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Anesthetic Management of Head Trauma

Head trauma or traumatic brain injury (TBI) is one of the most serious, life-threatening conditions in trauma victims. Prompt and appropriate therapy is necessary to obtain a favorable outcome. Anesthesiologists manage these patients throughout their perioperative course, taking them from the emergency room to the neuroradiology suite, the operating room, and the neurointensive care unit.
The perioperative management of patients with head injuries focuses aggressively on the stabilization of the patient and the avoidance of the systemic and intracranial insults that cause secondary neuronal injury. These secondary insults, while potentially preventable and treatable, can complicate the course of patients with head injuries and adversely affect outcome.

I. Head injury practice guidelines

Evidence-based guidelines for the management of severe TBI were published in 2000 after an extensive review of the literature. Three standards on the basis of Class I evidence and several guidelines on the basis of Class II evidence were recommended. In March 2006, the Brain Trauma Foundation and the Congress of Neurological Surgeons published new guidelines. This review presents literature-based recommendations for the surgical management of TBI.

II. Classification of head injury

Head injury is classified into primary injury and secondary injury. This classification is useful when considering therapeutic strategies.
Primary injury is the damage produced by a direct mechanical impact and the acceleration-deceleration stress onto the skull and brain tissue, resulting in skull fractures (cranial vault, skull base) and intracranial lesions. The intracranial lesions are further classified into two types: diffuse injury and focal injury.
Diffuse brain injury includes two categories.
Brain concussion is loss of consciousness lasting <6 hours.
Diffuse axonal injury is traumatic coma lasting >6 hours.
Focal brain injury includes the following types:
Brain contusion is usually located either below or opposite the region of impact.
Epidural hematoma is often caused by skull fracture and laceration of the middle meningeal artery.
Subdural hematoma is usually caused by the tearing of the bridging veins between the cerebral cortex and draining sinuses. Acute subdural hematoma is often associated with high mortality.
Intracerebral hematoma is usually located in the frontal and temporal lobes and visualized as a hyperdense mass on a computed tomographic (CT) scan. Brain tissue destroyed by the primary impact will not be saved. Therefore, functional outcome is improved by prompt surgical intervention and medical therapy.
Indications for surgery. Presently, no definitive therapeutic measure exists to treat diffuse axonal injury. Most open and depressed skull fractures and compound skull fractures with dural laceration require early surgical repair. Uncomplicated basal fractures usually do not require operation. The presence of compression of the basal cisterns from a brain contusion indicates operative intervention because of the risk of herniation (usually of the temporal lobe). Intracranial hematoma is the most common sequela of head trauma requiring surgical treatment.
Secondary injuries develop within minutes, hours, or days of the initial injury and cause further damage to nervous tissue. The common denominators of secondary injury are cerebral hypoxia and ischemia. Secondary injuries are caused by the following disorders:
Respiratory dysfunction (hypoxemia, hypercapnia).
Cardiovascular instability (hypotension, low cardiac output).
Elevation of intracranial pressure (ICP).
Biochemical derangements.

