well-organized, coherent history! In fact, labeling the patient a poor historian often signifies one thing only: the physician is not trained to assemble a comprehensive history. Instead of blaming the patient for an inadequate history, emphasis should be on the vitally important "verifiable past medical history." Verifiable PMH covers events one can document, usually meaning specific past medical contacts (doctor, emergency room, pharmacy, laboratory, radiology department, etc.). Pity the poor house officer who, after spending an hour with a patient eliciting every nuance of her vague symptoms, has failed to learn of a recent complete evaluation at another hospital for the same complaints! (Oh? Then why didn't the patient say so? Simple: because the house officer didn't ask.) It is amazingly common that patients we see in the hospital, the ER, or the outpatient clinic, have verifiable, recent medical history pertinent to their current problem(s): lab tests; x-rays; office visits to other physicians; pharmacy prescriptions; hospital discharge summaries; workers' compensation records; operative reports. It is also amazingly common how often this verifiable history goes undetected by the treating house officer. You will be amazed how often your patients have been treated and evaluated for the same problems you are treating them for; or how often they are taking medications pertinent to their current problem which they "forgot" to tell you about. When you learn that important verifiable information exists, take advantage of those modern medical tools the phone and fax machine and work to get the information. Questions Regarding Verifiable Medical History What physicians have you seen in the past year? Where? What for? When was the last time you saw a doctor for any reason? And the time before that? Have you had any operation in the past 5 years? Have you spent the night in a hospital in the last 5 years? Have you visited an emergency room or urgent care center in the last 5 years? 24 Have you seen a podiatrist, chiropractor, or psychologist recently? When was the last time you had a prescription filled? Do you remember what it was for? What drugs do you take? What else do you take? What else do you take when these drugs don't work? Where do you get your medicine? Where else do you get your medicine? The task may not be easy. Say you've learned that verifiable information does exist, and you've requested it be sent via fax. How long should you wait for it to arrive? Not long. You can minimize delays by remembering three rules. Rule 1: Always record the name and phone number of the person you speak with, the one who agrees to send you the information. Rule 2: Records mailed will never arrive in time to help an already-hospitalized patient. They must be faxed or, alternatively, important information relayed verbally over the phone. Rule 3: Since record-keeping departments are often under-staffed and chaotic, the best intentions may not result in the records being sent to you. The record personnel may forget the request, or their fax machine may be inoperable, or the old records may not be found. After a reasonable wait (a few hours at most) call back: "Hello, this is Dr. Jones. I spoke with you earlier about records on my patient, Mr. Smith. We still haven't received those records. Have they been sent? Oh? Well, we need to make some important decisions; could you please fax them now?" Summary: Don't blame the patient for an inadequate medical history. Always assume verifiable past medical history exists and work hard to find out what and where it is. If you need prior records, find out where they are and set out determinedly to obtain them. Be polite but aggressive. Summary: No one pays doctors for time-consuming, high-quality history taking. Nonetheless, it stands to reason that the more thorough your history, the better will be your care of the patient. HISTORY, PHYSICAL, & NOTES Introductory Sentence This sentence should include the number of hospital admissions or clinic visits followed by the patient's age, race, parity, sex, occupation, and the patient's chief complaint or complaints (C.C.) in his own words. Source Source of history and assessment of reliability. Present Illness The present illness should be told in chronological sequence with reference to calendar date or time prior to admission, outlining the course of the illness from its beginning. Expound on each symptom thoroughly and its course. Previous treatment and hospitalizations should be noted; identify all significant medications received. Items of past medical history, family history, occupational history or social history that might have a bearing on the present illness should be included. Any symptoms suggested by the clinical picture, which are not present, should be noted and denied, i.e. "pertinent negatives". Past Medical History PMH General Health: Patient's general health throughout life. Childhood Health: General health and development. Note important deviations. Also, specifically mention acute febrile illnesses of childhood. Medical Illnesses: List and/or describe all illnesses requiring hospitalizations or a physician's care. Give dates. Operations and Injuries: Describe briefly and date each operation. Identify the hospital and surgeon, if known. Give dates of severe lacerations, head trauma, sprains, broken bones, or gunshot wounds. Describe sequelae. Medications: List all prescription and OTC medications including dosages. Allergies and Immunizations: Record all known allergies, specifically allergies to drugs. Remark on the state of immunization of the patient. Family History 25 Ask about diseases in parents, siblings, and children including present age, age at death, and the cause of death where applicable. Specific diseases to be asked about are: cancer, diabetes, gout, Tb, bleeding disorders, arthritis, anemia, hypertension, migraine headaches, allergies, mental or nervous disorders, or diseases of the cardiovascular system. Personal and Social History Inquire about: alcohol use (quantity and type), smoking (how much, how long), unusual drug habits, occupation, economic status, leisure activities, home, family and marital history. Review of Systems Skin: moisture, temperature, color, texture, changes in hair or nails, itching, rashes, lesions Head: headache, head injury Eyes: vision, glasses, pain, photophobia, proptosis, diplopia, scotomata, lacrimation, inflammation, infection, discharge Ears: hearing acuity, pain, tinnitus, vertigo, infection, discharge Nose: head colds, discharge, epistaxis, obstruction, sinus pain, anosmia Mouth & Throat: lesions in mouth, tongue or lips, pain in mouth or tongue, condition of teeth and gums, sore throats, postnasal discharge, speech difficulty, hoarseness Neck: stiffness, pain, limitations of motion, goiter, swelling Breasts (both sexes): pain, swelling, discharge, masses Respiratory: cough sputum (character, amount), hemoptysis, chills, fever, night sweats, dyspnea, wheezing, asthma, pain, pleurisy, bronchitis, and pneumonia CVS: cyanosis, exertional dyspnea, paroxysmal nocturnal dyspnea, edema, palpitations, irregular rhythm, precordial pain (character, radiation, duration, location; relation to exercise, posture, eating, effect of medication), known hypertension, heart disease, or lipid disorder, claudication, varicose veins, phlebitis GI: appetite, food intolerance, dysphagia, belching, water-brash, heart-burn, sour stomach, nausea, vomiting, hematemesis, rectal pain, hemorrhoids, jaundice, hernia, "gas" (flatus, belching, borborygmus), change in bowel habits (regularity, frequency, laxative use), stools (color, consistency, size, shape, odor, bloody or tarry), epigastric distress (rel. to meals, relief by antacids, belching or food), abdominal pain (loc. & radiation; sharp, knife-like, colicky, dull, aching, gnawing; constant or intermittent; severity; relationship to eating, defecation, urination or menstruation; relieved by belching, vomiting, doubling up, defecation, urination, enema or drugs) GU: dysuria, urgency, frequency, nocturia, polyuria, incontinence, hesitancy, dribbling, size of stream, retention, oliguria, anuria, smoky urine, hematuria, pyuria, back or CVA pain, history of UTI, stones or gravel, gonorrhea and syphilis by name or symptoms OB-GYN: age of menarche, menses (freq., regularity, duration, amount, dysmenorrhea, recent changes in cycle, passage of clots, intermenstrual bleeding), menopause (spontaneous or surgical, date, complications, subsequent vaginal bleeding), vaginal discharge, genital lesions, infertility, past use of birth control pills, pregnancies (number, abortions, complications) Bones, Joints, and Muscles: pain, tenderness, swelling, stiffness limitations of movement, previous injuries and deformities Endocrine: general (weight change, easy fatigability, behavioral changes), diabetes (polyuria, polydipsia, infections), change in size of features, hands, feet, impotence, decrease in libido, change in body hair or distribution, thyroid disease (goiter, heat or cold intolerance, sweating, exophthalmos, tremor, skin and hair changes) Neurological: syncope, convulsions, unconsciousness, dizziness, vertigo, ataxia, tremor, weakness, paralysis, incoordination, pain, numbness, paresthesias, difficulty with speech or swallowing, difficulty with bladder or bowel control, localized or generalized symptoms Psychiatric: rapid changes in mood, memory loss, phobias, hallucinations, antisocial behavior, sleep disturbances, previous emotional illness and treatment Physical Examination General Appearance: A brief sentence to characterize the overall appearance of the patient including body habitus, muscular development, nutrition, and whether the patient appears to be of stated age, acutely ill, in acute distress, pain, dyspneic, coughing, etc. Vital Signs: ht, wt, (percentiles and FOC in pediatrics), temp, blood pressure (which arm and whether supine, sitting, or standing), pulse, and respiration. Skin: hands, nails, hair; color, pigmentation, texture, moisture, temperature, and lesions. Lymph Nodes: posterior auricular, submaxillary, cervical, epitrochlear, axillary, and inguinal. Head: symmetry, deformities, skull size, scars, tenderness, tumors, or lesions. Eyes: visual acuity and fields, exophthalmos, EOM, nystagmus, strabismus, inflammation, discharge, conjunctivae, sclera, corneal scars, opacity, ulcerations, arcus. Iris (iridectomy or lesions). Pupil size, regularity, equality, and reaction to light and accommodation (PERRLA). Lens (cataract, or dislocation). Fundi: disc (color, margins, cupping, and papilledema); vessels (size, tortuosity, AV nicking); hemorrhages, exudates, or lesions. Ears: hearing acuity, symmetry, tenderness, discharge, perforation, tophi; Weber, and Rinne test results. Nose: deformity, septal deviation or perforation, obstruction, mucosa (discharge, bleeding, polyps). Mouth and Throat: lips and mucous membranes (colors, lesions), tongue (size, color, papillae, lesions). Teeth and gums. Soft Palate. Uvula. Tonsils and pharynx (inflammation, exudate, and tonsillar size). Neck: symmetry, scars, ROM, stiffness, tenderness; thyroid (size, symmetry, nodules, and tenderness); trachea midline; JVD, carotid pulses; masses. 26 Spine: curvature, symmetry, mobility, tenderness. Chest: shape, symmetry, respiratory excursions, masses, tenderness, fremitus, percussion, rales, rhonchi, breath sounds, egophony, wheezes, friction rubs. Heart: heart sounds, rhythm, precordial heave or thrill, PMI location and character, pulsations, enlargement, murmurs (intensity, timing, location, and radiation), rubs and gallops. Breast: shape, retractions, discharge, masses, tenderness, scars. Abdomen: contour, scars, striae, venous pattern, abnormal movements; auscultation for bowel sounds (frequency and character) and bruits; percussion for liver and splenic dullness, ascites (shifting dullness); palpation for liver, spleen, kidneys, bladder, colon, masses, aortic pulsations; CVA tenderness, abdominal tenderness (direct and rebound), hernias. Genitalia: Male--size and development of penis and testes, hydrocele, varicocele, masses, discharge, lesions. Female-External genitalia, Bartholin's glands, urethral orifice, clitoris, cystocele, rectocele, prolapse, vaginal or cervical discharge, lesions, bleeding, cervix, uterus, adnexa, or masses (note size, location, mobility, and tenderness), Pap smear. Rectal: hemorrhoids, fissures, ulcerations, bleeding, sphincter tone, masses, tenderness, prostate, and stool for occult blood test. Extremities: atrophy, tremor, clubbing, edema, redness, tenderness, limitation of joint motion, deformities. Neurological: mental status, behavior, alertness, orientation, mood, memory (recent and remote), speech; gait, Romberg, cranial nerve function, muscle (coordination, strength, tremor, abnormal movements), sensation (light touch, pin prick, temperature, position, vibration, two point discrimination), reflexes (abdominalis, cremasteric, biceps, triceps, radials, Hoffman, patellar, Achilles, plantar), clonus. Stick figures are helpful for reflexes. Summary One or two sentences that contain only those points of the history and physical which contribute directly to the establishment of a diagnosis. Problem List Numbered in order of importance, include date of entry. Impression List of tentative diagnosis based on the history and physical exam to explain the problems noted under the problem list. This section should express your impressions diagnostically as to possible explanations for the problems found and most importantly why you feel these diagnoses should be considered. Likewise, reasons you feel certain disease processes are operative should also be discussed. Plan Record all planned diagnostic and therapeutic procedures and plan for education of the patient based on the problem list generated. MEDICAL HISTORY (alternative) A. Identification and Vital Statistics 1. Name, (residence), age; birth date, place of birth where relevant 2. Nationality, race, marital status, occupation where relevant 3. Informant- relationship to patient, name B. Chief Complaint(s) - problem/condition that motivated patient to seek care-duration C. Present Illness 1. Symptoms and pertinent negatives 2. Onset and duration; associations with specific events 3. Character and quality of condition 4. Current level of activity and degree of disability D. Past Medical History 1. General Health- lifetime summary, list of relevant risk factors 2. Infectious Diseases- dates, complications, therapies 3. Operations, Injuries- names, dates, operative diagnoses 4. Previous hospitalizations- dates and names of hospitals 5. Transfusion History E. Medications - names, doses, allergies F. Review of Systems 1. Integument a. Skin: color, pigmentation, temperature, moisture, lesions, pruritus, scaling, bleeding b. Hair: hair color, texture & distribution c. Nail: color, changes, brittleness, ridging, pitting, clubbing 2. Lymph Nodes - enlargement, pain, suppuration, draining sinuses, location 3. Connective Tissue a. Bones: fractures, dislocations, sprains, b. Joints: arthritis, pain, swelling, stiffness, migratory distribution, degree of disability c. Muscles: weakness, wasting, atrophy, pain, night cramps 4. Hematopoietic System a. Anemia (type, therapy, response) b. Bleeding (spontaneous, traumatic, familial, transfusions c. Lymphadenopathy, Infections 5. Endocrine 27 a. General : history of growth, body configuration and weight, head, and feet b. hair distribution, skin pigmentation, dryness of skin and hair c. Thyroid: goiter, exophthalmos, heat or cold intolerance, tremor d. Diabetes: polyphagia, polydipsia, polyuria, glycosuria e. Secondary sex characteristics, impotence, sterility, treatment 6. Allergic/Immunologic System a. Vaccinations and immunizations b. Vasomotor rhinitis, asthma, hay fever, c. Dermatitis, urticaria, angioneurotic edema, conjunctivitis, eczema d. Seasonal incidence of the foregoing, known sensitivity to pollen, food, drugs, e. Previous skin tests & results, desensitization, serum injections f. TB test results 7. Head- headaches, migraines, trauma, vertigo, syncope, convulsive seizures 8. Ears- deafness, tinnitus, vertigo, discharge, pain, mastoiditis, operations 9. Eyes- visual loss, color blindness, diplopia, hemianopsia, trauma, inflammation, glasses 10. Nose- coryza, rhinitis, sinusitis, discharge, obstruction, epistaxis, frequency of colds 11. Mouth- soreness, symptoms referable to teeth 12. Throat- hoarseness, sore throats, tonsillitis, voice changes 13. Neck- swelling, lymph node character, goiter, stiffness, range of motion 14. Breasts a. Development, lactation, gynecomastia b. Trauma, lumps, pain, nipple discharge and/or changes 15. Respiratory System a. Dyspnea: nocturnal, rest, exertional, orthopnea, pain, and cyanosis b. Wheezing, cough, sputum, night sweats, pleurisy, bronchitis, smoking c. Pneumonia, hemoptysis, other respiratory infections, tuberculosis (exposure) 16. Cardiovascular System a. Chest pain, shortness of breath, exertional, rest, smoking, hypertension b. Palpitation, tachycardia, irregular rhythms, cyanosis c. Exercise tolerance, edema, ascites, and claudication d. Cardiac Drugs, rheumatic fever, syphilis, diphtheria e. Cold extremities, phlebitis, postural or permanent skin color changes f. Cocaine abuse, other recreational drug abuse 17. Gastrointestinal System a. Appetite, changes in weight, dysphagia, flatulence, abdominal pain or colic b. Nausea, vomiting, diarrhea, constipation, frequency, consistency c. Hematemesis, jaundice (pain, fever, duration, color of urine) d. Stools - color, frequency, consistency, odor, gas, cathartics), hemorrhoids e. Change in bowel habits. 18. Genitourinary System a. Urine: color, polyuria, oliguria, nocturia, dysuria, hematuria, pyuria, urinary retention, frequency, incontinence, pain, passage of stones or gravel. b. Menstrual history - age at onset, frequency, regularity, duration, amount of flow, leukorrhea, dysmenorrhea, date of last period, date & character of menopause, postmenopausal bleeding. c. Pregnancy history -number, abortions, miscarriages, stillbirths, chronologic sequence, complications. d. Venereal history - chancre, buboes, papillomas, penile discharge, treatment 19. Nervous System a. Cranial Nerves - disturbance of smell or vision, orofacial paresthesias and chewing difficulty, facial weakness, disturbed hearing and/or equilibrium, difficulty with speech, swallowing and/or taste, limited neck motion. b. Motor system - paralyses, atrophy, involuntary movements / seizures, gait, coordination c. Sensory system - pain, lightning pain, girdle pain, paresthesia, hypesthesia, anesthesia d. Autonomic system - control of urination and defecation, sweating, erythema, cyanosis, pallor, reaction to heat and cold. 20. Psychiatric History a. Reactions to and influences of parents, siblings, spouse, children, friends and associates b. Sexual adjustments, successes and failures, illnesses, lability of mood, hallucinations c. Grandiose ideas, nervous breakdowns, sleep disturbances PHYSICALEXAMINATION A. General 28 1. Overall appearance, nutritional status, weight, height 2. Communication skills, behavior, awareness, orientation, cooperation with examination B. Vitals 1. Blood pressure, pulse, respiratory rate, temperature 2. Oxygen saturation where indicated C. Skin 1. Color, integrity, texture, temperature, hydration, diaphoresis, edema 2. Lesions 3. Hair, nails D. Head 1. Size, contour, scalp appearance, symmetry and spacing of facial features 2. Edema, puffiness, erythema, other lesions E. Eyes 1. Appearance of orbits, conjunctivae, sclerae, eyelids, eyebrows 2. Extraocular movements, 3. Corneal light reflex 4. Pupil shape, consensual response to light (and accommodation) 5. Visual fields (acuity optional) 6. Ophthalmoscopic findings a. Retina, optic disc, macula b. Retinal vessel size, caliber, arteriovenous crossings (optional cornea, lens findings) F. Ear 1. Configuration, position, and alignment of auricles 2. Otoscopic findings: canals and tympanic membrane 3. Hearing Assessment a. Weber Test: base of vibrating tuning fork on vertex midline of head вЂў normally hear sounds best in both ears вЂў if better in one ear, then sound is lateralized вЂў occlude this ear with finger and repeat the test вЂў sound lateralized to deaf ear in conductive loss, to better ear in sensorineural loss b. Rinne Test: base of vibrating tuning fork on mastoid вЂў time the interval until sound no longer heard вЂў then move fork to place vibrating tines with 1-2cm of auditory canal вЂў normally, hearing is ~2X longer with air than bone вЂў conductive loss: bone heard longer than air; sensorineural air is less than 2X bone G. Nose 1. External appearance, nasal patency, discharge, crusting, flaring 2. Internal Exam: appearance of turbinates, polyps, septal alignment 3. Presence of sinus swelling or tenderness, odor discrimination H. Throat/Mouth 1. Appearance of lips, tongue, buccal and oral mucosa 2. Condition of teeth, presence of dental appliances 3. Floor of mouth, pharynx, tonsils, hard and soft palates, uvula 4. Gag reflex, voice quality I. Neck 1. Mobility, suppleness (range of motion), strength, trachea position 2. Thyroid size, shape, tenderness, anomalies (eg. masses) 3. Lymphadenopathy, swollen salivary glands J. Chest 1. External Appearance a. Anteroposterior diameter b. Symmetry of movement with respiration, respiratory rate, use of accessory muscles 2. Auscultation a. Air movement b. Abnormal sounds - rales (crackles), rhonchi, wheezes, stridor, rubs K. Breasts 1. External Appearance: Symmetry, masses, scars, discharge, dimpling, erythema 2. Palpation: Tenderness, thickening, masses 3. Lymph node examination: esp axillary L. Cardiac 1. Surface location of apical impulse, rate, rhythm, amplitude 2. Contour and symmetry of apical impulse and pulse in extremities 3. Comparison between extremities 4. Findings on auscultation a. Characteristics of S1 and splitting of S2 b. Presence of murmurs: first listen for systolic murmurs, then diastolic (usually quieter) c. Gallops: suspect S4 in young persons, or hypertension, or hypertrophic cardiomyopathy d. Suspect S3 in systolic congestive heart failure, low ejection fraction 29 e. Clicks (synthetic valve), snaps (mitral valve prolapse) 5. Signs of Heart Failure a. Jugular venous distention b. Hepatojugular reflux c. Peripheral edema d. Presence of S3 gallop 6. Signs of Vascular Disease a. Presence of carotid, abdominal, renal, or femoral bruits b. Strength of distal pulses, temperature of extremities M. Abdomen 1. Shape, contour, visible aorta pulsations 2. Auscultation findings (Bowel Sounds) a. Normal b. Normal pitch, hyperactive: gaseous distension, partial obstruction c. High pitch: partial or complete mechanical obstruction d. Decreased or absent: ileus (functional obstruction), peritonitis, perforation 3. Palpation findings a. Each of four quadrants b. Pelvic area c. Costovertebral angle d. Spleen - not a sensitive test in low risk patients 4. Percussion findings a. Liver - total span b. Spleen N. Rectum / Anus 1. External Structures a. Hemorrhoids, fissures, skin tags b. Sphincter control: "Anal Wink" test 2. Rectal Digital Examination a. Rectal wall contour, tenderness, prostate size, contour and consistency b. Color and consistency of stool, occult blood O. Genitalia 1. Female a. Appearance, pubic hair, external genitalia b. Palpation findings c. Vaginal speculum exam: appearance, lesions, discharge (Pap smear) d. Bimanual findings: size, tenderness of uterus, adnexa and ovaries 2. Male a. Appearance, circumcision status, location and size of urethral opening b. Discharge, lesions, pubic hair, palpation findings c. Scrotum: hernia, scrotal swelling, pain P. Extremities 1. Temperature, color, hair distribution, skin texture and nails of lower extremities, edema, 2. Swelling, venous distention, 3. Evaluation of Thrombosis: tenderness, erythema, cord, Homans' sign 4. Pulses: a. Radial pulse, (brachial pulse) b. Femoral, Dorsalis pedis and posterior tibial pulses, (Popliteal Pulse) Q. Neurologic 1. Cranial Nerves (findings for each or specify those tested) 2. Cerebellar and motor function (gait, balance, coordination) 3. Sensory function and symmetry 4. Deep tendon reflexes (symmetry and grade) 5. Mental status (thought processes, cognitive function, speech and language) R. Musculoskeletal 1. Alignment of extremities and spine, symmetry of body parts 2. Muscle strength 3. Joints a. Joint appearance, deformities b. Range of motion passive and active, presence of pain, tenderness, crepitus S. Lymphatic 1. Size, shape, tenderness, discreetness, mobility 2. Presence in neck, epitrochlear, axillary, or inguinal areas 30 CARDIAC PHYSICAL EXAM SIGNS PULSES: Paradoxes: fall in BP >10 w/inspiration -seen in Tamponade & Obstructive Lung Dz. Pulsus Parvus: weak upstroke due to decreased stroke volume(hypovolemia, LV-failure, AS, MS Pulsus Tardus: delayed upstroke (AS) APICAL IMPULSES: -Lat & Downward: LV dilatation -Prominent Presystolic Impulse: HTN, AS, Hypertrophic Cardiomyopathy -Double Systolic Apical Impulse: Hypertrophic cardiomyopathy HEART SOUNDS: S1: shutting of mitral valve Very Loud: MS Very Soft: CHF, MR, COPD S2: Closing of the Aortic Valve Wide Split: MR, Pulm Stenosis Fixed Split: ASD Narrow Split: Pulm HTN Paradoxical Split: narrow sw/inp: AS Loud A2: systemic HTN Soft A2: AS Loud P2: Pulm Art Htn Soft P2: Pulm Stenosis S3: Rapid Ventricular Filling heard best w/bell @ apex nml in kids. In Adults indicated Volm Overload S4: Atrial Contraction w/reduced vent contraction heard best w/bell @ apex reflects noncompliant Ventricle heard in AS, HTN, ischemic & HTN cardiomyopathy Opening Snap: Mitral Valve Opening follows S2 heard @ LLSB (in MS) (apex in MS): MURMERS SEM: related to blood flow across semiLunar valves: "midsystolic" + Spaces between S1 & S2 PANSYSTOLIC: no space between S2: Occurring w/regurgitant flow across AV valves. EARLY DIASTOLIC: typically w/regurgitant flow Across incompetent semilunar valves AS: Loud Crescendo / Decrescendo (SEM) - heard best @ base & rad to neck - increase w/ squatting - decrease w/ Valsalva, standing - Late slow rising carotid upstroke w/ decreased intensity - strong apical impulse - narrow pulse pressure(in severe AS) MR: Holosystolic w/radiation to axilla - increase w/ squatting - decrease w/ Valsalva, standing - no correlation between intensity of murmur & severity of MR ** LOUD S1 AI: Low Pitched Early Diastolic murmur Immediately after S2 - early SEM - high pitched - widened pulse pressure(sig > SBP) - Bounding pulses - Water Hammer pulse @ wrist w/ rapid rise & sudden collapse - Capillary pulsation @ nail bed base ** absent or diminished S1 PI: same as AI MS: Mid-to-Late Diastolic: low pitched -increase w/ L lat position or cough -diastolic rumble & opening snap - accentuated S1 31 MINI-MENTAL STATUS EXAM EYE SIGNS IN NEURO EXAMINATION Frontal Eye Fields: in each lobe normally: Rt side moves eyes to Lt Lt side moves eyes to Rt Lesion: eyes deviate toward area of 32 lesion. Dolls Eyes: Oculocephalic Reflex (valid only if pt unconscious) Nmlly: eyes move opp of head mvt Lesion: front eye fields: can't move eyes away on head mvt on side of lesion brainstem: can't move bilat PUPILS: Asymmetrical: idiopathic or Trauma Pinpoint: Pontine lesion Oval (other one=pinpoint): midbrain --occulomotor N. damage Argyle-Robinson: No light Reflex w/ intact accommodation Optokinetic Reflex: move stripped tape to Lt - nml eyes w/nystagmus to right Calorics: Cold water: nystagmus away Warm water: nystagmus same side Cold in both ears: nystagmus up Warm in both ears: nystagmus down In COMA: cold H2O: slow deviation to side of stim- may fixate ICP: papiledema no venous pulsations check for increased blind spot MLF: (from ?MS vs DM) opposite eye stops @ midline on lateral gaze / converges normally Progress/SOAP Note (non-ICU) Hospital day #__ Postop day #__ Antibiotic day #__ Subjective: how the patient feels, new complaints, continuing complaints, dizziness, pain, bowel movement, flatus, nausea, vomiting, etc. Objective: Vital signs PE by system including any surgical wounds Labs Studies (CXR, MRI, EEG, etc.) Assessment: List each problem and its current status, eg #1 IDDM--still poorly control, patient doesn't understand disease #2 HTN--well controlled on current meds Plan: What are you going to do? eg: #1--increase insulin to 30 units NPH q am, will contact diabetic teaching for education #2--continue current meds and doses Progress Note (ICU) System oriented. Objective, assessment and plan done for each system in turn. Vitals (can include weight, growth esp. if pedi) Meds: list all medications pt is on Systems: Remember you have 11 systems in alphabetical order and you'll do great: A/B: airway, breathing, vent settings, apneic episodes, ABG's, pO2 by pulse ox, etc. CVS: heart, pulses CNS ("Da brain"): F/E/N: fluids, electrolytes, nutrition (include I/OвЂ™s, TPN and residuals, Chem. 7 (lytes)) GI: abdominal exam, pertinent studies, BM's, flatus, guaiac Heme: jaundice, CBC with differential, PT/PTT, etc. ID: infectious disease (include antibiotics, peak and trough levels, fever status, etc.) 33 Joints/Bones/Muscles: Kidney: Lines: List each and number of days it has been in place, whether local erythema, etc. Skin: rashes, decubitus ulcers Grade I = superficial Grade II = subcutaneous Grade III = muscle exposed Grade IV = bone exposed Operative Note Date of procedure: Procedure performed: Pre-op diagnosis: Post-op diagnosis: Surgeon: Assistant(s): Type of anesthesia: Anesthesiologist: Pump Time(if applicable): Clamp Time(if applicable): Findings: Specimen(s): Tubes/drains: (NG, ETT, Foley, wound drains) EBL: estimated blood loss, ask anesthesiologist Fluids in: type and amount Fluids out: eg. urine output, NG drainage Complications: (if not "none", a resident/attending should be writing this note) Pt's condition/disposition (eg. pt transferred to RR awake, extubated and stable) Procedure Note Procedure: type, date, time, indications, who performed Consent form: explained, signed, and on chart Description: Pt draped and prepped in a sterile manner. Local anesthesia achieved with ... Findings: Describe fluid withdrawn, specimens sent to lab or pathology, how pt tolerated. Complications: (if there are complications, best to have resident or attending write the procedure note) Discharge Summary Dictated by ____, medical student, for ____, MD/DO on ____(date) Patient name, medical record number Admit date, admit diagnosis Discharge date, discharge diagnosis Date and type of surgery, procedure(s) this admission Brief summary of pt's history & physical Summary of hospital course Pathology reports (if any) Disposition: discharge medications, follow-up instructions, discharged to home/nursing home/etc., discharge diet and activity Copies to: Repeat dictated by ____ for ____ on ____(date) Pt name and medical record number Labor and Delivery H&P CC: age, race, female, gravida, parity Dates: LMP, CGA and EDD by dates, with ultrasound on date, and CGA by scan Current labor: presents with contractions (regularity, interval, duration, radiation to back, associated fever, vaginal bleeding, mucus show, SROM, meconium Prenatal history: 34 prenatal care: where, since date, # of visits, EGA at first visit prenatal screening labs (on POPRAS) should include following and dates: PAP smear; CBC; UA; ABO; Rh; antibody screen; GTT glucose screen, PRP; rubella titer; HSsAg titer; urine cx; chlamydia cx. Medications: prenatal vitamins (PNV), Fe, other prescription meds Complications: substance abuse (alcohol, tobacco, IVDA); UTI's HTN; DM; gestational DM; PIH; large babies; h/o twins; h/o congenital anomalies Past OB history: for each pregnancy (not each child) note date of birth, location, sAb/tAb/c-section/NSVD/forceps; at gestational age; anesthesia used; fetal sex; weight; complications Past GYN history: age at menarche, interval, duration, flow, regularity use of contraceptives; h/o STD's treatment Past Med hx: highlight DM, HTN, asthma, renal disease, hepatitis Past Surg hx: procedure, age, location, surgeon, complications; any trauma Social hx: tobacco, alcohol; IVDA, animal exposure (Toxo) Family hx: medical hx; birth complications PE: vital signs, head to toe, and including Extremities: reflexes, edema are important Fundal height, Fetal heart tones (type of monitor, BTBV, rate, reactivity, decels), Pelvic exam: dilation/efface/present/station/membranes eg. dilation = FT to 10 cm efface = 0 to 100% present = vertex, breech (footling or frank), LOA, ROA, etc. station = +3 to -3 membranes = intact, SROM/AROM, time of rupture, +meconium A/P: 1) Term IUP in active labor 2) Routine labor room care and admitting lab work 3) Expectant management Glucose Screening in OB--glucose screening between 24 and 28 weeks gest. Fasting 100 mg/dl 1 hour after 50-gm glucose load 135 2 hour after 100-gm glucose load 140 if a fasting, or 1 hour, or 2 hour screening Serum Glucose level is above, order a 2 hour or 3 hour Glucose Tolerance Test Delivery Note (example) Diagnosis: Term IUP s/p NSVD over a 2o MLE with extension to 3o Anesthesia: epidural/local with 3-5 cc anesthetic agent Physician: MS/Resident Episiotomy/Lacerations: 2o midline episiotomy was cut with extension to 3o. Repaired with ___(suture types/sizes) in ___ layers. EBL: Estimated blood loss Findings: Term male/female infant, APGAR's 81/95, weight 7lb 5oz born at 08:12 with nuchal cord x 1, easily moved. Placenta delivered at 08:21, Schultze (or Duncan) and intact with 3 vessel cord noted. Cord blood and placental cultures sent to lab. Complications: none Disposition: Mother to recovery room in good condition; baby to TCN (or NICU) in ___ condition. INCOMPLETE ABORTION ADMIT ORDERS 1.Admit to... 2.NPO 3.Bedrest 4.IV D5RL @ 8hour rate with 2 amps Pitocin 5.Vitals Q2hours or routine 6.Watch for excessive bleeding 7.CBC, Astra 8, T & S 2u PRBC 8.Tetnus toxoid .5cc IM 9.OCOR: Bicitra 30cc PO 10.Rhogam if indicated PREGNANCY AND DRUGS TO BE AVOIDEDCoumarin compounds, colchicine, doxycycline, ergotamine, erythromycin estolate, ethacrynic acid, griseofulvin, lindane, lisinopril, mebendazole, metolazone, metronidazole, misoprostol, norfloxacin, phenylbutazone, piroxicam, tetracycline, tolazamide, tolbutamide, valproic acid. APGAR Score APGARS 35 _____________________________________________________________ 0 1 2 Hear rate none <100 >100 Respiration none slow, irreg good cry Tone none floppy active Color blue acrocyanotic all pink Reflex irritability none grimace cry _____________________________________________________________ Neonatal/Birth H&P DOB___ DOL#___ Gestational age (WBD=wks by dates/WBE=wks by exam), birth wt, SGA/AGA/LGA male/female: BTA (born to a): mom's age, parity (GPA), labs (ABO/ HepB /RPR/Rub),> complications of pregnancy (maternal DM, PIH, PTL,chorio, smoking, ETOH/drug abuse, HIV, etc), maternal temp at delivery /fever during labor Delivered via: SVVD/C-sect with nuchal cord x 1, ROM (spontaneous or artificial) at 05:20 with meconium Perinatal course: Infant to NICU warmer, suctioned with ETT x 1 with NBTC (no meconium below the cords), suctioned by NGT x 1 with ___ cc of meconium-stained fluid removed, dried & stimulated, APGARS 81/95. Infant transferred to TCN for transitioning PE: Vitals, weight, length, FOC (%tiles) HEENT: fontanelles, red reflex Heart/Lungs/Abd/GU Extremities: hip click Neuro: reflexes of infancy Labs: Infant's ABO Primitive Reflexes of Infancy Reflex Age of Appearance Moro Grasp Rooting Placing Crossed extension Tonic neck Trunk incurvation Landau birth birth birth birth birth birth birth 6-8 months Age of Disappearance 4-6 months 4-6 months 4-6 months 4-6 months 4-6 months 4-6 months 9-6 months 15 mo-2 yrs Pediatric H&P Chief complaint Informant (parent, guardian, etc.) HPI PMH: Hosp/surgeries Allergies Medications Complete birth history for child and siblings Dietary history Immunizations Developmental milestones Travel Pets Fam Hx: Include Tb exposure Psych / SocHx: who cares for, day care ROS: PE: Vitals Growth: weight, height, FOC (and %tiles) HEENT: fontanelles, red reflex Neck: stiffness, adenopathy Lungs/Heart/Abd GU: Tanner staging Mental Status Neuro and developmental 36 Estimating Body Surface Area in Children Weight (lb) Body Surface Area (m2) 3 6 12 18 24 30 36 42 48 60 >60 0.1 0.2 0.3 0.4 0.5 0.6 0.7 0.8 0.9 1.0 add 0.1 for each additional 10 lb Abbreviated Psych History Organizational components: identifying data, referral source, chief complaint, history of present problem, medical history, drug and alcohol history, mental status exam, formulation, diagnostic impression, treatment plan. HPI: Onset of problems (time, setting) Duration and course (chronic vs. episodic) Psychological symptoms Symptoms of psychoses Cognitive Problems Mood Changes (irritability, depression, elation) Somatic symptoms Medical conditions Vegetative signs (anorexia, weight loss, insomnia, anergy, agitation or retardation, decreased sexual energy and interest, diurnal mood variation) Neurological symptoms Somatic complaints without organic basis Severity of problems-degree of impairment in functioning Possible precipitants. Past History: Family relations (father, mother, siblings, others at home, important family relationships, major losses and separations) Infancy (birth order, birth history, developmental milestones) Childhood (health-hospitalizations, preschool years, friendships) Adolescence (onset of puberty, early sexual experiences, peer relationships, experimentation with drugs, smoking, ETOH) Adulthood (education, military experience, employment, social life & friendships, romantic relationships, sexual history, marriage, children) Mental Status Exam: Appearance and behavior (dress and grooming, posture and gait, physical characteristics, facial expressions, eye contact, motor activity, specific mannerisms) Speech (rate, pitch, volume, clarity, abnormalities) Emotions (mood, affect-variability, intensity, lability, appropriateness) Thought Process (flow of ideas, quality of associations) Content (Distortions -delusions, ideas of reference, depersonalization) (PreoccupationвЂ™s - obsession, phobias, somatic concerns) (Suicidal or homicidal ideation) Perception (Illusions or hallucinations) Sensorium and Intellect Consciousness Orientation Time- "What is today's date?" Place- "What is the name of this place?" Person- "What is your full name?" Concentration: Serial 7's (or 3's)- ask patient to subtract 7's (or 3's) in succession, starting from 100. Memory Immediate- Digit span (Ask patient to repeat a series of random numbers, first forward, then backward) Recent- Ask patient to remember 3 unrelated objects then recall them after 15 minutes. Remote- Ask about names and dates in patients earlier life; ask patient to name the U.S. Presidents beginning with the current one and going backwards. Fund of Knowledge ("Who is the Vice-president of the U.S.?", "What are the colors of the American flag?", "How far is it from New York to Los Angeles?", What is a thermometer?") Abstraction Proverbs- Ask patient to interpret a Proverb (a stitch in time saves nine, the grass is always greener on the other side of the fence, a rolling stone gathers no moss, etc.) 37 Similarities-ask the patient what two things have in common (a table and chair, an orange and a baseball) Judgment - Ask what the patient would do in a social situation that requires judgment (smelling smoke in a crowded theater; finding a stamped, addressed, sealed letter on the street) Insight- Ask patient if he knows why he is in hospital or if he thinks that he currently has any problems. Attitude toward interviewer ABBREVIATED NEUROLOGICAL EXAM Mini Mental Status Exam Orientation What is the year, season, month, day, date? {1 point each} Where are we (state, county, city, hospital, floor)? {1 point each} Registration Name 3 objects taking one second to say each. Ask pt. To repeat all 3 immediately after you say them. Repeat until he/she learns all three. {1 point each} Attention & Calculation Serial 7's (stop after 5 correct), or spell "world" backwards. {1 point each up to 5} Recall Ask pt. to name the three objects named above. {1 point each} Language Name 2 objects that you show (i.e. pencil, pen, cup). {1 point each} Repeat "no ifs, ands, or buts". {1 point} Follow a three step command (i.e. take the piece of paper, fold it in half, and toss it on the floor). {1point each step} Write a sentence. {1 point} Copy a complex polygon. {1 point} Total 30 points <27 considered abnormal Serial exams will reveal progress, no change, or deterioration. Glasgow Coma Scale Eye opening: Spontaneous To voice To pain None 4 3 2 1 Verbal response: Oriented Confused Inappropriate words Incomprehensible sounds None 5 4 3 Motor response: Obeys commands Purposeful movement Withdrawn Flexion Extension None 2 1 6 5 4 3 2 1 Cranial Nerves, Motor, Cerebellar, Sensory, Gait Cranial Nerves I test sense of smell II visual acuity III, IV, VI extraocular movements (LR6,SO4,all others3) V facial pinprick/touch (optional corneal reflex) VII upper/lower facial muscles (optional taste test for Bell's Palsy) VIII hearing (check for nystagmus) IX, X midline palate elevation XI turn head in both directions XII tongue protrudes in midline Motor Tone: degree of stiffness Strength: selected distal and proximal muscle groups C5 = elbow flexors C6 = wrist extensors C7 = elbow extensors 38 C8 = finger flexors T1 = small finger abductors L2 = hip flexors L3 = knee extensors L4 = anterior foot dorsiflexors L5 = long toe extensor Reflexes biceps = C5 brachioradialis = C6 triceps = C7-8 knee = L2-4 ankle = S1 Pathological Reflexes: i.e. Babinski, clonus Cerebellar Finger-to-nose Heel-to-shin Rapid alternating movement Sensory compare side vs. side, upper vs. lower in ability to discern pinprick, light touch, vibration, and proprioception. Gait heel walking, toe walking Dermatomes, anterior view 39 Dermatomes, posterior view 40 41 EKG Leads Medical Orders Admission Orders (Remember "ABC VANDALISM") Admit to: (floor, service, MD) Diagnosis: (Because) Condition: (good, fair, poor, critical, guarded) Vital Signs: (q shift, q 4o, per routine, etc.) Allergies: Nursing: (I/OвЂ™s, daily weights, turn patient q 4o, etc.) Diet: (regular, clear or full liquid, 4 g Na, low or hi protein, ADA calories, etc.) Activity: (ad lib, bedrest with/without bathroom privileges, OOB tid, etc.) Labs: (also x-rays, EKG's, etc.) IV Fluids: (type, added KCl, rate) Studies: (CXR, MRI, CT, EKG, EEG, etc.) Meds: Call house officer if T> 101, BP>170/110 or <90/50, HR>120 or <50 Pre-op Orders Diagnosis: Procedure planned: Labs: (lytes, CBC, PT/PTT, UA, amylase if applicable) CXR EKG (if > 35 yo or h/o heart disease) Type and crossmatch Prep and shave surgical field NPO after midnight Void on call to OR Foley catheter (if indicated) Consent form signed and on chart History and Physical on chart 42 SIGN-OUT Note An effective sign-out system saves everyone time. Use a printed, pocket-sized sign-out card. Interns complete a card on each patient, updating the information as needed. The cards are delivered to the covering house officer and retrieved the following morning. The card is printed with the following information, and the intern caring fills in the blanks for the patient. If the covering intern interacts with the patient, it also is noted on the card. Team_________________ Intern_____________________ Res._____________________ Pt____________________ ID#_______________________ Ward____________________ Age__________________ Allergies__________________________________________ Code: DNR FC IV: Yes No CX: Yes No Problems: Main Meds: Potential Problems (if this, then ______________): To Do List: Discharge Orders Discharge: when and to where Diagnosis: Discharge Medications: (also need to fill out prescriptions) Diet: Condition: Activity: (eg. ad lib with 4 weeks pelvic rest for postpartum patients) Follow up: (eg. return to clinic in 1 week) Presenting Patients Now that you've got the history, what do you do with it? One of your more important tasks is to transmit the information you've gathered to other health care professionals. This is frequently accomplished through a combination of written documentation (the medical record) and verbal presentation (face to face or over the telephone). Developing these skills is essential for your medical career. The following outline summarizes the elements of a good case presentation. Documenting vs. Communicating Keep in mind that a case presentation is not simply reading your write-up. The medical record and your presentation are complimentary. The former serves as the primary documentation of the patient's clinical situation. The latter is a formalized way of communicating the patient's story to your colleagues. A good case presentation includes all the "important" details in a very terse, easy to assimilate package. Knowing which details are important and which can be left out is an acquired skill that comes with practice. Finally, the length of the presentation (and thus the level of detail) will vary depending on the purpose. In a busy clinic this might be only 1 or 2 minutes. A formal case presentation to a large group might last as long as ten minutes or more. Opening Statement Begin with an arresting sentence; close with a strong summary; in between speak simply, clearly, and always to the point; and above all be brief. - William J. Mayo The opening statement sets the stage for the presentation, so it is worth looking at in detail. You should include a bit of demographic information ("Jean Smith is a 40 year old woman who...") and a description of the patient's problem or chief complaint ("...came to clinic because of increasing dyspnea.") Note that, unlike the subjective section of the written record, it is okay to use medical terms and state exactly what you think. The entire presentation is your interpretation of what is going on. 43 Personal Information The opening statement may also contain additional information about who the person is as an individual (what they do for a living, their general level of health, where they live). Including this information helps the listener paint a more complete mental picture of the patient and prevents the discussion from becoming totally focused on the disease. Source and Validity Finally, you may want to comment about the source(s) and validity of the information you are reporting. If you don't otherwise state it, your listener will assume that you got the history from the patient and that you consider the information valid. If the patient is mentally incapacitated or otherwise unable to communicate well (e.g. speaks a language you don't understand), say so! Time Course Remember that you are telling a story. As with any story, the events of the patient's illness unfold in a specific sequence. This sequence is referred to as the clinical time course or chronology. Think of it as the scaffold on which all the other details of the history of present illness (HPI) will hang. Elements of the time course should include: When did the problem start? (Onset) How has it progressed? What is its current status? Influential Factors Once you've established the time course, you should fill in the details that are "pertinent" to the case. These include other elements of the HPI such as: Precipitating and exacerbating factors Relieving or moderating factors Prior treatment and response to it Note that what is not present is often more important as what is. These are called pertinent negatives and should always be included. For example, in a patient with shortness of breath, the absence of chest pain is significant because it makes certain diagnoses less likely. Analysis At this point your listeners will expect you to "put it together" for them. What pathologic processes might explain the symptoms you've presented? As part of your analysis you will be expected to develop and prioritize a list possible causes (differential diagnosis). You should bring in elements of the HPI; family, social, and past medical history; review of systems; and physical exam that support or oppose each diagnosis. At the end of this process you should have narrowed the field to one or two possibilities. These are your working diagnoses - what you think is actually going on. The remainder of your presentation should explain what you intend to treat or better characterize these diagnoses. Keep in mind that medicine has a bias towards simpler explanations. A single cause is always preferred over a combination of causes. This doesn't mean that a patient can't have more than one thing going on. If you believe there are two distinct symptom complexes present, say so at the beginning of your presentation and develop a differential diagnosis for each. Acute Pain Management Special considerations for Elderly Persons 44 Elderly people often suffer multiple chronic, painful illnesses and take multiple medications. They are at greater risk for drug-drug and drug-disease interactions. Pain assessment presents unique problems in the elderly, as these patients may exhibit physiologic, psychologic, and cultural changes associated with aging. Misunderstanding of the relationship between aging and pain is common in the management of elderly patients. Many health care providers and patients alike mistakenly consider pain to be a normal part of aging. Elderly patients sometimes believe that pain cannot be relieved and are stoic in reporting their pain. The frail and oldest-old (>85 years) are at particular risk for under treatment of pain. Aging need not alter pain thresholds or tolerance. The similarities of pain experience between elderly and younger patients are far more common than are the differences. Cognitive impairment, delirium, and dementia are serious barriers to assessing pain in the elderly. Sensory problems such as visual and hearing changes may also interfere with the use of some pain assessment scales. However, as with other patients, the clinician should be able to obtain an accurate self-report of pain from most patients. When verbal report is not possible, clinicians should observe for behavioral cues to pain such as restlessness or agitation. The absence of pain behaviors does not negate the presence of pain. NSAIDS can be used safely in elderly persons, but their use requires vigilance for side effects, especially gastric and renal toxicity. Opioids are safe and effective when used appropriately in elderly patients. Elderly people are more sensitive to analgesic effects of opiate drugs. They experience higher peak effect and longer duration of pain relief. 45 46 Evidence Based 47 48 CENTRAL LINES: PLACEMENT AND PROBLEMS Immediate Questions When Line's Not Working A. Does it change with respiration? A CVP should have a slowly undulating waveform that varies with the patient's respirations, if properly positioned in the chest. B. Does it flush and can it be aspirated? C. When was the last chest x-ray? The tip should be in the superior vena cava. Differential Diagnosis A. Catheter in incorrect position. B. Kinked catheter. C. Other mechanical problems. D. Infected catheter. Any question of sepsis originating in a central venous line requires expeditious evaluation. The best technique involves drawing cultures through the catheter, removing the line, and culturing the tip. Remove & replace @ an alternate site Plan: A. Unless the line is infected, it can be changed over a guide wire. All line manipulations should be performed using sterile technique with the patient in Trendelenburg (head-down) position to prevent air embolus. B. A line thought to be clotted can often be declotted safely with a syringe. The catheter can be gently aspirated or flushed with a 1 cc tuberculin syringe. Internal Jugular Insertion: 49 A. Materials for central line placement are available in a kit, which you can obtain on the hospital unit. B. IJ lines have less risk of pneumothorax and are preferred if hyperinflation or mechanical ventilation are present. Because direct pressure can be applied, the IJ line also is preferred if coagulopathy is present. For IJ lines use a 25 gauge needle and 1% lidocaine to raise a small skin wheal. Change to a 22-gauge needle to anesthetize the deeper layers, and then use gentle aspiration, with the same needle, to initially locate the internal jugular vein. Direct the needle through the skin wheal, directed toward the ipsilateral nipple and at a 30-degree angle to the frontal plane. If the vein is not entered, withdraw the needle slightly and redirect it 5 to 10 degrees more laterally. Subclavian Insertion: A. Materials for central line placement are available in a kit, which you can obtain on the hospital unit. B. Subclavian lines usually are more comfortable for the patient and easier to fix to the skin. However, it results in a pneumothorax in 1 to 2% of insertions. C. Most commonly for subclavian lines, the patient is placed in Trendelenburg position, with a roll between the scapulae. This presumably makes the clavicles flatten and vein more prominent and simplifies puncture. The artery is above and behind the vein, so slow entry will allow going into the vein before the artery. The needle is passed below the clavicle and aimed toward the sternal notch, with the bevel upward. Turn the bevel to 3:00 when the vein is entered. Other lines: Femoral lines are acceptable when there is no upper body alternative and when rapid access is needed during cardiopulmonary resuscitation. Complications: Pneumothorax, hemothorax, hydrothorax, arterial puncture with hematoma and catheter tip embolus. A. Obtain help from an experienced house officer to assist with line placement. B. Always obtain and review a CXR following line placement. C. Air can enter an open system when intrathoracic pressure decreases, (as during an inspiration). An air embolus obstructs the pulmonary artery and can produce acute right heart failure. If you suspect that air embolization has occurred, place the patient head down and turned left side down to keep air in the right atrium. Obtain a stat CXR to look for air in the atrium. D. If you suspect a pneumothorax, order a stat portable CXR in the upright position in expiration. Hypotension, tachypnea and pleuritic chest pain after central line insertion are suggestive of a pneumothorax. Order O2 by mask at 10 L/min. E. Tension pneumothorax is a medical emergency requiring urgent treatment. F. Massive unilateral pleural effusion can occur if the IV line is emptying into the pleural space. Stop the IV fluid, and thoracentesis will be required if the patient is markedly SOB. Hemothorax can occur when a vessel is perforated. DRAIN MANAGEMENT Immediate Questions: A. What operative procedure did the patient have and what surgical sites are being drained? B. What type of drain was placed intraoperatively? Surgical drains are of two basic types: passive or active. Passive drainage is accomplished by gravity or capillary action. Drainage is further facilitated by transient increases in intraabdominal pressure, as with coughing. Passive surgical drains include Penrose, Foley, Malecot, and Word catheters. Active drainage is accomplished by suction from a simple bulb device or a suction pump. These systems may be closed, like the Hemovac and Jackson-Pratt drains. C. What is the nature of the drainage fluid? Examine the fluid for color, odor and volume. Also examine the tube for clots or other obstructing material. Differential Diagnosis: 50 A. Increased drainage Increased bloody drainage can be due to vessel leakage and may be caused by catheter erosion into a vessel. Document rate of bleeding every 30-60 minutes. Increased serous drainage may be from increased lymph drainage, particularly with increased activity. Drainage of urine may represent fistulas anywhere along the urinary tract. B. Purulent drainage This indicates infection. C. Sudden cessation of drainage Tissue debris, especially in smaller catheters, is a principal source of catheter occlusion. Drains can be walled off from the general peritoneal cavity within about 6 hours. Intra-abdominal fluid can be collecting without drainage from the catheters. Therefore, regular examinations of the abdomen are necessary for early identification of intra-abdominal fluid collections. D. Drain exit wound infection Erythema, induration and pain at the drain exit site are indicators of infection in the subcutaneous tract. Misc. Drain Management Usually drain management does not require emergent or urgent action with the exception of mediastinal tubes on the cardiac surgery service. 1. Increased output. Almost always due to blood. Document rate of bleeding by accurately noting output every 30-60 minutes and following serial hematocrits. Measure coagulation parameters and correct as needed. 2. Decreased output. A sudden decrease in output may be due to a clot in the tube and lead to an episode of cardiac tamponade. FOLEY CATHETER PROBLEMS Immediate Questions: A. What has the urine output been? If the urine output has slowly tapered off, then the problem may be oliguria rather than a nonfunctioning Foley. B. Is the urine grossly bloody and are there clots in the tubing or bag? C. Is the patient complaining of any pain? Bladder distention often causes severe lower abdominal pain. Differential Diagnosis: A. Low urine output. If the catheter irrigates freely, evaluate for decreased urine output (see section on Oliguria below). B. Obstructed or improperly positioned Foley catheter 1. Kinking of catheter or tubing 2. Clots and tissue fragments (especially if after a TURP) 3. Sediment/stones Management: A. Verify function. A rule of thumb is that a catheter that will not irrigate is in the urethra and not in the bladder. Start by irrigating the catheter with aseptic technique using a catheter-tipped 60 mL syringe and sterile normal saline. Catheter irrigation or replacement in any patient who has undergone bladder surgery must be done with extreme care. B. Spasms. A patient with bladder spasms may complain of severe suprapubic pain, pain radiating to the perineum, or urine loss from around the catheter. Spasms are common after bladder surgery. Bladder spasms can be treated with oxybutynin (Ditropan), propantheline (Pro-Banthine) or belladonna and opium (B&O) suppositories. C. Faulty balloon. There are several techniques to deflate a balloon that will not empty. 1. Injecting 5-10 mL of mineral oil into the inflation port will cause the balloon of a latex catheter to rupture in 5-10 minutes. 2. Threading a 16 French central venous catheter into the inflation channel (after the valve is removed) may bypass the obstruction. 3. As a last resort, ultrasound-directed transvesical needle puncture of the balloon may be needed. 51 NASOGASTRIC TUBE MANAGEMENT Immediate Questions: A. How long has the NG tube been in place? A tube that has just been placed may have bloody drainage from the trauma of insertion or as a result of recent gastric surgery. B. What is the volume and description of the output? How much bloody drainage has there been? Is the patient having abdominal distress? Database: An abdominal radiograph is useful to identify the tube's location. Look for a large stomach bubble indicating poor gastric emptying. Check the position of the tube tip and verify that it is in the stomach. Plan: A. Decreased output: 1. Verify position. This is based on x-ray confirmation. Flushing the tube with 40-60 cc of air and listening over the stomach results in a typical crackle or pop; however, this may also be heard with the tube in the distal esophagus or duodenum. Based on x-ray findings, you may want to advance or retract the tube, as needed. 2. Verify function. Sump tubes should whistle continuously on low suction. Most tubes need to be flushed with saline (30 mL) every 3-4 hours to maintain patency. 3. If the tube's position and function are not problems, then decreased output can indicate return of bowel function. B. Increased output: 1. Poor gastric emptying (no obstruction). 2. Distal obstruction 3. Ileus C. Blood in the NG output (See GI Bleeding Below): 1. Determine whether the cause of bleeding is serious enough to require specific aggressive therapy. Is there hypotension or hemodynamic instability? For either and signs of significant bleeding, place a large-bore IV and begin fluid and blood replacement. Bleeding may be due to trauma, all the causes of upper GI bleeding, and a coagulopathy. Place in ICU! NG irrigation; H2 blockers or antacids. NEEDLE STICKS and OTHER EXPOSURES TO BLOOD and BODY FLUIDS All exposures (needle sticks, splashes, scrapes, etc.) should be reported as soon as possible. During working hours, report to Employee or Student Health, and after hours, report to the Emergency Department. A team of experts available will do evaluation and management for both the exposed and the exposure source. In several epidemiologic studies, 7% - 35% of house officers, depending on prevalence of HIV in the patient population, had a reported needle or mucous membrane exposure to HIV. However, closer study of these groups indicated that only one-third of house staffs' exposures were reported due to concern regarding confidentiality and lack of knowledge about reporting procedures. Blood and body fluid exposures are evaluated for infectious disease transmission and wound care. HIV, hepatitis B and hepatitis C checked by lab studies. Prophylactic treatments and boosters are offered appropriately. Risks of tetanus are evaluated and boosters given when needed. The exposure source will be evaluated for other blood borne pathogens as well. Detailed algorithms for evaluation and management of blood or body fluid exposure are available. Remember: * Always use universal precautions. Always be careful. * Immediately wash affected area with soap and water. * Always report blood or body fluid exposures as soon as possible. WOUND COMPLICATIONS Immediate Questions: 52 A. Is there a wound dehiscence, and if so, to what extent? Did any fluid leak from the wound? Always evaluate the wound yourself as soon as possible; see how much of the wound has opened and if there is an evisceration. An "open wound" is not a dehiscence unless the fascia opens. B. Are there findings of an infection? Plan: A. Initial management. Determine by wound examination if there is an evisceration, fascial disruption without evisceration, or a superficial wound separation. In all cases, it is safe to make the patient NPO and start antibiotics to cover skin organisms, until a final plan is formulated. B. Evisceration/fascial dehiscence. Cover the wound with saline soaked sterile gauze, then cover with a large sterile dressing. Notify the senior staff since evisceration requires operative repair. C. Fascial dehiscence with evisceration. If the overlying skin and subcutaneous tissues are intact but there is clearly a fascial defect, it may be treated by operative repair or observation. Without treatment, a ventral hernia will develop. D. Superficial wound separation. Healing by secondary intention is mandatory when there is an associated superficial wound infection, and is the safest management in any case. E. Wound infection. Culture and antibiotics selected based on type of surgery. See the Stanford/Parkland guide for antibiotic choice, which varies with surgery type for: 1. surgery not involving GI or female GU tract 2. surgery involving GI tract (including oropharynx) and female GU tract 3. extremity, +/- sn sepsis PROCEDURES Blood Tube Type CBC: purple top PT/PTT: blue top Chem. 7: small red top Chem. 20: large red top ABGs: heparinized syringe with air bled out and on ice TFT's: red top Ammonia: green top on ice Others: call lab but usually red top Body Fluid Routine Labs Lumbar Puncture Tube 1: Gram stain & cultures Tube 2: protein, glucose Tube 3: cell count with differential Tube 4: special studies Thoracentesis specific gravity, protein, LDH, pH, cell count with differential, glucose, Gram stain, cultures, AFB smear & cultures, fungal smear & culture Paracentesis cell count with differential, Gram stain & cultures, lactic acid, pH, protein, glucose, LDH, specific gravity, amylase, cytology Arthrocentesis Un-heparinized tube: viscosity, mucin clots 53 heparinized tube: glucose, Gram stain, culture, cytology, cell count & differential glass slide for polarized light examination Pleural/Peritoneal Effusions Exudate (IU/dl) Transudate (IU/dl) Fluid LDH >200 <200 Fluid protein >3 g <3 g Fluid/serum LDH ratio >0.6 <0.6 Fluid/serum protein ratio >0.5 <0.5 Specific gravity >1.016 <1.016 Gram Stain 1.Air dry specimen after smearing thinly on slide. 