Vasospasm occurs after SAH in a significant number of patients. It is one of the most important causes of the high morbidity and mortality related to SAH. It is related to the amount of blood in the basal cisterns and can occur at any time following the bleed but most commonly in the initial 3-10 days.
This clinical syndrome is caused by a critical reduction of cerebral blood flow (CBF) brought on by a pathologic luminal narrowing of the cerebral arteries after SAH. Vasospasm typically starts around day 3 following SAH and can last for up to 10 days. Vasospasm can be symptomatic or asymptomatic. Symptomatic vasospasm otherwise called delayed ischemic neurologic deficit (DIND) represents a major cause of morbidity and mortality in patients with SAH. Diagnosis of symptomatic vasospasm was based on the following criteria: clinical deterioration in the patient’s neurologic condition, including insidious onset of confusion, anxiety, disorientation, or decline in level of consciousness or focal deficits that may fluctuate in severity. It is important to exclude structural causes of neurologic worsening such as hydrocephalus by appropriate investigations including head CT scanning. Other possible causes of confusion such as serum electrolyte or glucose disturbances, hypoxia, hypercapnia, or seizures (clinical or electrographic) should be actively searched for and corrected.
Symptomatic vasospasm has been reported in 22% to 40% of patients with SAH and may result in high frequency of morbidity (34%) and mortality (30%). Vasospasm is treated (prevented?) in some cases by prescribing Nimodipine for all patients with SAH. Hypertensive, hypervolemic and hemodilution therapy for vasospasm is also widely practiced. This is called the Triple H therapy.
Hypertension can be induced by intravenously administered phenylephrine, norepinephrine, and/or dopamine, and hypervolemia was achieved by intravenously administered crystalloid and colloid solutions. Patients with asymptomatic vasospasm are treated with modest hypervolemic therapy (central venous pressure, 5–8 mm Hg).
More aggressive hypervolemia (central venous pressure, 8–12 mm Hg) or elevation of blood pressure (mean arterial pressure, 110–130 mm Hg) was instituted in patients with symptomatic vasospasm. In those patients with history of heart disease or pulmonary edema, pulmonary artery catheters were inserted to maintain pulmonary artery occlusion pressures of 12–18 mm Hg. Careful clinical assessment of blood pressure, haematocrit and the blood chemistry are important in order to minimize any additional morbidity.
Hypertension and hypervolemia do not seem to increase the risk of hemorrhage from unsecured, unruptured aneurysms in the acute setting or in their short-term natural history.
Endovascular procedures such as angioplasty of the narrowed cerebral arteries and intra-arterial administration of papaverin are the other important modalities of treatment for symptomatic vasospasm in patients who do not respond to medical therapy.
Transcranial Doppler
by Pete Coles
Transcranial Doppler (TCD) is used to manage cerebral vasospasm following SAH. TCD is often performed with highly portable compact and easy to use machines at the patients bedside. It could also be performed in the angiography suite if necessary.
The routine for admitted patients is often to perform routine TCD recordings daily following admission or treatment for SAH. It is then performed daily for as long as necessary but usually about 7-14 days. The normal TCD is performed to insonate the middle cerebral arteries, and the anterior cerebral arteries bilaterally, measuring the velocity of blood flow in the arteries. Other vessels such as the posterior cerebral, basilar, ophthalmic and carotids can be examined.
The normal values are |
