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NEUROSURGICALANESTHESIA part 2ma_attari@med.mui.ac.irA and B, The sitting position. The patient is typically semirecumbent rather than sitting. In A, the head holder support is correctly positioned such that the head can be lowered without the need to detach the head holder first. The configuration in B, with the support attached to the thigh portion of the table, should be avoided.

Venous Air EmbolismThe common sources of critical VAE are the major cerebral venous sinuses, in particular, the transverse, the sigmoid, and the posterior half of the sagittal sinus, all of which may be noncollapsible because of their dural attachments.Venous Air EmbolismThe most common situation involve tumorsMost often parasagital or falcin meningiomas and craniosynostosis.Pin sites and trappped gas can lead to VAE.The common sources of critical VAE are the major cerebral venous sinuses.Detection of Venous Air EmbolismThe monitors employed for the detection of VAE should providea high level of sensitivity,a high level of specificity,a rapid response,a quantitative measure of the VAE event,an indication of the course of recovery from the VAE event.The combination of a precordial Doppler and expired CO2monitoring meet these criteria and are the current standard of care. Detection of Venous Air EmbolismDoppler placement in a left or right parasternal location between the second and third or third and fourth ribs has a very high detection rate for gas embolization, and when good heart tones are obtained, maneuvers to confirm adequate placement seem to be unnecessary. TEE is more sensitive than precordial Doppler to VAE and offers the advantage of identifying right-to-left shunting of air.The relative sensitivity of various monitoring techniques to the occurrence of venous air embolism (VAE). BP, blood pressure; CO, cardiac output; CVP, central venous pressure; ECG, electrocardiogram, ET-CO2, end-tidal carbon dioxide; PAP, pulmonary arterial pressure; physiol, physiological; T-echo, transesophageal echo.

Venous Air EmbolismRate of occurrence:Procedure Posterior fossaPosition SittingDetection method Doppler precordial 40% TEE 76% In cervical spine procedure 25%

Posterior Fossa, Doppler, Nonsitting 12%VAE in nonsitting Position has Smaller volume.

Management Of Acute Air Embolic Events1. Prevent further air entryNotify surgeon (flood or pack surgical field)Jugular compressionLower the head2. Treat the intravascular airAspirate via a right heart catheterDiscontinue N20FI02: 1.0(Pressors/ inotropes)(Chest compression)Electrocardiogram (ECG) configurations observed at various locations when a central venous catheter is used as an intravascular ECG electrode. The configurations in the figure are observed when lead II is monitored and the positive electrode (the leg electrode) is connected to the catheter. P indicates the sinoatrial node. The heavy black arrow indicates the P wave vector. Note the equi-biphasic P wave when the catheter tip is in the mid right atrial position.

Right Heart CatheterEssentially all patients who undergo sitting posterior fossa procedures should have a right heart catheter.Although catastrophic, life-threatening VAE is relatively uncommon, a catheter that permits immediate evacuation of an air-filled heart occasionally is the sine qua non for resuscitation.Which Vein Should Be Used for Right Heart Access?Although some surgeons may ask that neck veins not be used, a skillfully placed jugular catheter is usually acceptable.Positioning the Right Heart CatheterA multi-orificed catheter should be located with the tip 2 cm below the superior vena cavalatrial junction, and a single-orificed catheter should be located with the tip 3 cm above the superior vena cavalatrial junction.Paradoxical Air EmbolismThere has been much concern about the possibility of the passage of air across the interatrial septum via a patent foramen ovale (known to be present in approximately 25% of adults).

Fluid TherapyThe intraoperative fluid management of neurosurgical patients presents special challenges for the anesthesiologist. Neurosurgical patients often experience:Rapid changes in intravascular volume caused by hemorrhageThe administration of potent diureticsOr the onset of diabetes insipidus.Intravenous Fluid ManagementThe general principles 1.Maintenance of normovolemia 2.Avoidance of a reduction in serum osmolarity.Half-normal saline is probably a reasonable choice for maintenance fluid To replace blood and third-space loss: Normal saline(308mOsm/L ) and lactated Ringer's solution (273mOsm/L) [plasma (295mOsm/L)]. Intravenous Fluid Management (cont.)In situations: multiple trauma, aneurysm rupture, cerebral venous sinus laceration, fluid administration to support filling pressure during barbiturate coma, combination of isotonic crystalloid and colloid may be appropriate. (Albumin to be a reasonable choice as a colloid solution)Fluid TherapyIntracranial hypertension secondary to cerebral edema is now known to be one of the most common causes of morbidity and mortality in the intraoperative and postoperative periods.Fluid TherapyWe examine:Some of the physical determinants of water movement between the intravascular space and the central nervous system.Specific clinical situations and make suggestions for the types and volumes of fluids to be administered.Fluid TherapyFor physiologic solutions, osmolality is commonly expressed as milliosmoles (mOsm) per kilogram of solvent, whereas the units of measure for osmolarity are milliosmoles per liter of solution.Fluid TherapyWater has a tendency to move from the solution of lower osmolality, across the membrane, and into the solution of higher osmolality.