2.Heat fix by quickly passing the slide through a flame 2-3 times. 3.Cover the entire slide with Crystal Violet for 30 seconds. 4.Rinse with water.* 5.Cover slide with Iodine for 1 minute. 6.Rinse with water. 7.Hold slide at 45&degree; and decolorize with acetone/ethanol for 5 10 seconds or until no more blue runs off. 8.Rinse with water. 9.Cover slide with Safranine for 30 seconds. 10.Rinse with water and blot dry with bibulous paper. *NOTE: use distilled water for rinsing when available Urinalysis 1.Dipstick urine and record values. Pour sample of urine off into test tube for dipstick. Do not contaminate sterile specimen cup with dipstick. 2.Spin urine in centrifuge for 3-5 minutes. 3.Pour most of the supernatant off, leaving a few drops in the bottom of the test tube. 4.Put a few drops of the remaining mixture on each of 2 slides, put a cover slip on one (wet prep) and examine under the microscope while the other dries. 5.If there are more than 5 WBC's per high-powered field in spun urine, then it is considered infected. If you see WBC's then you will probably want to gram stain the slide you left to dry to see if you can see any bacteria. If the wet prep is clear, there is no reason to gram stain the other slide. 6.Other things to look for include: RBC's, yeast, Trich, sperm, epithelial cells, etc. If the specimen contains many epithelial cells it is considered a dirty catch and you had best start with another specimen from that patient. 54 Fluids & Electrolytes NORMAL PHYSIOLOGIC VALUES Hemodynamic Values Heart Rate..........................вЂ¦вЂ¦вЂ¦.60-100 beats/min. Pressures Systemic Arterial Peak Systolic/End-Diastolic.........100 - 140/60 - 90mmHg Mean (MAP).......................... 70 - 105 mmHg (2 * diastolic + systolic)/3 Left Ventricle Peak Systolic/End-Diastolic.........100 -140/3 - 12 mmHg Left Atrium (PCWP) Mean................................2 - 12 mmHg a wave..............................3 - 10 mmHg 55 v wave..............................3 - 15 mmHg Pulmonary Artery Peak Systolic/End-Diastolic.........15 - 30/4 - 14 mmHg Mean................................9 - 17 mmHg Right Ventricle Peak Systolic/End-Diastolic.........15 - 30/2 - 7 mmHg Right Atrium Central Venous Pressure (CVP).......less than 5 mmHg Mean................................2 - 6 mmHg a wave..............................2 - 8 mmHg v wave..............................2 - 7 mmHg Resistances Systemic Vascular Resistance (SVR)...700 - 1600 dyne-sec/cm-5 SVR = [(MAP-CVP)/CO] * 80 Pulmonary Vascular Resistance (PVR)..100 - 300 dyne-sec-cm-5 PVR = [(PAP-PCWP)/CO] * 80 Flow Cardiac Output (CO)...................3.5-5.5 liters/min CO = HR * SV Cardiac Index (CI)...................2.4 - 3.8 L/min/m2 CI = CO/BSA Ejection Fraction = (SV/End-Diastolic Volume) * 100 Arterial Blood Gases pH.....................................7.4 pCO2...................................40 mmHg pO2....................................90 mmHg SaO2...................................90+ % Mixed Venous Blood Gases pH.....................................7.36 pCO2...................................45 mmHg pO2....................................40 mmHg SvO2...................................0.75 Oxygen Content-Arterial Blood .....19 ml/100cc CaO2 = (1.34 * Hgb * (SaO2/100)) + (0.003 * PaO2) Oxygen Content-Venous Blood........14 ml/100cc CvO2 = (1.34 * *Hgb * (SvO2/100)) + (0.003 * PvO2) Oxygen Content-Capillary Blood.....22 ml/100cc (FiO2=1) CcO2 = (1.34 * *Hgb) + (0.003 * (713-PaCO2)FiO2) Alveolar Gas Equation PAO2 = PiO2 - PaCO2/R = (PB-PH2O)(FiO2) - (PaCO2/R) = (760-47)(0.21) - (40 * 1.25) = 100 at sea level, room air Simplified Alveolar Gas Equation PAO2 = (700 * FiO2) - (PaCO2 * 1.25) Alveolar-Arterial Gradient A - a = PAO2 - PaO2 56 Acid-Base Disorders See below for much more 57 Normal Lab Values 58 59 60 61 Acid-Base Metabolic Acidosis Acute Respiratory Acidosis Metabolic Alkalosis Respiratory Alkalosis Approach to interpreting Acid-Base Status Metabolic Acidosis A. Anion Gap Acidosis (Normal Anion Gap = Na - [Cl + HCO3] = 8 - 14) Paraldehyde Ketones (DKA, AKA, rarely starvation) Uremia (BUN usually >=40, gap 15-25) Salicylates (associated with respiratory alkalosis) Methanol (retinal edema, papillitis) Ethylene glycol (calcium oxalate crystals) Lactic acid B. Normal Gap Acidosis 1. Normokalemic Obstructive uropathy Hypoaldosteronism 2. Hypokalemic GI loss Acetazolamide Ileal loop RTAs (lithium, amphotericin, hyperparathyroidism., autoimmune, etc.) Acute Respiratory Acidosis Pulmonary CNS depression Chest wall weakness (Guillain-BarrГ©, drugs [e.g., succinylcholine]) Metabolic Alkalosis A. Chloride responsive (saline responsive) urine Cl <10 mEq/L Vomiting, NG suction Diuretics "Contraction" alkalosis B. Chloride unresponsive BartterвЂ™s Severe potassium depletion Mineralocorticoid excess Respiratory Alkalosis CNS (tumor, inflammation, infection, anxiety, cirrhosis) Hypoxia Airway irritation (tumor, fibrosis, pulmonary emboli) Drugs (ASA, progesterone, xanthines) Pregnancy Approach to Interpreting Acid-Base Status A. Measure electrolytes and ABGs B. Compare calculated and measured HCO3 to r/o lab error; H+ = 24 (PaCO2 / HCO3) C. Compute anion gap D. Compare PaCO2 and pH to see whether pH change is directly related PaCO2 change or other processes are ongoing 62 H+ 70 60 50 40 32 25 pH 7.16 7.22 7.3 7.4 7.5 7.6 Useful Mnemonic MUDPILES (for causes of increased anion gap) ELM PARK AMPLE SUDS Methanol Uremia Diabetic ketoacidosis Paraldehyde, Phenformin, Metformin, Propylene glycol Iron, INH Lactic acidosis Ethanol, Ethylene glycol Salicylate, Starvation BEDROCK LAB TESTS Arterial blood gases (pH, PaO2, PaCO2, SaO2) Chest x-ray (PA and lateral) Complete blood count (hematocrit, WBC, differential, platelet count) Electrocardiogram (12-lead) Serum electrolytes, BUN and blood glucose Spirometry Sputum analysis (Wright's stain, Gram's stain) Urinalysis Arterial Blood Gas Lecture Slides ABGs Pulse Oximetry 63 Accuracy of Pulse Oximetry 64 ABGвЂ™s in Pulmonary Embolism 65 Normal ABG Ranges 66 Oxyhemoglobin Desaturation Curve 67 Oxygen Transport System 68 Oxygen Dosing 69 Scoring for Acute Lung Injury and Acute Respiratory Distress Syndrome 70 Acute Lung Injury ALI Acute Respiratory Distress Syndrome ARDS 71 72 73 Anion Gap 74 Bicarbonate Gap Anion Gap Gap Delta Gap 75 Acid Base Algorithm 76 Anion Gap 77 Bicarbonate Gap Anion Gap Gap Delta Gap 78 79 80 Arterial Blood Gas Diagnostic Worksheet Normal Ranges Equations Aa O2 Diff <= 1.1 x (2.5 + .21 x Age) [H+] = 24 x (PaCO2/HCO3) OH Dissociation 20@30%; 30@60%; 60@90%; 90@100% AG <= (.5 xHCO3) +16 Not Organic Acidosis AG gap = AG вЂ“ 12 [24 вЂ“ AG gap = HCO3] SOsm - [ (2xNa) + (BUN/2.8) + (BS/18) ] <= +/- 10 mOsml Aa Diff = [ (760 вЂ“ 47) FiO2 вЂ“ (pCO2/0.8)] вЂ“ pO2 Bicarb Gap = Na вЂ“ Cl вЂ“ 39 (AG + vCO2 on lytes) = +/- 6 pH = 7.38-7.42 PaCO2 = 38-42 PaO2 on 21% O2 >= .9 x (104.2 - .27 x Age) Normoxia >=.8 x вЂњ Mild Hypoxia >= 55 вЂњ Moderate Hypoxia < 55 mm Hg Severe Hypoxia Compensation for Simple Acid-Base Disorders (Narins, RG, Medicine, 1980; 59, 161-187) Primary Disorder Metabolic Acidosis Initial Change HCO3 Decrease Compensatory PaCO2 Decrease Metabolic Alkalosis HCO3 Increase PaCO2 Increase Respiratory Acidosis PaCO2 Increase HCO3 Increase Respiratory Alkalosis PaCO2 Decrease HCO3 Decrease Age: Temp: Ht: BP: Ventilatory Mode: FiO2 = % Wt: AR: Primary Process? COHb= / Barometric Pressure: RR: Settings: - emia ? pH = PCO2 = PaO2 = SaO2 = SpO2 = H&H= Anion Gap = LFTвЂ™s = Glucose = Expected Range *PCO2= [1.5( HCO3)+8] +/-2 *PCO2 = Last 2 digits of pH deltaPCO2=1 to1.3x(deltaHCO3) PCO2 Variable Increase PCO2 = (.9 x HCO3) + 9 PCO2 .6 Incr per 1 Incr HCO3 Acute: delta[H+] = .8 x delta PCO2 pH = 7.40 вЂ“ [ .008 * ( pCO2-40) ] HCO3 Inc 1 for 10 Inc PCO2 Chronic: delta[H+] = .3 x delta PCO2 pH = 7.40 вЂ“ [ .003 * ( pCO2-40) ] HCO3 Inc 3.5 for 10 Inc PCO2 Acute: delta[H+] = .8 x delta PCO2 pH = 7.40 + [ .008 * ( 40 - pCO2)] HCO3 dec 2 for 10 dec PCO2 Chronic: delta[H+] = .17 x delta PCO2 pH = 7.40 вЂ“ [ .0017 * ( 40 - pCO2)] HCO3 dec 5 for 10 dec PCO2 Compensation Appropriate? MetHb= Na = CL= BUN= Toxic= K= CO2= Creat= Urine = Diagnoses: 81 Lactate= Ketones= ETOH = Acute or Chronic Calculations: HCO3 = AaDif = OHD = PaO2/FiO2= Hb= PCO2 Compensation = HCO3 Compensation = pH Compensation = Serum Osm calc = Acute Respiratory Failure Lecture Slides ARF 82 Systemic Inflammatory Response Syndrome SIRS 83 Multiorgan Dysfunction Syndrome MODS 84 85 ARDS 86 Hypoxia-Hypoxemia 87 Respiratory Muscles and Innervations 88 89 90 91 92 93 94 Mechanical Ventilation in Acute Respiratory Failure ARF 95 HYPERCALCEMIA Immediate Questions: A. Vital signs? Mental status? B. Underlying condition(s)? Differential Diagnosis: A. Among outpatients, malignancy and primary hyperparathyroidism are leading diagnoses. Malignancy predominates as an etiology for hypercalcemia among hospitalized individuals. B. Potential etiologies: 1. Malignancy: bone mets, ectopic PTH, osteoclast activating factor 2. Primary hyperparathyroidism 3. Myeloma 4. Vitamin D excess 5. Sarcoid / granulomatous disease 6. Milk alkali 96 7. Other: hyperthyroidism, thiazide diuretics, lithium, immobilization (especially children) Therapy: Patients usually are profoundly volume depleted and can require several liters of NS volume replacement. Volume replacement is the initial step in management. Lasix can be added to help increase a saline diuresis (>2500 ml urine/day) and calcium excretion but should only be used following volume replacement. Agent Dose Comments Saline + furosemide 40-80 mg IV each 2 hours monitor hourly urine output, (Diuretic only if adequately hydrated) output plus NS equal to urine monitor electrolytes frequently Mithramycin 25 mcg/kg IV every response takes 24 hours; can 2-3 days cause bone marrow suppression Pamidronate 60-80 mg IV over 6 to response in 3 to 4 days, which (mainstay of therapy) 24 hours lasts up to 7 to 14 days Prednisone 40-60 mg per day antagonizes actions vitamin D; decreases calcium absorption and increases calcium excretion; in most cases, effect lasts only for a few days HYPERCALCEMIA- (HC). HC is most commonly caused by cancer and primary hypoparathyroidism. In cancer patients the parathyroid hormone is low, and in primary hyperparathyroidism the parathyroid is high. Hypercalcemia in cancer patients and primary hyperparathyroidism is due to parathyroid-like hormone and parathyroid hormone, respectively, which stimulates osteoclast reabsorption of bone. Also, these two hormones stimulate renal tubular reabsorption of calcium, which further elevates the calcium. The hypercalcemia itself interferes with reabsorption of sodium and water and this leads to polyuria and dehydration. Moreover, many cancer patients are immobilized which further increases the calcium. SYMPTOMS OF HYPERCALCEMIA: HC can be divided traditionally into Gastrointestinal (anorexia, nausea, vomiting, constipation and pancreatitis), Renal (polyuria, polydipsia and nephrocalcinosis), CNS (drowsiness, coma, apathy) and Cardiovascular (short QT interval on EKG, digitalis sensitivity, and hypertension depending on degree of hydration). OTHER CAUSES OF HYPERCALCEMIA: Sarcoidosis, histoplasmosis, coccidioidomycosis, tuberculosis, leprosy, lithium, thiazide diuretics, estrogens and antiestrogens, multiple myeloma, Vitamin A and D toxicity, familial hypocalciuric hypercalcemia, milk alkali syndrome, immobilization, acute and chronic renal insufficiency, parenteral nutrition, pheochromocytoma, thyrotoxicosis, vasoactive intestinal polypeptide hormone- producing tumor and thyrotoxicosis. If the serum calcium after being corrected for albumin is 14 mg/dl, then immediate therapy is indicated. If the albumin is elevated then the calcium should be adjusted downward. If the albumin is low, then the calcium should be adjusted upward. TREATMENT OF HYPERCALCEMIA: The decision to treat is usually clear-cut if the calcium is 14 or greater. However, calcium levels between 10.5 and 14 depend on several factors such as age, concomitant conditions, stage of cancer, and symptoms. There are four classes of treatment and include: hydration, enhance the renal excretion of calcium, inhibit bone resorption and treating the underlying condition. These will subsequently be discussed. Hydration with isotonic saline is usually the first step. Various amounts and time schedules have been used, but in general give 2.5 to 4 liters of saline daily with attention to the cardiovascular and renal status. When there has been restoration of intravascular volume then one could reasonably expect a diminution of 1.6 to 2.4 mg reduction of the calcium level. This occurs because of increased renal calcium clearance, decreased calcium absorption in the proximal renal tubule, and obligatory kaluresis with increased presentation of sodium and water to the distal renal tubule. Furosemide is usually given along with isotonic saline in order to inhibit reabsorption of calcium in the thick ascending loop of Henle, and to protect the patient from saline overload. Thiazide diuretics should never be given as they increased the absorption in the distal tubule. Always precede loop diuretic agents as furosemide with saline hydration, because furosemide depends on the delivery of calcium to the loop. Depending on the degree of hypercalcemia and symptoms, the furosemide needs to be adjusted possibly from 20 mg every 6 hours to 80 mg every two hours. Careful attention must be given to electrolyte depletion. Etidronate works by inhibiting osteoclasts. The reduction in calcium begins at about 2 days and has a peak reduction at 7 days. The patient should be well hydrated as the etidronate works better under this situation. The dose is 7.5 mg/kg IV over a four-hour period daily for 3-7 days. The length of treatment depends on the response. Etidronate is safe with transient increases in creatinine and phosphate. Pamidronate is more potent than etidronate. Giving a single 24-hour IV infusion of up to 90 mg will normalize the serum calcium in 70-100% of patients. Other schedules include giving a slow IV infusion of 15-45 mg daily for up to six days depending on the response. Pamidronate can also be given orally as 1200 mg daily for up to 5 days, but many hypercalcemic patients are unable to tolerate orally because of nausea and vomiting. Onset of action and peak action is about the same as Etidronate. Side effects are mild with transient increase of temperature, which is usually less than 2 degrees C, transient hypophosphatemia and leukopenia. 97 Plicamycin is given at 25 micrograms/kg over a 4-6 hour period and can be repeated at 1-2 day intervals depending on limiting side effects of the drug which include: hepatic and renal toxicity, thrombocytopenia, and cellulitis with extravasation of the drug. The onset of lowering the calcium starts at 12 hours and peaks at 48-72 hours. Calcitonin is usually given as salmon calcitonin at 4 units/kg every 12 hours and is the drug of choice if a rapid reduction of calcium is needed. The calcium starts to drop after a few hours and the peak drop is at 12-24 hours. The drawback is that calcitonin is fairly weak and doesn't lower the calcium to degrees that the bisphosphonates and plicamycin do. In spite of this, severe hypercalcemia can be treated with a combination of calcitonin, which can be given for 1 to 2 doses and either plicamycin, bisphosphonates or gallium nitrate. Calcitonin also possesses pain relief properties that can relieve metastatic bone pain. Calcitonin is safe and causes mild nausea, flushing, abdominal cramps and allergic reactions to salmon. Skin testing with 1 unit of salmon calcitonin prior to therapy is recommended. Gallium nitrate is given as a continuous IV infusion at 200-mg/square meter of body surface in 1 liter of fluid daily for 5 days. Gallium appears to be more effective in lowering the calcium to normal and prolonging this effect than calcitonin. However, normal calcium levels are not obtained until the 5 days of therapy is completed and the lowest levels are at 3 days post infusion. Also, it appears that gallium is more effective than etidronate in normalizing the calcium by about 50%. The main side effect is nephrotoxicity and should not be given if renal insufficiency is present. Patients should not be given other renal toxic drugs, as aminoglycosides and hydration should be maintained. Decreased hemoglobin and phosphates can also occur. Steroids useful if the patient has multiple myeloma, lymphoma, vitamin D intoxication, or granulomatous disease and is given as 200-300 mg of hydrocortisone IV daily for 3-5 days. Hyperkalemia Immediate Questions: A. What are the vital signs? B. Is the lab result correct? Consider pseudohyperkalemia, especially if the ECG shows no changes of hyperkalemia. There are a number of causes of factitious hyperkalemia, the most common being the tourniquet method of drawing blood. A tight tourniquet around an extremity can elevate the potassium. Hemolysis of a blood sample prior to the chemical determination is another source of error. Extreme leukocytosis (>70,000) or thrombocytosis (>1,000,000) can elevate the serum potassium. If there is a question, obtain a plasma potassium. C. What is the patient's urine output? D. What does the ECG show? The ECG is the most important test, (besides the potassium level). It provides more of a "bioassay" than the serum potassium. Changes seen with potassium increase include peaked T waves, flat P waves, prolonged PR interval and a widened QRS complex, progressing to a sine wave and arrest. E. Is the patient taking any medication that could raise the potassium level? Is the patient receiving potassium in an intravenous solution? If the patient is receiving spironolactone, triamterene, indomethacin and other NSAIDS; ACE-inhibitors, trimethoprim / sulfamethoxazole, pentamidine, succinylcholine; stop these medications immediately. Differential Diagnosis: A. Redistribution 1. Acidosis drives potassium out of the cells and can cause hyperkalemia 2. Cellular breakdown a. Rhabdomyolysis b. Hemolysis c. Tumor lysis syndrome B. Increased total body potassium 1. Inadequate excretion a. Renal caused (acute or chronic renal failure) b. Mineralocorticoid deficiency or Addison's disease c. Drug-induced (potassium sparing diuretics [e.g., spironolactone] and ACE-inhibitors) 2. Excessive intake C. Pseudohyperkalemia 1. Hemolysis of the specimen 2. Prolonged period of tourniquets occlusion prior to blood draw 3. Thrombocytosis/leukocytosis Plan: The severity of hyperkalemia (as judged by the serum level and the ECG) dictates treatment. A. Repeat any abnormal value, taking care to avoid hemolysis, while assessing for increased WBC or platelets. B. Prevention of further hyperkalemia; discontinue any potassium administration and any contributing drugs. C. Calcium administration. Calcium counteracts membrane effects and protects the heart. Calcium antagonizes the membrane effects of hyperkalemia and restores normal excitability within minutes. Administer one to two ampules of calcium gluconate, (10-20 mL of a 10% solution IV over 3-5 minutes), with the patient on a cardiac monitor. 98 D. Potassium can be quickly shifted into cells by the administration of alkali or glucose plus insulin (one ampule D50 and 10 units regular insulin).Sodium bicarbonate (1 ampoule [44 mmol] of bicarbonate) may be administered intravenously over several minutes. E. Remove potassium from body. Kayexalate may be administered orally or as an enema. Remember that this will trade potassium for sodium and result in a sodium load. Normal saline diuresis can assist removal of potassium. ACUTE THERAPY OF HYPERKALEMIA Condition: ECG changes of hyperkalemia Therapy: Calcium gluconate (10%) 10 ml IV over 3 minutes. Repeat in 5 minutes if needed. Follow with 10 units regular insulin IV; the insulin may be by IV push, but must be followed with 1 ampule D50 IV push; alternatively, 10 units regular insulin in 500cc D20 may be infused over 30 to 60 minutes. Comment: Lasts only 30 to 60 minutes. No bicarbonate after calcium. Condition: After acute phase or if no ECG changes Therapy: Kayexalate: Oral dose of 30 to 60 grams in 50 ml sorbitol (20%). Rectal dose of 50 grams in 200 ml sorbitol (20%) as retention (30 to 45 minutes) enema. Comment: Oral dose preferred (enemas are only if patient cannot take po). Condition: If renal failure Therapy: Hemodialysis as soon as possible. Kayexalate also will be effective, but not immediately. HYPERKALEMIACalcium gluconate 10%: 10-30 ml IV. Lasts 30-60 min. Glucose and insulin: 50 grams glucose hourly and 5 units regular insulin q 15 min. Duration 2 hrs. Sodium bicarbonate: 50-100 mEq IV. Duration 3-6 hrs. Albuterol: 10-20 mg by inhaler. Duration 2 hrs. Sodium polystyrene sulfonate (Kayexalate) 15-60 gms with sorbitol PO or 50-100 gms with retention enema (retain for 30-60 min). Furosemide: 40-240 mg IV over 30 min. Ethacrynic acid: 50-100 mg IV over 30 min. Bumetanide: 1-8 mg over 30 min. Hemodialysis which is much more effective than peritoneal dialysis. HYPERNATREMIA Immediate Questions: A. What is the patient's mental status? B. What have been intake, output and serial weights? Clinical Findings: A. Na+ serum is usually 150 mEq/L before symptoms manifest; a rapid rate of increase is more likely to result in problems B. Na+ 160 mEq/L: irritability, anorexia, ataxia, cramping C. Na+ 180 mEq/L: confusion, stupor, and seizure Diagnostic Considerations: Extracellular Fluid Volume State Management: A. B. 99 Assess the extracellular fluid volume. "Hypernatremia with increased volume": Therapy is diuresis (e.g., furosemide), and replacement of the urine output with water (D5W). C. "Hypernatremia with " normal volume": Hypovolemia usually is not evident because of the large intracellular water reserve. Acute therapy is water (D5W) replacement, and evaluation for possible DI. D. "Hypernatremia with decreased volume", (i.e., water loss Na+ loss): Estimate the degree of volume depletion by using: Water depletion approximately (0.6 X body weight) X [measured serum sodium / 140] -1) *Correct volume with normal saline, and follow with half-normal saline. * If initial serum Na+ >175, prevent cerebral edema by monitoring serum Na+ hourly until it reaches 155 mEq/L, allowing a decline of at most 2 mEq/L/hr. Replace one-half this volume over the first 24 hours, the remainder over the next 1-2 days. HYPOKALEMIA Immediate Questions: 100 A. Is the patient symptomatic? Symptoms of hypokalemia include weakness, nausea, vomiting and abdominal tenderness. Severe hypokalemia can depress reflexes and cause weakness. B. What medications is the patient taking? Loop diuretics and amphotericin causes potassium wasting by direct renal effects. C. Is there a history of vomiting, nasogastric suction, diarrhea or renal problems (such as renal tubular acidosis)? Database: Because potassium is the principle intracellular cation, measured serum hypokalemia usually represents a significant loss of body potassium. Thus, serum levels of 3.0 meg/L (mmol/L) often reflect total deficits of 100-200 mEq or more. Look for coexisting hypocalcemia and hypomagnesemia. Check ABG's, as acid-base disorders may coexist and obtain an ECG. Severe hypokalemia can cause blunting of reflexes, paresthesia and paralysis. Plan: A. Aggressive potassium replacement should be performed only after adequate renal function has been documented. B. Parenteral replacement should be considered for digoxin toxicity, significant arrhythmia, and severe hypokalemia (<3.0 mmol/L). Maximum concentrations of KCl used in peripheral veins generally should not exceed 10-meq/100 cc, due to the damaging effects of high concentrations on the veins. C. For lesser degrees of hypokalemia that require parenteral replacement, 10 to 15 mEq/h may be infused peripherally. The maximum infusion rate is 10 mEq/hour. Check serum levels frequently (every 2-4 hours depending on clinical response) to avoid hyperkalemia. ICU monitoring is required if arrhythmias are present or for rapid infusions of KCl. D. Oral replacement includes liquids and tablets. Slow-release pills typically contain 8, 10 or 20-mEq tablet. Thus, it will take several days to replete the potassium depletion. Replacement doses should be 40-120 mEq qd in divided doses, depending on the patient's weight and level of hypokalemia. More than 20 mEq in one dose can cause GI upset. HYPOMAGNESEMIA Immediate Questions: A. What are the patient's vital signs? Cardiac arrhythmias including atrial fibrillation, ventricular tachycardia and ventricular fibrillation can occur. B. Is the patient tremulous? Tremor, tetany, muscle fasciculations, and seizures are all associated with magnesium deficiency. Determining the presence of these neurologic problems will help guide the urgency of treatment. Differential Diagnosis: Hypomagnesemia can be caused by medications; especially diuretics, antibiotics (ticarcillin, amphotericin B), aminoglycosides, cisplatin, and cyclosporin, often cause hypomagnesemia. Alcoholism and reduced intake/ malabsorption also can cause hypomagnesemia. Laboratory Data: Electrocardiograph findings may include prolongation of the PR, QT, and QRS intervals, as well as ST depression and T wave changes. Rhythm disturbances include supraventricular arrhythmias, as well as ventricular tachycardia and ventricular fibrillation. Plan: A. Asymptomatic individuals can be treated with oral magnesium. Oral magnesium oxide (20 meq of magnesium per 400 mg tablet) can be administered as 1 or 2 tablets per day; oral administration is most appropriate for chronic maintenance therapy. B. Magnesium sulfate 1 g (2 mL of a 50% solution of MgSO4) equals 98 mg of elemental magnesium. For moderate depletion, infuse 6 GMs (12 ml of 50% MgSO4 = 6 GMs) in 500 ml saline can be given IV over 3 hours, followed by 5 gm in 500 ml saline over the next 6 hours. The 50% solution must be diluted for IV use. For slightly less urgent situations, 1 g/h may be given q3-4h with close monitoring of deep tendon reflexes. As long as signs and symptoms of hypomagnesemia are improving, the infusion can then be slowed so that the patient receives approximately 10 g of magnesium sulfate in the first 24 hours. Intramuscular magnesium sulfate. Give 1-2 g IM q4h for 5 doses during the first 24 hours. 101 HYPONATREMIA Important Questions: A. Is the lab value real? Repeat any abnormal lab. Was it drawn above IV site? What's the glucose? What are lipids? B. What's the volume state, based both on the patient's history and current exam? What fluids have been administered? C. CNS sx? Are there any recent prior sodium levels to document the chronicity of the hyponatremia? The urgency of correction depends on the patient's symptoms and the acuteness of the hyponatremias onset. Differential Diagnosis: The initial differentiation is between true hyponatremia and laboratory artifact. True hyponatremia may be classified according to the volume status of the patient: hypovolemic, euvolemic or hypervolemic. Hypovolemic hyponatremia may be further classified by serum and urine chemistries. DIFFERENTIAL DIAGNOSIS of SIADH 102 1. Malignant neoplasia a. Carcinoma (bronchogenic, duodenal, pancreatic, Ureteral, prostatic, bladder) b. Lymphoma and leukemia c. Thymoma, mesothelioma, and Ewing's sarcoma 2. CNS disorders a. Trauma, subarachnoid hemorrhage, subdural hematoma b. Infection (encephalitis, meningitis, brain abscess) c. Tumors d. Porphyria e. Stroke 3. Pulmonary disorders a. Tuberculosis b. Pneumonia c. Mechanical ventilators with positive pressure d. Lung abscess 4. Drugs (including vasopressin, chlorpropamide, thiazide diuretics, oxytocin, vincristine, haloperidol, nicotine, phenothiazine, tricyclic antidepressants) 5. Others a. "Idiopathic" SIADH b. Hypothyroidism HYPONATREMIA CLASSIFIED BASED ON SERUM OSMOLALITY, VOLUME STATE and URINE SODIUM Calculated Na Deficit = 0.6 (Wt. in kg) (140 - Na) + (140) (Volume deficit in L) (mEq) Corrected Na for LIPID, PROTEIN and GLUCOSE % serum H2O = 99 - 1.03 (lipids in gm/L) - 0.73 (protein in gm/dl) corrected Na = measured Na X 93/% serum H2O change in Na = 0.016 (measured glucose - 100) corrected Na = 0.016 (measured glucose - 100) + measured Na HYPOPHOSPHATEMIA Immediate Questions: A. Is the patient an alcoholic, recovering from DKA or refeeding orally or parenterally? B. Symptoms or signs of weakness? (Clinical findings may not be prominent, despite PO4 of less than 1.0 mg/dl). Treatment: A. IV replacement is used for levels less than 1.0 mg/dl (even without symptoms). B. Monitor K, Mg, Ca, as abnormalities of other cations often coexists. MAGNESIUM TOXICITY (Consideration when treating preeclampsia) Immediate Questions: A. What dose of magnesium sulfate was the patient receiving? Most patients receive 1-2 MgSO4 IV every hour. This dose is regulated by following serum levels and changes in physical examination such as decreased patellar reflexes, which are suggestive of high serum magnesium levels. Magnesium sulfate used in patients with premature labor may require doses of up to 3g/h. 103 B. What was her last serum magnesium level? Clinically significant hypermagnesemia can begin to be seen at levels as low as 4 mEq/L. Most patients who are being maintained on magnesium sulfate for the prevention of eclampsia will be held at 4-6 mEq/L. Management: 1. Magnesium. Toxicity may be seen at levels as low as 4 mEq/l. Most patients are maintained at 4-6 mEq/l to prevent eclampsia. Respiratory depression can appear at magnesium levels of 8-10 mEq/l, and cardiotoxicity, while not usually seen until levels exceed 10 mEq/l, can occur at any serum magnesium level. 2. Electrocardiogram. Obtain a baseline study. Hypermagnesemia may manifest itself as a shortened Q-T interval up through complete heart block. 3. Calcium gluconate. Administer 1 g IV over approximately one minute, while waiting for serum magnesium and electrolyte values. If calcium administration improves the patient's status, then magnesium toxicity is most likely the correct diagnosis: magnesium is a calcium antagonist, and calcium should reverse its toxicity. 4. Urine output. The kidneys secrete magnesium. Urine output should be maintained at a minimum of 30 mL/h. CONVERSIONS Equations TEMP: 40C=104F/39=102.2/38=100.4/37=98.6 C=(F-32) x 5/9 F=(C x 1.8) + 32 1inch=2.54cm 1cm=0.3973 1lb=0.454kg 1kg=0.45kg 1L=1.06qt=33.81oz RENAL FUNCTION CREATININE CLEARANCE: (cockroft-gault eq) (140-Age) (wgt in Kg) --------------------- (X 0.85 if Female) (72) (Serum Cr) Endogenous Creatinine: primarily excreted by glomerular filtration Affected by: age, sex, dietary protein exercise, drugs & Dz DRUGS requiring dose change w/renal fxn - H2 BLOCKERS: accumulates w/renal dz & may interfere w/Cr excretion thus increasing serum levels - AMINOGLCOSIDES: - Some Beta LACTAM Antibiotics: - Some Beta BLOCKERS: Renal FXN & the Elderly: Cr Clearance may decrease w/age from nml renal aging & GFR may decline @ 10cc/min for each decade over 40 REF: Friedman: Corr of Est Renal Fxn JAMA 37:145-149,1989 ACUTE RENAL FAILURE A. Symptoms 1. Polyuria, Oliguria or Anuria 2. Hematuria 3. Dysuria 4. Uremia a. Definition: symptomatic azotemia b. Acidosis (В± tachypnea) 104 c. Mental Status changes d. Hypervolemia / Hypertension e. Hyperkalemia f. Pericarditis 5. Duration <3 months B. Etiologies 1. Location of Lesion a. Prerenal - ~70% of cases b. Intrinsic - ~25% of cases c. Post-renal (obstructive) - <5% of cases 2. Pre-renal azotemia a. Renal Artery Stenosis (atherosclerosis, fibromuscular dysplasia) b. CHF - reduced ejection fraction, hypoperfusion c. Hepatorenal syndrome (cirrhosis with ascites may show similar picture) d. Shock - renal hypoperfusion (usually hypovolemia and/or hypotension) 3. Parenchymal Damage a. Nephritis (inflammation): glomerular vs. interstitial b. Tubular Injury: most common cause of ARF c. Nephrotic Syndrome (total protein losses) 4. Obstruction of Outflow (~5%) a. Urinary Tract Infection (UTI) with Pyelonephritis b. Urinary Calculus disease (renal stones) c. Crystal Deposition d. Bladder tumors with extensive invasion e. Prostatic Enlargement: BPH vs. Carcinoma f. Unilateral obstruction with only one functioning kidney 5. Vascular a. Hypertension b. Atherosclerotic (atheroembolism) - cholesterol emboli, 5-10% of hospitalized ARF [8] c. Trauma d. Vasculitides e. Post-operative - aortic aneurysm repair, aortic cross-clamping 6. Pathophysiology a. Ischemia is the underlying problem in many patients with ARF b. This leads to depletion of cellular ATP and release of calcium c. Reactive oxygen species are produced leading to further cell death d. Calcium release leads to phospholipase activation e. Neutrophils may mediate reperfusion injury (ICAM-1 is involved) f. Many nephrotoxins are renal vasoconstrictors (eg. cyclosporine, radiocontrast) C. Initial Evaluation 1. Consider possible etiologies and direct evaluation towards these 2. Medications should always be suspected in contributing to or causing ARF a. Non-steroidal anti-inflammatory drugs (NSAIDS) b. ACE Inhibitors c. Aminoglycoside d. Radiocontrast Agents e. Amphotericin f. Cyclosporine g. Cisplatin h. Interstitial Nephritis - sulfonamides, NSAIDS, other antibiotics 3. Standard Blood Testing a. Electrolyte and renal panel, Ca2+, Phosphate, Mg2+, Albumin b. Complete Blood Count (В± reticulocyte count and ESR) 4. Foley catheter must be placed to rule out bladder obstruction 5. Urine for electrolytes, dipstick and microscopic analysis a. Osmolality, creatinine, Na+, K+, Clb. Urine spot protein to creatinine ratio (normal is <0.2) c. Pigment: Hemoglobin (myoglobin) d. Cells, Casts, Crystals, Organisms e. Consider Urine culture 6. Renal and Pelvic Ultrasound - stones, hydronephrosis, mass compression 7. Consider Abdominal radiograph if ultrasound is not done to rule out stones 8. Consider sedimentation rate, ASO titer, ANA, Complement Levels, Anti-GBM Abs 9. Renal Biopsy should be considered in rapidly progressing disease a. ANCA and Anti-GBM diseases вЂ“ consider cyclophosphamide + glucocorticoids b. Idiopathic rapidly progressive glomerulonephritis is often ANCA positive c. However, other inflammatory diseases such as bacterial endocarditis can given ANCA+ D. Pathology Summary 1. Glomerular Involvement a. Diffuse: all glomeruli in a tissue section are diseased 105 b. Focal: some glomeruli in a section are diseased c. Segmental: some parts of an individual glomerulus are affected 2. Focal Glomerulonephritis: a. Some of the glomeruli are dead b. Death can include necrosis, collapse, or sclerosis c. Acute or chronic inflammation is often seen 3. Crescent Glomerulonephritis a. Crescent (moon shaped) formation in glomerulus b. Affected glomeruli are non-functional c. Very poor prognosis 4. Focal and Segmental Glomerulosclerosis: portions of many glomeruli are destroyed 5. Minimal Change Glomerulonephritis a. Glomeruli appear okay, but function is poor b. Electron microscopic evidence of basement membrane disease c. Response to glucocorticoids is usually very good 6. IgA Deposition a. IgA nephropathy b. Deposition of IgA immune complexes c. Differential includes Systemic Lupus and Henoch-SchГ¶nlein Purpura 7. Proliferative Glomerulonephritis a. Increase in mesangial cell number b. Usually follows insults (eg. Post-Streptococcal) c. May be seen in collagen vascular disease, especially Systemic Lupus 8. Collapsing Glomerulonephritis a. Major form seen in HIV nephropathy b. Usually late stage c. Rapid progression to renal failure (weeks to months) d. No effective therapy to date 9. Tubular Necrosis a. Tubular cells die and slough off basement membrane b. The dead tubular cells form casts, which can occlude lumen c. Glomerular basement membrane may also be damaged E. Management 1. Renal Diet a. Low phosphate, potassium, sodium, and protein b. High calcium and vitamin D c. Various multivitamin formulas available for renal patients, eg. Nephro-ViteВ® d. Low protein diet may slow progression slightly in chronic renal disease [3] 2. Phosphate and Calcium a. Dangerous if product of Calcium and Phosphate > ~70 (mg/dl) (will lead to precipitation) b. If product is close to 70, then phosphate should be lowered with aluminum compounds c. These compounds should be given with meals to bind the phosphate directly d. If product is <60, then calcium should be given 500-1000mg po tid with meals e. If calcium is low but phosphate normal, then calcium should be given before meals f. Consider using 1,25 dihydroxyvitamin D supplements 3. Acidosis a. Renal tubular acidosis (RTA) is common in early renal failure b. Oral Bicitra (citrate replaces bicarbonate) may be used c. Bicitra is contraindicated in edematous states due to high sodium content 4. Hyperuricemia a. Check uric acid levels b. Uric acid deposition in renal tubules may worsen progression of renal failure c. Allopurinol may be given (100-200mg po qd) to attempt normalization of uric acid 5. Adjust medication dosages for the renal failure a. 24 hour urine collection for accurate GFR determination b. Discontinue NSAIDS and other nephrotoxic medications 6. Hypertension a. ACE inhibitors generally contraindicated in moderate to severe renal failure b. Calcium blockers such as nifedipine are effective c. Labetalol is also very effective but patient should have LV EF>50% and no bronchospasm d. Consider Hydralazine for afterload reduction e. Pure alpha-adrenergic blocking agents may be effective, but tachyphylaxis may occur f. Diuretic agents may improve hypertension and volume overload 7. Volume overload a. Attempt to maximize cardiac output and improve intravascular volume b. Diuretics often worsen renal failure but may be necessary to prevent pulmonary edema c. In general, potassium sparing diuretics should be avoided (high risk hyperkalemia) d. Dopamine or mannitol can be tried, but are usually not effective e. Albumin infusions are probably not helpful, but may help diuresis in low albumin states f. Dialysis may be required particularly in severe volume overload situations 106 8. Protein Load a. Thought to reduce incidence of azotemia b. Appears to slow progression of chronic renal failure [4] c. Patients with moderate renal disease вЂ“ some decrease in progression on low protein diet d. Patients with severe renal disease show no benefit on low protein diet [3] 9. Hospital inpatients with acute renal failure have ~50% mortality rate 10. Newer Agents a. Atrial natriuretic factor (ANF) are dilators with diuretic activities b. ANF (AuriculinВ®) may have some efficacy in oliguric renal failure [6] c. ANF may increase renal dysfunction in diabetics receiving radiocontrast [7] d. Other vasodilators (eg. calcium channel blockers) are not effective e. Renal growth and regeneration factors are under investigation F. Dialysis Indications 1. Serum abnormalities unresponsive to medical therapy a. Severe Acidosis b. Severe Hyperkalemia 2. Uremia a. Mental status changes (usually delirium) b. Nausea and vomiting c. Pericarditis (pericardial friction rub) 3. Volume Overload 4. Renal function and initiation of dialysis a. Native kidneys may continue with minimal function for 6-12 months b. After that, native kidneys usually shut down permanently G. Kidney Transplantation 1. Excellent (and improving) results with cadaveric grafts 2. New kidney usually placed in extraperitoneally in the pelvis 3. Cyclosporin usually required for life 4. Prednisone В± azathioprine may be required for life 5. Other immune suppression, eg. OKT3, mycophenolic acid, FK506 may also be used OLIGURIA (Sudden)PRERENAL AZOTEMIA: BUN: creatinine > 20:1; urine osmolality > 500; urine spot urine sodium < 20; FEna < 1%; urine sediment may show hyaline casts; Signs of intravascular volume depletion include low cardiac output states as CHF, tamponade, arrhythmias, cardiogenic shock, massive pulmonary embolism, OR intravascular volume depletions secondary to hemorrhage, renal losses with diuretics, osmotic diuresis, sequestration of fluid in a third space such as diarrhea, pancreatitis, peritonitis, skin looses from burns, excessive sweating OR increased renal/systemic vascular resistance such as vasodilation from antihypertensive drugs, anaphylaxis, anesthesia, sepsis, drug overdose, OR renal vasoconstriction from alpha adrenergic agonists or high dose dopamine, surgery, anesthesia, hepatorenal syndrome, OR impaired renal autoregulation from prostaglandin synthesis inhibitors such as NSAIDS in the presence of CHF, nephrotic syndrome, cirrhosis, hypovolemia or preexisting liver disease, ACE inhibition in the presence of bilateral renal artery stenosis or CHF. POSTRENAL AZOTEMIA: (Obstructive uropathy) BUN: creatinine > 20:1; urine osmolality variable; urine spot sodium is variable, may be < 20; FEna variable; may be < 1%; urine sediment is normal or may contain RBCs, WBCs, or crystals; urine volumes fluctuate day to day; bilateral hydronephrosis or hydroureter on sonography; enlarged bladder or prostate. Ureteral obstruction may be caused by papillary necrosis, blood clots, sulfonamide or uric acid crystals, fungus balls, stones, retroperitoneal hemorrhage and fibrosis, ureteral ligation during pelvic surgery, and tumors of the prostate, cervix and uterus. Bladder outlet obstruction can be caused by bladder carcinoma, stones, clots, functional impairment from neuropathy or ganglionic blocking agent, prostatic hypertrophy or malignancy. Urethral obstruction is caused by congenital valves, strictures, and phimosis. INTRINSIC RENAL DISEASE: acute tubular necrosis will produce a BUN: creatinine < 20:1; urine osmolality < 350; urine spot sodium > 20; FEna > 1%; urine sediment shows granular casts, renal tubular epithelial cells, and cellular debris, pigment, and crystals. There may be a history of significant hypotension and renal hypoperfusion, and exposure to nephrotoxins. Nephrotoxins include aminoglycoside, amphotericin B, radiographic contrast media, immunosuppressive drugs as cyclosporin, heavy metals as lead, arsenic, chemotherapeutic agents as cisplatin, methotrexate, organic solvents as ethylene glycol, myoglobin, hemoglobin, calcium, uric acid and oxalates. Acute glomerulonephritis and vasculitis will produce a BUN: creatinine > 20:1; urine osmolality > 500; urine spot sodium < 20; FEna <1%. The urine sediment shows RBCs and RBC casts. There may be systemic evidence of vasculitis as SLE or other collagen vascular disease. There may be a history of sore throat and strep infections. The causes include glomerulonephritis, toxemia of pregnancy, hemolytic uremic syndrome, DIC, malignant hypertension, and radiation injury. Acute interstitial nephritis shows a BUN: creatinine less than 20:1; urine osmolality is variable; urine spot sodium is variable; FEna variable; urine sediment shows WBC and WBC casts and eosinophils. There may be a history of allergic reaction, drugs, infections, peripheral eosinophilia and thrombocytopenia. Causes include fungal infections, bacterial infections, viral infections, drugs as beta lactam antibiotics, sulfonamides, rifampin, NSAIDS, cimetidine, and phenindione. Renovascular occlusion (Arterial) shows a BUN: creatinine < 20:1; urine osmolality is variable; urine spot 107 sodium is variable; FEna is variable; urine sediment is variable; renal vein thrombosis is associated with nephrotic syndrome or with compression or invasion of the renal vein by tumor. The causes include renal artery embolism, thrombosis, dissection (postangioplasty or traumatic), aortic aneurysm, and thrombotic microangiopathy. Renovascular occlusion (Venous) shows a BUN/creatinine < 20:1; urine osmolality variable; urine spot sodium variable; FEna variable; urine sediment variable. Renal vein thrombosis is associated with nephrotic syndrome or with compression or invasion of renal vein by tumor. Causes include renal vein thrombosis and compression, Individuals with sudden occlusion of one or both of their main renal arteries may have acute flank pain, fever, livedo reticularis, marked elevation of LDH (found in large quantities in renal cells), increased ESR, decreased serum complement levels, thrombocytopenia, eosinophilia and/or evidence of thrombotic thrombocytopenic purpura. There may be abdominal bruits, aneurysms, reduced or absent femoral pulses, or peripheral or cerebral vascular diseases. There may be atrial fibrillation, recent MI or endocarditis that embolizes. A history of aortic catheterization may point to cholesterol embolization. The FEna (fractional excretion of sodium) = Una x Pcr / Pna x Ucr x 100 where the Una=urine sodium (mEq/L), Pna=plasma sodium (mEq/L), Pcr=plasma creatinine (mg/dL), and the Ucr=spot urine creatinine (mg/dL). ACUTE TUBULAR NECROSIS (ATN) A. Pathophysiology [1] 1. Renal medulla receives blood supply after oxygen has been extracted in the cortex 2. In addition, low blood flow in medulla is required to maintain osmotic gradients 3. Therefore, medulla is especially susceptible to hypoxia, usually from hypoperfusion 4. ATN is the most common cause of acute renal failure in hospital 5. Renal Vasodilators help prevent ischemic injury a. Nitric oxide b. Prostaglandin - especially PGI2 (prostacyclin) c. Adenosine d. Dopamine e. Urodilatin 6. Renal Vasoconstrictors a. Endothelin b. Angiotensin II c. Vasopressin 7. Electrolyte transport inhibitors can also limit damage (by reducing energy needs) a. Prostaglandin E2 b. Adenosine c. Dopamine d. Platelet activating factor B. Etiology 1. Drugs a. Aminoglycoside b. Cis-platinum, methotrexate, mitomycin c. Cyclosporin d. Radiocontrast Agents (Intravenous) e. Amphotericin 2. Myoglobinuria (Rhabdomyolysis) and possibly Hemoglobinuria (hemolysis) 3. Ischemia / Hypotension a. Hemorrhage / Shock / Anesthesia (intubation) b. Sepsis c. Pre-renal azotemia prolonged (eg. dehydration, hypotension) d. Obstetric Complications 4. Factors Contributing to Likelihood of Renal Damage a. Underlying renal disease вЂ“ especially diabetes mellitus, hypertension, myeloma b. Non-steroidal anti-inflammatory drugs (NSAIDS) c. Baseline hypoxemia - COPD mainly C. Signs and Symptoms 1. Oliguria or anuria 2. Epithelial ("muddy brown") Casts in Urine 3. Previous Toxin Exposure 4. Rapidly progressive azotemia вЂ“ creatinine elevation 0.5-1mg/dl per day 5. Urine sodium usually high due to inability to reclaim electrolytes 6. Uremia D. Treatment 1. Hydration - usually the most effective method, least toxicity 2. Mild diuresis to hasten toxin removal a. Mannitol: increases lumen fluids, may prevent obstruction by casts and dead cells b. Furosemide: increases toxin removal, theoretical sparing of tubules by blocking ATPase c. Mannitol and furosemide are not effective in preventing contrast nephropathy 3. Dopamine (low dose, 2-4Вµg/kg/min) may improve urinary flow 108 a. Especially in patients with poor renal perfusion such as heart failure b. However, no clear benefit in patients after major vascular surgery [3] c. Use reasonable in patients who require diuresis with poor cardiac function and perfusion d. This agent is probably worth trying in many patients, especially with above medicines 4. Discontinue any renal toxins and implicated medications 5. Dialysis 6. Atrial Natriuretic Protein (ANP, ANF; AuriculinВ®) a. Produced in cardiac atria in response to elevated atrial pressures b. Induces natriuretic diuresis c. May improve outcome in oliguric renal failure CHRONIC RENAL FAILURE (CRF) A. Etiology 1. Azotemia means abnormally high BUN (>28) and creatinine (>1.5) levels due to reduced GFR 2. Prerenal azotemia a. Renal hypoperfusion b. Usually with heart failure or liver failure c. Renal artery stenosis 3. Intrinsic Renal Azotemia a. Intrinsic disease, usually glomerular b. Hypertension (~28%) and Diabetes (~33%) are the most common causes c. Glomerulonephritis accounts for ~12% of current cases d. Renal (glomerular) deposition diseases 4. Postrenal azotemia - obstruction of some type 5. Long-term progression of (cumulative) insults to kidney 6. CRF requires duration >3 Months 7. Common Underlying Causes of CRF a. Hypertension - systolic BP >210 or diastolic >120 mm has 22X increased risk of CRF [3] b. Diabetes - over 30% of persons with CRF have diabetes mellitus c. Renal Deposition Diseases вЂ“ amyloidosis and others d. Renal Vascular Disease - renal artery stenosis, atherosclerotic vs. fibromuscular e. Medications - especially causing tubulointerstitial diseases B. Electrolyte Abnormalities 1. Excretion of Na+ is initially increased, probably due to natriuretic factors 2. As glomerular filtration rate (GFR) falls, fractional sodium excretion rises a. Maintain volume until GFR <10-20ml/min, then edema will occur b. In renal failure with nephrotic syndrome, edema occurs early c. Can not conserve Na+ when GFR <25ml/min, and Fe Na rises with falling GFR 3. Tubular K+ secretion is decreased a. Aldosterone mediated. Also increased fecal loss of K+ (up to 50% of K ingested) b. Can not handle bolus K+, so must avoid drugs high in K+ c. Do not use K+ sparing diuretics 4. Control of acids a. Normally, produce ~1mEq/kg/day H+ b. When GFR <40ml/min then decrease NH4+ excretion adds to metabolic acidosis c. When GFR <30ml/min then urinary phosphate buffers decline and acidosis worsens d. Bone CaCO3 begins to act as the buffer and bone lesions result (renal osteodystrophy) e. Usually will not have wide anion gap even with acidosis if can make urine f. Acidosis caused by combination hyperchloremia and hyper sulfatemia (SID reduction) g. Defect in renal generation of HCO3-, as well as retention of nonvolatile acids 5. Loss of urine diluting and concentrating abilities a. Osmotic diuresis due to high solute concentration for each functioning nephron b. Reduce urinary output only by reducing solute excretion c. Major solutes are salt and protein, so these should be decreased 6. Bone metabolism a. GFR reduction leads to elevated blood phosphate, low calcium and acidosis b. In addition, reduced tubular resorption of calcium augments hypocalcemia c. Other defects include acidosis and decreased dihydroxy-vitamin D production d. Bone acts as a buffer for acidosis, leading to chronic bone loss in renal failure e. Low vitamin D causes poor calcium absorption and hyperparathyroidism (high PTH) f. Increased PTH maintains normal serum Ca2+ and PO42- until GFR <30ml/min g. Chronic hyperparathyroidism and bone buffering of acids leads to severe osteoporosis 7. Other abnormalities a. Slight hypermagnesemia with inability to excrete high magnesium loads b. Uric acid retention occurs with GFR <40ml/min 109 c. Vitamin D conversion to dihydroxy-Vitamin D is severely decreased d. Erythropoietin (EPO) levels fall and anemia develops 8. Accumulation of normally excreted substances, "uremic toxins", MW 300-5000 daltons C. Uremic Syndrome 1. Symptomatic azotemia 2. Fever, Malaise 3. Anorexia, Nausea 4. Mild neural dysfunction D. Associated Problems and Treatment 1. Immunosuppression a. Patients with CRF, even pre-dialysis, are at increased risk for infection b. Cell mediated immunity is particularly impaired c. Hemodialysis seems to increase immunocompromise d. Complement system is activated during hemodialysis e. Patients with CRF should be vaccinated aggressively 2. Anemia a. Due to reduced erythropoietin production by kidney b. Occurs when creatinine rises to >2.5-3mg/dL c. Rarely clinically significant until 6-12 months prior to dialysis 3. Hyperuricemia 4. Hyperphosphatemia a. Decreased excretion by kidney b. Increased phosphate load from bone metabolism (by high PTH levels) 5. Hypertension a. ACE inhibitors shown be most effective at preserving renal function [ 1, 6] b. Blood pressure control is very important to slowing progression of renal failure c. Patients with grade IV (severe) HTN have 22X-increased risk vs. normal for CRF [3] d. Targeted mean pressure 92-98mm Hg in patients with renal failure and proteinuria [2] e. ACE inhibitors are avoided in patients with serum creatinine >2.5-3mg/dL 6. Poor coagulation a. Platelet dysfunction - usually with prolonged bleeding times b. May be partially reversed with DDAVP administration 7. Proteinuria >0.25gm per day is an independent risk factor for renal decline [2] E. Evaluation 1. Search for underlying causes (see above) 2. Laboratory a. Full Electrolyte Panel b. Calcium, phosphate, uric acid, magnesium and albumin levels c. Urinalysis, microscopic exam, quantitation of protein in urine (protein: creatinine ratio) d. Calculation of creatinine clearance and protein losses e. Complete blood count - anemia can occur, low erythropoietin levels f. Consider complement levels, protein electrophoresis, and antinuclear antibodies, ANCA g. Renal biopsy - particularly in mixed or idiopathic disease 3. Radiographic Evaluation a. Renal Ultrasound - evaluate for obstruction, stones, tumor, kidney size, chronic change b. Duplex ultrasound or angiography or spiral CT scans to evaluate renal artery stenosis c. Magnetic resonance angiography preferred over contrast agents 4. Bone Evaluation a. Severe secondary hyperparathyroidism can lead to osteoporosis b. Some patients will require parathyroidectomy to help prevent this c. Unclear when bone densitometry should be done on patients with CRF F. Pre-Dialysis Treatment 1. Maintain normal electrolytes a. Potassium, calcium, phosphate are major electrolytes affected in CRF b. Discontinue ACE inhibitors in most patients with creatinine >3.0mg/dL c. Reduce or discontinue other renal toxins (including NSAIDS) d. Diuretics (eg. furosemide) may help maintain potassium in normal range e. Renal diet including high calcium and low phosphate 2. Reduce protein intake to <0.6gm/kg body weight [5] a. Appears to slow progression of diabetic and non-diabetic kidney disease b. In type 1 diabetes mellitus, protein restriction reduced levels of albuminuria 3. Underlying Disease a. Diabetic nephropathy should be treated with ACE inhibitors until creatinine >2.5-3mg/dL b. Hypertension should be aggressively treated (ACE inhibitors may be preferred) [1] c. Caution with use of ACE inhibitors in renal artery stenosis G. Hemodialysis 1. Indications a. Uremia - azotemia with symptoms and/or signs b. Severe Hyperkalemia 110 c. Volume Overload - usually with congestive heart failure (pulmonary edema) d. Toxin Removal - ethylene glycol poisoning, theophylline overdose, etc. 2. Procedure for Chronic Hemodialysis a. An arteriovenous fistula in the arm is created surgically b. Catheters are inserted into the fistula for blood flow to dialysis machine c. Blood is run through a semi-permeable filter membrane bathed in dialysate d. Composition of the dialysate is altered to adjust electrolyte parameters e. Electrolytes and some toxins pass through filter f. By controlling flow rates (pressures), patient's intravascular volume can be reduced g. Most chronic hemodialysis patients receive 3 hours dialysis 3 days per week 3. Efficacy a. Some acids, BUN and creatinine are reduced b. Phosphate is dialyzed, but quickly released from bone c. Very effective at reducing intravascular volume and potassium levels d. Once dialysis is initiated, kidney function is often reduced further e. Not all uremic toxins are removed and patients generally do not feel "normal" f. Response of anemia to erythropoietin is often suboptimal with hemodialysis [4] 4. Chronic Hemodialysis Medications a. Anti-hypertensives - often labetalol, calcium blockers, ACE inhibitors b. Erythropoietin (EpogenВ®) - given for anemia, in ~80% of dialysis patients c. Vitamin D Analogs - calcitriol given intravenously d. DDAVP may be effective for patients with symptomatic platelet problems MYOCARDIAL ISCHEMIA A. Symptoms 1. Classical a. Chest Pain, squeezing b. Radiation to left, both, or right arms (shoulders) c. Nausea and vomiting d. Diaphoresis e. Shortness of Breath f. Responds to rest or to nitroglycerin 2. Non-Classical a. Burning chest pain - may be increased in women b. Tingling in arms c. Abdominal or Epigastric Pain d. No symptoms (silent ischemia) 3. Silent Ischemia a. Most common in diabetics and women [27] b. Patients with heart transplants have no somatic pain inputs from new heart c. Both peripheral and central nervous systems are involved in lack of pain sensation d. Frontal cortical activation is present in patients with pain, absent without pain [28] 4. Initial Evaluation a. History, especially cardiac risk factors, previous cardiac events b. Targeted physical exam вЂ“ jugular venous distension, lungs, heart, extremities (edema) c. Comorbid conditions: stroke, peripheral vascular disease, and renovascular disease d. Vital signs including pulse-oximetry or arterial blood gas e. ECG; old ECG is very helpful for interpretation of ECG abnormalities f. Consider Chest Radiograph g. Women should be evaluated similar to men, particularly post-menopausal patients 5. Assess Coronary Artery Disease (CAD) B. ECG Changes 1. Reversible ST segment Depression a. Down-sloping depression most specific b. Horizontal depression is less specific c. Up-sloping (with J point) is most likely a normal variant d. Patients may have abnormal (CAD) or normal (Syndrome X) Coronary Arteriograms 2. Variant Angina (Prinzmetal's) a. ST segment elevation b. Vasospasm induced, relieved when spasm stops c. May be due to underlying plaque / thrombus which is variably lodged / dislodged d. Overall good prognosis; related to tobacco use e. Other vasospastic diseases are commonly found (eg. migraine, Raynaud's Disease) C. Stable Angina 1. Definition 111 a. Angina on exertion, relieved by resting В± nitrates b. Cardiac etiology confirmed by ECG or ETT c. Most patients have demonstrable epicardial coronary artery disease (CAD) 2. Etiology a. Epicardial coronary artery disease (CAD) present in most patients b. Stable atherosclerotic plaques present in majority c. TRUE cardiac angina in patients with normal epicardial vessels is called "Syndrome X" or microvascular angina d. Syndrome X patients may have vasospasm, abnormal vessel dilation (see below) 3. Evaluation a. Medical history suggestive of cardiac angina b. Concomitant risk factors c. Exercise Treadmill Test d. Dobutamine echocardiography e. Catheterization for high-risk patients who are candidates for PTCA or cardiac surgery f. The most important part of evaluation is patients history and cardiac risk factors g. This provides a pre-test probability of coronary disease h. Tests are done to rule out coronary disease and avoid unnecessary cardiac angiography 4. Exercise Treadmill Testing (ETT) a. Walking (or arm) ergometry to increase myocardial workload b. Workload includes increased heart rate, blood pressure, and myocardial vessel dilation c. In general, attempt to achieve >90% of maximal heart rate: max HR ~ 220 - Age d. Monitor symptoms and ECG for specific changes (ST depressions most specific) e. Test is gauged by Rate Pressure product (RPP) = SBP x Maximum HR f. A "good" (interpretable) test usually has RPP > 20,000 g. Combination with thallium or technetium (MIBI) improves specificity and sensitivity h. Patients with the following abnormal results have high risk for coronary disease: вЂў Decrease in or no change in blood pressure during test вЂў Global ischemia вЂў Lung uptake (thallium) вЂў Reversed cavity dilatation i. ETT may be less useful in women and in persons with poor exercise tolerance [27] j. Women have increased number of false positives with ETT vs. men k. However, nuclear tests often show large number of false positives in low risk patients l. In women and patients with baseline ECG anomalies, especially LBBB, nuclear studies or dobutamine (stress) echocardiography must be used m. However, in patients with normal ECG, nuclear scans add cost but no information [1] n. Due to low pre-test probability of CAD for normal ECG 5. Stress-Echocardiography [2] a. Assessment of wall motion abnormalities (implies ischemia) at high cardiac work b. Similar sensitivity and specificity as other pharmacologic stress tests c. Dobutamine (10-40Вµg/kg/min) is usually used to increase cardiac work (as above) d. Atropine (0.25-1mg iv) may be added to increase heart rate to >90% predicted e. Ultrasound (echocardiogram) is used to detect work-induced wall motion abnormalities f. Wall motion abnormalities usually occur prior to development of symptoms g. Test is useful for evaluation of chest pain to rule out myocardial source h. Extremely useful in preoperative assessment in patients who cannot exercise i. Negative predictive value for late cardiac events ~87% in patients with suspected coronary disease j. Positive predictive value ~25%; therefore, best used to rule out cardiac ischemia 6. Classification a. Class I: Angina with prolonged exertion b. Class II: Angina with walking >2 blocks c. Class III: Angina with walking <2 blocks d. Class IV: Angina with minimal or no exertion D. Therapy of Exertional Angina [3] 1. Control of Cardiac Risk Factors a. Hypertension itself can cause angina b. Cholesterol reduction is critical c. Diabetes control d. Tobacco abuse 2. Pharmacologic Agents a. Goal is control of rate-pressure product (ie. control pulse and blood pressure) b. Гџ-Blockers are preferred over calcium channel blocking agents вЂў Гџ-blockers have been proven to reduce mortality in angina as well as MI вЂў Use Calcium blockers only when Гџ-Blockers are contraindicated вЂў Calcium blockers reduce anginal symptoms but do not reduce mortality 112 c. All patients should be on ASA if tolerated (consider sulfinpyrazone as substitute) d. Vitamin E (alpha-tocopherol) supplementation, but not Гџ-carotene, provided a minor decrease in incidence of angina in persons with no known coronary artery disease [25] 3. Specific Therapy a. Atenolol/Metoprolol (Гџ-blockers) are excellent agents for the treatment of stable angina b. Adding nifedipine or IsordilВ® (or both) to atenolol does not improve overall symptoms c. Long acting nitrates reduce anginal symptoms but do not reduce mortality d. Some calcium blockers cause vasodilatation, increased ischemia, and coronary "steal" 4. In patients not controlled on monotherapy, further evaluation of angina may be indicated a. Patients with high-risk ETT results should undergo coronary angiography b. Other causes of angina should be considered E. Unstable Angina 1. Definitions a. Originally defined as angina at rest b. Now includes new onset angina and accelerating angina also c. Crescendo (accelerating or increasing) non-rest angina 2. Mechanisms a. Likely similar to that for MI; may be precursor lesion b. Vasospasm and transient clot formation are likely contributors c. Non-occlusive thrombi often form on top of severely obstructed coronary lesions d. Vasoconstrictors (Serotonin, thromboxanes, ADP, PAF, etc.) are likely involved e. Many of the patients with unstable angina have multi-vessel disease 3. Evaluation a. Medical history is the key element here b. Exercise treadmill test is contraindicated in unstable angina c. Patients with recurrence, on medications, should undergo coronary angiography d. Dobutamine echocardiography may be reasonable pre-angiography screening test 4. Decision to Treat [4] a. Risk stratification important: high or moderate risk patients are admitted to hospital b. Patients with known CAD, age >60-70, ECG changes, hemodynamic changes are high risk c. Diabetes - very important risk factor, especially since patients may not have pain d. 2-10% of hospitalized patients with unstable angina will progress to MI 5. Treatment of High Risk Patients (hospitalized) a. Aspirin: All patients without contraindications should be given one EC-ASA (325mg) qd b. Aspirin must be given prior to stopping heparin to prevent recurrent ischemia c. Ticlopidine (TiclidВ®) should be considered in patients intolerant to aspirin d. IIb/IIIa in route to cath lab e. Heparin (standard): therapeutic levels important f. Low Molecular Weight Heparin - Nadroparin more effective than standard heparin] g. Hirudin or Hirulog, direct platelet inhibitors, are about as effective as heparin h. Morphine for resistant pain (and consider further evaluation) i. Reduce Heart Rate - ischemia is exacerbated by high HR; Гџ-blockers preferred j. Angioplasty in appropriate candidates k. Angioplasty probably safer than atherectomy l. Patients with pre-infarction angina who do progress to MI are likely to have very rapid reperfusion (mean ~40 minutes) with thrombolytic therapy m. Thrombolytics of no benefit overall in patients with unstable angina (without MI) n. Nitrates: sublingual given initially, iv nitroglycerin if pain continues, otherwise paste 6. Outpatient Management a. Begin Гџ-blocker (preferred) or calcium blocker to HR 50-60 b. Control blood pressure with systolic 130-150 and diastolic <80 if possible c. Begin ASA (81-325mg qd) or ticlopidine (250mg po bid; monitor blood counts) d. Consider nitrates (eg. patch or oral formulation) 7. Additional Therapy [6] a. Consider coumadin or low molecular weight heparin in outpatients [24] b. Consider ticlopidine for patients allergic to aspirin c. Aspirin / coumadin combinations d. In hospitalized patients to receive anti-coagulation, Hirulog has less bleeding than heparin [21] e. Abciximab (ReoProВ®), an anti-platelet antibody, is safe and effective in unstable angina F. Microvascular Angina [16] 1. Definition a. Chest Pain b. Abnormal ECG, ETT with ST depressions c. No significant coronary artery stenosis on angiography d. ~5% of patients with myocardial infarction will have normal coronaries e. Previously called "Syndrome X" (distinct from insulin resistance syndromes) 2. Etiology [ 8, 9] a. Vasospasm vs. microvascular disease b. Abnormal arterial dilatory responses (inadequate vasodilator reserve) 113 c. Role of hyperinsulinemia, insulin resistance, and dyslipidemia 3. Treatment [10] a. Agents above, but also agents to reduce vasospasm (eg. diltiazem, nicardipine) b. Aspirin should probably be used as described below c. Ca agents probably more effective than Гџ-blockers in this syndrome (no real data) d. Tricyclic antidepressants may have efficacy (eg. Imipramine 25-50mg po qhs) e. Prognosis is excellent; disease is benign (communicate this to the patient) G. Summary of Pharmacologic Agents 1. Nitrates a. Vasodilation: Nitroglycerin (iv or paste): short acting primarily venodilator b. Isosorbide Dinitrate (IsordilВ®): direct, long acting vasodilator, mainly venous action c. Isosorbide Mononitrate (ISMOВ®): 20mg bid (7 hours apart) or qd, reduced tolerance and rebound compared with dinitrates d. The Mononitrate is the major active metabolite of dinitrate with ~100% bioavailability 2. Aspirin a. 325mg po qod or 81mg qd (strongly consider H-2 blocker to prevent GI ulcers) b. Sulfinpyrazone is not effective c. Ticlopidine 250mg bid may be as effective as ASA; consider in ASA-allergic patients 3. Гџ-Blockers a. Excellent anti-ischemic agents (anti-inotropic, anti-chronotropic) b. Also control premature ventricular contractions (PVC) and other arrhythmias c. Demonstrated benefit on survival d. Contraindications: bronchospasm, diabetes, low-EF states, impotence e. Suggest Metoprolol 50-100mg bid-tid or Atenolol 50-100mg qd (both oral) 4. ACE inhibition a. Excellent afterload reduction / anti-hypertensives b. Strongly recommended in diabetics with hypertension c. Effective and safe in patients with COPD, arrhythmias, peripheral vascular disease d. Examples: captopril, enalapril, lisinopril, etc. 5. Heparin [14] and other anti-coagulants a. IV bolus then drip for 2-3 days in all patients with unstable angina or rule out MI b. Consider warfarin in patients with PTCA, diabetes, high risk of MI or ASA intolerant c. ASA must be given before heparin is stopped or recurrent unstable angina likely to occur d. Hirudin, a direct thrombin inhibitor from leeches, has reduced early events after PTCA compared with heparin, but no improvement in late events [20] e. Hirulog, a synthetic direct thrombin inhibitor, has reduced bleeding compared with heparin, more easily dosed, but no overall improvement in mortality outcomes 6. Calcium Antagonists a. Verapamil most effective for hypertrophic cardiomyopathy and to slow heart rate b. Diltiazem excellent for slowing heart rate with less anti-inotropic activity c. Nifedipine: peripheral vasodilation, good for BP reduction, but causes reflex tachycardia d. Felodipine, amlodipine, isradipine, nicardipine have less anti-inotropic effects e. Calcium blockers can induce coronary steal syndromes вЂў Non-diseased vessel dilatation is greater than that of diseased vessel вЂў Therefore, blood is shuttled into dilated healthy vessels, away from ischemic areas f. In general, calcium antagonists are not recommended post-MI g. They should be considered if patients are intolerant of Гџ-blockers 7. Cholesterol Reduction a. Clear data that secondary prevention (post-MI) is beneficial b. Cholesterol reduction, especially in patients with coronary artery disease, as a primary measure is still debated but very reasonable. c. Cholesterol reduction leads to plaque stabilization and sometimes regression [17] d. Increased dietary fiber intake reduced risk of CAD independent of cholesterol [26] 8. Antioxidant Vitamins a. Oxidized form of LDL is major contributor to atherosclerosis b. Antioxidants can prevent LDL oxidation c. Vitamin E >100U per day po supplement reduced coronary artery disease progression d. Main effect occurred only in patients on colestipol-niacin for high cholesterol [18] e. Vitamin E slightly reduced incidence of angina in primary prevention cohort [25] f. Randomized studies are complete and pending publication 9. Other Agents a. Ticlopidine may be used in aspirin intolerant / allergic patients b. Lamifiban - platelet aggregation inhibitor with efficacy in unstable angina c. Newer anti-platelet agents (RGD inhibitors of platelet integrin function) 114 Myocardial Infarction (MI) RISK FACTORS A. Risk Factors for MI 1. Smoking a. Responsible for ~21% of all mortality from heart disease b. Quitting within 5 years decreased risk 50-70%; quit >5 years has near non-smoker risk c. Smoking d. Smoking + Oral Contraceptives ~39X increased risk 2. Lipid Profile a. 2-3% decrease in risk for each 1% decrease in serum cholesterol b. Low HDL (<35mg/dl) is independent risk factor c. Hypertriglyceridemia is a risk factor only in setting of high LDL:HDL ratio d. High lipoprotein a {Lp(a)} levels is a risk factor in hypertriglyceridemic white men e. High Lp(a) levels is best correlate of CAD in patients with high LDL-C [37] f. Lowering cholesterol improves coronary artery endothelial dilatory responses g. Reduction of cholesterol in persons with high cholesterol reduces MI risk ~37% 3. Hypertension a. 2-3% decrease in risk for each 1mm diastolic BP decreased to DBP ~85 mm b. Interaction with diabetes, cholesterol c. HTN also major risk for stroke 4. Left Ventricular Hypertrophy (LVH) a. LVH appears to be an independent risk factor for MI and premature death b. LVH as a risk is also independent of coronary artery disease c. LVH is a more important single risk factor than HTN, smoking, high cholesterol 5. Genetic a. Family History b. Male Sex; Post-menopausal women c. Other genetic disease (hyperlipidemias, homocystinuria, thrombotic disorders, etc) 6. Hyperhomocystinemia a. Autosomal recessive genetic trait affecting 1:20,000 persons b. Many patients with atherosclerosis have high homocysteine serum levels c. ~20% of patients with hereditary homozygous disease (cystathionine Гџ-synthase deficiency) will have a thromboembolic event by age 20 d. Patients with CAD should probably take B vitamin complex to lower serum homocysteine e. Folic acid 1mg po qd will usually reduce homocysteine levels; may add vit B6/B12 also f. Studies ongoing to determine role of high serum homocysteine levels in CAD [35] g. Appears that each 5ВµM increase in homocysteine increases cardiac risk as much as a 20mg/dL increase in total cholesterol h. Low serum folate is a risk factor for heart disease, may correlate with homocysteine [3] 7. Cocaine a. Potent vasoconstrictor, also increase cardiac oxygen demand b. Synergistic with smoking to cause ischemia and myocardial infarctions 8. High levels of fibrinogen, von Willebrand factor antigen, tissue plasminogen activator are mild risk factors for CAD (~2 fold increase each compared to low levels) [25] 9. Summary of Risk Factors For MI a. Left Ventricular Hypertrophy (LVH) b. Male age >45 or Female age >55 yrs. c. Hypercholesterolemia d. Low HDL (<35mg/dl) e. Smoking f. Hypertension g. Diabetes h. Family History i. Sedentary Lifestyle j. Obesity k. Fibrinogen Elevation [15] l. Cocaine abuse m. Serum Homocysteine Elevations B. Cardiovascular Risk Reduction 1. Exercise [ 5, 6] a. Fairly good data show risk reduction ~50% for active life style b. Aerobic activity may be of maximal benefit c. Sudden exertion in sedentary persons is definite risk for infarction 2. Aspirin, Low Dose a. PHS (Physicians' Health Study) 115 b. Randomization to ASA or not (325mg qod) for 22,071 male physicians c. Total MI ~50%; 75% in fatal MI in ASA group (p<.006 in all groups) d. Stroke incidence increased ~15% though p>0.1 in all (fatal, nonfatal, total) groups e. Data on low (160mg and 80mg po qd) dose not yet available f. Risk of bleeding and possibly stroke are increased 3. Estrogen Replacement Therapy (ERT) a. Cardioprotective effects of estrogen b. Estrogen may be inotropic agent as well as anti-atherosclerotic (alters lipid profile) c. ~45% decreased risk in women who take estrogen vs. those who do not d. Progesterone may partially decrease estrogen's protective effect 4. Elevated HDL Levels a. HDL subtypes 2 and 3 are major cardioprotectant b. They are anti-atherosclerotic c. Levels of total HDL > 60mg/dL are considered protective 5. Alcohol: Mild-Moderate consumption may decrease risk of MI 25-45% a. Appears to correlate with decrease HDL2 and HDL3 sub fractions [7] b. No significant changes in total cholesterol or triglycerides c. Moderate alcohol also increase endogenous tissue plasminogen activator levels [8] 6. Anti-Oxidants [36] a. No clear benefit of anti-oxidant vitamin C, trend benefit only for Гџ-carotene, in CAD b. Vitamin E taken for 2 years reduces risk of CAD in men and women 30-60% c. Probucol + lovastatin may improve dilation of atherosclerotic coronary arteries 7. Other Factors a. High Fish Oil (marine n-3 fatty acids) does not decrease risk of coronary disease b. Moderate n-3 fatty acid (seafood) intake does reduce risk of cardiac arrest [32] c. Highest quartile dietary fiber intake was independently associated with 40% risk reduction for MI compared with lowest quartile intake [38] d. High doses of folate and/or vitamin B6 (pyridoxine) may reduce serum homocysteine C. Symptoms of Coronary Artery Disease 1. Crushing or squeezing substernal chest pain 2. Usually radiates to left shoulder 3. High suspicion with shortness of breath, vomiting, and/or diaphoresis 4. Must distinguish from gastrointestinal pain (usually esophageal pain) 5. In women, diabetics, elderly, symptoms may be atypical, very mild or even absent 6. Good correlation between suspicion of CAD from history and physical and results of testing 7. Physician suspicion and exercise stress (thallium) tests correlate well D. Blood Test Results 1. Creatine Kinase (CK) elevation (normal 25-125) a. MB isozyme specifically (MM=striated muscle; BB=brain) b. Note that skeletal muscle <5% MB form c. Peaks 20-24 hours post MI d. Specific CK MB isozyme analysis may detect MI within 6-12 hr [17] 2. Cardiac Troponin T testing is available for diagnosis of MI 3. Lactate Dehydrogenase a. LDHI/LDHII > 1 implies MI b. Peaks 2-3 days post event c. Note LDH not useful in hemolytic or megaloblastic anemia or renal insufficiency 4. AST peaks 24-48hrs post-MI 5. Leukocytosis - due to stress response: epinephrine and cortisol production E. Pathophysiology of MI [ 18, 19, 20] 1. Prevalence of coronary occlusion during early hours of transmural MI a. ~90% of patients seen within 4 hours of onset of symptoms have total occlusion b. ~65% of patients seen 12-24 hours of onset had total occlusion 2. Etiology of Occlusion [40] a. Total arterial thrombotic occlusion is found in most cases of infarction b. The thrombus has formed on a newly ruptured atherosclerotic plaque c. Coronary artery vasospasm is responsible for occlusion in minority of cases d. Unstable angina is usually caused by a non-total thrombotic occlusion (mural thrombus) e. The underlying problem is initial formation of atherosclerotic plaque, which ruptures f. Platelets adhere to exposed surface of ruptured plaque and activate thrombus formation 3. Involvement of Vasoconstrictors a. Thromboxane A2 b. Serotonin - vasoconstrictive effects on diseased (but not healthy) arteries c. Platelet activating factor (PAF) d. Thrombin e. ADP 4. Lack of Vasodilator Substances a. Insufficient nitric oxide (EDRF) b. Adenosine c. Prostacyclin 116 5. Occlusion often resolves over next 24-48 hours without treatment 6. Reperfusion Injury a. Tissue ischemia and necrosis stimulates complement and other systems b. Increase in neutrophil migration into dead / dying tissue c. Release of toxic oxygen species may contribute to injury F. Prognosis 1. Ejection Fraction (EF) is most accurate predictor of prognosis a. Echocardiography usually used to determine EF b. Radio ventriculography more accurate but gives no valve function data c. Cardiac catheterization can provide a good estimate of EF d. Note that cardiac output, not just EF, is important for determining heart function 2. Complications post-MI indicate poor prognosis (eg. arrhythmias, bundle branch block, CHF) 3. Even asymptomatic ventricular arrhythmias have 2 fold increased incidence of death. 4. Stress thallium test may be done 3-6 weeks post-MI a. Exercise test preferred to evaluate functional status b. Thallium should be used to assess dead vs. ischemic myocardium c. Determine if coronary angiography is indicated d. That is, is there additional myocardium at risk? The Use of Beta-Blockers for Acute Myocardial Infarction Contraindications Bradycardia of < 50 beats/min Significant first-degree atrioventricular block (pulse rate > 240 ms) Systolic blood pressure of less than 90 mm Hg High-degree atrioventricular block Acute congestive heart failure Severe asthma Recommended IV Dosage of Beta-Blockers for Patients with Acute Myocardial Infarction on Admission Propranolol 0.1 mg/kg (IV) divided into three equal doses given at 5-minute intervals Metoprolol (Lopressor) three 5 mg (IV)doses given at 2-minute intervals. If 15mg tolerated, start 50mg PO dose 15 minutes after IV dose finished. Esmolol (Brevibloc) Loading dose: 0.5 mg/kg/min for 1 minute followed by a maintenance infusion of 50 ug/kg/min. If an inadequate therapeutic effect is observed, the loading dose should be repeated over 1 minute followed by an increased maintenance dose and orally administered beta-blockers without intrinsic sympathomimetic activity (e.g., atenolol, metoprolol, propranolol, or timolol) are then used 30 to 60 minutes after the intravenous dose. (See PDR for additional titration information.) Thrombolytic Agents in Acute Myocardial Infarction Administration of Thrombolytic Agents 1. Start two 18-g peripheral intravenous lines. 2. No ABGs or central lines may be used or started before treatment. Streptokinase (Kabikinase, Streptase) 1.Dilute two 750,000-unit vials of streptokinase with 5 ml of 5% dextrose in water. 2.Gently swirl to dissolve. 3.Add this dose of 1.5 million units to 150 mL of 5% dextrose in water. 4.This should be infused over 60 minutes. 5.Monitor for the first few hours for signs of anaphylaxis or allergic reaction. Infusion should be slowed if the blood pressure drops 25 mm Hg or terminated if asthmatic symptoms appear. 6.Begin a 5,000- to 10,000-unit bolus dose of heparin followed by 1,000 units per hour approximately 3 to 4 hours after completion of streptokinase infusion or when partial thromboplastin time is < 100 seconds. 7.Monitor prothrombin time, partial thromboplastin time, and fibrinogen levels during therapy. Alteplase, recombinant (tPA Activase) 1.Dilute two 50-mg vials with sterile water for injection provided in the package. 117 2.Gently swirl to dissolve. 3.The total dose is 100 mg over 1.5 hours. (For patients who weigh < 65 kg, use 1.25 mg/kg.) 4.Add this dose to a 100-mL bag of 0.9% sodium chloride for a total volume of 200 mL. 5.Infuse 15 mg (30 ml) over 1 to 2 minutes. 6.Infuse 50 mg (100 ml) over the remainder of the first 30 minutes. 7.Begin a 5,000- to 10,000-unit bolus dose of heparin followed by continuous infusion of 1,000 units per hour. 8.Infuse 35 mg over the next hour. 9.Check partial thromboplastin time 3 to 4 hours after the end of the infusion. Contraindications to Thrombolysis Absolute Active bleeding Possible Aortic dissection Prolonged CPR Head injury Central nervous system neoplasm Hemorrhagic retinopathy Pregnancy Streptokinase or anistreplase allergy Blood pressure > 200/120 mm Hg after sublingual nifedipine Prior cerebral bleeding Trauma or surgery within 2 weeks Relative Trauma/surgery longer than 2 weeks Chronic severe hypertension Active peptic ulcer disease History of cerebrovascular accident Bleeding diathesis Anticoagulant medication Liver dysfunction Previous Streptokinase / Alteplase CONGESTIVE HEART FAILURE (CHF) A. Introduction to Cardiac Pump Function 1. Cardiac output depends on filling of heart (preload) and resistance to emptying (afterload) 2. Starling Curve is a graphic relationship between cardiac output and Preload/Afterload a. Relationship between venous return to the LV (Preload, or Left Atrial Filling Pressure) b. And Afterload (vascular resistance) as they determine the cardiac output (LV) 3. The curve shows that as left ventricular end diastolic volume (LVEDV) increases, LV stroke volume also increases a. This probably occurs up to a maximal LV output b. After this, further filling of the heart may lead to decreased cardiac output 4. The curve also shows that as afterload (resistance to emptying) increases, Cardiac Output decreases 5. For a given clinical situation, preload and/or afterload may be suboptimal 6. It should be noted that preload here refers to LV preload, or return from the lungs 7. The central venous (R sided) pressure may not be a reliable indicator of LV preload 8. Invasive monitoring with a may be indicated a. A catheter is inserted through the RA, to the RV, into the pulmonary artery b. The catheter balloon is inflated ("wedged") to estimate LA pressures c. This LA pressure, pulmonary capillary wedge pressure (PCWP)are usually related d. LVEDV ~ LV end diastolic pressure ~ pulmonary capillary wedge pressure e. SEE BELOWвЂ¦ B. Considerations in Evaluation of CHF 1. Underlying Etiology a. By anatomy b. By function (systolic or diastolic) c. Hypertension is/was present in >90% of CHF patients [32] 2. Anatomy of the failing heart 118 3. Severity and Disability 4. Polypharmacy C. Anatomic Types [1] 1. Hypertrophic a. Hypertensive b. Aortic Stenosis c. Hereditary 2. Dilative a. Viral b. Alcoholic c. Post-MI (ie. infarction due to coronary disease) d. Mitral Regurgitation e. Familial f. Small Vessel: microvascular angina g. Hemochromatosis h. Cobalt toxicity i. Tachycardia induced dilation - may be reversible 3. Restrictive a. Pericardial process (usually post-inflammatory) b. Amyloidosis c. Hemochromatosis d. Scleroderma e. Sarcoidosis D. Major Symptoms and Signs 1. Left Sided Failure a. Rales (pulmonary congestion) b. S3 Gallop - rapid filling of dilated ventricle c. Displaced point of maximal impact / Left heart border d. Tachycardia / arrhythmia - tachycardia can also induce LV dysfunction e. Narrow pulse pressure due to peripheral vasoconstriction f. Acute pulmonary edema with hypoxia, dyspnea, may progress to hypercarbia g. Cardiac Cachexia (weight loss, muscle loss) partly due to high heart rate [6] and TNF [7] 2. Right Sided Failure a. Usually seen with L sided failure, but may be unilateral (eg. patients with lung disease) b. Jugular venous distension c. Pedal Edema (pitting) d. Hepatojugular reflex / Hepatomegaly e. Hypotension 3. Elevated BUN and Creatinine (due to renal hypoperfusion) E. Newer Classification of CHF [ 2, 3] 1. Systolic Dysfunction a. LV Ejection Fraction (EF) < 40% b. Loss of heart muscle with inability to pump; remodelling then occurs (including fibrosis) c. Good filling (preload) of ventricle, poor unloading d. Compensation by increased preload, tachycardia, hyperadrenergic ("cold, clammy") state e. Occurs in ~60-70% of CHF cases [28] 2. Diastolic Dysfunction (see Below) a. Diastole, with LV muscle relaxation, requires ATP b. Poor ventricular filling (impedence to filling) c. Typically hypertensive cardiomyopathy, aortic stenosis, diabetics with LVH d. Patients tend to be older and have less coronary disease than patients with systolic CHF e. Growth factors, including angiotensin II, may be responsible for LVH f. Occurs in ~30-40% of CHF cases [28] g. Diastolic dysfunction also occurs in constrictive and restrictive pericarditis 3. Clinical signs are unreliable indicators of type of CHF 4. Echocardiography is indicated for evaluation of CHF and proper management [30] F. Mortality from Heart Failure 1. Arrhythmias a. Bradycardia, VT, VF b. May be asymptomatic until sudden cardiac death occurs c. Amiodarone may prolong survival in CHF with asymptomatic ventricular arrhythmias [26] 2. Cardiogenic shock 3. Fulminant Respiratory Failure due to Pulmonary edema 4. Mortality Rates 119 a. Class II or III: 50% mortality at 5 years b. Class IV: 50% morality < 1 year 5. Over 750,000 new cases per year; >250,000 deaths per year G. Therapy of Systolic Failure 1. General Considerations [20] a. Fluid Restriction 1.5-3L per day depending on symptoms b. Low Salt Diet - 3gm/d initially; lower to 2gm/d if continued fluid retention c. Diuretics as needed for symptomatic relief d. TEDs stockings - very effective and underutilized e. Oxygen as needed f. ETOH restricted to 30ml/day g. Activities as tolerated 2. Types of Agents a. Afterload reduction b. Vasodilators, nonspecific c. Diuretics (preload reduction) d. Inotropic Agents e. Anti-ischemics f. Low dose Гџ-adrenergic blockers 3. Afterload Reduction a. ACE inhibitor: most efficacious agents for symptomatic and asymptomatic CHF [25] b. Enalapril appears to lower mortality more than the hydralazine - nitrate combination c. Hydralazine (see below) d. Amlodipine (NorvascВ®) may show some benefit in improving symptoms in early studies 4. ACE Inhibitors in heart failure a. A large number of studies have been done using ACE Inhibitors in heart failure b. Overall reduction in mortality (usually from progressive CHF) was ~30% c. Additional reduction in hospitalizations for progressive CHF d. Patients with lowest ejection fraction (EF) have the greatest benefit e. These agents are highly preferred as first line therapy in CHF f. Long term (2-4 year) followup of ACE inhibitor (trandolapril) use 3-7 days post-MI with reduced EF confirmed the mortality and morbidity benefits of shorter term studies [29] 5. Vasodilator Combinations [ 9, 10] a. Combination of isosorbide dinitrate and hydralazine decreases morbidity for CHF b. Prazosin in high dose (20mg qd) is no better than control c. Recent comparison of captopril + IsordilВ® vs. hydralazine + IsordilВ® shows ACE better 6. Inotropic Agents [11] a. Digitalis decreases mortality from CHF only combined with diuretics b. Should be avoided in diastolic dysfunction c. Should be avoided in elderly, patients on quinidine, etc. [12] d. Digitalis + ACE Inhibitors more effective (improved symptoms, EF, delayed progression) than ACE inhibitor therapy alone in EF 35% Class II or III CHF [13] e. Milrinone is a new positive inotropic agent developed for treatment of heart failure - Increases cellular cAMP - Dosing 10mg po qid - Therapy with milrinone increases morbidity and mortality in severe CHF [14] f. Vesnarinone, 60mg po qd, shown to have impressive effect in improving quality of life and preventing mortality in late stage heart failure. Higher doses worsen condition [15] 7. Гџ-Blocking agents [ 16, 27] a. Low doses of metoprolol may prolong survival in patients with LV EF<40% b. Appear to prevent high output failure and improve responses to other agents c. Overall mean EF was actually increased and hospital admissions were decreased d. Begin at 6.25mg bid and increase to 50mg po bid (then consider qd agent) e. Bisopropyl had significant improvement in CHF symptoms, trend improved survival [24] f. Carvedilol therapy showed moderate improvement in symptoms, EF, exercise [27] g. Carvedilol reduced hospitalization and mortality in patients with EF<35% [31] h. Bucindolol is another new Гџ-blocker for CHF in Phase III trials ("BEST" Trial) 8. Anti-Coagulation a. Many experts recommend anti-coagulation for EF <15-20% b. This is independent of rhythm or presence of intracardiac clots c. No compelling data to support empiric anticoagulation in CHF in normal sinus rhythm [21] d. Patients with known clots or in atrial fibrillation should be anti-coagulated 9. Diuretics a. Useful for symptomatic relief and acute therapy b. Generally use furosemide (LasixВ®) or other loop diuretic c. Thiazide type diuretic (distal tubule function) can be added 120 d. Diuretics long term may deplete thiamine, leading to poorer LV function e. Supplementation with thiamine in such patients may improve LV dysfunction (~4%) and diuresis (~500cc/day) 10. Arrhythmia Therapy a. High risk of sudden cardiac / arrhythmia associated death with dilated cardiomyopathy b. Patients with CHF and frequent ventricular arrhythmias have mortality ~15% per year c. Amiodarone may provide some benefit in patients with non-ischemic dilated cardiomyopathy and asymptomatic ventricular arrhythmias [26] d. However, AICD devices are usually recommended for symptomatic arrhythmias e. Гџ-blockers may provide some benefit (low doses) in CHF with arrhythmias 11. Endstage Failure a. Heart Transplant b. Cardiomyoplasty c. Role of bypass surgery is unclear but may improve function in ischemic disease [22] d. Risk of surgery greatly increases as EF declines; EF~10% carries ~30% mortality risk e. Angioplasty can be considered in patients with moderate-severe LV dysfunction and CAD 12. Severe CHF (ICU Setting) a. Inotropic support with Dobutamine initially (В± dopamine) b. If chronotropic activity not tolerated, substitute amrinone iv for dobutamine c. Afterload reduction with nitroprusside may be required if tolerated d. Further inotropic support with vasopressor activity may require epinephrine e. Aortic balloon pump support may be required as bridge to surgery or transplantation f. Magnesium levels should be maintained high (may reduce arrhythmias) [17] H. Current Recommendations: Step Therapy for Systolic CHF 1. ACE Inhibition: afterload reduction and remodeling a. Captopril to 50mg po tid b. Enalapril to 10mg po bid c. Lisinopril to 20mg po qd or bid d. Newer Agents (early studies only; eg. ramipril, fosinopril) e. Note: these agents were only effective at (near) maximal doses (lower doses not studied) 2. Hydralazine for afterload reduction (if failed ACE inhibitor) a. Cardiac remodeling has not been studied with these agents b. Doses 10-75mg po qid (100mg po tid) as tolerated by blood pressure c. Concern for development of lupus-like syndrome 3. Digitalis: adds inotropism in low (eg. <35%) EF states. a. Titrate to therapeutic levels b. Should be avoided in hypertrophic cardiomyopathy and diastolic dysfunction 4. Diuretics a. Primarily symptomatic relief (peripheral and pulmonary edema) b. Titrate to desired patient weight c. Loop diuretics (furosemide, bumetanide, torsemide) usually first line d. Caution when initiating diuretics with ACE inhibitors 5. Гџ-Blockers a. Systolic Dysfunction: Low to moderate dose only in systolic dysfunction b. Consider higher doses in diastolic dysfunction c. Reduce hyperadrenergic states; decrease high cardiac output failure conditions d. Mortality benefit likely; clear benefit on morbidity 6. Nitrates a. Major effect is to lower preload b. Provide rapid symptomatic relief, may decrease ischemia induced cardiac dysfunction c. May worsen CHF caused by diastolic dysfunction or aortic stenosis (preload reduction) 7. Consider vesnarinone for additional inotropic support I. Therapy of Diastolic Failure 1. Treat underlying hypertension aggressively a. ACE inhibitors, especially in diabetics or with accompanying systolic dysfunction b. ACE inhibitors may be preferred agents because they may inhibit hypertrophy c. Calcium blockers, especially verapamil or nifedipine (if severe) 2. Slow Heart Rate a. Гџ-Blockers are highly preferred by most cardiologists (high dose if tolerated) b. Verapamil (or diltiazem, if co-existent systolic dysfunction) c. Anti-inotropic agents are recommended to improve diastolic relaxation d. Nodal blocking agents are very useful atrial fibrillation associated with diastolic CHF 3. Other a. Low dose diuretics for symptomatic improvement b. Low dose nitrates for ischemia (which may worsen diastolic dysfunction) c. The use of preload reducing agents (venodilators, diuretics) should be limited d. This is because diastole in LVH is highly dependent on adequate preload for filling 121 e. Digoxin and other inotropes are contraindicated in diastolic CHF patients 4. Efficacy a. Many patients with severe diastolic CHF will improve b. No change in exercise capacity with verapamil or nadolol in mild-moderate hypertrophy J. Treatment of Acute Pulmonary Edema Due to CHF 1. Nitrates: sublingual or paste a. Dilation of coronary vessels b. Preload reduction c. Some afterload reduction d. Should be used iv in severe situations e. IV preferred in diastolic dysfunction, since preload reduction may worsen condition 2. Loop Diuretics, Given Intravenously a. Furosemide (LasixВ®) or Bumetanide (BumexВ®) b. Reduced preload volume by increasing urine output c. Direct vasodilators (when given iv) d. May be combined with thiazides or mixed diuretics in patients with renal insufficiency 3. Morphine a. Coronary vasodilator b. Decreases respiratory drive (decreases tachypnea) and anxiety 4. Reduces Blood Pressure (Afterload) a. ACE inhibition b. Hydralazine c. Severe hypertension should be treated aggressively with IV nitroprusside d. Nifedipine (may use sublingual or 10mg po tid-qid) 5. Dilative cardiomyopathy a. Consider digitalis loading: Digoxin: 0.25mg iv q8 hours. b. Decrease preload and afterload 6. Mnemonic: "LMNOP" a. LasixВ® (Furosemide) or Ethacrynic acid in patients with allergy to furosemide b. Morphine c. Nitrates d. Oxygen e. Posture (upright) 7. Intensive Care Setting a. IV Nitroprusside or Nitroglycerin b. IV furosemide or bumetanide c. ACE Inhibition d. Intubation may be required; usually it is not prolonged (eg. 1-3 days) e. Morphine f. If ischemic cause, consider aspirin and heparin g. Consider invasive monitoring, especially with intubation and/or sepsis DIASTOLIC HEART FAILURE (DHF) 40% all CHF w /nml systolic Fxn - w/ diastolic dysfxn w/better prog than w/systolic dysfunction (Systolic dysfxn is often complicated by sig diastolic component) INCREASED DIASTOLIC FILLING PRESSURE FROM NON-COMPLIANT VENTRICLE: 1. enlarged heart reaches limits of pericardial expansion 2. hypertrophic myocardium stretches less than nml myocardium 3. Interstitial or regional fibrosis causes restricted diastolic filling Seen in Pts w/ -mild-moderate HTN or ischemic Heart Dz Dx of Diastolic Dysfunction: NO GOLD STD (Dx of Exclusion) 1. Maintain high index of suspicion 2. Consider complete CHF Dif-Dx 3. r/o systolic dysfxn: nml EF & size 4. ECHO: LVEF & heart size 122 5. Assessment of rate of diastolic filling & Г»rate of filling in both rapid phase & atrial contraction phase: w/worsening diastolic fxn, amt of filling from atrial contrac increases & ratio of filling from atrial contraction/rapid phase is > 1. (complicated by changes in preload, afterload, age, MR CAUSES OF CHF: 1. Restrictive diastolic filling: pericarditis & mitral stenosis 2. Myocardial Overload: MR & AS 3. Myocardial Dysfxn: MI, myocarditis or idiopathic cardiomyopathy TX: - No Dig: - No Afterload Reduction: assumes poorly fxning heart & won't improve CO *Cautious Diuresis: overdiuresis may lead to low output state from increased filling pressures for nml CO. -Ca+ blockers & ГЎ-blockers may improve fxn (particularly in IHSS) -Ca+ blockers may improve active relaxation & passive filling -ГЎ-blockers slow rate for increased filling time Systolic Dz: -Dig: Inotropy -Nitrates & diuretics: reduce Preload -ACEI's: reduce afterload Torsades Des Pointes (Polymorphic VT) stop 1a antiarrhythmics may use overdrive pacer or iv magnesium due to low mg, quinidine follow corrected q-t int: corrected for rate: q-t/square root of r-r IF UNSTABLE cardiovert + lidocaine + ISOPROTERONOL PULMONARY ARTERY CATHETERIZATION A. Description 1. Catheter is a flow directed, balloon tipped devise inserted through a large vein 2. Fed through Right Atrium into ventricle then "wedged" into the Pulmonary Artery (PA) 3. Wedging is accomplished by inflating a balloon at the end of the catheter. 4. Pressures are recorded with balloon inflated while catheter is inserted forward 5. Allows determination of R sided pressures, PA pressures, and "Wedge" pressure 6. The "wedge" pressure is approximately the pulmonary capillary pressure (hence "PCWP") 7. Generally, PCWP = LAEDP (end diastolic pressure) = LV filling pressure (LVEDP, see below) 8. Other Uses of PA Catheter a. Permits determination of oxygen consumption and cardiac output b. Pacing from atrial and ventricular sites c. Measurement of core body temperature d. Measurement of intracavitary potentials e. Infusion of medications and fluids B. Theoretical Pressure Tracing 1. Catheter is fed through a dilator-sheath device ("cordice") 123 2. This devise is usually inserted into the R-Internal Jugular, L-Subclavian, or femoral veins 3. Balloon is inflated when RA is reached a. Central venous pressure can be determined b. Catheter is further inserted with balloon up into the RV c. Arrhythmias are often seen (usually briefly) as tricuspid valve is passed 4. Once in the RV (note pressure tracing change), further advance into the pulmonary artery a. In the wedged, balloon-up position in PA, PCWP is determined b. The PCWP is used to estimate LV filling (see above) 5. Order of pressures is IVC/SVC (0-6cm) leads RA (0-8cm) leads to RV (20-25/6-12cm) leads to PA (20-25/10cm) leads to Wedge (6-12 cm) C. Indications 1. General Considerations a. Majority of patients are hypotensive and/or with low (or no) urine output b. Catheter is used to determine whether problem is with volume or heart pump function c. This will help guide volume manipulations and choice of vasopressor agents d. Especially useful in patients with >2 components of hypotension e. Thus, volume status and pump function are determined from catheter data 2. Complicated MI See Card "MI-Complications" a. Cardiogenic Shock b. Severe Left Ventricular Failure c. Right Ventricular (RV) Failure d. Acute Mitral Regurgitation e. Ventricular Septal Rupture f. Cardiac Tamponade g. Recurrent severe post-infarction ischemia 3. Respiratory Distress a. Severe respiratory dysfunction of any cause b. Adult Respiratory Distress Syndrome (ARDS) c. Cardiogenic or non-cardiogenic pulmonary edema d. Massive pulmonary embolism (PE) e. Toxic inhalations f. Mechanically ventilated patients, especially with high PEEP 4. Evaluation of specific causes of CHF a. Dilative Cardiomyopathy b. Constrictive vs. Restrictive Disease c. Pre-capillary pulmonary hypertension 5. High Risk Obstetric Patients a. Pre-existing Cardiac Disease b. Pre-eclampsia and Eclampsia c. Abruptio placentae 6. Multiorgan-System Failure Syndromes (MODS) a. Severe Sepsis b. Extensive Burns c. Pancreatitis d. Extensive Trauma e. Persistent low output syndrome 7. Shock a. Septic Shock b. Hypovolemic Shock c. Cardiogenic Shock d. RV Failure due to Pulmonary Embolism e. Cardiac Tamponade 8. Other Indications a. Acute Renal Failure for volume management b. Cirrhosis with ascites - volume management c. Post- and intra-operative open heart and other surgeries D. Limitations of PCWP and LVEDP Equivalency 1. PA inflated balloon pressure increase PCWP a. Increased PVR b. Heart Rate > ~120 beats per minute c. Veno-occlusive disease (VOD) 2. PCWP increase Pulmonary Venous Pressure a. Catheter tip location b. Severe hypovolemia c. PEEP 3. Pulmonary Venous Pressure increase LA Pressure a. Veno-occlusive disease b. Tumor venous occlusion 4. LA Pressure increase LVEDP a. Mitral Valve disease 124 b. Increased intrapleural pressure c. Aortic Valve disease d. Decreased LV compliance (with increased atrial systole) E. Complications of Swan-Ganz Catheter Placement 1. Arrhythmia 2. Complete heart block or R bundle branch block 3. Thrombosis 4. Infection 5. Pulmonary Infarction 6. Balloon rupture 7. Pulmonary artery rupture / hemorrhage 8. Cardiac Tissue injury 9. Catheter knotting F. Normal Values and Calculations 1. Cardiac Output (CO) a. Various methods for calculation b. Fick Method uses assumed oxygen consumption and is good for cardiac disease VO2i (=OCI) CI = -----------------------------------CaO2-CvO2 c. Thermodilution measures flow and is good in septic patients d. Normal value 3.0-7.0L/min, cardiac index (CI) 2.5-4.5 L/min/m2 (CI=CO/BSA) 2. Systemic Vascular Resistance (SVR) = (Mean SBP-CVP) Г· CO (nl 1000-1500 dyne/sec/cm2) 3. Pulmonary Vascular Resistance (PVR) = (Mean PAP-PCWP) Г· CO (nl 120-250 dyne/sec/cm2) 4. Mixed venous saturation can be obtained from blood sample during insertion / proximal port a. Normal MVO2 ~ 75% b. MVO2 is decreased in cardiogenic shock c. MVO2 is increased in septic shock (due to AV shunting and poor perfusion) 5. Stroke index = cardiac index/heart rate (nl 50-75ml/contraction) 125 Hemodynamic Examples H. Additional Notes and Waveforms 1. Acute Tricuspid Regurgitation a. Increased CVP, right atrial, and RV end diastolic pressures b. Blunted "X" descent, steep "Y" descent c. RA and RV pressures equalized 2. Constrictive Pericarditis a. Increased RA and PCW pressures b. Dip and plateau in RV pressure c. "M" or "W" shaped jugular venous pressures d. Preserved "X" and steep "Y" descents 3. Restrictive Cardiomyopathy a. PCWP may be higher than RA pressure b. Similar findings to constrictive pericarditis 4. Acute Ventricular Septal Rupture a. Reduced CO, increased SVR, tachycardia, hypotension b. Oxygen step-up from RA to RV and PA (due to Left to Right shunt 126 Swan Ganz Catheter Wave Forms 127 Goldman Multifactorial Cardiac Risk Index (MCRI) Variable S3 gallop or JVD MI in past 6 mos Rhythm other than sinus or PACs on last preop EKG Age >70 years 5 Emergency operation Intraperitoneal, intrathoracic, or aortic operation Suspected critical aortic stenosis Poor general medical condition K<3.0, HCO3<20, pO2<60 or pCO2>50, BUN>50 or Creat>3.0, abnormal LFTs, bedridden Points 11 10 7 4 3 3 3 Stage Points Risk of life threat complications/death I 0-5 0.7% / 0.2% II 6-12 5% / 2% III 13-25 11% / 2% IV >=26 22% / 56 HYPERTENSIVE CRISISNITROPRUSSIDE: Give 0.5-1.5 ug/kg/min to start with, then maintenance up to10 ug/kg/min. Add 50 mg of reconstituted sodium nitroprusside to 250 ml of either 5% dextrose in water or normal saline. The solution should be covered with an aluminum foil or paper bag to protect it from light. Nitroprusside has its onset of action within 3-5 min. It acts directly on vascular smooth muscle producing mostly arterial, and to a lesser extent, venous dilation. The heart rate (HR), cardiac output (CO) and extracellular fluid (ECF) all may increase or have no change. There is a decrease of systemic resistance (SVR). The pulmonary capillary wedge pressure (PCWP) will decrease or have no change. There will be an increase of the plasma renin activity (PRA), and angiotensin II (ANG II). SIDE EFFECTS: Side effects are cyanide and thiocyanate toxicity. Clinical signs of thiocyanate toxicity include headache, nausea and vomiting, tremulousness, confusion, drowsiness, psychosis and coma. Deaths due to cyanide poisoning are extremely rare. If the patient is given an infusion of nitroprusside for more than 24 hours, serum thiocyanate levels should be done daily. Concentration > 10 mg/dL are associated with toxicity; > 20 mg/dL could be fatal. Always monitor the renal status as thiocyanate is excreted via the kidney. Oral antihypertensives should be started as soon as possible; usually when the diastolic reaches 100 mm Hg. If needed hemodialysis is used for treating thiocyanate toxicity. Nitroprusside is indicated for hypertension associated with CNS events, CHF, and aortic dissection and hypertensive encephalopathy. LABETALOL: Use 20 mg IV over 2 minutes to start with by bolus. If a response is not seen, then double the dose q 10 min to a total of 300 mg. Onset of action is in minutes and lasts for 4-6 hours. A labetalol infusion may be prepared by adding 200 mg of labetalol (40 mL) to 160 mL of either 5% dextrose in water or normal saline. The infusion rate is 0.5 mg/min. This is then titrated to obtain the desired blood pressure. In most cases, hypertension is under control when labetalol is given at a dose of 2 mg/min. Infusion rates up to 4 mg/min may be used. There is a decrease or no change in the HR and CO. There is a decrease of the SVR. The PCWP and ECF may either increase or have no change. There is a decrease in both the PRA and ANG II. Labetalol is a sympatholytic agent and is unique in that there is both post synaptic non-cardioselective Beta blockade and Alpha1 blockade. Since there is an oral form, the patient can be switched to oral labetalol after BP is controlled. SIDE EFFECTS: There is a relative contraindication in patients with CHF, bradydysrhythmia, and bronchospastic lung disease. Watch for paradoxical hypertension that occasionally happens. Also, there may be orthostatic dizziness. Labetalol is useful in hypertensive encephalopathy, angina, renal failure, pheochromocytoma, antihypertensive withdrawal, and interactions between monamine oxidase inhibitors and drugs or food. PHENTOLAMINE: Give a test dose of 1 mg IV over 2 minutes. If there is no marked hypotension then give 5-10 mg (.1-.2 mg/kg IV) over the next 4 minutes. It can be given every 5-15 minutes. Phentolamine is useful in hyperadrenergic states such as pheochromocytoma, but has a very short half life and the BP will start to rise again in 10 minutes, at which time the phentolamine can be given in intermittent boluses or a drip of 100 mg/hr. Because of a reflex tachycardia, a beta blocker should be used. ENALAPRILAT (Vasotec): Start with 1.25 mg (1 ml of a 2 ml vial) given over a 5 minute period. Increase to 5-10 mg as needed, then give q 6 hours. The peak effect usually is seen in 30 minutes, but may not be until 4 hours. Hypotension is very infrequent but can be treated with fluids. Diuretics will enhance the effect. Enalaprilat has no effect on the HR but does cause a decrease in the SVR, PCWP, and ECF. The CO is increased. The PRA is increased and the ANG II is decreased. Enalaprilat is excreted primarily by the kidneys. Enalaprilat is useful in CHF. HYDRALAZINE: The initial dose is 10-20 mg IV ever 20 minutes as needed or 10-50 mg IM (onset of action in 30 minutes) every 6 hours IM. The peak effect occurs at about 60 minutes. If hydralazine is used as a continuous infusion, 200 mg of drug is added to 1 liter of 5% dextrose in water or normal saline, and infused at 0.2 mg/min initially, and subsequently titrated. The onset of action by continuous infusion occurs within 10 to 20 minutes. Peak effect is seen at 20-40 minutes with continuous infusion. Hydralazine should not be used in myocardial ischemia. It is most useful in pre-eclampsia and eclampsia. Hydralazine is a direct acting arterial vasodilator. It exerts little effect on the venous system. Reflex tachycardia, increased myocardial oxygen consumption and increased cardiac output are 128 the major effects. There is a decreased SVR and increase in PCWP and ECF. The PRA and ANG II are both increased. Hydralazine is metabolized primarily by the liver by acetylation. Some patients, genetically, are rapid acetylator and metabolize hydralazine rapidly, and therefore a more frequent dosing schedule may be needed. SIDE EFFECTS: Side effects include headache, palpitations, orthostatic dizziness and edema. There may be exacerbation of angina. Drug induced lupus erythematosus occurs rarely with parenteral administration and much more commonly with oral hydralazine. In this syndrome there may be rash, fever, arthralgias, arthritis, serositis, elevated sedimentation rate and antinuclear antibodies. NITROGLYCERIN: Nitroglycerine is given as an infusion of 5-100 ug/min by adding 50 mg/250 ml of 5% dextrose and water and then titrating to desired BP. Can give up to 300ug/min. Nitroglycerin is useful in myocardial infarction, pulmonary edema, and unstable angina. NIFEDEDPINE [FELT Contraindicated in HTN Crisis d/t risk of stroke!]: Can be given as 10 mg, and then biting and swallowing or sublingually. The peak effect is seen in 30-45 minutes. Nifedipine should be avoided in unstable angina or evolving MI as it may lower perfusion pressure. Nifedipine maintains or increases the cerebral blood flow. Nifedipine causes an increase or no effect in the cardiac output, and conduction in the sinoatrial node and atrioventricular node. There is an increase in the HR and coronary blood flow. There is a decrease or no change of myocardial contractility. There is a fairly marked decreased in PVR and an increase in sodium retention. There is a lack of a predictable response to nifedipine. The duration of response is 2-6 hours. CLONIDINE: Clonidine is given initially as .1-.2 mg orally followed by .1 mg/hr to a total dose of 0.6 - 0.7 mg over 6-7 hours. The onset of action is at 30-60 min and peaks at 2-4 hours. It does not cause reflex tachycardia and can be used in CHF and myocardial ischemia. It can be useful in hyperadrenergic states as cocaine toxicity, clonidine withdrawal, MAO inhibitors with tyramine ingestion and phenylpropanolamine. The major disadvantage is sedation. Therefore, it shouldn't be used in hypertensive encephalopathy, stroke, or subarachnoid hemorrhage. It can cause significant bradycardia and rebound hypertension if stopped abruptly. CAPTOPRIL: Give as a 25 mg tablet and onset will occur in 15 minutes and peak in 2-3 hours. There may be a precipitous drop if used in patients with CHF, scleroderma crisis, renovascular disease and those on diuretics and vasodilators. Lisinopril and enalapril have slower onsets and shouldn't be used when a rapid reduction is needed. It doesn't cause reflex tachycardia or salt retention. It will maintain cerebral blood flow. It is useful in malignant hypertension, CHF, renovascular and cerebrovascular disease. There is an increase in the CO and PRA and a decrease in SVR, PCWP, ECF and ANG II. Side effects are rash, agranulocytosis, and angioedema. MINOXIDIL: The initial dose is 5 mg with a repeat dose in 6 hours if needed. It should be used with a beta blocker and diuretic. It doesn't cause a rapid decrease in blood pressure and should not be used with CHF, myocardial ischemia or pheochromocytoma because of the reflex tachycardia. DIAZOXIDE: Diazoxide can be given at 50-150 mg (1-2 mg/kg) IV over a 5-10 second period, and can be repeated every 10-15 minutes as needed, or can be given as a 7.5-30 mg/min IV infusion. Diazoxide acts directly on vascular smooth muscle. There is an increase of HR, CO, PCWP, ECF, PRA and ANG II. There is a decrease in SVR. There is onset of action within 5 minutes and a peak effect within 3-5 minutes if given as an IV bolus. The duration of effect ranges from 4-12 hours. SIDE EFFECTS: The most serious effect is prolonged hypotension. This occurs less frequently when mini boluses are given rather than the full 300 mg given as a bolus. There may be palpitations and tachyarrhythmias and peripheral edema. It may produce hyperglycemia by inhibiting Beta islet cell function. If extravasation occurs there may be superficial thrombophlebitis, cellulitis and necrosis as diazoxide is very alkaline. TRIMETHAPHAN CAMSYLATE: Trimethaphan can be started as a .3 -.5 mg/min IV infusion by adding 500 mg in 500 ml of 5% dextrose in water and then titrating to the desired level. In most patients the hypertension is controlled by giving 1-4 mg/min. Trimethaphan is a ganglionic blocking agent and will decrease the HR, CO, SVR, PCWP and increase the ECF. SIDE EFFECTS: Trimethaphan can cause postural hypotension and patients should be kept at bed rest and may be placed in a 15 degree reverse Trendelenburg position to optimize the hypotensive effect. Other side effects include adynamic ileus, urinary retention and mydriasis. In very high doses of greater than 5 HYPERTENSIVE CRISIS AND SPECIFIC DRUG THERAPYMost hypertensive crisis can be controlled with the following drugs: Nitroprusside, labetalol, diazoxide, nimodipine, nitroglycerin, calcium antagonists, nicardipine and hydralazine. However, it is important that the appropriate drug be matched up with the condition producing the hypertensive crisis, and that certain drugs not be given as they may exacerbate the hypertension or underlying disease. In most cases hypertensive crisis can be defined as an elevation of the diastolic pressure greater than 120. However, this rule needs to be modified in some cases depending on whether the patient has had pre-existing hypertension or normal blood pressure. If a patient has had normal blood pressure in the past, and then suddenly develops a diastolic BP of 100-110 this rapid change could be disastrous. On the other hand, if a patient has chronic elevation of the BP and suddenly develops elevation of the diastolic pressure the results may not be as severe with diastolic pressures greater than 120 mm Hg. Hypertensive crisis usually affects patients that have pre-existing elevation of the BP. Blacks, smokers and men tend to be affected. Hypertensive crisis, to place it in perspective, will only occur in about 1-2% of those that have hypertension. 129 AORTIC DISSECTION: In this disease the blood pressure should rapidly be reduced to around 120/80 in order to reduce the shearing force and reduce the chance of further dissection. Aortic dissection is suspected if the patient has chest, back or abdominal pain associated with abnormal abdominal pulsation, aortic regurgitation, peripheral pulse deficits, and widening of the mediastinum on chest x-ray. Aortic dissection of the ascending aorta is a surgical emergency whereas dissection beyond the left subclavian artery is treated medically. MRI, transesophageal echocardiography, CT and angiography all have been used for diagnosis. Recently MRI and transesophageal echocardiography have emerged as the procedures of choice. DRUGS USED IN AORTIC DISSECTION: Beta blockers plus nitroprusside or trimethaphan, OR labetalol used alone. Avoid hydralazine and diazoxide. SUBARACHNOID HEMORRHAGE: Subarachnoid hemorrhage may be due to rupture of a berry aneurysm or an arteriovenous malformation. Reduction of BP in the face of subarachnoid hemorrhage is somewhat controversial because of possible induction of cerebral spasm. However, if the BP is severely elevated, a cautious, slow reduction over several hours may be attempted to reduce the pressure to around 170/100 or 20% of the patient's BP. Nimodipine is now standard therapy in subarachnoid therapy as it has been shown to reduce death, disability and the vegetative state by about 40%. Nimodipine will help reduce the cerebral spasm, but in the recommended oral dose, the BP is not significantly lowered. DRUGS USED IN SUBARACHNOID HEMORRHAGE: Nimodipine: 60 mg po QID for 21 days. Start within 96 hours of the subarachnoid hemorrhage. Nitroprusside and labetalol may be used. Avoid beta blockers, diazoxide, clonidine, and methyldopa. ISCHEMIC STROKE: The same precautions for reduction of hypertension in ischemic stroke should be followed as for subarachnoid hemorrhage because decreases can precipitate decreased cerebral perfusion. Reduce slowly and by about 20%. DRUGS USED IN ISCHEMIC STROKE: Nitroprusside and labetalol. Avoid diazoxide, methyldopa, clonidine and beta blockers. INTRACEREBRAL HEMORRHAGE: Treatment should only be given if the BP is exceedingly high such as greater than 200/130. The outcome prognosis is usually poor with intracerebral bleeds and treatment doesn't usually change the course. TREATMENT FOR INTRACEREBRAL HEMORRHAGE: Treat with Labetalol or nitroprusside only if BP is greater than 200/130. Otherwise, no treatment is required. ISCHEMIC HEART DISEASE OR MYOCARDIAL INFARCTION: An effort should be made to decrease peripheral vascular resistance, sympathetic activity and increase coronary perfusion which will in turn decrease oxygen demands and wall tension. TREATMENT OF ISCHEMIC HEART DISEASE AND MYOCARDIAL INFARCTION: Nitroglycerine is the drug of choice and should be given IV, titrated to reduce the ischemic pain and/or reduction of diastolic BP to 100 mm Hg. Labetalol given IV as well as calcium channel blockers may also be used as they will favorably influence the BP. Nitroprusside should be reserved for those that are refractory to the above measures. Avoid hydralazine and diazoxide. LEFT VENTRICULAR FAILURE: Treatment of left ventricular failure associated with a hypertensive crisis should be treated with drugs that will reduce preload and or afterload. TREATMENT USED IN LEFT VENTRICULAR FAILURE: Nitroprusside and nitroglycerin are the drugs of choice. Avoid beta blocker and labetalol. HYPERADRENERGIC STATES : Hyperadrenergic states can be caused by cocaine overdose, pheochromocytomas, clonidine withdrawal and amphetamines. All of these conditions can cause arrhythmias and myocardial ischemia. TREATMENT USED IN HYPERADRENERGIC STATES: Phentolamine, labetalol, and nitroprusside are the drugs of choice. Reinstitution of clonidine is used for clonidine withdrawal. ECLAMPSIA: TREATMENT FOR ECLAMPSIA: Hydralazine, magnesium sulfate, labetalol and calcium antagonists. Avoid diuretics, ACE inhibitors, and trimethaphan. POST-OPERATIVE HYPERTENSION: TREATMENT FOR POST-OPERATIVE HYPERTENSION: Labetalol, nitroglycerin, nitroprusside, nicardipine. Avoid trimethaphan. and ACUTE RENAL INSUFFICIENCY: TREATMENT FOR ACUTE RENAL INSUFFICIENCY Labetalol, nitroprusside, and nicardipine. Avoid beta blockers and trimethaphan. SPECIFIC DRUGS: Propranolol (Inderal): Give a loading dose of 1-10 mg, then 3 mg/hour IV followed by 80-640 mg/day orally in divided doses. Nitroprusside (Nipride): 0.25-10 ug/kg/min IV with titration to desired BP. (Add 50 mg to 250 ml of D5W). Trimethaphan camsylate (Arfonad): Give 2-4 mg/min IV infusion. (Add 500 mg to 500 ml D5W). Labetalol (Trandate): Give 20 mg IV bolus (0.25 mg/kg), then 20-80 mg boluses IV 130 every 10 minutes and titrate to desired BP. (maximum of 300 mg). For infusion give 0.5-2 mg/min. (max 300 mg/day). Follow orally with 100-400 mg po BID. Magnesium sulfate: Give 1-2 grams (2-4 ml) 50% solution (8-16 mEq) IV bolus over 5-15 minutes. For infusion drip, add 2 grams of Magnesium sulfate to 250 ml of D5W and drip at 3-20 mg/min. Start at 10 mg/min or 75 ml/hour. Hydralazine (Apresoline): 10 mg IV every 20 minutes prn to keep diastolic below 100. Nicardipine: 20 mg tid initially po. Maximum of 120 mg daily. Nicardipine SR (Cardene): 30-60 mg bid. Nitroglycerin: 5100 ug/min IV, titrated to desired BP up to 300 ug/min. Add 50 mg of nitroglycerin to 250 ml of D5W. Nimodipine: 60 mg QID for 21 days. Diazoxide: 50-150 mg IV over 5-10 seconds, repeat every 10 minutes as needed or give infusion at 7.5-30 mg/min IV. Phentolamine (Regitine): Give 5-10 mg IV and repeat as needed up to 20 mg. Clonidine (Catapres): Give .2 mg po initially, Hypertensive Emergencies Lancet 2000; 356: 411 вЂ“ 417 A hypertensive emergency is a situation in which uncontrolled hypertension is associated with acute end-organ damage. Most patients presenting with hypertensive emergency have chronic hypertension, although the disorder can present in previously normotensive individuals, particularly when associated with pre-eclampsia or acute glomerulonephritis. The pathophysiological mechanisms causing acute hypertensive endothelial failure are complex and incompletely understood but probably involve disturbances of the renin-angiotensin-aldosterone system, loss of endogenous vasodilator mechanisms, upregulation of proinflammatory mediators including vascular cell adhesion molecules, and release of local vasoconstrictors such as endothelin 1. Magnetic resonance imaging has demonstrated a characteristic hypertensive posterior leucoencephalopathy syndrome predominantly causing oedema of the white matter of the parietal and occipital lobes; this syndrome is potentially reversible with appropriate prompt treatment. Generally, the therapeutic approach is dictated by the particular presentation and end-organ complications. Parenteral therapy is generally preferred, and strategies include use of sodium nitroprusside, Гџ-blockers, labetelol, or calcium-channel antagonists, magnesium for preeclampsia and eclampsia; and short-term parenteral anticonvulsants for seizures associated with encephalopathy. Novel therapies include the peripheral dopamine-receptor agonist, fenoldapam, and may include endothelin-1 antagonists. Causes of hypertensive emergencies Essential hypertension Renal parenchymal disease Acute glomerulonephritis Vasculitis Haemolytic uraemic syndrome Thrombotic thrombocytopenic purpura Renovascular disease Renal-artery stenosis (atheromatous or fibromuscular dysplasia) Pregnancy Eclampsia Endocrine Phaeochromocytoma Cushing's syndrome Renin-secreting tumours Mineralocorticoid hypertension (rarely causes hypertensive emergencies) Drugs Cocaine, sympathomimetics, erythropoietin, cyclosporin, antihypertensive withdrawal Interactions with monoamine-oxidase inhibitors (tyramine), amphetamines, lead intoxication Autonomic hyper-reactivity 131 Guillain-BarrГ© syndrome, acute intermittent porphyria Central-nervous-system disorders Head injury, cerebral infarction/haemorrhage, brain tumours End organ Aorta 132 Complications Therapeutic considerations Aortic dissection Гџ-blockade, labetalol (decrease dp/dt), sodium nitroprusside with Гџ-blockade, avoid isolated use of pure vasodilators Brain Hypertensive Avoid centrally acting antihypertensive drugs encephalopathy such as clonidine Cerebral infarction Avoid centrally acting agents; avoid rapid or haemorrhage decreases in blood pressure Heart Myocardial ischaemia Intravenous glyceryl trinitrate, Гџ-blockade Myocardial infarction Diuretics and ACE inhibitors useful, ГџHeart failure blockers with caution Kidney Renal insufficiency Diuretics with caution, calcium antagonists useful Placenta Eclampsia Hydralazine, labetalol, calcium antagonists useful; avoid sodium nitroprusside dp/dt=change in pressure/change in time. Table 1: End-organ complications of hypertensive emergencies Drug Sodium Dose 0В·25-10 Вµg kg1 min1 Onset Duration Adverse effects Hypotension, Immediate 1-2 min nausea, nitroprusside * Labetalol Hydralazine vomiting, cyanate 20-80 mg bolus (every 10 min) 2 mg/min infusion 10-20 mg bolus 5-10 min 2-6 h 2-6 h 10-15 Fenoldopam 0В·1-0В·6 Вµg kg1 min1 5-10 min min Glyceryl trinitrate Enalaprilat 5-100 Вµg/min Nicardipine 2-10 mg/h 10 min 1-3 min 1В·25-5В·00 mg bolus 15 min toxicity Nausea, vomiting, heart block, bronchospasm Reflex tachycardia Hypotension, headache 5-15 min Headache, vomiting 4-6 h 5-10 min 2-4 h Hypotension, renal failure Reflex tachycardia, flushing Reflex tachycardia Phentolamine 5-10 mg/min 1-2 min 3-5 min *Risk of toxic effects in patients with renal impairment. Table 2: Commonly used parenteral antihypertensive drugs PERICARDITISCOMMON CAUSES OF PERICARDITIS: 133 Most causes are idiopathic or due to a viral infection. Most cases can readily be diagnosed in the clinical setting. For instance, if a patient has a malignancy and develops pericarditis, there is a possibility of metastatic disease to the pericardium. In a young healthy person, viral or idiopathic would be suspected. Pericarditis that develops a few weeks after cardiac surgery could be due to post-pericardiotomy syndrome. Pericarditis in a uremic patient could be due to advanced kidney disease. VIRAL: Viral pericarditis can be caused by echovirus, Coxsackie, adenovirus, mumps, varicella, mononucleosis, hepatitis and AIDS. Males under the age of 50 are the most susceptible to viral etiologies. Confirmation may be obtained by rising viral titers in paired sera. Cardiac enzymes may be slightly elevated. Pericarditis usually starts after an upper respiratory infection. Indomethacin 100-150 mg/day in divided doses or ASA 650 mg QID is usually effective, but if not, prednisone may be added. Most cases will resolve after a few days to weeks. However, there may be recurrences and rarely this may cause constrictive pericarditis. Tamponade occurs in < 5%. TUBERCULOUS: Tuberculous pericarditis is rare in the USA. Associated clinical involvement of the lungs may be absent, but pleural effusions are common. The patients may have fever, fatigue, night sweats with a subacute presentation for days to months. Spread is usually by lymphatics or hematogenous. The effusions are usually small or moderate. Pericardial biopsy has a higher yield than pericardiocentesis fluid and diagnosis may be made at another site of involvement. Patients usually respond to standard anti-tuberculous pharmacologic therapy, but constrictive pericarditis may be a sequela. MALIGNANT: Common causes of neoplastic pericarditis include carcinoma of the breast and lungs, renal carcinoma, leukemia, lymphomas, Hodgkin's disease and melanoma. Neoplastic pericarditis is a common cause of pericardial tamponade and frequently is painless, but presenting with hemodynamic consequences. Diagnosis is by cytologic exam of the pericardial effusion and/or pericardial biopsy, which may be difficult if the patient has had mediastinal radiation within the last year. CT and MRI may be of some benefit in visualizing proximal tumor. Once the patient has malignant invasion of the pericardium, the prognosis is very poor with only a few surviving for a year. Palliation can be achieved by drainage, followed by instillation of chemotherapeutic agents or tetracycline in an effort to reduce recurrence of fluid accumulation. Partial pericardiectomy may be of some benefit while pericardial windows are rarely helpful. Be careful not to assume that the cause is neoplastic in a patient that has cancer, as radiation, infection and autoimmune disorders may be instrumental. Rarely, mesotheliomas are causative. RADIATION: Radiation for neoplastic disease may present months or years after radiation. The patients may present as acute, or subacute pericarditis or constrictive pericarditis due to fibrinous and scar formation of the pericardium as well as the myocardium, conducting system and coronary arteries. Radiation pericarditis usually develops if there is more than 4000 cGy delivered to ports including more than 30% of the heart. POST MI AND DRESSLER'S SYNDROME: Dressler's syndrome is probably an autoimmune disease. It occurs weeks to months after open heart surgery or MI, and can be recurrent. The sedimentation rate is elevated, there is leukocytosis, pain, malaise, and fever, and pleural effusions. The pericardial effusions tend to be large and tamponade is rare after MI, but not so in postcardiotomy pericarditis. Treatment is with NSAIDS and corticosteroids. Pericarditis accompanying MI usually occurs 2-5 days post MI. Large effusions are rare. Differential from progressive ischemic changes may be difficult as evolutionary repolarization changes of the pericarditis may simulate ischemic changes. There is usually a rub. Spontaneous resolution usually occurs after a few days. NSAIDS or ASA will help the pain. ACUTE BACTERIAL INFECTION: Staphylococcus, pneumococci, streptococci, Legionella, Neisseria gonorrhoeae, Neisseria meningitidis. INFLAMMATORY DISEASE: SLE, rheumatoid arthritis, scleroderma, polyarteritis nodosa, amyloidosis, sarcoidosis, acute rheumatic fever, and inflammatory bowel disease. DRUGS: Procainamide, hydralazine, isoniazid, phenytoin, dantrolene, phenylbutazone, methysergide and cyclophosphamide. CARDIAC TAMPONADECardiac tamponade occurs when ventricular and atrial filling are compromised by increased intrapericardial volume and pressure, with subsequent decreased cardiac output and hypotension. Pericardial effusions may be due to fungal infections, TB, malignancy, trauma, thyroid disease, autoimmune diseases, acute and chronic renal failure, aortic dissections, endocarditis and in postcardiac surgery. Echocardiography can ascertain if there is pericardial effusion and/or tamponade. Tamponade criteria include right ventricular diastolic or right atrial systolic collapse, swinging heart, respiratory variation in the left and right ventricular chamber sizes and right atrial indentation. Confirmation of these findings may be necessary by inserting a balloon flow directed pulmonary artery catheter and determining equalization of right atrial, left atrial and ventricular end-diastolic pressures. Ancillary bedside findings of a pulsus paradoxus (augmented respiratory variation in the pulse pressure of greater than 10 mm Hg), along with distended neck veins, dyspnea, orthopnea, tachycardia, tachypnea, decreased heart sounds and hypotension are usually present. Electrical alternans on ECG, and water bottle cardiomegaly may also be present. 