III. Pathophysiology of head trauma

Comprehensive management requires an understanding of the pathophysiologic responses to TBI.
Systemic effects of head trauma
Cardiovascular responses to head trauma are commonly observed in the early stage. They include hypertension, tachycardia, and increased cardiac output. Patients with severe head injuries and those suffering from multiple systemic injuries with substantial blood loss, however, may develop hypotension and a decrease in cardiac output. Systemic hypotension (systolic blood pressure of <90 mm Hg) at the time of admission to the hospital is associated with significantly increased morbidity and mortality.
Respiratory responses to head trauma include apnea and abnormal respiratory patterns. Respiratory insufficiency and spontaneous hyperventilation often occur. Patients may also suffer from aspiration of vomitus and central neurogenic pulmonary edema.
Temperature regulation may be disturbed, and hyperthermia, if it occurs, can provoke further brain damage.
Changes in cerebral circulation and metabolism.
In focal brain injury, cerebral blood flow (CBF) and cerebral metabolic rate for oxygen consumption (CMRo₂) decrease in the core area of injury and in the penumbra, an area of hypoperfused tissue that surrounds the damaged tissue. When ICP increases, diffuse and more marked hypoperfusion and hypometabolism ensue.
In diffuse brain injury, hyperemia may occur. In most cases, however, CBF decreases within a few hours of head trauma. The combination of hypotension and impaired autoregulation exacerbates cerebral ischemia. The chemical-metabolic regulation of CBF may also be impaired. The combination of these pathophysiologic responses to head injury creates a complicated management scenario.
Acute brain swelling and cerebral edema
Acute brain swelling is provoked by a decrease in vasomotor tone and a marked increase in the volume of the cerebral vascular bed. In this situation, increases in blood pressure can easily lead to further brain swelling and an increase in ICP.
Cerebral edema following head trauma is often a mixture of vasogenic and cytotoxic types caused by blood-brain barrier disruption and ischemia, respectively.
Following head trauma, both acute brain swelling and edema ensue concurrently. When these pathologic conditions occur in association with an intracranial hematoma, the resultant intracranial hypertension causes a further reduction in CBF with cerebral ischemia. Eventually, intracranial hypertension, if untreated, leads to herniation of the brain stem through the foramen magnum.
Excitotoxicity. Head trauma causes excessive release of glutamate from neurons and glia, increasing the concentration of glutamate in the cerebrospinal fluid (CSF). The biochemical changes associated with the excessive release of glutamate and the activation of glutamate receptors are closely related to an increase in intracellular calcium ion, which triggers a number of events that lead to the damage. These include an activation of phospholipase, protein kinase, proteases, nitric oxide synthase, and other enzymes. Activation of these enzymes also produces lipid peroxidation, proteolysis, free radical formation, deoxyribonucleic acid (DNA) damage, and finally, neuronal death (Figure -1).

 

Figure-1. Excitotoxicity in head injury. AMPA, alpha-amino-3-hydroxy-5-methyl-4-isoxazoleproprionate; NMDA, N-methyl-d-aspartate; [Ca]i, intracellular Ca.

Inflammatory cytokines and mediators. The cytokines are major mediators in the initiation of inflammatory and metabolic responses to injury. Cytokines increase in response to cerebral ischemia. Interleukin-6 (IL-6) and tumor necrosis factor alpha are known to be released after TBI. Patients who have Glasgow Coma Scale (GCS) scores of <8 show a higher and more sustained elevation of IL-6. The cytokines released after TBI stimulate the production of free radicals and arachidonic acids and upregulate the activity of the adhesion molecules, which produce disturbances in the microcirculation. All of these changes contribute to secondary brain injury.

IV. Emergency management

Initial assessment of the patient's condition
Neurologic assessment. There is usually little time initially to evaluate the patient's neurologic condition thoroughly. However, a quick neurologic assessment can be performed while stabilizing the patient to achieve adequate ventilation (oxygenation and carbon dioxide [CO₂] elimination) and hemodynamic stability.
GCS (Table -1) is a simple and universally accepted method for assessing consciousness and neurologic status in patients with head injuries. The GCS has low interobserver variability and is a good predictor of outcome.
(1) GCS score of <8 characterizes severe head injury.
(2) GCS score of 9 to 12 represents moderate injury.
(3) GCS score of 13 to 15 represents mild injury.
Pupillary responses (size, light reflex) and symmetry of motor function in the extremities should be quickly assessed.
Assessment of injuries to other organs. Trauma patients often suffer from injuries to multiple organ systems. Particular attention should be paid to determine whether there is evidence of intrathoracic or intraperitoneal (intrapelvic) hemorrhage. If bleeding is suspected, the thorax or abdomen should be explored without delay.
Treatment of hemorrhagic shock takes precedence over neurosurgical procedures. The patient's hemoglobin must be measured immediately, and blood and fresh-frozen plasma should be set up and made available for infusion.
Establishment of airway and ventilation
Tracheal intubation. The first step in emergency therapy is to secure an open airway and ensure adequate ventilation. Because all trauma patients are considered to have a full stomach and frequently (approximately 10%) have an associated cervical spine injury as well, cricoid pressure and in-line stabilization of the cervical spine are used during laryngoscopy and intubation.
If facial fractures and soft tissue edema prevent direct visualization of the larynx, either fiberoptic intubation or intubation with an illuminated stylet may be attempted. In the presence of either severe facial injuries or laryngeal trauma a cricothyrotomy may be required. Nasal intubations are avoided in the presence of a suspected basal skull fracture, severe facial fractures, and bleeding diathesis.

