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Intracranial Hypertension
• Intracranial hypertension is defined as a sustained increase in intracranial pressure (ICP) above 15 mm Hg. Intracranial hypertension may result from an expanding tissue or fluid mass, depressed skull fracture, interference with normal absorption of cerebrospinal fluid (CSF), excessive cerebral blood flow (CBF), or systemic disturbances promoting brain edema.
• Clinical manifestations: Headache, nausea, vomiting, papilledema, focal neurologic deficits, and altered consciousness; Periodic increases in arterial blood pressure with reflex slowing of the heart rate (Cushing response) are often observed and can be correlated with abrupt increases in ICP lasting 1 to 15 minutes. When ICP exceeds 30 mm Hg, CBF progressively decreases, and a vicious circle is established: ischemia causes brain edema, which in turn increases ICP, resulting in more ischemia. If left unchecked, this cycle continues until the patient dies of progressive neurologic damage or catastrophic herniation.
• Cerebral edema: An increase in brain water content can be produced by several mechanisms. Disruption of the blood–brain barrier (vasogenic edema) is most common and allows the entry of plasma-like fluid into the brain. Common causes of vasogenic edema include mechanical trauma, inflammatory lesions, brain tumors, hypertension, and infarction. Cerebral edema after metabolic insults (cytotoxic edema), such as hypoxemia or ischemia, results from failure of brain cells to actively extrude sodium and progressive cellular swelling. Cerebral edema can also be the result of intracellular movement of water secondary to acute decreases in serum osmolality (water intoxication). Interstitial cerebral edema is the result of obstructive hydrocephalus and entry of CSF into brain interstitium.
• Treatment: Treatment of intracranial hypertension and cerebral edema is ideally directed at the underlying cause. Metabolic disturbances are corrected and operative intervention undertaken whenever possible. Vasogenic edema often responds to corticosteroids. Tight blood glucose control should be maintained when steroids are used to reduce cerebral edema. Regardless of the cause, fluid restriction, osmotic agents, and loop diuretics are usually effective in temporarily decreasing brain edema and lowering ICP until more definitive measures can be undertaken. Diuresis lowers ICP chiefly by removing intracellular water from normal brain tissue. Moderate hyperventilation (PaCO2 30–33 mm Hg) is often very helpful in reducing CBF.
• Mannitol, in doses of 0.25 to 0.5 g/kg, is particularly effective in rapidly decreasing ICP. Its efficacy is primarily related to its effect on serum osmolality. Treatment can transiently decrease blood pressure by virtue of its weak vasodilating properties, but its principal disadvantage is a transient increase in intravascular volume initially, which can precipitate pulmonary edema in patients with borderline cardiac or renal function. It is important to remember that mannitol should not be used in patients with intracranial aneurysms, arteriovenous malformations (AVMs), or intracranial hemorrhage until the cranium is opened. Osmotic diuresis in such instances can expand a hematoma as the volume of the normal brain tissue around it decreases. The combined use of mannitol and furosemide may be synergistic but requires close monitoring of the serum potassium concentration.
Craniotomy Surgery
Craniotomy is commonly undertaken for primary and metastatic neoplasms of the brain.
• Glial cells: astrocytoma, oligodendroglioma, or glioblastoma
• Ependymal cells, ependymoma
• Supporting tissues: Meningioma, schwannoma, or choroidal papilloma
• Childhood tumors: Medulloblastoma, neuroblastoma, and chordoma
Clinical manifestations: Headache, seizures, cognitive decline, neurologic deficits; supratentorial masses: seizures, hemiplegia, aphasia; infratentorial masses: cerebellar dysfunction (ataxia, nystagmus, and dysarthria); brainstem compression: cranial nerve palsies, altered mental status, and respirations
Preoperative Management
• Review CT and MRI scans for evidence of brain edema, midline shifts, and ventricular size.
• Neurologic examination, including mental status and existing sensory or motor deficits
• Medications reviewed for corticosteroid use, diuretic, and anticonvulsant therapy
• Premedication is best avoided when intracranial hypertension is suspected. Corticosteroids and anticonvulsant therapy should be continued until the time of surgery.
Intraoperative Management:
• Direct intraarterial pressure monitoring (A-Line) to obtain arterial blood gases (ABGs) closely regulate PaCO2.
• Bladder catheterization is necessary because of the frequent use of diuretics, the long duration of most procedures, and its utility in guiding fluid therapy.
Monitoring
• ICP monitored perioperatively with a ventriculostomy or subdural bolt can be beneficial and is most commonly used and is usually placed by the neurosurgeon preoperatively.
Induction: Induction of anesthesia and tracheal intubation are critical periods; prevention of ICP increases is of critical importance.
• The most common induction technique uses thiopental or propofol together with hyperventilation to lower ICP and blunt the noxious effects of laryngoscopy.
• All patients are hyperventilated with controlled ventilation, and a neuromuscular blocking agent (NMBA) is given to facilitate ventilation and prevent straining or coughing. Succinylcholine may increase ICP but may be the agent of choice in patients at increased risk for aspiration or with a difficult airway because hypoxemia and hypercarbia are even more detrimental.
• Hypertension during induction can be blunted by one of three ways: β-blockade, deepening anesthesia with additional propofol, or hyperventilation with low-dose IAs.
• ICPs can be improved by osmotic diuresis, steroids, or removal of CSF via a ventriculostomy drain immediately before induction.
Intraoperative
• Anesthesia can be maintained with IAs or by total intravenous agents (TIVA): propofol or dexmedetomidine and remifentanil.
• Hyperventilation should be continued intraoperatively to maintain PaCO2 between 30 and 35 mm Hg.
• Intravenous (IV) fluid replacement should be limited to glucose-free isotonic crystalloid or colloid.
Emergence
• Extubation in the operating room requires special handling during emergence. Straining or bucking on the tracheal tube may precipitate intracranial hemorrhage or worsen cerebral edema.
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