134 TREATMENT: The first line of treatment is fluid loading and dopamine in order to stabilize the patient until pericardiocentesis can be accomplished which is essential for treatment and diagnosis. Under echocardiographic, fluoroscopic or electrocardiographic guidance, an intrapericardial catheter should be introduced using the Seldinger method. Having a tube in place for at least 24 hours will allow drainage of large effusions, and provide access for instillation of chemotherapeutic, sclerosing or anti-infective agents. In patients that have malignant effusions from lung cancer, breast cancer, melanoma, leukemia, lymphoma or Hodgkin's disease, sclerotherapy with bleomycin, tetracycline or fluorouracil may decrease the recurrence of tamponade. If the patient has a life expectancy of > 6 months or the effusion cannot be controlled with sclerosis, pericardiectomy may be indicated. Open surgical drainage has the advantage of a generous biopsy sample, lysis of adhesions for loculated fluid and less danger of laceration of a coronary artery or muscle. Hemodialysis patients are treated by increasing the frequency of dialysis or pericardiocentesis and triamcinolone instillation. AORTIC DISSECTIONAortic dissection occurs when there is a tear in the aortic intima. The etiology of this tear may be degenerative changes in the smooth muscle and elastic tissue of the media. Sometimes there is associated cystic medial necrosis. Hypertension is the most common cause of medial degeneration, and about 66% of patients will have hypertension. The peak age for hypertension depends on the etiology, but in general is in the 6th and 7th decade. Patients that have proximal dissections tend to be somewhat younger. Approximately 60% of patients have intimal tears in the proximal ascending aorta. Males predominate in a ratio of 3:1. Marfan's syndrome as a cause of aortic dissection commonly presents in the 3rd and 4th decade. Other causes of aortic dissection include Marfan's and Ehlers-Danlos syndromes, Turner's syndrome, relapsing polychondritis, coarctation of the aorta, bicuspid aortic valves, patent ductus arteriosus, arteriosclerosis, trauma, and injury from arterial catheterization and other vascular procedures such as cross clamping injuries. As the tear progresses the media is separated from the adventitia with production of a false channel which extends distally, and to a lesser extent proximally. The proximal dissection will produce incompetency of the aortic valve. Distal dissections may occlude vital tributaries of the aorta with symptoms contingent upon the vessels that are compromised. The most common site of origination of the tear is within about 5 cm of the aortic valve, and in the descending aorta near the ligamentum arteriosum and just distal to the origin of the left subclavian artery. Rupture may occur into the pericardial cavity or left pleural space and produce mortality. Without treatment 90% will be dead in 3 months. If the patient is fortunate enough to be treated 60% of those that are released from the hospital after treatment will be alive 5 years later, and 40% 10 years later. CLASSIFICATIONS OF DISSECTIONS: Aortic dissections are considered acute if they are less than 2 weeks or chronic if > 2 weeks. There are two main systems used for classification. The DeBakey system has been in place for many years and reflects the site of the intimal tear while the Stanford University system does not address the site of the tear, but only involvement of the ascending aorta. In the Stanford type A tear, all ascending aorta tears are addressed, and type B dissections address all tears that do not involve the ascending aorta. In the DeBakey classification there are 3 types of dissection. Type I starts in the proximal aorta and extends beyond the brachiocephalic tributaries. Type II originates at the same place but is confined to the ascending aorta. Type III originates in the descending thoracic aorta just beyond the origin of the left subclavian artery. CLINICAL: Patients present with sudden pain that has been described as ripping or tearing and is excruciating. There is no crescendo tempo to the pain. The pain is maximal at the start. If the dissection is proximal, the pain tends to be in the anterior chest, while pain in the back in the interscapular area suggests a distal dissection. As the dissection extends, the initial pain will migrate to another area. This can be an important diagnostic feature. Other symptoms depend on the tributaries that are occluded. Some may develop myocardial infarction, stroke, or paraparesis. There may be pain in an arm due to ischemia or there may be abdominal pain secondary to mesenteric insufficiency or infarction. Syncope may be caused by rupture into the pericardium producing tamponade. Congestive heart failure may develop secondary to severe aortic regurgitation. If blood flow is interrupted to the kidneys there is renal dysfunction and further elevation of the blood pressure due to excessive renin release from the ischemic kidney. Physical exam may reveal the BP to be elevated with a difference in BP between the arms. There may be jugular vein distention, pericardial friction rub and pulsus paradoxus suggesting rupture into the pericardium. Other patients may present with hypotension, become clammy and complain of chest pain simulating a myocardial infarction. Hypotension suggests rupture into the 135 peritoneal cavity, cardiac tamponade or pleural space. Check the femoral and brachial pulses as a decrease in these will reflect a distal aortic dissection. About 16% of patients with distal dissections will have diminished or absent pulses. About 50% with proximal dissections will have diminished pulses. Check the brachiocephalic branches for dissection of the proximal ascending aorta. Aortic regurgitation associated with proximal dissection occurs in about 2/3 of cases. This will produce a diastolic murmur. If the aortic regurgitation is severe, as well as acute, the murmur may be difficult to hear, and the patient may develop congestive heart failure. LABORATORY: The patient may have an elevated LDH, bilirubin and anemia secondary to hemolysis of the RBCs in the false lumen of the aorta. The BUN and creatinine may be elevated if there is compromise of the renal blood flow to the kidneys. If the dissection extends into the coronary arteries there may be EKG, and enzyme changes secondary to myocardial infarction. The AST and CK are usually normal unless there is a concomitant myocardial infarction. A precise diagnosis must be made before thrombolytic therapy is given for a myocardial infarction. The chest x-ray will demonstrate widening of the aorta in about 90% of cases. There may also be displacement of an aortic plaque of 5-10 mm or more. If there is rupture into the pericardium, the heart may be enlarged. There may be a left pleural effusion. IMAGING PROCEDURES: TRANSESOPHAGEAL ECHOCARDIOGRAPHY (TEE) has a specificity of 90% or greater and a sensitivity of almost 100%. It can be done fairly rapidly, is portable, can show the status of the coronary arteries and can demonstrate aortic regurgitation. A typical exam can be done in about 15 minutes. At the present time with the new multiplane probe, images can be imaged in the transverse and longitudinal planes and various in-between planes. TEE can show the true and false lumens and the intimal flap as well as the branch vessels and thrombi in the false lumen. Pericardial effusions may also be detected. With the advent of the multiplane probe, false positive intimal flaps have been eliminated to a large degree. Transthoracic echocardiography has a sensitivity at the best of about 85% and a 63-96% specificity. It is best for detection of ascending aorta dissection. MAGNETIC RESONANCE IMAGING has a sensitivity and specificity of 99%. However, it can not be used in an emergent situation because it is too time consuming. It also is not available at all institutions and is very expensive. Intravenous contrast is not needed which is an asset if there is renal compromise or allergies. The true and false lumens are visualized. The intimal flap is best seen when the blood flow is rapid. Secondary signs of aortic dissection may be seen as widening of the aorta and thickening of the aortic wall. If cine-MRI is used, aortic regurgitation can be diagnosed with correlation paralleling Doppler studies. However, utilizing cine-MRI will extend the imaging time by another 15-30 minutes so that the total time of imaging can be over an hour. This is unacceptable in acute unstable aortic dissections. Disadvantages include the inability to visualize branch vessels and coronary arteries. MRI cannot be used in patients with mechanical prosthetic valves, metal implants, surgical clips or pacemakers. COMPUTED TOMOGRAPHY has a sensitivity of about 90% and specificity of 95%. Most institutions now have CT machines. It can demonstrate both the true and false lumens and flap. False positives can occur due to motion and streak artifacts, and false negatives may occur due to insufficient contrast in the false lumen. It is non-invasive but does require intravenous contrast agents. Branch vessels and coronaries are not visualized. AORTOGRAPHY is mandatory if surgical therapy is planned. It will define the origin and extent of the dissection, the magnitude of aortic regurgitation, and involvement of the branches of the aorta and any coronary occlusion. It has a sensitivity of 90% and specificity of 95%. It is invasive, requires contrast and is somewhat time consuming. TREATMENT: For dissections of the proximal aorta, surgery is usually required while distal aortic dissections are treated medically. Patients should have intra-arterial catheters inserted for blood pressure monitoring. Pulmonary artery catheters also are helpful, monitoring for pulmonary edema and volume changes due to dissection and rupture. The goal in medical treatment is to reduce the systemic blood pressure and the rate of pressure change in the aorta (dP/dT). The systolic blood pressure should be reduced to around 120 mm Hg. The combination of sodium nitroprusside and propranolol is a useful combination. Nitroprusside should not be used alone because it can increase the dP/dT initially. Nitroprusside is prepared by adding 50 mg in 250 ml of 5% D5W with a starting drip rate of 25ug/min and then titrating to the desired BP level. Propranolol may be given at .5-1 mg every 3-5 minutes to a total of .15 mg/kg or until the pulse slows to around 60 beats/min. IV labetalol can also be used with nitroprusside. The dose is 10-20 mg initially and then 20-40 mg every 15 minutes until the BP is controlled. The total dose should not be greater than 300 mg. Additional doses of labetalol in the same range may be given prn every 4-8 hours. Constant infusions of labetalol can also be used by giving the drug at 1-2 mg/min. Other 136 beta blocker alternatives that can be used are esmolol, metoprolol and atenolol. If patients are not candidates for beta blockers because of congestive heart failure, bradycardia, heart block, asthma or left ventricular systolic dysfunction, calcium channel blockers, and nifedipine may be used. Verapamil may be given at .05-.1 mg/kg IV and nifedipine 10-20 mg sublingually every 2-4 hours. Trimethaphan camsylate may be used alone at a dose of 1-5 mg/min IV. It is initially effective, but tachyphylaxis may rapidly develop. Furthermore, blurred vision, urinary retention and ileus are side effects. SURGERY is usually indicated in acute dissections of the ascending aorta. Complications as stroke and myocardial are not absolute contraindications for surgery. Unless there is dissection into branch vessels or impending rupture, dissections of the aortic arch and distal aorta are treated medically. The mortality associated with aortic dissection is about 15%. The dissected portion of the aorta is excised with reconstitution of the aorta with a synthetic graft. If there is significant aortic regurgitation, valve replacement should be done. All patients, whether they are initially treated with surgery or by medical means, should be chronically treated with a combination of beta blockers or calcium antagonists plus an ACE inhibitor. Hydralazine, minoxidil or beta blockers that possess intrinsic sympathomimetic properties, as acebutolol or pindolol, should not be used. All patients should be followed for any recurrence of dissection, aneurysmal development or progressive aortic valve insufficiency. SYNCOPECARDIOVASCULAR CAUSES OF SYNCOPE: COMMON: 1....Aortic stenosis 2....Arrhythmia - slow or fast 3....Carotid sinus hypersensitivity 4....Drugs 5....Low cardiac output with cardiomyopathy 6....Neurally mediated 7....Orthostatic hypotension 8....Vasovagal UNCOMMON: 1....Atrial myxoma 2....Cardiac tamponade 3....Congenital lesions as tetralogy of Fallot, EisenmengerвЂ™s complex. 4....Obstructive hypertrophic cardiomyopathy 5....Primary pulmonary hypertension 6....Pulmonary stenosis CAUSES OF ORTHOSTATIC HYPOTENSION: COMMON: 1....Decreased circulating volume as bleeding, dehydration, fever, widespread burns, pregnancy, diabetes insipidus, hemodialysis 2....Deconditioning 3....Drugs UNCOMMON: 1....Autonomic nervous system dysfunction as: 2....Bradbury Eggleston syndrome (sympathetic dysfunction in older men) 3....Shy-Drager syndrome 4....Riley Day syndrome 5....Alcoholic or diabetic neuropathies 6....Subacute combined sclerosis 7....Tabes dorsalis 8....Spinal cord disease or trauma 9....Adrenal insufficiency 10...Pheochromocytoma 11...Amyloidosis DRUGS THAT COMMONLY CAUSE SYNCOPE: 1....Antidepressants 2....Antihypertensives 3....Beta blockers 4....Calcium channel blockers 5....Cardiac glycosides 6....Nitrates 7....Phenothiazine derivatives 137 8....Diuretics 9....Antiarrhythmics - causes proarrhythmia 10...Antidepressants - causes arrhythmias 11...Cardiac glycosides - causes arrhythmias 12...Phenothiazine--causes arrhythmias TREATMENT OF REFRACTORY ORTHOSTATIC HYPOTENSION: 1....Atrial pacing 2....Caffeine 3....Clonidine 4....Diet high in sodium 5....Fludrocortisone acetate(Florinef) 6....Indomethacin 7....Elastic stockings 8....Monoamine oxidase inhibitors 9....Inderal CARDIAC WORKUP FOR SYNCOPE: 1....CAROTID SINUS MASSAGE - Put in an IV line in place and continuous EKG monitoring and appropriate medication such as atropine sulfate should be available. Response may be slowing of the heart (cardioinhibitory) or fall in BP (vasodepressor response) or a combination of the two. One half seconds of pressure per side should be done. Only unilateral pressure should be applied. An abnormal response is 5 seconds or more of ventricular asystole or a fall in systolic BP of more than 30 mm Hg. 2....EKG - look for arrhythmias, left ventricular hypertrophy as in hypertension or aortic stenosis, previous MI that may predispose to arrhythmias, prolonged QT interval and WPW. 3....HOLTER - The diagnostic yield is low. 4....ECHO - Look for valvular lesions, poor contraction, and pericardial effusion. 5....EXERCISE STRESS - Look for a positive test for ischemia. 6....SIGNAL AVERAGED EKG - This test is most useful for assessing the possibility of ventricular tachycardia in a patient with coronary artery disease. A high percentage of patients with sustained VT or subsequent sudden cardiac death show late potentials on the surface EKG. It has a high sensitivity but low specificity. It is most useful when used in patients with known organic heart disease in whom the absence of late potentials makes significant ventricular arrhythmias unlikely as a cause of syncope. 7....ELECTROPHYSIOLOGIC STUDY - is expensive and is invasive and uncomfortable and may result in complications. It should be used only when a complete noninvasive workup is unrevealing. 8....TILT TABLE TESTING - Beta blocker, Norpace, Transderm or dual chamber cardiac pacing have been used with varying degrees of success. a....Head up tilt testing should be done in young patients who have no history of cardiac disease initially. In older patients LV function should be assessed by echo or radionuclide isotope imaging. Echo can also identify LV outflow obstructive syndromes. Head up tilt testing will identify patients that have neurocardiogenic dysfunction. b....Head up tilt test - Patients lie on a tilt table that has a footboard for support. The head of the table is elevated to 70 degrees from horizontal. They remain in this position for 15 minutes during which arterial pressure and EKG leads are monitored continuously. If syncope occurs the test is discontinued. If after 15 minutes there is no syncope the table is placed in the horizontal position and infusion of Isoproterenol is started to raise the heart rate by 20% over the baseline. The table is then placed in 70 degrees for another 15 minutes. c....If the head up tilt test is negative then an electrophysiologic study should be done to evaluate sinus node dysfunction, AV conduction abnormalities, supraventricular tachycardia and rarely ventricular tachycardia. Supraventricular tachycardia remains an important cause of syncope in young patients with or without evidence of overt ventricular preexcitation. d....If the patient has had an old myocardial infarction, or has Q waves on EKG from previous MI or has LV ejection fraction less than 40 % then ventricular tachycardia must be ruled out if the patient has syncope. A signal averaged electrocardiogram may be useful. If this reveals abnormalities then electrophysiologic studies to induce ventricular tachycardia is higher. Twenty four hour ambulatory Holter monitoring has a low yield for detection of arrhythmic syncope. e....Get potassium and magnesium levels as these can precipitate ventricular tachycardia, as can transient myocardial ischemia, orthostatic hypotension, LV outflow obstruction, antihypertensives, vasodilator therapy or autonomic dysfunction. TREATMENT OF CARDIAC SYNCOPE: 1....Patients with sinus node dysfunction or AV block do well with permanent pacing. In selected cases, radiofrequency modification and ablation may help supraventricular tachycardia arising in the AV junction. Flecainide and Encainide are the most effective drugs. However, class I agents are useful. 2....For ventricular tachycardia, class I and III, catheter or surgical ablation and implantation of an automatic cardioverter defibrillator may be used. 138 3....For Neurocardiogenic dysfunction, drugs that decrease the force of myocardial contraction as beta blockers and disopyramide (Norpace) are helpful. Beta blockers are the best. To predict the efficacy of oral beta blocking agents head up tilt testing sessions after treatment with IV Esmolol (Brevibloc) are useful. Oral theophylline and Transderm-Scop may also be helpful. SYNCOPE CAUSESCardiovascular: carotid sinus syncope, vasodepressor syncope, aortic, mitral and pulmonary stenosis, pulmonary hypertension, myxoma, hypertrophic cardiomyopathy, tetralogy of Fallot, neurocardiogenic, arrhythmic, structural abnormalities, cardiovascular drugs, postural hypotension, brain stem ischemia, cardiac tamponade, pulmonary embolism, aortic dissection, brady and tachyarrhythmias, pump failure due to myocardial infarction and cardiomyopathy. Neurologic diseases: cerebrovascular disease, seizures, trigeminal and glossopharyngeal neuralgia, autonomic neuropathies. Psychiatric disorders: panic disorder, hysteria, orthostatic hypotension, drug induced syncope, metabolic and endocrine disorders, hypovolemia, hypoglycemia, hyperventilation. SYNCOPE- CARDIAC SYNCOPE: The most common cause of obstructive stenosis is aortic valvular stenosis. However, other causes would include hypertrophic cardiomyopathy which is typically exertional, but can be due to arrhythmia or conduction system disease. Primary pulmonary hypertension and severe pulmonic stenosis are occasionally associated with effort syncope. Tetralogy of Fallot and other cyanotic congenital heart defects with right to left shunting and pulmonary hypertension and/or right ventricular outflow obstruction also can cause exertional syncope. Left atrial myxomas may occur with change of position secondary to obstruction of the mitral orifice by the mass. Thrombosis of a prosthetic valve may cause sudden obstruction and syncope. Arrhythmic syncope should be a concern if there are palpitations, and underlying cardiac disease. Advanced or high degree AV block is the most common arrhythmia causing syncope as the Stokes-Adams syndrome. Most of these defects involve the His-Purkinje system post MI or in the elderly. The ECG may demonstrate various combinations of fascicular block. Heart block may also be caused by drugs such as digitalis, calcium blockers and beta blockers. Ventricular tachycardia and fibrillation, and prolonged QT interval may degenerate into torsades de pointes causing syncope. The Romano-Ward syndrome is associated with a prolonged QT interval, as well as the JervellLange-Nielsen syndrome which also has associated congenital deafness. Supraventricular arrhythmias may be associated with the sick sinus syndrome that is prevalent postoperatively in congenital heart diseases or the elderly. Paroxysmal atrial tachyarrhythmias may cause syncope, particularly in the elderly with associated cerebrovascular disease. Occasionally, young patients without structural heart disease will develop syncope due to polymorphic ventricular tachycardia. Patients with acute myocardial infarction present with syncope in about 5-10% of patients, usually with Q wave inferior infarctions. EVALUATION: The resting ECG may provide clues to the cause of the syncope. A prolonged QT interval may be associated with polymorphic ventricular tachycardia. Q waves may represent an old MI with related ventricular arrhythmias or hypertrophic cardiomyopathy that may also cause ventricular arrhythmias. A bifascicular block might indicate the patient has developed bradycardic syncope. Other findings as Wolff-Parkinson-White, atrial and ventricular ectopy may be a clue. Cardiac monitoring will only reveal the cause in about 15% of cases. Patient activated recorders may be helpful. Echocardiography can diagnose aortic stenosis, hypertrophic cardiomyopathy and atrial myxoma. Exercise testing for exertional syncope may uncover exercise induced ischemia or arrhythmias. Invasive electrophysiologic studies are important for arrhythmic syncope and can diagnose the mechanism of syncope in about 66% of patients. It can elicit ventricular and supraventricular tachycardia and the response to pacing and pharmacologic interventions. Neurally mediated syncope may be diagnosed with a positive response to tilt testing with or without isoproterenol provocation. The signal averaged ECG is important for defining post MI after potentials that are associated with sudden death and arrhythmias. Electrophysiologic testing is important in elucidating a bradyarrhythmia or heart block as the cause of syncope. For example a prolonged HV interval longer than 100 milliseconds, a prolonged sinus node recovery time, or a pacing induced infranodal block would all be helpful. If the patient has a negative electrophysiologic study there is only a 20% likelihood of recurrent syncope and a low mortality risk. Other tests that may be needed to rule out non-cardiac causes would include serum glucose, electrolytes, hematocrit, toxicology screen for alcohol and drugs, head CT, EEG, hyperventilation testing, cough, micturition, and pain syncope, orthostatic testing, and testing for carotid sinus syncope. This type of syncope usually occurs from pressure to the neck as tight 139 collars, trauma and tumors. Autonomic dysfunction syncope can be caused by Parkinson's disease, Shy-Drager syndrome or Wernicke's encephalopathy. In about 35% of patients with recurrent syncope, no cause can be found. They have a 6% 1 year mortality. Syncope due to cardiac etiologies have a 20-30% 1 year mortality. Patients with bradyarrhythmias due to diffuse conduction system disease can be treated with the appropriate type of pacemaker. DDD or DVI pacemakers may be indicated in these patients with sinus rhythm and primary conduction system disease. Pacemaker + pharmacologic therapy is needed in the tachycardiabradycardia syndrome. Radiofrequency ablation, antitachycardia pacemakers, implantable AICDS, and revascularization may be needed. SYNCOPE (Neurocardiogenic)Head up tilt testing includes continuous monitoring of arterial pressure by an intra-arterial cannula place in the brachial or femoral artery. Initially, the test is carried out for 20 minutes at 70 degrees in a drug free state. If the test does not show hypotension with or without bradycardia, the patient is place in the supine position and IV isoproterenol is started at 1 ug/min. The infusion is increased gradually until there is a 20% elevation in the heart rate. At this point the test is repeated at 60 degrees for 20 min. The treatment of choice is a beta blocker. Some patients do not respond to a beta blocker and in some the patient's symptoms are aggravated. Prediction of long term efficacy for a beta blocker can be achieved by a negative tilt test with esmolol infusion. Disopyramide, theophylline, ephedrine, fludrocortisone and scopolamine patches have all been used with varying degrees of success. CHRONIC OBSTRUCTIVE PULMONARY DISEASE Current Concepts: Management of Chronic Obstructive Pulmonary Disease The New England Journal of Medicine -- April 8, 1993 -- Vol. 328, No. 14 Gary T. Ferguson, Reuben M. Cherniack: Table 1: Risk Factors for COPD. 140 Figure 1: Typical Regimen for Treating COPD. 141 Outcome was measured in terms of improvement in the FEV1, FEV1:FVC, and peak flow; improvement in the distance covered in a 6or 12-minute walk; and objectively observed reduction in dyspnea, medication use, and nocturnal symptoms. MDI denotes metereddose inhaler. Table 2: Characteristics of Bronchodilators Delivered by Metered-Dose Inhalers. 142 Table 3: Indications for Supplemental Oxygen for COPD. 143 (COPD) A. Symptoms 1. Definition: Chronic cough for >3 consecutive months in two consecutive years 2. Production of sputum (usually thick, white-yellow, yellow-green) 3. Other symptoms include: shortness of breath, tachypnea, right heart (RV) failure 4. Chronic airflow obstruction is underlying defect B. Occurrence 1. Smokers - current or previous; account for >90% of cases of COPD 2. Elderly (progressive loss of lung function with aging) 3. Alpha1-Antitrypsin Deficiency вЂ“ homozygous only C. Pathophysiology [7] 1. Chronic inflammation of airways due to irritations 2. Cigarette smoke, including second hand smoke, is major irritant 3. Destruction of normal lung tissue is chronic process, accelerated by irritants a. Non-smokers lose FEV1 at ~10-15cc/year after age 35 b. Smokers lose FEV1 at 25-30cc/year 4. Mechanisms of Lung Tissue Destruction a. Thought to be due to neutrophil proteases released during inflammation b. Alpha-1 antitrypsin is a protease inhibitor essential for protection of lung tissue c. A1-antitrypsin deficiency causes pan-alveolar destruction, pan-lobular emphysema d. Smokers typically develop centrilobular fibrosis e. Proteases destroy alveoli as well as cilia 5. Causes of Inflammation a. May be related to inability to clear organisms efficiently from lungs b. Pollutants and cigarette smoke inhibit alveolar macrophage function and ciliary motion c. Result is increased bacterial load which leads to chronic inflammation d. The inflammation in bronchitis is characterized by sputum overproduction and fibrosis 144 e. Contrast with asthma, where inflammation causes airway constriction 6. Net Result is Hypoxemia a. Several mechanisms of hypoxemia exist b. Mucus plugging with shunting and V/Q mismatch appears to make major contribution c. Destruction of lung tissue prevents O2 exchange 7. Response to Hypoxemia [9] a. Increased ventilatory drive вЂ“ decreases pCO2, increases pO2 and work of breathing b. Non-pulmonary vascular beds dilate - decreased systemic vascular resistance (SVR) c. Decreased SVR induces tachycardia and increased stroke volume (cardiac output up) d. Pulmonary vascular resistance (PVR) increases to improve ventilation perfusion matches e. This increase in PVR leads to pulmonary hypertension and right heart failure f. Hypoxia also leads to increased erythropoietin production, increased red cell mass g. The increased RBC mass increases cardiac work h. Supplemental oxygen, particularly at night, may slow or prevent progression [8] 8. Etiology of CO2 retention in COPD is controversial a. Appears to be mainly due to mucus plugging with V/Q mismatch b. Increasing O2 in patients with COPD may increase CO2 retention c. Likely due to increased V/Q mismatch and hypoventilation due to reduced hypoxic drive d. Respiratory drive in CO2 retainers is most pH (not CO2 level) dependent 9. Emphysema a. Emphysema is a pathologic diagnosis with destruction of lung tissue b. Centriacinar, panacinar and distal acinar pathologies are seen c. Patients are typically hypoxic and hypocarbic, late stage O2 dependent with tachypnea d. Cor pulmonale (R heart failure) may occur due to pulmonary hypertension e. Often referred to as "pink puffer" (pink because CO2 level is low with low normal O2) f. PFTs show markedly reduced DLCO, increased residual volume and reduced FEV1/FVC 10. Chronic Bronchitis a. Clinical diagnosis with definition of cough and sputum production as for COPD b. Specifically refers to chronic inflammation of the bronchial tubes c. Patients with prominent bronchitis are borderline hypoxic but retain CO2 (hypercarbic) d. They typically have a compensated respiratory acidosis (ie. with high bicarbonate) e. Often referred to as "blue bloaters" (blue because of high CO2 levels) f. Cor pulmonale often occurs due to pulmonary hypertension g. Polycythemia is common due to chronic hypoxemia h. High dose O2 administration (>2-4L/min may exacerbate CO2 retention (see above) i. PFTs show nearly normal DLCO, increased total lung capacity, reduced FEV1/FVC D. Common Organisms Found in COPD Patients 1. Streptococcus pneumoniae 2. Haemophilus influenza 3. Moraxella catarrhalis (Branhamella): G- diplococci 4. Other gram-negative organisms 5. Thus, antibiotic use in COPD should cover the above organisms 6. In general, TMP/SFX, second (or third) generation cephalosporin, AugmentinВ®, are useful E. Treatment of Chronic Disease 1. Stop smoking 2. Bronchodilators a. Ipratropium (AtroventВ®): 2-4 puffs po qid; anti-cholinergic, preferred for chronic disease b. Гџ2 agonists, eg. Albuterol (VentolinВ®), also effective; more so in acute exacerbations c. In chronic COPD treatment, efficacy of ipratropium is better than Гџ2-agonists 3. Theophylline may increase respiratory muscle strength mildly (~10%) [3] a. Use in difficult / severe cases is strongly recommended b. May prevent overnight attacks c. Improvement in exercise tolerance in moderate to severe COPD cases d. Improvement often seen on patients on ventilator with low tidal volume, apnea, etc. 4. Antibiotic Therapy a. In most patients, there is no benefit to chronic suppressive therapy with antibiotics b. In general, antibiotics should be reserved for mild to moderate exacerbations 5. Decongestants a. Pseudoephedrine b. EntexВ® or DeconsalВ® (Pseudoephedrine with Gauifenesin) c. Anti-histamines are not recommended (dry up secretions) 6. Glucocorticoids a. Inhaled agents of clear benefit in COPD (not in exacerbations) b. Use high dose (eg. 80mg iv q8- Solu-MedrolВ®) in COPD exacerbations (see below) 7. BronkosolВ®: to thin out thick secretions, make easier to clear 8. Organidin: iodinated mucolytic, thins mucus, easier to clear. 9. Supplemental Oxygen [ 8, 9] a. Usually for patients with pO2 at rest of <55mm b. Clear benefits in exercise tolerance when given over long term c. Improvement in cardiac function (including right heart pressures) 145 d. Unclear effect on mortality e. Some patients do not respond at all, and there are currently no predictors of response F. Inhaled Glucocorticoids in COPD 1. Recent study of all comers with obstructive airway disease (COPD / Asthma) a. Patients given baseline Гџ2-agonist; randomized to second therapy: b. Inhaled steroid (beclomethasone) vs. inhaled anti-cholinergic (Ipratropium Bromide) 2. Results show much greater efficacy of inhaled steroid a. No difference between placebo and AtroventВ® b. Note that all patients were on Гџ2-agonists, however 3. Strongly indicate that patients with COPD (and asthma) should be treated with inhaled glucocorticoids 4. Oral Glucocorticoids [5] a. In stable disease will benefit only ~10% of patients b. Not usually indicated in stable disease due to high side effect profile G. Treatment of COPD Exacerbations 1. Low dose Oxygen (concern about CO2 retention with higher levels O2) 2. Rule out CHF contribution (wheezing may be cardiac vs. bronchospastic) 3. Chest Radiograph - rule out frank pneumonia 4. Nebulizers a. Гџ2 agonists b. May add MucomystВ® (N-acetyl cysteine to loosen secretions) c. Ipratropium 500Вµg + albuterol вЂ“ more effective for FEV1 increase than Гџ2-agonist alone d. Consider also for patients on home nebulizer therapy 5. Steroids iv - may be most important therapy (eg. 80-100mg iv Solu-MedrolВ® q8-) 6. Antibiotics a. No frank pneumonia - still need to cover H. influenza, Moraxella, Pneumococcus, etc. b. Ceftriaxone or Cefuroxime iv c. Oral: BactrimВ® good initial choice; Cefuroxime or Cefixime (SupraxВ®) if allergic d. Other excellent po antibiotics include Ofloxacin, Clarithromycin and AugmentinВ® e. Ampicillin out of favor due to increased resistance of H. influenza and M. catarrhalis. f. Patients treated with antibiotics recover more rapidly and have less deterioration [ 4, 6] 7. Ipratropium bromide a. Adjunct to Гџ2-agonist therapy; combination more effective than Гџ2-agonist alone b. Available for combination nebulizer treatment with Гџ2-agonists c. Only mild cardiac effects. 8. Theophylline See Card "Theophylline Toxicity" a. Mild bronchodilator See Card "Asthma" b. Increases Respiratory muscle (diaphragmatic) strength c. Mild diuretic d. Intubated patients who fail to wean due to poor muscle strength may benefit greatly e. IV aminophylline load is usually preferred (~5mg/kg slow bolus, then 0.5mg/kg/hr iv) f. Tachycardia, tremors, palpitations, and hypertension may occur 9. Diuretics - may improve oxygen transit if pulmonary edema is present 10. Mechanical Ventilation a. Endotracheal Intubation is usually used b. Positive pressure, non-invasive ventilation is very effective in some patients [10] c. In general, non-invasive methods should be considered 11. Prognosis [11] a. In hospital mortality was 24% for patients in intensive care for COPD exacerbation b. Most in hospital mortality was associated with non-respiratory organ dysfunction c. For >65 year old patients, 1 year after hospital discharge, mortality was 60% H. Surgical Treatment of COPD [12] 1. Indications a. Incapacitating dyspnea b. Compression of relatively normal lung parenchyma by diseased lung tissue 2. First performed by Brantigan in 1957 3. Bullectomy and volume reduction pneumoplasty are performed 4. 30% of lung is excised with aim to reduce total lung capacity and residual volume 5. Allows diaphragmatic contour to return to baseline, thus improving respiratory mechanics 6. Variable Success a. No definite predictors of successful outcome with respect to PFTs or imaging b. Poor six minute walk test pre-operatively may predict good outcome c. Improved lung function, reduction in pCO2, and increased RV function was seen [12] DIFFERENTIAL DIAGNOSES OF PULMONARY ABNORMALITIES A. Lung Cavitation 1. Tuberculosis 146 2. Fungus Histoplasmosis, Nocardia, Actinomyces, Aspergillus 3. Lung Cancer: usually non-small cell carcinoma 4. Pulmonary infarction 5. Aspiration Pneumonia with Abscess formation 6. Lymphoma - usually non-Hodgkin's 7. Bacterial Abscess: anaerobic / mixed 8. Inflammatory: Wegener's Granulomatosis, Rheumatoid Arthritis (necrobiotic), sarcoidosis 9. Cystic Bronchiectasis 10. Developmental Cysts 11. Parasitic Disease - hydatid, paragonimiasis 12. Silicosis - very rarely cavitary B. Hemoptysis 1. Diseases a. Pulmonary Embolus b. Arterio-venous malformation (AVM) c. Goodpasture's (anti-basement membrane Antibodies) Syndrome d. Vasculitis e. Sarcoidosis f. Mitral Stenosis - with high pulmonary pressures; called "cardiac apoplexy" 2. Infection (Bronchiectasis, bronchitis) a. Bacterial pneumonia b. Tuberculosis (most common world-wide) c. Nocardia d. Lung abscess e. Unusual: fungal balls, fungal infection (aspergillosis), parasitic infections 3. Neoplastic a. Lung Carcinoma b. Lymphoma (unusual) c. Carcinoid Tumors Syndrome" C. Pulmonary Edema 1. Etiology a. Acute Cardiac Decompensation вЂў Mitral Regurgitation вЂў Ischemia вЂў Arrhythmia вЂў Infarction вЂў Heart Failure (Left Sided) b. ARDS c. Hypoproteinemia вЂў Liver Failure вЂў Nephrotic Syndrome d. Inflammatory Response e. Pulmonary Embolism and Infarction 2. Symptoms a. Hypoxia due to poor gas exchange b. Shortness of Breath (including "cardiac asthma") c. Pain, usually over the lower lung fields d. Paroxysmal Nocturnal Dyspnea, Orthopnea D. Interstitial Lung Disease (ILD) 1. Hypersensitivity Pneumonitis 2. Atypical pneumonia: Mycoplasma, Legionella, Pneumocystis, Viral, Chlamydia 3. Granulomatous Diseases a. Sarcoidosis b. Wegener's Granulomatosis c. Tuberculosis - unusual 4. Interstitial pulmonary fibrosis (IPF) a. Usual interstitial pneumonitis (UIP) b. Desquamative interstitial pneumonitis (DIP) 5. Connective Tissue Disease a. Usually lower lobes: Rheumatoid Arthritis (RA), Scleroderma, SLE, Myositis b. RA: HLA linked, often with pleural involvement c. Usually upper lobes: ankylosing spondylitis 6. Asbestosis (pleural involvement) 7. Silicosis, Berylliosis 8. Radiation pneumonitis: >4000 R total dose; Fibrosis 9. Metastatic Infiltration: lymphangitic spread (breast CA, lymphoma, etc) 10. Drug Reaction: bleomycin, nitrofurantoin, ?methotrexate 11. Others a. Idiopathic pulmonary hemosiderosis 147 b. Eosinophilic granuloma c. Lymphangioleiomyomatosis (LAM) E. Solitary Pulmonary Nodule 1. Usually defined as < 3 - 4cm opacity without atelectasis or hilar adenopathy 2. Etiology a. Bronchogenic Ca (35-50%): non-small cell cancers were more common than SCLC b. Metastatic Cancer (breast, colon, renal, Kaposi's Sarcoma) c. Carcinoid Tumor (total 10%) d. Granulomatous Process: TB, Histoplasma, Coccidiomycosis, Cryptococcus, Aspergillus e. Other: Bronchial Cyst, AV Fistula, Fibroma, Rheumatoid Nodule, Hematoma, Sarcoid f. Rounded Atelectasis, Hamartoma g. Resolving pneumonia, infarction 3. Factors Favoring Malignancy a. Older age of patient b. Smoker c. Margins Not Sharp d. Uncalcified, or Calcification NOT laminated, homogeneous or popcorn e. Change in size on Chest Radiograph over 2 years f. A very rapid doubling in size (<7 days) favors benign histology g. Size >2cm 4. Evaluation a. Chest radiography is most common initial test b. Nodules <2cm require thin section CT study c. >2cm is nearly always a bronchogenic CA; staging with chest and abdominal CT d. Sputum Cytology: diagnostic 20% of malignancies (endobronchial tumors often exfoliate) e. Fiberoptic Bronchoscopy: Diagnostic yields 50-75%; drops off for lesions <2cm f. Transthoracic Aspiration: Diagnostic <2cm ~60%, >2cm ~85% 5. Chest Radiographic (CXR) Results of Benign Lesions a. Calcification usually means benign (<1% malignancies appear calcified on CXR) b. Benign Calcifications: laminated (granuloma), popcorn (hamartoma), homogeneous c. No change in size over 2 years d. CT scan gives better assessment of size and calcification Pulmonary Function Testing PFT PULMONARY EMBOLI: Origin of Emboli: -(80-90%) large lower extremity & pelvic veins -Rt Atrium (CHF, A-Fib, indwell cath) 148 -Hepatic & Renal Veins -Tricuspid Endocarditis or upper extremity thrombi in IV drug abusers Predisposing Pathology: 1) Stasis, 2) Endothelial Damage 3) Hypercoagagulable State Predisposing factors: immobility BCP's, IBD, shock, CHF pregnancy, stroke, neoplasm, obesity, SLE, nephrotic syndrome, polycythemia, -HIP & Knee surgery/any surgery -Any pt in Hosp approx 30% will have DVT PROPHYLAXIS: low dose heparin: decr risk fro 30-5 Adj Dose Heparin: PTT in high nml range -effective 24h prior to surg Coumadin 2mg/d 1-2d prior to surg -followed by full Tx post-op Pressure compression device: cause sys -anticoagulation Venous Thrombi(Red): Fibrin & RBC's Art Thrombi (white): Plt dense Etiologic Factors: 1. Lack of Endogenous Anticoag Factors a) antithrombin III b) protien C c) protein S 2. TPA - impaired synth & release 3. Plasminogen - abnml fxn or quantity 4. Antiphospholipid Atibodies - in SLE cause of Art & Venous thrombi 5. Exogenous Estrogen: dose related hypercoagulable state (risk unrelated to duration of use) Presentation: -uncomplicated embolus w/dyspnea -pulm infarct syndrome(pleuritc CP +/- hemotysis -circulatory collapse (<10%) RISK: -compounded w/age, obesity, CHF, presence of CA, acute MI, prior DVT or PE & immobilization 1. Low: age<40 w/uncomplicated surg age>40 w/minor surg 2. Moderate: age >40 w/gen surg>30min 3. High: major orthoSurg on low limbs or age>40 w/extensive abd/ pelvic surg for malignant dz (fatal PE in 1-5%) SX: 1.Common: Most common Tachypnea (>50%): Dyspnea, tachypnea, tachycardia, cough, rales, pleuritic CP, angina 2. Less Common(10-40%): hemoptysis, low fever, JVD, DVT signs syncope, altered MS 3. Rare(<10%) weezing, DIC, abd pain EKG Signs: Sinus Tachycardia S1 Q3 T3 (40% w/nonspec T wave changes) 149 S-T wave abnormalities PACs, PVCвЂ™s, atrial tach Rt atrial strain, RBBB, RAD(or LAD) CXR: Atelectasis elevation of hemidiaphragm (lost volume) pleural effusion "knuckle sign" PA tapers abruptly pulm infarction: pre-existing CV dz LAB Signs: -98% of all PE Pts w/abnml A-a grad or w/ PaCO2 <36 (sens not specific) V/Q scan: inj radiolabeled albumin & - inhaled inert hot xenon ** (Pos: 50% false + rate) ** 1. Nml: reliably excludes PE 2. Low Prob: 20-40% are pos (same for intermit & matched result) 3. Int Scan: abnml perf + infl on CXR 4. Matched defect: due to bronchoconstriction 5. High Prob: 86% accuracy if large perfusion defect or segmental -only 37% if sub segmental (confirmed by pulm angio) PAgram:Pulm Arteriogram: definitive Dx - Morbidity: 4-6%- increased in Pts w/ RV-EDP > 20mmHg - must do prior to thrombolysis, embolectomy, or anticoag in Pt w/ bleeding risk FX of PE on Right Ventricle: - Massive PE leads to increased RV afterload- enlarged RV, shifts vent septum to Lt & decreased LV preload - leading to decreased CO - leads to RV dilation & ischemia from reduced coronary flow in systol -----------------------------------TREATMENTS: Heparin: indicated in PE, suspected PE & DVT - 1/2 life=60-90 min - Bolus dose: give prior to definitive *** Dx to prevent early mediatorinduced pulm vasoconstriction & bronchoconstriction by thrombin activation & PLT aggregation - Acts by binding Antithrombin III which inactivates Thrombin & inhibits coagulation - Duration of TX: gen continued 7-10d - Early Ambulation is Discouraged since fresh thrombi may embolize prior to adherence to vein wall (7-10 days) - Maintainance Drip or Sq post bolus - IV 12,000 - 18,000 IU/hour - SQ 12,000 - 14,000 IU q12 hour (test PTT midway between sq inj) -------------------------------- 150 Coumadin: for long term maintainance - antagonist of Vit K - depleates clot factors II, VII, IX, X - Effectivenes depends on depletion of clotting factors - FacII(Prothrombin) 1/2 life =60 hours- no use in rushing - Give 10mg PO x 3d, get PT on 1st & 3rd day - To prevent recurrent PE: 6mo of TX unless definitive studies show cleared DVT & PE (IPG & Lung Scan) ---------------------------THROMBOLYTIC TX: 1. hemodynamically unstable Pts 2. rTPA within 3 days of surgery Streptokinase, Urokinase, & TPA - act to facilitate fibrinolysis by converting plasminogen to PLASMIN which hydrolyses fibrin,fibrinogen & blood coag factors - TRIALS show thrombolytic Tx superior to heparin in improving PAgrams, hemodynamic indices, & perf scans ***-particularly in massive PE's - F/U TRIALS: thrombolysis w/<longTerm residual pulm clots & pulmonary diffusion capacity than w/Heparin (seen @ 2weeks, 1yr, & 7yrs) - NO dif w/TPA by IV or intrapulm Cath - UROKINASE: direct act of plasminogen (isolated from human urine) - STREPTOKINASE: must bind plasminogen & then become plasmin activator (isolated from grpC B-hem Strep) - rTPA: "CLOT SPECIFIC" thrombolysis Activates Plasminogen-plasmin only significantly inpresence of fibrin which facilitates conversion of plasminogen, **** thus producing localized FCTs - 100mg infusion x 7 hours may be superior to 50 mgX 2hrs ---------------------------CONTRAINDICATIONS to THROMBOLYSIS: Absolute Contraindications: -active internal bleeding -recent surgery -? aortic aneurysm -recent head trauma/CNS TUMOR/CVA -Ophthal bleed--?DM -BP> 200/120 -------------------Relative Contraindications -recent minor trauma -Hx: chronic severe HTN -active PUD /bact endocarditis -Bleeding diathesis/Anticoag Tx -sig Liver/ kidney Dysfxn -age > 75 -prior streptokinase (particularly -within initial 6-9mo period) Complication of thrombolysis: - bleeding (1% intracraneal) - antibody formation (w/SK) - allergic Rxn (w/SK) 151 - fever (w/SK) - resistance to thrombolysis ISOPROTERONOL: beta agonist: bronchodil, pulm/syst vasodilator, & +inotrope - in Pt w/ MILD PE & cardiac failure - lowers pulm HTN & increases CO TX FOR UNSTABLE PT w/PE 1. Thrombolysis 2. Embolectomy(only for central emboli) 3. Tranvenous Catheter Embolectomy 4. IVC Filter Recurrent PE: may lead to pulm HTN and Cor Pulmonale REF: Biebuyck JF: PulmThromboembolism: Dz Recog. & Pt Mgt.Anesthesiology 73:146-64,1990 Pulmonary Embolism Lecture Slides(Dr. Goff) 152 153 154 155 156 157 158 159 160 161 Anticoagulation 162 163 TB Mycobacterium Tuberculosis SOURCE: human transmission especially pulm TB pt =pts w/tubercle bacilli in sputum are most infectious) =pt in whom are TB+ by sputum cult alone are much < infectious =transmitted by aerosol drops & penetrate bronchi & lungs ---------------------------------------Pathophysiology..................... PRIMARY INFECTION: usually latent but sometimes w/clin signs: either skin, fever, nodes, or x-ray focus SKIN RESPONSE/PPD: + after few weeks of exposure to tuberculin EARLY POST PRIMARY RESPONSE: miliary TB, meningitis or pleuricy LATE POST PRIMARY TB: lesions in lymph nodes, joints, bones or abd REAACTIVATION OF PRIMARY TB FOCUS: usually following wakening of immune fxn or exogenous reinfection --> leads to caseous focus in lung that liquifys & proliferates microbes. -once drained via bronchi-> the focus remains as a TB pulm cavity ---------------------------------------DIAGNOSIS: SITE: Most often lungs but 30% extrapulm **Pulmonary TB**: 164 AGE: all ages >>in 20-35 year old males Sx: persistant cough +/- fever, anorexia hemoptysis. TUBERCULIN TEST: neg result r/o dz unless pt is moribund/cachectic, has measles/pertussis virus, on steroids or in 3rd trimester of pregnancy **POSITIVE RESULT:Little Dx value since could mean either past BCG vac or old primary inf w/o active dz. SPUTUM: Imperitive to get 2 sputum smpls 2cc/each for micro smear exam **Extrapulmonary TB** TEN RULES FOR READING CHEST X-RAYS (http://www.mtsinai.org/pulmonary/books/house/rules-a.html) (Especially for House Officers in Clinical Specialties) 1. The only way to learn to read chest x-rays is to read chest x-rays. Daily. 2. Always check the name and date on the film. Five percent of the time the film will be of someone else. 3. When confronted with an abnormal chest x-ray, always seek out prior films for comparison. Unless absolutely, positively certain, always assume that old films are available somewhere. 4. Don't ignore the lateral film. It can often clarify the presence or absence of lower lobe disease. 5. "Technique" accounts for much of the variation in serial chest x-rays. Don't confuse this change (e.g., the amount of x-ray penetration, or rotation of the patient) with change in disease. 6. Consider everything on the film that might provide some potentially useful information: endotracheal tube? (respiratory failure); surgical clips? (thoracotomy); absent breast shadow? (mastectomy); chest leads? (AP film); large amount of soft tissue? (obesity); etc. 7. The presence of clear lung fields (no infiltrate, no vascular redistribution) and normal-sized heart rules out left-sided congestive heart failure as a cause of the patient's symptoms. 8. Lung fields can never be called clear on a portable chest x-ray until you've identified the left hemi-diaphragm and lack of infiltrate behind the heart. 9. The chest x-ray never lies. 10. Ask for help. Help is always available. 165 Chest Radiography Lecture by Dr. Goff 166 167 168 169 170 171 172 173 174 175 176 177 178 179 180 181 Rules on Oxygen Therapy -- What Every House Officer Should Know (http://www.mtsinai.org/pulmonary/books/house/rules-a.html) Physiology 1. PO2, SaO2, CaO2 are all related but different. 2. PaO2 is a sensitive and non-specific indicator of the lungs' ability to exchange gases with the atmosphere. 3. FIO2 is the same at all altitudes. 4. Normal PaO2 decreases with age. 5. Oxygen from the wall outlet is always 100%. 6. The body does not store oxygen. Therapy & Diagnosis 7. Supplemental O2 is an FIO2 > 21%. 8. Supplemental O2 is a drug. 9. Supplemental O2 is the most commonly-prescribed drug in hospitals. 10. A reduced PaO2 is a non-specific finding. 11. A normal PaO2 and alveolar-arterial PO2 difference (A-a gradient) do not rule out pulmonary embolism. 12. High FIO2 doesn't affect COPD hypoxic drive. 13. A given liter flow rate of nasal O2 does not = any specific FIO2. 14. Face masks cannot deliver 100% oxygen unless there is a tight seal. 15. Oxygen masks migrate. 182 SIGNS OF OBVIOUS BREATHING (WOB) (http://www.mtsinai.org/pulmonary/books/house/rules-a.html) If a patient's breathing is obvious on initial contact (for example, when you first see the patient on walking into the room) it is abnormal. Normal breathing at rest is simply not obvious; one has to look very closely for chest movement to appreciate breathing. Six signs that may make someone's breathing obvious to the observer - all abnormal - are listed below. flaring of nostrils with breathing tachypnea (generally, to be obvious, respiratory rate is > 24 breaths/min) noisy breathing (wheezing, stridor, moaning, etc.) use of accessory breathing muscles (neck muscles, intercostal muscles, etc.) pursed lip breathing (often seen in severe COPD) Cheyne-Stokes breathing (alternating periods of apnea with tachypnea; apnea periods may last up to 30 seconds) THE FOUR MOST IMPORTANT EQUATIONS IN CLINICAL PRACTICE (http://www.mtsinai.org/pulmonary/books/house/rules-a.html) Pulmonary, Acid Base, ABG 1. The PaCO2 equation PaCO2 = CO2 produced by metabolism (ml/min) x k/alveolar ventilation (L/min) where alveolar ventilation = minute ventilation minus dead space ventilation k = 0.863. REASON IMPORTANT: This equation explains why one cannot assess PaCO2 clinically, i.e., with only bedside observations such as respiratory rate, depth of breathing, level of discomfort, breath sounds, etc. There are no clinical variables in this equation. For example, a patient with fast and/or deep breathing can still be retaining CO2 if most of the air goes to dead space (either because of shallow tidal volumes or ventilation-perfusion mismatch). Since there is nothing clinical in this equation, one cannot use clinical criteria to assess PaCO2 (i.e., adequacy of alveolar ventilation). A patient may appear to be "hyper-ventilating" but in fact be hypoventilating, i.e., have a high PaCO2. 2. The alveolar gas equation PAO2 = FIO2 (B.P. - 47) - 1.2 PaCO2 where PAO2 = alveolar PO2 FIO2 = fraction of inspired oxygen B.P. = barometric pressure 47 = water vapor pressure in airway in mm Hg Alveolar-arterial PO2 difference [A-a gradient] = calculated PAO2 - measured PaO2 REASON IMPORTANT: You need the calculated PAO2 to know if arterial PO2 (PaO2) is abnormal or not. Specifically, the variables in this equation (B.P., FIO2 and PaCO2) must be known to properly interpret any PaO2 value. Is a PaO 2 of 28 mm Hg normal? (Yes, if breathing mountain air at the summit of Mt. Everest, where B.P. is only 253 mm Hg). Is a PaO2 of 100 mm Hg abnormal? (Yes, if the patient is breathing 100% oxygen). Does a PaO2 of 50 mm Hg indicate a problem of ventilationperfusion mismatch? (Yes, if the A-a gradient is increased; no, if the A-a gradient is normal, in which case the low PaO2 may be solely from elevated PaCO2). 3. The Henderson Hasselbalch equation pH = pK + log HCO3/.03(PaCO2) 183 REASON IMPORTANT: Helps diagnose presence and type of acid-base disorder, and the body's compensation for it. The abbreviated version is adequate in most clinical situations. Equation shows there are only four primary acid-base disorders: two where the first change is in HCO3- (metabolic alkalosis and acidosis) and two where the first change is PaCO2 (respiratory alkalosis and acidosis). 4. The arterial oxygen content (CaO2 ) equation CaO2 content = amount O2 bound to hgb + amt.O2 dissolved = (1.34 x hgb x SaO2) + (.003 x PaO2) where O2 content = ml O2 /100 ml blood 1.34 = ml O2 that can maximally bind to a gram of hgb hgb = hemoglobin content, in grams/dl SaO2 = saturation of hemoglobin with oxygen in arterial blood .003 = ml O2 that can dissolve in plasma per mm Hg PaO2 per 100 ml blood REASON IMPORTANT: Incorporates factors for adequate arterial oxygen content, most important of which is hemoglobin; over 97% of arterial oxygen content is normally carried by hgb. Note that oxygen content is the only readily available value that directly reflects the number of oxygen molecules in the blood. In assessing degree of hypoxemia (as opposed to the cause), CaO2 is more useful than either PaO2 or SaO2. A patient can be profoundly hypoxemic with a normal PaO2 (for example, from severe anemia or carbon monoxide intoxication) or with a normal SaO2 (from severe anemia). 5. And the fifth most important equation? (http://www.mtsinai.org/pulmonary/books/house/rules-a.html) Anion gap equation Fick equation for oxygen uptake Equation for oxygen delivery Conversion equations for: centigrade to Fahrenheit; cm H2O to mm Hg; kg to lbs. Resistance equation (for blood flow or air flow) Compliance equation for a solid organ (heart, lungs) Harris-Benedict nutrition equations Creatinine clearance equation Equation for fractional excretion of sodium Equation for calculating serum osmolality 184 185 PAO2 = FIO2(PBO2-47) - 1.2(PaCO2) ALT. = altitude in feet PB = barometric pressure FIO2 = fraction of inspired oxygen PIO2 = pressure of inspired oxygen in the trachea PaCO2 = arterial PCO2, assumed to = alveolar PCO2 PAO2 = alveolar PO2, PAO2 is calculated using an assumed R value of 0.8 except for the summit of Mt. Everest, where 0.85 is used 24 PaO2 = arterial PO2, assuming a P(A-a)O2 of 7 mm Hg at each altitude; each PaO2 value is normal for its respective altitude CaO2 = (SaO2 x Hb x 1.34) + .003(PaO2) 186 Figure 1. PaCO2 vs. alveolar ventilation (VA). The relationship is shown for carbon dioxide production rates of 200 ml/min and 300 ml/min. Changes in PaCO2 are shown for a one liter decrease (short horizontal lines) in VA starting at two different PaCO2 values, 30 and 60 mm Hg. A decrease in alveolar ventilation in the hypercapnic patient will result in a greater rise in PaCO2 than will the same V.A change when PaCO2 is low or normal. Also, note that an increase in carbon dioxide production when VA is fixed will result in an increase in PaCO2 . 187 Figure 2. Normal range of P(A-a)O2 from FIO2 of .21 to 1.00, based on data obtained from 16 healthy subjects aged 40 to 50 years.23 Lines represent mean values and + or - 2 standard deviations. The P(A-a)O2 increases up to an FIO2 of 0.6, then plateaus with further increases in FIO2. Note that P(Aa)O2 may normally exceed 100 mm Hg on an FIO2 of 1.00. Figure 3. PaO2 vs. SaO2 and oxygen content. The oxygen dissociation curve relates PaO2 to SaO2. The shape and position of the curve are the same regardless of hemoglobin content. The right ordinates show arterial oxygen contents for two different concentrations of hemoglobin: 15 gm% and 10 gm%. Normal P50 (the PaO2 at which hemoglobin is 50% saturated with oxygen) is approximately 27 mm Hg. "X" represents measured PaO2 and oxygen saturation of Case 4. 188 Shunt Equation Normal Ranges for Ventilatory Values Respiratory Rate (RR)= 8-16 b/m (*<=38) Core Temperature = 36-38 C (96.8-100.4 F) Esophageal Pressure (Pes=PESmax-PESmin)=< 15 cmH2O Airway Pressure (Paw) <= 40 cmH2O Tidal Volume (Vt)= 7-10 cc/kg (*>=325) Tidal Volume(cc)/Weight(kg) *>=4 Work of Breathing (WOBp)= .05 J/L (<= .8 J/L max sustained) TransPulmonary Pressure (PTP)= 6-8 cm H2O Respiratory Time Fraction (Ti/Ttot)= .3-.4 (abn if >.4 or > .1 increase) Mean Inspiratory Flow (VT/Ti)<= .4 VT/RR= .05-.075 L/s (*<= 105 b/m/l) Airway Resistance (Raw)= 2-5 cmH2O/L/s Dynamic Compliance (Cdyn)= 50-100 cc/cmH2O (*>=22) Static Compliance (Cstat)= *>=33 cc/cmH2O Respiratory Drive (P0.1)= 3-4.5 cm H2O (<= 6 cm H20) PTP/Pmax <= .4 (sustained) Pressure Time Index (PTI)<= .15 (sustained) Minute Ventilation (Ve)= 7-10 l/m (*<=15) Maximal Inspiratory Pressure (Pmax, NIF, MIP) *<= -15 cm H2O PaO2/PAO2 ratio *>=.35 CROP index** *>=13 * Threshold Values of Indexes Used to Predict Weaning Outcome ** CROP Index=(Cdyn*Pimax*[PaO2/PAO2])/R Tobin et al, NEJM 1991; 324: 1445-50 189 Pleural Effusions Pathophysiology of Pleural Effusion Starling Equation: F = K((Pcap - Pif) - (Ocap - Oif)) F = Flow in cc/sec K = Permeability Constant cc/sec/cmH2O/cm^2 P = Hydrostatic Pressure in cmH2O/cm^2 O = Oncotic Pressure in " cap = capillary if = Interstitial Fluid Pd = (Pcap - Pif) - (Ocap - Oif) Pd = Driving Pressure = 8 - 9 cm H2O favoring fluid movement from parietal capillaries into pleural space = 10 -11 cmH2O favoring flux from pleural space into visceral pleural capillaries (Reabsorption) Therefore Increased Flow & Pl Ef : 1. Increased K (Capillary Permeability) a. eg. pneumonia; inflammation; PE; Empyema; CVD Uremia, pancreatitis, Subphrenic abscess Whipple, hepatic abscess, Dresslers, XRT, Vasculitis, Chronic Hemothorax b. w/ Decreased Lymphatic Flow --> exudate CA, TB 2. Increased Pcap (Hydrostatic Pressure) a. With decreased Oncotic------> transudative eg. CHF, cirrhosis, nephrosis, myexedema (rarely exudative), peritoneal dialysis, hypoprotein, Meig's (left eff, benign ovarian fibroma w/ ascites rarely exudative) 3. Decreased Pif (Increased Negative Intrapleural Pressure) -eg. Atelectasis----->transudate early 4. Decreased Ocap (Oncotic capillary Pressure) -eg. Nephrotic Syndrome, hypoalbuminemia 5. Increased Oif (Oncotic Pleural Fluid) -eg. Pleural tumor, inflammation, infection 6. Decreased Lymphatic Flow / Exudative -Chylothorax, Sarcoid, Yellow Nail, Milroy's Ds 7. Other: CVP catheter, Postpartum pl ef 8. Drug & Hypersensitivity ----> exudate -Macrodantin, Methylsergide, Nitrogen mustard, Quinicr, Sclerotherapy for esoph varices -HALF OF ALL PLEURAL EFFUSIONS ARE CAUSED BY CANCER; WHILE THE MOST COMMON CAUSE IS CHF... -2/3 OF ALL MALIGNANT EFFUSIONS ARE FROM LUNG, BREAST OR LYMPHOMA ANY TUMOR CAN CAUSE IT; GU / REPRODUCTIVE / GI ---> 15% 15% OF ALL EFFUSIONS ARE FROM UNKNOWN CA ORIGIN. -50% OF PATIENTS W/ BREAST OR LUNG CA WILL DEVELOP PLEURAL EFFUSION Symptoms 190 Dyspnea, Cough & Chest Pain are the commonest symptoms (especially w/ CA.) The cough may be positional. Physical Signs: Amount of P.E. Resp Rate Expansion Fremitus Sounds Tracheal Shift Small (< 300cc) n-^ n n vesc none Moderate (300-1500) n, ^^ n-lo n-lo lo-vesc " Large (>1500) ^^^ lo lo lo lo lo BV none maybe Less than 300 cc's usually not found on Physical Exam; may here a rub though. Greater than 10 cm layering free flowing fluid on decubitus CXR OK to TAP. With > 1500 cc; there is usually mediastinal shift away. If this does not occur r/o: a. Obstruction of Main Stem Bronchus w/ Volume loss b. Trapped Lung (As in Mesothelioma) c. Fixation of Mediastinum (Tumor, Nodes Lymphoma) Sometimes Large ( >1000cc ) of Subpulmonic Fluid can be Occult on CXR Causes of Pleural Effusion TRANSUDATES Increased Hydrostatic Pressure --------------------------- Miscellaneous ------------- CHF Acute Atelectasis Constrictive Pericarditis Subclavian Catheter misplaced SVC obstruction Idiopathic Urinary Obstruction Decreased Oncotic Pressure -------------------------Cirrhosis w / Ascites Nephrotic Syndrome Hypoalbuminemia Peritoneal Dialysis Acute Glomerulonephritis Myxedema USUALLY BILATERAL EFFUSIONS EXUDATES 191 Pulmonary Embolism (30-50%) Infectious Drug Induced ------------------------------ Pleural Disease ---------------------------- Bacteria, TB, Fungi, parasites Virus, mycoplasmal Hepatitis Pulmonary Infarction ---------------------------Neoplastic Chylo / Pseudochylothorax --------------------------------------------------------Metastatic, Bronchogenic, lymphoma, leukemia, mesothelioma, chest wall Miscellaneous tumor ---------------------------Esophageal rupture, Sarcoidosis Collagen Vascular Diseases Chronic Atelectasis, Trapped -----------------------------lung, Uremia, Asbestos, RA, SLE, Drug-Induced SLE, Sjogren's Familial Mediterranean Fever Wegners, etc PostMI, Lyphedema (Yellow Nail Syndrome), Obstructive Uropathy Intra-abdominal Diseases (urinoma), XRT, Myxedema, ----------------------------Immunoblastic Lymphadenopathy Abd Sx, Pancreatitis, Subdiaph Abscess, Incarcerated diaphr hernia, Intrahepatic Idiopathic Abscess Meig's Syndrome Thoracentesis 1. Safe & simple Dx'tic & Tx'tic procedure. Made even safer by Ultrasonic localization. Rarely severe bradycardia & hypotension as needle passes parietal pleura (PLEURAL SHOCK): Vasovagal rxn...may pretx w/ atropine. Can get Reexpansion Pulmonary Edema if > 1000-1500 cc 's removed too quickly (based on pleural pressure and if kept <= 20 cm H2O unlimited volume can be removed...manometry). Pleural Effusion GROUP 1 Pts w/ previously dx'ed New Pl Ef & No Dx Pl Ef w/ Asbestos GROUP 2 CA & Pl Ef exposure &/or Hx PE GROUP 3 Tcentesis Or Xray like Mesothel + Pleural bx GROUP 4 Undx'ed Effusions After Conventional methods have failed. -cytogenetics -Pleuroscopy -Thoracotomy Multiple thoracenteses may be needed to dx a Malignancy: #1 ----> 53% yield #2 ----> 64% #3 ----> 69% #4 ----> 72% Some Ca have a lower yield on thoracentesis: -Hogdkin's only 23% yield -Lung, Breast, Ovary & Lymphosarcoma 63-73% When Pleural Bx is combined with Thoracentesis the yield is increase to 81-90%. [ COPE or ABRAHAMS NEEDLE ] Coupling Cytology & Cytogenetic analysis yields a 92% positive dx'tic 192 yield for malignancy (perform after 2 negative thora's and pleural bx). Pleuroscopy has a 93-96% yield for malignant Pl Ef. In 10-20% of exudative effusions are enigmatic. Malignant Pleural Mesothelioma Dull aching non-pleuritic chest pain, dyspnea & cough of insidious nature. Very difficult Dx. Hemoptysis, fever, weight loss, hypertrophic pulmonary osteoarthropathy and hypoglycemia (the latter 2 are w/ benign mesothelioma). Hx asbestos exposure in only 50% - 70%. Peak age 50-70 with male : female 2:1 to 5:1. 