Top 10 Pitfalls of Emergency Medicine
Tony Johnson, DVM, DACVECC
Veterinary Information Network (VIN)
Email: [email protected]
3 Rivers Conference 2016
The aim of this monograph is to highlight ten (fairly random) aspects of emergency veterinary
medicine that I find to be particularly vexing.
NUMBER TEN: Rectal exam There are only 2 reasons NOT to do a rectal exam – NO rectum
and NO finger. Evaluation of stool consistency and color (many GI bleeds have been
discovered this way), palpation of the prostate and sublumbar lymph nodes are just a few of the
physical findings that can be found on rectal exam.
NUMBER NINE: Urinalysis and urine culture In order to adequately assess renal function –
you need a U/A. Remember – the usual chemistry panel is an insensitive indicator of renal
function; 3/4 of nephrons have to be no-functional before the renal values elevate.
Urine cultures also deserve mention. They should be part of the diagnostic workup for
unexplained fever, any case of acute renal failure (or acute-on-chronic), and all cases of diabetic
ketoacidosis. I try and save a sample for culture any time I submit a UA. Additionally, all CRF
patients should be cultured routinely every 6 months – many will have a low-grade
pyelonephritis or UTI that can escape detection on a routine UA due to the dilutional effects of
their PU/PD state.
NUMBER EIGHT: Endotracheal and transtracheal wash Patients with thoracic pathology
(such as suspected neoplasia or infectious conditions like fungal disease or pneumonia) may
benefit (at least diagnostically) from this procedure. Simply done and available to the general
practitioner, this does not require referral. The notes below are used with permission from Dr.
Garrett Pachtinger of the University of Pennsylvania.
Endotracheal wash is best for small dogs or cats.
Transtracheal washes can be done in medium to large sized dogs.
May be falsely negative if antibiotic therapy has already begun
Do not attempt in patients with severe respiratory compromise
Approximate injection volume of sterile saline:
Cat:
2-3 ml per attempt
Small Dog: 2-4 ml per attempt
Large Dog: 4-6 ml per attempt
Approach - Endotracheal wash:
Prior to anesthesia, check to ensure all equipment is accessible
Prepare the sterile syringes - After the saline, draw up another 3-5 ml of air into the
syringe to help
flush in the saline.
Anesthetize and sterilely intubate the patient.
Once intubated, insert the suction catheter down the ET tube until it cannot pass any
further.
Flush the saline followed by air down the tube
Have your assistant gently coupage the chest, while applying suction to the catheter.
Immediately after obtaining a sufficient sample for submission, attach the patient to the
anesthesia machine to supply oxygen to the patient.
If you need to repeat the saline flush and aspiration, ideally this should be performed
prior to connection of the ET tube to the anesthesia machine to prevent contamination.
Submit the sample for cytology and aerobic culture, +/- mycoplasma and fungal.
Approach - Transtracheal wash:
Clip and scrub the ventral neck
Elevate the head and palpate between two rings of cartilage, 3-4 rings below the larynx
Locally block this area with lidocaine.
With the bevel down insert the needle of the sampling catheter into the skin
Advance perpendicular to the trachea into the tracheal lumen between to cartilage rings
on the midline of the trachea, feeling a “pop” as you enter the tracheal lumen.
Raise needle slightly to advance catheter another 2-3 mm towards the lower airways.
Advance the sampling catheter completely into the tracheal lumen.
Once inserted, pull the needle back out of the skin and place needle guard on the needle
to reduce risk of tracheal laceration, or cutting the sampling catheter which is located in the
trachea.
Inject sterile saline followed by air.
Coupage the chest and aspirate back on the syringe.
Repeat as needed.
Submit sample for cytology and aerobic culture, +/- fungal and mycoplasma.
NUMBER SEVEN: Pneumothorax Pneumothorax is typically evident through elevation of the
cardiac silhouette off of the sternum on the lateral projection, retraction of lung lobes from the
thoracic wall and blunting of the costophrenic angles.
