Complications
This seems to be a reaction of basal cerebral blood vessels to the breakdown products of the subarachnoid blood. It is related to prolonged and intense smooth muscle contraction associated with smooth muscle cell proliferation, fibrosis, and inflammatory changes.[67]
It is the main cause of delayed morbidity or death and occurs in up to 30% of patients with SAH.[68] Vasospasm typically occurs 7 to 10 days after hemorrhage onset and correlates with the amount of subarachnoid clot adjacent to the basal vessel. It clinically manifests as acute neurologic deficit.
The Fisher grade uses a 4-point scale to describe the amount of blood on noncontrast CT of the head and has been shown to correlate with the complication of vasospasm.[35]
Transcranial Doppler is effective for monitoring the degree of vasospasm.
Nimodipine is the standard treatment for preventing ischemia related to vasospasm.[20] Medical management is with triple H therapy (hypertension, hemodilution, and hypervolemia).
Intra-arterial vasodilator or balloon angioplasty may be required if medically refractory.
Hyponatremia may be due to syndrome of inappropriate antidiuretic hormone secretion (SIADH) or cerebral salt wasting (CSW).[68] SIADH is a primary disruption in water regulation, with intact sodium and volume regulation. In CSW, hyponatremia results from renal sodium loss, leading to intravascular volume loss (an opposite mechanism to that found in SIADH).
Fluid restriction to an amount less than urinary output (while attempting to maintain normal sodium intake) gradually corrects hyponatremia in most cases due to SIADH.
CSW should be treated with enteral sodium and intravenous hypertonic saline.[68]
The risks of endovascular obliteration include arterial dissection, parent artery occlusion, and thromboembolic complications. Intraprocedural rupture of the aneurysm during advancement of the catheter into the aneurysm is one of the most serious complications.
The risks of surgical aneurysm repair include vessel injury, stroke, infection, and injury to the brain parenchyma.
Risks of flow-diverter devices include aneurysm re-rupture, device thrombosis, and complications of associated dual antiplatelet therapy. Flow-diverter devices are not recommended for use in ruptured aneurysms, and should only be considered when no other method of effective aneurysm treatment is feasible.[56][57]
Even with immediate obliteration of the aneurysm with coiling, recurrence is an issue that may potentially increase the risk of rebleeding.[24] Larger aneurysms that are coiled tend to recanalize. The risks associated with aneurysm recanalization after coil embolization are yet to be defined. Aneurysms that are clipped tend to not recur.
Aneurysm recurrence after coiling or clipping is usually treated with further endovascular embolization.
This is usually diagnosed after an acute neurologic decline and more subarachnoid hemorrage (SAH) on noncontrast head CT. Aneurysmal rebleeding carries significant morbidity and mortality. Highest incidence occurs within the first 24 hours after hemorrhage.
Endovascular coiling or surgical clipping for aneurysm obliteration is the primary means of eliminating risk of rebleeding.
Measure intracranial pressure invasively in a critical care setting with intraparenchymal or intraventricular probes. Maintain cerebral perfusion pressure (cerebral pressure = mean arterial pressure minus intracranial pressure) at 50 mmHg to 70 mmHg with a beta-blocker, such as labetalol.
Seizures are more often witnessed in the prehospital setting.
Start anticonvulsants after witnessed seizure. Some initiate anticonvulsants prophylactically, but then discontinue them days after the aneurysm has been definitively treated.
One retrospective study of 383 cerebral aneurysms treated with endovascular coiling showed that 33.6% of treated aneurysms that were followed up showed aneurysm recurrence at a mean of 1 year. Major recurrences presented in 20.7% at a mean time of 16 months.[69]
Acute hydrocephalus usually occurs after intraventricular hemorrhage or from excess blood in the basal cisterns. It clinically manifests as an abrupt onset of stupor or persistence of coma after initial rupture. Noncontrast head CT is the primary means of diagnosis.
Subacute hydrocephalus develops days to weeks after SAH and presents as progressive drowsiness or a quiet abulic state. Ventriculostomy with external ventricular drain can be given. Acutely, the ventricular drainage system may be left open to drain at 10 cm above the external auditory meatus. Improvement may be immediate and dramatic.
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