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The following is an abstracted summary, not a verbatim transcript, of the lectures/discussions on this audio program. If, after reviewing this written summary, you would like to hear the contents and/or earn CME/CE credit: View Main Program Listing Visit Audio-Digest Home Page Anesthesiology Program Info |
Neuroanesthesia Update Educational Objectives The goal of this program is to improve neurosurgical anesthesia technique and the management of venous air embolisms (VAEs). After hearing and assimilating this program, the clinician will be better able to: 1. Determine which patients with head trauma are most likely to require ventilatory support after surgery. 2. Explain the importance of attention to patient positioning during neurosurgery. 3. Describe the effect of different anesthetic agents on intracranial pressure. 4. Identify neurosurgical patients at greatest risk of developing VAE. 5. Apply techniques to reduce the risk for VAE in patients undergoing head-elevated surgical procedures. Faculty Disclosure In adherence to ACCME Standards for Commercial Support, Audio-Digest requires all faculty and members of the planning committee to disclose relevant financial relationships within the past 12 months that might create any personal conflicts of interest. Any identified conflicts were resolved to ensure that this educational activity promotes quality in health care and not a proprietary business or commercial interest. For this program, the following has been disclosed: Dr. Gelb has received honoraria as a speaker for Abbott India and Abbott Korea, is a consultant for Eisai, and has received research funding from Hospira. Dr. Schubert and the planning committee reported nothing to disclose. Acknowledgements Dr. Gelb spoke at the California Society of Anesthesiologists Annual Meeting and Clinical Anesthesia Update, held May 15-17, 2009, in Monterey, CA, and sponsored by the California Society of Anesthesiologists. Dr. Schubert was recorded at the Comprehenive Anesthesiology Review, held March 28 to April 2, 2009, in Cleveland, OH, and sponsored by the Cleveland Clinic Anesthesiology Institute. The Audio-Digest Foundation thanks the speakers and the sponsors for their cooperation in the production of this program. Neuroanesthesia for the Very Occasional Neuroanesthesiologist Adrian W. Gelb, MB, ChB, Professor of Anesthesiology, University of California, San Francisco Diagnosis and operation: information provided on operating room schedules often scant; anesthesiologist should ask surgeon about details of surgery Common trauma scenarios: epidural hematoma — com-puted tomography (CT) or magnetic resonance imaging (MRI) may be available; smooth outline distinguishes hematoma on imaging; patients often have lucid interval after head injury, then coma; trauma tears middle meningeal artery or arterial branch, which bleeds slowly; patients become comatose when volume of blood becomes sufficient to produce compression; usually no underlying brain injury; plan anesthesia on assumption that patient starts procedure comatose, with elevated intracranial pressure (ICP), but may be “reasonably neurologically intact” and able to be extubated after procedure; acute subdural hematoma — more common; bleeding occurs beneath dura, which remains adherent to bone; blood overlies brain; almost always associated with some degree of underlying brain injury; therapeutic challenge to lower ICP; “if they come to the operating room (OR) comatose, there is a 99.9% chance they will leave the OR comatose”; plan anesthetic accordingly; chronic subdural hematoma — typical patient elderly person with recent history of fall, who experiences progressive neurologic deterioration over several days or weeks; in older people, cortical atrophy often increases intracranial space, which allows more blood to collect before significantly increasing ICP and causing symptoms; fall may rupture small veins carrying blood from dura to brain surface, without much underlying brain injury; patients do not generally require mannitol; may benefit from transient hyperventilation while surgery performed; once hematoma drained, fill as much cranial space as possible (CO2 should be normal or slightly above normal); vapor-based anesthetic may help fill space Patient position: varies