Anesthetic goals for intracranial procedures include hypnosis, amnesia, immobility, control of ICP and CPP, and a “relaxed brain” (ie, optimal surgical conditions). Whenever possible, promptly following the procedure, the anesthetist should endeavor to provide an awake and interactive, extubated patient who can be evaluated neurologically by the neurosurgical team.

1. Induction of anesthesia must be accomplished without increasing ICP or compromising CBF. Hypertension, hypotension, hypoxia, hypercarbia, and coughing should be avoided.
   1. While thiopental ([not available in the United States] 3-7 mg/kg), propofol (1.0-2.5 mg/kg), midazolam (0.2-0.4 mg/kg), and etomidate (0.3-0.4 mg/kg) are all reasonable IV induction agents, the hemodynamic effects caused by these agents should be carefully considered.
   2. An adequate mask airway is essential to prevent hypoventilation and increased PaCO₂. After induction, hyperventilation by mask can be started with either a nitrous oxide–oxygen mixture or 100% oxygen.
   3. An intubating dose of muscle relaxant is given. Nondepolarizing agents are commonly chosen. Adequate relaxation should be obtained before laryngoscopy and intubation to avoid coughing and straining.
   4. Opioids cause minimal changes in cerebral hemodynamics and are useful in blunting responses to intubation and craniotomy. Because intubation, placement of head pins, and craniotomy (skin incision and manipulation of the periosteum) are the most physiologically stimulating periods during intracranial procedures, generous doses of narcotics are given before these manipulations. Fentanyl (5-10 μg/kg) and remifentanil are most commonly used because both have rapid onset and high potency. Lidocaine (1.5 mg/kg IV) or esmolol (~0.5 mg/kg IV) can also be used to attenuate the cardiovascular and ICP responses to intubation.
   5. Low concentrations of a potent volatile agent are occasionally added to prevent hypertension during the initial surgical stimulation.
   6. After intubation, the eyes are covered with watertight patches to prevent irritation from surgical preparation solutions, and the head is carefully checked after final positioning to ensure good venous return. Because access to the airway is limited during neurosurgical procedures, breath sounds and ventilation should be checked after final positioning to ensure proper placement of the endotracheal tube, the tube should be adequately secured, and all connections in the breathing circuit should be securely tightened.
2. Maintenance
   1. Adequate brain relaxation is necessary before opening the dura. This is achieved by ensuring adequate oxygenation, venous return, muscle relaxation, anesthetic depth, a PaCO₂ of 33 to 35 mm Hg (hyperventilation if dictated by surgical field), and often the administration of furosemide (10-20 mg IV), mannitol (0.5-1.5 g/kg IV), and dexamethasone before the craniotomy is completed. The surgeon can then assess the need for further brain relaxation by checking the tension of the dura. If necessary, additional IV thiopental can be administered or CSF can be drained through a previously placed lumbar subarachnoid catheter.
   2. Anesthetic requirements are substantially lower after craniotomy and dural opening because the brain parenchyma is devoid of sensation. If supplemental narcotics are needed, small doses of morphine or fentanyl can be given. A continuous infusion of propofol (50-150 μg/kg/min) and/or remifentanil (0.1-0.5 μg/kg/min) produces a stable level of anesthesia and allows for a rapid emergence. Large doses of long-acting narcotics and sedatives are usually avoided during the last 1 to 2 hours of the procedure to facilitate neurologic examination at the end of surgery and avoid potential drowsiness and hypoventilation.
   3. Muscle relaxants are frequently continued throughout the procedure to prevent movement. Patients receiving anticonvulsants (eg, phenytoin) may require more frequent administration of muscle relaxants.
3. Emergence should occur promptly without straining or coughing. IV lidocaine may be administered to suppress the cough reflex but may delay emergence. Toward the end of the procedure, PaCO₂ is normalized gradually if hyperventilation was employed. Hypertension should be controlled to minimize bleeding; rapidly acting IV agents such as labetalol, esmolol, sodium nitroprusside, and nitroglycerin are often used. Muscle relaxation is usually maintained until the head dressing is completed and then reversal agents are administered. Before leaving the operating room, the patient should be awake and responsive so that a brief neurologic examination can be performed. The differential diagnosis of persisting unconsciousness after discontinuation of all anesthetics should include residual anesthesia, narcosis, hypothermia, hypoxia, hypercapnia, partial neuromuscular blockade, metabolic causes, and surgically induced increases in ICP (bleeding, edema, and hydrocephalus). Physostigmine (0.01-0.03 mg/kg IV) or naloxone (0.04-0.4 mg IV) may help antagonize pharmacologically induced CNS depression. The presence of new localized or generalized neurologic deficits should be immediately addressed and may be evaluated by CT and/or surgical reexploration.
4. Perioperative fluid management is designed to decrease brain water content, thereby reducing ICP and providing adequate brain relaxation, while maintaining hemodynamic stability and CPP.
   1. The blood-brain barrier is selectively permeable. Gradients for osmotically active substances ultimately determine the distribution of fluids between the brain and intravascular spaces.
      1. Water freely passes through the blood-brain barrier. Intravascular infusion of free water may increase brain water content and may elevate ICP. Isoosmotic glucose solutions (eg, 5% dextrose in water) have the same effect because the glucose is metabolized, and free water remains. As such, these are usually avoided during neurosurgery.