80-90% of pts will have xray evidence of Pl Ef, often with scoliosis and shift of the mediastinum toward the effusion. Associated rib destruction, pleural plaquesor calcifications, intrapulmonary nodules, pleural thickening or rind in fissures & paramediastinal structures; most often in the lung bases & posteriorly. Pleural Fluid Analysis TEST EXUDATE VALUE Specific Gravity > 1.016 <= Protein pleural > 3 g/dl <= > 0.5 Pleural/Serum Protein LDH pleural > or > 2/3 upper normal Pleural/Serum LDH > 0.6 Glucose < 60 Pleural/Serum Glucose < Prostaglandin E TRANSUDATE <= 200 IU/L <= <= <= >= .5 >= 280 pg/ml <----------> 27 pg/ml Bedside Refractometer as Poor Man's Test of SG & Total Protein --------------------------------------------------------- Lipid Profiles: Milky or opalescent persisting after centrifuge Chylous Effusions: > 400 mg Total Lipids / dl 65 - 220 mg Cholesterol / dl Triglyceride > 110 mg/dl & > 2 x serum SUDAN III is + + Chylomicrons on Lipoprotein electro is dx'tic of CHYLOTHORAX Chyliform Effusions : (Pseudochylous Effusion) has Increased Lipids with Triglycerides < 50 mg / dl - SUDAN III Elevated Cholesterol No chylomicrons (Chronic Fluid usually 5 yrs old) 193 Other Pleural Fluid Tests - pl CEA : > 2.5 - 12.5 ng/ mL is malignant adeno CA (poor screening test) - Gm Stain; Aerobic & Anaerobic Cultures; AFB; Fungal; Silver Stain - Counterimmune electrophoresis (CIE) - Directogens - Increased Pleural Creatinine : Urinothorax (from Urinary Tract Obstruction) - Hyaluronic Acid > 0.8 mg/ml ------> Mesothelioma - Adenosine Deaminase (ADA) > 30 IU/L in all with TB (lower in all w/ parapneum / CA) - Pleural Bx: In TB & CA will be + in 50% of Exudates In TB > 80% will be + for AFB or Granulomata & TB c/s 75% of pt In CA w/ fluid & Bx 90% yield Low yield in Mesothelioma - Pleuroscopy - Cytogenetic (Chromosomal Studies) - Bronchoscopy: Epecially with Parenchymal Abnormalities R/O Obstructing Lesion with will cause fistula w/ Chest Tube Pleural Fluid Descriptions: C = Clear ..............Most Transudates & SC = Straw Colored....... some Exudates T = Turbid ............. Infectious P = Pus................. Empyema Y = Yellow.............. & turbid = infection SS = Serosanguineous G = Green...............& turbid rheumatoid Pleurisy B = Bloody..............Trauma, Tumor, Pulm Infarct Cloudy Milky White......Chylothorax (chylous effusion) Thoracic duct trauma, tumor, lymphangio Lymphoma, Surgical Thick yellow metallic...Pseudo-chylothorax = chyliform effusion Sheen................as in chronic tb, ra, trapped lung Viscous Hemorrhagic.....Malignant Mesothelioma Anchovy Color...........Amebic Liver Abscess ruptured into Pleural Cavity Cellular Descriptions: Small Lymphocytes (>50% of Cells) r/o CANCER!!! Eosinophilia : pneumothorax or air; benign asbestos pleurisy < 5% CA Exudates & is good Px Disease States w/ Pleural Fluid Transudative Diseases: Congestive Heart Failure: C,SC; <1000 RBC & WBC; Mononuclear; Normal GLUC,pH & Amylase....With Tx of CHF may become exudative!!! Cirrhosis w/ Ascites : C,SC; < 1000rbc <500wbc; mono; normal G,Ph,Am Exudative Diseases: Malignancy : T,B; 5000-100,000RBC 100-10000wbc; Mononuclear; gluc < 60 to normal; maybe < 7.3; Variable amylase Uncomplicated Parapneum : T; 5000-100000rbc&wbc; pmn; >40 gluc; >7.2; nor am Complicated Parapneum : T,P; " ; pmn; < 40 ; <7.2; " Chest Tube especially if Glu < 40 or pH < 7.00!!!!! Pulmonary Embolism : SC,B; 100-200000rbc, 100-50,000wbc; pmn/mono; norm Pancreatitis : SS,B; 1000-100000rbc, 1000-50000wbc;pmn; p/s amy >2 194 or > 160 U; pseudocyst, CA, esoph rupture Rheumatoid Pleuritis : T,Y; <1000rbc, 1000-20000wbc; pmn/mono; g<25; ph<7.2 80% men; subq nodules; pleural RF >= 1:320 Low Complement & Immune Complexes Systemic Lupus : " ; except normal glucose & pH; ANA LE cells ANA >= 1:160 or p/sANA >1 Tuberculosis : SC,SS; <10000rbc <5000wbc; PMN early, MONO late; <60; >=7.3; < 5% mesothelial cells; pleural bx 90% dx Treatment of Pleural Effusions A. Malignant Effusions: -Some tumors are amenable to chemotherapy and can be used as a therapeutic index (eg. Germ Cell tumor, HodgkinвЂ™s, Lymphoma, small cell lung ca, Breast Ca {hormone responsive},) -Treatment depends on the condition & life expectancy as to how aggressive one should be and how symptomatic the patient is. Most malignant effusions will reaccumulate rapidly w/out treatment. -Thoracentesis alone: Mean time for re-accumulation was 4.2 days with most recurring in 1-3 days & by 1 month 97% were back. Repeated thoracentesis carries increased risk of pneumothorax, bleeding, empyema, fluid loculation & HYPOPROTEINEMIA (which favors transudation and more fluid.) Effective immediate symptom relief by effecting pressure - volume curves & length-tension relationship of the diaphragm. -Tube Drainage: closed drainage is inefficacious; but Denver pleuroperitoneal shunt a good alternative(?). Tube drainage is a necessary prelude to pleurodesis (the drainage should be less than 50-100 cc/24 prior to instillation therapy.) Pleurodesis: Tetracycline: (No longer available) 1500 mg +/lidocaine in 50-100 cc. 15mg/kg 70% pts free of Pl Ef @ 1 month. Bleomycin : 40 IU / m^2 90 IU intracavitary dose... 78-85% success rate 1.24 U/kg 1.25 milligrams per kilogram (not to exceed 40 milligrams per square meter in elderly patients) Doxycycline : 500 mg Talc : By slurry or Poudrage via Pleuroscopy.5 grams of talc via insufflation during thoracoscopy or as a slurry via chest tube Quinacrine : Not used The presence of Hilar or mediastinal masses, atelectasis or endobronchial lesions are associated with an increased failure rate of sclerosing agent. -Pleurectomy: Major operative procedure with 23% complication rate (air leaks, bleeding, pneumonia, empyema, chf, pe, resp insuf.) High morbidity & mortality w/ 90-100% response rate. -External Beam Radiation: is of limited use in malignant eff. 1400-2300 rads. effective in lymphomatous effusions 195 ABDOMINAL PAIN Immediate Questions (Determine whether the patient has an acute "surgical" [i.e., requiring surgery] abdomen): A. What are the patient's vital signs? Orthostatic blood pressure and pulse changes help ascertain the patient's volume status. Fever occurs in inflammatory conditions. Tachycardia and hypotension would suggest circulatory or septic shock from perforation, hemorrhage, or fluid loss into the intestinal lumen or peritoneal cavity. B. Where is the pain located? When did the pain begin? Sudden onset suggests perforated ulcer, mesenteric occlusion, ruptured aneurysm or ruptured ectopic pregnancy. What is the quality of pain? Intestinal colic occurs as cramping abdominal pain interspersed with pain-free intervals. C. Are there any associated symptoms? Vomiting may result from intestinal obstruction or could result from a visceral reflex caused by pain. D. If the patient is a woman, what is her menstrual history? CHARACTERISTIC PHYSICAL FINDINGS IN THE ACUTE ABDOMEN Peritonitis Generalized guarding, tenderness, rebound tenderness, hypoactive or absent bowel sounds Appendicitis Right lower quadrant tenderness, guarding and rebound, discrete tenderness at McBurney's point, peak age 10-20. Acute cholecystitis Right upper quadrant tenderness and guarding, positive Murphy's sign, may radiate to right scapula. High Small Bowel obstruction Severe vomiting, dehydration, no distention Low Small Bowel obstruction Distention, hyperactive and high pitched bowel sounds, vomiting. Bowel Infarction Pain out of proportion to tenderness, rectal bleeding if venous infarction. Ruptured aortic aneurism Pulsatile tender mass, hypotension, back pain Pancreatitis Steady, severe, LUQ and epigastric pain radiating to the back; pain less when sits forward; decreased BS; diffuse tenderness. Plan: The initial goal in evaluating a patient with abdominal pain is to determine whether or not surgical treatment is indicated to prevent further morbidity. A. The abdominal films can help differentiate between: 1. Several diagnoses can cause a surgical abdomen, the most life-threatening considerations are perforated or ruptured viscus, intraabdominal hemorrhage, and necrosis of a viscus, (e.g., necrosis of an intraabdominal viscus due to intussusception, volvulus, strangulated hernia, or ischemic colitis). Other specific conditions that may not cause an acute "surgical" abdomen should be considered: pancreatitis, intraabdominal abscess, peptic ulcer disease or gastritis, pyelonephritis, renal stones, infectious gastroenteritis, ovarian cyst, tumor and salpingitis. 196 2. Among the elderly and those on steroids, abdominal pain may be mild despite the presence of an acute abdomen. One should not underestimate the seriousness of mild abdominal pain in the elderly, especially if it is associated with acute confusion, fever, an elevated WBC or a metabolic acidemia. B. Laboratory tests to consider are a CBC with a differential, amylase, liver function, urinalysis, and pregnancy test. C. Flat and upright abdominal films. These films can be readily obtained and may provide important information. Observe for the following: gas pattern, evidence of bowel dilation, air-fluid levels, presence or absence of air in the rectum, pancreatic calcifications, biliary and renal calcifications, aortic calcifications, loss of psoas margin. D. Observation. With the exception of those conditions that require urgent surgical exploration, most cases of abdominal pain can be initially managed with close observation, correction of any fluid or electrolyte disturbances, and judicious use of analgesics. In general, any patient on a medical service developing acute abdominal pain should receive an evaluation by a general surgeon. In those cases in which mechanical obstruction is suspected or vomiting is present, nasogastric decompression should be initiated. Patients who appear in septic or circulatory shock should receive vigorous intravenous volume replacement, cultures, empiric antibiotics and be in an ICU setting. GASTROINTESTINAL BLEEDING (Acute upper)The mortality for acute upper gastrointestinal bleeding is about 8-10% and in part is due to underlying diseases of the liver, kidney, CNS, pulmonary and neoplastic disease. CLINICAL: The most common presentation is that of hematemesis and melena. Hematemesis is suggestive of bleeding that is proximal to the ligament of Treitz. Hematemesis may be either frank bright red blood or "coffee ground". Bright red blood infers that the hematemesis occurred immediately after bleeding, whereas coffee ground emesis is due to blood that has interacted with hydrochloric acid. Patients may also have melena (black, tarry, foul smelling stools). Melena must be differentiated from those patients that are taking iron, licorice or bismuth. Melena is due to degradation of the hemoglobin in the GI tract by bacteria to hematin or other homeochrome. Melena can takes several days to clear after there has been cessation of the upper GI bleeding. Approximately 50-100 ml of blood is needed in order to produce melena. PHYSICAL: Physical examination is important, for it can provide a clue as to the etiology of the bleeding. For example, if the patient has spider angiomas, splenomegaly, asterixis, ascites, testicular atrophy, jaundice and gynecomastia, the possibility of esophageal varices or alcoholic gastritis arises. Abdominal tenderness in the epigastric area is suggestive of peptic ulcer disease. Hyperactive bowel sounds may indicate that the bleeding is in the upper GI tract. If hyperpigmented macules are seen on the lips this would suggest the Peutz-Jeghers syndrome. Soft tissue masses may be associated with Gardner's syndrome. Lymphadenopathy, abdominal masses and Kaposi's sarcoma lesions would be suggestive of a malignant process as the etiology. Perioral telangiectasias would point toward hereditary hemorrhagic telangiectasia, whereas blue subcutaneous nodules can be associated with blue rubber bleb nevus syndrome. History is also important in providing clues as to the cause of the bleeding. Inquire as to the use of NSAIDS, and if the patient is being treated for peptic ulcer disease. If the patient had violent coughing or retching prior to the GI bleeding, Mallory-Weiss syndrome would be in the differential diagnosis. Mallory-Weiss tears are lacerations that occur in the gastric cardia or the gastroesophageal junction. They are usually about 1-2 cm in length. They typically occur with persistent vomiting or wrenching, but have been seen following heavy lifting, hiccups, straining at the stool, trauma, asthma, cardiopulmonary resuscitation, childbirth, and endoscopy. In about 50% of cases no etiology can be found. Mallory-Weiss tears account for about 15% of all upper GI 197 bleeding. Mallory-Weiss bleeding usually stops spontaneously in greater than 90% of cases. If bleeding does not stop, epinephrine injection and thermal therapy may be effective. In patients who fail endoscopic therapy, angiographic embolization or intra-arterial vasopressin can be used, which is effective in 70%. Also, inquire about the patient's alcohol use and if there has been liver disease in the past, as this would indicate that the bleeding originated from esophageal variceal bleeding. A history of previous aortic graft surgery indicates the possibility of an aortoenteric fistula. Aortoenteric fistulas are rare, with most of these occurring in the third portion of the duodenum. Most of the patients have had Dacron graft surgery. The fistula may occur at the suture line or into the graft. There may be associated sepsis and positive blood cultures. The first bleed from an aortoenteric fistula is known as the herald bleed, usually is brief, and usually stops spontaneously. However, this is deceiving, as the bleeding resumes in a few hours or days and can be massive. CT scanning can show air bubbles in the wall of the aorta, or evidence of perigraft infection. Angiography may not demonstrate the fistula unless there is active bleeding. Upper endoscopy should be done in all patients that have had an aortic graft placed and GI bleeding, to rule out other potential causes for the bleeding. LABORATORY: Serial CBCs should be done. The initial Hct may be deceiving because it does not accurately reflect the degree of blood loss. However, as the intravascular volume is restored, the hematocrit will drop. This may take up to 3 days. Platelets should be assessed as thrombocytopenia may be due to portal hypertension. If patients are actively bleeding, and the platelet count is less than 70,000/ul, platelet transfusions should be given. Prolongation of the prothrombin time is compatible with liver disease and is treated with subcutaneous vitamin K and fresh frozen plasma if the patient is actively bleeding. Elevated BUNs are commonly found in upper GI bleeding, due to absorption of blood proteins and intravascular volume depletion. Patients needing multiple blood transfusions should have frequent calcium and potassium determinations. DIFFERENTIAL DIAGNOSIS: Most cases of upper GI bleeding are due to peptic ulcer disease, with duodenal ulcers more common than gastric ulcers. The remaining causes consist mostly of varices, Mallory-Weiss lacerations and gastric erosions. TREATMENT: The first step in treatment is a rapid assessment of the urgency of the bleed. A patient that presents with a BP of 95-100 systolic, and tachycardia suggests that the patient has lost 50% of blood volume. If the patient is not in shock, BPs should be checked in the supine and upright positions. A systolic blood pressure that drops to less than 90 mm Hg on standing suggests a loss of 25-40% of the blood volume. If there is a decrease of 10 mm Hg or more in the systolic blood pressure, or an increase in heart rate above 120, a loss of 20% of the blood volume is probable. Patients that have active bleeding should be immediately treated with IV normal saline or Ringer's solution administered through two large bore 14 to 18 gauge peripheral catheters. Blood should be obtained for immediate type and cross match, CBC, platelet count, PT, PTT and chemistries. EKGs should be done in patients over the age of 40, those with chest pain, or a history of coronary artery disease. Oxygen should be given if large amounts of blood have been lost. Some patients will need endotracheal intubation to prevent aspiration, particularly those with esophageal variceal bleeding. In some emergencies, non-crossed matched O negative blood may be necessary. Patients with questionable bleeding sites will need a nasogastric tube inserted. A return of bright red blood indicates active, recent upper GI bleeding. However, the absence of a bloody return does not rule out upper GI bleeding, for the bleeding may be coming from the duodenum, or the nasogastric tube may be curled in the fundus of the stomach. Likewise, bile stained aspirates do not rule out an upper source. Following the assessment, the nasogastric tube can be removed. GASTRIC LAVAGE: In the past, iced saline has been used extensively. Recently, however, the effectiveness of this has been questioned, and studies have shown increases in bleeding times, and prothrombin times. Therefore, iced saline is probably of no proven benefit, and, in fact, may be detrimental. Likewise, the addition of epinephrine to the lavage fluid, is of no benefit. ACID REDUCERS: There has been no single trial that has shown consistent, overall benefit of H2 antagonists in stopping acute GI bleeding. Omeprazole, which is a proton pump inhibitor, has been shown in some reports to be successful in stopping GI bleeding. Other reports have shown no significant differences between placebo and omeprazole in terms of rebleeding, transfusion requirements, morbidity, and the need for surgery. Tranexamic acid has also been used in upper GI bleeding with inconsistent data. Furthermore, the side effects associated with the use of tranexamic acid, has limited its use. Somatostatin and octreotide (its analogue) have no proven benefit in active upper GI non-variceal bleeding. The benefits of sucralfate is also questionable at the present time. Vasopressin has not shown any particular benefit in stopping acute non-variceal upper GI bleeding. 198 ENDOSCOPIC THERAPY: There are 2 types of endoscopic therapy; the thermal method, such as heater probe, electrocoagulation, laser therapy, AND the injection therapy. Studies have found that thermal methods and injection therapy can reduce the need for emergency surgery by 60-80%, and reduce recurrent bleeding when used in patients with active hemorrhage or visible vessels seen at endoscopy. Laser therapy is not used much because of its high cost, lack of portability, and associated technical problems. Monopolar electrocoagulation has been used for coagulation of blood vessels, but there is the potential for sparking, deep tissue destruction and perforation. The use of multipolar coagulation , however, results in more controlled tissue destruction. The degree of tissue destruction is determined by the amount of pressure that is placed on the tissue by the multipolar probe. The heater probe, like the multipolar coagulation system, controls the amount of destruction by the amount of probe pressure applied to the tissue. Endoscopic injection therapy can achieve hemostasis by using 98% alcohol, epinephrine, sclerosant and saline. Epinephrine functions by constricting the blood vessels, and producing edema in the surrounding tissues. Sclerosant and 98% alcohol cause inflammation in the blood vessels with shrinkage of the surrounding tissues which leads to vessel thrombosis. Most GI specialists would recommend multipolar electrocoagulation, heater probe or injection therapy because of their low cost, efficacy, safety and ease of use. Most series show a perforation rate of less than 1%. SURGERY AND ANGIOGRAPHY: Patients that fail endoscopic hemostasis will need surgery. Patients that are not good candidates for surgery and fail endoscopic therapy can be treated with angiographic embolization or intra-arterial vasopressin. ALCOHOLISM A. History: "CAGE" 1. Have you ever tried to Cut Down on your drinking? 2. Do you get Angry when people talk to you about your drinking? 3. Have you ever felt Guilty about drinking? 4. Do you ever have an "Eye Opener" in the morning? B. Diseases Associated with Alcoholism 1. Gastrointestinal Irritation a. Gastritis and Gastric Ulcers b. Esophagitis 2. Pancreatitis a. Acute Pancreatitis b. Chronic pancreatitis with complications c. Pancreatic carcinoma 3. Metabolic Abnormalities a. Increased NADH/NAD ratio causes: вЂў increased conversion of acetaldehyde to beta-hydroxybutyrate (BHB) вЂў lactic acidosis - increased lactate synthesis from reduction of pyruvate b. Folate Deficiency: Mean Corpuscular Volume (MCV) >105 fl c. Iron Deficiency (may be due to gastrointestinal bleed) d. Thiamin Deficiency - may be exacerbated by glucose therapy (ie. give thiamine first) e. Note that chronic liver disease may also cause an increased MCV f. Alcoholic Ketoacidosis g. Decreased urinary excretion of uric acid (due to lactate inhibition) h. ETOH Anemia: slightly increased MCV (~103 fl) 4. Hepatitis a. Fatty Liver (enlarged) b. Cirrhosis (Micronodular or LaennecвЂ™s) 5. Buccal Hyperplasia 6. Neurologic Disease a. Encephalopathy: Wernicke type, Hepatic encephalopathy (usually cirrhotic) b. Cerebellar Degeneration c. Nutritional polyneuropathy (peripheral) d. Seizures 7. Wernicke's Encephalopathy a. Due to Thiamine (Vitamin B1) deficiency b. Mental Confusion, nystagmus, ophthalmoplegia, gait ataxia c. Medical Emergency d. Requires immediate thiamin 50mg iv (or im) to prevent further brain damage e. Thiamine should be given before other iv infusions (or Wernicke's may be exacerbated) f. Often with Korsakoff's syndrome вЂ“ gross disturbance in recent memory 8. Seizures a. Alcoholic (during intake) b. Withdrawal (24-60 hours after intake) c. Delirium Tremens (usually 48-96 hours post intake) d. Trauma (focus) 199 9. Myopathy [1] a. Skeletal muscle weakness and atrophy b. Dilated cardiomyopathy - women appear more susceptible than men [4] c. Usually requires >10 years of heavy drinking 10. Other a. Poor Dentition b. Trauma c. Internal Bleeding d. Increased risk of serious infection - pneumonia, aspiration, tuberculosis [5] e. Increased risk (>2 fold) of developing ARDS with chronic alcohol abuse vs. none [8] f. Low level alcohol ingestion appears to reduce cholesterol and may be cardioprotective g. Depression [10] 11. Fetal Alcohol Syndrome [2] a. Exposure to EtOH during pregnancy b. First trimester exposure probably: bland face, microcephaly, retardation c. Later exposure probably: behavioral abnormalities d. Timing and peak level of EtOH most important e. Newborns with syndrome may have withdrawal symptoms, tremors, hypotonia f. Neuroligc abnormalities, Septal defects, Renal hypoplasia also occur g. Complete abstinance from EtOH recommended during pregnancy C. Metabolism of Ethanol [7] 1. Ethanol is oxidized by alcohol dehydrogenase producing acetaldehyde 2. This is converted to acetate, and 2 NAD molecules are reduced to NADH 3. High NADH levels favor conversion of pyruvate to lactate leading to lactic acidosis a. High lactic acid levels inhibit renal urate excretion leading to hyperuricemia b. High NADH levels also oppose gluconeogenesis, Krebs cycle, and fatty acid oxidation c. Inhibition of gluconeogenesis predisposes to hypoglycemia and seizures 4. Acetaldehyde a. Inhibits repair of alkylated nucleoproteins b. Promotes cell death by depleting cells of glutathione (an anti-oxidant) c. Binds tubulin leading to inhibition of protein secretion and hepatocyte ballooning d. Crosses placenta, impairs fetal fetal DNA methylation, leads to fetal alcohol syndrome 5. Induction of microsomal ethanol-oxidizing system (MEOS) a. Long term ethanol consumption induces MEOS b. This permits metabolic tolerance to alcohol c. This oxidizing system can convert many substances to very toxic agents d. Acetaminophen (TylenolВ®), isoniazid, cocaine are converted to toxic molecules e. The MEOS also generates toxic oxygen species f. Depletion of reduced glutathione and anti-oxidant vitamins contributes to toxicity g. Short term alcohol consumption competes with other drugs for MEOS D. ETOH Withdrawal 1. Minor symptoms occur 1-2 days after withdrawal, usually after stopping chronic EtOH use 2. Major symptoms: 1-2% of ETOH abusers. Cannot predict which ones 3. Pathophysiologic and Symptomatic Changes a. Autonomic Nervous System Dysfunction: nausea and vomiting b. Increased sympathetic outflow: Locus ceruleus (norepinephrine) activation c. Neuronal Excitation: Seizures d. Mental Clouding: hallucinations, delirium 4. Mnemonic for withdrawal: "THE DTs" a. Tremulousness - 8-12 hours b. Hallucinations - 24-48 hours c. Epilepsy (Seizures) - 8-24 hours d. Delirium e. Tremors with Delirium - >48 hours after ETOH stopped f. Note that ETOH level is not necessarily zero (0) during withdrawal 5. Delirium Tremens a. Medical Emergency b. ICU Monitoring c. Adequate sedation d. Control of cardiovascular system E. Therapy for Withdrawal 1. Block sympathetic discharge a. Clonidine 0.2mg po or patch as needed; excellent for hypertension, tachycardia b. Benzodiazepines - will reduce sympathetic discharge c. Гџ-Blockers - especially with esophageal varices. Proprandol qid or Atenolol qd 2. Prevent (Reduce) Withdrawal [ 3, 9] a. Benzodiazepines are first line and may also prevent or reduce seizures b. Lorazepam (AtivanВ® 1-2mg q2-4 hrs) IM or IV; avoid diazepam (ValiumВ®, long half life) c. Oxazepam (SeraxВ® 15-30mg q4-6-), Chlordiazepoxide (LibriumВ® 25-50mg q8-), others d. Originally recommended standing dose with taper over 3-7 days 200 e. Suggest prn dosing, fairly liberally, for inpatients, as effective, decreased side effects f. Benzodiazepines have never been prevent to prevent DTs 3. Fluid resuscitation - most alcoholics are dehydrated 4. Nutritional Supplementation a. Thiamine 100mg iv - give first; prior to any glucose to prevent acute Wernicke Syndrome b. Glucose 1 Amp D50 - give after thiamine as glycogen stores are depleted c. Folate 1mg iv qd d. Multivitamins F. Alcoholic Liver Disease 1. Pathophysiology a. Metabolism via alcohol dehydrogenase (ADH) and MEOS (induced by EtOH) b. Toxic effects of metabolites (eg. acetaldehyde), highly reactive with biomolecules c. Acetaldehyde (CH3CHO) is made from ETOH oxidation (CH3CH2OH) 2. Pathology a. Fatty Liver - can begin within days of heavy drinking b. Alcohol induced cirrhosis - often occurs in absence of hepatitis intermediate c. Cirrhosis results from reduction in collagen degradation d. Fibrosis results from necrosis of liver cells with inflammation 3. Symptoms a. Hepatomegaly, Jaundice b. Ascites, Encephalopathy 4. Effects on liver a. AST mildly increased; ALT may not be increased b. Typically AST:ALT > 2 (ETOH induces AST) c. Jaundice may occur in early moderate or severe disease d. Fatty liver change leads to hepatomegaly and eventually liver failure e. Micronodular cirrhosis and fatty liver may be seen on biopsy specimens G. Abstinence 1. Difficult for most persons 2. Family history of alcoholism predicts recurrent alcoholism 3. Social reinforcement of abstinence, usually with Alcoholics Anonymous, is critical 4. Disulfiram (AntabuseВ®) - causes a severe reaction when taken with alcohol 5. Naltrexone (ReViaВ®) a. An opioid receptor antagonist, recently FDA approved for treating alcohol dependence b. Reduces craving in abstinent patients c. Blocks reinforcing effects of alcohol in patients who do drink d. Dose is 50mg po qd and acts for ~24 hours; duration of treatment usually 12 weeks e. Adverse effects - mild nausea, mild sedation, may cause mild hepatitis f. Drug interactions - with thioridazine can increase sedation; avoid hepatotoxic drugs g. Agent should not be started until patient is alcohol (and opiate) free h. Long term trials are lacking but may prevent relapses 6. Desipramine [10] a. High rates of depression in alcoholics suggest use of anti-depressants b. In alcoholics without depression, desipramine did not reduce alcohol abuse c. In alcoholics with depression, desipramine increased abstinence from alcohol ALCOHOLIC WITHDRAWALThiamine 100 mg IV or IM prior to glucose then 50 mg qid x 5-10 days. Magnesium sulfate 50% soln 2 ml IM q12h x1 day then once daily x 3 days. Lorazepam 1-4 mg po or IV q4h OR Librium 25-100 mg po or IV q4-6h the first day then reduce by 100 mg each following day. Tenormin 50-100 mg daily for tachycardia, increased BP and tremors. Folic acid 1 mg po daily. Hydrate. For seizures use valium, dilantin. ALCOHOLSEIZURES: Withdrawal from acute alcohol intoxication may cause seizures. Most occur 12-48 hrs after a drinking binge, but may occur at any time. Dilantin 1 gram IV over 30 minutes with continuous monitoring ECG and BP. Renal and liver function studies should be obtained. CT of head is considered. Lumbar puncture should be seriously considered in patients with sepsis or persistent fever in whom a readily evident cause for the temperature elevation cannot be found. 201 DELIRIUM TREMENS: This is the most serious complication of alcohol withdrawal. Usually starts a day or so after drinking is stopped and may last for 1-2 days. Characterized by agitated, confusional state, tremulousness and autonomic hyperactivity. Need hydration and sedation. WERNICKE'S ENCEPHALOPAHTY AND KORSAKOFF'S PSYCHOSIS: WernickeвЂ™s encephalopathy usually manifests as a triad of encephalopathy, ophthalmoplegia and ataxia due to thiamine deficiency. Neuropathologic changes are seen in the tissues surrounding the 3rd and 4th ventricles, most prominently in the mamillary bodies and may be seen on MRI or CT. KorsakoffвЂ™s psychosis is a disabling memory disorder related to WernickeвЂ™s encephalopathy and may result from thiamine deficiency. Patients should be given 100 mg of thiamine hydrochloride (Betalin S) IV daily for 5 days. CEREBELLAR DEGENERATION: is seen in long term alcoholics. Clinical manifestations include gait ataxia and dysarthria. Treatment is supportive. Abstention from alcohol and improvement in nutrition have reduced the rate of progression and in some cases even reversed symptoms. MARCHIAFAVA-BIGNAMI DISEASE: is rare and may be acute, subacute or chronic in nature. Clinically it results in dementia, dysarthria, spasticity and gait apraxia and may progress to coma. Neuropathologic cause is necrosis of the corpus callosum and subadjacent cortical white matter. MRI may visualize. CENTRAL PONTINE MYELINOLYSIS: There may be an aberrant mental state, quadriparesis, paraparesis, and lower cranial nerve dysfunction. The syndrome occurs following the rapid reversal of chronic and subacute hyponatremic states, and may result from conditions other than alcoholics such as chronic liver disease, and burns. In severe cases it may result in a locked in syndrome (complete paralysis except for the eyes). Neuroanatomically there is demyelination of the base of the pons. Treatment is non-specific. Slow correction of sodium deficiency by means of restriction of water consumption or closely monitored administration of small amounts of hypertonic saline solution should be carried out. FETAL ALCOHOL SYNDROME: Features include cranial-facial dysmorphisms, systemic and mental retardation and developmental anomalies of several organ systems. Occurs in about .1.3% of live births in the USA and accounts for about 5% of congenital abnormalities. Partial expressions of full blown clinical syndrome have been described. PERIPHERAL NERVOUS SYSTEM EFFECTS: They may correlate with the extent and length of alcohol use, and are most often those of a symmetric, distal polyneuropathy involving sensory, motor, and autonomic nerves. Paresthesia, dysesthesia, numbness and ataxia are common as are symptomatic mononeuropathies resulting from local trauma or compression of larger peripheral nerves. MYOPATHIES: affect about 50% of chronic alcohol abusers. May occur shortly after a drinking binge, manifested clinically by pain and tenderness of an affected muscle, usually a proximal skeletal muscle. Lab reveals myoglobulinuria and an elevation of serum CPK-MM. EMG may show myopathy and muscle biopsies often demonstrate involvement of type I fibers. Complications may include cardiac dysrhythmias, renal failure and electrolyte abnormalities. A chronic state of alcoholic myopathy, evidenced by muscle cramping and atrophic changes particularly of the hip and shoulder girdles is even more common. Involvement of type II fibers is often seen on muscle biopsy in patients with chronic myopathy. VIOLENT PATIENTSThe violent patient is usually calmed by using either a benzodiazepine or haloperidol. If the patient is not psychotic, lorazepam is usually used. Patients that have psychotic episodes such as schizophrenia or bipolar affective disorders, haloperidol or droperidol are the best drugs. In some patients, both of these drugs may be used. This combination is usually composed of 5 mg of haloperidol and 2 mg of lorazepam given IM every 2-3 hours until sedation. This combination should not be given IV. Lorazepam is preferred over diazepam because it has a faster onset of action and shorter duration of action. Do not use oral lorazepam. IV lorazepam should be used judiciously because of vein irritation. Lorazepam given sublingually has been effective and works just as fast as IM injection. If both lorazepam and haloperidol are being given, the two can be mixed in the same syringe and given IM. Lorazepam is given at 1-2 mg every 1-2 hours, either sublingually or IM until the patient is sedated or up to a maximum of 4 mg. For patients with renal, or COPD or the elderly, downward adjustments will have to be made. In these patients you should start with .5 mg. Haloperidol is given in small intramuscular boluses to treat schizophrenia and other psychoses. Extrapyramidal complications are side effects. IV haloperidol is not routine even though the literature supports its safety and efficacy. It can be used if a violent patient needs alleviation of agitation immediately. Sedation usually reaches its peak at about 20 minutes after an IM dose and 5-10 minutes after IV. Start with 5-10 mg of Haloperidol as a slow IV push, which may be repeated every 10 minutes until calm is established. Elderly patients are only given 1-2 mg IV every 10 minutes for 3 doses, and then the dose may be escalated to 5 mg every 10 minutes if it 202 is tolerated. Patients that are severely agitated may need up to 50-75 mg IV every 30-60 minutes. Use caution in patients that are ethanol intoxicated or other drug intoxications. Haloperidol may also lower the seizure threshold. Haloperidol usually doesn't impact on the patient's vital signs or respiratory function when given IV. Extrapyramidal reactions are rare and tend to be milder with IV Haloperidol use, and usually do not occur during the first 24 hours. Diphenhydramine is used to reverse the symptoms. A very rare side effect is neuroleptic malignant syndrome. Droperidol, may have fewer side effects than haloperidol. The dosage is 2.5 to 5.0 mg via IV push. RANSON'S CRITERIA: For Determining Prognosis of Acute Pancreatitis UPON ADMISSION: 1.Age > 55 2.Blood Glucose > 200 mg/dl 3.WBC count > 16,000 / cu mm 4.Serum LDH > 700 IU% 5.SGOT > 250 SF units % (56 units/dl) AFTER 48 HOURS: 1.HCT decrease > 10% 2.Serum Ca2+ < 8mg % (mg/dl) 3.Base Deficit > 4 mEq/l 4.BUN increase > 5mg % (mg/dl) 5.est. fluid retention > 6L 6.Arterial 02 tension < 60 mm/dg < 3 signs - better prognosis, < 1% mortality. > 3 signs - serious acute pancreatitis - may be 25% mortality. Modified Child's Index for Grading Severity of Liver Dz Clinical or Lab Feature 123 Encephalopathy None Mild-moder Severe Ascites None Slight Moderate Bilirubin < 2mg/dl 2-3 mg/dl > 3 mg/dl Albumin > 35 g/l 28-34 g/l < 28 g/l Prothrombin time <4 sec 4*6 sec > 6 sec (prolonged) 5-6 points: good operative risks 7-9 points: moderate operative risks 10-15 points: poor operative risks ACUTE BLINDNESS Immediate Questions: A. What is extent of visual loss? Monocular? Visual Field, hemianopsia (one-half visual field), homonymous (same half), bitemporal (pituitary tumor) or binasal (rare)? B. Prior symptoms? Eye pain? Differential Diagnosis of Acute Monocular Blindness: A. Retinal detachment. Often preceded by floaters or flashing lights; painless; detachment visible on funduscopic exam. Risks are extreme myopia and trauma. Emergency ophthalmologic consult is needed for urgent reattachment. 203 B. Central retinal vein occlusion. No prodrome; painless. Funduscopic shows edema, hemorrhages and dilated veins. Associated with hypertension. Requires emergent ophthalmologic consult. C. Central retinal artery occlusion. Acute onset; painless; may be history other thromboembolic disease, atrial fibrillation or carotid disease. Funduscopic reveals pale disc and cherry red spot in the macula. Requires emergent ophthalmologic evaluation. D. Acute (narrow angle) glaucoma. E. Ischemic optic neuritis: Temporal arteritis. Elderly white woman; may be history of headache; elevated ESR. Abrupt onset blindness. Begin empiric high dose steroids, if diagnosis is suspected. F. Trauma. G. Optic Neuritis. Decreasing vision over several days; associated with multiple sclerosis. H. Infiltrate or compression due to tumor or aneurysm. Data to Document Eye Findings: A. Inspection B. Extraocular muscle movement C. Pupil response direct and consensual D. Visual acuity and fields E. Funduscopic F. Obtain emergent ophthalmologic exam ACUTE DYSTONIC REACTION Immediate Questions: A. What are the vital signs? B. What medications is the patient receiving? C. Is IV Benadryl (diphenhydramine) available on the floor? Diagnosis and Management: A. Dystonias are idiosyncratic drug reactions that involve acute involuntary muscle movements and spasms. Although any muscle group in the body can be involved, the commonest manifestations are torticollis, facial grimacing, and opisthotonos. B. Because of their antidopaminergic properties, anti-psychotic agents often are associated with a variety of motor disorders. The use of drugs of this class, Compazine for example, can cause an acute dystonic reaction. C. Treatment is diphenhydramine 50 mg IM or IV, or benztropine 2 mg IM or IV; improvement generally occurs within seconds or within 15 to 30 minutes. These doses can be repeated in 30 minutes. Even if the agent is discontinued, oral treatment with either agent may be helpful for the next 3 to 21 days, since symptoms can recur. 204 SEIZURES A. Definitions and Background 1. Seizures are abnormal spontaneous firing of nerve tissue 2. May affect part (focal) or all (general) of the brain 3. Over 2 million patients with seizure disorder (epilepsy) in USA 4. Medications control ~80% of these patients very well 5. Thus, over 400,000 patients with intractable or poorly controlled seizures B. Causes in Infants 1. Trauma 2. Infection / Fever 3. Tumor 4. Degenerative 5. Aminoaciduria 6. Metabolic a. Hypoglycemia b. Hyponatremia c. Hypocalcemia 7. Developmental a. Arteriovenous Malformation (AVM) b. Hyperactive focus - usually a scar 8. Idiopathic C. Causes in Children 1. Hemorrhage 2. Toxins - drugs 3. Renal Failure 4. Cerebrovascular Abnormalities 5. Metabolic 6. Infection / Abscess 7. Fever D. Causes in Adults 1. Idiopathic 2. Post-Traumatic 3. Post- or peri-stroke 4. Tumor - ~10% of new onset seizures 5. Alcohol - withdrawal seizures more common than during use 6. Eclampsia 7. Vasculitis 8. Medial Temporal Sclerosis 9. Metabolic - As above 10. Abscess / Encephalitis / Meningitis 11. Medications a. Anti-psychotics - lower seizure threshhold b. Lidocaine c. Гџ-Lactams - especially imipenem, high dose penicillin d. Meperidine (Demerol(r)) - metabolites are epileptogenic 12. Multiple Sclerosis - very rare cause E. Differential Diagnosis 1. Syncope, Presyncope 2. Transient ischemic attack 3. Transient global amnesia 4. Cardiac Arrhythmia 5. Migraine (atypical) 6. Vertigo 7. Tremor 8. Breath-Holding / Functional F. Types of Seizures and Therapy [ 1, 6] 1. Level of Consciousness a. Simple: no loss of consciousness b. Complex: impairment or alteration of consciousness 2. Focus of Seizure activity a. Partial: begins at specific focus (may be idiopathic or structural or due to injury) b. Generalized: appear to begin diffusely in large part of the brain, loss of consciousness 3. Tonic Clonic: grand mal. Entire body is involved 4. Absence Seizures (Petit mal) a. 1-2 minute staring episodes b. Infrequent patient with very short (1-10 second) "spells" who have absence seziures 5. Complex Partial: lip smacking, fumbling, staring, guttural vocalization, confusion 6. Myoclonic Seizures: associated with anoxia, ischemia, drug overdose, idiopathic 205 7. Treating Symptomatic Partial Epilepsy [7] a. Simple partial seizures: cbz > pht=vpa b. Complex partial seizures: cbz > pht and/or gaba > vpa > pb = prim c. Evolution to Generalized (tonic-clonic) seizures: cbz > pht > pb > vpa 8. Treating Idiopathic Generalized Epilepsy (mainly children) a. Absence seizures: esm = vpa > clonazepate b. Myoclonic seizures: vpa > clonazepate c. Generalized tonic-clonic seizures: vpa > cbz > pht > pb = prim 9. Surgery for Seizures G. International Classification of Epileptic Seizures 1. Partial Seizures a. Simple Partial Seizures (no impaired consciousness) b. Complex Partial Seizures (impaired consciousness) c. Partial Seizures evolving into secondary generalized seizures 2. Generalized Seizures a. Absence Seizures b. Myoclonic Seizures c. Clonic Seizures d. Tonic Seizures e. Tonic-Clonic Seizures f. Atonic Seizures 3. Unclassified Seizures H. Specific Anti-Convulsant Agents [7] 1. Acute Therapy for Generalized Seizures a. Dilantin 1gm load iv (hypotension common side effect) b. Phenobarbital 30-60mg iv repeated every 5-10 minutes c. Benzodiazepine вЂў Diazepam (Valium(r)) more effective than lorazepam (Ativan(r)) вЂў Especially useful for alcoholic and alcohol withdrawal seizures d. Pentobarbital: status epilepticus; induce coma 2. Benzodiazepines a. Diazepam (Valium(r)): grand mal (tonic-clonic), alcoholic related seizures; 5mg iv/im b. Lorazepam (Ativan(r)): shorter t1/2 than diazepam; easier to use for withdrawal c. Clonazepam (Klonopin(r)): myoclonic seizures, also useful for anxiety 3. Phenytoin (pht; Dilantin(r)) a. Use: Partial Epilepsy, Generalized Tonic-Clonic seizures b. Side Effects: cognitive changes, gum hyperplasia, hirsutism, nystagmus c. Hypotension often occurs with intravenous loading (usually 50mg per minute to 1gm) d. Overdose: ataxia, nystagmus (especially vertical), induction of seizures, lethargy e. Note that phenytoin overdose usually occurs when patients on drug are given iv loading 4. Carbamazepine (cbz; Tegretol(r)) a. Use: Complex-partial seizures, Generalized Seizures, Second Line Myoclonic Seizures b. Side Effects: Drowsiness, diplopia, GI upset, low WBC (5-10%), Rash, allergy c. Severe Side Effects: Agranulocytosis, platelet decrease, aplastic anemia (1/20,000) d. WBC and Platelets should be monitored each week initially, then each month e. Drug Interactions (hepatic metabolism): warfarin, estrogens, theophylline, alcohol 5. Valproic Acid / Valproate (vpa; Depakene(r), Depakote(r)): a. Use: All seizure types, especially generalized epilepsy b. Side Effects: gastrointestinal upset, weight and apetite increase, fatigue, tremor, hair loss (510%; reversible) c. Severe: hepatotoxic reactions (usually on other drugs). Monitor liver function tests. d. Fatal Hemorrhagic Pancreatitis. 6. Phenobarbital (pb) or Primidone (prim; Mysoline(r)) a. Second line therapy in adults with resistant seizures b. Side Effects: Sleepiness, depression, personality changes c. Encephalopathy and hyperammonemia can also occur in adults 7. Ethosuximide: petit mal only (without other seizure types) 8. Phenyl Dicarbamates a. Meprobamate (Equanil(r)) b. Felbamate (Felbatol(r)): Oral only; approved for partial seizures В± generalization c. May block sodium channels, enhance g-aminobutyric acid (GABA) d. Less behavior and other side effects than earlier agents e. Side Effects: mild to moderate, HA, insomnia, fatigue, A/N/V, aplastic anemia, hepatitis f. Aplastic anemia risk high enough with Felbamate to warrant close monitoring [5] 9. Gabapentin (GABA, Neurontin(r)) a. Efficacy for partial and secondary generalized seizures, as add on agent b. Decrease incidence in secondary generalized seizures c. Enhances activity of GABA neurotransmission, inhibits sodium channels d. Drug interactions: does not alter plasma concentrations of other agents 206 e. Side Effects: mild in general; somnolence, dizziness, ataxia, fatigue, nystagmus, nausea 10. Lamotrigine (lamo, Lamictal(r)) a. Approved in USA for use in partial seizures in adults b. Blocks voltage dependent sodium channels c. Metabolism by glucuronidation, does not induce P450 enzymes, few drug interactions d. Valproate inhibits metabolism of lamotrigine, and lamotrigine decrease valproate levels e. Generally very well tolerated when added to other drugs or used alone f. Most patients begin at 50mg po qd x 2 weeks, increase slowly to 300-500mg/day g. Effective in children with the Lennox-Gastaut Syndrome 11. Other Agents (not yet available in USA) [9] a. Oxcarbazepine: analog of carbamazepine, pro-drug requires liver metabolism b. Clobazam: benzodiazepine with reduced cognitive effects, used in refractory seizures c. Tiagabine: blocks GABA reuptake, refractory epilepsy d. Topiramate: blocks sodium channels, attenuates kainite responses, enhances GABA effect e. Vigabatrin: inhibits GABA breakdown, effective in resistant and new epilepsy f. Zonisamide: blocks sodium and calcium channels, effective in partial seizures 12. Experimental Agents a. Losigamone b. Remacemide c. Levetiracetam d. Fosphenytoin 13. All of the studied agents cause birth defects with 1% Risk of spina bifida (see below) 14. Choice of agent a. Use of single agent recommended whenever possible (~65% of patients) b. Above section (E) outlines preferred agents c. Surgical evaluation may be considered if drug combinations fail 15. Discontinuing Agents a. >60% of persons who remain free of seizures can have medications discontinued b. Most physicians wait 2-5 yearsof seizure-free time before slow reductions in dose I. Summary Of Uses Of Anti-Convulsive Agents Drug Generalized Absence Myoclonic Phenobarbital ++ + Phenytoin(Dilantin(r)) ++ Carbamazepine(Tegretol(r)) ++ Valproate (Depakote(r)) +++ ++ ++ Ethosuximide ++ Clonazepam(Klonopin(r)) + + + Diazepam(Valium(r)) + + Felbamate(Felbatol(r)) ++ Clonazepate + ++ J. Drug Treatment During Pregnancy [7] 1. Seizures are generally well controlled during pregnancy 2. Phenytoin levels may fall during pregnancy 3. Small increase in serious fetal malformations (~3% vs. 2% for average pregnancy) 4. Women on valproate or carbamazepine should take folic acid 5mg po qd during pregnancy 5. Slight increase in risk of Vitamin K depletion on cbz, pht, pb, and prim 6. Recommend 20mg vitamin K during last few weeks of pregnancy if on these medications K. Temporal Lobe Epilepsy 1. Arise in: a. Medial temporal lobe b. Amygdaloid Nucleus c. Hippocampus 2. Propagation to amygdala 3. Symptoms a. Feelings of depersonalization b. Emotionality c. Automatic Behavior d. Loss of memory during bizarre behavior 4. Cannot distinguish from partial complex seizures arising from frontal lobes without EEG 5. Treatment a. Carbamazepine b. Dilantin c. Valproate d. Phenobarbital 207 Status Epilepticus Definition: According to the International Classification of Seizures, it is ''a condition characterized by an epileptic seizure that is so frequent or so prolonged as to create a fixed and lasting condition". From a practical standpoint, continuous, generalized, tonic-clonic seizure activity lasting 30 minutes or longer, i.e., grand mal status epilepticus, is most worrisome and represents a life threatening emergency. Diagnostic evaluation: Immediately send off a CBC, a serum chemistry profile, and drug screen. Assess for possible drug intoxication or drug withdrawal as effectively as possible. Keep in mind that anticonvulsant drug withdrawal is a common cause of status epilepticus. Obtain an arterial blood gas if there is evidence of respiratory compromise. Obtain a brain scan (CT or MRI), with and without contrast as quickly as feasible to assess for a possible mass lesion. Evaluate for lumbar puncture, especially if there is clinical evidence of an infectious process and there is no contraindication by brain scan and bleeding studies. An EEG, on an emergency basis, may be indicated if there is an atypical presentation or a suboptimal response to medical intervention. Management: It is important to establish that there is no respiratory compromise and no evidence of cardiovascular collapse. Preparation for possible intubation and respiratory support should be made. Correction for metabolic disturbance, if present, is clearly indicated. Low serum Na+, glucose, Ca++, or Mg++ can result in recurrent seizure activity. Drug or alcohol withdrawal, or certain drug intoxication, can be precipitating factors. It is important to recognize that withdrawal from phenobarbital generally requires resumption of phenobarbital with a loading dose which will necessitate intubation with respiratory support. An intravenous line is mandatory. Initial, i.e., short-term, control of generalized seizure activity can often be obtained with either intravenous lorazepam, at a dose of 0.1 mg/kg, or diazepam at 0.2 mg/kg. Either agent is infused over two minutes. It is important to recognize that these agents can promote respiratory depression at relatively small doses in certain individuals. If either of these agents is used, it is with the understanding that longer term, i.e., maintenance, therapy must also be initiated unless there is a recognized metabolic derangement that can be rapidly corrected. Fosphenytoin is now available as the replacement for parenteral phenytoin. Each fosphenytoin vial contains 75 mg/ml which is equivalent to 50 mg/ml of phenytoin ( 1.5 equivalents). Its primary advantages over phenytoin include: significantly reduced risk of cardiovascular depression, markedly improved local infusion tolerance, and the ability to give it intramuscularly. Its dosing is expressed as phenytoin equivalents (PE). The loading dose in status epilepticus is 15 to 20 mg PE/kg at a maximum intravenous infusion rate of 150 PE/min. (For example the order for a 67 kg man would be: "Fosphenytoin 1000mg PE to be infused IV over 10 minutes". In such a circumstance, intravenous administration is preferred to intramuscular because the intravenous route allows less time to achieve a therapeutic plasma concentration. Fosphenytoin is converted to phenytoin after parenteral administration. It is recommended that phenytoin blood levels not be measured until the conversion of fosphenytoin to phenytoin is complete. This occurs approximately two hours after completion of the intravenous infusion. If the patient continues to have seizure activity despite adequate intravenous loading with fosphenytoin, then phenobarbital loading is indicated. Phenobarbital is given at an intravenous dose of approximately 20 mg/kg at an infusion rate of no more than 1.5 mg/kg/min. This translates into approximately 100 mg/min in adults. If this is unsuccessful, then intravenous pentothal is given at a loading dose of 3 to 4 mg/kg over two minutes followed by a continuous infusion at a rate of 0.2 mg/kg/min. The dose is then adjusted upward, every 3 to 5 minutes by 0.1 mg/kg/min, until the EEG becomes isoelectric. LUMBAR PUNCTURE TESTS 1.Cell Count 2.Gram Stain, AFB, KOH, Bacteria and Fungal 208 Cultures (CIE) 3.Glucose, Protein, LDH, VDRL 4.Cell Count, RBC, WBC 5.Viral Culture - CIE Indications: 1.CNS infection 2.Determine CNS Bleeding Contraindications: 1.Infection at site 2.Any Bleeding Disorder 3.Mass Lesion 4.Papilledema CSF ANALYSIS PRESSURE: 75-150mmH2O in lat decub pos PROTIEN: 15-45 mg/dl LD: 1/10 of serum GLUCOSE: 45-85 (60-70% of blood) COLOR: if yellow (xanthochromic) may indicate subarach bleed(previus bleed) or dark yellow indicating subarach block. -abnml color seen w/prot >100 CELLS: total cell CT: 0-5/cu. mm 2-10=borderline pleocytosis 25-50=elevated pleocytosis >50=severe pleocytosis (>500 usually purulent meningitis w/ predominant granulocytes) (300-500 w/predom lymph or monos -viral, syphilis, TB, lyme, partially tx'd bact inf, MS in 50%, sarcoid) (>40% MONOs c/w subarachnoid bleed) Stroke Risk Factors and Prevention Therapy Stroke Prevention Therapy for Patients with Atrial Fibrillation Age < 65 - Risk factors Present: Warfarin (maintain INR at 2-3) Age < 65 - Risk factors Absent: Aspirin Age 65 to 75 - Risk factors Present: Warfarin (maintain INR at 2-3) Age 65 to 75 - Risk factors Absent: Warfarin or aspirin Age > 75 - Risk factors Present or Absent: Warfarin (maintain INR at 2-3) (INR = international normalized ratio) Risk Factors for Stroke hypertension diabetes mellitus CHF coronary artery disease mitral stenosis prosthetic heart valves 209 left atrial enlargement global left ventricular dysfunction thyrotoxicosis history of TIA or stroke COMA (Common Causes)INFECTION: Meningitis, subdural empyema, encephalitis, and brain abscess. TUMORS: Primary tumors with gliomas being the most common. Metastatic disease most commonly from breasts, lungs, GI, and kidney. VASCULAR DISEASE: Subdural hematoma, epidural hematoma, subarachnoid hemorrhage and intracerebral hemorrhage. DRUGS AND TOXINS: Heavy metals, alcohol, salicylates, barbiturates, opiates, tranquilizers, sedatives. FLUID, ELECTROLYTE AND ACID BASE DISORDERS: All are capable of causing coma if severe. HYPOXIA: Anemia, hypo and hypertension, respiratory failure, decreased cardiac output. ENDOCRINE DISEASE: Hypo and hyperglycemia. Hypo and hyperthyroidism, hypo and hyperadrenalism, hypo and hyperparathyroidism, hypo and hyperpituitarism. OTHER: Uremia, heat stroke and hypothermia, Vitamin deficiencies as thiamine which can cause Wernicke's encephalopathy, seizures, concussion, status epilepticus. COMA CAUSESINFECTION: Sepsis, encephalitis, meningitis, abscess, granulomatous, viral encephalitis. TRAUMA: concussion, contusion, laceration, subdural and epidural hematoma. NEOPLASTIC: metastatic and primary. TOXIC: antidepressants, ethanol, tranquilizers, barbiturates, narcotics, anticonvulsants, anticholinergics, cimetidine, bromides, cyanide, carbon monoxide, cyanide, heavy metals, digoxin, lithium, methemoglobinemia, phenothiazine, organophosphates, salicylates, radiation. SYSTEMIC: renal failure, hypoventilation, hepatic failure. HYPOPERFUSION AND HYPOXEMIA: respiratory failure, status epilepticus, post cardiac arrest, severe anemia, aortic stenosis, altitude edema, arrhythmias, DIC, carotid sinus hypersensitivity, fat and post bypass emboli, pulmonary emboli, hyperventilation, hypertensive encephalopathy, hyperviscosity, malaria, hypovolemia, malaria, syncope, SBE, vasculitis and autoimmune disease. METABOLIC: increased or decreased glucose, calcium and sodium, hyperosmolar state, severe acidosis and alkalosis, Addison's or CushingвЂ™s syndrome, hyper and hypothermia, carcinomatosis, hypopituitarism, increased and decreased magnesium, decreased phosphorous, superior vena cava syndrome, acute porphyria, toxic shock syndrome, increased and decreased thyroid, thiamine, niacin, B6 and B12 deficiency. ANTIBIOTICS & Infectious Disease 1. Aerobic GNR: 1)Aminoglycosides 2)Cephalosporins 2-3rd gen 3)TMP/SMX 2. Anaerobes: 1)PCN, Amp,tetra,cephI-III, Clinda. 2)Chloramphenicol 3) Metronidazole (only Chlor/Flagyl cross BBB) 3. GPC/GPR: 1)PCN 2)PCN Resistant AbTx/ Extended Spectrum: a)IV: ox,naf,meth b)PO: clox, diclox 3)Meth Resistant Organisms: (S.Aureus, St.Epi, S.Fecalis) a)S.Epi: vanco +/- gent b)MRSA: Vanco 4)ENTEROCOCCUS: 210 a)non SBE: AMP b)SBE: PCN/VANCO + AMINO 4. H FLU: (Assume Amp Resistance) 1)Chloramphenicol 2)TMP/SMX 3)3rd Gen Cepahalosporin 4)Amox + Clauvulanic Acid 5)Erythro + sulfa 5. Neisseria: 1) PCN, Chlor, Erythro, CephIII. 6. Pseudomonas: 1)Tobra, Amakacin, Gent 2)Ceftazidime 3)Imipenem-Cilastatin 4)Cipro 5)Cefipine . Cellulitis (usually due to grpA strep) 1. PCN VK 0.5-1gm PO QID 2. Erythro 500 mg po qid . Diabetic Cellulitis 1. Cefoxiten 1-2g IV q8 (good anaerobic coverage) . Meningitis: (most commonly S.Pneum or N.Mening) 1. For S. Pneumonia PCN 2million U IV q2 x 10-14d 2. For N. Meningitis: same as above 3. for H. Flu: Cefuroxime 3g IV q8 TMP/SMX 4. Gram - Rods= 3rd Gen Ceph w/ . UTI 1. Amp 500mg po qid 2. TMP/SMX DS one PO BID 3. cephalixin 500mg po qid C-DIF COLITIS: May suggest lactobaccili by yogurt ingestion caused partic by macrolides but any ABX TX: Flagyl, Vanco po, Bacitracin po HIV & AIDS Stats, etc RISK: Needlestick 0.3% infected male to female < 50% STAGING: majority pt ASx LABS Absolute CD4(helper) # (nml=350-1200) PERSISTANCE STAGE: low viral product w/ seroconversion CD4 to 200 range plateau for to several years CD4 > 500 low risk for opp infection CD4 <50: High risk for opp inf 211 (follow trend since labs vary by 20-30%) HIV Viral Burden B2 microglobulin level -sm mw prot synth & secreted by cell involved w/ HLA I maj histocomp Ag's (by interferon and infections) -HIV+ & +B2MG = inc risk of AIDS (>5mg/dL) HIV p24 level: Eliza for p24 Ag (not fed licensed) In late Dz pt may make more P24Ag HIV Ag & P24 may be detected prior to seroconversion Plasma HIV co-culture LABS: ELIZA & Western Blot ELIZA: Tests for HIV Ab: (tests against HIV Ag) False +'s occur partic if +ANA,RF,cryoglobs,or PREGNANT False -'s in early HIV <12mo due to lack of Ab production High + pred value in high incidence population inexpensive & widely available (high index of suspicion makes +result not repeated due to impr ELIZA) (if low seroprevalence group :+ is likely false lab error) WB: IMMUNOBLOT: viral Ag 4% false pos (usually screened out by eliza) High + pred value in high incidence population More Expensive Than ELIZA variable reproducibility indeterminate either: -early disease or cross Rx AB re check at 3months PT EVAL: ? VD hepatitis, toxoplasma, ? where do they live, ?pets 1st tests: PPD, toxo serology, Hep screen, VDRL CD4 T4 helper cell count if >500 check q6months if 200-500 begin AZT & check q6mo if close to 200 check q3months if <200 begin PCP prophylaxis & re-check q3-6 months (infection risk @ CD4 < 200) TX: TX for CD4 < 500 AZT: well tol if used early DATA: improves survival decreases opp infections increases CD4 transiently Decreases progression to AIDS Dose:500mg qd in 100mg po q4 212 TOXICITY: incr MCV in everyone anemia, leukopenia DDI: didanosine VIDEX -raises CD4 count -survival studies not in yet -thus only for those who cant take AZT TOXICITY:-pancreatitis (9%) can be fatal -priph neuropathy (34%) DOSE: must chew tabs >75kg 300bid <50kg 125bid 50-74kg 200bid PCP DZ TX: -Bactrim: 15-20mg/kg/d x 3wks -pentamidine: 3-4mg/kg/d x 3wks For mild to mod DZ: -Dapsone/TMP: 100mg qd & 20/mg/kg/d Experimental tx: clinda / primaquine trimetrexate/leucovorin STEROIDS: for po2<75 on RA PCP PROPHYLAXIS:(for all w/CD4<200 or if pt has had PCP) BACTRIM: 1 ds po qd PENTAMIDINE AERO: 300mg q month CRYPTOCOCCAL MENINGITIS: Ampho B:in initial episode FLUCONOZOLE: for chronic suppression (200mg qd) TB: if HIV+ - 10% chance of reactivation each year -if PPD+ >5mm INH prophylaxis TOXOPLASMA: 95% is recrudescence 80% relapse if not tx Typically: focal brain lesion (50-70% are toxo - others are: lymphoma, PML, herpes, TB, KaposiвЂ™s -lesion typically by basal ganglia .5-11.6cm vs 30cm for lymphoma) TOXO TX: - Sulfadiazine/PYM/folinic Acid - Clinda/PYM - Azithromycin/clarithromycin/???? HIV PNEUMONIA MALIGNANCY: lymphoma CVD AdenoCA SARCOID PROTAZOA: PCP VIRAL: Influenza RSV,Adenovirus EBV, Hsv, VSV, FUNGAL:Crypto Histo Blasto Aspergillis BACTERIA: Mycoplasma Legionella 213 HFlu, Pneomcoccus, TWAR & other Chlamydia Psitticosis MAI/TB PARASITES: strongaloidies DX: cults, cold agglut, legionella, CMV/viral studies, CD4 (majority of PCP w/CD4<200) Broch Specimen: for silver stain AFB, Viral, Fungal TX For PCP: sulfa better than pentamidine since faster acting than pentamidine & less expensive. --------------------------------------DIARRHEA bacteria: salmonella, shigella, camplyo, yersinia, C-dif, listeria, MTB/MAI protozoa: entamebae histolytica cryptosporidium, microsporidiosis isospora(tx w/bactrim), giardia, strongoloides virus: CMV, Adenovirus malignancy: lymphoma (sm bowel), KS drugs: ddi, megase, fungal: candida, histo(if from midwest) --------------------------------------Antiretroviral (AIDS) Agents, Daily Dosage and Major Toxicities Nucleoside analogs Zidovudine, AZT (Retrovir) 500-600 mg po (typically 200 mg po tid) Children 3 mo- 1 2 yr:180 mg/M2 q6h, not to exceed 200 mg q6h Bone marrow suppression, Severe anemia, Granulocytopenia, Symptomatic myopathy, myositis (with prolonged use) Didanosine, ddl, (Videx) Two 100 mg tablets bid (> =60 kg), One 100 mg tab Plus one 25 mg tab bid (< 60 kg) Powder: 250 mg bid (> =60 kg) Pancreatitis, Peripheral neuropathy, Liver failure, Retinal depigmentation and change in vision (in children) Zalcitabine, ddc (Hivid) 0.75 mg po tid (0.375 mg po tid for patients <30 kg), 0.75 mg po tid Severe peripheral neuropathy, Pancreatitis, Esophageal ulcers, Cardiomyopathy/congestive heart failure, Anaphylactoid reaction Stavudine, d4T (Zerit) 40 mg po bid (>=60 kg), 30 mg po bid (<60 kg) Delayed peripheral neuropathy, Hepatotoxicity, Anemia (but decreased bone marrow toxicity in comparison to zidovudine) Lamivudine, 3TC (Epivir) 150 mg po bid (>50 kg) with AZT, 2 mg/kg po bid (<50 kg) with AZT Headache, insomnia, fatigue, peripheral neuropathy, myalgia Protease inhibitors 214 Saquinavir mesylate (Invirase) 600 mg po tid Generally well tolerated. Ritonavir (Norvir) 600 mg bid Generally well tolerated. Indinavir (Crixivan) 800 mg tid Generally well tolerated. Prophylaxis of opportunistic infections AIDS 215 CDC Recommendations for Reducing Perinatal HIV Transmission 1. At 14 to 34 weeks of gestation, a CD4 count above 200 per uL and no previous antiretroviral therapy: three-phase zidovudine (Retrovir) therapy should be offered to the pregnant woman and to the infant after birth. 2. At more than 34 weeks of gestation: three-phase zidovudine therapy should be offered to the pregnant woman and to the infant after birth. 3. With a CD4 counts below 200 per uL: three-phase zidovudine should be offered for the woman's benefit. 4. With more than six months of any antiretroviral therapy before pregnancy: three-phase zidovudine therapy should be offered on a case-by-case basis. 5. For women who received no antiretroviral therapy during pregnancy and present in labor: zidovudine therapy should be offered intrapartum to the mother and to the infant after delivery as the clinical situation permits. 6. For infants born after no zidovudine prophylaxis: zidovudine therapy should be offered for the infant if therapy can be initiated within 24hours of birth. CDC = Centers for Disease Control and Prevention; HIV = human immunodeficiency virus. *_Implies no previous antiviral therapy has been used. Adapted from Recommendations of the U.S. Public Health Service Task Force on the use of zidovudine to reduce perinatal transmission of human immunodeficiency virus. MMWR Morb Mortal Wkly Rep 1994;43(RR-11):1-20. Perinatal Care of HIV-Infected Mothers and Their Infants Antenatal surveillance 216 1. Perform standard prenatal baseline laboratory tests and Papanicolaou smears, plus CD4 counts, toxoplasmosis and cytomegalovirus titers, liver enzyme levels, a tuberculin test (purified protein derivative) and a glucose-6-phosphate dehydrogenase (G6PD) level.7 2. Offer zidovudine (Retrovir) prophylaxis according to the guidelines formulated by the Centers for Disease Control and Prevention (see Table 4).37 3. Consider antenatal influenza, pneumococcal and hepatitis B immunizations (may wait until after the first trimester). 4 7 4. Perform a complete physical examination and a review. of systems during each trimester. 7 27 5. Maintain surveillance for HIV-related opportunistic infections based on CD4 staging; initiate prophylaxis as indicated. 7 6. Repeat sexually transmitted disease screening tests (rapid plasmin reagin test/VDRL test, gonorrhea culture and Chlamydia assay) and group B streptococcal culture in the third trimesters 7. If the pregnant woman is receiving zidovudine therapy, monitor the complete blood count and liver enzyme levels each month.37 8. Obtain a CD4 count each trimester if the count is under 600 per uL; repeat the CD4 count at six weeks and six months postpartum. 37 9. Discuss postpartum contraception and safe sexual practices. 7 Intrapartum management 1. Minimize internal fetal monitoring and fetal scalp sampling; fetal scalp lesions increase the risk of exposure to maternal blood. 7 27 36 2. Wear double gloves and eye shields to protect against exposure to body fluids. 4 4, 7 3. Avoid episiotomy, vacuum extraction and the use of forceps. 7,27 4. At this time, cesarean sections have no specific HIV-related indications. 