 

Table -1. Glasgow Coma Scale
Adult Scale		Pediatric Scale
Parameter	Score	Parameter	Score
Eye opening		Eye opening
Spontaneously	4	Spontaneously	4
To speech	3	To speech	3
To pain	2	To pain	2
None	1	None	1
Best verbal response		Best verbal responsea
Oriented	5	Oriented to place	5	>5 y
Confused	4	Words	4	>12 mo
Inappropriate	3	Vocal sounds	3	>6 mo
Incomprehensible	2	Cries	2	<6 mo
None	1	None	1
Best motor response		Best motor response in upper limbsa
Obeys commands	6	Obeys commands	6	>2 y
Localizes to pain	5	Localizes to pain	5	6 mo-2 y
Withdraws from pain	4	Normal flexion to pain	4	>6 mo
Flexes to pain	3	Spastic flexion to pain	3	<6 mo
Extends to pain	2	Extension to pain	2
None	1	None	1
aScore highest appropriate for age.

Nasal intubation also adds risk to patients who have basilar skull fractures because of the introduction of contaminated material into the brain. Basilar skull fractures are strongly suspected when hemorrhage of the tympanic cavity, otorrhea, petechiae on the mastoid process (Battle's sign), and petechiae around the eyes (panda sign) are observed.
Mechanical ventilation. As soon as the trachea has been intubated, a nondepolarizing muscle relaxant is administered and mechanical ventilation to a partial arterial pressure of carbon dioxide (Paco₂) of approximately 35 mm Hg is instituted. Aggressive hyperventilation (Paco₂ of <30 mm Hg) should be avoided unless transtentorial herniation is suspected. Hypoxemia, if present, should be corrected immediately. Hyperoxia may be recommended. If massive aspiration is suspected, bronchial suctioning using a fiberscope is advisable before transferring the patient to either the neuroradiology suite or the operating room.
Cardiovascular stabilization. Systemic hypotension is one of the major contributors to poor outcome after head trauma. When necessary, fluid resuscitation is initiated immediately and inotropic and vasopressor drugs are administered as required to stabilize the blood pressure.
Fluid resuscitation. Hypovolemia is often masked by a relatively stable blood pressure secondary to either sympathetic hyperactivity or the reflex response to increased ICP. Therefore, fluid resuscitation should be guided not only by blood pressure but also by urinary output and central venous pressure (CVP).
Crystalloid and colloid solutions. Isotonic and hypertonic crystalloid solutions and colloid solutions may be given to maintain adequate intravascular volume.
(1) Lactated Ringer's solution is slightly hypotonic relative to plasma, which precludes the use of a substantial amount. If administered, serum osmolarity should be measured periodically. When large-volume resuscitation with crystalloid is required, an isotonic crystalloid, such as normal saline, is preferable.
(2) Hypertonic saline (3%, 7.5%) can be beneficial in small amounts after TBI. Large volumes may produce a lethal increase in serum sodium concentration.
(3) Hydroxyethyl starch (HES) and human plasma products can be administered to maintain intravascular volume for longer periods. No more than 1.5 L of HES should be administered in conjunction with careful monitoring of blood coagulation. The incidence of coagulopathy in patients with head injuries is approximately 20%, and HES in large amounts is known to interfere with blood coagulation. The reported incidence of coagulopathy is less with pentastarch.