Thoracocentesis should be performed bilaterally, generally above the level of the costochondral
junction, and anywhere from the 6-10th intercostal space (ICS). Because of the presence of the
neurovascular bundle caudal to the ribs, the needle should be introduced cranial to the rib. For
smaller patients, an 18-21 ga butterfly catheter connected to a stopcock and a 20cc syringe may
be sufficient. Larger patients may require a 1 ½ “ needle attached to an extension set. Tapping
the chest does not generally require sedation or local anesthetic. Any fluid obtained should be
saved for analysis (PCV/TP, cytology, culture).
Management of pneumothorax (PTX) can either be very simple or very complex. Some patients
with PTX can be managed with a single thoracocentesis, while others will need a thoracostomy
tube placed. Decision-making in regards to PTX depends on the number of times the chest must
be tapped, the volume of air (or fluid) removed and patient stability. In general, if the chest must
be tapped more than 3 times in a 24-hour period, a chest tube is indicated. Ideally, chest tubes
are placed under general anesthesia and under controlled conditions, but thoracostomy tubes are
rarely placed as an elective procedure. Most chest tubes are placed with a combination of
chemical and physical restraint and local anesthesia. Chest tube diameter should be roughly
equivalent to the diameter of a mainstem bronchus. Chest tubes should enter the thoracic cavity
at the level of the 8th ICS and exit the skin at the level of the 10th ICS. This subcutaneous tunnel
can be formed by having an assistant pull the skin on the lateral thorax cranially before tube
insertion. A routine prep and draping of the lateral thorax is performed and sterile gloves are
worn. A small stab incision is made in the skin and the chest tube (with trocar) is grasped 2-3
cm from the tip to keep it from advancing too far into the chest. A sharp blow is delivered to the
end of the chest tube to place it into the thoracic cavity and the skin is released to form the
tunnel. Alternatively, the trocar can be removed and the tube tip can be grasped with a pair of
Carmalts and bluntly dissected through the chest wall until it is in the thoracic cavity. The tube
is then clamped and connected to either a suction apparatus (if continuous suction is needed) or
an appropriate stopper is fashioned and the tube is secured to the skin. A Chinese-finger-trap
pattern or tape butterflies can be used.
NUMBER SIX: Pericardial effusion This condition is often misdiagnosed as cardiomegaly
on thoracic films. Prompt thoracocentesis can make a dramatic impact on a patient’s status.
This condition is one that needs to be considered in any geriatric, large-breed dog with a history
of collapse, lethargy and weakness. Mucous membranes may be pale, and PCV/TP is often in
the normal range. This constellation of clinical signs, while by no means pathognomonic, should
prompt an evaluation of the pericardial space. A good discussion of the topic can be found in the
proceedings from this conference in 2009: Diagnosis and Treatment of Pericardial Effusion,
Western Veterinary Conference 2009; L. Ari Jutkowitz, VMD, DACVECC; Matthew W. Beal,
DVM, DACVECC Michigan State University, East Lansing, MI.
Patients with known or suspected pericardial effusion should not be administered furosemide as
this can cause a disastrous drop in blood pressure and perfusion. Prompt pericardiocentesis,
through the cardiac notch on the right side of the chest at the 4th-6th intercostal space, in concert
with IV fluid therapy is the initial therapy of choice. Patients should have continuous EKG
monitoring and evaluation for recurrence of fluid buildup post-pericardiocentesis. Thorough
diagnostic workup would include CBC/chemistry panel and urinalysis, as well as coagulation
assays and abdominal and thoracic imaging.
In addition to the clinical signs outlined above, patient may exhibit jugular venous distension,
pulsus paradoxus (diminishing of the palpable pulse on inspiration) or electrical alternans
(alternating large and small QRS complexes on EKG), although these findings are variably
present and somewhat unreliable. Echocardiography is the diagnostic test of choice, and fluid
analysis of the effusion has little diagnostic value unless in-house evaluation demonstrates a
suppurative effusion or visible infectious agents; the effusion should be then submitted for
bacteriologic analysis. Coagulation status of patients should be assessed before
pericardiocentesis. In many cases, the effusion is due to an aggressive malignancy such as atrial
hemangiosarcoma and the prognosis is poor if this can be confirmed as the cause. Other
measures that may be indicated include pericardiectomy and/or right atrial appendage removal.
