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Neurosurgical Anesthesia Does the Choice of Anesthetic Agents Matter?

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Neurosurgical Anesthesia Does the Choice of Anesthetic Agents Matter? medigraphic Artemisaen línea E A NO D NEST A ES Mexicana de IC IO EX L M O G O I ÍA G A E L . C C O . C Revista A N A T Í E Anestesiología S G S O O L C IO I S ED TE A ES D M AN EXICANA DE CONFERENCIAS MAGISTRALES Vol. 30. Supl. 1, Abril-Junio 2007 pp S126-S132 Neurosurgical anesthesia Does the choice of anesthetic agents matter? Piyush Patel, MD, FRCPC* * Professor of Anesthesiology. Department of Anesthesiology University of California, San Diego. Staff Anesthesiologist VA Medical Center San Diego INTRODUCTION 1) Moderate to severe intracranial hypertension 2) Inadequate brain relaxation during surgery The anesthetic management of neurosurgical patients is, by 3) Evoked potential monitoring necessity, based upon our understanding of the physiology 4) Intraoperative electrocorticography and pathophysiology of the central nervous system (CNS) 5) Cerebral protection and the effect of anesthetic agents on the CNS. Consequent- ly, a great deal of investigative effort has been expended to CNS EFFECTS OF ANESTHETIC AGENTS elucidate the influence of anesthetics on CNS physiology and pathophysiology. The current practice of neuroanes- It is now generally accepted that N2O is a cerebral vasodila- thesia is based upon findings of these investigations. How- tor and can increase CBF when administered alone. This ever, it should be noted that most studies in this field have vasodilation can result in an increase in ICP. In addition, been conducted in laboratory animals and the applicability N2O can also increase CMR to a small extent. The simulta- of the findings to the human patient is debatable at best. A neous administration of intravenous anesthetics (barbitu- great deal of emphasis has been placed on the minor differ- rates, propofol, benzodiazepines, narcotics) can substantially ences in anesthetic induced changes in cerebral blood flow reduce this increase in CBF and CMR. The behavior of a (CBF), cerebral metabolic rate (CMR) and intracranial pres- combination of volatile agents and N2O is quite different. sure (ICP) that have been consistently demonstrated in a When administered in low doses, volatile agents can reduce variety of studies. Is this emphasis justified? It is not surpris- CBF and CMR. The addition of N2O to low dose volatile ing that, in the absence of controlled studies which demon- agent anesthesia increases both CBF and CMR. This N2O strate the superiority of one technique over another, inter- mediated vasodilation can be greater when higher doses of pretations of the available data differ and that opinions on volatile agents are administered. the optimal approach to the neurosurgical patient also dif- Volatile agents uniformly suppress CMR. At doses of 1.5 fer. A more important question to the practicing anesthesi- – 2.0 MAC, the commonly used agents isoflurane, desflu- ologist is not whether the minor differences in CNS physiol- rane and sevoflurane all produce burst suppression of the ogy induced by anesthetics are relevant to all neurosurgical EEG. At burst suppression, CMR is reduced by 50-60%. patients but the identification of clinical situations in which Volatile agents are also vasodilators. Their effect on CBF is anesthetic effects might be significant. edigraphic.combiphasic. At doses of about 0.5 MAC, the suppression in In the present discussion, a brief review of the cerebrovas- CMR balances the vasodilatory effects and CBF does not cular effects of anesthetic agents will be presented. Thereaf- change significantly. In doses greater than 1.0 MAC, the ter, situations in which the anesthetic selection has been vasodilatory effect predominates and CBF increases. The suggested to be relevant will be addressed: addition of N2O to volatile anesthetic anesthesia will in- S126 Revista Mexicana de Anestesiología Patel P. Neurosurgical anesthesia crease CBF and CMR. This increase in CBF may not neces- observation of the brain and the surgical conditions can sarily result in an increase in ICP. The effect of volatile then dictate the anesthetic regimen. agents on cerebral blood volume (CBV) parallel the CBF A similar logic may apply to the management of the acute- changes but are of a significantly lesser magnitude. ly head injured patient. Compensatory mechanisms are inad- Intravenous hypnotic agents, with the exception of ket- equate to offset the rapid increase in intracranial volume and amine, all decrease CMR and CBF substantially. In appro- ICP. In such patients, brain distortion and herniation can com- priate doses, barbiturates, propofol and etomidate produce promise regional brain perfusion, rendering the brain ischem- burst suppression of the EEG. Ketamine’s effect on CBF and ic. Moreover, experimental data have shown that hyperventi- CMR are regionally specific; in the limbic structures, CBF lation, which is often employed to minimize or counteract and CMR increase whereas within the cortex, reductions in volatile agent induced vasodilation, can be ineffective in CBF and CMR occur. doing so with acute