Blood and blood products. Patients who have a low hematocrit may require a transfusion to optimize oxygen delivery; the hematocrit ideally is maintained above 30%. Children require special attention because they can easily become hypovolemic by losing large volumes of blood into an intracranial or subgaleal hematoma or through a scalp laceration, even without blood loss in other organ systems.
Adverse effect of glucose-containing solutions. Glucose-containing solutions are avoided because hyperglycemia is associated with worsened neurologic outcomes. Glucose should be used only to treat hypoglycemia. The plasma level of 80 to 150 mg/dL is desirable; values above 200 mg/dL should be avoided and treated with insulin.
Inotropics and vasopressors. If the blood pressure and cardiac output cannot be restored through fluid resuscitation, the administration of intravenous inotropic and vasopressor drugs may be necessary. An infusion of either phenylephrine or dopamine is recommended to maintain cerebral perfusion pressure (CPP), the difference between the mean arterial pressure (MAP) and the ICP, above 60 mm Hg.
Management of elevated ICP. The reduction of elevated ICP and the maintenance of blood pressure are crucial in the management of intracranial hypertension because CPP is directly related to both MAP and ICP.
Hyperventilation. When evidence of transtentorial herniation in patients with severe head injuries exists, hyperventilation to a Paco₂ of 30 mm Hg should be instituted because hyperventilation can rapidly and effectively reduce ICP. Hyperventilation was previously thought to be more effective in children than in adults because of the idea that pediatric patients, unlike adults, responded to TBI with acute brain swelling from hyperemia. The accumulation of recent data has revealed, however, that hyperemia may not occur as commonly in severe pediatric TBI. The initial response of both adult and pediatric patients to TBI is more often hypoperfusion. Aggressive hyperventilation to a Paco₂ of <30 mm Hg can therefore aggravate ischemia through excessive vasoconstriction. To avoid this risk, other measures, including diuretic therapy, barbiturate therapy, and CSF drainage, should be instituted. The Paco₂ is allowed to return toward normal as soon as possible.
Diuretic therapy. Mannitol, 1 g/kg intravenously (i.v.) infused over 10 minutes, is administered to patients in whom transtentorial herniation is suspected. In less acute cases, an infusion of 0.25 to 1 g/kg may be administered over 10 to 20 minutes and repeated every 3 to 6 hours. The serum osmolarity is monitored frequently and should not exceed 320 mOsm/L.
Posture. A head-up tilt of 10° to 30° facilitates cerebral venous and CSF drainage and lowers ICP. This ICP-reducing effect is negated when systemic blood pressure decreases.
Corticosteroids. Corticosteroids were previously thought to be of value in reducing brain edema and hence ICP in patients with head trauma. However, recent reports have demonstrated worsened outcomes with the use of corticosteroids. Steroids also increase blood glucose levels, which can adversely affect the injured brain. Corticosteroids, therefore, have no place in the treatment of head injury despite their proven efficacy in spinal cord injury.
Barbiturates. Barbiturates are known to exert cerebral protective and ICP-lowering effects. High-dose barbiturate therapy may be considered in patients with severe head injuries whose intracranial hypertension is refractory to maximal medical and surgical ICP-lowering therapy. When considering the institution of high-dose barbiturate therapy, hemodynamic stabilization of the patient is a prerequisite. The prophylactic use of barbiturate coma is not indicated.

