Regional Anesthesia www……………………………. → www.nerveblocks.net → www.miller.sps.co.uk → www.manbit.com Regional Anesthesia - definition !!!! no loss of consciousness No pain=analgesia No motor response=muscles relaxation No reflexes 1/ surgery-orthopedics, obstetrics, vascular surgery, urology 2/ acute pain - postoperative analgesia, acute pancreatitis, intermittent claudication, trauma 3/ chronic pain History • cocaine, an extract of the coca leaf (=Erythroxylon coca bush) , was the first effective local anesthetic • had been known for centuries in Peru, where folk surgeons performing trepanations of the skull chewed coca leaves and allowed their saliva to fall onto the surfaces of the wound (both the operator and his patient shared the effects of the same drug) • in 1884, Koller reported the first use of a local anesthetic - cocaine for ophthalmologic surgery. Local anesthetics • inhibit reversibly impulse conduction along the nerve fibres by blocking sodium channels. • block the generation and propagation of impulses in spinal cord, spinal nerve roots, and peripheral nerves • with progressive increases in concentrations of local anesthetics, the transmission of: 1/ autonomic 2/ somatic sensory and 3/ somatic motor impulses is interrupted, producing: 1/ autonomic nervous system blockade 2/ sensory anesthesia and 3/ skeletal muscle paralysis in the area innervated by the affected nerve. Neural cell wall with sodium channel Strategies to find nerves include: • looking for the landmarks • seeking a paresthesia (recall the old saying, "No paresthesia, no anesthesia") or • using an "electric nerve stimulator." Electric nerve stimulator This is a device that gives a short pulse of electrical current and is attached to a needle. Electrical impulses reaching a nerve are transmitted along the nerve fibres. If the nerve contains • motor fibres, the electrical current will induce contraction at the effector muscle. • sensory fibres they cause parasthesia in the distribution of the nerve. Local anesthetics • aminoesters and the aminoamides • lidocaine (Xylocaine) intermediate acting (water soluble jell and a 4% solution, as a 5% solution with dextrose for spinal administration, and for injection as 1% and 2% solutions) • bupivacaine (Marcaine) long acting local anesthetic (as 0.5% solution) • mepivacaine • ropivacaine Aminoamide local anesthetics are primarily cleared from the bloodstream by metabolism in the liver. Local anesthetic toxicity intravascular injection or systemic absorption → systemic effects • allergic reactions – very rare • neurotoxicity • cardiotoxicity The cardiovascular system (CVS) is generally more resistant to local anesthetic toxicity than is the CNS Neurotoxicity NEUROTOXICITY OF LIGNOCAINE-SYMPTOMS: • Lightheadness • Tongue Numbness, metallic taste in the mouth • Visual disturbances • Generalised twitching • Convulsions • Profound Coma • Respiratory Arrest • CVS Depression The important thing about this list is to notice that cardiovascular depression occurs only at very high blood concentrations. Thus, if the other symptoms occur, ask the patient to hyperventilate, provide oxygen and prepare to secure the airway and treat a seizure. Mechanisms : → initially inhibition of inhibitory pathways→convulsions → later inhibition both inhibitory and facilitatory pathways→generalized state of CNS depression Neurotoxicity • general relationship between anesthetic potency and CNS toxicity Convulsions have been reported at venous blood levels of approximately: • 2 to 4 ng/ml of bupivacaine, dose limits is 2 mg/Kg plain and 3 mg/Kg with epinephrine (150 mg) • 10 ng/ml of lidocaine, dose limits 5 mg/Kg of plain solution or 7 mg/Kg if the solution contains epinephrine (200mg, 500mg with epinephrine) Cardiovascular System Toxicity • Lidocaine – agent used for treating ventricular arrhythmias Mechanisms : • unidirectional block and a reentrant type of cardiac arrhythmia • decreased myocardial contractility • vasodilation CHARACTERISTICS OF LOCAL ANESTHETIC TOXICITY • (I) CNS toxicity: a) Excitation Phase: tinnitus, confusion, restlesness, perioral numbness or tingling, metallic taste, lightheadness, sense of dread and impending doom. b) Convulsive Phase: grand-mal clonic-tonic seizure c) Depression Phase: CNS depression with drowsiness and unconsciousness. d) Repiratory depression and apnea. • (II) CVS Toxicity: a) Excitation Phase: - hypertension, tachycardia (with convulsions) b) Depression Phase: Negative inotropic effect with decreased blood pressure, cardiac output and stroke volume. Peripheral vasodilation with further hypotension. c) Cardiovascular Collapse LOCAL ANESTHETIC - FACTORS INFLUENCING SYSTEMIC ACTIVITY→Toxicity • choice of drug • dosage - relation between dosage and maximum plasma concentration is linear • addition of Epinephrine • site of injection - absorption from any site depends on the blood supply to that site. The highest concentrations occurred after intercostal block and the lowest after subcutaneous abdominal infiltration. Sites are generally ranked: intercostal>epidural>brachial plexus>spinal Addition of epinephrine to