NUMBER FIVE: Anticoagulant Rodenticide Anticoagulant rodenticide (hereafter
abbreviated AR) toxicity can present in any number of ways, depending on the site of bleeding.
Additionally, many pets will present after ingestion but not be showing clinical signs. It is
important in these cases to ascertain whether exposure could have occurred in the past, or if this
is the first possibility of exposure. Additionally, the owners may not be aware (or may not be
forthcoming) of a pet’s possibility for exposure. It is important NOT to rule out AR intoxication
because an owner claims that they do not know of any exposure. Patients may show no clinical
signs for several days after ingestion, as it takes time for clotting factors to be used up. ARs
inactivate vitamin K1 epoxide reductase, which recycles inactive, vitamin K-dependent clotting
factors (II, VII, IX and X) to the active form.
Patients who have ingested an AR within the prior 1-2 hours, but have no clinical signs should
undergo general decontamination. If there is a possibility of prior exposure, coagulation assays
should be run, preferably in-house if available. If there is no possibility of prior exposure and
PT/PTT are within normal range the patient may be treated as an outpatient with 2.5mg/kg
vitamin K1 PO q12h for 4 weeks after decontamination and activated charcoal administration.
The PT and PTT should be assessed 2-3 days after starting therapy to make sure the dose is
sufficient and 2-3 days after cessation of therapy to ensure that they were treated for long
enough. Elevated PT/PTT should prompt either a dose increase or extension of the vitamin K.
Patients showing clinical signs of bleeding can have extremely variable clinical signs depending
on the site of hemorrhage. Management may include the administration of blood products (such
as FFP for replacement of clotting factors, or fresh whole blood or PRBC if there has been
significant blood loss), oxygen therapy and other supportive measures. Fluid therapy may be
needed in cases of hemorrhage until blood can be obtained, and crystalloid resuscitation should
be titrated to a systolic BP of 90mmHg to prevent exacerbation of further bleeding.
Thoracocentesis should only be performed in cases where there is confirmed pleural space
bleeding, and only if there is significant respiratory compromise. If there is documented thoracic
cavity bleeding, but the patient is not dyspneic, they should be closely monitored and treated
aggressively with plasma and vitamin K. Plasma doses needed for AR intoxication are in the
range of 10-30ml/kg, and are usually rounded to the nearest plasma unit size. Very small
patients needing plasma should have the unit thawed normally, and the initial dose drawn from
the unit and administered over 4 hours. The remainder of the unit should be refrigerated and
used within 24 hours. Vitamin K1 should not be given IV due to the risk of severe anaphlaxis. If
possible, it should be given PO with a meal as it has superior absorption by this route, and Sq
absorption may be diminished in hypovolemic or hypotensive patients.
NUMBER FOUR: Spontaneous hemoabdomen Management of patients presenting with
spontaneous (non-traumatic) hemoabdomen present a management challenge. There are many
ways to stabilize and diagnose their condition, and also assess the extent of their disease; I
present only one way of looking at this condition here. While a diagnosis of neoplasia should
never be made without histopathological confirmation, studies show that roughly 60 to 75% of
dogs presenting with spontaneous hemoabdomen have neoplastic conditions, and the vast
majority of these are hemangiosarcomas which carry a poor prognosis (roughly 3 months with
surgery alone, 6 months or more with chemotherapy). Counseling of owners is therefore of vital
importance when dealing with these cases. (The odds of a neoplastic condition are approximately
50% if a mass is found in the spleen and it is not associated with hemorrhage).