V. Anesthetic management

Anesthesia. The major goals of anesthetic management are to (a) optimize cerebral perfusion and oxygenation, (b) avoid secondary damage, and (c) provide adequate surgical conditions for the neurosurgeons. General anesthesia is recommended to facilitate control of respiratory and circulatory function.
Induction of anesthesia. Most patients who have severe head injury have already had an endotracheal tube inserted either during triage in the emergency department or for their CT examination. The patient who comes to the operating room without endotracheal intubation is treated with immediate oxygenation and securing of the airway. Anesthesiologists must be aware that these patients often have a full stomach, decreased intravascular volume, and a potential cervical spine injury.
Direct arterial pressure monitoring by an indwelling arterial catheter inserted before the induction of anesthesia is recommended. Either the radial artery or the dorsalis pedis artery may be cannulated, depending on other sites of injury.
Several induction techniques are recommended. The patient's presentation and hemo-dynamic stability determine the choice.
Rapid sequence induction may be desirable in hemodynamically stable patients, although this procedure can produce an elevation in blood pressure and ICP. During administration of 100% oxygen, an induction dose of thiopental, 3 to 4 mg/kg, or propofol, 1 to 2 mg/kg, and succinylcholine, 1.5 mg/kg, is administered and the trachea is intubated. Etomidate, 0.2 to 0.3 mg/kg, may be administered in patients in whom the circulatory status is concerning. In hemodynamically unstable patients, the dose of induction drugs is substantially decreased or even omitted. However, cardiovascular depression is always a concern, especially in hypovolemic patients.
Succinylcholine has been shown to increase ICP. The prior administration of small doses of a nondepolarizing muscle relaxant may prevent this increase but not predictably. Succinylcholine remains a good choice, however, to facilitate rapid laryngoscopy and to secure the airway. Rocuronium, 0.6 to 1 mg/kg, is an excellent alternative because of its rapid onset of action and lack of effect on intracranial dynamics.
Intravenous induction. When the patient is stable and does not have a full stomach, anesthesia can be induced by titrating the dose of either thiopental or propofol to minimize circulatory instability. An intubating dose of a nondepolarizing muscle relaxant is given with or without priming to facilitate intubation within a short period of time. For example, rocuronium, 0.6 to 1 mg/kg, allows satisfactory intubating conditions within 60 to 90 seconds. Fentanyl, 1 to 4 mcg/kg i.v., is administered to blunt the hemodynamic response to laryngoscopy and intubation. Lidocaine, 1.5 mg/kg i.v., given 90 seconds before laryngoscopy, can help prevent the increase in ICP.
A large-bore oral gastric tube is inserted after intubation, and gastric contents are initially aspirated and then passively drained during the operation. Nasal gastric tubes are avoided because of the potential presence of a basilar skull fracture.
Maintenance of anesthesia. The ideal drug for maintenance of anesthesia should reduce ICP, maintain adequate oxygen supply to the brain tissue, and protect the brain against ischemic-metabolic insult. No gold-standard anesthetic drug fulfills these requirements for head injury. The selection of anesthetic drugs is based on a consideration of the intracranial pathology as well as systemic conditions such as cardiopulmonary disturbances and the presence of multisystem trauma.
Anesthetics
(1) Intravenous anesthetics
(a) Barbiturates. Thiopental and pentobarbital decrease CBF, cerebral blood volume (CBV), and ICP. The reduction in ICP with these drugs is related to the reduction in CBF and CBV coupled with metabolic depression. These drugs will also have these effects in patients who have impaired CO₂ response.
Thiopental and pentobarbital have been shown in animal models to protect against focal brain ischemia. In head injury, ischemia is a common sequela. Although barbiturates might be effective in head injury, no prospective, randomized clinical trial has demonstrated that they definitely improve outcome after TBI. In addition, barbiturates can be detrimental in patients with head injuries because of their cardiovascular-depressant effect. Also, when barbiturates are administered for prolonged periods, their duration of action is increased.
(b) Etomidate. As with barbiturates, etomidate reduces CBF, CMRo₂, and ICP. Systemic hypotension occurs less frequently than with barbiturates. Prolonged use of etomidate may suppress the adrenocortical response to stress.