more in neurosurgery than in general surgery; speaker recommends that anesthesiologist practice positions mentally and with surgical team; should know which way patient will be turned and where patient’s head will be; when patient lies prone, gravity can extend tongue from mouth, which may cause swelling and prolapse; axillary roll goes on chest wall to prevent axillary compression; always maintain control of endotracheal tube while neurosurgeon positioning patient; avoid brachial plexus injury by pushing patient’s shoulder into position before having individual at end of table apply tape; anesthesiologist should help position mandible; the more head turned away from midline or neutral position, the greater the risk for venous obstruction (warn surgeon before procedure begins); document everything Bleeding and blood loss: if surgeon estimates loss of 50 mL, plan on 500 mL; if estimate 500 mL, plan on 5 liters; will help anesthesiologist have sufficient blood available; intraparenchymal brain tumors — usually not well-vascularized; most blood loss from craniotomy; blood loss generally £250 to 400 mL; lesions that may bleed “torrentially” include large arteriovenous malformations (preoperative angiography and embolization help limit blood loss, but potential remains); meningiomas — often highly vascular meningeal tumors originating in dura; growth causes compression of brain; blood supply derived from dura, overlying bone, and below; without extreme caution by surgeon, patient may lose several liters during craniotomy and opening dura alone; if case involves meningioma, anesthesiologist should inquire about vascularity (presurgical vascular imaging recommended), anticipated blood loss, and embolization Ischemia: ask whether ischemia anticipated; also ask whether cross-clamping of carotid artery or intracranial vessels planned, and whether surgeon prefers any specific “pseudoneuroprotectant”; no human studies demonstrate cerebroprotection by any anesthetic during neurosurgery; speaker advises complying with surgeon’s choice of agent Neuromonitoring: most often used during spinal surgery; prevents central nervous system (CNS) injury and allows corrective maneuvers Most common types of neuromonitoring: electromyography (EMG) — monitors placed on relevant muscle groups; surgeon stimulates appropriate neural structures with probe and observes for twitching; requires avoidance of muscle relaxants during this part of procedure; somatosensory evoked potentials (SSEP) — surgeon stimulates peripheral nerve and monitors at selected points; nerves frequently stimulated include median or posterior tibial; common monitoring sites include C7 and over cortex; potentials small and not easily seen, but with 500 to 1000 stimulations, remainder of electroencephalography (EEG) can be filtered out and intact sensory conduction pattern discerned; motor evoked potentials (MEPs) — transcranial stimulation to test integrity of motor tracts; change earlier than SSEPs during spinal surgery; motor function most vulnerable part of spinal activity; anterior (motor) portion of cord has single blood supply; more vulnerable than posterior (sensory) portion, which has dual blood supply; no trials show any benefit of either type of evoked potential during spinal cord surgery; SSEPs sensitive to anesthetics; still inducible if volatile anesthetics limited to <0.7 minimum alveolar concentration (MAC); anesthetic-related suppression occurs at >1.0 MAC; MEPs more sensitive to anesthetics (especially volatile anesthetics) than SSEPs Anesthetic guidelines for neuromonitoring: if patient has no myelopathy, limited volatile anesthetic acceptable (£0.5 MAC), combined with opioid-propofol infusion; total intravenous anesthetic (TIVA) preferable; ketamine and etomidate can increase size of evoked potentials when necessary; desflurane and sevoflurane also good choices; avoid vapor anesthetics in patients with myelopathy (very sensitive) whenever possible; avoid muscle relaxants whenever EMG or MEPs planned (can be used with SSEPs); if using muscle relaxant with MEP, keep drug level absolutely constant; maintain communication with neuromonitoring technician regarding signals and level of anesthetic; advise of any changes; if blood pressure drops, bring it back to (or slightly above) baseline; decrease vapor if using; consider adding