head injury(3). A cogent argument can therefore be made that one should avoid nitrous oxide and 1) MODERATE TO SEVERE INTRACRANIAL volatile agents in the anesthetic management. HYPERTENSION “TIGHT BRAIN” DURING SURGERY Patients with intracranial hypertension (ICH) have symp- toms of headache, nausea, vomiting and visual disturbance. Adequate brain relaxation facilitates neurosurgery and re- Patients with severe ICH also have a reduced level of con- duces the need for excessive brain retraction. Although un- sciousness. CT scans demonstrate mass lesions, ventricular common, brain swelling can occur intraoperatively during effacement, midline shifts of the brain and full basal cis- surgery. This is most commonly seen during AVM surgery terns. The brain’s capacity to accommodate increases in CBV but it can occur during tumor surgery as well. The etiology is exhausted and even slight increases in intracranial vol- of brain swelling is not clear. Clearly, engorgement of the ume can result in dramatic increases in ICP. In patients with brain with blood plays a significant role. When brain swell- acute increases in ICP (for example, with traumatic brain ing does occur, the brain is placed at risk for ischemic inju- SUSTRAÍDODE-M.E.D.I.G.R.A.P.H.I.C injury, epidural and subdural hematomas), the effect of an ry. In addition, brain swelling interferes with surgery and on increase in CBV on ICP is even greater. It is in these patients occasion, can prevent closure of the dura. This represents an :ROP ODAROBALE FDP that the choice of anesthetic agents must be considered care- urgent problem that demands the attention of the anesthesi- fully. ologist and the neurosurgeon. The approach to this difficult VC ED AS, CIDEMIHPARG Agents that produce vasodilation can increase CBF and problem is reasonably well established and the following more importantly, CBV. The potential for a further increase maneurvers may be instituted: ARAP in ICP is therefore apparent. Minor increases in ICP can be readily treated by modest hyperventilation and the use of • Check ventilation. Moderate hypocapnia (target PaCO ACIDÉMOIB ARUTARETIL :CIHPARGIDEM 2 diuretics. Consequently, for the majority of patients, it is 25-30 mmHg) will produce cerebral vasoconstriction and unlikely that anesthetic induced increases in ICP will be the consequent reduction in brain bulk. Measurement of substantial enough to compromise the brain. For example, end-tidal CO2 tension is occasionally misleading. Arteri- in patients with intracranial tumors, there were no differenc- al blood gas analysis should be utilized judiciously to es in outcome in patients anesthetized with propofol-fenta- confirm hypocarbia. nyl, isoflurane-nitrous oxide or fentanyl-nitrous oxide(1). • Ensure normal oxygenation. Nontheless, other studies have shown that dural tension is • Control blood pressure. Target is normotension (within higher with isoflurane-fentanyl and sevoflurane-fentanyl 10% of baseline blood pressure). anesthesia in comparison to propofol-fentanyl anesthesia(2). • Ensure adequate venous drainage from the brain. Neck In patients in whom the ability of the brain to compensate torsion or the placement of endotracheal tube ties around for further increases in CBV is exhausted, a technique that the neck can impede venous drainage from the brain. reduces CMR, CBV and ICP may be preferable. In such pa- • Head elevation (30° optimum) tients, it is the author’s practice to avoid nitrous oxide and • Check intrathoracic pressure. Rule out pneumothorax volatile agents until such time as the dura is opened. An (especially if central line has been placed). anesthetic technique based on the infusion of propofol and • Maintain adequate neuromuscular relaxation. narcotics may be a more prudent approch in so faredigraphic.com as the • Administer mannitol. reserve of the brain to compensate for increases in CBV is not encroached upon and may in fact be increased (reduc- If these measures are not adequate, then consideration tion in CBV). Volatile agents may be introduced once the should be given to the potential deleterious effect of anes- cranium has been opened and the dura has been reflected; thetic agents. In particular, attention should be focused on Volumen 30, Suplemento 1, abril-junio 2007 S127 Patel P. Neurosurgical anesthesia those agents that can increase brain bulk by producing cere- results in a very good signal is a total intravenous anesthet- bral vasodilation. The manipulation of anesthetic adminis- ic technique. The combination of propofol and a narcotic tration can effect dramatic reductions in brain bulk: infusion results in excellent signals in most patients(7). In addition, the variability in the amplitude of the evoked po- • Make sure that the concentration of volatile agent is less tential is reduced by this technique in comparison to a N2O than 0.5 MAC -volatile agent-narcotic technique. This is an important con- • Discontinue the administration of N2O sideraton in those patients with CNS abnormalities in whom • Discontinue the administration of volatile anesthetics the EP is already compromised by the primary disease. If the • Switch to an intravenous anesthetic technique.
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