(c) Propofol. The cerebral hemodynamic and metabolic effects of propofol are similar to those of barbiturates. Propofol might be useful in patients who have intracranial pathology if hypotension is avoided. Because the context-sensitive half-life is short, emergence from anesthesia is rapid, even after prolonged administration. This may offer an advantage over other intravenous anesthetics in providing the opportunity for early postoperative neurologic evaluation. Because of propofol's potent circulatory depressant effect, however, meticulous care should be exercised to maintain adequate CPP, including the correction of hypovolemia prior to administering propofol. Recent studies have shown a reduction in jugular bulb oxygen saturation during propofol anesthesia. Propofol can also reduce CBF more than CMRo₂, producing ischemia under certain conditions. Therefore, care should be taken when hyperventilating patients during propofol anesthesia.
(d) Benzodiazepines. Diazepam and midazolam may be useful either for sedating patients or inducting anesthesia because these drugs have minimal hemodynamic effects and are less likely to impair cerebral circulation. Diazepam, 0.1 to 0.2 mg/kg, may be administered for inducting anesthesia and repeated, if necessary, up to a total dose of 0.3 to 0.6 mg/kg. Midazolam, 0.2 mg/kg, can be used for induction and repeated as necessary.
(e) Narcotics. In clinical doses, narcotics produce a minimal to moderate decrease in CBF and CMRo₂. When ventilation is adequately maintained, narcotics probably have minimal effects on ICP. Despite its small ICP-elevating effect, fentanyl provides satisfactory analgesia and permits the use of lower concentrations of inhalational anesthetics. Some reports have shown that sufentanil increases ICP in patients with severe head injuries. This could result from the autoregulatory response (i.e., cerebral vasodilatation) to the sudden decrease in systemic blood pressure. When these drugs are used, measures to maintain systemic blood pressure need to be implemented.
(2) Inhalational anesthetics
(a) Isoflurane. A potent metabolic depressant, isoflurane has less effect on CBF and ICP than halothane has. Because isoflurane depresses cerebral metabolism, it may have a cerebral protective effect when the ischemic insult is not severe. Data favor the use of isoflurane over either halothane or enflurane. Isoflurane in concentrations of >1 minimum alveolar concentration should be avoided, however, because it can cause substantial increases in ICP.
(b) Sevoflurane. In the rabbit cryogenic brain-injury model, the elevation of ICP occurring in association with an elevation in blood pressure was higher in the animals anesthetized with sevoflurane than with halothane. Clinical studies have demonstrated, however, that sevoflurane's effect on cerebral hemodynamics is either similar to or milder than that of isoflurane. The disadvantage of sevoflurane is that its biodegraded metabolite may be toxic in high concentrations. There is no evidence of an adverse effect at clinically used concentrations, however, unless sevoflurane is administered in a low-flow circuit for prolonged periods. Rapid emergence from anesthesia with sevoflurane may be an advantage because it facilitates early postoperative neurologic evaluation.
(c) Desflurane. Desflurane at high concentrations appears to increase ICP.
(d) Nitrous oxide (N₂O). N₂O dilates cerebral vessels, thereby increasing ICP. Patients who have intracranial hypertension or a decrease in intracranial compliance should, therefore, not receive this drug. N₂O should also be avoided in the presence of pneumocephalus or pneumothorax because it diffuses into an airspace more rapidly than the nitrogen diffuses out, thereby increasing the volume within the airspace.
(3) Local anesthetic. The infiltration of either lidocaine 1% or bupivacaine 0.25%, with or without epinephrine, in the skin around the scalp incision and the insertion sites for the pin head holder is helpful in preventing systemic and intracranial hypertension in response to these stimuli and avoiding the unnecessary use of deep anesthesia.
(4) Muscle relaxants. Adequate muscle relaxation facilitates appropriate mechanical ventilation and reduces ICP. Coughing and straining are avoided because both can produce cerebral venous engorgement.
(a) Vecuronium appears to have minimal or no effect on ICP, blood pressure, or heart rate and would be effective in patients with head injuries. This drug is given as an initial dose of 0.08 to 0.1 mg/kg followed by infusion at a rate of 1 to 1.7 mcg/kg/minute.
(b) Pancuronium does not produce an increase in ICP but can cause hypertension and tachycardia because of its vagolytic effect, thereby increasing the patient's risk.
(c) Atracurium has no effect on ICP. Because of its rapid onset and short duration of action, a bolus dose of 0.5 to 0.6 mg/kg followed by a continuous infusion at a rate of 4 to 10 mcg/kg/minute is administered with monitoring of neuromuscular blockade.
(d) Rocuronium is useful for intubation because of its rapid onset of action and lack of effect on intracranial dynamics. For maintenance, drugs with longer durations of action are recommended.
Intraoperative respiratory and circulatory management
Mechanical ventilation. Mechanical ventilation is adjusted to maintain a Paco₂ of around 35 mm Hg. The fraction of inspired oxygen (Fio₂) is adjusted to maintain a Pao₂ of >100 mm Hg.
Patients, especially those who have pulmonary contusion, aspiration, or central neurogenic pulmonary edema, may require positive end-expiratory pressure (PEEP) to maintain adequate oxygenation. Excessive PEEP should be avoided, however, because the elevation in intrathoracic pressure can compromise cerebral venous drainage and increase ICP.