      2. The blood-brain barrier is impermeable to most ions including Na⁺. Unlike the peripheral vasculature, total osmolality, rather than colloid oncotic pressure, determines the osmotic pressure gradient across the blood-brain barrier. Consequently, maintenance of high-normal serum osmolality can decrease brain water content, while administration of a large amount of hypoosmolar crystalloid solution may increase brain fluid content.
      3. Large, polar substances cross the blood-brain barrier poorly.Albumin has little effect on brain ECF because the colloid oncotic pressure contributes to only a small portion of total plasma osmolality (approximately 1 mOsm/L).
      4. If the blood-brain barrier is disrupted (eg, by ischemia, head trauma, or tumor), permeability to mannitol, albumin, and saline increases so that these molecules have equal access to brain ECF. Under such circumstances, isoosmolar colloid and crystalloid solutions seem to have similar effects on edema formation and ICP.
   2. Severe fluid restriction can produce marked hypovolemia, leading to hypotension, reduced CBF, and ischemia of the brain and other organs, while only modestly decreasing brain water content. Excessive hypervolemia may cause hypertension and cerebral edema.
   3. Specific treatment recommendations are outlined below. The overarching goal is to maintain normal intravascular volume and to produce a hyperosmolar state.
      1. Fluid losses. The fluid deficit incurred by an overnight fast is usually not replaced. Physiologic maintenance fluids are given. Third spacing of fluids during intracranial surgery is minimal and usually does not warrant replacement. Two-thirds to total intraoperative urine output is replaced with crystalloid. If signs of hypovolemia develop, additional fluid is administered.
      2. Assessment of blood loss may be difficult during intracranial procedures because significant amounts can be hidden under the drapes. Also, irrigating solutions are used generously by the neurosurgeon. As such, the anesthetist should keep track of total irrigation fluids used during the procedure.
      3. The serum osmolality is increased to 305 to 320 mOsm/kg. If large fluid requirements are anticipated, isoosmolar crystalloid solutions such as 0.9% normal saline (309 mOsm/kg) may be preferable to hypoosmolar solutions such as lactated Ringer (272 mOsm/kg). However, large volumes of 0.9% normal saline may cause a metabolic acidosis that can be deleterious to end-organ function. Therefore, it is prudent to follow the arterial blood gases and change to lactated Ringer if indicated. Mannitol (0.5-2.0 g/kg IV) and/or furosemide (5-20 mg IV) are also often administered. The marked diuresis produced by these agents demands close monitoring of intravascular volume and electrolytes.
      4. Hypokalemia may develop from the use of steroids or potassium-wasting diuretics and is exacerbated by hyperventilation. Nevertheless, intraoperative administration of potassium is rarely necessary.
      5. Hyponatremia may be produced by diuretics or syndrome of inappropriate antidiuretic hormone secretion (SIADH).
      6. Hyperglycemia may worsen neurologic outcome after ischemia (Section II.E.2.d). Glucose-containing solutions are avoided in patients at risk for CNS ischemia.
5. Immediate postoperative care. Patients are observed closely in an intensive care setting after most intracranial neurosurgical procedures.
   1. The head of the bed should be elevated 30° to promote venous drainage.
   2. Neurologic function, including the level of consciousness, orientation, pupillary size, and motor strength, should be assessed frequently. Deterioration of any of these may indicate development of cerebral edema, hematoma, hydrocephalus, or herniation.
   3. Adequate ventilation and oxygenation are essential in patients with reduced consciousness.
   4. Continuous monitoring of ICP may be indicated if intracranial hypertension exists at the time of dural closure or is anticipated in the postoperative period.
   5. Serum electrolytes and osmolarity should be checked and corrected as appropriate.
   6. SIADH can be diagnosed by hyponatremia and low serum osmolality with high urine osmolality and is treated by restricting free water intake.
   7. Cerebral salt-wasting syndrome can occur in the setting of brain tumors or injury to the brain. It is characterized by hyponatremia and polyuria. Polydipsia, extreme salt cravings, and dehydration may also be seen. It is a diagnosis of exclusion and can be difficult to distinguish from SIADH, with the main difference being volume status (hypovolemia in cerebral salt wasting syndrome and normal to hypervolemia in SIADH).
   8. Diabetes insipidus may occur after any intracranial procedure but is most common after pituitary surgery. Polyuria is associated with hypernatremia, serum hyperosmolality, and low urine osmolality. Conscious patients can compensate by increasing their fluid intake; otherwise, adequate IV replacement is mandatory. Aqueous vasopressin (5-10 USP units subcutaneously or 3 units/h by IV infusion) may be given. Larger doses may cause hypertension. Alternatively, desmopressin (1-2 mg IV or subcutaneously every 6-12 hours) can be used and is associated with a lower incidence of hypertension than vasopressin.
   9. Seizures may indicate the presence of an expanding intracranial hematoma or cerebral edema. If a seizure occurs, airway patency, oxygenation, and ventilation must be ensured. The patient should be protected from injury and the IV secured. For acute therapy, thiopental (50-100 mg IV), midazolam (2-4 mg IV), or lorazepam (2 mg) may be used. Fosphenytoin (15-20 mg/kg IV, 100-150 mg/min) can be administered to prevent recurrence.
   10. Tension pneumocephalus may occur and should be suspected after failure to awaken from anesthesia. Skull radiographs or head CT scans confirm the diagnosis; treatment consists of opening the dura to release the air.