7,27 5. To avoid needle sticks, repair of all lacerations and episiotomies should be performed by the most experienced personnel available. Postpartum management 1. Counsel the mother about the proper disposal of sanitary pads and the need for careful hand washing before she handles the infant.7 2. Circumcision is not specifically contraindicated. 3. Breast feeding should be discouraged in developed countries. 4,7 36 4. Provide routine postpartum and HIV-related care to the mother as indicated. 7 5. The child may require referral to a specialist familiar with the care of infants at risk for HIV infection. 37 HIV = human immunodeficiency virus. FEVER CLUES- DIAGNOSTIC SIGNIFICANCE BY MAGNITUDE OF THE TEMPERATURE: Extreme pyrexia > 106 F includes CNS fevers (hemorrhagic, neoplastic, trauma or infection), drug fever, heat stroke, HIV infection and malignant hyperthemia. FEVER WITH RELATIVE BRADYCARDIA: CNS lesions, Dengue, drug fever, Epidemic typhus, Legionnaires disease, Leptospirosis, lymphomas, malaria, psittacosis, typhoid fever, and yellow fever. To find out if there is a relative bradycardia take the last digit of the temperature in Fahrenheit and decrease this by one and then multiply that number by 10 and then add it to 100. For example if the temperature is 104, the pulse rate is calculated as 4-1=3x10 + 100=130. Therefore, if a patient has a temperature of 104, then a pulse lower than 130 constitutes relative bradycardia. This works best if the temperature is 102 or above. 217 DIAGNOSTIC SIGNIFICANCE OF DURATION AND DEGREE OF FEVER: Prolonged obscure fevers less than 102 include any malignancy, cirrhosis, CMV infection, hepatitis (B or non Anon B), infectious mononucleosis (Epstein Barr), SBE, TB, untreated legionnaires disease, Mycoplasma pneumonia, and Zoonoses. Prolonged obscure fevers greater than 102 include drug fever, hypernephroma, intraabdominal, renal-perinephric or pelvic abscess, Kawasaki disease, lymphoma, metastasizing carcinoma to the liver or CNS, pulmonary hypersensitivity diseases, SBE, TB (especially disseminated or extrapulmonary). DIAGNOSTIC SIGNIFICANCE OF FEVER IN THE HOSPITAL PATIENT WITHOUT LOCALIZING SIGNS AND TEMP < 102: Catheter associated bacteriuria, hepatitis B and non A non B, dehydration, delirium tremens, nonspecific inflammation, resolving hematomas, postoperative anesthesia related fever, and thyroid storm. DIAGNOSTIC SIGNIFICANCE OF FEVER IN THE HOSPITAL PATIENT WITHOUT LOCALIZING SIGNS AND TEMP > 102: Anesthetic induced hepatitis, intraabdominal or pelvic peritonitis or abscess, IV line sepsis, prosthetic valve endocarditis, urosepsis, adrenal insufficiency, CNS fever, drug fever, malignant hyperthermia secondary to anesthesia, transfusion reactions, and vasculitis. DIAGNOSTIC SIGNIFICANCE OF FEVER IN THE HOSPITAL PATIENT WITH LOCALIZING SIGNS AND TEMP < 102: Cholecystitis, Clostridium difficile diarrhea, decubitus ulcers, pharyngitis, postperfusion syndrome, pyelonephritis, uncomplicated wound infection, atelectasis, gout, myocardial infarction, pancreatitis, phlebitis, post pericardiotomy syndrome, and pulmonary emboli. DIAGNOSTIC SIGNIFICANCE OF FEVER IN THE HOSPITAL PATIENT WITH LOCALIZING SIGNS AND TEMP > 102: Clostridium difficile colitis, cholangitis, intraabdominal or pelvic peritonitis or abscess, IV line sepsis, nosocomial pneumonia, procedure related bacteremias, suppurative thrombophlebitis, pancreatic abscess, infected pseudocyst, and vasculitis. FEVER OF UNKNOWN ORIGIN- FUO INFECTION: pulmonary abscess, empyema, pneumonia, bronchiectasis, endocarditis, sinusitis, dental abscess, pharyngeal abscess, brain abscess, epidural abscess, meningoencephalitis, abdominal or hepatic abscess, cholangitis, hepatitis, peritonitis, diverticulitis, perinephric or cortical abscess, pyelonephritis, prostatitis, septic arthritis, osteomyelitis, decubitus ulcer. AUTOIMMUNE CAUSES: Giant cell arteritis, Goodpasture's disease, Crohn's disease, ulcerative colitis, Adult Still's disease, polyarteritis, relapsing polychondritis, sarcoidosis, rheumatic fever, SLE, Wegener's granulomatosis, vasculitis. ONCOLOGIC CAUSES: cancer of the lung, pleura, GI tract, renal cell carcinoma, hepatocellular cancer. HEMATOLOGIC: cyclic neutropenia, hemolytic disease, leukemia, lymphoma, pernicious anemia. ALLERGIC: drug reaction to antibiotics, iodides, phenobarbital, methyldopa, streptokinase, quinidine, cimetidine, phenytoin, insect bites and horse serum. METABOLIC: alcoholic hepatitis and cirrhosis, alcohol withdrawal and DTs, Fabry's disease, gout, familial Mediterranean fever, recurrent acute porphyria, hyperthyroidism, hyperlipidemia type I, hypothalamic damage secondary to infection, infarct, tumor, trauma, hyperthermic damage, neuroleptic malignant syndrome. TISSUE PRODUCTS: gangrene, blood collection in the gut or cavities, portal vein thrombosis, myocardial infarction, toxic shock syndrome, venous thrombosis, pulmonary embolism or infarction. UNCOMMON BACTERIA: Listerosis, brucellosis, salmonellosis, tularemia, plague. FUNGAL: as coccidioidomycosis, histoplasmosis. RICKETTSIAL: SPIROCHETAL: Leptospira, Borrelia, syphilis. VIRAL: as infectious mononucleosis, HIV, CMV. PARASITIC: as amoeba, malaria, filaria, toxoplasma. 218 MYCOBACTERIAL: TB. FEVER WITH RELATIVE BRADYCARDIA- The pulse should rise approximately 10 beats/minute for each degree F increase in temperature. Exclude patients that take beta blockers, verapamil, hypothyroidism and adrenal insufficiency. The following infectious disease will produce a fever with a low pulse: Legionellosis, Leptospirosis, Brucellosis, Dengue fever, Psittacosis, Rocky mountain spotted fever, Typhoid fever, tuberculosis, yellow fever. Also, consider non-infectious causes as drug fever, factitious fever, lymphoma, CNS tumor or trauma causing increased intracranial pressure. HEAT STROKE A. Types [1] 1. Exertional a. Young People b. Sporadic c. Common: Rhabdomyolysis, Lactic Acidosis, Renal Failure d. Severe: Disseminated Intravascular Coagulopathy (DIC) 2. Classic a. Elderly b. Heat Waves [2] c. No sweating d. Acute renal failure and Rhabdomyolysis are rare e. Social isolation and lack of air conditioning are risk factors [2] f. Increased Risk: Heart Failure, Diabetes, ETOH intoxication, severe Scleroderma 3. Heat stroke definition requires >40.5-C (105-F) B. Signs an Symptoms 1. Loss of Consciousness may be presenting symptom 2. CNS a. Headache, Vertigo, Faintness, b. Confusion / Coma c. Seizures d. Stroke (Focal Deficit) 3. Abdominal Distress 4. Temp >41- common (106-F): Pyrexia and Prostration 5. Skin Hot and Dry 6. Hyperpnea, Rapid pulse, BP usually low 7. Flaccid muscles, decreased deep tendon reflexes 8. Cardiovascular a. Hypotension b. CHF C. Laboratory 1. Leukocytoses and Hemoconcentration 2. Proteinuria 3. BUN elevation - probably due to increased tissue destruction at high temperatures 4. Respiratory alkalosis and Metabolic Acidosis 5. Common - lactic acidosis 6. DIC may occur - petechiae, purpura, hematemesis, epistaxis 7. Liver damage can occur 24-36- post-admission 8. Renal failure - myoglobulinuria, oliguria, anuria D. Therapy 1. Remove all clothing 2. Immediate shower, lukewarm water recommended 3. Fan (cool air) to dissipate heat 4. Lower rectal temperature to 100-102- within 1 hour 5. Ice bath not effective 6. Good fluid resuscitation 7. Watch for electrolyte imbalance and arrhythmias 8. May need Central Venous or Pulmonary Artery Measurements 9. Avoid large doses of tylenol and NSAIDs E. Differential of Very High Fever 1. Malignant Hyperthermia (Heat Stroke) 2. Neuroleptic Malignant Syndrome 3. Severe Hyperthyroidism 4. Meningitis (sepsis occasionally gives very high fevers) 219 5. Rocky Mountain Spotted Fever 6. Drug Reaction 7. Cerebral Malaria 8. Heat Stroke 9. Still's Disease NEUROLEPTIC MALIGNANT SYNDROMEThe neuroleptic malignant syndrome (NMS) is a potentially fatal syndrome, characterized by fever, muscle rigidity, autonomic instability, and an altered sensorium caused by neuroleptic drugs as phenothiazines, thioxanthenes, butyrophenones, loxapine and clozapine. There is no relation to the duration or dose of the medications, but there appears to be an increased incidence of the syndrome when the dosage is suddenly increased from a previously stable level. The incidence of the syndrome in patients taking neuroleptic drugs is .5 - 1%. Many of these neuroleptic drugs are used to treated conditions such as Tourette's syndrome, Huntington's chorea, Sydenham's chorea, emesis and in managing dissociative anesthesia. The syndrome appears to be more common in young men who have disorders as depression, mania and schizoaffective disorders. At particular risk are those taking lithium along with neuroleptic medications. Also, any person taking the very potent drugs, haloperidol (Haldol), and trifluoperazine (Stelazine) and fluphenazine (Permitil, Prolixin) are at increased risk. There seems to be an increased incidence of neuroleptic malignant syndrome in those in whom the dose of neuroleptic has recently been increased, and in patients that are using the depot preparations of fluphenazine decanoate (Prolixin). The major criteria of NMS includes fever, rigidity and elevated creatine phosphokinase. The minor criteria consist of tachycardia, blood pressure alteration, diaphoresis, tachypnea, leukocytosis and an altered state of consciousness as excitement, coma and stupor. To make a diagnosis of NMS requires 3 major criteria or two major criteria and four minor criteria. The temperature usually is between 101 and 104 F, but higher temperatures have been seen. The rigidity may be associated with dysarthria, dysphagia, tremors, opisthotonos, blinking eyes and a positive Babinski. The tempo of the evolution of the disease may be characterized as being fairly swift, usually developing over 24-72 hours unless treatment is instituted. Once treated, the syndrome slowly subsides over about 10 days, unless there is intervening complications. Those patients that have received depot medications as Prolixin may take 10-30 days to recover. COMPLICATIONS: There may be 20-30% mortality over a 3-30 day period. Complications that may be life threatening include acute renal failure developing from myolytic heme pigment tubular necrosis, dehydration, decreased renal perfusion from autonomic instability. There may be cardiovascular collapse which can be due to rhythm disturbances and electrolyte alterations. Disseminated intravascular coagulation may develop as well as thromboembolism. The decreased level of consciousness may result in dysphagia and aspiration. The rigidity may cause decreased chest compliance with its attendant complications. LABORATORY: The creatine phosphokinase levels are extremely high, being reported up to 100,000 IU/L, but more typically between 2000 and 15000. The aldolase may be elevated. There is a leukocytosis usually in the range of 15,000 to 30,000 with a leftward shift. UA may reveal hematuria due rhabdomyolysis. Liver function tests may be elevated. CSF sometimes shows increased protein but otherwise is benign. At autopsy there has been no specific findings. The EEG may reveal only non-specific changes. DIFFERENTIAL DIAGNOSIS: Several other diseases may be simulated, but usually can be distinguished by subtle differences. For example, patients that are taking MAO inhibitors may develop hypertension if exposed to tyramine, which can cause rigidity and hyperthermia. The distinction between NMS and the MAO syndrome is extremely important, because treating the MAO syndrome with levodopa and bromocriptine (drugs used in treating NMS), may augment the hypertensive hyperthermic crisis of the MAO syndrome. Infections of the central nervous system are differentiated by changes in the CSF. Phenothiazine induced heat stroke may be confusing, but in this disorder there is no diaphoresis or rigidity. Malignant hyperthermia is an autosomal dominant condition which is associated with anesthetic exposure. In the so-called anticholinergic crisis there is dry skin, no rigidity or diaphoresis, but there are dilated pupils. In lethal catatonia there is a history of schizophrenia and an absence of neuroleptic medication. Any hypertonic state as tetany, strychnine poisoning and stiffman syndrome must be ruled out. CNS AIDS, viral encephalitis and Wilson's disease may also be considered in the differential. 220 TREATMENT: Treatment starts with stopping the offending neuroleptic. Dialysis is of no help because of high protein binding and lipid solubility. The patient should be hydrated to help prevent and control myoglobinuric renal failure. Control of fever with cooling blankets and adequate nutrition is essential. Prevention therapy with subcutaneous Heparin should be given to avert pulmonary thromboembolic disease. Measures should be taken to keep the lungs clear of secretions, prevent pulmonary aspiration, use antibiotic therapy as needed, and provide ventilatory support as needed. Bromocriptine 2.5-10 mg po tid and amantadine 100-200 mg po bid have been used. Dantrolene can be given as 50 mg IV, as needed to help the rigidity, but 10 mg/kg/day should not be exceeded. Dantrolene may also be given orally 50-200 mg qd. Monitor liver function tests when using Dantrolene. l-DOPA and electroshock therapy have been used as well as Nitroprusside IV and minoxidil when Dantrolene failed. Any patient after recovering from NMS, must be evaluated individually for re-institution of neuroleptics in order to control their underlying disease. Several points should be mentioned. It is critical that informed consent be obtained, and that from 10-30 days elapse after remission from the syndrome. The dopamine agonist used in treatment should be continued for at least 10 days following remission of NMS, and even longer, if depot drugs were involved. Try to use low potency neuroleptics at low dosages, and titrate very slowly. Creatine phosphokinase levels should be monitored frequently. It is estimated that about 25% of patients will re-develop the NMS after the original episode and another 25 % will develop at least one feature of the neuroleptic malignant syndrome. The other 50% of patients must be watched indefinitely, because re-development is always a possibility. MENINGITIS- Common causes of meningitis by age: Neonatal: E coli 50-60%; Group B streptococcus 20-40%; Listeria monocytogenes 2-10%. Children: Haemophilus influenzae 40-60%, Neisseria meningitidis 10-35% S. Pneumoniae 1020%; Adults: S pneumoniae 30-50%, N. meningitidis 10-35%, Gram negative bacilli 10-20%, Listeria 510%. Patients with otitis/sinusitis / mastoiditis are prone to S. pneumoniae, H. influenzae. With CSF rhinorrhea S. pneumoniae is common. Closed head trauma may lead to S. pneumoniae, H. influenzae meningitis. Penetrating head trauma can cause S. aureus, Gram negative bacilli meningitis. Asplenic patients are susceptible to S. pneumoniae, N. meningitidis, H. influenzae, Sickle cell anemia patients are more prone to Salmonella, H. influenzae, S. pneumoniae. Alcoholic patients are susceptible to Klebsiella and S. pneumoniae. HIV infection can cause meningitis by C. neoformans, Toxoplasma, L. monocytogenes, Cytomegalovirus. (Immunosuppressed patients are subject to L. monocytogenes and C. neoformans. Neurosurgical procedure can be complicated by S. aureus, and gram negative bacilli meningitis. Differential: Herpes encephalitis is nonseasonal, may have a focal neurologic defect, seizures and temporal lobe lesions on MRI/CT scan. Sarcoid meningitis causes cranial nerves palsies and there will be evidence of systemic disease. Viral meningitis may produce a maculopapular rash, diarrhea and is seasonal. Chemical meningitis will have a history of spinal anesthesia or tap. Bacterial endocarditis have septic emboli, positive blood cultures and heart murmur. Early TB meningitis shows a preponderance of PMN leukocytes initially followed by lymphocytes, cranial nerve abnormalities and the chest x-ray is abnormal in 50%. Amebic meningoencephalitis gives a history of freshwater swimming. Parameningeal infection will show the lesions on MRI/CT imaging. Carcinomatous meningitis usually has no fever, but cranial nerve involvement common, and patient has known cancer. Lyme disease is seasonal, history of tick bite, cranial nerve 7 palsy and flulike symptoms. MENINGITIS (Causes)- CAUSES: Haemophilus is the leading cause in children. Pneumococcus is the top cause in adults. Occurs suddenly, and frequently presents with seizures or coma. Meningococcus patients present with a characteristic rash, but the rash may be seen with ECHO and staphylococcus. Listeria is usually seen in immunosuppressed patients. Tuberculosis usually presents as a smoldering subacute or chronic disease. Cranial nerve involvement is common. 221 Viral patients usually have a viral syndrome. Most will have a short and uncomplicated course. Most are caused by enteroviruses as ECHO and Coxsackie. Gram negative meningitis is usually associated with trauma or following surgery. Klebsiella, E. coli and Pseudomonas are the most common. Cryptococcus is seen in immunosuppressed patients. Coccidiodes is present in the southwest USA. Candida may also cause. Neoplastic disease can result from metastases to the CNS or leukemia. Sarcoid and SLE meningitis are not common. MENINGITIS (CSF Profiles)BACTERIAL: The leukocyte count is >500 with a predominance of PMNs. The protein is increased. The glucose is decreased while the pressure is increased. Gram stain will be positive in 80%. FUNGAL, TB AND PARTIALLY TREATED BACTERIAL: The leukocyte is < 500 with a predominance of lymphocytes. The protein is normal or slightly increased. The glucose is decreased. The pressure is normal or increased. Mycobacteria are rarely seen. India Ink is positive for cryptococcus. VIRAL: The leukocyte count is <500 with a predominance of lymphocytes. The protein is normal or slightly decreased. The glucose is normal, while the pressure is normal or increased. Microscopic exam is negative. Elevated protein with no other CSF abnormalities, including a normal cell count can be seen in stroke patients, diabetics, chronic alcoholics and uremic patients. MENINGITIS CSF TESTSBacterial: cell count usually 1000-5000 with > 80% granulocytes. Protein 100-500. Glucose < 40. Gram stain positive 75-80%. Culture 70-85%. Acid fast, India ink, cytology, wet mount negative. Counterimmunoelectrophoresis positive. Lactate positive at > 35 mg/dl. Limulus lysate positive in gram negative meningitis > 90%. Cryptococcal antigen negative. Adenosine deaminase negative. Cyclic adenosine monophosphate decreased. LDH often elevated. Aseptic meningitis: Cell count usually 100-500 with less than 50% granulocytes, but may be > 50% in early tuberculous, amebic, fungal, viral or spirochetal meningitis. Protein 100-500. Glucose is normal but may be low in meningitis secondary to M. tuberculosis, C. neoformans, and other fungi, chemicals, sarcoidosis, neoplasms, syphilis, and subarachnoid hemorrhage. In viral meningitis it is < 40 in less than 5% of viral cases, especially mumps and lymphocytic choriomeningitis. Gram stain is negative, but may be positive in fungal meningitis (40% with Candida species). Culture is negative, but is positive in > 80% in tuberculosis and cryptococcal (50%), and rarely with viral. The acid fast stain is positive in TB in 15 to > 60%. The India ink is positive in cryptococcal meningitis in 50-75%. Wet mount is positive in amebic meningitis. CIE, Limulus lysate, and lactate are negative. Cryptococcal antigen is positive in cryptococcal (>95%). Adenosine deaminase is positive in TB (>80%). LDH is often elevated. 222 MENINGITIS (Meningococcal)Meningococcal meningitis (MM) can be a severe illness, with uncomplicated meningococcal meningitis causing death in about 10-20%. If the disease is fulminant the mortality may reach over 50%. The incidence in the USA is about 1.2 cases /100,000. MM is caused by Neisseria meningitidis, a gram negative, oxidase positive, nonmotile, non spore forming organism that contains endotoxin in the cell wall. The organism will grow well on chocolate agar with 2-5% carbon dioxide. It is distinguished by metabolizing glucose, and usually maltose but not lactose. Group B now is the most important serogroup which accounts for approximately 40% of cases. Group C accounts for 30%, group Y for 20% and Group A 2%. The peak incidence of meningococcal disease is late winter and early spring and is spread by droplet contamination. The risk is highest in crowded areas such as day care centers, school classrooms and army camps. Most of the cases involve children or adolescents. About 40% of the population are nasopharyngeal carriers of meningococci, but fewer than 1% of carriers will develop the disease. Meningococcal infection may take on several presentations. Meningococcemia is a fulminant form of septicemia and may occur with or without meningitis. There may also be chronic meningococcemia, septic arthritis, pneumonia, pericarditis, otitis media, vaginitis, and conjunctivitis. CLINICAL: MENINGOCOCCEMIA: Meningococcemia usually starts with an upper respiratory infection and is then followed by headache, hypotension and fever. Petechiae, and purpura develop over the trunk, palms, soles and extremities very rapidly. CHRONIC MENINGOCOCCEMIA: Patients with chronic meningococcemia have episodic fever, headaches, arthritis and arthralgia, and bouts of petechiae. Between these episodes the patient may have no symptoms and appear non-toxic. Splenomegaly may be present. The mean duration of this disease is about 6-8 weeks. FULMINANT MENINGOCOCCEMIA: Fulminant meningococcemia, also known as the Waterhouse-Friderichsen syndrome, occurs in 10-20% of patients with meningococcemia, has a high fatality rate and is characterized by shock, disseminated intravascular coagulation and extensive mucosal and skin hemorrhage. MENINGOCOCCAL MENINGITIS: Meningococcal meningitis is the second most common cause of bacterial meningitis after the neonatal period. In childhood it is second to H. influenza and in the adult it is second to pneumococcus. The patient usually presents with chills, headache, high fever, abdominal and back pain, and vomiting. There is nuchal rigidity with a positive Brudzinski and Kernig signs. Cranial nerve palsies, especially the third, fourth, sixth, seventh and eighth cranial nerves are common complications which usually resolve with treatment, but hearing deficits may not resolve. The skin rash consists of patches of ecchymosis, petechiae and purpura. DIFFERENTIAL DIAGNOSIS: HENOCH-SCHONLEIN PURPURA: Henoch-SchГ¶nlein purpura (HSP) is an immune vasculitis that also presents with purpura. It is usually seen in children but may be seen in adults. HSP will often follow a viral infection. There is microscopic hematuria, fever, abdominal pain and polyarthralgia. The purpuric skin rash characteristically affects the extensor surfaces of the feet and legs, buttocks and the extensor surfaces of the arms. There also may be swelling of the ankles, hands, knees, wrists and elbows. SYSTEMIC LUPUS ERYTHEMATOSUS WITH LUPUS ANTICOAGULANT: Some lupus patients are very ill when first seen and may have purpura. There may be widespread skin necrosis with secondary hemorrhage. GONOCOCCEMIA: One shouldn't have too much difficulty in diagnosing gonococcemia because the characteristic skin lesions are scattered pustulo-papules rather than extensive hemorrhagic purpura. ROCKY MOUNTAIN SPOTTED FEVER AND ENTEROVIRUS INFECTION These two diseases may simulate meningococcemia and would be included in the differential diagnosis. LABORATORY: The patient will need a lumbar puncture which will show the CSF to be cloudy or purulent with increased protein, decreased glucose and elevated pressure. The cell count is usually greater than 1000 cells/uL with a predominance of polymorphonuclear cells with gram negative intracellular diplococci. Latex agglutination for the capsular polysaccharide antigen is positive in about 60-80%. This antigen may be detected in the CSF, urine or serum. The organism may be seen by smear or culture of the CSF, blood or aspirated petechiae. Blood culture is positive in about 2/3 of the cases of meningococcemia with or without meningitis. Gram stain of the buffy coat may show the gram negative cocci if there is fulminant meningitis. Isolation of N. meningitidis from the nasopharynx is not helpful because of the high incidence of colonization. Any adult patient that develops invasive meningococcal disease should be suspected of having an immunoglobulin defect or abnormality of the complement system. Total immunoglobulins, IgG2 subclass, C3, and total hemolytic complement (CH50) should be done. If DIC is present the prothrombin time is prolonged, the platelets are decreased and the fibrinogen levels are low. 223 TREATMENT: Treatment is with IV aqueous penicillin G 2 million units every 2 hours, given until the patient has been afebrile for about 5-7 days. If the patient is allergic to penicillin, chloramphenicol should be used at 1-1.5 grams IV every 6 hours. Patients should be in isolation for the first 24 hours of treatment. PROPHYLAXIS: Close contacts and family members should receive prophylaxis with rifampin for 2 days. In the adult use 600 mg po bid. For children from 5-12 years give 10 mg/kg bid and for neonates 3-12 months use 5 mg/kg bid. Meningococcal vaccine is used to control epidemics or for travelers to epidemic areas. MENINGITIS (Treatment)- The following is the IV empiric therapy of meningitis directed at various levels of age and special situations: In all of the following situations, ceftriaxone may be substituted for cefotaxime, with the exception of neonates < 1 month, in which ceftriaxone is not recommended because it can displace bilirubin from albumin binding sites. The pediatric dose for ceftriaxone is 100 mg/kg in divided doses q12h. The adult dose of ceftriaxone is 2 grams given in divided doses q12h. NEONATAL (< 1 month): Ampicillin is given at 200 mg/kg in divided doses every 4 hours + gentamicin 7.5 mg in divided doses q8h (or tobramycin 6 mg/kg in divided doses q8h or amikacin 20 mg/kg in divided doses q8h). Alternatively, cefotaxime given at 200 mg/kg in divided doses q4h + aminoglycoside can be given. This treatment will cover Group B streptococcus, Listeria monocytogenes, and Escherichia coli. INFANTS (1-3 months): Ampicillin 200 mg/kg in divided doses q4h + cefotaxime given at 200 mg/kg in divided doses q4h OR alternatively ampicillin 200 mg/kg in divided doses q4h + aminoglycoside (amikacin 20 mg/kg in divided doses q8h, or gentamicin 7.5 mg in divided doses q8h, or tobramycin 6 mg/kg in divided doses q8h). These antibiotics will cover Haemophilus influenzae, Streptococcus pneumoniae, Listeria monocytogenes, Neisseria meningitidis, and Group B streptococci. CHILDREN 3 months- 7 years: Cefotaxime 200 mg/kg in divided doses q4h, OR alternatively ampicillin 200 mg/kg in divided doses q4h + chloramphenicol 75 mg/kg in divided doses q6h (monitor serum levels of chloramphenicol). These antibiotics will cover Haemophilus influenzae, Neisseria meningitidis, and Streptococcus pneumoniae. OLDER CHILDREN (> 7 years) AND ADULTS: Penicillin G 250,000 U/kg in divided doses q4h (Pediatric) or 24 million U given as divided doses q4h (ADULT), OR alternatively, cefotaxime 200 mg/kg given in divided doses q4h (Pediatric) or 12 grams given in divided doses q4h (ADULT). This will cover Neisseria meningitidis and Streptococcus pneumoniae. CSF SHUNTS: Vancomycin 10 mg/kg q8h + ceftazidime 150 mg/kg given in divided doses q8h (Pediatric) or 6 grams in divided doses q8h (Adults). This will cover Staphylococcus aureus and epidermidis and Gram negative bacilli. Consideration must be given for shunt removal and intraventricular vancomycin). ASPLENIA: Cefotaxime 200 mg/kg in divided doses q4h (Pediatric), or ceftazidime 12 grams in divided doses q4h (Adult). This will cover Neisseria meningitidis, Haemophilus influenzae, and Streptococcus pneumoniae. POST NEUROSURGICAL PROCEDURES: Nafcillin 200 mg/kg in divided doses q4h (Pediatric) or Nafcillin 12 grams in divided doses q4h (Adults) + ceftazidime 150 mg/kg in divided doses q8h (Pediatric), or ceftazidime 6 grams in divided doses q8h (Adult). This will cover Pseudomonas aeruginosa, Staph aureus and epidermidis, and Gram negative bacilli. CLOSED HEAD TRAUMA: Penicillin G 250,000 U/kg in divided doses q4h (Pediatric), or Penicillin G 24 million U in divided doses q4h (Adult). This will cover Streptococcus pneumoniae. TRANSPLANT PATIENTS: Ampicillin 200 mg/kg in divided doses q4h (Pediatric), or Ampicillin 12 grams given in divided doses q4h (Adult) + aminoglycoside (Amikacin 20 mg/kg in divided doses q8h (Pediatric) or Amikacin 15 mg/kg in divided doses q8h (Adult), OR Gentamicin 7.5 mg/kg in divided doses q8h (Pediatric) or Gentamicin 5 mg/kg in divided doses q8h (Adult), OR Tobramycin 6 mg/kg in divided doses q8h (Pediatric), or tobramycin 5 mg/kg in divided doses q8h (Adult). This will cover Listeria monocytogenes. ALCOHOLIC PATIENTS: Penicillin G 24 million units in divided doses q4h + cefotaxime 200 mg/kg in divided doses q4h. This will cover Streptococcus pneumoniae and Gram negative bacilli. RECURRENT MENINGITIS: Penicillin G 250,000 U given in divided doses q4h (Pediatric), or Penicillin G 24 million U in divided doses q4h (Adult). This will cover Streptococcus pneumoniae. ELDERLY PATIENTS: Penicillin g 24 million U in divided doses q4h. This will cover Streptococcus pneumoniae. TERMINAL COMPLEMENT DEFICIENCY: Penicillin G 250,000 U in divided doses q4h (Pediatric), or Penicillin G 24 million U in divided doses q4h (Adults). This will cover Neisseria meningitidis. TREATMENT BASED ON MORPHOLOGY BY GRAM STAIN: Gram positive bacilli could represent Listeria monocytogenes and is treated with ampicillin +/- aminoglycoside, or alternatively trimethoprim-sulfamethoxazole. Gram negative cocci could represent Neisseria meningitidis, and is treated with Penicillin G or alternatively cefotaxime, ceftriaxone or chloramphenicol. Gram positive cocci in short chains and pairs could represent Streptococcus pneumoniae, or Group B streptococci, and is treated with Penicillin G, or alternatively with cefotaxime, ceftriaxone, or 224 chloramphenicol. Gram positive cocci in clusters could represent Staphylococcus aureus, and is treated with nafcillin or alternatively with vancomycin (has variable CSF penetration). Gram negative coccobacilli represents Haemophilus influenzae, and is treated with cefotaxime or ceftriaxone, or alternatively with ampicillin + chloramphenicol. Gram negative bacilli could represent Pseudomonas aeruginosa or Klebsiella (treated with ceftazidime + aminoglycoside), or Escherichia coli (treated with cefotaxime or alternatively with Trimethoprim-sulfamethoxazole). If no Gram stain organisms are seen, treat empirically with ampicillin + cefotaxime or ceftriaxone. DIABETIC KETOACIDOSIS DKA Presentation 1. DKA often presents as anorexia, N/V, and abdominal pain. a. Abdominal pain be sufficiently severe to suggest an acute surgical abdomen. b. Abdominal tenderness, guarding, decreased bowel sounds, and increased WBC may be present. c. Abdominal pain from DKA almost always subsides in 6-8 hours after institution of therapy. 2. DKA is often proceeded by a period of polydipsia, polyphagia, polyuria, weight loss, increasing weakness, and mental obtundation. 3. The onset is usually gradual over several days. 4. Hypothermia is the rule and does not preclude infection. DIFFERENTIAL DIAGNOSIS DKA HNKC Onset DKA Gradual HYPOGLYCEMIA Sudden Skin Warm, dry Cool, clammy Respirations Rapid and deep (Kussmaul) not as profound Breath Odor Sweet, fruity Ketosis Blood sugar Osmolarity Na+ Metabolic acidosis DKA Present Not deep, but may be rapid Very profound MNKC Absent Usually < 600 Usually > 900 Never < 600 Usually < 350 Usually > 350 ~ 28 ~ 80 Usually low Usually high Usually severe Usually not severe ( acidosis < 7.35 ) PRECIPITATING FACTORS (There is always a precipitating factor) 1. Infection - most common - usually UTI, URI, infected decubitus 2. Silent MI 3. Non-compliance is taking Meds 4. Intraabdominal catastrophes 5. Pancreatitis (Note increased amylase seen in 2/3 of patients with DKA) 6. Stroke 7. Trauma, surgery, psychological stress MANAGEMENT 225 ALWAYS MAKE A FLOW SHEET! Initial labs: 1. SMA-7 a. Glucose - use Dextrostix initially and PRN. b. Bun - often increase d/t dehydration. c. Creatinine - may be increased out of proportion to BUN 2o interference by acetoacetate with picric acid in assay. 2. Acetone - Bedside: Dilute plasma 1:1 with NS or water and test with crushed Acetest tablet; > 2+ reaction = significant ketosis (may use undiluted serum instead). 3. CBC a. HCT - often increase d/t dehydration. b. WBC - leukocytosis is common even without infections and may be masked. 4. ABG's 5. Calcium and Phosphorus - baseline 6. Lactate - Not increased in ordinary DKA; acidosis not accounted for by ketoacidosis may be 2o lactic acidosis, especially in elderly, hypotensive patients. 7. U/A - glucose, ketones, UTI Calculate: 1. Correct the Na+ for glucose For every 100 mg/dl increase in glucose > 100, add 2.5 mEq/l to the measured serum Na+. 2. Fluid deficit a. Normal TBW - 0.6 x IBW (kg) b. Current TBW - Normal serum Na+ (Normal IBW) Corrected serum Na+ c. Body water deficit - Nl TBW - Current TBW d. Correct half the deficit in the first 8 hours and the rest over the next 16-24 hours. 3. Serum Osmolarity 2 (corrected Na+) + (glucose) + (BUN) 18 2.8 - A patient in coma with osmolarity < 340 is probably not in DKA; look for stroke or severely decreased phosphate. Treatment: 1. FLUIDS - use NS or 1/2NS a. Use 1/2NS if: Corrected serum Na+ > 150 Bicarb is being given. Otherwise use NS initially. b. Usually give 1-2 liters over the first hour. c. Severe hypotension: may need albumin, whole blood, or continuous NS. d. Monitor CVP if: heart disease, renal disease, hypotension, elderly, susceptible to overload. e. Swan-Ganz catheter preferred if: severe shock, pulmonary hypertension, MI. f. Follow initial rapid hydration with 1/2NS at 300-500 cc/hr. 2. Insulin: a. Peak action of regular insulin: IV - 5-10 mins. IM - 1-2 hours SQ - 4 hours b. Two routes preferred: continuous IV or IM. c. Dose: 0.1 unit/kg/hr IV 0.1 unit/kg/dose IM 7 units/hour d. Give IV bolus of 10 - 20 units (0.33 units/kg) first (both routes) e. Continuous IV: 50 units in 250 cc 1/2NS 1 unit/5cc via infusion pump at 35 cc/hour - (addition of albumin to set-up is not necessary) f. Measure glucose, acetone, electrolytes and ABG's every hour. g. Blood sugar should decrease 10% per hour or 100 mg/dl per hr. - if not, increase (double) the infusion rate or repeat the loading dose. 226 h. At blood sugar = 250: switch to 5 units of insulin 250 cc D51/2NS, and continue the infusion until the plasma is cleared of ketones. - (Average dose is 50 units over 5 hours to decrease blood sugar to 250). i. Maintain the blood sugar at 250 and continue the infusion until the acidosis is corrected (pH normal, HCO3, AG). j. Criteria for stopping insulin infusion: (1) Normal pH (acidosis corrected) (2) Negative serum and urine acetone (3) Eating (4) Looks good and feels good k. The patient should be out of DKA in 10 - 16 hours. If not out of DKA in 16 hours there is an increased incidence of mucormycosis (headache, drainage of pink nasal secretions) l. To establish the insulin regimen: (1) Usually the patient will be clear by the next morning (2) If the infusion is still running give half of the previous insulin dose as NPH or give 0.1 units/kg of NPH as the a.m. dose (3) If the infusion is discontinued: (a) Begin sliding scale regular insulin SQ every 4 hours. OR: (b) Give 10 units NPH empirically as the AM dose. (most people will tolerate this dose). (c) Get 7 AM and 4 PM blood sugars daily. Regulate the insulin dose if the 4 PM blood Sugar is > 200. (d) When 4 PM blood sugar is < 200, get qid blood sugars (7 AM, 11 AM, 4 PM, and 10 PM) to refine dosage. 3. BICARBONATE a. Indications: (1) pH < 7.1 (2) Hypotension, shock or both when pH < 7.2 (3) Consider bicarbonate when low pCO2 (already maximally compensated) or lung disease (can't compensate) b. Dose: 2 amps (88 mEq) diluted in 1 liter of l/2NS given over 1 - 2 hours. Repeat dose until pH > 7.2 c. Do not give as bolus unless in resuscitation, shock or if initial pH <7.0. 4. POTASSIUM a. Monitor q 1 hour. b. Make sure there is urine output. c. If K is normal or low, start K at once; if increased, give when K+ reaches 5.5 d. Give 40 mEq in the first liter and 20 - 40 mEq/L thereafter. 5. PHOSPHATE a. If possible, get an initial phosphate (and calcium) as a baseline and monitor every 4 - 6 hours. b. Decrease in phosphate will usually not be seen until 8 - 12 hours; replace phosphate if and when it falls to low levels. c. Prevention of hypophosphatemia in DKA (1) 20 mEq/L of K+ replacement may be given as K Phosphate. (2) K Phosphate = 4.4 mEq K+ + 3mmole phosphate/ cc (3) 5 cc of K phosphate/L = 22 mEq K+ + 15mmole (466 mg P) phosphate/L (4) Rate of K phosphate solution must not exceed 10mmole/hr. (5) Some authorities should give the first 10 - 30 mEq of K+ replacement as K phosphate. d. Danger of phosphate therapy is that too much phosphate binds calcium leading to hypocalcemia. e. Low phosphate leads to deficiency of ATP and 2.3 DPG which shifts the Hb dissociation to the left and impairs oxygen delivery to the tissues. 227 6. ADDITION MEASURES a. If obtunded: Endotracheal intubation prior to NGT to prevent aspiration b. Foley catheter if obtunded, urinary outlet obstruction, or oliguria after several hours of treatment. c. Tagamet 300 mg. IVPB every 8 hours to prevent stress ulcerations. d. Search for precipitating factors (1) Cultures (2) Spinal Tap (3) Serial EKG's and cardiac enzymes e. Cerebral Edema is a risk if fluid deficit is corrected too fast or if markedly hypotonic fluids are used. -Usually seen in adolescent diabetics. -S/S: progressive obtundation, increased ICP (papilledema, blown pupil), and hypothalamic dysfunction (hyperpyrexia, diabetes insipidus) f. Diet (1) Liquids when PO fluids tolerated (2) Regular ADA diet in 24 - 48 hours g. Monitor Calcium and Phosphate daily h. Unexplained or refractory shock: think of MI, sepsis, bowel infarction, or lactic acidosis. i. Remember that patients with lousy kidneys do not spill glucose! j. Sliding scale for glucometer: Blood sugar: > 400 Regular insulin SQ: 20 units > 300 15 units > 200 10 units Hemoglobin A1c [Glycohemoglobin] and Blood Glucose Approximate Relationship Between HbA1c and Average Blood Glucose -----------------------Average HbAlc Glucose (mg/dl) (%) -----------------------360 14 330 13 300 12 270 11 240 10 210 9 180 8 150 7 120 6 90 5 ------------------------ Diabetic Glucose Target Goals: Pre-meal glucose-- 80-120 mg/dl Bedtime glucose--- 100-140 mg/dl Hb1c-------------- < 7% 228 THYROID DISEASE INTRODUCTION A. Occurrence 1. Thyroid problems are extremely common 2. ~5% of population has palpable thyroid abnormality 3. More common in women than men (10:1) 4. Anomalies ~2X more likely to be carcinoma in men than in women B. Disease Entities 1. Hyperthyroidism a. Subtle in elderly, often presents with atrial fibrillation or CHF b. In young persons, often presents as resting tachycardia, weight loss, heat intolerance c. Graves' Disease: autoimmune stimulation of TSH receptor (anti-TSH-R antibodies) 2. Hypothyroidism a. Commonly caused by drugs: lithium, sulfonylureas, amiodarone b. Hashimoto's Thyroiditis: autoimmune destruction of thyroid follicles c. Common complication of treatment for hyperthyroidism 3. Thyroid Inflammation - thyroiditis a. Diffuse enlargement is most common b. Painful or painless helps with differential diagnosis 4. Subclinical Thyroid Disease [9] a. Increased use of TSH as screening has increased number of cases b. Subclinical disease implies normal thyroid hormones (T4, T3) with abnormal TSH c. Low TSH (eg. <0.5) with normal T4 and T3 is subclinical hyperthyroidism d. High TSH (eg. >5.0) with normal T4 and T3 is subclinical hypothyroidism e. However, patients may have subtle symptoms from these thyroid abnormalities 5. Drug Induced Thyroid Disease a. Decrease TSH Secretion: dopamine, glucocorticoids, octreotide b. Decrease T4 Secretion: lithium, iodide, amiodarone c. Increase T4 Secretion: iodide, amiodarone d. Decrease T4 Adsorption: colestipol, cholestyramine, aluminum, iron, sucralfate e. Increase Serum TBG: estrogen, tamoxifen, heroin, methadone, mitotane, fluorouracil f. Decrease Serum TBG: androgens, danazol, slow release niacin, glucocorticoids g. Displace T4 from Binding Sites: furosemide, salicylates h. Increase Hepatic T4 Metabolism: phenobarbital, rifampin, phenytoin, carbamazepine i. Decrease T4 to T3 Conversion: propylthiouracil, amiodarone, Гџ-blockers, glucocorticoids 6. Thyroid Mass (Thyroid Nodule) a. Multinodular vs. Solitary Nodule b. Previous head and neck irradiation has 5-10% risk of developing nodule over 20 years c. Diagnosis is usually made by needle biopsy C. Evaluation of Goiter (Thyroid Enlargement) 1. Consider endemic causes - deficiency or adverse drug effects 2. History a. Symptoms of hypo- or hyperthyroidism b. Medication History c. Symptoms of mechanical obstruction: airway problems, dysphagia 3. Physical Exam a. Observation of gland size is very important; normal gland rarely visible b. Palpation should be performed from behind the patient c. Characterize the enlargement: Single Nodule, Multinodular, Diffuse d. Prominent glands should be measured with a ruler 4. Fine Needle Aspiration of Thyroid Nodule(s) D. Causes of Diffuse Thyroid Enlargement 1. Hyperthyroidism a. 95% Graves' Disease b. 5% Hashimoto's or other type of thyroiditis c. Evaluation: eye findings, Thyroid Stimulating Antibodies, TSH, T4 index d. Radioiodide uptake: determine if condition is transient (eg. thyroiditis) vs. longer term 2. Euthyroid: usually preclinical stage of either Graves' or Hashimoto's Disease 3. Hypothyroid - Usually Hashimoto's Thyroiditis E. Multinodular Goiter 1. Hyperthyroidism a. Plummer's Disease 229 b. Foci of functional autonomy develop within simple goiter (?) c. Ablative Therapy (radioactive iodine) 2. Euthyroid a. Most patients are women b. Autonomously functioning nodules more common c. Hormone suppression 3. Hypothyroid a. Unclear etiology (? Hashimoto's disease) b. Hormone replacement therapy is indicated F. Causes of Solitary / Dominant Nodules 1. Classification a. Previously classified by ability of nodule to take up radio-isotope ("hot" nodule) b. However, nearly all nodules are initially evaluated by fine-needle aspiration (FNA) c. Main issue is to rule out presence of carcinoma in the nodule d. Thyroid Function Tests are generally only useful in patients with systemic symptoms 2. Benign FNA Results a. Hashimoto's Thyroiditis is most common b. Colloid only may be seen - usually patient is observed 3. Follicular Neoplasm a. Most are adenomas; size is crucial determinant b. In elderly 25% >4cm present with T3 Thyrotoxicosis c. Radionucleotide scanning will help delineate hot from cold nodules d. Carcinoma is major concern here, but hot nodules are usually benign e. Full TFTs including T3 levels should be obtained 4. Frank Malignancy a. Consider ultrasound, CT or MRI of neck for more extensive evaluation b. Papillary, Follicular, and Medullary (~5%) Carcinomas are found 5. Some specialists prefer initial radio-iodine scan to classify "hot" vs. "cold" nodules a. ~5% of all thyroid nodules are hyperfunctioning ("hot") b. The remainder are "cold" or "warm" and these are most suspicious for carcinoma 6. Causes of Solitary Nonfunctional ("Cold") Thyroid Nodules a. Adenoma (~75-80%) b. Carcinoma (~15%) c. Cyst (simple and other) d. Multinodular goiter e. Inflammatory diseases, Abscess, Dermoid, Teratoma (all rare) 7. Causes of "Hot" Nodules a. Hot nodules are far more common in woman than men (F:M 13:1) b. Patient may be euthyroid or hyperthyroid ("toxic") G. Evaluation of Thyroid Nodules [ 1, 3] 1. Fine Needle Aspiration (FNA) [ 1, 2, 6] a. Most effective method for diagnosing malignancy b. Overall yield is: Benign 69%; Suspicious 10%; Malignant 4%; Non-Diagnostic 17% c. Yield of non-diagnostic is extremely operator dependent d. False negative ~5%, False positive ~5%; Sensitivity 68-98%; Specificity 72-100% e. Non-diagnostic FNAs should be repeated with ultrasound guidance f. If FNAs are non-diagnostic twice, surgical biopsy and/or resection should be considered 2. Thyroid Function Tests (TFTs) a. For evaluation of thyroid hormone levels (usually done, but rarely useful) b. Majority of the nodules are "cold" - that is, do not produce T4 hormone c. Even some "hot" nodules will release near-normal amounts of thyroid hormone 3. Ultrasound a. Mainly done to ascertain gland size, number and size of nodules b. Detection of cysts (>2mm) or nodules (>3mm) and calcifications c. May delineate extra-thyroid from intra-thyroid masses d. Evaluate lymph nodes in patients with thyroid cancer e. Useful for aiding fine needle aspiration (biopsy) 4. Radio-iodine scan (123-I) a. Assesses organification and uptake b. Thus, will determine "hot" vs.вЂќ cold" nodules; diffuse vs. local uptake c. Generally, these are preferred over technetium scans 5. Technetium scan a. Assesses blood supply and uptake of gland (not organification) b. Useful for determining anatomy of gland and in patients allergic to iodine 6. MRI and CT Scanning a. Mainly for evaluation of complicated cases, particularly with carcinoma b. Evaluate Masses for regional extension and symptoms due to local effects H. Treatment of Thyroid Nodules 1. Carcinomas should generally be resected followed by T4 suppressive/replacement therapy 2. Adenomas causing symptoms (local compression, T4 production) should usually be resected 230 3. Cold Nodules a. Suppression therapy is often very effective b. Both Levothyroxine and iodine are both effective [7] 4. Hot (Hyperfunctioning) Nodules a. Ablative therapy with iodine is one option b. Surgical resection can be performed THYROTOXIC CRISISCLINICAL: Patients present with exaggerated symptoms of hyperthyroidism. The precipitating factor usually is a pulmonary infection, diabetic complications, pulmonary embolism, or myocardial infarction. The use of haloperidol, recent iodine or surgical therapy, cessation of antithyroid drugs may also be causative. There may be diarrhea and altered mental state, and young females are commonly involved. There may be atrial fibrillation, elevated temperature, increased pulse pressure, goiter, exophthalmopathy, lid lag, arthritis, pretibial myxedema, tender hepatomegaly, gynecomastia, lymphadenopathy, fine tremor, galactorrhea, and delirium. LAB: There may be increase glucose unless there is adrenal insufficiency, increased calcium normocytic normochromic anemia, increased transaminases, BUN and bilirubin. The ECG shows sinus tachycardia or supraventricular arrhythmias. A T4 should be done (the T4 may be decreased to normal in the acutely ill). Also obtain a thyroid panel, TSH, cultures, chemistries and CBC. TREATMENT: Cooling blankets and acetaminophen may be used for hyperthermia >104 F. Salicylates should not be given because they will displace thyroid hormones from binding protein, exacerbating the condition. Cardiac monitoring should be carried out. Use B-complex and IV fluid maintenance. CHF should be treated and small doses of propranolol may be beneficial by slowing the heart rate. Propranolol is given at 2-5 mg IV at 1 mg/min or 40-80 mg PO q6h. Propranolol will block peripheral conversion of T4 to T3 and decrease the hyperadrenergic effects. It should not be used in asthma or CHF that is not due to tachyarrhythmia. Sodium iodide 1 gm IV q8h or Lugol's solution 30 cc po daily is started 2 hours after Propylthiouracil is given. Iodine will block thyroid hormone release. Propylthiouracil is given at 1 gm through a nasogastric tube or by rectum as a loading dose, then 400 mg PO daily for 3-6 weeks. Dexamethasone is given at 2 mg q6h until patient is stable. Dexamethasone will block the peripheral conversion of T4 to T3 and correct any relative adrenal insufficiency. Thyroid Storm SX: HTN, Palpitations, febrile, Tachy High suspicion if pt is FEBRILE other SX: n/v/ :due to stress infection -Tx Lugol's Soln: K+ Iodide: prevents iodine metab of thy hormones propylthiouracil: ?Steroids: usually must give in myxedema coma due to immune syndrome(SchmidtвЂ™s) from co-antibody against thyroid & adrenals (so must give steroid w/Synthroid since Synthroid will stim adrenals) ADRENAL INSUFFICIENCYAdrenal insufficiency (AI) can be a medical emergency and the failure to recognize it could have catastrophic consequences. The incidence of AI may be rising with AIDS and the increasing use of steroids. CAUSES: The causes can be divided into two categories: primary adrenal disease and secondary. PRIMARY can be caused by the following: Granulomatous disease (TB, Histoplasmosis and other fungal infections, and sarcoidosis), Neoplastic infiltration, Amyloidosis, Hemochromatosis, Drugs (ketoconazole, mifepristone, anticoagulants), meningococcemia with Friderichsen-Waterhouse syndrome, adrenal hemorrhage, adrenoleukodystrophy in boys, autoimmune adrenalitis, and acquired immunodeficiency syndrome. SECONDARY hypothalamic and or pituitary disorders can be caused by pituitary and hypothalamic tumors, lymphocytic hypophysitis, and withdrawal from glucocorticoid therapy. Idiopathic autoimmune adrenalitis is the most common cause accounting for 80% of adrenocortical insufficiency. There are several 231 endocrine disorders associated with this disease: (diabetes mellitus, thyrotoxicosis, thyroiditis, alopecia, vitiligo, myasthenia gravis, hypoparathyroidism, pernicious anemia, ovarian failure, hypercalcemia, chronic moniliasis, and Schmidt's syndrome). Several antibodies are often found as; gastric antibodies (20%), parathyroid antibodies (20%), adrenal antibodies (60%) and thyroid antibodies (40%). Metastatic disease involves the adrenal glands in 25% of oncologic patients. Ninety percent of the adrenal gland has to be destroyed before a patient is symptomatic. Most cancer patients don't have this amount of involvement. AIDS can cause adrenocortical insufficiency by infiltration with Mycobacterium avium-intracellulare, Cytomegalovirus, Kaposi's sarcoma, and Cryptococcus. Ketoconazole can also cause AI. CLINICAL DIAGNOSIS: Weakness and fatigue are the most frequent findings (94%) followed by the following in decreasing frequency: Skin hyperpigmentation manifested as tanning, freckles, vitiligo, blue-black discoloration of the areolas and mucous membranes (91%), Anorexia and weight loss (88%), Postural hypotension (81%), Hyponatremia (67%), Nausea and vomiting (66%), Hyperkalemia (55%), Azotemia (52%), Diarrhea and abdominal pain (23%) and hypoglycemia (19%. Dermal hyperpigmentation is seen in primary adrenocortical insufficiency, but is not seen in secondary insufficiency. Look especially at the palmar creases and in scars where there is increased pigmentation. The entire body can be affected but look especially at the face, neck, upper extremities, scrotum, penis, axillary areas and the periumbilical area. Dilutional hyponatremia is more common in secondary insufficiency than primary. It is caused by increased arginine vasopressin secretion and reduced free water elimination by the kidneys. Hyperkalemia only occurs in primary adrenocortical insufficiency because of the aldosterone deficiency. LABORATORY: RAPID ACTH TEST- Give cosyntropin 250 ug IV and measure plasma cortisol and aldosterone levels at baseline and after 30 min. The normal response at 30 min should be an increase of > 7 ug/dL of cortisol and aldosterone OR double the baseline value OR an absolute value of 20 ug/dL of cortisol and aldosterone. In primary AI there is a decreased cortisol and aldosterone level. In secondary, there is a decreased cortisol level and increased aldosterone level. PLASMA ACTH- Measure the ACTH at baseline before the rapid ACTH test is done. The normal diurnal plasma ACTH level is 0-70 pg/ml. In primary AI there is increased ACTH level and in secondary AI there is decreased ACTH levels. If you suspect acute adrenal insufficiency, baseline levels of cortisol, aldosterone and ACTH should be done along with routine blood chemistries. Give 5% dextrose in normal saline, about 2 liters in the first 6 hours. Give dexamethasone, 4 mg IV initially then 4 mg every 6 hours. Next, for diagnosis, give cosyntropin, 250 ug IV and determine the plasma cortisol after 30 minutes. Investigate the possible causes, get TB skin test and cultures and MRI of the adrenals. TREATMENT: Give 20 to 30 mg of hydrocortisone daily, 2/3 in the early AM and the remainder in the early afternoon. If there is primary insufficiency give .05 to .3 mg of fludrocortisone daily to maintain fluid and electrolyte balance. Before surgery and major stress give hydrocortisone 100 mg IV followed by 10 mg/hour during the procedure and postoperatively give 100 mg of hydrocortisone every 8 hours until the patient is stable; then taper the dose over 3-5 days. ANTICOAGULATION TREATMENT General Treatment with Heparin 1.Baseline Study 2.Loading Dose 80U/Kg (Range = 5000-10,000U) Heparin IVPB 3.Follow immediately by constant IV infusion 1000-1500 units/hour or 18U/Kg/Hr not to exceed 1500U/Hr. 4.4 hours later get PTT 5.Aim = 1 1/2 - 2 x control, or 15 - 30 sec over control. IF: 1.< 5 seconds above normal - reload with 10,000 units and increase transfusion rate by 200 units/hr. 2.5-20 seconds above normal - reload at 5000 units (1/2 dose) and increase transfusion rate by 100 units/hr. 3.10-15 seconds above normal - increase infusion rate by 100 units/hr. 4.15-30 seconds above normal - maintain at same rate 5.> 30 seconds above normal -hold IV 1-1 1/2 hours (decrease PTT rise by 1/2) and restart infusion decrease by 200-300 units/hr. Recheck PTT in 4-6 hours! 232 Notes: 1.Adjust dose according to PTT, continue until coag. rate as measured by PTT stabilizes within the desired range, then may extend interval between PTT's to 12 hours then 24 hours. 2.CBC with platelet count after 3 days of treatment and on the 7th day. CONVERSION GUIDELINES Heparin ---> Coumadin Day 1 - Baseline PT ----> Begin (at 10 mg/day) Day 2 - Draw PT ----> Give 10 mg Coumadin - if PT > 1 1/2 control or INR > 2.5 decrease by 5mg Day 3 - Draw PT ----> Give 10 mg Coumadin - if PT > 1 1/2 control or INR > 2.5 decrease by 2.5 mg Day 4 - Draw PT ----> Give 5mg Coumadin - if PT > 2 x control or INR > 3 decrease by 1-2 mg Day 5 - Draw PT ----> Give 5 mg if PT > 2 x control or INR > 3 decrease 1-2 mg Day 6 and on: Draw PT &LT1 1/2 control (INR &LT1 2) 1 1/2 - 2 Control (INR 2-3) > 2 control (INR > 3) inc 1-2mg/day No Changes dec dose 1-2mg/day | | | | \|/ | ------------------> Draw PT 5-7 days later <---------------Once a stable PT of 1 1/2 - 2 x control or INR of 2 to 3 is established, PT's may be obtained every 2 weeks, then 3 weeks, then monthly. Notes: 1.Baseline PT taken on day 1 (after 4-5 days of Heparin) is necessary to ID a patient who is debilitated or malnourished and who as a result may have low clotting factors and prolonged PT. This patient may be sensitive to effects of Coumadin. 2.Before 2nd dose, have PT drawn to check for sensitivity. ALTERNATIVE CONVERSIONS Start Coumadin 15 mg/day. When PT starts to move out, give 2.5 (times number of days to move out) for daily dose. Minidose Heparin 5000 units SQ Bid ANTICOAGULANT INR RECOMMENDATIONS FOR VARIOUS SITUATIONSProphylaxis of venous thrombosis in high risk surgical procedures: 2-3 INR. Treatment of pulmonary embolism: 2-3 INR. 233 Prevention of venous thrombosis: 2-3 INR. Mechanical prosthetic heart valves at high risk: 2.5-3.5 INR: Prevention of embolization in acute myocardial infarction: 2-3 INR. Prevention of embolization in tissue heart valves: 2-3. Prevention of embolization in valvular heart disease: 2-3 INR. Prevention of embolization in atrial fibrillation: 2-3 INR. Prevention of embolization in patients with recurrent systemic embolism: 23 INR. BLEEDING DISORDERSKEY QUESTIONS IN HISTORY TAKING: 1....Have you ever had excessive bleeding during surgery? 2....Have you ever had excessive bleeding during dental extractions? 3....Have you had excessive menstrual bleeding? 4....Do you get spontaneous bruises or nose bleeds? 5....Do you have a family history of bleeding problems? 6....Have you had liver disease, renal disease, collagen vascular disease, cancer, nutritional deficiencies, Cushing's disease or dysproteinemias? 