All act to draw fluid from the capillaries and into the extracellular space of the tissue:Capillary pressureTissue pressure (negative in nonedematous tissues)Tissue oncotic pressure.

In peripheral tissues, the only factor that serves to maintain intravascular volume is the plasma oncotic pressure, which is produced predominantly by albumin and to a lesser extent by immunoglobulins, fibrinogen, and other high-molecular-weight (HMW) plasma proteins.The clinical effects of altering one or more of the variables in the Starling equation may frequently be observed in the operating room. Many patients who have been resuscitated from hemorrhagic hypovolemia with large volumes of crystalloid solutions demonstrate pitting edema, caused by a dilution of plasma proteins.

Fluid Movement between Capillaries and the BrainThe brain and spinal cord are unlike most other tissues in the body in that they are isolated from the intravascular compartment by the blood-brain barrier. Morphologically, this barrier is now thought to be composed of endothelial cells that form tight junctions in the capillaries supplying the brain and spinal cord.

Fluid moves in and out of the central nervous system according to the osmolar gradient (determined by relative concentrations of all osmotically active particles, including most electrolytes) between the plasma and the extracellular fluid.Administration of large volumes of iso-osmolar crystalloid results in peripheral edema caused by dilutional reduction of plasma protein content but does not increase brain water content or intracranial pressure (ICP).Osmolarity is the primary determinant of water movement across the intact blood-brain barrier. The administration of excess free water (either iatrogenically or as a result of psychogenic polydipsia) can result in an increased ICP and an edematous brain.Hyperosmolar solutions are used daily in operating rooms throughout the world as standard therapeutic agents to treat intracranial hypertension.What occurs when the brain is injured with disruption of the barrier?In patients at risk for intracranial hypertension. The infusion of colloids is often recommended to maintain intravascular volume in such patients, implying that maintaining or increasing plasma oncotic pressure reduces cerebral edema.In the case of the intact blood-brain barrier, neither theoretical nor experimental evidence suggests that colloids are more beneficial than crystalloids for either brain water content or ICP.

SOLUTIONS FOR INTRAVENOUS USEThese fluids may be categorized conveniently on the basis of:OsmolalityOncotic pressureDextrose content.Osmolarity of Commonly Used Intravenous FluidsOncotic Pressure(mm Hg)Osmolarity (mOsm/L)Fluid0273Lactated Ringers solution0525D5 lactated Ringers solution03080.9% saline0406D5 0.45% saline01540.45% saline0109820% mannitol31310Hetastarch (6%)169300Dextran 40 (10%)69300Dextran 70 (6%)19290Albumin (5%)26295PlasmaThe term colloid denotes solutions that have an oncotic pressure similar to that of plasma. Some commonly administered colloids are:6% hetastarch (Hespan)5% and 25% albuminThe dextrans (40 and 70)PlasmaDextran and hetastarch are dissolved in normal saline, so the osmolarity of the solution is approximately 290 to 310 mOsm/L with a sodium and chloride ion content of about 145 mEq/L.Hyperosmolar Solutions Although an acute beneficial effect has been demonstrated, the longer-term (24-48 hours) effect of such hyperosmotic fluid therapy remains unknown.Acute increases to values that exceed 170 mEq/L sodium are likely to result in a depressed level of consciousness or seizures.30mL of 23.4% saline brought prompt and sustained decreases in ICP.Despite these impressive results, it is unclear why hypertonic saline should be more effective than mannitol.In clinical studies, hyperglycemia has been associated with worsened neurologic outcome after traumatic brain injury (glucose > 200 mg/dL), acute ischemic stroke, and subarachnoid hemorrhage.