local anesthetic →vasoconstriction • commercially available solutions of local anesthetic containing epinephrine are prepared at a low pH to prevent degradation of the epinephrine • concentration of 1:200,000 • purposes: 1) prolongs the action of the local anesthetic 2) blunts systemic uptake and thereby limits systemic toxicity 3) decreases bleeding at the site of injection 4) serves as a marker of intravascular injection 5) improves the quality of spinal blockade, probably on the basis of spinal alpha receptors 1/Topical Anesthesia • local anesthetics may be applied topically-on the eye, skin, tympanic membrane, oral mucosa, tracheobronchial tree, and rectum. • to be effective topically, high concentrations of local anesthetics are required • onset of anesthesia usually occurs in 5–10 minutes when applied to mucous membranes and in 30–60 minutes when applied to the skin • systemic absorption is greater from mucous membranes-risk of toxicity if large volumes of local anesthetic are used 1/ Topical Anesthesia EMLA® cream provides an alternative for topical anesthesia • is a eutectic mixture of lidocaine and prilocaine containing approximately an 80% concentration of active base • has been particularly useful for providing topical anesthesia for venipuncture in infants and children • onset of anesthesia after application requires at least 1 hour • absorption is relatively low • maximum depth of anesthesia that can be achieved is approximately 5 mm 2/ Infiltration Techniques Local anesthetic is given: • Subcutaneously, intracutaneously, intramuscularly • Intravenously =Bier’s block Intravenous Block =Bier’s block • Needle is inserted into a distal vein in the extremity. • Wide rubber band is tightly wrapped starting distally and working proximally to remove blood from the superficial veins of limb. • Pneumatic cuff is inflated to prevent venous outflow from the extremity. • 50 to 60 ml of lidocaine 0.5% is injected through the distal IV. • The cuff may remain inflated for up to two hours (ischemic pain limits the time) • At the end cuff is re-inflated over several minutes 3/ Central Blockades • The target of the local anesthetic molecules in central blokade are the neural pathways traversing the spinal column. • Spinal cord is protected by the cushion of CSF that is enclosed with the dura sac. 3/ Central Blockades • Local anethetics injected within dura sac (into CSF) penetrate the nerve fibres rapidly and provide the rapid spinal anesthesia. • Local anesthetics injected outside the dura mater produce the slower onset of epidural blockade. • Approaches: paramedian and lateral • Subarachnoid space contains CSF • Epidural space surrounds the dura sac and contains fat, air and veins Needle Tip Designs Features of note are: 1. The presence of a cutting tip on the Quincke type needle. 2. The dimensions of the terminal hole. - A large hole contributes to a rapid flashback. - A long hole increases the possibility of injecting part of the intended sub-arachnoid dose into the epidural space. 3. The original pencil point needle (HART) is illustrated. > Spinal block • The local anesthetic is injected into the cerebral spinal fluid (CSF). • As the nerves are unprotected here, a very small amount of anesthetic will cause the rapid onset of the block. • The local anestetic may be hyperbaric, hypobaric or isobaric relative to CSF. • By having a different baricity from CSF the anesthetic solution spread and the extent of the block may be controlled by positioning the patient. Spinal block • In 3% of the population the cord ends at L1 or above. • In 94% of the population the cord ends at L1 or L2. • In 3% of the poulation the cord ends at L3. Spinal block -paramedian approach • The needle passes through : 1/ skin 2/ superspinous ligaments 3/ interspinous ligaments 4/ ligamentum flavum 5/ dura sac Lateral position for performance of spinal anesthesia • Lateral positionknee down up toward the chest and head flexed down toward the knee Sitting approach for spinal anesthesia • Sitting position-feet supported on the stool and the shoulders hunched forward to increase flection of the spine. Spinal block Extent of spinal block depends on: • Baricity of solution (density) • Position of patient (except isobaric solutions) • Dose and volume of the drug • Level of injection • Speed of injection Spinal block LEVEL OF SPINAL ANESTHESIA REQUIRED FOR COMMON SURGICAL PROCEDURES T4–5 (nipple) T6–8 (xiphoid) pelvic surgery upper abdominal surgery gynecologic pelvic surgery,ureter, renal and T10 (umbilicus) transurethral resection, obstetric vaginal delivery, and hip surgery L1 (inguinal ligament) transurethral resection, if no bladder distension; thigh surgery; lower limb amputations L2–3 (knee and below) foot surgery S2–5 (perineal) perineal surgery, hemorrhoidectomy Spinal block-complications • Hypotension • Bradycardia-thoracic sympathetic segments (T1-5) are blocked Sympathetic blockade above the level of the cardiac accelerator fibres (T1 - T4) will cause a bradycardia • Total spinal block • Neurological complications-damage of the nerves, hematomas, infections. • Post dural