Circulatory management. CPP should be maintained between 60 and 110 mm Hg. The transducer for direct monitoring of arterial blood pressure is zeroed at the level of mastoids to reflect the cerebral circulation.
When hypotension persists despite adequate oxygenation, ventilation, and fluid replacement, careful elevation of the blood pressure with a continuous infusion of an inotrope or vasopressor may be necessary. Phenylephrine, 0.1 to 0.5 mcg/kg/minute, and dopamine, 1 to 10 mcg/kg/minute, are appropriate drugs in this setting. A bolus dose of vasopressor must be used cautiously because abrupt increases in blood pressure can elevate ICP to dangerous levels, especially in patients who have disordered autoregulation.
Hypertension is treated cautiously because the elevation in blood pressure may reflect compensatory hyperactivity of the sympathetic nervous system in response to elevated ICP and compression of the brain stem (Cushing's reflex). Adequate oxygenation, ventilation, volume replacement, and analgesia should be first assessed and corrected. When necessary, an antihypertensive drug, such as either labetalol or esmolol, which has minimal cerebral vasodilating effects, should be administered. When treating hypertension, maintenance of CPP is a major concern.
Intraoperative management of elevated ICP
Patient's posture. A slight head-up tilt of 10° to 30° is desirable. CPP might not be improved, however, if systemic blood pressure decreases substantially. When the surgeon requests either rotation or flexion of the head and the neck, the anesthesiologist must ensure the adequacy of venous return.
Ventilation. The Paco₂ is maintained at around 35 mm Hg. Hyperventilation is best avoided unless monitoring ensures adequate brain oxygenation.
Circulation. Both hypotension (systolic blood pressure of <90 mm Hg) and hypertension (systolic blood pressure of >160 mm Hg) should be corrected when indicated.
Diuretics
(1) Mannitol decreases cerebral volume and reduces ICP.
(2) Furosemide may be coadministered in severe cases as well as in the patient who has compromised cardiac function and the potential for heart failure. Furosemide, 0.1 to 0.2 mg/kg, is given 15 minutes before mannitol administration. When furosemide and mannitol are administered, careful monitoring of intravascular volume either by CVP or pulmonary artery pressure is necessary.
Ventilation, oxygenation, depth of anesthesia, and last dose of diuretics should be assessed in the patient if protrusion of the brain is observed after craniotomy. If all are adequate, additional thiopental (or pentobarbital) may be indicated. More vigorous hyperventilation is also an option with careful monitoring of brain oxygenation. If these measures fail, decompressive craniectomy may be necessary.
CSF drainage. If an intraventricular catheter is in place, CSF drainage is an effective and reliable technique for reducing ICP.
Monitoring
Standard monitoring includes heart rate and rhythm (electrocardiogram), noninvasive and direct arterial blood pressure measurement, pulse oximetry, end-tidal CO₂, body temperature, urinary output, CVP, and neuromuscular blockade. Arterial blood gases, hematocrit, electrolytes, glucose, and serum osmolarity should be measured periodically.
Monitoring for air embolism. Detection of venous air embolism by Doppler ultrasound should be considered for surgical procedures in which veins in the operative site are above the level of the heart.
Brain monitoring as with an electroencephalogram, evoked potentials, jugular venous bulb oxygen saturation (Sjo₂), flow velocity measured by transcranial Doppler (TCD), brain tissue Po₂ (btPo₂), and ICP may be used.
1. Sjo₂. The Sjo₂ provides continuous information about the balance between global cerebral oxygen supply and demand. An Sjo₂ of <50% for >15 minutes is a poor prognostic sign and is often associated with a poor neurologic outcome. The decrease in Sjo₂ could be caused by excessive hyperventilation, decreased CPP, cerebral vasospasm, or a combination. The major causes of a decrease in Sjo₂ and their treatment are listed in Table -2.
2. Flow velocity of basal cerebral arteries as measured by the TCD technique is helpful in assessing the cerebral circulatory state at the bedside. However, it does not provide an absolute value for the CBF. High-normal values may indicate hyperemia or vasospasm. The TCD waveform can differentiate between these two conditions. A disadvantage of this monitor is that the application of the Doppler probe is not always possible during the surgical procedure.
3. Near-infrared spectroscopy, currently available in clinical practice, provides relative information about changes of oxy- and deoxyhemoglobin and the cytochrome oxidase redox status in the brain tissue of interest in a noninvasive and continuous fashion.
4. ICP. The association between severity of ICP elevation and poor outcome is well known. Monitoring ICP is useful, therefore, not only as a guide to therapy, but also for assessing the response to the therapy and determining the prognosis.