Pediatric NeuroanesthesiaIntraoperative Fluid and Electrolyte ManagementBecause CBF constitutes 55% of total cardiac output in 2- to 4-year old patients, sudden blood loss or venous air embolus can rapidly deteriorate to cardiovascular collapse.52Normal saline is commonly used as the maintenance fluid during neurosurgery because it is mildly hyperosmolar (308 mOsm/kg) and should minimize cerebral edema. However, rapid infusion of large quantities of normal saline (>60 mL/kg) can be associated with hyperchloremic acidosis.Estimated Blood Volume in ChildrenEstimated Blood Volume (mL/kg)Age100Preterm neonate90Full-term neonate801 year751-12 years70Adolescents and adultsDecision to transfuse should be dictated by:The type of surgeryUnderlying medical condition of the patientPotential for additional blood loss both intraoperative and postoperative.Pediatric NeuroanesthesiaHematocrit values of 21% to 25% should provide some impetus for blood transfusion. Packed red blood cells (10 mL/kg) will raise the hematocrit by 10%. Initially, blood losses should be replaced with 3 mL of normal saline for each 1 mL of lost blood or a colloid solution such as 5% albumin equal to the blood loss.Additional fluid administration at 3 to 10 mL/kg/hr may be necessary.Pediatric NeuroanesthesiaPediatric patients, particularly infants, are at particular risk for hypoglycemia. Small premature infants, who have limited reserves of glycogen and limited gluconeogenesis, require continuous infusions of glucose at 5 to 6 mg/kg/min to maintain serum levels.

Pediatric NeuroanesthesiaSurgery elicits a stress response, and children are generally able to maintain normal serum glucose levels without exogenous glucose administration

Pediatric NeuroanesthesiaIn any case hyperglycemia is always best avoided, because it may exacerbate neurologic injury if ischemia occurs.follow a conservative approach that keeps randomly measured serum glucose levels below 180 mg/dL.Pediatric NeuroanesthesiaMannitol can be given at a dose of 0.25 to 1.0 g/kg IV. This agent will transiently alter cerebral hemodynamics and raise serum osmolality by 10 to 20 mOsm/kg.Furosemide prevent the rebound swelling due to mannitol.Daily Water Loss for an AdultAmount (mL/day)Type/LocationInsensible losses:350Skin350Lungs1400Urine100Sweat200Feces2400TOTAL

PERIOPERATIVE MANAGEMENT OF ADULT PATIENTS WITH SEVERE HEAD INJURYDuring fluid resuscitation of the head-injured patient, the goals are to maintain:Serum osmolalityAvoid profound reduction in colloid oncotic pressureRestore circulating blood volume.PERIOPERATIVE MANAGEMENT OF ADULT PATIENTS WITH SEVERE HEAD INJURYImmediate therapy is directed at preventing hypotension and maintaining cerebral perfusion pressure (CPP) above 60 mm Hg.PERIOPERATIVE MANAGEMENT OF ADULT PATIENTS WITH SEVERE HEAD INJURYHypertonic saline solutions (3%, 7.5%) can be very useful for low-volume resuscitation in the head-injured patient because they lower ICP, raise blood pressure, and may improve regional cerebral blood flow (CBF).PERIOPERATIVE MANAGEMENT OF ADULT PATIENTS WITH SEVERE HEAD INJURYA minimum hematocrit value between 30% and 33% is recommended to maximize oxygen transport.Intraoperative FluidsIntraoperative maintenance fluid administration usually consists of lactated Ringers or normal saline solution. These fluids are crystalloids and are approximately equiosmolar to normal plasma. As a general rule, hypo-osmolar solutions and dextrose-containing solutions should be avoided.Intraoperative FluidsIso-osmolar crystalloids are given at a rate sufficient to replace the patients urine output and insensible losses milliliter for milliliter. Blood loss is replaced at about a 3:1 ratio (crystalloid/blood) down to a hematocrit value of approximately 25% to 30%.