Fluids used for resuscitation of these patients should be carefully titrated, and every effort should
be made to keep systolic blood pressure at levels that are sufficient to provide organ perfusion
but that will not disrupt forming clots and potentiate hemorrhage. I will try and tailor fluid
resuscitation with low volumes of crystalloids and colloids to keep BP near 90mmHg and not
above if this is possible; avoid blousing large volumes of fluids without checking BP
periodically. Administration of whole blood, if available, should be considered for patients who
are going to surgery on an emergency basis. An acceptable alternative is FFP and PRBCs if
whole blood is not available. While controversial, an abdominal counterpressure wrap can help
slow bleeding and aid in the stabilization of patients perioperatively, but this can decrease vital
organ perfusion. Unfortunately, the decision on when to go to surgery on these patients is often
clouded by the availability of a willing surgeon, the status of the patient, available post-operative
facilities and the degree of pre-operative workup performed by the clinician (or desired by the
owners). Ideally, thoracic films, coagulation assays, CBC/chemistry panel/urinalysis and
possibly abdominal ultrasound should be considered before surgery, depending on availability
and patient status. Additionally, the ideal surgical candidate should have improved
hemodynamics prior to surgery, but this may not be achievable in actively bleeding patients.
Some patients can be stabilized to allow time to gather the surgical staff and further stabilize the
patient (as well as perform a more thorough diagnostic assessment) while others must go to
surgery under less-than ideal conditions, or with a partial workup. If at all possible, different
scenarios should be discussed pre-operatively with owners so rapid decision-making can be
facilitated based on intraoperative findings. Owners should also be counseled about common
post-operative complications such as cardiac arrhythmias that may prolong the hospital stay.
In patients who are not in pain or dyspneic, hospice care at home is a humane option for those
owners who do not wish to go to surgery but are not prepared to euthanize when the diagnosis is
made.
NUMBER THREE: Blood pressure Adequate organ perfusion occurs when blood pressure is
at or near 60mmHg mean arterial pressure. This typically correlates to a systolic BP of
90mmHg. The three elements of arterial blood pressure are systolic arterial pressure (SAP),
diastolic arterial pressure (DAP) and mean arterial pressure (MAP). Systolic arterial pressure is
generated by the contractions of the beating heart. Mean arterial pressure reflects the average
pressure across the vasculature during the cardiac cycle, and is therefore the main determinant of
organ perfusion. Diastolic pressure is the lowest pressure in the arteries during cardiac filling or
diastole. MAP can be approximated from measured values for SAP and DAP by the following:
SAP - DAP
MAP = ------------------------- + DAP
3
Blood Pressure Homeostasis Several mechanisms work in concert in the normal animal to
maintain systemic arterial blood pressure within physiologic range. Both neural and endocrine
regulatory mechanisms are determinants of blood pressure, thus any condition that disrupts this
internal milieu of the animal can alter blood pressure.
Blood pressure can be expressed by the relationship of cardiac output (CO) to total peripheral
vascular resistance (TPR): BP = CO X TPR
Cardiac output, in turn, is determined by the heart rate (HR) and stroke volume (SV) in the
following way:
CO = HR X SV
All of these variables, HR, SV, and TPR are the determinants of blood pressure, and are the
physiological points of control acted on by the various neurohormonal mechanisms used to keep
blood pressure within a specified range.
Hypertension is a common entity in the emergency room and ICU; many patients are
hypertensive due to their primary disease, and many (perhaps many more) are hypertensive due
to fear, pain or anxiety. My approach to mild to moderate systolic hypertension (in the range of
120mmHg to160mmhg) in patients without pathology referable to the hypertension alone
(typically acute renal failure, retinal detachment or seizures) is to look for an underlying cause
such as pain or anxiety and correct it with analgesia or sedation. Patients with symptomatic
hypertension, however, warrant prompt therapy. In cases of severe hypertension (systolic BP
>200 with repeated measurement) or hypertension causing clinical signs, therapy (typically with
IV nitroprusside) can be instituted to control BP. This requires ICU-level care and rigorous BP
monitoring.