Table -2. Major causes of decreased Sjo2a and treatment
Cause	Clinical condition	Treatment
Cao2	Hypoxemia	Correction of hypoxemia
	Anemia	Blood transfusion
CBF	Hypotension	Fluid replacement; inotropics and vasopressors
	Hyperventilation	Correction of Paco2
	Intracranial hypertension	Mannitol, furosemide, barbiturate, propofol
CMRo2	Hyperthermia	Cooling
	Seizures	Barbiturate, propofol
Cao2, oxygen content in arterial blood; CBF, cerebral blood flow; CMRo2, cerebral metabolic rate for oxygen consumption.
aSjo2 OC[Cao2-CMRo2/CBF].

5. btPo₂. A probe for the determination of btPo₂ is available. A btPo₂ of <10 mm Hg is assumed to convey the risk of hypoxic injury. The disadvantages of btPo₂ monitoring include the facts that it (a) only provides focal monitoring, (b) cannot be used in the surgical field during operation, and (c) has a critical threshold that is not well determined.

VI. Cerebral protection

Hypothermia. A reduction of body temperature to 33°C to 35°C may confer cerebral protection. Protective mechanisms include a reduction in metabolic demand, excitotoxicity, free radical formation, and edema formation. In an animal ischemia model, mild hypothermia of approximately 34°C to 36°C markedly attenuated ischemic injury. In clinical practice, controversy concerning the effectiveness of hypothermia in head injury still continues. The multi-institutional study of postoperative mild hypothermia in patients with head injury was terminated by its Safety Monitoring Board after enrolling 392 patients (see Clifton G et al.). The results showed no difference in mortality between patients with hypothermia and normothermia, and patients with hypothermia experienced more medical complications. Subgroup analysis revealed that younger patients (45 years of age or younger) who were hypothermic on admission and assigned to the hypothermic group tended to have better outcomes than those assigned to the normothermic group. A new study of this group with an earlier induction of hypothermia and more consistent critical care has been initiated.
When induction of hypothermia is elected, meticulous care is necessary to avoid adverse side effects such as hypotension, cardiac arrhythmias, coagulopathies, and infections. Rewarming should be carried out slowly. Temperature monitoring at two or more sites is recommended and may include the tympanic membrane, nasopharyngeal area, esophagus, and blood.

VII. Postoperative management

Emergence and extubation. Anesthesiologists often receive requests to awaken patients promptly to allow early postoperative neurologic assessment. Patients who had a normal level of consciousness before the operation and who have undergone an uneventful procedure can be awakened and their tracheas extubated in the operating room, assuming that emergence criteria have been satisfactorily met. Smooth emergence with control of systemic blood pressure and avoidance of coughing is necessary to prevent postoperative cerebral edema and hematoma formation.
Contraindications to extubation. Extubation in the operating room is discouraged for patients whose level of consciousness was depressed preoperatively and in whom brain swelling is either marked during operation or expected to occur postoperatively. Patients who have sustained multiple traumatic injuries are also candidates for postoperative ventilation. Patients who are hypothermic during emergence should be mechanically ventilated postoperatively and their tracheas extubated after careful rewarming.

VIII. Summary

The major goal of perioperative management of patients with head injuries is to prevent secondary damage. Therapeutic measures based on established guidelines and recommendations must be instituted promptly and continued throughout the perioperative course. Appropriate selection of anesthetics and meticulous general management of respiration, circulation, metabolism, fluid replacement, and temperature are all essential to improve outcome.