Generally treated with nimodipine (controversial, probably works not by dilating vessels but as a neuroprotectant, if at all) and triple-H therapy (hypertension, hypervolemia, and hemodilution, also controversial). Increased blood flow, as opposed to pressure, may be more important.
In the aftermath of subarachnoid hemorrhage, when nimodipine & HHH fail to avert cerebral vasospasm, balloon angioplasty may be performed to forcibly dilate constricted vessels & restore perfusion to the affected (ischemic) brain regions. In addition to angioplasty, vasodilating agents such as papaverine or verapamil, can be infused directly (intra-arterially) to relieve the spasm.
Hypertension, hypervolemia, and hemodilution (triple-H therapy) is often utilized to prevent and treat cerebral vasospasm after aneurysmal subarachnoid hemorrhage (SAH). Methods include intravenous fluids (IVF) +/- inotropes/pressors with targets of CVP 10-12mmHg, PAOP 15-18mmHg, CI 3-3.5L/min/m2, Hct 30-35%, SBP 160-200mmHg if aneurysm clipped and 120-150mmHg if unclipped. Although this paradigm has gained widespread acceptance over the past 20 years, the efficacy of triple-H therapy and its precise role in the management of the acute phase of SAH remains uncertain. In addition, triple-H therapy may incur significant medical morbidity, including pulmonary edema, myocardial ischemia, hyponatremia, renal medullary washout, indwelling catheter-related complications, cerebral hemorrhage, and cerebral edema.
What is Vasospasm? Narrowing intracranial arteries with impaired autoregulation Seen in 35% of pts with SAH / cerebral aneurysm rupture 3-10 days after SAH, #1 cause of delayed cerebral ischemia, usually starts resolving after 10-14 days Seen in 60% of pts w/ SAH but only 50% have symptoms
- Altered level of consciousness (drowsiness, disorientation) or new focal neurologic deficit. May have HA, meningismus, fever
- Differential: rebleeding, hydrocephalus, seizure, hyponatremia
- Cerebral angiography (gold standard) – detect # and location of vessels involved
- Transcranial Doppler (TCD) – increased arterial velocity (>200cm/s high risk infarct) however changes from baseline generally more useful
- Nimodipine – CCB (60mg PO q4h x21days) – cytoprotective by decreasing avail intracellular Ca in ischemic cells
- Removal of subarachnoid blood as soon as possible
- Instillation of thrombolytic agents (e.g. urokinase)
- Antiinflammatory agents (steroids or NSAIDs)
- HHH Therapy – (Hypervolemia, HTN, Hemodilution) – controversial
- IVF +/- Inotropes/vasopressors
- CVP 10-12mmHg, PAOP 15-18mmHg, CI 3-3.5 L/min/m2, Hct 30-35%, SBP 160-200 if aneurysm clipped and 120-150 if unclipped
- Complications: pulmonary edema, myocardial ischemia, rebleeding, rupture of new aneurysm, vasogenic edema/hemorrhagic infarction insetting of compromised BBB.
- HHH refractory – Selective intra-arterial verapamil, papaverine, or nitroprusside or Angioplasty
- Mathew Joseph, Saleem Ziadi, Joseph Nates, Mark Dannenbaum, Marc Malkoff Increases in cardiac output can reverse flow deficits from vasospasm independent of blood pressure: a study using xenon computed tomographic measurement of cerebral blood flow. Neurosurgery: 2003, 53(5);1044-51; discussion 1051-2
- Kendall H Lee, Timothy Lukovits, Jonathan A Friedman “Triple-H” therapy for cerebral vasospasm following subarachnoid hemorrhage. Neurocrit Care: 2006, 4(1);68-76