Our experts specialize in evaluating and treating cerebral vasospasm. Vasospasm occurs when a brain blood vessel narrows, blocking blood flow. It can occur in the two weeks following a subarachnoid hemorrhage or brain aneurysm. Diagnostic tests will help determine the source of the bleeding. Treatment for SAH varies, depending on the underlying cause of the bleeding and the extent of damage to the brain.
Treatment may include lifesaving measures, symptom relief, repair of the bleeding vessel, and complication prevention. For 10 to 14 days following SAH, the patient will remain in the neuroscience intensive care unit NSICU , where doctors and nurses can watch closely for signs of renewed bleeding, vasospasm, hydrocephalus, and other potential complications.
Medication Pain medication will be given to alleviate headache, and anticonvulsant medication may be given to prevent or treat seizures. Surgery If the SAH is from a ruptured aneurysm, surgery may be performed to stop the bleeding. Options include surgical clipping or endovascular coiling. Controlling hydrocephalus Clotted blood and fluid buildup in the subarachnoid space may cause hydrocephalus and elevated intracranial pressure.
Blood pressure is lowered to reduce further bleeding and to control intracranial pressure. Excess cerebrospinal fluid CSF and blood can be removed with: 1 a lumbar drain catheter inserted into the subarachnoid space of the spinal canal in the low back, or 2 a ventricular drain catheter, which is inserted into the ventricles of the brain.
Controlling vasospasm Five to 10 days after an SAH, the patient may develop vasospasm. Vasospasm narrows the artery and reduces blood flow to the region of the brain that the artery feeds.
A patient in the NSICU will be monitored for signs of vasospasm, which include weakness in an arm or leg, confusion, sleepiness, or restlessness. Transcranial doppler TCD ultrasounds are preformed routinely to monitor for vasospasm.
TCDs are used to measure the blood flow through the arteries Fig. Although the direct cause of the disease is largely unknown, it is thought that is caused by an imbalance in the chemicals that cause vasoconstriction blood vessel narrowing and vasodilation blood vessel widening. Most patients with subarachnoid hemorrhages are given drugs to prevent strokes from cerebral vasospasm.
Kevin White, Justin F. A second-line hemodynamic intervention, after optimization of blood pressure, of increasing cardiac output with inotropes is recommended by many centers. When hemodynamic management fails to reverse a focal neurologic deficit consistent with vasospasm or is contraindicated, endovascular management is preferred.
In contrast, patients with medically refractory symptomatic vasospasm should be treated with the same urgency as an acute ischemic stroke. Early aggressive treatment with an optimal time window of less than 2 hours is the best strategy to prevent cerebral infarction. Different vasodilators have been infused to brain vessels through selective or superselective transarterial catheters, although none has been studied in randomized controlled clinical trials.
Papaverine, which was widely used in the past, is no longer used in current practice because of reported neurotoxicity. Nicardipine, verapamil, and to a lesser degree, nimodipine, fasudil, and milrinone are the preferred agents. Intra-arterial infusion can be used as a standalone therapy with the advantages of safety and more diffuse vasodilatory action. Disadvantages of intra-arterial infusion alone are the delayed and short duration of action that may necessitate repetition of the procedure and the possibility of intracranial hypertension and systemic hypotension.
Prevention, effective monitoring, and early detection are the keys to successful management. Oral nimodipine 60 mg every 4 hours improves neurologic outcomes for patients with vasospasm or DCI. For patients who do not respond to nimodipine, prompt stepwise therapy starting with hemodynamic optimization euvolemia plus hypertension progressing to urgent aggressive therapy with balloon angioplasty and infusion of vasodilators may be needed.
Because vasospasm is a more complex pathophysiologic process than previously understood, more research regarding multimodal approaches and new therapeutic targets is needed. Macdonald RL.
Nimodipine—oral or intravenous? World Neurosurg. Neurocrit Care ;15 2 Pathogenesis of cerebral vasospasm following aneurismal subarachnoid hemorrhage: putative mechanisms and novel approaches.
J Neurosci Res. Prediction of cerebral vasospasm in patients presenting with aneurismal subarachnoid hemorrhage: a review. Amount of blood on computed tomography as an independent predictor after aneurysm rupture.
Comparison between clipping and coiling on the incidence of cerebral vasospasm after aneurysmal subarachnoid hemorrhage: a systematic review and meta-analysis. Neurosurg Rev. Clipping versus coiling for ruptured intracranial aneurysms: a systematic review and metanalysis. Definition of delayed cerebral ischemia after aneurysmal subarachnoid hemorrhage as an outcome event in clinical trials and observational studies: proposal of a multidisciplinary research group.
Predictors of cerebral infarction in aneurysmal subarachnoid hemorrhage. Delayed neurological deterioration after subarachnoid hemorrhage.
Nat Rev Neurol. Predicting the lack of development of delayed cerebral ischemia after aneurysmal subarachnoid hemorrhage. Early prediction of delayed cerebral ischemia after subarachnoid hemorrhage: development and validation of a practical risk chart.
0コメント