ketamine; keep temperature >35.5o C; severe anemia also reduces evoked potentials by decreasing oxygen delivery to muscles and nerves Intracranial pressure: ask whether elevated; also ask about lesion size Effect of anesthetics on ICP: barbiturates and propofol reduce ICP at higher concentrations; sevoflurane has neutral effect at £1.3 MAC; desflurane and isoflurane most vasoactive anesthetics (autoregulation essentially abolished at concentrations >1.0 MAC, with corresponding increases in ICP); hyperventilation — reduces ICP during neurosurgery, but evidence lacking to distinguish this from effect of opening dura (ICP becomes atmospheric); in randomized trial involving »260 patients with supratentorial tumors, hyperventilation (lowering Paco2 from 38 to 28 mm Hg) associated with significant reduction in ICP, although patient responses varied widely; also associated with improved operating conditions; aggressive hyperventilation may increase risk for ischemia, but no outcome studies show long-term adverse effects; recommendation — hyperventilate patient until surgeon debulks mass and can operate comfortably, then let Paco2 rise to lower risk for ischemia Patient’s postoperative destination: if patient remains intubated, longer-acting anesthetics acceptable; when planning to keep patient awake or to awaken soon after surgery, use shorter-acting agent; speaker recommends newer vapors; remifentanil has advantages as transitional analgesia; if patient remains drowsy after using desflurane, sevoflurane, or remifentanil, recommend CT (not likely due to anesthetic) Air Embolism in Neurosurgical Patients Armin Schubert, MD, MBA, Professor of Anesthesiology, Cleveland Clinic, Lerner College of Medicine of Case Western Reserve University, Cleveland, OH Clinical significance of venous air embolism (VAE): risk for complete and possibly fatal cardiovascular collapse; paradoxic embolism may result in stroke and coronary or renal insufficiency; outcome may be acute respiratory distress syndrome (ARDS) and pulmonary edema; anatomy of head conducive to development of VAE because many venous structures noncollapsible; VAE likely if patient sitting up and venous pressure low (due to pumping of heart and inability of venous sinus to collapse); may also occur in spontaneously breathing patient Predisposing factors in neurosurgery: entry of air into noncollapsible vein (eg, dural sinuses, emissary veins); with sufficient gradient between heart (right atrium) and incision site, venous subatomspheric pressure can develop in vein when operative field pressure greater than central venous pressure (CVP); patient may be protected if CVP high and open vein bleeds rather than takes in air; classically described when patient in sitting position, but can occur in lateral, supine, and prone positions Commonly associated neurologic tumors: any located near great venous sinuses (eg, parasagittal tumors, craniosynostosis tumors) Clinical presentation: awake patient — tachypnea, chest pain, coughing, sneezing, and gasping; under anesthesia — rapidly decreasing end-tidal CO2, increase in pulmonary artery pressure and CVP, and hypoxemia; later developments —arrhythmias, changes on electrocardiography (ECG) (mill wheel murmur), profound hypotension, and decreased cardiac output Incidence: depends on patient’s position; if patient seated, incidence 40% to 50%; incidence may be higher when patient seated for such procedures as posterior fossa surgery; in other positions (including supine), reported incidence 10% to 15%; also depends on method of detection; if end-tidal CO2 used, incidence »9%; if Doppler used, incidence 40% to 50%; with transesophageal echocardiography (TEE), incidence in sitting position as high as 75% to 100%; surgical site — incidence higher in cranial than lower cervical surgery; however, some cervical procedures performed with patient seated; risk lower if patient has had previous surgery at same site; incidence among pediatric patients higher than in adults; lethal levels — data lacking on humans; animal studies suggest >100 mL Sensitivity of air embolism detection methods: TEE most sensitive, followed by Doppler; intermediate sensitivity —pulmonary artery pressure, end-tidal nitrogen, end-tidal CO2, transcutaneous CO2, Paco2; during routine clinical practice, patient monitored with precordial