Complications of SAH


The most common complications of SAH are rebleeding, cerebral vasospasms, hydrocephalus and myocardial ischemia.

Rebleeding within the first 24 hours is the leading cause of death in persons who survive the initial bleed. The incidence of rebleeding episodes starting with day 7 correlates with normal clot dissolution via natural fibrinolysis. There is a higher risk of rebleeding in patients classified as grades III-V due to labile blood pressure; however, it is important to realize that all patients with a SAH are at risk for rebleeding. Signs and symptoms of rebleeding include

Prevention of rebleeding is an important nursing function. Dramatic or rapid changes in blood pressure must be avoided in the patient recovering from a SAH. Current literature indicates that the risk of rebleeding appears to be more related to variations in blood pressure rather than to mean blood pressure.

Antifibrinolytic drugs that prevent the dissolution of the fibrin that forms the foundation of an aneurysmal blood clot may be used to prevent rebleeding. The antifibrinolytic agent aminocaproic acid (Amicar) may be given as a continuous infusion from the day of admission to the day of surgery in patients whose CT scan indicates that they are at low risk for the development of vasospasms. Antifibrinolytic therapy is controversial due to the increased risk of thrombus formation. In patients who are poor surgical risks or for whom surgery is delayed, the benefits of antifibrinolytic therapy may outweigh the risk.


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The most important preventative measure to prevent aneurysmal rebleeding is to avoid sudden variations in blood pressure.
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Cerebral vasospasm is the narrowing of a cerebral blood vessel due to irritation. Vasospasm results in reduced cerebral perfusion, cerebral ischemia, potential infarction, and further deterioration of neurological function. The mortality rate from vasospasm is between 40 and 50%.

The most common time span for vasospasm is between days 4 and 14, with a peak between days 7 and 10 after hemorrhage. It is thought that agents that cause vessel spasms may be released into the cerebral circulation as the clot breaks down between days 7 to 10. The initial CT scan is very useful in estimating the probability and location of vasospasms. A decreased level of consciousness, the presence of focal signs consistent with a stroke, together with a CT scan that correlates the symptoms to a specific vascular area, point to vasospasm when no other changes can explain neurological deterioration. When either significant or subtle neurological changes occur, the nurse can quickly alert the physician so that quick intervention can prevent extension of the neurological deficits or death. The most common signs and symptoms of cerebral vasospasm are a gradual neurological deterioration related to a specific vascular territory. Depending on the area of the brain deprived of blood supply due to cerebral ischemia; the patient may exhibit the following symptoms:

Hypovolemia is a risk factor for vasospasm. Adequate perfusion is accomplished by promoting a slightly hypervolemic and hypertensive state using controlled fluid administration to expand extracellular volume. Crystalloid and colloid fluids are given intravenously to expand volume and improve cerebral perfusion. The goal of therapy is to maintain the following physiologic parameters:

Communicating hydrocephalus, the type seen after SAH, occurs when CSF cannot be absorbed normally through the arachnoid villi. Blood in the subarachnoid space from the SAH plugs the arachnoid villi, interfering with CSF absorption. The diagnosis of communicating hydrocephalus after an SAH is made on the basis of a CT scan, which will reveal blood dilating the brain's ventricles. Acute hydrocephalus occurs within the first 24 hours after hemorrhage and is associated with a large amount of bleeding in the basal cisterns. Acute hydrocephalus is characterized by the abrupt onset of stupor or a persistent comatose state. Management involves an immediate ventriculostomy to drain the CSF to avert a dangerous increase in intracranial pressure. Subacute hydrocephalus occurs within a week after the initial SAH and is characterized by the gradual onset of drowsiness or changes in the patient's level of consciousness. A ventriculostomy or serial lumbar punctures to drain CSF from the cisterns is used to manage subacute hydrocephalus. Delayed hydrocephalus occurs 10 or more days after SAH. This type of hydrocephalus is characterized by a gradual onset of behavioral symptoms seen while the patient is recovering from surgery, and is managed with the surgical placement of a vetriculoperitoneal shunt. Because the signs and symptoms of hydrocephalus are nonspecific, it is important for the nurse to maintain an high index of suspicion for this potential complication of SAH. Changes in the patient's responsiveness are often attributed to other problems, thus delaying appropriate treatment for hydrocephalus. Monitoring of the patient at risk for hydrocephalus after SAH includes assessment of the following symptoms that indicate increasing intracranial pressure:


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