Section V

26

Cerebral Vasospasm after Subarachnoid Hemorrhage

Characteristics of Vasospasm

Radiographic CVSs are seen in 30 to 70% of angiograms,1,2 as opposed to clinical spasms, which are seen in ~20 to 30% of patients after SAH. Radiographic spasm may occur in the absence of clinical spasm and vice versa (i.e., patients may have a small vessel spasm, causing neurologic deficit, but an angiogram may not be able to detect it). Mild CVSs are usually reversible, whereas severe CVSs can result in permanent deficits and death in 7% of patients. CVSs that occur early are associated with the worst neurologic deficits.

In 1980, Fisher et al³ revealed a correlation between the thickness of the subarachnoid blood on CT scan and the risk of developing CVS. Patients classified as Fisher III (localized clot and/or vertical layer >1 mm thick within the subarachnoid space) are at greatest risk of developing symptomatic CVS. Twenty-three of the 24 patients in Fisher et al’s study who were grade III developed clinical CVS.

Diagnosis of Vasospasm

Transcranial Doppler (TCD) ultrasound is the most utilized method of diagnosing and monitoring clinical CVSs. It measures blood velocity in major intracranial arteries (ICAs), which is used to determine if there may be arterial narrowing. Not only the actual velocity but also the relationship between the relative velocity of the ICA and the velocity of flow in the internal carotid artery is important. This relationship is referred to as the Lindergaard ratio. It is commonly used to express the difference in velocity between the MCA and the ICA, but it is also used in velocity measurements of all large intracranial vessels. The Lindergaard ratio may help to distinguish vasospasm from hyperemia (Table 26–1).⁴

Cerebral angiogram can detect vessel narrowing in larger vessels. Half of the patients with angiographic spasm will be asymptomatic. Angiograms may miss spasm of small arteries in patients who are symptomatic.

Xenon 133, xenon CT, single-photon emission computed tomography (SPECT), and positron emission tomography (PET) scanning are among the other methods used to detect low-flow arterial states. However, these may not be routinely available at many institutions, and they may not be practical for daily or frequent use. TCD ultrasound is less time consuming, less costly, and can be used daily to monitor CVS and its response to treatment.

CVS, cerebral vasospasm; LR, Lindergaard ratio.

Treatment of Vasospasm

Hyperdynamic, or “triple-H,” (hypertensive, hypervolemic, and hemodilution) therapy is the mainstay of treatment in patients with surgically or endovascularly treated aneurysms. A mild form of this type of therapy can be used in unsecured aneurysms, but it may cause the aneurysm to rerup-ture. Hyperdynamic therapy should not be started if there is a new cerebral hemorrhage, a new large infarct, or severe cerebral edema.5

Some experts advocate starting therapy prior to the onset of CVS to combat the common occurrence of hypovolemia in patients with SAH.⁶ In a randomized control trial, Lennihan et al⁷ found that the prevention of hypovolemia rather than the promotion of hypervolemia was critical in the prevention of cerebral ischemia. Induction of hypervolemia can be done with isotonic/hypertonic crystalloids and with colloids (albumin) or blood.

After the ruptured aneurysms have been clipped or coiled, the neurosur-geon has greater freedom to use certain medicines to raise blood pressure. Vasopressors can be used to augment blood pressure to improve cerebral perfusion. In this approach, increase blood pressure in 10 to 15% increments until neurologic function shows improvement. This may require increasing systolic blood pressure (SBP) to 240 mm Hg or mean arterial pressure (MAP) to 150 mm Hg (for clipped aneurysms). Wean pressors upon improvement and allow blood pressure to fall to sustain an acceptable neurologic function. Targets for central venous pressure (CVP) are 6 to 8 mm Hg; pulmonary capillary wedge pressure (PCWP), 16 to 18 mm Hg.

Once a patient has evidence of symptomatic vasospasm, he or she should be treated with hyperdynamic therapy for at least 14 days or until symptoms resolve and there is no angiographic evidence of vasospasm.

Complications of triple-H therapy include exacerbation of cerebral edema, pulmonary edema, intracerebral hemorrhage (ICH), worsened infarctions, rebleeding of unsecured aneurysms, myocardial infarction, and problems related to pulmonary artery catheter.

Transluminal Balloon Angioplasty

Transluminal balloon angioplasty allows the neurosurgeon to direct mechanical opening of a vessel using neuroendovascular techniques. It is reserved for patients with clinical vasospasm not improving using hyperdynamic therapy and with radiographic evidence of vasospasm. The best results are seen if the procedure is done within 24 hours of neurologic decline.8–11 Up to 70% of patients can have clinical and lasting improvement.

Angioplasty should be avoided if there is a new cerebral hemorrhage or a large area of infarction because of the risk of re-perfusion injury. Furthermore, angioplasty, if clinical and radiologic benefits do not persist, may need to be repeated.

Endovascular use of intra-arterial papaverine is sometimes recommended; however, the clinical benefits are short-lived. It is helpful in placing angioplasty balloons and in treating vessels inaccessible to angioplasty catheters.

