1. Admit to an intensive care setting for constant hemodynamic and neurologic monitoring.

Patients with SAH are at risk for hemodynamic instability and neurologic deterioration.

2. Endotracheal intubation

Indications: Glasgow Coma Scale (GCS) score ≤8, elevated intracranial pressure (ICP), poor oxygenation or hypoventilation, hemodynamic instability, and requirement for heavy sedation or paralysis.

3.Cerebral Angiogram

To localize and define the anatomic details of the aneurysm and to determine if other unruptured aneurysms exist

4. Endovascular coiling or surgical clipping

Endovascular coiling or surgical clipping is strongly recommended to reduce the rate of rebleeding. Aneurysmal rebleeding may be secondary to uncontrolled hypertension or aneurysmal clot fibrinolysis.

The choice between coiling and clipping usually depends on the location of the lesion, the neck of the aneurysm, and the availability and experience of hospital staff.

5. Deep venous thrombosis (DVT) prophylaxis with pneumatic compression stockings is started prior to aneurysm treatment. Subcutaneous unfractionated heparin 5000 units three times daily can be added for DVT prophylaxis once the aneurysm is treated.

6. Intravenous fluid administration should target euvolemia and normal electrolyte balance.

7. Hyponatremia, in particular, is common and sodium levels should be checked at least daily.

8. Patients are given stool softeners and analgesia (eg, morphine sulfate) and kept at bedrest to diminish hemodynamic fluctuations and lower the risk of rebleeding.

9. Prophylactic therapy for gastrointestinal ulcers is typically provided. (

taking of medicine, usually proton pump inhibitors or H2 blockers

a. Esomeprazole Sodium

10. Treat:

●Hypoxemia (arterio-alveolar gradient >125 mmHg)

●Metabolic acidosis (serum bicarbonate <20 mmol/L)

●Hyperglycemia (serum glucose >180 mg/dL [10 mmol/L])

●Blood pressure instability (mean arterial pressure [MAP] <70 or >130 mmHg)

Blood pressure control — The optimal therapy of hypertension in SAH is not clear. No blood pressure target has been defined in acute aneurysmal SAH with an unsecured aneurysm. The 2012 American Stroke Association guidelines suggest that a decrease in systolic blood pressure to <160 mmHg is reasonable [7]. When blood pressure control is necessary, the use of vasodilators such as nitroprusside or nitroglycerin should be avoided because of their propensity to increase cerebral blood volume and therefore ICP. Labetalol, nicardipine, and enalapril are preferred.

While lowering blood pressure may decrease the risk of rebleeding in a patient with an unsecured aneurysm, this benefit may be offset by an increased risk of infarction. Cerebral perfusion pressure (CPP) equals the MAP minus the ICP. Thus, with increased ICP, cerebral perfusion may be impaired and increases in MAP may be the only means to maintain CPP at a level necessary to prevent infarction. One study's results suggest that this CPP threshold may be 70 mmHg [43]. In one report of 134 patients with SAH, 80 received antihypertensive therapy to lower the diastolic pressure below 100 mmHg [44]. The patients given antihypertensive therapy had a lower incidence of rebleeding (15 versus 33 percent) that was offset by a higher incidence of infarction (43 versus 22 percent).

In the absence of ICP measurement, antihypertensive therapy is often withheld unless there is a severe elevation in blood pressure [45]. The patient's cognitive status may be a useful guide. If the patient is alert, CPP is adequate and lowering the blood pressure may decrease the risk of rerupture; we typically keep the systolic blood pressure in such patients below 140 mmHg. In contrast, antihypertensive therapy is generally withheld in those with a severely impaired level of consciousness since the impairment may be due to a reduced CPP.

Control of Blood Pressure

The optimal therapy of hypertension in SAH is not clear. No blood pressure target has been defined in acute aneurysmal SAH with an unsecured aneurysm. The 2012 American Stroke Association guidelines suggest that a decrease in systolic blood pressure to <160 mmHg is reasonable [1]. [

Antihypertensive agents when mean arterial pressure exceeds 130 mm Hg
]

Avoid nitroprusside or nitroglycerin because of their propensity to increase cerebral blood volume and therefore ICP.

Labetalol, nicardipine, and enalapril are preferred.

While lowering blood pressure may decrease the risk of rebleeding in a patient with an unsecured aneurysm, this benefit may be offset by an increased risk of infarction.

Cerebral perfusion pressure (CPP) equals the MAP minus the ICP. Thus, with increased ICP, cerebral perfusion may be impaired and increases in MAP may be the only means to maintain CPP at a level necessary to prevent infarction.

One study's results suggest that this CPP threshold may be 70 mmHg [43]. In one report of 134 patients with SAH, 80 received antihypertensive therapy to lower the diastolic pressure below 100 mmHg [44]. The patients given antihypertensive therapy had a lower incidence of rebleeding (15 versus 33 percent) that was offset by a higher incidence of infarction (43 versus 22 percent).

In the absence of ICP measurement, antihypertensive therapy is often withheld unless there is a severe elevation in blood pressure [45]. The patient's cognitive status may be a useful guide. If the patient is alert, CPP is adequate and lowering the blood pressure may decrease the risk of rerupture; we typically keep the systolic blood pressure in such patients below 140 mmHg. In contrast, antihypertensive therapy is generally withheld in those with a severely impaired level of consciousness since the impairment may be due to a reduced CPP.

Control Arterial Mean Blood Pressure

• Avoidance of nitrates (which elevate ICP) when feasible
• Hydralazine and calcium channel blockers
Angiotensin-converting enzyme (ACE) inhibitors (not first-line agents in acute SAH)

 

 

●Fever of infectious and noninfectious origin is a common complication of SAH, particularly in those with a higher neurologic grade, and is associated with a poor prognosis [27,28]. In one nonrandomized study, the use of external cooling devices in patients with fever after SAH appeared to be associated with improved outcomes [29].

