Update on the Management of Subarachnoid Hemorrhage

Katja E Wartenberg


Future Neurology. 2013;8(2):205-224. 

In This Article

General Emergency & Critical Care Management

In acute SAH, the sudden rise of intracranial pressure (ICP) up to levels of the mean arterial pressure (MAP) creates an arrest of cerebral circulation resulting in loss of consciousness[60] and the development of global cerebral edema as well as acute ischemic injury on neuroimaging (Figure 5).[61–64] Initial care should focus on: stabilization of systemic oxygenation and hemodynamics to optimize cerebral perfusion and oxygen supply; control of ICP caused by hydrocephalus and/or global cerebral edema; blood pressure control; seizure control; and prevention of aneurysm rebleeding.

Figure 5.

Diffusion-weighted imaging of a patient with Hunt and Hess IV subarachnoid hemorrhage, obtained on admission, showing acute ischemic injury in the distribution of the bilateral anterior cerebral artery territory (arrows).
Reproduced with permission from Oxford University Press, NY, USA.219

The resuscitation goals for SAH are presented in Table 1. Recurrent hemorrhage occurs in 9–17% of patients in the first 72 h, 40–87% of those occur within the first 6 h. Patients with high-grade SAH, loss of consciousness at index bleed, larger aneurysms, sentinel bleeds, angiography within 3–6 h of symptom onset, delay to treatment and incomplete aneurysm repair are at a higher risk for recurrent hemorrhage.[65–68] The literature reports available are not sufficient for specific recommendations regarding blood pressure reduction and administration of antifibrinolytic therapy with tranexamic acid or aminocaproic acid prior to cerebral angiography or aneurysm repair. Lowering blood pressure to a systolic value of 140–160 mmHg with a titratable agent is recommended.[29] A MAP of 110 mmHg can be tolerated. However, care should be taken to adjust the MAP and cerebral perfusion pressure (CPP) to maintain cerebral blood flow (CBF).[29,56] A short course of antifibrinolytic therapy may be undertaken until aneurysm repair for a maximum of 72 h. This therapy should be discontinued 2 h prior to endovascular aneurysm repair. Thromboembolic events present a contraindication, and the patients should be monitored closely for deep venous thrombosis.[29,56,68] The use of steroids is not supported by any controlled trials.

The patients diagnosed with SAH should be treated at high volume centers (>35 cases per year) with appropriate specialty neurointensive care units (NICUs), neurointensivists, vascular neurosurgeons and interventional neuroradiologists.[29,69–71]

Treatment of Increased ICP

SAH is associated with intracranial hypertension caused by hydrocephalus, space-occupying intracerebral hemorrhage, and global and focal cerebral edema. Hydrocephalus occurs in 20–30% of patients after SAH.[72–74] The treatment of choice is insertion of an extraventricular drain (EVD),[29] which may result in a prompt clinical response such as improvement of consciousness.[75] The risk of infection ranges from 2.2 to 21.9% depending on the number of manipulations and sterile techniques used. If there is no improvement after 36–48 h and the ICP is low, a poor neurological state is likely due to primary brain injury related to the acute effects of hemorrhage. Weaning of the EVD should begin after ICP is controlled for 48 h, either by trials of intermittent clamping or raising the EVD level with ICP monitoring. Clamping the EVD and subsequent weaning within 24 h, as opposed to a gradual increase in EVD level, resulted in a decreased length of stay in the intensive care unit, but did not reduce the need for a ventriculoperitoneal shunt.[76] Serial lumbar puncture[77] or placement of a lumbar drain[78] present alternatives to prolonged or repeated EVD placement if the basal cisterns are open. Approximately 18–26% of all SAH patients require a ventriculoperitoneal shunt for persistent hydrocephalus.[73,79]

Space-occupying intraparenchymal hemorrhages should be treated by craniotomy and surgical decompression. Decompressive craniectomy is indicated in patients with life-threatening cerebral edema with and without intracerebral hemorrhage, due to infarction or recurrent hemorrhage, and should be performed rapidly to avoid herniation.[80]

Apart from head-of-bed elevation, sedation, temperature control, administration of isotonic fluids, maintaining CPP >60 mmHg and an arterial partial pressure of carbon dioxide of 35 mmHg, bolus administration of hypertonic saline may be the preferred treatment for ICP crisis. Hypertonic saline (23.5%) given for ICP control resulted in an increase in CBF in ischemic regions and in brain tissue oxygenation, as well as in a decrease in ICP.[81,82]

Multimodal monitoring including ICP, MAP, CPP, partial pressure of cerebral tissue oxygen, cerebral lactate, pyruvate, glucose, glycerol and glutamate by microdialysis and reactivity indices may help to determine the optimal CPP threshold. The pressure reactivity index is calculated as the correlation coefficient between ICP and MAP to reflect cerebral autoregulation states. If autoregulation is disturbed, MAP changes are directly transmitted passively through a nonreactive vasculature to ICP (Figure 6). The optimal CPP is defined as the CPP at the lowest pressure reactivity index observed within a range of CPP (usually 50–90 mmHg).[83]

Figure 6.

Relationship between extremes of cerebral perfusion pressure and intracranial pressure in states of reduced intracranial compliance.
In the vasodilatory cascade zone, CPP insufficiency and intact pressure autoregulation leads to reflex cerebral vasodilation and increased ICP: the treatment is to raise CPP. In the autoregulation breakthrough zone, pressure and volume overload, which overwhelms the brain's capacity to autoregulate, leads to increased cerebral blood volume and ICP: the treatment is to lower CPP.
CPP: Cerebral perfusion pressure; ICP: Intracranial pressure.
Reproduced with permission from.221

Volume Status

Intravascular volume status should be monitored since reduced intravascular volume may cause cerebral ischemia and infarction.[84–87] Although placement of a central venous catheter is recommended for large volume access and monitoring, central venous pressure was found to be an unreliable marker of intravascular volume.[88,89] Assessment of fluid status should not be based solely on central venous pressure, but should include clinical examination of the patient, records of input and output, hourly urine output and stroke volume variation in intubated patients. Routine placement of pulmonary artery catheters is not recommended.[56] In general, intravenous fluid management for patients with SAH should target euvolemia.[29,56] Prophylactic hypervolemia may be harmful.[90–93] Isotonic fluids such as 0.9% saline at 1–1.5 ml/kg/h can be used. Supplemental 250 ml boluses of crystalloid (0.9% saline) or colloid (5% albumin) solution can be given every 2 h. However, crystalloids are preferred.[56] Hypertonic saline solutions are an alternative to normal saline for patients suffering from refractory intracranial hypertension or symptomatic intracranial mass effect. Hypotonic fluids should be avoided.[29]

Treatment of Seizures

The frequency of seizures in SAH has been reported to be 1–7% at onset. Approximately 5% of patients experience seizures during hospitalization and 7% will develop epilepsy during the first year after discharge.[94,95] The most important trigger for seizure is focal pathology such as large subarachnoid clots, intracerebral or subdural hematoma and cerebral infarction. A seizure at the onset of SAH does not predict an increased risk for epilepsy.[94] Routine use of phenytoin or fosphenytoin may worsen functional and cognitive outcome after SAH[96,97] and is no longer recommended.[29,56] If seizure prophylaxis with other anti-epileptic drugs is warranted to prevent rebleeding, they should be administered for only 3–7 days.[56]

Comatose patients may have nonconvulsive seizures or status epilepticus (8–19%).[98–100] Therefore, continuous electroencephalography is recommended in poor-grade SAH patients in stupor or coma. The effect of treatment of nonconvulsive seizures in these patients is less clear.[56]