Recent investigations measuring cerebral lactate to pyruvate ratios and brain tissue oxygen tension before and after balloon angioplasty show data that may be able to provide an early diagnosis of CVS and allow monitoring of threatened cerebral tissue regions.¹²

Cerebral Salt Wasting Syndrome and Subarachnoid Hemorrhage

Hyponatremia is a frequent finding in the neurosurgical intensive care unit (NICU) patient, and it can be a common cause of neurologic deterioration in a patient with aneurysmal SAH, especially in anterior communicating artery aneurysms. In the 1950s, when the condition was first described, NICU patients with hyponatremia were initially thought to have cerebral salt wasting (CSW); but as the description of SIADH became more popular later in that decade, CSW fell out of favor, and many hyponatremic patients with CSW were treated with fluid restriction.13 CSW is associated with hyponatremia and extracellular volume depletion. Harrigan¹⁴ summarized the evidence in favor of CSW as follows:

1. A negative salt balance is present with hyponatremia in many patients with intracranial disease.
   
2. These patients were found to be volume depleted, which is incompatible with SIADH.
   
3. They improved with volume and salt replacement.

Clinical manifestations of hyponatremia include confusion, lethargy, seizures, and coma. It is likely that both humoral and neural mechanisms are involved in the renal wasting of sodium. Atrial natriuretic factor involvement is likely, but it does not appear to be the primary factor. No solid laboratory studies are available to reliably distinguish SIADH and CSW. In fact, laboratory tests may be identical.

Findings in CSW

Treatment of CSW

It is crucial to make a correct diagnosis, because treatment plans for CSW and SIADH are opposite. Patients with cerebral injury who are already hypovolemic will be at greater risk of ischemia and infarction. In one study, the administration of normal saline 50 cc/kg/day and oral salt 12 g/day was shown to be effective in restoring serum within 3 days.15 Three percent saline is also used for severe hyponatremia, especially if the patient is symptomatic. Correction of sodium should occur no faster than 0.5 to 1.0 mEq/L/hour, and maximum correction should not exceed 20 mEq/L in the first 48 hours. Correct initially to a serum sodium level of 130 to 134 mEq/L and the remainder of the salt deficit over 1 or 2 days.

Hyperdynamic Syndrome after Carotid Endarterectomy

Hyperdynamic syndrome following carotid endarterectomy (CEA) occurs in ~0.3 to 1.0% of patients, and usually >24 hours after surgery. Heralding signs and symptoms include ipsilateral frontal headache within the first week (better with sitting), focal motor seizures that are characteristically difficult to control,16 and etiology thought to be the return of blood flow to areas previously rendered chronically ischemic and with poor autoregulation.^17,18

Risk factors for hyperdynamic syndrome are

• Carotid stenosis > 90%
  
• Poor collateral hemisphereic flow
  
• Contralateral carotid occlusion
  
• Evidence of ipsilateral chronic hypoperfusion
  
• Pre- and postoperative hypertension
  
• Preexisting ipsilateral cerebral infarction (especially recent)
  
• Preoperative anticoagulation or antiplatelet treatment

CT Findings of hyperdynamic syndrome may show mild edema, petechial hemorrhages, and ICH ipsilateral to the side of the CEA.

Intracerebral Hemorrhage after Carotid Endarterectomy

ICH is the most catastrophic complication of the hyperperfusion syndrome. It occurs in ~0.5 to 0.7% of patients after CEA and accounts for ~20% of peri-operative strokes. In one study, all ICHs occurred between days 1 and 10 postprocedure.19 The cause of ICH is most likely the blood–brain barrier being overcome by a rapid increase in the cerebral blood flow that occurs after CEA. The mortality is ~30%, with the highest risk factor appearing to be relief of high-grade stenosis.

Treatment of ICH after CEA

Arteriovenous Malformations and Rebleeding

The most common cause for postoperative ICH after AVM surgery is retained AVM, which needs to be meticulously searched for. However, hemorrhagic complications can occur after total extirpation of cerebral AVMs.20–32 AVMs that are large and with the highest flow rates are at greatest risk. The incidence is 0.01 to 0.10%.

There are two theories to explain rebleeding. The normal perfusion pressure breakthrough theory, as outlined by Spetzler²² in 1978, says that chronic hypoperfusion leads to impaired autoregulation around the AVM; after excision, the return of normal pressure causes local hyperemia and capillary leakage. The occlusive hyperemia theory, first proposed by al-Rodhan et al²⁹ in 1993, maintains that the obstruction of the venous outflow system of adjacent brain causes passive hyperemia and a stagnant arterial flow in the former AVM feeders.

Exact pathophysiological and hemodynamic mechanisms are not fully understood, and it is likely that combinations of the above theories in conjunction with a yet unidentified mechanism are at play.

The treatment of ICH after fully resected AVM surgery may require evacuation of ICH, careful blood pressure management, and antiedema medication. Adequate hydration and blood volume since dehydration can promote further venous thrombosis. Serum hematocrit <35 is recommended. If the patient is in poor neurologic condition, barbiturate coma may be helpful by globally reducing blood flow and allowing the normal brain to develop normal autoregulation.