Description

• Cerebral vasospasm is defined as the constriction of one or more major cerebral arteries, usually secondary to subarachnoid hemorrhage (SAH) or craniocerebral trauma.
• The amount of blood in the basal cistern and the presence of intraventricular blood correlate with the risk of developing clinically significant cerebral vasospasm.
• The diagnosis can be made clinically, angiographically, or by transcranial Doppler (TCD).
• The resulting decrease in cerebral blood flow (CBF) can lead to ischemia and infarction, and is a main cause of permanent neurologic injury and death after SAH.

Etiology/Risk Factors

• The cause of vasospasm following SAH is still unknown. It is thought that the presence of blood in the subarachnoid space can lead to cerebral vasoconstriction. Various components and breakdown products have been proposed as mediators. Oxyhemoglobin has several properties that make it one of the most likely candidates.
• The Fisher grade on initial presentation is highly predictive of the development of clinically significant cerebral vasospasm. The presence of thick blood in the basal cistern and intraventricular or intraparenchymal hemorrhage is associated with the highest risk of poor neurologic outcome.
• Although patients > 68 years of age are more likely to develop symptomatic vasospasm, younger patients are more likely to show angiographic evidence of vasospasm.
• Female gender, hypertension, elevated intracranial pressure (ICP), smoking, and cocaine use also increase the risk of developing vasospasm.

Physiology/Pathophysiology

• Contraction of smooth muscle in the vessel wall leads to lumen narrowing and restricted blood flow. Cerebrovascular resistance shifts from the penetrating arterioles to the major branches of the Circle of Willis, which undermines the brain's ability to autoregulate. BP then becomes the main determinant of CBF beyond the affected vessels.
• There is also evidence that histological changes occur. These include thickening of all three vascular layers, periadvential inflammation, and myointimal hyperplasia. However, the extent of the clinical significance of these findings is unclear.

Anesthetic GOALS/GUIDING Principles

• Since autoregulation in the brain is impaired, hypotension should be avoided throughout the perioperative period; flow is pressure dependent.
• Hypertension, hypervolemia, and hemodilution (triple-H therapy) can potentially minimize the risk of ischemia; however, it is associated with a significant risk of morbidity that must be carefully weighed against this unproven benefit. Invasive monitoring is recommended.
• Consider avoiding volatile agents. Uncoupling of CBF and cerebral metabolic rate of oxygen consumption (CMRO₂) may lead to lower cerebral vascular resistance in unaffected areas of the brain. This can decrease perfusion distal to spastic vessels. Intravenous agents such as propofol have a more favorable profile in the setting of vasospasm.

Symptoms

• Decreased level of consciousness is the most common finding indicative of cerebral vasospasm.
• Rarely, patients can present with focal neurologic findings without a global decrease in level of consciousness.

Treatment History

• Patients with cerebral vasospasm may have had an aneurysm surgically clipped or endovascularly embolized.
• Triple-H therapy is widely used.

Medications

• Most patients with symptomatic vasospasm are treated with calcium channel blockers. Nimodipine has been shown to provide some benefit. Its intravenous equivalent nicardipine, on the other hand, has demonstrated inconclusive results.
• Other medications that have been experimented with include fibrinolytic therapy, sodium nitroprusside, magnesium, cyclosporine, erythropoietin, and clazosentan.

CONCOMITANT ORGAN DYSFUNCTION

• Cardiovascular
  • Cerebral vasospasm may, in and of itself, lead to hypovolemia for unknown reasons.
  • Reversible myocardial stunning can occur in the setting of SAH. Its severity is associated with the degree of neurologic injury.
  • Aneurysms occur more frequently in certain genetic conditions such as polycystic kidney disease, coarctation of the aorta, fibromuscular hyperplasia, and connective tissue disorders.
• Pulmonary function should be assessed in patients who are smokers. Also, patients with compromised neurologic status are at an increased risk of aspiration.
• Patients on triple-H therapy are at risk of developing cardiac, pulmonary, and renal complications.

Circumstances to delay/Conditions

• Delay in surgical clipping after SAH or interventional radiologic procedures to treat vasospasm can have severe consequences, including rebleeding and devastating neurologic injury.
• If ischemic heart disease is suspected, an echocardiogram may be helpful in guiding intraoperative management.

Classifications

• The Fisher grade classifies the appearance of SAH on CT scan and correlates it to the risk of clinically significant vasospasm:
  • Grade 1: No hemorrhage evident
  • Grade 2: SAH < 1 mm thick
  • Grade 3: SAH > 1 mm thick
  • Grade 4: SAH of any thickness with intraventricular hemorrhage or parenchymal extension.

Bed Acuity

Patients at high risk for vasospasm, based on clinical and radiologic findings post-SAH, should be monitored at least every 2 hours for neurologic changes. This is usually done in an intensive care unit (ICU) setting. Lower risk patients can be monitored every 4 hours.

Medications/Lab Studies/Consults

• Patients at risk for cerebral vasospasm are almost always placed on a nicardipine drip. They may further be placed on a pressor such as norepinephrine to maintain MAPs that are 10–20% above baseline.
• Daily labs should include CBC, chemistry panel, and measures of urine function.
• TCD can be a useful screening tool but is fraught with technical limitations. Magnetic resonance angiography (MRA) is more reliable. Cerebral angiography is the gold standard for diagnosis.
• Consults should be obtained as clinically indicated if cardiac, pulmonary, or renal complications are detected.

Complications

• One should be prepared for the risk of significant bleeding intraoperatively. This can lead to malignant brain swelling with devastating consequences. Brain protection and brain relaxation techniques should be immediately instituted in such an event.
• As with any neurosurgical procedure, there is risk of intracranial hemorrhage. Patients should be monitored closely for changes in neurological function for at least 24 hours postoperatively.
• There is also the potential for developing an intraoperative infarct, especially if hypotension is maintained. This may present in the postoperative period as delayed emergence, altered mental status, or focal neurologic deficits.
• Any of the above complications resulting in neurologic injury can lead to compromised airway reflexes, which puts the patient at risk for aspiration.
• Triple-H therapy can lead to additional complications, such as cerebral edema, cardiac ischemia, pulmonary edema, and hyponatremia. Patients should be closely monitored in an ICU. Central venous pressure monitoring is recommended.

• Craniotomy, Cerebral Aneurysm Clipping
• Cerebral Embolization
• Cerebral Blood Flow

ICD9

435.9 Unspecified transient cerebral ischemia

ICD10

G45.9 Transient cerebral ischemic attack, unspecified

Victor Duval , MD