7....Have you ever taken anticoagulant drugs? Normal PT, PTT and bleeding time do not eliminate the possibility of a significant bleeding disorder. Von Willebrand's disease is the disorder found most commonly in combination with normal results on screening. Diagnosis requires von Willebrand's factor antigen assay and ristocetin cofactor assay. In some cases electrophoretic analyses of the multimer, that constitute Von Willebrand's factor proteins, is also needed. Initial diagnosis of Von Willebrand's disease in adulthood is not uncommon, especially if the patient has not undergone any surgical procedures in the past. MILD Hemophilia A or B may also present in adulthood. Mild cases may not adversely affect the PTT. In fact, a PTT may be normal even in some patients who have factor VIII or IX levels as low as 20% of normal. Less common conditions that may be missed when screening tests are normal are afibrinogenemia, hypofibrinogenemia, dysfibrinogenemia, factor XIII deficiency and inherited qualitative platelet defects. ISOLATED PTT ELEVATION: A....Poor collection of venous blood with some clotting present. B....Lupus anticoagulant. (Mixing the patients plasma with normal plasma doesn't correct the prolonged PTT in patients with lupus inhibitors. Patients with lupus anticoagulant usually do not experience bleeding complications, but one of the most common clinical manifestations is thrombosis. C....Factor XII deficiency, high molecular weight kininogen, or prekallikrein can cause PTT prolongation, but these patients do not have a significant hemostatic defect. D....Hemophilia A & B E....Von Willebrand's disease F....Acquired Factor VIII inhibition, and circulating anticoagulants may cause significant bleeding problems. ISOLATED BLEEDING TIME ELEVATION: A....Thrombocytopenia B....Von Willebrand's disease C....Medications such as alcohol, antihistamines, beta lactam antibiotics, cardiovascular agents as calcium channel blockers, disopyridamole, quinidine and NSAIDS. D....Faulty testing technique. ISOLATED PT PROLONGATION: A....Deficiency of vitamin K-dependent factors (factors II, VII, IX, and X, which result from poor nutrition, therapy with warfarin or liver disorders). B....Acquired coagulation factor inhibitors are seen rarely in patients with lymphoma or collagen vascular disease and can lead to prolongation of the PT. BLOOD TRANSFUSION COMPLICATIONSBlood transfusion complications can be due to hemolytic reactions, non hemolytic reactions, transfusion reactions associated with anti IgA antibodies, delayed hemolytic transfusion 234 reactions, febrile transfusion reactions, urticarial transfusion reactions, circulatory overload, and infectious contamination of donor blood. ACUTE HEMOLYTIC REACTIONS: These are usually due to ABO incompatibility. These may occur after infusion of RBCs, white cells, platelets or fresh frozen plasma. In most cases, the donor will have an A or B antigen on the RBCs. Other hemolytic causes include patient antibodies to donor Duffy, Kidd, and Kell RBC antigens which will cause a hemolytic anemia. Females are more at risk for transfusions reactions since they become sensitized through pregnancy and blood transfusions secondary to obstetrical complications. Age also is a risk factor because older patients receive more transfusions. Hemolytic transfusion reactions include pain at the site of infusion, fever, chills, chest, back and abdominal pain, apprehension, nausea, flushing and dyspnea. The patient may develop hypotension, hemoglobinuria, renal failure, and bleeding secondary to DIC. The severity of the reaction is proportional to the amount of blood the patient has received. Therefore, the transfusion should be stopped immediately when suspected. The patient should be given generous amounts of IV normal saline and furosemide to increase renal cortical blood flow, keeping the urine output at 100 ml/hour. If hypotension does not respond to hydration, dopamine may be started at a low dose of less than 2ug/kg/min in an attempt to increase renal blood flow. The use of heparin for DIC is controversial. The blood bank should be notified immediately. Blood samples are drawn from the recipient and the serum is checked for a pinkish or red color which would indicate hemoglobin, and a direct Coomb's test. DELAYED HEMOLYTIC REACTIONS: Usually occur about 5-7 days after transfusion, but occasionally may be seen up to 3 weeks after transfusion. These are usually asymptomatic, but can be quite severe with the symptoms resembling acute hemolytic reactions. Most of these are due to exposure to a previous antigen from pregnancy or transfusion. The antibody that is produced is usually below detectible limits. These antibodies include anti-Fy, anti-E, anti-Jk, anti-C, antiD and anti-K. No specific treatment is usually needed for delayed hemolytic disease. URTICARIAL REACTIONS: Occurs in about 2% of transfused patients. These patients are treated by stopping the transfusion. There is no evidence of acute hemolysis and the urticaria are due to a reaction to plasma proteins. For prevention, these patients are treated with antihistamines and washed RBCs. ANAPHYLACTIC IGA DEFICIENT REACTIONS: These produce sudden onset respiratory distress, shock and urticaria. They may also develop flushing, back pain, hypotension, chest and abdominal pain, hives, and nausea. They are rare and are usually found in patients who are IgA deficient and have formed anti-IgA antibodies during prior transfusion or pregnancy. The anaphylaxis usually begins before the patient has received 10 ml of blood. These patients are treated with IV epinephrine .5 mg 1:10,000 every 5-10 minutes as needed, fluids, steroids and dopamine if shock is present. To prevent future episodes, autologous blood, washed RBCs or RBCs from an IgA deficient donor should be given. TRANSFUSION ASSOCIATED ADULT RESPIRATORY DISTRESS SYNDROME: This disorder is clinically similar to fluid overload, but occurs less commonly. It causes dyspnea by 6 hours, hypotension, normal pulmonary capillary wedge pressure, bilateral pulmonary infiltrates and fever. The patients usually recovers rapidly within 24-48 hours. It is usually due to an anti white cell antibody in the donor blood of a multiparous female. This antibody reacts with an antigen on the patient's white cells with subsequent leukoagglutination and obstruction of blood flow. There also is a release of toxic granulocyte products that can cause capillary vasoconstriction producing increased pulmonary vascular resistance. Confirmation of this disorder requires a search of the donor plasma for antigranulocyte and/or antilymphocyte antibodies which is time consuming. The treatment is supportive, with many patients needing a ventilator with positive end expiratory pressure, furosemide and dopamine. Some patients may also need large doses of methylprednisolone sodium succinate 30 mg/kg given once or twice. Prevention is with leukocyte filters and washed RBCs. FLUID OVERLOAD: Fluid or circulatory overload can cause a dry cough, tightness of the chest and acute pulmonary edema. It is fairly common, especially in infants and the elderly. Treatment includes pretreatment with furosemide and slowing the transfusion to about 1/2 unit of packed RBCs given over 4 hours or about 100 ml/hour. BACTERIAL CONTAMINATION OF THE DONOR BLOOD: This is a serious consequence of blood transfusions that can have a high mortality with death occurring within 6-12 hours. The patient presents with fever, chills, dyspnea, nausea, vomiting and hemoglobinuria. Gram negative rods are commonly involved, since they can grow at cold temperatures. Yersinia enterocolitica has been very common, but clinically is rare. It can be diagnosed by obtaining a gram stain of the donor blood obtained from the blood bag. FEBRILE TRANSFUSION REACTIONS: Febrile reactions are characterized by chills, fever, flushing, tachycardia, and headache that starts within one hour after transfusion begins, and may last 235 for 8-10 hours. It has a frequency of about 1% of all transfusions. Febrile reactions are usually due to antibodies toward donor white cells, with a history of previous transfusion or pregnancy. The blood should be stopped immediately, because acute hemolytic transfusions reactions can also produce fever. In febrile reactions there is no hemolysis. If no hemolysis is found, the treatment is supportive with antipyretics and use of leukocytic filters and washed RBCs. VIRAL HEPATITIS: NON-A, NON-B HEPATITIS: Less than 1% of transfused patients will develop viral hepatitis with a risk of infection of 0.1%/unit transfused. Non-A, Non-B is the most common cause of post transfusion hepatitis (90%). The duration from exposure to seroconversion varies between 6 weeks to 1 year. Clinically, the patient has elevation of liver enzymes and a positive hepatitis C antibody. Other causes of hepatitis must be ruled out as alcoholic hepatitis, hepatitis A, B, and D, and Epstein-Barr and CMV hepatitis. Chronic hepatitis secondary to non-A, non-B hepatitis develops in 50%, cirrhosis (20%), and hepatocellular cancer in 5%. If a patient has been accidentally exposed to a blood transfusion with a test suggestive of non-A, non-B hepatitis, immune serum globulin should be given as some studies have suggested protection. HEPATITIS B: Hepatitis B causes about 10% of post-transfusion hepatitis. The incubation period is about 3 months. The sequelae are similar to non-A, non-B hepatitis. Treatment is with hepatitis B immune globulin, 5 ml, + hepatitis B vaccine given IM in the deltoid at 0, 1, and 6 months. CMV INFECTION: This infection occurs when there is infusion of infected white cells (usually B lymphocytes). The primary risk is when immunosuppressed transplant patients and premature neonates are infected. The mortality in transplant patients is about 60-85%, while neonates may have a mortality of 40% and a morbidity of 50%. Because of this high morbidity and mortality, all CMV negative transplant patients, and all CMV negative premature neonates weighing less than 1250 grams, should only be given CMV negative blood if needed. The clinical symptoms consist of hepatitis, pneumonia, hepatosplenomegaly and production of cytopenias. Adults can develop colitis, esophagitis, gastritis, arthritis, retinitis and encephalitis. OTHER TRANSFUSIONS COMPLICATIONS: Other rare post transfusion complications include malaria, post-transfusion purpura, Graft-versus-host disease, leukemia (HTLV I) and paroxysmal nocturnal hemoglobinuria. Medical Evaluation of Surgical Risk Operative Risk Profiles Typical: 0 - 0.01% Low but increased: 0.01 - 0.9% Significant: 1 - 5% Moderate: 5 - 10% High: 10 - 20% Very high: >20% Periop deaths = .3% 10% during induction of anesthesia 35% intraop 55% within 48 hrs after surgery Causes of periop deaths: 1. Inadeq ventilation 2. Aspiration 3. Arrythmias 4. Drug-related myocardial depression 5. Refractory hypotension Causes of postop deaths: 1. Pneumonia (20%) 2. Non-pulm infections (peritonitis, G sepsis) 3. Cardiac arrest 4. Pulmonary embolism 5. Renal failure 6. Hypovolemic shock 7. Inoperable cancer 8. Stroke Increased risk for periop mortality: 1. Age 2. Emergency surgery 3. Cancer 236 Anesthesia: spinal -> wide fluctuations in blood pressure, greater anxiety, less airway and ventilatory control, peripheral vasodilatation ASA Classification of Periop Morbidity and Mortality: I - normal II - mild disease III - severe disease limiting activity but not incapacitating IV - severe incapacitating, a constant threat to life V - expected to die in 24 hours Periop Morbidity & Mortality Detsky Modified Multifactorial Index Variable Points ------------Coronary artery disease MI within 6 mos 10 MI >6 mos 5 Canadian Cardiovascular Society angina Class III 10 Class IV 20 Unstable angina within 6 mos 10 Alveolar Pulmonary Edema within 1 week 10 ever 5 Valvular disease suspected critical aortic stenosis 20 Arrhythmias Rhythm other than sinus or sinus+APC's on last 5 pre-op EKG More than 5 VPB's at any time prior to surgery 5 Poor medical status 5 Age over 70 5 Emergency operation 10 Detsky Modified MFI Pulmonary Risk: Less than cardiovascular risks. Primary risk is COPD. Restrictive disease much less worrisome. Need to produce a good cough. Factors that increase risk of postop pulmonary complic: 1) smoking hx 2) obesity 3) age>60 years 4) length of anesthesia > 3 hours 5) type of surgery (upper abdominal and thoracic greatest risks) PFT are most reliable predictor of operative risk. Obtain on pts with pulmonary symptoms (dyspnea, chronic cough) and those undergoing thoracic operations. Low risk: FEV1 > 2,000 ml Medium risk: FEV1 1,000 ml to 2,000 ml High risk: FEV1 < 1,000 ml (might require prolonged respiratory support postop) FEV1 (% of pred) < 75% assoc w/ incr rate of pulm complic MVV (maximal voluntary ventilation) < 50% pred - 237 serious operative risk On ABG an incr pCO2 may indicate a pt who will be difficult to wean off a ventilator Preop Preparation: Stop smoking at least 1 week prior to operation (2 months is better) If signs of reversible airway disease (15% improvement in FEV1 after bronchodilators) then consider theophylline or aerosilized bronchodilator Postop: Incentive spirometry every few hours Early mobilization Peak incidence of post-op MIs: 3rd day postop - can be silent secondary to analgesics Surgery post-MI: 3 months - risk=30% >=6 months - risk=5% Risk factors for CAD: age>70, DM, HTN, LVH, PVD, carotid artery disease CHF: 2% in pt with no prior hx of CHF 6% in pt with h/o CHF but no current evidence of CHF (on CXR or exam) >30% in pts with preop S3 gallop or JVD 2 peaks of occurrence: 1) immediately post-op 2) 24-48 hours later (secondary to fluid mobilization) Arrhythmias: Generally do not pose a significant hazard for periop morbidity or mortality. SVT occurs in about 4% of postop patients - has a high morbidity - should search for CHF, MI, pericarditis, infection, hypoxemia, acidosis, hypokalemia, anemia or aggravating meds (ie. epinephrine). Resolves spont in 40%, responds to meds in 47%, needs electr CV in 6%. Valvular Heart Disease: Most murmurs benign. Greatest risk with AS. Significant stenosis or regurgitation of mitral or aortic valves are each associated with a 20% incidence of new or worsening CHF in the postop period. If not sure can treat with antibiotics for endocarditis prophylaxis and w/u valves afterwards. HTN: mild is not a surgical risk factor. Risk only increases with diastolic bp>110. Can exhibit exaggerated fluctuations in bp (hyper and hypo) periop. Continue anti-HTN meds until AM of surgery - should be restarted postop. Can use IV, IM or SQ forms if pt can't take pos (hydralazine, labetalol, Inderal, Procardia, Vasotec, Cardizem). IV nitroprusside for control of severely elevated bp. Dental: 238 if anticoag then keep PT<20 sec - can continue AC. Can use local epinephrine and atropine in small quantities. Endocarditis prophylaxis in patients with valve disease. Anemia: usually treat to Hct >= 30 (unless chronic - then >=20) transfuse at least 24 hrs prior to surgery Platelets: >=100,000 for major surgical procedures >=30,000 for minor operations Can transfuse - each unit will raise platelet count by about 10,000 Platelets can also be dysfunctional with a normal count - can see this by prolonged bleeding time (but may not correlate with surgical blood loss). Common causes are drugs (ie. ASA, NSAIDS) and von Willebrand's disease. Should D/C ASA 5-7 days prior to surgery and NSAIDS 1-2 days prior. PT/PTT: if elevated are the result of a drug or disease PT - elev by coumadin - need to stop 3-4 days prior to the surgery (if elective). If urgent can give Vit K (10 mg SQ & repeat 12 hrs later) &/or transfuse with FFP. Vit K will interfere with coumadin for days afterwards where FFP will not. - also elevated by chronic liver disease, malabsorb of Vit K and DIC. PTT - elev by heparin - short half life. If need to reverse effects immed then can use protamine. - also elevated by hemophilia and lupus anticoagulant Tight AC control: for pts with MV prosthesis, dialysis pts with shunts prone to clot off and pts prone to embolization. Stop Coumadin 3-4 days preop - start full-dose heparin - stop heparin 6-12 hrs pre-op and restart postop when bleeding risk is minimal (can also start at half-dose and then increase to full-dose several days later). Loose AC control: for pts with AoV prosthesis, remote history of TIA or DVT. Stop Coumadin 3-4 days preop and restart several days postop. Thromboembolism Prophylaxis in Surgical Procedures -------------------------------------------------Type of Surgery Prophylaxis Regimen* --------------------------------------------------------General Low dose heparin 5,000u sq bid-tid Urology** Low dose heparin 5,000u sq bid-tid Gynecology** Low dose heparin 5,000u sq bid-tid Neurosurgery Extracranial Low dose heparin 5,000u sq bid-tid Intracranial Pneumatic compression 239 Orthopedic (hip Two step warfarin Begin 10 d before surgery and knee surgery - keep PT reconstruction) 2-3 sec prolonged Give twice preop dose postop- keep PT 1.5x control Adjusted dose Begin 2 d before heparin surgery at 3,500 units sq tid. Check PTT 6 hrs after AM dose and incr or decr by 500-1000 units to keep PTT 30-40 s. Dihydroergotamine- 2 hrs preop and heparin (Embolex) bid postop Dextran-40 Give 10 ml/kg as 12 hr infusion on day of surgery, followed by 7 ml/kg/d as constant infusion x 5 days Use cautiously w/ h/o CHF Pneumatic compression * duration of prophylaxis should be 5-7 days or until pt is ambulatory ** for open prostatectomies and for gyn cancer operations consider stronger prophylaxis (ie one of the orthopedic regimens) Postop DVT occurs in about 25% of above operations. Incidence of fatal pulmonary embolism 1-5%: Diabetes: most common postop complication besides hyperglycemia is infection (wound or UTI) and cardiovascular events (MI or CHF). Pts on insulin as outpts should receive some insulin preop but at a reduced dose. One regimen is giving half the pts normal intermediate acting insulin preop and supplementing with short acting insulin postop. If insulin is given preop then pt should be on a glucose containing infusion (ie D5W at 125 ml/hr). If on oral agents then can be maintained with possible periop insulin if glucose is >250-300. Long acting oral agents should be stopped 3 days preop to prevent intraop or periop hypoglycemia and shorter acting agents should be stopped the day before surgery. Greatest risk occurs in pts with chronic liver dysfunction, especially those with progressive hepatic failure. Antibiotics for Endocarditis Prophylaxis Site Std Regimen Reg for PCN allergy --------------------------------------------------------Dental and oral/ PCN V 2.0gm po Erythromycin 1.0g respir tract 1 hr before then po 1 hr before 1.0gm 6 hrs after then 500mg 6 hrs after GI and GU tract Ampicillin 2.0gm 240 Vancomycin 1.0gm IM or IV + Gent IV over 1 hr + 1.5 mg/kg IM or Gent 1.5 mg/kg IM IV given .5-1 hr or IV given 1 hr before then 8 hrs before then 8 hrs after after POISONING [Initial management] Provide airway, ventilation and vital signs. Protect yourself from organophosphate & carbamate insecticides and cyanide. If the patient is unconscious and convulsing, give Dextrose, and naloxone (2 mg in child or adult. If there is ingestion of propoxyphene, pentazocine or butorphanol then more than 2 mg may be required), and Oxygen. If the patient is alcoholic, give Thiamine 100 mg IV or IM before dextrose. If unable to give drug IV then may give atropine, epinephrine, lidocaine and naloxone through an endotracheal tube. Diazepam can be given rectally. SEIZURES: If the seizures are due to theophylline then they may be refractory to usual therapeutic medications, and the patient may need general anesthesia. Seizures due to hypoglycemia must be treated immediately with glucose. Seizures due to isoniazid will respond to pyridoxine. Seizures related to anticholinergic agents may respond to physostigmine, if the usual anticonvulsants are not effective. Hemodialysis may be needed for seizures due to salicylates or lithium. Be aware that alcoholic withdrawal may cause seizures. Tricyclic seizures may need bicarbonate. INVESTIGATIONS: EKG (for dysrhythmias or conduction defects from tricyclics). Chest x-ray (for aspirations & non cardiogenic pulmonary edema). Measure the anion gap and electrolytes (salicylates, methanol, ethylene glycol, carbon monoxide, toluene, cyanide, and hydrogen sulfide). Get serum osmolality & calculate the osmolality (2x sodium) + (glucose/18) + (BUN/2.8). The difference between these two is the osmolar gap. If more than 10 mOsm/liter then think methanol, ethylene glycol, or isopropanol poisoning. UA (for crystals of ethylene glycol) Qualitative drug screening of urine, serum & possibly gastric contents). Specific drug levels are useful in acetaminophen, anticonvulsants, digoxin, aspirin, ethanol, methanol, ethylene glycol, iron, isopropyl alcohol, lithium & theophylline overdoses. Contact the poison center. For salicylates & ethanol treat with urine alkalinization & hemodialysis. For methanol & ethylene glycol treat with hemodialysis. Breath analysis will reveal clues. Petroleum distillates have a characteristic odor, fruity odor (ketoacidosis & ketones of ethanol and isopropyl alcohol), almond odor (cyanide), garlic odor (arsenic or organophosphates), glue odor (chronic toluene abuse) and rotten egg odor (hydrogen sulfide or disulfiram). Do a physical exam to look for focal neurological signs (CVA, subdural hematoma), nuchal rigidity (meningitis), needle tracts (arms, feet, groin, under the tongue, neck, supraclavicular), drugs in the rectum, vagina & swallowed drug packets, and cardiac arrest (cocaine). Get family members to bring in prescription bottles and call the pharmacy to get a list of drugs. Search the clothing, home & garbage. Look for drug paraphernalia. ANTIDOTES: 1....Benzodiazepines [Flumazenil] 0.2 mg over 30 seconds. If ineffective after 30 seconds give .3 mg over 30 seconds. If no response after 30 seconds give .5 mg over 30 seconds at 1 minute intervals up to a total dose of 3 mg. Flumazenil should not be given if benzodiazepines are being given for convulsions or there is simultaneous ingestion of tricyclics. 2....Tricyclics antidepressants [Bicarbonate] 3....Digitalis [Digoxin specific antibody fragments] If the amount ingested and the serum digoxin concentration are both unknown then given 10-20 vials IV if there is a life threatening dysrhythmia. If the number of milligrams is known then divide that by 0.6 to ascertain the number of vials to give OR if the serum digoxin concentration is known, the number of vials = the digoxin concentration in ng/ml x 5.6 x weight in kg/600. 4....Opiates [Naloxone] Start at 2 mg IV. Less may be needed to prevent withdrawal symptoms. More may be needed if synthetic narcotics have been taken as propoxyphene, pentazocine & butorphanol. 5....Anticholinergic agents [Physostigmine] 1-2 mg IV over 5 minutes. May be useful to treat tachydysrhythmia or seizures. Should only be used for severe delirium. 6....Methanol, ethylene glycol [Ethanol] Give loading dose of 10 ml of 10% solution /kg of body weight. Maintenance dose 0.15 ml/kg/hr. If the patient is on dialysis, double the maintenance dose. Titrate to blood ethanol level of 100 mg/dl. 7....Calcium channel blockers, hydrofluoric acid, and fluorides [Calcium] 1 g calcium chloride given over 5 min by IV infusion with cardiac monitoring. Monitor the calcium level. 8....Organophosphate or carbamate insecticides [Atropine] Give an initial test dose of 2 mg IV. Repeat in larger doses until there is drying of pulmonary secretions. 9....Isoniazid, hydrazine, monomethylhydrazine in Gyromitra species mushrooms [Pyridoxine]. If the amount of ingestion is unknown, start with 5 g IV. Overdose can cause neuropathy. If amount ingested is known then given gram per gram equivalent of pyridoxine. 10....Beta blockers [Glucagon] Start with 5-10 mg IV. ACETAMINOPHEN TOXICITYIf the patient is seen within 12 hrs of ingestion and is alert, ipecac 30 ml with fluids is given. Repeat in 15 minutes or gastric lavage. Do not give charcoal or cathartics. LAB: acetaminophen level 4 hrs post ingestion, liver tests, BUN, creatinine, glucose, PT. 241 THERAPY: Within 24 hrs of ingestion give Mucomyst loading dose of 140 mg/kg PO, diluted 3:1 in juice, soda or water, then maintenance of 70 mg/kg PO q4h for 17 doses. Beyond 24 hrs of ingestion supportive therapy is indicated without Mucomyst. Avoid diuresis, sedatives and drugs that are metabolized in the liver. Obtain daily labs for at least 4 days. For a prolonged PT give vitamin K 10 mg IM. Refractory bleeding may require fresh frozen plasma. The toxic dose in adults is > 7.5 grams, with hepatic damage > 10 grams. The symptoms are malaise, nausea, vomiting and sweating. Use Rumack-Matthew Nomogram For Acetaminophen Overdose CARBON MONOXIDE POISONINGCarbon monoxide is a colorless, odorless gas that is produced by the combustion an any type of carbon containing material. It may be found in automobile exhaust, coal and gas heaters, and as a toxin in smoke inhalation patients from fires. As many as 40% of smoke inhalation victims die of carbon monoxide poisoning. The most common sources for exposure include automobile exhausts, faulty space heaters and furnaces, fires, improperly vented wood stoves and fireplaces, and engines used without ventilation in enclosed spaces. Cigarette smokers are constantly exposed to CO and can reach a COHb level as high as 10% in chronic smokers. The 242 severity of carbon monoxide (CO) varies depending on the ambient CO concentration, the minute ventilation of the individual, the health status of the individual, and the duration of exposure. Equilibrium is reached much more rapidly in individuals who engage in vigorous physical activity. Patients with underlying heart and lung disease cannot tolerate hypoxia produced by even small or moderate CO levels. Infants are even more at risk to CO poisoning, because fetal hemoglobin has a very high affinity for CO. CO poisoning occurs as a metabolic breakdown product of methylene chloride. Fumes from paint strippers that contain methylene chloride which are metabolized to CO. CO is rapidly absorbed through the lungs and is eliminated by the lungs. It produces toxicity by hypoxemia, cellular asphyxia and ischemia. It combines with hemoglobin with an affinity that is about 250 times that of oxygen. Therefore, even at low levels of CO, there can be excessive saturation of hemoglobin binding sites, severely limiting the blood's oxygen carrying capacity. As little as 0.1% CO (1000 ppm) can produce potentially fatal 50% saturation of hemoglobin at equilibrium. Exposure at workplaces is restricted to 50 ppm as an eight hour average. Levels approaching 1500 ppm are considered dangerous to life. CO binding to hemoglobin changes the shape of the oxygen hemoglobin dissociation curve, which causes a left shift, resulting in further decreases of intracellular oxygen concentrations. Decreased cardiac output occurs, probably due to intracellular binding of CO with myoglobin, causing decreased output and hypotension. CO may also bind to intracellular cytochromes, which negates oxygen utilization. The consequent tissue hypoxia results in ischemic and cellular damage, a conversion to anaerobic metabolism, a reactive hyperglycemia secondary to liver glycogen breakdown, and a severe metabolic acidosis. CO poisoning accounts for almost 50% of all fatal poisoning occurring yearly in the USA. CLINICAL: The symptoms depend on the carbon monoxide hemoglobin levels. Individuals with 010% usually have no symptoms. Levels of 10-20% will cause complaints of headache, tightness across the forehead, dilation of cutaneous vessels, dyspnea with minor exertion and angina in coronary artery patients. Patients with levels between 20-30% have throbbing headaches, dyspnea, nausea, and dizziness. Levels between 30-40% have vomiting, very severe headaches, and poor judgment. Levels between 40-50% have syncope, confusion, tachycardia, and tachypnea. Levels between 50-60% have seizures, syncope and coma. Levels between 60-70 present in coma, hypotension, arrhythmias or death. Levels greater than 70% usually leads to respiratory failure and death. The diagnosis cannot be made unless you suspect exposure. If the patient is found in a car with the engine running, your suspicion should be heightened, just as in finding multiple victims in a common room. Cans of paint strippers and solvents that contain methylene chloride found with the victim in a poorly ventilated room should also arouse your suspicion. Carbon monoxide may commonly be diagnosed as influenza with headache, nausea and vomiting. Most textbooks stress the cherry red coloration of the skin, but in reality this is very rare, and cannot be relied upon for diagnosis. Sometimes retinal hemorrhages may be seen. Arterial blood gases usually show a metabolic acidosis, due to the tissue hypoxia and ischemia. The arterial PO2 and the calculated oxygen saturation is typically normal because dissolved oxygen in the serum is not affected by CO. Pulse oximetry oxygen saturation usually remains normal despite severe CO poisoning. The diagnosis is confirmed by the laboratory measurement of COHB levels in the blood. High COHb levels greater than 20% indicate a dangerous exposure. Patients that seemingly recover from CO poisoning may not recover fully. CO poisoning can produces a neuropsychiatric syndrome days to weeks following recovery consisting of dull mentation, behavioral changes, loss of memory, cognitive changes and garrulousness. Complications include blindness, deafness, parkinsonism, seizures, incontinence, cortical blindness, aphasia, apraxia, psychosis, cogwheel rigidity, rhabdomyolysis, myoglobinuria and renal failure. DIFFERENTIAL DIAGNOSIS should include head trauma, hypoglycemia, meningitis, alcohol and drug intoxication. Cyanide, hydrogen sulfide and other toxic gases should also be considered in the differential. TREATMENT: Treatment begins with the administration of 100% oxygen provided with a tight fitting mask or a non-re breather mask with oxygen reservoir, or by an endotracheal tube at a flow of 10 liters/min. Hypotension is treated with 1-2 liters of crystalloid solution. Low potassium is frequently seen and should be treated in order to avert cardiac arrhythmias. Patients with mild to moderate metabolic acidosis (pH 7.2-7.3) should not be treated because the acidosis can facilitate oxygen deliver to the tissues by moving the oxygen hemoglobin dissociation curve to the right. Administration of 100% oxygen will also shorten the CO half life from 5 hours in room air to 40-80 minutes. With hyperbaric oxygen at 2-3 atmospheres, the arterial pO2 is raised as high as 2000 mm Hg and the COHb half life can be further reduced to 23 minutes. The indications for hyperbaric oxygen include any one who has lost consciousness due to CO exposure or a symptomatic patient with a COHb level extrapolated to 25% at the time of the initial exposure. Children with COHb levels of 20% or higher at the time of exposure can be candidates. Pregnant patients exposed to COHb levels as low as 20% are also candidates. If patients are treated by hyperbaric oxygen, urgency is the key. Patients that were treated within 6 hours had a 13.5% mortality, while 30.1% died if treated later than 6 hours. 243 CIGUATERA FISH POISONINGMany patients with Ciguatera fish poisoning that seek medical attention from symptoms of gastroenteritis are missed. A patient that presents with nausea, vomiting, diarrhea, diaphoresis and numbness and tingling, particularly around the mouth, may be mis-diagnosed as hyperventilation syndrome plus viral gastroenteritis. Key points to differentiate Ciguatera fish poisoning from the garden variety gastroenteritis are: Ciguatera fish poisoning produces a phenomenon known as sensory reversal dysesthesia, whereby a patient perceives cold objects as warm and vice versa. The second key point is that alcohol will produce a return of the symptoms or a worsening of the symptoms. The third point is that Ciguatera fish poisoning will last for about 1-2 weeks and about 50% of patients will still have symptoms at 2 months. The neurologic symptoms persist much longer than the gastrointestinal symptoms. Ciguatera poisoning is contracted by eating fish that harbor the single cell toxic producing parasite, Gambierdiscus toxicus. There are more than 400 fish species that live around coral reefs and harbor the parasite. Gambierdiscus toxicus attaches itself to marine algae, and small fish will eat the algae. Larger fish will eat the smaller fish and thus a poisoning chain is set up. In particular, grouper, red snapper, amberjack, barracuda, sturgeon fish, jack tuna, sea bass, moray eels and king mackerel are the common fish involved with this infestation. The larger the fish, the larger the concentration of the poisonous toxin, and the greater the magnitude of the symptoms. Fish under 5 pounds are relatively safer to eat than those over 25 pounds. Ciguatoxin cannot be deactivated by cooking, freezing, drying, smoking, marinating, salting, or pickling, and gastric enzymes and acids will not inactivate it. The toxin is tasteless and odorless. The toxin doesn't cause any ill affects in the fish, even though there are high concentration in the viscera such as the gonads and liver. Florida and Hawaii are common states that have a higher incidence, but with modern transportation any state can be affected. Ciguatera fish poisoning is endemic in tropical regions as the Caribbean and the Indo-Pacific islands. CLINICAL: Approximately 2-24 hours after ingesting the affected fish, nausea, vomiting, watery diarrhea, abdominal cramps, myalgias and diaphoresis will begin. The abdominal symptoms usually last about 3 days but can be longer. Eighty percent of patients will develop paresthesias of the extremities, numbness and tingling around the mouth and hot and cold reversal as mentioned above. The patient may also have dizziness, ataxia, pruritus, facial pain, rash, tremors, nuchal rigidity, and rarely audio and visual perturbations, confusion and coma. TREATMENT: Treatment is mainly supportive with IV fluids and electrolyte replacement. The pruritus may be managed with terfenadine 60 mg bid. Amitriptyline, 25 mg bid may help the pruritus and the dysesthesias. Mannitol 20%, 1 gram/kg given over 30 minutes may help in the severe cases. The patient should be told to avoid alcohol and further fish ingestion. Anaphylaxis -Anaphylactic -- IgE-mediated -Anaphylactoid -- not IgE-mediated prob Complement mediated Presentation Airway: wheezing, stridor, laryngeal edema Cardiac: incr vasc perm, circulatory collapse, hypotension GI:incr motility from histamine, diarrhea Skin: urticaria, flushing Treatment Airway -- intubate prn Breathing -- ventilate prn, consider breathing treatments Circulation - epinephrine 1:1000 1cc SQ or .3cc q5min 1:10,000 10cc IV .3-5cc Antihistamines H1 blockers -- 50-100mg diphenhydramine H2 blockers -- cimetidine Steroids 200 mg of Solu-Cortef 100 mg of Solu-Medrol Consider Phenylephrine drip Levo drip Epinephrine drip DYE RXN: high prob of having another reaction 244 SCABIESScabies is caused by a small female itch mite Sarcoptes var. hominis. The adult female measures about 400 microns and is extremely difficult to see. It causes a significant amount of morbidity in the family and also in nursing homes. The most frequent location of the rash is on the wrists and hands followed by the extensor elbows, feet, ankles, penis, scrotum buttocks and axillae. Scabies is usually acquired by sleeping with a person who is infested, or in the bed of an infested person. The entire family can be affected. The mite is incapable of jumping or flying but can cover about 2.5 cm of warm skin per minute. The mite seems to be attracted to the skin by host odor and body heat. The mite is transferred between hosts by direct contact, infested clothing and linens. Live mites can be found from the dust of bedroom floors, mattresses, chairs, floors, curtains and dirty laundry of nursing homes. CLINICAL: The eruption consists of burrows, pustules, papules, nodules and occasionally urticaria. Itching is extreme and usually occurs at night. The onset of symptoms usually are delayed for several weeks after the first infestation. The pruritus is caused by sensitization to the mite. Usually only a few mites are present with most patients having around 10. There are epidemics of scabies which occur in cycles. The lesions are typically seen on the volar aspect of the wrists, breasts, axillae, interdigital webs of the hands and genitalia. Females may have lesions around the areolae of the nipples and male patients may have the lesions on the penis. In young children, the palms and soles may be involved with vesicular and pustular lesions. In immunosuppressed patients the lesions may occur on the face and scalp which are usually spared except possibly in infants. The burrow is a 2-3 mm track, but may be difficult to see in about a quarter of the patients. The mite, eggs and stool reside in this track which is formed by the female mite tunneling under the stratum corneum epidermidis. The female mite in the burrow lays eggs at about 2-3 per day for up to 2 months. The egg hatches in about 3-4 days. Only about 10% of the eggs will eventually become adults. As the larvae emerge after a few days from the burrow, papules are formed around hair follicles which become pruritic. The larvae become adults in about 10-14 days. The adult female burrows into the skin and is eventually fertilized starting the entire cycle again. Continuous scratching can lead to thickening of the skin and nodule formation. with hyperpigmentation. Some of these lesions become infected with group A beta-hemolytic Streptococcus pyogenes or coagulase positive Staphylococcus aureus. Atypical presentations may occur in two different forms: Scabies incognito and Norwegian scabies. Scabies incognito causes a widespread non-inflammatory distribution due to previous use of topical corticosteroid preparations. Norwegian scabies or crusted scabies is a rare presentation seen in immunocompromised or neurologically impaired patients. Typical patient populations would include the malnourished, mentally retarded, AIDS patients, leukemia, diabetes mellitus or those receiving immunosuppressive therapy. In this form there is crusting of the face, scalp, hands, feet and pressure bearing areas. Generalized body distribution may occur affecting even the nails. The pruritus is minimal. DIAGNOSIS: Diagnosis is made from the history of contact with an infested person along with the typical presentation of lesions in the interdigital web spaces, axillae and genitalia. The patient should be asked if anyone else in the household or nursing home is itching and scratching. The definitive diagnosis depends on microscopic identification of the mite. Several non excoriated lesions should be chosen and scraped with an #15 mineral oil impregnated scalpel. This debris is then transferred to a slide with cover and viewed under the microscope. The mite, larvae, eggs and excrement all may be seen. TREATMENT: LINDANE: Lindane should not be used in pregnant patients, infants and those that have excoriations. It is relatively safe when used appropriately. In older patients lindane is no longer considered the first line treatment. Rare cases of seizures in neonates has occurred. Lindane (1% gamma benzene hexachloride) is available as Kwell, G-well and Scabene. It should not be applied to damp skin which will increase the absorption. Typically, 1 oz of lotion or cream is applied from the chin down to the toes and is then showered off 8-12 hours later. This should be repeated in one week in order to eliminate late hatching larvae. Lindane does not kill the eggs. PERMETHRIN: Permethrin 5% cream is now considered the treatment of choice. It is available as a 5% cream base known as Elimite. It was originally marketed as Nix, a 1% cream rinse. Permethrin is often times effective when lindane fails. It is poorly absorbed and is rapidly metabolized and excreted making it safer than lindane. It may safely be used in infants aged 2 months to 5 years of age. Permethrin 5% cream is probably the drug of choice if the patent is pregnant. The cream is massaged into the skin from head to toe and left on the body for 8-12 hours. A repeat application is given in one week. CROTAMITON: Crotamiton (Eurax) 10% cream or lotion is applied from chin to toes for 8-12 hours for 5 nights. It is far less effective than the above two. The cure rate is only about 50-66% that of lindane. It may used in children and pregnant or lactating women. For itching, topical .1% fluorinated corticosteroid ointment may be used BID. The pruritus often takes about 2 weeks to subside after the patient is treated with lindane or permethrin. In severe cases a short course of prednisone, 40 mg daily, and tapered over 2-3 weeks may be necessary for refractory pruritus. All clothes that have been worn within 48 hours of treatment along with bedclothes and towels must be machined-washed in hot water or dry cleaned. Shoes should be placed in plastic bags for 1 week before these are worn again. Floors should be swept, chairs and mattresses should also be cleansed, as it has been shown that the mite can live 245 for more than 2 days on floors and furniture. There should be simultaneous treatment of all members of the household, sexual contacts and household guests that frequent the domicile. ACUTE ARTHRITIS Immediate Questions: 1. Is it really arthritis? When examining an individual with "joint" pain, you will ask yourself a series of questions. First, does the patient have arthritis, or some other form of musculoskeletal pain? There are four categories of etiologies for "joint" pain. A. Arthritis: Hx- pain in the joint, or in the reference area of the joint; pain will increase with any joint movement; that is, all ranges of motion will cause pain. PE- tenderness over "entire" joint, especially joint line; swelling of "entire" joint, either soft tissue or bony; joint effusion; limitation of and pain in range motion in all directions. B. Periarticular: (e.g., tendinitis, bursitis, ligamentous) Hx- pain in or near the joint; usually localized to one aspect of the joint; pain with certain movements of the joint. PE- localized tenderness and swelling, often along the outline of the involved structures; no joint effusion; usually normal passive range of motion, but decreased active range of motion when the involved structure is moved. C. Nonarticular: (e.g., fibrositis, endocrine/metabolic, myalgia) Hx- pain unrelated to joint or joint movement; atypical pain pattern. PE- usually normal articular exam; often with relatively normal physical exam. D. Referred: (e.g., visceral, neurogenic, psychogenic) Hx- pain following a dermatome or peripheral nerve distribution; neurological symptoms; non-musculoskeletal symptoms. PE- neurological abnormalities: strength, sensation, reflexes; non-musculoskeletal abnormalities. Joint Aspiration: Joint tap is needed to determine the etiology of acute arthritis. An infection can destroy a joint, so treatment must be initiated rapidly. future link to See pages (?) for information on joint aspiration techniques. Diagnostic Considerations for Acute Arthritis: Acute arthritis is a serious condition. Failure to recognize and treat an infection can lead to rapid joint destruction. The disorders that require prompt, specific treatment are infectious and crystal-induced arthritis. Pyogenic infections of the joints in adults are seen primarily in the debilitated, the elderly and those who are parenteral drug abusers. Among healthy adults with acute monarthritis, the probability of nongonococcal joint sepsis is estimated to be less than 10%. That is, other than GC 246 arthritis, infections are infrequent. Findings that suggest gonococcal disease include a prodromal of myalgias, migratory arthralgias, fever, dermatitis or tenosynovitis. These associated findings occur in about 65% of patients. Gram-positive organisms account for 80 to 90 percent of acute nongonococcal infectious arthritis, and staphylococci are responsible for the majority of those cases. Such infections especially occur in rheumatoid joints, those patients receiving corticosteroids and individuals with a prosthetic joint. Gout typically presents among men over age 45, (women usually do not have gout until postmenopausal). Acute gouty arthritis is typically an episodic, monarticular arthritis that develops rapidly to exquisite pain, heat, erythema and swelling. Severe first metatarsophalangeal arthritis (podagra) is common. The onset is abrupt and may follow trauma, surgery or no discernible stimulus. Fever (101 to 103deg.F) can be present. Pseudogout is a microcrystalline synovitis induced by crystals of calcium pyrophosphate dihydrate and associated with calcification of hyaline and fibrocartilage (chondrocalcinosis). More properly, this disorder is named calcium pyrophosphate dihydrate (CPPD) crystal deposition disease. Unlike gout, the large joints are preferentially involved in CPPD crystal deposition disease, especially the knee, (found in over half the cases). Involvement of the shoulder, hip, wrist, elbow, and MCP joints also occurs. Generally, episodes of pseudogout are less intense and more protracted than those of gout. However, they also may mimic gout in intensity, duration and joint involvement. Pressure Ulcers in Adults: Prediction and Prevention The staging of pressure ulcers recommended for use by this panel is consistent with the recommendations of the National Pressure Ulcer Advisory Panel (NPUAP): Stage I: Nonblanchable erythema of intact skin; the heralding lesion of skin ulceration. Note: Reactive hyperemia can normally be expected to be present for one-half to three-fourths as long as the pressure occluded blood flow to the area; it should not be confused with a Stage I pressure ulcer. Stage II: Partial thickness skin loss involving epidermis and/or dermis. The ulcer is superficial and presents clinically as an abrasion, blister, or shallow crater. Stage III: Full thickness skin loss involving damage or necrosis of subcutaneous tissue that may extend down to, but not through, underlying fascia. The ulcer presents clinically as a deep crater with or without undermining of adjacent tissue. Stage IV: Full thickness skin loss with extensive destruction, tissue necrosis or damage to muscle, bone, 247 or supporting structures (for example, tendon or joint capsule). Note: Undermining and sinus tracts may also be associated with Stage IV pressure ulcers. Staging definitions recognize these limitations: Assessment of Stage I pressure ulcers may be difficult in patients with darkly pigmented skin. When eschar is present, accurate staging of the pressure ulcer is not possible until the eschar has sloughed or the wound has been dГ©brided. The guideline is intended for clinicians who examine and treat persons at risk of developing pressure ulcers. These clinicians include family physicians, internists, geriatricians, dietitians, occupational and physical therapists, nurses, and nurse practitioners working in a variety of health care settings such as acute care, rehabilitation, geriatric care, and home- and community-based settings. After an extensive review of the scientific literature, the panel used the following criteria to grade the evidence supporting each recommendation: A There is good research-based evidence to support the recommendation. B There is fair research-based evidence to support the recommendation. C The recommendation is based on expert opinion and panel consensus. Risk Assessment Tools and Risk Factors Goal: Identify at-risk individuals needing prevention and the specific factors placing them at risk. Bed- and chair-bound individuals or those with impaired ability to reposition should be assessed for additional factors that increase risk for developing pressure ulcers. These factors include immobility, incontinence, nutritional factors such as inadequate dietary intake and impaired nutritional status, and altered level of consciousness. Individuals should be assessed on admission to acute care and rehabilitation hospitals, nursing homes, home care programs, and other health care facilities. A systematic risk assessment can be accomplished by using a validated risk assessment tool such as the Braden Scale or Norton Scale (reproduced here). Pressure ulcer risk should be reassessed periodically. (Strength of Evidence = A.) All assessments of risk should be documented. (Strength of Evidence = C.) 248 249 250 Pulmonary Bedside Reference 251 Central Line Placement Site 252 cm insertion . Right IJ Right SC Left IJ Left SC (Ht (cm)/10) - 1 ~ 15 cm (Ht (cm)/10) - 2 ~ 14 cm (Ht (cm)/10)+2 ~ 18 cm (Ht (cm)/10)+4 ~ 20 cm Endotracheal Tube Placement Lip Line @ 23 cm in MEN 21 cm in WOMEN Check CXR Massive Hemoptysis (any of the below) Massive Hemoptysis 200 - 300 cc in 12 hrs 400 - 600 cc in 24 hrs 16 - 25 cc/hr or >= 100 cc in any 4 hr time period Respiratory Distress associated with any volume of Hemoptysis '7-3' - Rule for fluid monitoring Initial PCWP Fluid < 10 mmHg 200 ml in 10 minutes 10-15 mmHg 100 ml in 10 minutes > 15 mmHg 50 ml in 10 minutes Reaction Therapy PCWP increases > 7 mmHg Stop PCWP increases 3 - 7 mmHg Wait 10 minutes Always > 3 mmHg Stop PCWP increases < 3 mmHg More fluid 253 254 Guidelines For Fluid Challenges By CVP or PCWP PCWP PCWP PCWP PCWP 255 < 10 mmHg 10 - 15 mmHg 16 - 20 mmHg > 20 mmHg 250 cc/hr 150 cc/hr 60 cc/hr Reseal IV Evidence Based Medicine Lectures 256 257 258 259 260 261 262 263 264 265 266 267 268 269 270 271 272 273 Worksheet for Using an Article About Therapy or Prevention Citation: _______________________________________________ _______________________________________________ _______________________________________________ Guide Comment s п‚· Are the Results of the Study Valid? 1. Was the assignment of patients to treatment randomized? [ ] Yes [ ] No [ ] Can't Tell - was follow-up complete? - were patients analyzed in the groups to 2. Were all patients who entered the trial properly which they were randomized accounted for and attributed at its conclusion? (intention to treat analysis)? [ ] Yes [ ] No [ ] Can't Tell 3. Were patients, their clinicians, and study personnel 'blind' to treatment? [ ] Yes [ ] No 274 [ ] Can't Tell 4. Were the groups similar at the start of the trial? - Baseline prognostic factors (demographics, co-morditity, disease severity, other known confounders) balanced? - If different, were these adjusted for? [ ] Yes [ ] No [ ] Can't Tell Cointervention? Contamination? Compliance? 5. Aside from the experimental intervention, were the groups treated equally? [ ] Yes [ ] No [ ] Can't Tell 6. Overall, are the results of the study valid? [ ] Yes [ ] No [ ] Can't Tell п‚· What are the Results 1. How large was the treatment effect? Absolute risk reduction? Relative risk reduction? 2.How precise was the estimate of the treatment effect? Confidence intervals? п‚· Will the Results Help Me in Caring for My Patients? 1. Can the results be applied to my patient care? Patients similar for demographics, severity, co-morbidity and other prognostic factors? Compelling reason why the results should not be applied? [ ] Yes [ ] No [ ] Can't Tell 2. Were all clinically important outcomes considered? [ ] Yes [ ] No [ ] Can't Tell Are substitute endpoints valid? 3. Are the likely treatment benefits worth the potential harms and costs? [ ] Yes [ ] No [ ] Can't Tell 275 NNT for different outcomes? 276 277 278 279 280 281 282 283 284 285 286 287 288 289 290 Worksheet for Using an Article About Assessing Diagnostic Tests Citation: _______________________________________________ _______________________________________________ _______________________________________________ Guide Comment s п‚· Are the Results of the Study Valid 1. Was there an independent, blind comparison with a reference standard? Is reference standard used acceptable? Were both reference standard and test applied to all patients? [ ] Yes [ ] No [ ] Can't Tell 2. Did the patient sample include an appropriate spectrum of patients to whom the diagnostic test will be applied in clinical practice? [ ] Yes [ ] No [ ] Can't Tell 3. Did the results of the test being evaluated influence the decision to 291 "Verification" or "workup" bias? perform the reference standard? [ ] Yes [ ] No [ ] Can't Tell 4. Were the methods for performing the test described in sufficient detail to permit replication? Preparation of patient? Performance of test? Analysis and interpretation of results? [ ] Yes [ ] No [ ] Can't Tell 5. Overall, are the results of the study valid? [ ] Yes [ ] No [ ] Can't Tell п‚· What Were the Results? How big or small is this LR? Magnitude of charge from pre-to post-test probability 1. Are likelihood ratios for the test results presented or data necessary for their calculation provided? Size of L.R п‚· 0.1 or 10 large/conclusive 0.1-0.2 or 5п‚· moderate 10 0.2-0.5 or 2-5 small but sometimes 0.5-1 or 1-2 NB small, rarely NB [ ] Yes [ ] No [ ] Can't Tell п‚· Will the results Help Me in Caring for My Patients? 1. Will the reproducibility of the test result and its interpretation be satisfactory in my setting? [ ] Yes [ ] No [ ] Can't Tell 2. Are the results applicable to my patient? Similar distribution of disease severity? Similar distribution of competing diseases? Compelling reasons why the results should not be applied? [ ] Yes [ ] No [ ] Can't Tell 3.Will the results change my management? 292 Test and treatment thresholds? High or low LR's? [ ] Yes [ ] No [ ] Can't Tell Is target disorder dangerous if left undiagnosed? Is test risk acceptable? 4. Will patients be better off as a result Does effective treatment exist? of the test? Information from test will lead to change of Management beneficial to patient? [ ] Yes [ ] No [ ] Can't Tell Worksheet for Using an Article About Prognosis Citation: _______________________________________________ _______________________________________________ _______________________________________________ Guide Comment s п‚· Are the Results of the Study Valid? 1. Was there a representative and well-defined sample of patients at a similar point in the course of the disease? Inclusion and exclusion criteria? Selection biases? Stage of disease? [ ] Yes [ ] No [ ] Can't Tell 2.Was follow-up sufficiently long and complete? Reasons for incomplete follow-up? Prognostic factors similar for patients lost- and not lost-tofollow-up? [ ] Yes [ ] No [ ] Can't Tell 3. Were objective and unbiased outcome criteria used? Outcomes defined at start of study? Investigaotors 'blind to prognostic factors? [ ] Yes [ ] No [ ] Can't Tell 4. Was there adjustment for important prognostic factors? [ ] Yes [ ] No [ ] Can't Tell 5. Overall, are the results of the study valid? 293 [ ] Yes [ ] No [ ] Can't Tell п‚· What are the Results 1. How large is the likelihood of the outcome event(s) in a specified period of time? Survival curves? Confidence intervals? 2. How precise are the estimates of likelihood? п‚· Will the Results Help Me in Caring for My Patients? 1. Were the study patients similar to my own? Patients similar for demographics, severity, co-morbidity, and other prognostic factors? Compelling reason why the results should not be applied? [ ] Yes [ ] No [ ] Can't Tell 2. Will the results lead directly to selecting or avoiding therapy? [ ] Yes [ ] No [ ] Can't Tell 3. Are the results useful for reassuring or counselling patients? [ ] Yes [ ] No [ ] Can't Tell Worksheet for Using an Article About Causation of Harm Citation: _______________________________________________ _______________________________________________ _______________________________________________ Guide Comment s п‚· Are the Results of the Study Valid? RCT, cohort, base-control? 1.Were there clearly identified comparison groups that were similar with Other known prognosis respect to important determinants of outcome, other than the one of factors similar or adjusted interest? for? [ ] Yes [ ] No [ ] Can't Tell 2. Were the outcomes and exposures measured in the same way in the groups being compared? 294 Recall bias? Interviewer bias? Exposure opportunity similar? [ ] Yes [ ] No [ ] Can't Tell 3.Was follow-up sufficiently long and complete? Reasons for incomplete follow-up? Risk factors similar in those lost and not lost to followup? [ ] Yes [ ] No [ ] Can't Tell 4. Is the temporal relationship correct? [ ] Yes [ ] No [ ] Can't Tell 5. Is there a dose-reponse gradient? [ ] Yes [ ] No [ ] Can't Tell Exposure preceded outcome? Risk of outcome increases with quantity or duration of exposure? 6. Overall, are the results of the study valid? [ ] Yes [ ] No [ ] Can't Tell п‚· What are the Results? 1. How strong is the association between exposure and outcome? 2. How precise is the estimate of risk? RR's or OR's? Confidence intervals? п‚· Will the Results Help Me in caring for My Patients? 1. Are the results applicable to my practice? Patients similar for demographics, morbidity and other prognostic factors? Are treatments and exposures similar? [ ] Yes [ ] No [ ] Can't Tell 2.What is the magnitude of the risk? [ ] Yes [ ] No [ ] Can't Tell 295 Absolute rsk increase (and its reciprocal)? 3.Should I attempt to stop the exposure? Strength of evidence? Magnitude of risk? Adverse effects of reducing exposure? [ ] Yes [ ] No [ ] Can't Tell Worksheet for Using Clinical Practice Guidelines Citation: _______________________________________________ _______________________________________________ _______________________________________________ Guide Comment s п‚· Are the Recommendations Valid? 1. Were all important options and outcomes clearly specified? [ ] Yes [ ] No [ ] Can't Tell 2. Was an explicit and sensible process used to identify, select, and combine evidence? [ ] Yes [ ] No [ ] Can't Tell п‚· 3. Was an explicit and sensible process used to consider the relative value of different outcomes? [ ] Yes [ ] No [ ] Can't Tell 4. Is the guideline likely to account for important recent developments? [ ] Yes [ ] No [ ] Can't Tell 5. Has the guideline been subject to peer review and testing? [ ] Yes [ ] No [ ] Can't Tell 6. Overall, is the guideline valid? [ ] Yes [ ] No [ ] Can't Tell п‚· What are the Recommendations? 1. Are practical, clinically important, recommendations made? [ ] Yes 296 [ ] No [ ] Can't Tell 2. How strong are the recommendations? [ ] Yes [ ] No [ ] Can't Tell 3. What is the impact of uncertainty associated with the evidence and values used in the guidelines? [ ] Yes [ ] No [ ] Can't Tell п‚· Will The Recommendations Help You in caring for Patients? 1. Is the primary objective of the guideline consistent with your objective? [ ] Yes [ ] No [ ] Can't Tell 2. Are the recommendations applicable to your patients? [ ] Yes [ ] No [ ] Can't Tell Worksheet for Using a Systematic Review Citation: _______________________________________________ _______________________________________________ _______________________________________________ Guide Comment s п‚· Are the Results of the Study Valid? 1. Did the overview address a focused clinical question? [ ] Yes [ ] No [ ] Can't Tell 2. Were the criteria used to select articles for inclusion appropriate? [ ] Yes [ ] No [ ] Can't Tell 3. Is it unlikely that important, relevant studies were missed? [ ] Yes [ ] No [ ] Can't Tell 297 4. Was the validity of the included studies appraised? [ ] Yes [ ] No [ ] Can't Tell 5. Were assessments of studies reproducible? [ ] Yes [ ] No [ ] Can't Tell 6. Were the results similar from study to study? [ ] Yes [ ] No [ ] Can't Tell п‚· What are the Results? 1. What are the overall results of the review? 2. How precise were the results? п‚· Will the Results Help Me in Caring for My Patients? 1. Can the results be applied to my patient care? [ ] Yes [ ] No [ ] Can't Tell 2. Were all clinically important outcomes considered? [ ] Yes [ ] No [ ] Can't Tell 3. Are the benefits worth the harms and costs? [ ] Yes [ ] No [ ] Can't Tell Worksheet for Using an Article About An Economic Analysis Citation: _______________________________________________ _______________________________________________ _______________________________________________ Guide 298 Comment s п‚· Are the Results of the Study Valid? Costs and outcomes for each strategy? 1. Did the analysis provide a full economic comparison of health Whose viewpoint? care stragegies? Cost-effectiveness/benefit/utility study? [ ] Yes [ ] No [ ] Can't Tell Clinical effectiveness established? 2. Were the costs and outcomes properly measured and Costs measured accurately? Data on costs and outcomes appropriately valued? integrated? [ ] Yes [ ] No [ ] Can't Tell 3. Was appropriate allowance made for uncertainties in the analysis? Sensitivity analysis? Statistical significance? [ ] Yes [ ] No [ ] Can't Tell 4. Are estimates of costs and outcomes related to the baseline risk in the treatment population? [ ] Yes [ ] No [ ] Can't Tell What are the Results? 1. What were the incremental costs and outcomes of each strategy? 2. Do incremental costs and outcomes differ between sub-groups? [ ] Yes [ ] No [ ] Can't Tell 3. How much does allowance for uncertainty change the results? п‚· Will the Results Help in Caring for My Patients? 1. Are the treatment benfits worth the harms and costs? [ ] Yes [ ] No 299 Strong dominance? Weak dominace? Non-dominance? Incremental costeffectiveness? Sub-group analyses by risk? [ ] Can't Tell 2. Could my patients expect similar health outcomes? Study patients similar to my patients? Study clinical management similar to my local practice? [ ] Yes [ ] No [ ] Can't Tell 3. Could I expect similar costs? Study/local resource consumption similar? Study/local prices similar? [ ] Yes [ ] No [ ] Can't Tell Worksheet for Using an Article Reporting Variations in the Outcomes of Health Services Citation: _______________________________________________ _______________________________________________ _______________________________________________ Guide Comment s п‚· Are the Results of the Study Valid? 1. Are the outcome measures accurate and comprehensive? [ ] Yes [ ] No [ ] Can't Tell 2. Were there clearly identified sensible comparison groups? [ ] Yes [ ] No [ ] Can't Tell 3. Were the comparison groups similar with respect to important determinants of outcomes, other than the one of interest? - Important factors measured? - Measures reproducible and accurate? - Groups similar for important factors? [ ] Yes [ ] No [ ] Can't Tell 4. Were appropriate analyses undertaken to reduce the effect of dissimilarities between comparison groups? [ ] Yes 300 - Multivariate analyses? - Low risk sub-group analyses [ ] No [ ] Can't Tell 5. Overall, are the results of the study valid? п‚· What are the Results 1. How strong is the association between exposure and outcome? 2. How precise is the estimate of risk? п‚· Will the Results Help Me in Caring for My Patients 1. Are the results applicable to my practice? [ ] Yes [ ] No [ ] Can't Tell 2. What is the magnitude of the risk? [ ] Yes [ ] No [ ] Can't Tell 3. Should I attempt to stop the exposure? [ ] Yes [ ] No [ ] Can't Tell 301 IndexВ (I/OвЂ™s ........................................................................... 42 '7-3' - Rule for fluid monitoring ............................ 24, 255 Abciximab ................................................................. 113 ABDOMINAL PAIN ................................................... 198 ABG ................................ 34, 66, 67, 101, 185, 228, 240 ABGвЂ™s in Pulmonary Embolism ................................... 66 ABORTION ................................................................. 35 abscess............................. 103, 148, 192, 199, 212, 220 Abscess .................................... 148, 194, 196, 207, 232 Accuracy of Pulse Oximetry........................................ 65 ACE.... 98, 105, 106, 107, 110, 111, 114, 120, 121, 122, 131, 138 ACE inhibitors ................................... 106, 110, 111, 121 acetaminophen ......................................... 233, 243, 244 ACETAMINOPHEN TOXICITY ................................. 244 Acid Base............................................................ 76, 185 Acid Base Algorithm.................................................... 76 Acid-Base........................................................ 57, 62, 81 acid-base disorders........................................... 101, 186 Acidosis................... 23, 81, 98, 105, 106, 107, 109, 221 ACIDOSIS............................................................. 13, 14 ACLS........................................................................... 13 Acquired Factor VIII inhibition ................................... 236 ACTH ........................................................................ 234 Actinomyces.............................................................. 148 ACUTE ABDOMEN................................................... 198 Acute arthritis ............................................................ 249 ACUTE ARTHRITIS.................................................. 248 ACUTE BLINDNESS ................................................ 205 ACUTE DYSTONIC REACTION............................... 206 ACUTE HEMOLYTIC REACTIONS .......................... 237 Acute Lung Injury ........................................................ 71 acute myocardial infarction ....................................... 236 Acute renal failure ..................................................... 221 Acute Renal Failure .................................................. 124 ACUTE RENAL FAILURE......................................... 104 ACUTE RENAL INSUFFICIENCY ............................ 131 Acute Respiratory Distress Syndrome ........................ 71 Acute Respiratory Failure ........................................... 82 acute tubular necrosis............................................... 107 ACUTE TUBULAR NECROSIS ................................ 108 Addison's ............................................................ 98, 212 adrenal ...................................................... 220, 221, 233 Adrenal insufficiency ......................................... 138, 233 ADRENAL INSUFFICIENCY .................................... 233 Advanced Cardiac Life Support .................................. 13 afterload ............ 106, 114, 118, 121, 122, 123, 131, 151 Afterload.................................... 118, 120, 121, 122, 123 AIDS.... 12, 135, 213, 214, 215, 216, 217, 222, 233, 247 Albumin ..................................................... 105, 107, 205 Albuterol.............................................................. 99, 146 Alcohol .............................................. 116, 202, 203, 207 Alcoholic............................ 119, 138, 201, 202, 203, 223 alcoholic withdrawal .................................................. 243 ALCOHOLIC WITHDRAWAL.................................... 203 Alcoholism......................................................... 101, 201 ALCOHOLISM .......................................................... 201 Algorithm..................................................................... 76 ALI............................................................................... 71 Allergic ........................................................................ 28 Alpha-1 antitrypsin .................................................... 145 Alpha1-Antitrypsin Deficiency ................................... 145 alpha-tocopherol ....................................................... 113 Alteplase ................................................................... 118 alveolar gas equation................................................ 185 alveolar ventilation ............................................ 185, 189 302 aminoglycosides ................................. 98, 101, 107, 226 Aminoglycosides....................................... 105, 108, 212 Aminophylline ............................................................. 22 amiodarone............................................................... 231 Amphotericin..................................................... 105, 108 amphotericin B.................................................. 101, 107 amyloidosis....................................................... 109, 135 Amyloidosis .............................................. 119, 138, 233 Anaphylactic ............................................................. 246 ANAPHYLACTIC IGA DEFICIENT REACTIONS ..... 237 Anaphylactoid ................................................... 216, 246 Anaphylaxis .............................................................. 246 anemia26, 110, 111, 116, 137, 186, 208, 209, 212, 215, 216, 220, 223, 233, 234, 237, 240 Anemia ............................... 28, 110, 201, 212, 217, 241 anesthesia ..... 28, 34, 35, 107, 220, 222, 223, 238, 239, 243 aneurysm.......................... 105, 108, 131, 152, 198, 206 ANF .................................................................. 107, 109 angina 24, 112, 113, 114, 115, 116, 119, 129, 130, 150, 239, 245 Angina ...................................................... 112, 113, 114 ANGIOGRAPHY....................................................... 201 Angioplasty ....................................................... 113, 121 anion gap...................................................... 62, 63, 109 Anion Gap................................................. 62, 74, 77, 81 Anion Gap Acidosis .................................................... 62 Anion Gap Gap..................................................... 75, 78 Anti-Arrhythmic Drugs ................................................ 14 ANTIBIOTICS ........................................................... 212 anticholinergic................................................... 222, 243 anticoagulant .................................................... 236, 241 ANTICOAGULANT INR RECOMMENDATIONS FOR VARIOUS SITUATIONS- ..................................... 236 Anticoagulation ......................................................... 164 Anti-Coagulation ....................................................... 121 ANTICOAGULATION TREATMENT ........................ 234 Anti-Convulsant Agents ............................................ 208 anticonvulsants......................................... 132, 212, 243 ANTIDOTES ............................................................. 243 Anti-hypertensives .................................................... 111 Anti-Oxidants ............................................................ 116 Antiretroviral ............................................................. 216 anuria.......................................................... 26, 108, 221 AORTIC DISSECTION ..................................... 131, 136 Aortic stenosis .......................................................... 138 Aortic Stenosis.......................................................... 119 AORTOGRAPHY...................................................... 137 APGAR ................................................................. 35, 36 ARDS.................................................. 71, 124, 148, 202 ARF .............................................................. 82, 95, 105 Argyle-Robinson ......................................................... 33 Arrhythmia ................................ 121, 125, 138, 148, 207 Arrhythmias ...................................... 120, 124, 239, 240 Arterial Blood Gas Diagnostic Worksheet .................. 81 Arterio-venous malformation .................................... 148 Arthrocentesis............................................................. 54 ASA ............................ 62, 113, 114, 116, 135, 239, 241 asbestos ........................................................... 195, 196 Ascites .............................................. 193, 196, 203, 205 Aspergillus ........................................................ 148, 149 Aspirin............................................... 113, 114, 116, 211 asthma.... 26, 28, 35, 117, 138, 146, 147, 148, 200, 233 asthmatics .................................................................. 11 atenolol ..................................................... 113, 117, 138 Atenolol..................................................... 