●Anemia is common after SAH, occurring in 18 percent of patients during their hospital stay in one report [30]. Most studies suggest that anemia is associated with worse outcomes, while higher hemoglobin levels are associated with fewer cerebral infarctions and improved outcomes [31-34]. A goal hemoglobin for transfusion has not been defined in patients with SAH [7]; some experts recommend a target above 8 to 10 g/dL [35], however, one randomized trial found that a higher transfusion goal (11.5 g/dL versus 10 g/dL) appeared to be safe [36].

●Troponin levels and electrocardiogram (ECG) should be checked on admission [35]. If positive, follow-up levels and echocardiogram to evaluate possible left ventricular function should be considered.

●Hypothalamic pituitary dysfunction is common after SAH, but the clinical implications and appropriate treatment is uncertain [37]. Routine administration of glucocorticoids is not recommended after SAH, but may be considered in patients who are unresponsive to vasopressor therapy for vasospasm [35].

Antithrombotic discontinuation — Although there are few data, most experts favor reversal of all anticoagulation for acute SAH until the aneurysm is definitively repaired by surgery or coiling [38-40].

Guidelines from the American Heart Association/American Stroke Association issued in 2006 recommend that all anticoagulants and antiplatelet agents should be discontinued after SAH [40]. In addition, any anticoagulant effect should be reversed immediately with appropriate agents such as vitamin K, fresh frozen plasma, or unactivated prothrombin complex concentrate (which is also called factor IX complex). We use the therapeutic approach that is recommended for warfarin-associated intracerebral hemorrhage. (See "Reversal of anticoagulation in warfarin-associated intracerebral hemorrhage", section on 'Initial treatment'.)

Intracranial pressure — Patients with SAH often develop increased ICP that is usually due to acute hydrocephalus and reactive hyperemia after hemorrhage. (See "Clinical manifestations and diagnosis of aneurysmal subarachnoid hemorrhage", section on 'Hydrocephalus'.)

We generally place a ventriculostomy in appropriate patients (eg, those with enlarged ventricles on CT or World Federation of Neurosurgical Societies [WFNS] scale score ≥3 (table 2)); this allows direct measurement of ICP and also allows treatment by drainage of cerebrospinal fluid (CSF) when appropriate. While some concern has been raised about precipitating rebleeding with abrupt lowering of ICP, this has not been substantiated in clinical studies [41]. (See "Intraventricular hemorrhage", section on 'External ventricular drain' and "Evaluation and management of elevated intracranial pressure in adults", section on 'ICP monitoring'.)

Patients without a ventriculostomy can be managed medically with osmotic therapy and diuresis. Hyperventilation is generally avoided because it may precipitate or exacerbate vasospasm. The use of hypertonic saline has been evaluated in patients with elevated ICP related to traumatic brain injury and appears to lower ICP and may improve cerebral perfusion. A small observational study in 16 patients with poor-grade SAH suggests that it may also be useful in this setting, but further study is required [42]. (See "Evaluation and management of elevated intracranial pressure in adults", section on 'Osmotic therapy and diuresis'.)

In some cases, decompressive craniectomy may be needed for ICP control in the setting of intracerebral hemorrhage and/or severe cerebral edema. (See "Evaluation and management of elevated intracranial pressure in adults", section on 'Decompressive craniectomy'.)

 

Antiseizure drug therapy — The use of antiseizure drugs to prevent seizures in patients with SAH has been a widely debated topic [7,46,47]. Many experts believe that seizure prophylaxis in the setting of an unsecured aneurysm is reasonable, given the relatively low risk associated with antiseizure drug administration versus the potential deleterious effects of seizures on an already dysautoregulated brain [4,48]. However, evidence from a large case series suggests that antiseizure drug exposure to phenytoin may be associated with worse neurologic and cognitive outcome after SAH [49]. Therefore, the use of antiseizure drugs for seizure prophylaxis after SAH should probably be minimized whenever possible, and phenytoin is generally avoided.

The decision to treat with antiseizure agents may be based in part upon the distribution of blood on axial imaging studies. A higher threshold to start antiseizure drugs is warranted in the setting of perimesencephalic blood without cortical layering since this pattern of hemorrhage is associated with a particularly good prognosis. In contrast, initiation of antiseizure drugs in higher risk patients with poor neurologic grade, unsecured aneurysm, and associated intracerebral hemorrhage may be reasonable [7]. (See "Clinical manifestations and diagnosis of aneurysmal subarachnoid hemorrhage", section on 'Seizures'.)

Continuation of antiseizure drug therapy may not be necessary in most patients after undergoing aneurysmal clipping following a SAH, especially those without acute seizures who present with a good grade. (See 'Seizures' below.).

 

 

Laboratory studies for SAH should include the following: Serum chemistry panel - To establish a baseline for detection of future complications Complete blood count - For evaluation of possible infection or hematologic abnormality Prothrombin time (PT) and activated partial thromboplastin time (aPTT) - For evaluation of possible coagulopathy Blood typing/screening - To prepare for possible intraoperative transfusions Cardiac enzymes - For evaluation of possible myocardial ischemia Arterial blood gas (ABG) - Necessary in patients with pulmonary compromise

• In patients with signs of increased ICP or herniation, intubation and hyperventilation

Other interventions for increased ICP are as follows:

• Osmotic agents (eg, mannitol)
• Loop diuretics (eg, furosemide)
• IV steroids (controversial but recommended by some)

Additional medical management is directed toward the following common complications:

• Rebleeding
• Vasospasm
• Hydrocephalus
• Hyponatremia
• Seizures
• Pulmonary complications
• Cardiac complications