Mannitol may have a biphasic effect on ICP. Concomitant with the infusion.ICP may transiently increase, presumably because of vasodilation of cerebral vessels in response to the sudden increase in plasma osmolality.Subsequent reduction in ICP is achieved by the movement of water from the brains interstitial and intracellular spaces into the vasculature.Medium MW Hydroxyethyl Starch ProductsVoluven is an equally effective volume expander compared to hetastarch or HES 200/0.5 in the patient populations described.Plasma and Red Blood CellsRed blood cells should be given only to keep hematocrit at a safe level. This level varies from patient to patient; and even in a specific circumstance, it may be difficult to objectively define what constitutes safe.In general, healthy individuals easily tolerate hematocrits in the 20% to 25% range.SPECIFIC NEUROSURGICAL CHALLENGESFluid Management in Patients with Cerebral AneurysmsFluid Management of Diabetes InsipidusFluid Management of the Trauma Patient with Head InjuriesFluid Management in Patients with Cerebral AneurysmsVolume loading may be accomplished by infusing iso-osmolar crystalloids, colloids, or red blood cells in order to achieve hemodilution to a hematocrit of approximately 30%.Fluid Management in Patients with Cerebral AneurysmsFrequent assessment of pulmonary function with arterial blood gas measurements, chest radiographs, and physical examination is essential.Fluid Management of Diabetes InsipidusThe patient should be vigorously rehydrated with 0.45% saline until euvolemia is established. Because of the preexisting hyperosmolar/hypernatremic state, normal saline should not routinely be used for the initial rehydration of these patients.Fluid Management of the Trauma Patient with Head InjuriesThe ideal resuscitation fluid for patients who are hypovolemic with ongoing blood loss is fresh whole blood. Because whole blood is a colloid rather than a crystalloid.Fluid Management of the Trauma Patient with Head InjuriesSmaller volumes of whole blood are required to restore intravascular volume, thus producing a more rapid resuscitation. Whole blood replaces clotting factors and platelets that have been lost and may therefore prevent the emergence of a dilutional coagulopathy.

HypothermiaMild hypothermia (32-34C) in reducing the neurologic injuryMild hypothermia is perceived to hazards: Coagulation dysfunctionIncreased postoperative wound infection rateHypertension on emergence Modest overshoot in temperatureEmergence from AnesthesiaTo the prevention of coughing and straining: NarcoticN2ON2O + propofol (either bolus increments or infusion at rates in the range of 25-100 g/kg/min)LidocaineEmergence from AnesthesiaMost practitioners of neuroanesthesia believe that a premium should be placed on "smooth" emergence, that is, one free of coughing/straining and arterial hypertension.Avoidance of arterial hypertension is seen as desirable because of the belief that arterial hypertension can contribute to intracranial bleeding and increased edema formation.Emergence from AnesthesiaIn the face of a poorly autoregulating cerebral vasculature, hypertension also has the potential, through vascular engorgement, to contribute to elevation of ICP.Much of the concern with coughing/straining has a similar basis. Emergence from AnesthesiaThe sudden increases in intrathoracic pressure are transmitted to both arteries and veins, and the transient increases produced in both cerebral arterial and venous pressure have the same potential consequences: edema formation, bleeding, and elevation of ICP.Emergence from AnesthesiaCoughing is a specific concern with certain individual procedures.In the circumstances of transsphenoidal pituitary surgery in which the surgeon has opened and subsequently taken pains to close the arachnoid membrane to prevent leakage of CSF, it is believed that coughing has the potential to disrupt this closure because of sudden and substantial increases in CSF pressure.Emergence from AnesthesiaOpening a pathway from the intracranial space to the nasal cavity conveys a substantial risk of postoperative meningitis. In other procedures, notably those that have violated the floor of the anterior fossa, there is also the potential for air to be driven into the cranium and, in the event of a flap valve mechanism, cause a tension pneumocephalus. This latter event can take place only when coughing occurs after the endotracheal tube has been removed.

Emergence from AnesthesiaA common method for the management of systemic hypertension during the last stages of a craniotomy is the expectant or reactive administration (or both) of vasoactive drugs, most commonly labetalol and esmolol.Other drugs, including enalapril and diltiazem, have been used to good effect.

Emergence from AnesthesiaAdministration of dexmedetomidine during the procedure and up to 30 to 60 minutes before conclusion of the procedure has also been reported to lessen the requirement for antihypertensives during emergence.There are also many approaches to the prevention of coughing and straining. We encourage trainees to include in their anesthetic technique "as much narcotic as is consistent with spontaneous ventilation at the conclusion of the procedure."

Emergence from AnesthesiaThat practice is based on the same physiologic effect that justifies the administration of codeine and related compounds as antitussive medication, specifically, the depression of airway reflexes by narcotics. Emergence from AnesthesiaA common practice among neuroanesthetists near the conclusion of a craniotomy is the relatively early discontinuation of the volatile anesthetic and supplementation of residual nitrous oxide with propofol by either bolus increments or infusion at rates in the range of 25 to 100 g/kg/min.