Most cases of mild to moderate hypertension without clinical signs will resolve without direct
antihypertensive therapy. Cases where hypertension persists and the patient can tolerate oral
meds usually receive a calcium channel blocker (such as amlodipine), a beta adrenergic blocker
(such as atenolol) or an ACE inhibitor such as enalapril. Therapy for hypertension should be
undertaken based on known or suspected causes for it, therefore hard and fast rules for therapy
are problematic.
Hypotension is discussed below, but systolic BP should be kept above 90mmHg to minimize the
deleterious effects of hypotension.
NUMBER TWO: Analgesia Many patients suffer in silence, and therapy for pain is
problematic. In my experience, many clinicians are afraid of the ‘dysphoric’ effects of opioids in
cats, and this is rarely a problem. I also feel that butorphanol is an inadequate analgesic for
anything but mild pain – it is overused for severe pain as can be seen with traumatic injuries. For
mild pain, I prefer low-dose hydromorphone or buprenorphine, and for moderate to severe pain I
believe a full mu-agonist is indicated. A fentanyl continuous-rate infusion (CRI) of 1-5 ug/kg/hr
is an effective and adaptable way of controlling pain, and can be adjusted to compensate for
changes in pain level and sedation. Some cats on opiods (particularly transdermal fentanyl) will
develop a fever, although the mechanism for this phenomenon is unexplained. Transdermal
fentanyl patches are a popular way of providing pain relief in cats, but I feel that their effect is
too unreliable to be a viable option for actual pain. Some patients are oversedated, many are
undermedicated, and I feel that they lull the clinician into feeling like they are doing ‘something’
for pain, while in fact they are not. They may be helpful for leveling out the ‘peaks and valleys’
of intermittent opioid administration, but should not be counted on for complete analgesia.
Sublingual (not oral) administration of buprenorphine (at doses similar to IV or IM use) is a
reasonably effective means of providing analgesia to outpatients.
NUMBER ONE: Fluid therapy Both as a resuscitative measure and for rehydrating
hospitalized patients, fluid therapy is one area I struggle with daily. It seems like no other
therapeutic intervention is so fraught with the possibility of either under doing it or overdoing it
– both with potentially disastrous consequences. I will present my approach to fluid therapy – but
there are many schools of thought much controversy regarding this topic. It seems like the
temptation exists to just set the pump at ‘two times maintenance’ and call it a day. The actual
fluid plan should be calculated out based on an evaluation of the patient and changed to match
the changing status of the patient.
For resuscitation of hypotensive or hypovolemic patients, a stepwise approach is usually best
(crystalloids >> colloids >> pressors). Provision of external rewarming is vital to restoration of
normotension for cats, and will help avoid fluid overload.
Crystalloids are traditionally the first line of therapy for treating traumatic shock. The ‘shock
dose’ of crystalloids for cats is roughly 60ml/kg and 90ml/kg for dogs, which corresponds to one
blood volume. This dose should not be delivered all at once, but rather divided into 15-20ml/kg
aliquots and perfusion assessed after each dose. Improvement in mucous membrane color,
mental status, body temperature, extremity warmth, urine output and blood pressure (>90mmHg
systolic) are indicators that fluid therapy is achieving its goal. One should not rely on one
physiological variable alone, but rather an overall assessment of the patient’s status. Resolution
of metabolic acidosis, improved central venous oxygen saturation (>70%) and resolution of
hyperlactatemia are also good markers for adequacy of resuscitation. To avoid fluid overload in a
hypothermic patient, I will generally try and limit feline crystalloid boluses to 50-75ml at a time,
and administer additional boluses in response to continued hypotension.