puncture headache (PDPHA) is related to low CSF pressure due to leak of the fluid from the puncture hole in the dura sac with the spinal needle. A very powerful diagnostic feature of the headache is its positional nature. It is worse when the patient is sitting or standing and better when the patient is lying flat. PDPHA is treated with recumbency, hydration, caffeine, or more aggressively with an epidural blood patch of the leaking dural hole. Cardiovascular changes with epidural anesthesia Spinal block-complications • Hypotension • Bradycardia-thoracic sympathetic segments (T1-5) are blocked Sympathetic blockade above the level of the cardiac accelerator fibres (T1 - T4) will cause a bradycardia • Total spinal block • Neurological complications-damage of the nerves, hematomas, infections. • Post dural puncture headache (PDPHA) is related to low CSF pressure due to leak of the fluid from the puncture hole in the dura sac with the spinal needle. A very powerful diagnostic feature of the headache is its positional nature. It is worse when the patient is sitting or standing and better when the patient is lying flat. PDPHA is treated with recumbency, hydration, caffeine, or more aggressively with an epidural blood patch of the leaking dural hole. Epidural block • A needle for the epidural space takes a similar path to a spinal needle, but is stopped before the dura. • If the needle is advanced too far, the dura will be punctured and CSF will pour out when the syringe is removed. Epidural block • Single shot technique • Loss of resistance technique-ligamentum flavum gives the strong resistance to compression of the syringe barrel. As the epidural needle passes through the ligamentum flavum a sudden loss of resistance occurs • Hanging drop technique Epidural block Catheter Techniquecontinuous technique Epidural block • Epidural anesthesia requires about ten times the dose of local anesthetic to achieve a block as compared to a spinal. This raises the potential for systemic toxicity. • The blocks set up more slowly than spinal blocks, but is good for controlling blood pressure with fluid resuscitation. • Postoperative continuous epidural analgesia. • Epidurals are a frequent method of labor analgesia for pregnant women because they produce good analgesia • Testing dose • Abdominal and thoracic block Epidural block-complications • inadvertent dural puncture and total spinal blockade • total epidural blockade • epidural venous injection • local anesthetic toxicity • gaps • neurological complications -damage of the nerves, hematomas, infections, direct trauma to the spinal cord. • backache 1/ Sympathetic block 2/ Sensory block ( cold sensation, pain, touch) 3/ Motor block Assessing the quality of a block Methods of measurement of motor blockade The Bromage Scoring Method • 0: No motor block: full flexion of knee and foot. • 1: Inability to raise extended le. Just able to move knee. • 2: Inability to flex knee. Able to move foot only. • 3: Inability to flex ankle joint. Unable to move foot or knee. Assessing the quality of a block Methods of assessing the sensory level of the block • The sensory level may be determined by mapping out the distribution of loss of appreciation of pain to pinprick, cold sensation with ice and paraesthesiae to soft touch Assessing the quality of a block The assessment of sympathetic blockade (cardiovascular effects) • sympathetic blockade below the level of the cardiac accelerator fibres (T1 - T4) causes venodilatation→hypotension • sympathetic blockade above the level of the cardiac accelerator fibres (T1 - T4) will cause a bradycardia and hypotention 4/ Blockades of the Peripheral Nerves • Brachial plexus blockade →interscalene approach=Winnie’s approach →axillary approach • Lumbar plexus blockade (femoral, obturator and lateral femoral nerves) →psoas compartment block →femoral nerve block=3 in 1=inguinal block of the lumbar plexus • Sacral plexus blockade (sciatic nerve) →proximal sciatic nerve block=transgluteal= acording to Labat Brachial plexus blockadeinterscalene approach=Winnie’s Complications: • Phrenic nerve paralysis • Horner’s Syndrome • Reccurent laryngeal nerve paralysis • Vessel puncture Brachial plexus blockade- axillary approach • Gaps • Low risk method Commonly used needles in nerve blocks Contraindications absolute contraindications: • patient’s refuse • infection at the injection site • coagulopathy whether therapeutic or part of the patient's pathology • increased ICP - absolute contraindications when epidural or spinal is considered. relative contraindications: • sepsis, hypovolemia, • neurologic disease, psychologic instability, • antiplatelet drugs, • prolonged surgery, • certain cardiac diseases (idiopathic hypertrophic subaortic stenosis, aortic stenosis), and • uncooperative patient or surgeon. Benefits of local anasthesia • Diminish a predominant part of the physiologic response to surgical procedures=stress response • Prophylaxis of thromboembolic complications • Postoperative analgesia • Vasodilatation in artheriosclerosis • Cooperative patient
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