Vasospasm After Aneurysm Hemorrhage

Following brain hemorrhage, particularly aneurysmal subarachnoid hemorrhage, vasospasm often develops. The term “vasospasm” refers to cramping or narrowing of the cerebral arteries in response to the presence of blood in the fluid spaces that bathe the brain. Scientific evidence points to irritation caused by the degredation products of blood that cause vessel damage and muscle in the blood vessel walls to spasm resulting in severe narrowing or blockage of the cerebral arteries. Vasospasm typically develops around 4 to 12 days after the hemorrhage and is an extremely complication. It is believed that cerebral vasospasm is the most common cause of stroke and death in patients who are hospitalized after suffering from SAH,1 and may occur in as many as two-thirds of patients who experience aneurysms.2 If left untreated, vasospasm will lead to death or significant disability in more than 20% of patients.

Medications have contributed to a significant decrease in death and disability that vasospasm can cause.

Prevention and Treatment
In recent years, medications have become available that appear to help prevent vasospasm from developing or protect the brain from the effects of vasospasm. These medications have contributed to a significant decrease in death and disability that vasospasm can cause. Following subarachnoid hemorrhage of any cause, patients should receive a 21 day course of treatment with nimodipine, a calcium channel blocker, proven in a randomized trial to improve clinical outcomes in this patient population.

Angiography, or blood vessel picture taking, has previously been used to demonstrate that most patients develop some degree of vasospasm following subarachnoid hemorrhage. Angiography involves the insertion of dye into the blood vessels so that they can be examined through the use of x-ray technology.4 However, not all patients develop complications of vasospasm if the vasospasm is not too severe. More aggressive treatment to prevent stroke is warranted in some; but, due to the risks associated with invasive treatment, these more aggressive measures are applied in a step-wise fashion. When necessary, though, invasive measures to reopen the arteries in spasm and increased blood pressure to force blood through oxygenated blood through the brain can be life-saving.

As mentioned previously, all patients receive a 21 day course of the calcium channel blocking drug, nimodipine, to limit the effects of vasospasm. Patients with subarachnoid hemorrhage are usually kept in the intensive care unit for up to two weeks following their hemorrhage in order to watch closely for early signs of vasospasm-related complications. If a patient’s neurological status starts to decline, and there is no medical contra-indication to further medical intervention, most patients undergo what is commonly referred to as “Triple H therapy”.

Triple H therapy stands for three things: 1.) medically-induced high blood pressure or Hypertension; 2.) increased fluid in the blood space or Hypervolemia so that the heart has more blood to pump to the brain; and 3.) mild thinning of the blood or Hemodilution by reducing the percentage of red blood cells to around 30% to improve the bloods ability to pass through narrowed blood vessels. When properly administered in the intensive care unit by physicians with specific expertise in the care of subarachnoid hemorrhage, Triple H therapy can help prevent stroke and death in many patients.

Some patients will not respond well to Triple H therapy due to the severity of their vasospasm or because of other medical conditions that prevent the full use of Triple H therapy. It is in the care of this patient group that the interventional neuroradiologist is indispensable and can maek the difference between life without disability and death.

Some patients will develop very severe vasospasm in response to subarachnoid hemorrhage. The severity of vasospasm often relates to the amount of bleeding that occurred at the time of the original hemorrhage or the development of subsequent hemorrhages. Some patients, particularly young patients, have strong and highly reactive muscle in their cerebral blood vessels that can severely narrow or even cut off blood flow in the major brain arteries. In these patients, direct administration of strong muscle relaxers into the narrowed brain arteries or even the use of a tiny balloon to force the brain blood vessels back open has now been shown in a nation-wide study to result in a nearly 20% reduction in the risk of death due to vasospasm.