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A 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 Embolism The 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 Embolism The most common situation involve tumors Most 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 Embolism The monitors employed for the detection of VAE should provide (1) a high level of sensitivity, (2) a high level of specificity, (3) a rapid response, (4) a quantitative measure of the VAE event, (5) an indication of the course of recovery from the VAE event. The combination of a precordial Doppler and expired CO 2 monitoring meet these criteria and are the current standard of care.

Detection of Venous Air Embolism Doppler 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 Doppler to VAE 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-CO 2, end-tidal carbon dioxide; PAP, pulmonary arterial pressure; physiol, physiological; T-echo, transesophageal echo.

Venous Air Embolism Rate of occurrence: 1. Procedure Posterior fossa 2. Position Sitting 3. Detection 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 Events 1. Prevent further air entry Notify surgeon (flood or pack surgical field) Jugular compression Lower the head 2. Treat the intravascular air Aspirate via a right heart catheter Discontinue N 20 FI 02: 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 Catheter Essentially 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 Catheter A multi-orificed catheter should be located with the tip 2 cm below the superior vena caval–atrial junction, junction and a single-orificed catheter should be located with the tip 3 cm above the superior vena caval–atrial junction

Paradoxical Air Embolism There 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 Therapy The intraoperative fluid management of neurosurgical patients presents special challenges for the anesthesiologist. Neurosurgical patients often experience: 1. Rapid changes in intravascular volume caused by hemorrhage 2. The administration of potent diuretics 3. Or the onset of diabetes insipidus.

Intravenous Fluid Management � The 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(308 m. Osm/L ) and lactated Ringer's solution (273 m. Osm/L) [plasma (295 m. Osm/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 Therapy Intracranial 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 Therapy We examine: 1. Some of the physical determinants of water movement between the intravascular space and the central nervous system. 2. Specific clinical situations and make suggestions for the types and volumes of fluids to be administered.

Fluid Therapy For physiologic solutions, osmolality is commonly expressed as milliosmoles (m. Osm) per kilogram of solvent, whereas the units of measure for osmolarity are milliosmoles per liter of solution.

Fluid Therapy Water 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: 1. Capillary pressure 2. Tissue pressure (negative in nonedematous tissues) 3. 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 highmolecular-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 Brain The brain and spinal cord are unlike most other tissues in the body in that they are isolated from the intravascular compartment by the bloodbrain 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 USE These fluids may be categorized conveniently on the basis of: v. Osmolality v. Oncotic pressure v. Dextrose content.

Osmolarity of Commonly Used Intravenous Fluid Osmolarity (m. Osm/L) Oncotic Pressure (mm Hg) Lactated Ringer’s solution D 5 lactated Ringer’s solution 0. 9% saline D 5 0. 45% saline 20% mannitol Hetastarch (6%) Dextran 40 (10%) Dextran 70 (6%) Albumin (5%) Plasma 273 525 308 406 154 1098 310 ≈300 295 0 0 0 31 169 69 19 26

The term colloid denotes solutions that have an oncotic pressure similar to that of plasma. Some commonly administered colloids are: v 6% hetastarch (Hespan) v 5% and 25% albumin v. The dextrans (40 and 70) v. Plasma

Dextran and hetastarch are dissolved in normal saline, so the osmolarity of the solution is approximately 290 to 310 m. Osm/L with a sodium and chloride ion content of about 145 m. Eq/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 m. Eq/L sodium are likely to result in a depressed level of consciousness or seizures.

30 m. L 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/d. L), acute ischemic stroke, and subarachnoid hemorrhage.

Pediatric Neuroanesthesia

Intraoperative Fluid and Electrolyte Management Because 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.

Normal saline is commonly used as the maintenance fluid during neurosurgery because it is mildly hyperosmolar (308 m. Osm/kg) and should minimize cerebral edema. However, rapid infusion of large quantities of normal saline (>60 m. L/kg) can be associated with hyperchloremic acidosis.

Estimated Blood Volume in Children Age Preterm neonate Full-term neonate ≤ 1 year 1 -12 years Adolescents and adults Estimated Blood Volume (m. L/kg) 100 90 80 75 70

Decision to transfuse should be dictated by: q. The type of surgery q. Underlying medical condition of the patient q. Potential for additional blood loss both intraoperative and postoperative.

Pediatric Neuroanesthesia Hematocrit values of 21% to 25% should provide some impetus for blood transfusion. Packed red blood cells (10 m. L/kg) will raise the hematocrit by 10%. Initially, blood losses should be replaced with 3 m. L of normal saline for each 1 m. L of lost blood or a colloid solution such as 5% albumin equal to the blood loss. Additional fluid administration at 3 to 10 m. L/kg/hr may be necessary.

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

Pediatric Neuroanesthesia In 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/d. L.

Pediatric Neuroanesthesia Mannitol 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 m. Osm/kg.

Furosemide prevent the rebound swelling due to mannitol.