113, 114, 203 Ativan ................................................................ 203, 208 AtivanВ® ..................................................................... 203 ATN........................................................................... 108 atrial fibrillation .......... 101, 121, 122, 206, 231, 233, 236 Atrial Fibrillation .................................................. 18, 211 Atrial Flutter................................................................. 18 Atrial natriuretic factor ............................................... 107 Atrioventricular (AV) Heart Block during Anesthesia .. 22 Atropine............................... 13, 14, 18, 22, 23, 112, 243 AtroventВ® .......................................................... 146, 147 AuriculinВ® ......................................................... 107, 109 autoimmune ................................ 62, 135, 212, 231, 233 AVM .................................................................. 148, 207 azotemia ................................... 105, 107, 108, 110, 111 Azotemia ........................................................... 109, 234 AZT ................................................... 214, 215, 216, 217 Babinski .............................................................. 39, 222 balloon pump ............................................................ 121 BartterвЂ™s....................................................................... 62 belladonna .................................................................. 51 Benzodiazepine ........................................................ 208 Benzodiazepines....................................... 203, 208, 243 Beta Blocker................................................................ 18 Beta-Blockers................................................ 14, 22, 117 Bicarbonate................................................... 75, 78, 243 Bicarbonate Gap ................................................... 75, 78 Bicitra .................................................................. 35, 106 BLEEDING DISORDERS ......................................... 236 Bleomycin ................................................................. 197 BLOOD ............................................................... 52, 237 blood pressure ... 26, 112, 113, 117, 118, 121, 130, 131, 137, 198, 200, 222, 239 BLOOD TRANSFUSION COMPLICATIONS-........... 237 Blood Tube Type......................................................... 53 blue bloaters ............................................................. 146 BODY FLUIDS ............................................................ 52 bradyarrhythmia ........................................................ 141 Breasts............................................................ 26, 28, 29 Bretylium ..................................................................... 13 Brevibloc ........................................................... 117, 140 Bronchiectasis........................................................... 148 Bronchodilators ................................................. 144, 146 Bronchogenic Ca ...................................................... 149 bruises ...................................................................... 236 bumetanide ....................................................... 121, 122 Bumetanide......................................................... 99, 122 bypass surgery.......................................................... 121 CAD .................. 111, 112, 113, 114, 115, 116, 121, 240 CAGE........................................................................ 201 Calcitonin .................................................................... 98 Calcium ...... 14, 22, 23, 98, 99, 104, 105, 106, 110, 113, 114, 121, 139, 228, 230, 243 Calcium Antagonists ........................................... 14, 114 calcium channel blockers.................. 107, 131, 138, 236 Calculated Na Deficit ................................................ 103 Calorics ....................................................................... 33 captopril ............................................................ 114, 120 CAPTOPRIL.............................................................. 130 Carbamazepine......................................... 208, 209, 210 carbon monoxide .............................. 186, 212, 243, 245 Carbon monoxide...................................................... 245 CARBON MONOXIDE .............................................. 245 Carcinoid........................................................... 148, 149 Carcinoma......................................... 103, 105, 148, 232 Cardiac. 13, 14, 18, 28, 29, 56, 101, 112, 116, 117, 118, 119, 121, 124, 125, 129, 135, 138, 139, 140, 148, 207, 233, 238, 246 Cardiac Arrest ....................................................... 13, 14 Cardiac Dysrhythmias................................................. 18 303 cardiac output .. 106, 107, 117, 118, 121, 124, 129, 146, 212 cardiac tamponade ............................................. 51, 140 CARDIAC TAMPONADE.................................... 13, 135 Cardiogenic Shock ................................................... 124 cardiomyopathy ... 30, 31, 114, 119, 121, 122, 123, 138, 140, 202 Cardiomyopathy ................................. 31, 124, 127, 216 Cardiomyoplasty....................................................... 121 Cardiovascular...................... 28, 97, 116, 140, 221, 239 Cardioversion ....................................................... 18, 22 Carotid ................................................................ 22, 138 Carvedilol.................................................................. 120 Central Line Placement ............................................ 254 CENTRAL LINES ....................................................... 49 CENTRAL PONTINE MYELINOLYSIS..................... 204 Central retinal artery occlusion ................................. 206 Central retinal vein occlusion ................................... 206 Cerebellar ..................................................... 30, 39, 201 CEREBELLAR DEGENERATION ............................ 204 Chest Radiograph..................................... 111, 147, 149 Chest radiography .................................................... 149 chest x-ray .......................................... 49, 137, 167, 223 CHF ... 31, 105, 107, 117, 118, 119, 120, 121, 122, 123, 124, 129, 130, 147, 150, 192, 193, 196, 212, 221, 231, 233, 240, 242 Chloramphenicol............................................... 212, 213 Chlordiazepoxide...................................................... 203 Chloride responsive.................................................... 62 Chloride unresponsive................................................ 62 cholesterol ........................ 105, 108, 114, 115, 116, 202 Cholesterol ....................................... 112, 114, 195, 196 cholesterol embolization ........................................... 108 Chronic Bronchitis .................................................... 146 CHRONIC RENAL FAILURE.................................... 109 Chyliform Effusions................................................... 195 Chylous Effusions..................................................... 195 Cigarette ........................................................... 145, 245 CIGUATERA............................................................. 246 Ciguatera fish poisoning ........................................... 246 Cirrhosis ................................... 124, 193, 196, 201, 203 cisplatin............................................................. 101, 107 CLASSIFICATIONS OF DISSECTIONS .................. 136 Clonazepam ..................................................... 208, 209 Clonidine........................................... 130, 132, 139, 203 CLONIDINE .............................................................. 130 CMV INFECTION ..................................................... 238 CO poisoning............................................................ 245 Coagulopathy ........................................................... 221 cocaine ............................................. 130, 131, 202, 243 Cocaine .............................................................. 28, 115 COHb.......................................................... 81, 245, 246 collagen vascular disease ................................ 106, 236 Coma .................................................................. 38, 221 COMA................................................................. 33, 212 Confusion ......................................................... 201, 221 CONGESTIVE HEART FAILURE............................. 118 Contraindications to Thrombolysis ........................... 118 CONVERSIONS Equations ...................................... 104 COPD 31, 108, 114, 142, 143, 145, 146, 147, 184, 185, 204, 239 Cor pulmonale .......................................................... 146 coronary artery disease ... 112, 113, 114, 115, 139, 200, 212 Coronary Artery Disease .................................. 111, 116 cosyntropin ............................................................... 234 cough..... 26, 28, 32, 141, 145, 146, 150, 167, 193, 195, 237, 239 coumadin .................................................... 11, 113, 241 CPR .............................................................. 13, 14, 118 Cranial Nerves ................................................ 28, 30, 39 Creatine Kinase ........................................................ 116 creatinine clearance.................................................. 110 CREATININE CLEARANCE ..................................... 104 CRF................................................................... 109, 110 Cryptococcus ............................................ 149, 224, 234 CSF ANALYSIS ........................................................ 211 CT ...... 42, 110, 131, 135, 137, 141, 149, 200, 204, 210, 211, 223, 232 CVP............................... 49, 56, 126, 127, 192, 228, 257 CXR ........................ 33, 42, 50, 149, 151, 193, 240, 255 cyanide...................................................... 129, 212, 243 cyclosporin ........................................................ 101, 107 Cyclosporin ....................................................... 107, 108 Cytomegalovirus ............................................... 223, 234 DDAVP.............................................................. 110, 111 DDI............................................................................ 215 decubitus ulcers .......................................................... 34 Defibrillate ................................................................... 13 Defibrillation .......................................................... 18, 22 DELAYED HEMOLYTIC REACTIONS ..................... 237 delirium ............................... 45, 107, 202, 220, 233, 243 Delirium Tremens...................................................... 202 DELIRIUM TREMENS .............................................. 204 Delta Gap.............................................................. 75, 78 Depakote........................................................... 208, 209 Dermatomes ......................................................... 40, 41 Desipramine.............................................................. 203 Dexamethasone........................................................ 233 Dextran ..................................................................... 242 diabetes ..... 26, 108, 109, 110, 114, 115, 138, 212, 230, 234, 247 Diabetes...................... 28, 109, 112, 113, 115, 221, 242 DIABETIC KETOACIDOSIS ..................................... 227 diabetics............ 107, 111, 114, 116, 119, 121, 224, 230 dialysis ................ 99, 107, 110, 111, 136, 192, 241, 243 Dialysis...................................... 107, 109, 110, 193, 222 Diarrhea .................................................................... 234 Diastolic Dysfunction......................................... 119, 123 DIASTOLIC HEART FAILURE (DHF)....................... 122 Diazepam.................................................. 208, 209, 243 DIAZOXIDE............................................................... 130 DIC............................ 108, 151, 212, 221, 225, 237, 241 DIFFERENTIAL DIAGNOSES OF PULMONARY ABNORMALITIES ................................................ 148 DIFFERENTIAL DIAGNOSIS DKA HNKC................ 227 Digibind ....................................................................... 23 Digitalis ................................... 18, 22, 23, 120, 121, 243 Digoxin .................................................. 18, 23, 122, 243 Dilantin .............................................. 204, 208, 209, 210 Dipstick ....................................................................... 54 Ditropan ...................................................................... 51 Diuretic................................................................ 97, 106 diuretics 97, 98, 101, 103, 107, 109, 120, 121, 122, 123, 130, 131 Diuretics ...... 62, 107, 110, 120, 121, 122, 129, 139, 147 DKA............................................. 62, 103, 227, 228, 229 DNR ................................................................ 11, 12, 43 Dobutamine............................................... 112, 113, 121 Dopamine............................................ 21, 107, 108, 109 Doxycycline............................................................... 197 DRAIN......................................................................... 50 DRESSLER'S SYNDROME...................................... 135 DRUG OVERDOSE .............................................. 13, 14 DTs ........................................................... 202, 203, 220 Dyspnea........................................ 11, 28, 148, 150, 193 EC-ASA..................................................................... 113 ECG ..... 98, 99, 101, 111, 112, 113, 114, 136, 140, 204, 233 echocardiogram ........................................................ 112 304 Eclampsia ......................................... 124, 132, 134, 207 ECLAMPSIA ............................................................. 131 EKG ........ 12, 42, 97, 129, 137, 139, 151, 230, 239, 243 elderly 45, 116, 120, 140, 197, 199, 204, 228, 231, 232, 237, 249 Elderly................................. 45, 104, 145, 205, 206, 221 ELECTROPHYSIOLOGIC STUDY.......................... 139 Emboli....................................................................... 150 Emphysema.............................................................. 146 Enalapril............................................................ 120, 121 ENALAPRILAT ......................................................... 129 Encephalopathy................................ 201, 203, 205, 208 Endocarditis.............................................. 150, 241, 243 Endocrine ............................................................. 26, 28 ENDOSCOPIC THERAPY ....................................... 201 Endotracheal Tube Placement ................................. 255 Epinephrine .......................................... 13, 14, 201, 247 equation............................................................ 185, 186 ergometry ................................................................. 112 Erythropoietin ................................................... 110, 111 Esmolol....................................................... 22, 117, 140 Esophageal Pressure ............................................... 191 Esophagitis ............................................................... 201 Estrogen ........................................................... 116, 150 ethanol........................................ 54, 202, 205, 212, 243 Ethanol ....................................................... 63, 202, 243 Ethosuximide .................................................... 208, 209 ethylene glycol.......................................... 107, 111, 243 Etidronate ................................................................... 97 ETOH...................... 36, 37, 81, 120, 201, 202, 203, 221 ETOH Withdrawal..................................................... 202 ETT............................................... 34, 36, 112, 113, 114 euvolemic ................................................................. 102 Evidence Based.......................................................... 47 Evidence Based Medicine Lectures ......................... 258 Evisceration ................................................................ 53 exacerbations ........................................................... 146 Exercise.............................. 28, 112, 113, 116, 117, 140 EXUDATES .............................................................. 194 EYE SIGNS ................................................................ 33 family .......... 11, 25, 26, 37, 44, 226, 236, 243, 247, 250 Family History..................................................... 26, 115 fax................................................................... 11, 24, 25 FEBRILE TRANSFUSION REACTIONS.................. 238 Femoral lines .............................................................. 50 FEna ......................................................................... 107 FETAL ALCOHOL SYNDROME .............................. 204 FEV1 ......................................... 143, 145, 146, 147, 240 fever..... 11, 26, 28, 34, 35, 36, 108, 130, 135, 138, 151, 153, 166, 167, 195, 199, 204, 219, 220, 221, 222, 223, 225, 237, 238, 249 Fever ................................ 110, 194, 198, 207, 221, 249 FEVER.............................................. 219, 220, 221, 225 Fick Method .............................................................. 125 Fine Needle Aspiration ..................................... 231, 232 Fish Oil ..................................................................... 116 Fluids & Electrolytes ................................................... 55 Flumazenil ................................................................ 243 Folate................................................................ 201, 203 Folate Deficiency ...................................................... 201 FOLEY........................................................................ 51 Folic acid .......................................................... 115, 203 fractional excretion of sodium........................... 108, 186 Friderichsen-Waterhouse syndrome ........................ 233 fungal.......................... 53, 108, 135, 148, 216, 224, 233 FUO .......................................................................... 220 furosemide.......... 97, 100, 109, 110, 121, 122, 231, 237 Furosemide........................................... 97, 99, 109, 122 Gabapentin ............................................................... 209 galactorrhea.............................................................. 233 Gallium nitrate............................................................. 98 Gambierdiscus toxicus.............................................. 246 GASTRIC LAVAGE.................................................. 200 Gastric Ulcers ........................................................... 201 Gastritis..................................................................... 201 Gastrointestinal ............................................. 28, 97, 201 GASTROINTESTINAL BLEEDING........................... 199 Genitalia................................................................ 27, 30 Genitourinary .............................................................. 28 GFR .................................................. 104, 106, 109, 110 GI bleeding.................................................. 52, 199, 200 Glasgow Coma Scale ................................................. 38 glaucoma .................................................................. 206 Glomerulonephritis.................................... 106, 109, 193 Glomerulosclerosis ................................................... 106 Glucagon............................................................. 22, 244 glucocorticoids .................................. 105, 106, 147, 231 Glucocorticoids ................................................. 146, 147 Glycohemoglobin ...................................................... 230 Goodpasture's................................................... 148, 220 Gout .......................................................................... 249 Gram Stain.......................................................... 54, 211 grand mal .................................................................. 208 Graves ...................................................................... 231 Guidelines For Fluid Challenges............................... 257 gynecomastia.............................................. 28, 199, 233 Haemophilus influenza.............................................. 146 Hashimoto's ...................................................... 231, 232 HbA1c ....................................................................... 230 HDL................................................................... 115, 116 heart block ................................................ 104, 125, 141 Heart Failure ......................... 18, 30, 120, 148, 196, 221 HEART SOUNDS ....................................................... 31 Heart Transplant ....................................................... 121 heart transplants ....................................................... 111 HEAT STROKE......................................................... 221 Hematopoietic System ................................................ 28 Hemochromatosis ............................................. 119, 233 Hemodialysis............................... 99, 110, 111, 136, 243 hemodynamic................................ 18, 52, 113, 135, 152 Hemodynamic ............................................................. 55 Hemodynamic Examples .......................................... 127 Hemoglobin A1c........................................................ 230 Hemolysis ................................................................... 98 hemolytic................... 108, 116, 220, 225, 237, 238, 247 Hemolytic transfusion reactions ................................ 237 Hemophilia ................................................................ 236 Hemoptysis ............................................... 148, 195, 255 hemothorax ................................................................. 50 Henderson Hasselbalch equation ............................. 186 Henoch-SchГ¶nlein Purpura....................................... 106 Heparin ............. 113, 114, 150, 151, 152, 223, 234, 235 Hepatitis .................................................... 194, 201, 238 hepatomegaly ................................................... 203, 233 Hirudin............................................................... 113, 114 Hirulog............................................................... 113, 114 Histoplasmosis.................................................. 148, 233 history 11, 12, 24, 25, 26, 27, 28, 34, 35, 36, 37, 43, 44, 101, 102, 107, 112, 113, 116, 139, 198, 200, 203, 206, 212, 222, 223, 236, 238, 241, 247 HISTORY ................................................ 24, 25, 27, 236 HIV ........ 36, 52, 106, 213, 214, 215, 218, 219, 220, 223 Homocysteine ........................................................... 115 hydralazine........................ 120, 129, 130, 131, 135, 241 Hydralazine ....... 106, 120, 121, 122, 129, 131, 132, 138 HYDRALAZINE......................................................... 129 hydrocortisone .................................................... 98, 234 hydrothorax ................................................................. 50 hypercalcemia......................................... 96, 97, 98, 234 Hypercalcemia ............................................................ 97 305 HYPERCALCEMIA............................................... 96, 97 Hypercapnia ............................................................... 22 Hypercholesterolemia............................................... 115 Hyperhomocystinemia .............................................. 115 hyperkalemia ........................................ 98, 99, 101, 107 Hyperkalemia.............................. 98, 105, 107, 111, 234 HYPERKALEMIA............................................ 13, 14, 99 hypermagnesemia ............................................ 104, 110 Hypernatremia .......................................................... 100 HYPERNATREMIA..................................................... 99 hyperparathyroidism ....................... 62, 96, 97, 110, 212 Hyperphosphatemia ................................................. 110 hyperpigmentation ............................................ 234, 247 Hypersensitivity Pneumonitis.................................... 148 hypertension ...... 24, 26, 28, 30, 97, 106, 108, 114, 118, 121, 122, 124, 129, 130, 131, 136, 138, 139, 140, 146, 147, 200, 203, 206, 212, 222, 228 Hypertension ... 105, 106, 109, 110, 111, 112, 115, 119, 136 HYPERTENSIVE CRISIS AND SPECIFIC DRUG THERAPY ............................................................ 130 hyperthyroidism .......................... 97, 212, 220, 231, 233 Hyperthyroidism................................................ 221, 231 hypertrophic pulmonary osteoarthropathy ................ 195 Hyperuricemia .................................................. 106, 110 hypervolemic ............................................................ 102 Hypoalbuminemia..................................................... 193 hypocalcemia............................................ 101, 109, 229 Hypocalcemia ........................................................... 207 Hypoglycemia ........................................................... 207 hypokalemia ..................................................... 101, 240 HYPOKALEMIA.................................................. 14, 101 hypomagnesemia ..................................................... 101 Hypomagnesemia..................................................... 101 hyponatremia.................................................... 102, 234 Hyponatremia ................................................... 207, 234 HYPONATREMIA............................................. 102, 103 hypoparathyroidism ............................................ 97, 234 HYPOPHOSPHATEMIA........................................... 103 Hypotension. 22, 50, 108, 119, 129, 137, 208, 221, 229, 246 HYPOTHERMIA ................................................... 13, 14 Hypothyroidism........................................... 23, 103, 231 HYPOVOLEMIA ......................................................... 13 hypovolemic.............................................................. 102 hypoxemia ................................ 108, 146, 186, 240, 245 Hypoxemia.......................................................... 22, 146 Hypoxia..................................... 23, 62, 81, 87, 146, 148 HYPOXIA...................................................... 13, 14, 212 ICU ................................. 13, 33, 52, 101, 121, 199, 202 IgA nephropathy ....................................................... 106 IIb/IIIa........................................................................ 113 IJ lines ........................................................................ 50 Imipramine................................................................ 114 Infected catheter......................................................... 49 Infectious Disease .................................................... 212 Infectious Diseases .................................................... 27 Inotropic............................................................ 120, 121 Intensive Care .......................................................... 122 Intern ............................................................................ 1 Internal Jugular................................................... 50, 124 Intoxication ........................................................... 22, 23 INTRACEREBRAL HEMORRHAGE ........................ 131 INTRINSIC RENAL DISEASE .................................. 107 ipecac ....................................................................... 244 Ipratropium ....................................................... 146, 147 ischemic..... 31, 108, 114, 117, 121, 122, 123, 131, 135, 137, 199, 207, 245 ISCHEMIC STROKE ................................................ 131 ISOLATED BLEEDING TIME ELEVATION.............. 236 ISOLATED PT PROLONGATION............................. 236 ISOLATED PTT ELEVATION ................................... 236 Isoprenaline .......................................................... 18, 22 isopropanol ............................................................... 243 IsordilВ®...................................................... 113, 114, 120 Isosorbide Dinitrate ................................................... 114 Jervell-Lange-Nielsen syndrome .............................. 140 joint sepsis ................................................................ 249 Kaposi's sarcoma...................................................... 234 Kayexalate .................................................................. 99 KCl ...................................................................... 42, 101 ketoacidosis ................................................ 63, 228, 243 Ketoconazole ............................................................ 234 Klonopin ............................................................ 208, 209 Korsakoff's ........................................................ 202, 204 LAB ............................................... 11, 63, 151, 233, 244 labetalol............................. 111, 129, 130, 131, 138, 241 Labetalol ................................................... 106, 129, 131 LABETALOL ............................................................. 129 Labor and Delivery...................................................... 35 LAEDP ...................................................................... 124 Lamifiban .................................................................. 115 LAWS OF HOSPITAL PRACTICE.............................. 11 LEFT VENTRICULAR FAILURE............................. 131 Left Sided Failure...................................................... 119 left ventricular end diastolic volume.......................... 118 Left Ventricular Hypertrophy ..................................... 115 Legionella.................................................. 135, 148, 216 LibriumВ®.................................................................... 203 Lidocaine................................................. 13, 22, 23, 207 Lindane ..................................................................... 247 Lipid .................................................................. 115, 195 lithium.................................... 62, 97, 212, 222, 231, 243 lorazepam ......................................................... 204, 208 Lorazepam ................................................ 203, 204, 208 low molecular weight heparin.................................... 113 Low urine output ......................................................... 51 LOWN Classification ................................................... 23 Lugol's....................................................................... 233 Lugol's solution ......................................................... 233 Lumbar Puncture ........................................................ 53 LUMBAR PUNCTURE .............................................. 211 Lung Cancer ............................................................. 148 Lung Cavitation ......................................................... 148 Lupus ........................................................ 106, 197, 236 lupus anticoagulant ................................................... 236 LV dysfunction .................................................. 119, 121 LVEDP .............................................................. 124, 125 LVEDV ...................................................................... 118 LVH ................................................... 115, 119, 122, 240 Lymphangioleiomyomatosis...................................... 149 lymphoma ... 98, 136, 149, 194, 215, 216, 220, 221, 236 Lymphoma ................................ 103, 148, 193, 196, 197 magnesium ....... 101, 103, 104, 110, 123, 131, 139, 212 Magnesium ................... 22, 23, 101, 104, 121, 132, 203 MAGNESIUM TOXICITY .......................................... 103 MAGNETIC RESONANCE IMAGING....................... 137 malignancy.................. 96, 107, 135, 195, 216, 220, 232 MALIGNANT ............................................. 135, 192, 222 malignant hyperthemia.............................................. 219 Malignant Hyperthermia............................................ 221 Mallory-Weiss ........................................................... 200 mannitol .................................................................... 107 MARCHIAFAVA-BIGNAMI DISEASE ....................... 204 Marfan's .................................................................... 136 Massive Hemoptysis ................................................. 255 maximal voluntary ventilation.................................... 240 MB isozyme .............................................................. 116 Mechanical Ventilation ........................................ 95, 147 Medications. 25, 27, 35, 36, 43, 105, 109, 111, 207, 236 306 MENINGITIS............................. 215, 223, 224, 225, 226 meningococcemia............................................. 225, 233 Mental Status Exam ............................................. 37, 38 Meperidine................................................................ 207 Mesothelioma ........................................... 193, 195, 196 Metabolic Acidosis........................................ 62, 81, 221 Metabolic Alkalosis ............................................... 62, 81 methanol................................................................... 243 metoprolol................................................. 117, 120, 138 Metoprolol................................................. 113, 114, 117 Metronidazole ........................................................... 212 Milk alkali .................................................................... 97 Milrinone ................................................................... 120 MINI-MENTAL STATUS EXAM.................................. 32 MINOXIDIL ............................................................... 130 Mithramycin ................................................................ 97 Mitral Regurgitation .................................. 119, 124, 148 mitral stenosis................................................... 123, 212 Mitral Stenosis .......................................................... 148 Mnemonic ................................................... 63, 122, 202 Modified Child's Index for Grading Severity of Liver Dz ............................................................................. 205 MODS................................................................. 84, 124 moniliasis.................................................................. 234 Moraxella catarrhalis ................................................ 146 Morbidity ........................................................... 151, 239 Morphine........................................................... 113, 122 Mortality .................................................... 120, 121, 239 MRI ....... 33, 42, 131, 135, 137, 204, 210, 223, 232, 234 mucolytic................................................................... 146 Mucomyst ................................................................. 244 MucomystВ®............................................................... 147 Multinodular Goiter ................................................... 231 Multiorgan Dysfunction Syndrome.............................. 84 Multiple Sclerosis ..................................................... 207 MURMERS ................................................................. 31 mushrooms............................................................... 243 MVV.......................................................................... 240 myalgias ........................................................... 246, 249 myasthenia gravis..................................................... 234 Mycobacterium ................................................. 166, 234 Mycoplasma ............................................. 148, 216, 220 myeloma ....................................................... 97, 98, 108 Myeloma ..................................................................... 96 Myocardial depression................................................ 22 myocardial infarction... 24, 114, 136, 137, 139, 140, 220 Myocardial Infarction ........................................ 115, 117 MYOCARDIAL INFARCTION ............................. 13, 131 MYOCARDIAL ISCHEMIA ....................................... 111 Myxedema ........................................................ 193, 194 myxoma ............................................................ 138, 140 Na+ ..................................... 99, 100, 105, 109, 227, 228 N-acetyl cysteine ...................................................... 147 Naloxone .................................................................. 243 NASOGASTRIC TUBE............................................... 52 Nebulizers................................................................. 147 NEEDLE STICKS ....................................................... 52 neoplasia .................................................................. 103 nephrotic........................................... 107, 108, 109, 150 Nephrotic Syndrome......................... 105, 148, 192, 193 Nervous System ................................................. 28, 202 neurocardiogenic .............................................. 139, 140 Neurocardiogenic ............................................. 140, 141 neuroleptic malignant syndrome............................. 222 Neuroleptic Malignant Syndrome ............................. 221 Neurologic .................................................. 30, 140, 201 Neurological.................................................... 26, 27, 37 NEUROLOGICAL EXAM............................................ 38 NIFEDEDPINE ......................................................... 130 nifedipine .......................... 106, 113, 118, 121, 130, 138 Nifedipine .................................................. 114, 122, 130 nitrates ...................................................... 112, 113, 122 Nitrates.............................. 113, 114, 121, 122, 123, 139 Nitroglycerin ...................................... 114, 122, 130, 132 NITROGLYCERIN .................................................... 130 Nitroglycerine .................................................... 130, 131 Nitroprusside..................... 122, 129, 130, 131, 138, 223 NITROPRUSSIDE .................................................... 129 NMS .................................................................. 222, 223 Nocardia.................................................................... 148 Non-steroidal anti-inflammatory drugs .............. 105, 108 Normal ABG Ranges .................................................. 67 Normal Gap Acidosis .................................................. 62 Normal Lab Values ..................................................... 58 Normal Ranges for Ventilatory Values...................... 191 Norwegian scabies.................................................... 247 nose bleeds............................................................... 236 NSAIDS. 45, 98, 105, 106, 107, 108, 110, 135, 236, 241 nuchal rigidity .................................................... 225, 243 Nucleoside analogs................................................... 216 nystagmus............................... 26, 33, 39, 201, 208, 209 Obesity...................................................................... 115 occupational........................................................ 25, 250 Oliguria........................................................ 51, 104, 108 OLIGURIA................................................................. 107 Oncotic Pressure .............................................. 192, 193 Operative ............................................................ 34, 238 opium .......................................................................... 51 optic neuritis.............................................................. 206 Optic Neuritis ............................................................ 206 Optokinetic Reflex....................................................... 33 Oral Contraceptives .................................................. 115 Orders ................................................................... 42, 43 ORTHOSTATIC HYPOTENSION ............................. 138 osmolar gap .............................................................. 243 OUTPATIENT ............................................................. 11 overdose ........................................... 107, 111, 131, 208 Oxazepam................................................................. 203 oxybutynin................................................................... 51 Oxygen..... 29, 56, 69, 70, 120, 122, 127, 145, 146, 147, 184, 185, 200, 243 Oxygen Dosing ........................................................... 70 oxygen saturation.............................................. 190, 245 Oxygen Transport System .......................................... 69 Oxyhemoglobin ........................................................... 68 PA Catheter .............................................................. 124 Pacemaker.................................................... 18, 22, 141 PaCO2 .............. 56, 62, 63, 81, 151, 185, 186, 188, 189 Pain..................................... 45, 111, 114, 148, 193, 198 palmar creases ......................................................... 234 Pamidronate................................................................ 97 Pancreatic carcinoma ............................................... 201 Pancreatitis124, 194, 197, 198, 201, 205, 208, 216, 227 Paracentesis ............................................................... 53 Past Medical History ............................................. 25, 27 Pathophysiology of MI............................................... 116 PCWP .... 24, 55, 56, 118, 124, 125, 126, 127, 129, 130, 255, 257 pericarditis......................... 119, 123, 127, 135, 225, 240 Pericarditis ................................ 105, 107, 127, 135, 193 PERICARDITIS......................................................... 135 Peritonitis .................................................................. 198 Permethrin ................................................................ 247 pernicious.......................................................... 220, 234 PFT ................................................................... 146, 149 Phenobarbital............................................ 208, 209, 210 Phenothiazine ................................................... 139, 222 PHENTOLAMINE...................................................... 129 Phenytoin .................................................... 23, 208, 209 Phosphate................................. 105, 106, 111, 229, 230 307 PHYSICAL...................................... 25, 29, 31, 198, 199 Physical Examination ................................................. 26 physostigmine........................................................... 243 Physostigmine .......................................................... 243 pink puffer................................................................. 146 plaques ..................................................................... 112 platelet ........ 63, 111, 113, 115, 200, 208, 235, 236, 241 pleural effusion ........................................... 50, 137, 151 Pleural Effusions............................................... 192, 197 Pleurodesis............................................................... 197 Pleuroscopy...................................... 194, 195, 196, 197 Plicamycin .................................................................. 98 PMH................................................................ 24, 25, 36 Pneumocystis ........................................................... 148 Pneumonia ................................. 28, 103, 148, 213, 238 pneumothorax............................................. 50, 196, 197 poisoning .......................... 111, 129, 222, 243, 245, 246 POISONING ............................................. 243, 245, 246 Polycythemia ............................................................ 146 Polymorphic VT ........................................................ 123 Postrenal azotemia................................................... 109 POSTRENAL AZOTEMIA ........................................ 107 potassium ...... 62, 98, 99, 101, 106, 107, 110, 111, 139, 200, 246 Potassium............................................... 22, 23, 99, 110 Prazosin.................................................................... 120 Prednisone ......................................................... 97, 107 Preexcitation-Syndrome ............................................. 22 Pregnancy ............................................ 28, 62, 118, 209 PREGNANCY............................................................. 36 preload.............. 118, 119, 120, 121, 122, 123, 131, 151 Preload ..................................................... 118, 122, 123 Prerenal azotemia .................................................... 109 Pre-renal azotemia ........................................... 105, 108 PRERENAL AZOTEMIA........................................... 107 Pressure Ulcers ........................................................ 249 Presyncope............................................................... 207 Prinzmetal's .............................................................. 112 Pro-Banthine............................................................... 51 Procainamide...................................................... 22, 135 Prognosis.................................. 114, 117, 147, 205, 295 prolonged QT............................................................ 140 Prolonged QT-Interval ................................................ 22 Propafenone ......................................................... 18, 22 propantheline.............................................................. 51 Propranolol ................................. 22, 117, 131, 138, 233 propylthiouracil ................................................. 231, 233 prosthetic heart valves...................................... 212, 236 protease.................................................................... 145 Protease inhibitors.................................................... 217 protein intake ............................................................ 110 Proteinuria ........................................................ 110, 221 pruritus................................................ 27, 246, 247, 248 Pseudochylous ......................................................... 195 Pseudoephedrine ..................................................... 146 Pseudogout .............................................................. 249 Pseudohyperkalemia .................................................. 98 Psych.......................................................................... 37 Psychiatric .................................................... 26, 28, 140 psychiatry ................................................................... 12 PTH .................................................................... 96, 110 Pulmonary ..... 56, 62, 66, 103, 120, 122, 123, 124, 125, 126, 137, 138, 141, 146, 148, 149, 153, 167, 185, 193, 194, 197, 221, 238, 239, 253 pulmonary artery catheter......................................... 136 PULMONARY ARTERY CATHETERIZATION......... 123 pulmonary capillary wedge pressure ................ 118, 129 pulmonary edema.... 107, 111, 119, 121, 124, 137, 147, 237, 243 PULMONARY EMBOLI ............................................ 150 pulmonary embolism. 107, 124, 140, 184, 233, 236, 242 Pulmonary Embolism ........................ 124, 148, 193, 197 PULMONARY EMBOLISM ......................................... 13 Pulmonary Embolus.................................................. 148 Pulmonary Function Testing ..................................... 149 Pulmonary infarction ................................................. 148 Pulmonary vascular resistance ................................. 146 Pulse Oximetry............................................................ 64 Pulseless Electrical Activity ........................................ 13 Pulseless VT ............................................................... 13 PULSES...................................................................... 31 PUPILS ....................................................................... 33 PVR............................................. 56, 125, 126, 130, 146 pyrexia ...................................................................... 219 Pyridoxine ................................................................. 243 Quinidine......................................................... 18, 22, 23 RANSON'S CRITERIA.............................................. 205 Rate Pressure product .............................................. 112 Reflexes ................................................................ 36, 39 Renal biopsy ............................................................. 110 Renal Failure..................................................... 207, 221 Renovascular ............................................................ 108 ReoProВ® ................................................................... 113 Respiratory Acidosis ............................................. 62, 81 Respiratory Alkalosis ............................................ 62, 81 Respiratory System..................................................... 28 Retinal detachment ................................................... 206 Review of Systems ............................................... 26, 27 Rhabdomyolysis.......................................... 98, 108, 221 Rheumatoid............................................... 148, 149, 197 Rhogam ...................................................................... 35 Right Sided Failure ................................................... 119 Rinne Test................................................................... 29 Risk .. 112, 113, 115, 116, 121, 124, 129, 142, 209, 211, 212, 221, 238, 239, 240, 250, 297 risk factors................................... 27, 111, 112, 115, 221 Romano-Ward syndrome.......................................... 140 salicylates ................................................. 212, 231, 243 Sarcoid........................................ 96, 149, 192, 223, 224 sarcoidosis ................................ 135, 148, 220, 224, 233 Sarcoidosis ......................................... 97, 119, 148, 194 Sarcoptes var. hominis ............................................. 247 Scabies ..................................................................... 247 SCABIES .................................................................. 247 Scoring for Acute Lung Injury and Acute Respiratory Distress Syndrome ................................................. 71 Seizure...................................................................... 208 Seizures .................... 201, 202, 207, 208, 209, 221, 243 SEIZURES ................................................ 204, 207, 243 sensory reversal dysesthesia.................................... 246 Sepsis ....................................................... 108, 124, 212 Septic Shock ............................................................. 124 SeraxВ® ...................................................................... 203 serum osmolality ............................................... 186, 243 Shunt Equation ......................................................... 191 Shy-Drager........................................................ 138, 141 SIADH ....................................................................... 103 SIGN-OUT Note.......................................................... 43 Signs ............... 26, 30, 42, 107, 108, 119, 151, 193, 221 SIGNS OF OBVIOUS BREATHING (WOB) ............. 185 Silent Ischemia.......................................................... 111 Silicosis ..................................................................... 148 Sinus Bradycardia................................................. 18, 23 sinus tachycardia ...................................................... 233 Sinus Tachycardia ........................................ 18, 23, 151 SIRS............................................................................ 83 SLE ........................... 107, 135, 148, 150, 194, 220, 224 smoke ......................................................... 38, 145, 245 Smokers.................................................................... 145 smoking............. 26, 28, 36, 37, 115, 146, 239, 240, 246 308 Smoking.................................................................... 115 SOAP.......................................................................... 33 Social History.............................................................. 26 Sodium iodide........................................................... 233 Solu-MedrolВ®.................................................... 146, 147 sputum.................................. 26, 28, 145, 146, 166, 167 Sputum Cytology ...................................................... 149 Гџ-blockers......................................... 113, 114, 121, 231 Гџ-Blockers ................................ 113, 114, 121, 122, 203 Гџ-carotene ........................................................ 113, 116 ST depressions................................................. 112, 114 ST segment ...................................................... 111, 112 Starling Curve........................................................... 118 Starling Equation ...................................................... 192 Status Epilepticus ..................................................... 210 Steroids .............................................. 98, 147, 233, 247 Streptococcus pneumoniae .............................. 146, 226 Streptokinase............................................ 117, 118, 152 stroke. 31, 111, 115, 116, 118, 130, 131, 136, 138, 146, 150, 207, 212, 219, 221, 222, 224, 228 Stroke ....... 103, 116, 126, 211, 212, 221, 222, 227, 238 SUBARACHNOID HEMORRHAGE ......................... 131 Subclavian .................................................. 50, 124, 193 Suicide........................................................................ 12 Sulfinpyrazone.......................................................... 114 Supplemental Oxygen for COPD.............................. 145 supraventricular ................................ 101, 139, 140, 233 Supraventricular (SV) Tachycardia............................. 22 Supraventricular Extrasystole..................................... 18 surgery24, 34, 51, 52, 53, 107, 109, 112, 118, 121, 135, 136, 137, 138, 150, 152, 198, 200, 201, 224, 227, 234, 236, 238, 239, 241, 242, 249 Surgery Prophylaxis ................................................. 241 SVT........................................................................... 240 SWAN GANZ.............................................................. 24 Swan Ganz Catheter Wave Forms........................... 128 Swan-Ganz....................................................... 125, 228 Symptoms.... 27, 37, 101, 103, 104, 108, 111, 116, 119, 145, 148, 193, 203, 209, 221, 231 syncope ........................ 26, 28, 139, 140, 141, 212, 245 SYNCOPE ........................................ 138, 139, 140, 141 Syndrome X...................................................... 112, 114 systemic embolism ................................................... 236 Systemic Inflammatory Response Syndrome............. 83 Systolic Dysfunction ......................................... 119, 121 T4 214, 231, 232, 233 tachypnea .. 50, 105, 122, 136, 145, 146, 150, 185, 222, 245 Tamponade ........................................ 31, 124, 135, 136 TB 12, 28, 135, 149, 166, 167, 192, 194, 196, 211, 215, 216, 220, 223, 224, 233 TEE........................................................................... 137 Tegretol ............................................................ 208, 209 TEN RULES FOR READING CHEST X-RAYS ........ 167 TENSION PNEUMOTHORAX.................................... 13 thallium ..................................................... 112, 116, 117 THE LECTURER ........................................................ 12 theophylline ................ 11, 111, 140, 141, 208, 240, 243 Theophylline ..................................................... 146, 147 Therapy of Systolic Failure ....................................... 120 thiamin ...................................................................... 201 thiamine .................................... 121, 201, 203, 204, 212 Thiamine........................................... 201, 202, 203, 243 thiazide ............................................................... 97, 103 thoracentesis .............................................. 50, 194, 197 Thoracentesis ............................................. 53, 194, 197 Thromboembolism Prophylaxis in Surgical Procedures ............................................................................. 241 THROMBOLYSIS ..................................................... 152 thrombolytic .............................................. 113, 137, 152 Thrombolytic ............................................................. 117 Thyroid .......................................... 28, 29, 231, 232, 233 THYROID DISEASE ................................................. 231 thyroiditis........................................................... 231, 234 THYROTOXIC CRISIS ............................................. 233 thyrotoxicosis .............................................. 97, 212, 234 TIA .................................................................... 212, 241 ticarcillin .................................................................... 101 TiclidВ® ....................................................................... 113 ticlopidine .................................................................. 113 Ticlopidine................................................. 113, 114, 115 TILT TABLE TESTING.............................................. 139 Tobacco .................................................................... 113 Torsades Des Pointes............................................... 123 tPA ............................................................................ 118 Transderm-Scop ....................................................... 140 TRANSESOPHAGEAL ECHOCARDIOGRAPHY..... 137 Transfusion ................................................................. 27 TRANSFUSION ASSOCIATED ADULT RESPIRATORY DISTRESS SYNDROME ........... 237 TRANSUDATES ....................................................... 193 Travel .......................................................................... 36 Treadmill ................................................................... 112 Trendelenburg............................................... 49, 50, 130 Tricyclic ............................................................. 114, 243 TRIMETHAPHAN CAMSYLATE............................... 130 TSH................................................................... 231, 233 Tuberculosis........................ 12, 103, 148, 166, 197, 223 Tuberculous .............................................................. 135 Tubular Necrosis....................................................... 106 tubulointerstitial ......................................................... 109 Tumor lysis syndrome................................................. 98 Ultrasound................................... 13, 105, 110, 112, 232 universal precautions .................................................. 52 Uremia .......... 62, 63, 105, 107, 108, 111, 192, 194, 212 Uremic Syndrome ..................................................... 110 Urinalysis ...................................................... 54, 63, 110 URTICARIAL REACTIONS....................................... 237 Use Rumack-Matthew Nomogram For Acetaminophen Overdose.............................................................. 244 Valium ....................................................... 203, 208, 209 309 Valproic Acid............................................................. 208 Valsalva ................................................................ 22, 31 Valvular............................................................. 239, 240 Vascular Disease................................................ 30, 109 vasculitis ........................................... 107, 212, 220, 225 Vasospasm............................................... 112, 113, 114 Vasotec............................................................. 129, 241 venous thrombosis ................................................... 236 ventilators ................................................................. 103 VentolinВ® .................................................................. 146 Ventricular Dysrhythmia ............................................. 22 ventricular fibrillation................................................. 101 ventricular tachycardia.............................. 101, 139, 140 Verapamil ............................... 18, 22, 23, 114, 122, 138 Vertigo .............................................................. 207, 221 vesnarinone .............................................................. 121 Vesnarinone ............................................................. 120 VF ....................................................................... 13, 120 VIOLENT PATIENTS................................................ 204 Vitamin.. 96, 97, 110, 111, 113, 114, 116, 201, 209, 212 vitamin D....................................... 97, 98, 106, 109, 110 Vitamin D .................................................... 96, 110, 111 vitamin K........................................... 200, 209, 236, 244 Von Willebrand's....................................................... 236 warfarin............................................. 114, 208, 236, 242 Water depletion ........................................................ 100 Weber Test ................................................................. 29 Wegener's ........................................................ 148, 220 Wernicke's ................................ 141, 201, 202, 204, 212 WERNICKE'S ENCEPHALOPAHTY AND KORSAKOFF'S PSYCHOSIS .............................. 204 women ..... 111, 112, 115, 116, 202, 218, 231, 232, 248, 249 Worksheet for Using an Article About Therapy or Prevention............................................................ 276 Worksheet for Using an Article About Assessing Diagnostic Tests .................................................. 293 WOUND COMPLICATIONS....................................... 53 WPW ............................................................ 22, 23, 139 x 147, 244