If I have reached 50-75% of the calculated crystalloid shock dose without improvement, I will
generally administer a colloid bolus. Colloid ‘shock dose’ is 20ml/kg, but, as with crystalloids, I
divide this in to aliquots of 5 ml/kg and administer over 5-10 minutes. If I have administered a
full crystalloid and colloid bolus, rewarmed the patient, ruled out occult hemorrhage and cardiac
disease, pressor therapy is indicated. Ideally, monitoring central venous pressure (CVP) would
help guide therapy and avoid over- or under-resuscitation. Patients who are hypotensive with a
low CVP (<0 cm H2O) should be fluid loaded with either crystalloids or colloids (regardless of
the dose already administered) until the CVP is in the 0-5 range. Pressors should not be
administered to patients who are not fluid replete as ischemia will result. Dopamine (2-20
ug/kg/min), phenylephrine (1-3 ug/kg/min), norepinephrine (0.05-0.3 mcg/kg/min) epinephrine
(1 mL of 1:1000 epinephrine per 100 mLs of 0.9% NaCl, titrate drip-rate to effect) or
vasopressin (CRI dose not established) can be used. Higher doses of catecholamines (such as
epinephrine, phenylephrine, norepinephrine) can cause arrythmias and seizures at the higher end
of the dose range in cats.
For true hemorrhagic shock (which is more uncommon than traumatic or distributive shock),
replacement of lost volume with type-specific blood products and correction of the cause of
hemorrhage is indicated.
For cardiogenic shock, minimal to no fluid therapy is indicated. Rather, diuretic, venodilator
(nitroprusside or nitroglycerine) and/or pressor (dobutamine) therapy should be considered. For
many cats with hypertrophic cardiomyopathy, in which systolic function is usually normal to
supranormal, the development of cardiogenic shock is an indicator of catastrophic myocardial
failure and typically cannot be reversed.
Fluid therapy for rehydration in hospitalized patients is a different beast altogether. Once
hypotension has been addressed (or in dehydrated patients that present without hypotension) a
maintenance fluid therapy plan must be devised. A three part plan has served me well, and helps
to match the fluid therapy prescription to the patients needs.
Correction of estimated dehydration deficit is the first part and is usually accomplished with
isotonic crystalloids and spaced over 6-48 hours depending on patient factors (speed of
development, albumin level, cardiac function, etc). While a dismally inexact science, clinical
estimation of dehydration can serve as a guide for this phase of fluid therapy. Levels below 57% are generally not appreciable on examination. Patients who are between 7-10% dehydrated
generally will have poor skin turgor, and tacky mucous membranes. 10-12% dehydration will
typically show systemic signs of hypovolemia such as hypothermia, hypotension, sunken eyes,
etc. Hydration deficit greater than 12% is generally considered to have severe metabolic
consequences and may be lethal. Remember – these are very rough and inaccurate guidelines.
The volume of deficit is calculated as %estimate dehydration X body weight (in Kg). This gives
the volume to be administered over the chosen interval.
The second portion of the plan is provision of maintenance needs. Estimated daily maintenance
is 60ml/kg/day, and is provided through isotonic crystalloids. Maintenance fluids are calculated
to provide hydration to replace fluids lost through sensible (mostly urinary ~30-40ml/kg/day)
losses and insensible (metabolic and respiratory ~20ml/kg/day) losses. Again, much debate
exists over the actual numbers for maintenance, and this value should be used as a rough
guideline.
The third part of the fluid therapy prescription is provision of fluids to replace ongoing losses. In
my experience, this part is often overlooked. Losses exceeding the normal metabolic demands
(as outlined above – urinary and insensible) fall into this category. Polyuric patients (diabetes
mellitus or insipidus, renal disease, etc), body cavity effusions (especially through chest tubes
and abdominal drains), extensive burns or very exudative skin lesions, GI losses or hyperthermia
call all cause losses exceeding those calculated for maintenance fluid requirements alone. For
some of these conditions, volumes can be measured and replaced 1 to 1 with crystalloids – for
example thoracostomy tubes or excessive urinary losses. For others, such as vomiting, the
volume lost can be estimated and replaced. Monitoring patient weight can also be helpful in
guiding administration of fluids to correct deficits from ongoing losses.
Updated January 22, 2015