Daily Water Loss for an Adult Type/Location Insensible losses: Skin Lungs Urine Sweat Feces TOTAL Amount (m. L/day) 350 1400 100 2400

PERIOPERATIVE MANAGEMENT OF ADULT PATIENTS WITH SEVERE HEAD INJURY During fluid resuscitation of the head-injured patient, the goals are to maintain: 1. Serum osmolality 2. Avoid profound reduction in colloid oncotic pressure 3. Restore circulating blood volume.

PERIOPERATIVE MANAGEMENT OF ADULT PATIENTS WITH SEVERE HEAD INJURY Immediate therapy is directed at preventing hypotension and maintaining cerebral perfusion pressure (CPP) above 60 mm Hg.

PERIOPERATIVE MANAGEMENT OF ADULT PATIENTS WITH SEVERE HEAD INJURY Hypertonic saline solutions (3%, 7. 5%) can be very useful for low-volume resuscitation in the headinjured patient because they lower ICP, raise blood pressure, and may improve regional cerebral blood flow (CBF).

PERIOPERATIVE MANAGEMENT OF ADULT PATIENTS WITH SEVERE HEAD INJURY A minimum hematocrit value between 30% and 33% is recommended to maximize oxygen transport.

Intraoperative Fluids Intraoperative maintenance fluid administration usually consists of lactated Ringer’s or normal saline solution. These fluids are crystalloids and are approximately equiosmolar to normal plasma. As a general rule, hypoosmolar solutions and dextrose-containing solutions should be avoided.

Intraoperative Fluids Iso-osmolar crystalloids are given at a rate sufficient to replace the patient’s 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 brain’s interstitial and intracellular spaces into the vasculature.

Medium MW Hydroxyethyl Starch Products Voluven is an equally effective volume expander compared to hetastarch or HES 200/0. 5 in the patient populations described.

Plasma and Red Blood Cells Red 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 CHALLENGES q. Fluid Management in Patients with Cerebral Aneurysms q. Fluid Management of Diabetes Insipidus q. Fluid Management of the Trauma Patient with Head Injuries

Fluid Management in Patients with Cerebral Aneurysms Volume loading may be accomplished by infusing isoosmolar crystalloids, colloids, or red blood cells in order to achieve hemodilution to a hematocrit of approximately 30%.

Fluid Management in Patients with Cerebral Aneurysms Frequent assessment of pulmonary function with arterial blood gas measurements, chest radiographs, and physical examination is essential.

Fluid Management of Diabetes Insipidus The 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 Injuries The 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 Injuries Smaller 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.

Hypothermia �Mild hypothermia (32 -34°C) in reducing the neurologic injury �Mild hypothermia is perceived to hazards: �Coagulation dysfunction �Increased postoperative wound infection rate �Hypertension on emergence �Modest overshoot in temperature

Emergence from Anesthesia q. To the prevention of coughing and straining: �Narcotic �N 2 O + propofol (either bolus increments or infusion at rates in the range of 25 -100 μg/kg/min) �Lidocaine

Emergence from Anesthesia �Most 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 Anesthesia �In 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 Anesthesia �The 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 Anesthesia �Coughing 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 Anesthesia �Opening 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 Anesthesia �A 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 Anesthesia �Administration 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 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 Anesthesia �That 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 Anesthesia �A 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 Anesthesia �An 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 Anesthesia �Another 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 Anesthesia �Bolus 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 Anesthesia �In 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 Anesthesia �In 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 Tumors �Hypertension (due to irritation of the hypothalamus) �Disturbances in consciousness varying from lethargy to obtundation. �Diabetes insipidus �Cerebral 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 Malformations �Fluid management 1) SIADH 2) 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. ) �Vasospasm �Drowsiness 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 mm. Hg) (Phenylephrine and Dopamine are the most commonly employed pressors )

Aneurysms and AV Malformations (Cont. ) �ECG abnormalities �Canyon T waves �Nonspecific T-wave changes, QT prolongation, �ST-segment depression and U waves �QT>550 msec → Torsades de pointes

Anesthetic Technique �Important considerations include the following: �Avoidance of acute hypertension �Brain relaxation �Maintenance of high-normal MAP �Preparedness to perform precise manipulations of MAP as the surgeon attempts to clip the aneurysm or control bleeding from a ruptured aneurysm (or both)

Head Injury �Intubating a Head-Injured Patient �GCS of 7 to 8 �Trauma-related cardiopulmonary dysfunction �Uncooperative, to facilitate diagnostic procedures

Factors that may be relevant during intubation of a head-injured patient �Full stomach �Uncertain cervical spine �Uncertain airway: �Blood �Airway injury (larynx, cricoarytenoid cartilage) �Skull base fracture �Uncertain volume status �Uncooperative/ combative �Hypoxemia �Increased intracranial pressure

The Cervical Spine

Head Injury: Anesthetic Technique �Choice of anesthetics �All 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 (N 20 and all of the vapors) have some cerebral vasodilatory effect.