Emergence from AnesthesiaAn additional principle relevant to emergence from neurosurgical procedures that practitioners will learn either from a book or by bad experience is that emergence should be timed to coincide, not with the final suture, but rather with the conclusion of the application of the head dressing. Emergence from AnesthesiaAnother nuance of our practice has been to withhold the administration of neuromuscular antagonists as long as possible as a hedge against misjudgment while lightening anesthesia in a patient in the later stages of the procedure. An additional popular and apparently effective technique for reducing airway responsiveness and the likelihood of coughing/straining while reducing the depth of anesthesia is the administration of lidocaine.

Emergence from AnesthesiaBolus doses on the order of 1.5 mg/kg, often given as application of the head dressing begins, are appropriate for this purpose.Emergence from AnesthesiaIn some instances, one may be tempted to extubate patients before complete recovery of consciousness. This practice may be acceptable in some circumstances. However, it should be undertaken with caution when the circumstances of the surgical procedure make it possible that neurologic events may have occurred that will delay recovery of consciousness or when lower cranial nerve dysfunction may be present. Emergence from AnesthesiaIn these circumstances, it will generally be best to wait until the likelihood of the patient's recovery of consciousness is confirmed or until patient cooperation and airway reflexes are likely to have recovered (or until both)

Supratentorial TumorsHypertension (due to irritation of the hypothalamus) Disturbances in consciousness varying from lethargy to obtundation.Diabetes insipidusCerebral salt-wasting syndrome (after 12-24 hrs)Supratentorial Tumors (cont.)Frontal lobey: 1) Retraction and irritation of the inferior surfaces of the frontal lobes can result in a patient who is lethargic and does not awaken cleanly, and who may exhibit delayed emergence . 2) The phenomenon is more likely to be evident when there has been bilateral subfrontal retraction than when it occurs only unilaterally. Aneurysms and AV MalformationsFluid management 1) SIADH2) Cerebral salt wasting syndrome (Na, volume , urine Na>50 mmol/lit)management of both is simple: administration of isotonic fluids using intravascular normovolemia as the end point. Aneurysms and AV Malformations (cont.)VasospasmDrowsiness is a common initial clinical sign.Administration of Nimodipine has been shown to decrease the incidence of Vasospasm.Treatment: (triple H) Hypervolemia Hemodilution(Hct 30)Hypertension(20-30 mmHg) (Phenylephrine and Dopamine are the most commonly employed pressors )Aneurysms and AV Malformations (Cont.)ECG abnormalitiesCanyon T wavesNonspecific T-wave changes, QT prolongation, ST-segment depression and U wavesQT>550 msec Torsades de pointesAnesthetic TechniqueImportant considerations include the following:Avoidance of acute hypertensionBrain relaxationMaintenance of high-normal MAPPreparedness to perform precise manipulations of MAP as the surgeon attempts to clip the aneurysm or control bleeding from a ruptured aneurysm (or both)Head InjuryIntubating a Head-Injured PatientGCS of 7 to 8Trauma-related cardiopulmonary dysfunctionUncooperative, to facilitate diagnostic proceduresFactors that may be relevant duringintubation of a head-injured patientFull stomachUncertain cervical spineUncertain airway:BloodAirway injury (larynx, cricoarytenoid cartilage)Skull base fractureUncertain volume statusUncooperative/ combativeHypoxemiaIncreased intracranial pressureThe Cervical Spine

Head Injury: Anesthetic Technique Choice of anestheticsAll of the IV anesthetics, except Ketamine, cause some cerebral vasoconstriction and are reasonable choices, provided that they are consistent with hemodynamic stability. All of the inhaled anesthetics (N20 and all of the vapors) have some cerebral vasodilatory effect.Blood Pressure ManagementCareful maintenance of a CPP of 60-70 mmHg in the first 72 hours after TBI will be appropriate and is common practice in a head-injured adult. A CPP target of 45 mm Hg has been recommended for children.Posterior Fossa ProceduresProcedures involving dissection on the floor of the fourth ventricle can result in loss of control and patency of the upper airway The cardiovascular responses: Bradycardia and hypotension Tachycardia and hypertension Bradycardia and hypertension Ventricular dysrhythmiasTranssphenoidal Hypophysectomy Preoperative EvaluationHypocortisolism with associated hyponatremiaHypothyroidismHypertension, diabetes, and central obesity (Cushing's disease). Acromegaly: enlarged tongue and a narrowed glottis, and the airway should be evaluated .Transsphenoidal Hypophysectomy Diabetes insipidus (DI)DI usually develops 4-12 hours postoperatively and very rarely arises intraoperatively. Urine specific gravity is a useful bedside test.(