Doppler probe and capnography, but use of TEE increasing Mechanism for decreasing end-tidal CO2: CO2 exchange cannot occur when air obstructs one part of pulmonary circulation, but ventilation continues and results in growth of dead space; air from obstructed pulmonary circulation does not contain CO2; when mixed with perfused air from lung, CO2 drops precipitously, especially when embolism large Treatment: if VAE detected, notify surgeon, give 10 mg ephedrine, administer 1000 mL colloid, aspirate central line, and initiate cardiopulmonary resuscitation (CPR); surgeon ultimately responsible for immediate management of VAE; can plug hole and fill wound with fluid; anesthesiologist should discontinue nitrous oxide and lower head of bed Emergency treatment in sitting position: with high-risk patient, in addition to other measures, aspirate air through central venous line; can attempt compressing neck veins; VAE (especially if large) increases strain on right heart, possibly leading to right heart failure; anesthesiologist should maintain circulation and prepare to administer CPR Air lock phenomenon: highly lethal consequence of VAE; results in absence of output from right ventricle as it contracts against mixture of foam, air, and fluid; air aspiration may be lifesaving; if aspiration not possible, inject fluid through central line to “pump up” right heart Right heart support: essential; inotropic support may be necessary; start with norepinephrine; later, as hypotension resolves, milrinone or dobutamine may be used Pulmonary effects of VAE: obstruction of pulmonary tree; air interacts with endothelium, which releases vasoactive factors; may lead to leaky capillary syndrome, ARDS, and pulmonary edema Paradoxic embolism: incidence estimated at 1% of VAEs; most likely mechanisms transpulmonary passage or patent foramen ovale (PFO) Risk reduction strategies for patients undergoing head-elevated neurosurgical procedures: early detection through use of sensitive monitoring equipment; identify high-risk patients for large or paradoxical VAEs (screening for PFO performed in Europe and increasingly in United States; if PFO detected, surgeon can modify approach; Valsalva maneuver performed with TEE, air contrast, and color Doppler increases yield of PFO screening); positive end-expiratory pressure (PEEP) not routinely recommended (increases right-left gradient across intra-atrial septum and may increase risk for paradoxic VAE); generous fluid management decreases risk for VAE; optimal positioning of central venous catheter improves efficiency of venous air retrieval through aspiration; if patient has brain tumor, preoperative x-rays or MRI may show erosions into skull, which can also identify patient as high-risk for bleeding and VAE Suggested Reading Boisseau N et al: Comparison of the effects of sevoflurane and propofol on cortical somatosensory evoked potentials. Br J Anaesth 88:785, 2002; Crandon IW et al: A case report of chronic subdural haematomas in two elderly patients. West Indian Med J 56:547, 2007; Gelb AW et al: Does hyperventilation improve operating condition during supratentorial craniotomy? A multicenter randomized crossover trial. Anesth Analg 106:585, 2008; Gelb AW et al: Remifentanil with morphine transitional analgesia shortens neurological recovery compared to fentanyl for supratentorial craniotomy. Can J Anaesth 50:946, 2003; Head BP, Patel P: Anesthetics and brain protection. Curr Opin Anaesthesiol 20:395, 2007; Kawaguchi M et al: Neuroprotective effects of anesthetic agents. J Anesth 19:150, 2005; Kincaid MS: Transcranial Doppler ultrasonography: a diagnostic tool of increasing utility. Curr Opin Anaesthesiol 21:552, 2008; Mantz J et al: Recent advances in pharmacologic neuroprotection. Eur J Anaesthesiol July 15, 2009 [Epub ahead of print]; Mirski MA et al: Diagnosis and treatment of vascular air embolism. Anesthesiology 106:164, 2007; Morris C et al: Anaesthesia in haemodynamically compromised emergency patients: does ketamine represent the best choice of induction agent? Anaesthesia 64:532, 2009; Nathan N et al: Influence of propofol concentrations on multipulse transcranial motor evoked potentials. Br J Anaesth 91:493, 2003; Pasternak JJ, Lanier WL: Neuroanesthesiology update. J Neurosurg Anesthesiol 21:73, 2009.
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