Blood Pressure Management �Careful maintenance of a CPP of 60 -70 mm. Hg 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 Procedures �Procedures 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 dysrhythmias

Transsphenoidal Hypophysectomy Preoperative Evaluation �Hypocortisolism with associated hyponatremia �Hypothyroidism �Hypertension, 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. (<1. 002) �Fluid management regimen is hourly maintenance fluids plus 2/3 of the previous hour's urine output. (An acceptable alternative is the previous hour's urine output -50 m. L plus maintenance. ) �Half-normal saline and 5% dextrose in water are commonly used as replacement fluids. �If the hourly requirement exceeds 350 -400 m. L, Desmopressin (DDAVP) is usually administered.

Cerebrospinal Fluid Shunting Procedures �Hydrocephalus is particularly common after SAH. �The ventriculoperitoneal shunt is the most commonly employed device. �Ventriculoperitoneal shunts are done supine.

Anesthetic Management �Invasive monitoring is generally not required. �Moderate hyperventilation (Paco 2 25 to 30 mm Hg) is customary. �Blood pressure may decrease abruptly (as brainstem pressure is relieved) when the ventricle is first cannulated. Infrequently, brief pressor support is required. �Burrowing the subcutaneous tunnel can produce a sudden painful stimulus.

Parkinson's Disease �Management of anesthesia is based on an understanding of the treatment of this disease. �Levodopa therapy should be continued during the preoperative period (administered 20 min before induction). �Orthostatic hypotension, cardiac dysrhythmia and hypertension must be considered. �Droperidol, Alfentanil and Ketamine should not be used.

Multiple Sclerosis �Management of anesthesia �SCh should not be used (in GA) �Spinal anesthesia has been implicated in postoperative exacerbation of MS (vs EA and nerve block) �Efforts must be made during the perioperative period to recognize and prevent even modest increases in body temperature (>1°C), as this change might lead to deterioration of nerve tissue.

Protection of cervical spine �cervical spine Injury Awake fiberobtic intubation Three providers are required to: ventilate the patient, hold cricoid pressure, and provide in-line cervical stabilization; �a fourth provider to administer anesthetic medications

Traumatic Brain Injury �Brain injury after trauma is classified as mild, moderate, �or severe, depending on the GCS score on admission. �Mild: GCS=13 -15 �Moderate: GCS=9 -12 �Severe: GCS≤ 8

Airway and Ventilatory Management With adequate volume resuscitation, PEEP does not increase ICP, nor does lower cerebral perfusion pressure (CPP) Hyperventilation therapy, long a mainstay in the management of patients with TBl, is no longer an appropriate treatment unless signs of imminent herniation are present. Current guidelines suggest maintenance of Pa. CO 2 at 35 mm. Hg with hyperventilation to 30 mm. Hg only for episodes of elevated ICP that cannot be controlled with sedatives, CSF deranging, neuromuscular blockage, osmotic agents, or barbiturate coma.

Circulation ü Patients with severe TBI should have systolic SBP higher than 110 mm. Hg with a goa 1 of achieving MAP greater than 90 mm. Hg (to allow for a minimum CPP of 70 mm. Hg) until ICP monitoring is instituted and CPP can be directly targeted. ü Correction of anemia from blood loss is the first priority, with a goal of maintaining hematocrit greater than 30%

Management of Intracranial and Cerebral Perfusion Pressure Most authors support treatment of ICP greater than 20 to 25 mm. Hg. Patients with sever head injury (defined as a GCS <8) and abnormal head CT findings (hematoma, contusions, edema, or compressed basal cisterns) should be managed with the aid of ICP monitoring. In addition, patients should be monitored if they have severe TBI, normal head CT findings, and any of the following: age > 40 years, motor posturing, or SBP< 90 mm. Hg.

Escalating therapy for severe traumatic brain injury.

Spinal Cord Injury v. Cervical spine injuries causing quadriplegia are accompanied by significant hypotension because of inappropriate vasodilatation and loss of cardiac inotropy (neurogenic shock). v. Autonomic hyperreflexia develops in 85%, of patients with a complete injury above T 5 because of excessive sympathetic response to stimuli below the level of injury, absent the brain's normal damping effect.

Early Supportive Care q. Focused on preservation of adequate perfusion. Hypoxemia must be avoided at all costs, and MAP should be maintained at a normal to high level. q. Emergency intubations are performed, with inclusion of manual in-line axial stabilization. q. In the acute setting (< 24 hours from the moment of injury), succinylcholine can be safely used in patients with SCI. q. Ventilatory support is absolutely required for patients with a deficit above C 4 because they will lack diaphragmatic function. q. Patients with deficits from C 4 to C 7 will still need support, because of lost chest wall innervation, paradoxical respiratory motion, and inability to clear secretions.

Intraoperative Management of Spinal Cord Injury § Direct laryngoscopy with in-line stabilization is appropriate in the emergency setting and in unconscious, combative, or hypoxemic patients when the status of the spine is not known. § In the OR, an awake, alert, and cooperative patient can be intubated by a number of different methods known to produce less displacement of the cervical spine and presumably less risk of worsening an unstable SCI. § Awake fiheroptic intubation (the most common technique) § Blind nasal intubation § Intubating LMA § Bullard laryngoscope