Hemorrhagic strokes comprise 10-15% of all strokes. Subarachnoid hemorrhage (SAH) accounts for about 50% of hemorrhagic strokes. A thunderclap headache (TCH), which is a sudden and severe headache with maximal intensity at onset is a common presenting feature of SAH.

About 80% of cases of non-traumatic SAH are due to the rupture of a saccular arterial aneurysm. These aneurysms have a peak incidence at about the age of 50, and hence are a common cause of stroke in the 40-60 age group. SAH is also caused by arteriovenous malformations (AVMs), central nervous system (CNS) trauma, amyloid angiopathy, dural arteriovenous malformation, intracranial dissection, bleeding diathesis, and ingestion of cocaine and/or amphetamines.

  • Thunderclap headache: sudden and severe with maximum intensity at onset.

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  • Evidence of meningeal irritation: nuchal rigidity and Brudzinski’s and Kernig’s signs.

  • CNS features of bleeding, vasospasm or mass effect: nausea, vomiting, delirium, coma and/or cranial nerve palsies, subretinal hemorrhage, and seizures.

  • History of recent new onset headache, history of uncontrolled hypertension and/or abuse of sympathomimetic agents.

Classic presentation: 50 year old woman who presents with sudden onset of severe headaches, vomiting, low back pain and altered mental status. Evaluation in the emergency department (ED) reveals nuchal rigidity, right third cranial nerve palsy and retinal hemorrhage.

Clinical features are due to a combination of effects of meningeal irritation due to the bleed, location of vascular pathology, increase in intracranial pressure, and secondary effects of the SAH and its associated complications.

1. Headache: occurs in about 97% of cases. 30%-60% report a history of short-lasting headaches a few weeks before the typical presentation with a severe headache. Most of these preceding episodes are due to sentinel bleeds. Onset of the presenting headache may be preceded by some form of muscular activity in about 40% of cases.

2. Meningeal irritation: occurs in 40%-50% of cases. Neck stiffness and other features of meningeal irritation may not be obvious in the elderly and in comatose patients.

3. Increase in intracranial pressure: 50%-80% of cases have vomiting, visual impairment and altered mental status as part of their presenting symptoms.

4. Seizures: About 10% of patients with SAH have seizures in addition to the other usual presenting symptoms.

  • The most common causes of SAH are ruptured aneurysms and trauma. 80% of non-traumatic SAH are due to aneurysmal rupture.

  • 5% of the population above 20 years have saccular aneurysms. SAH has an incidence of about 6-8 cases/100,000 persons/year.

  • There is a higher incidence in women than in men. There is also a higher incidence rate in blacks compared to other racial groups.

  • 85% percent of aneurysms occur in the anterior circulation. In 20% of cases there are multiple aneurysms.

  • Hemodynamic stress accounts for the rupture of these aneurysms. The major risk factors for SAH are hypertension, smoking and heavy drinking (>150gm of alcohol per week).

  • Peak incidence is at 50 years. First degree relatives of patients with non-traumatic SAH have a higher incidence of SAH.

  • Genetic conditions associated with cerebral aneurysms include polycystic kidney disease, type III collagen deficiency, Marfan’s syndrome and other rare Collagen vascular diseases.

  • Angiogram-negative SAH accounts for about 15-20% of cases of SAH. The causes include bleeding diathesis as in sickle cell disease, amyloid angiopathy, vasculitis, intracranial artery dissection, cortical vein thrombosis, and illicit drug use, specifically cocaine and amphetamines. Do not ignore the middle-aged uncontrolled hypertensive woman who smokes and uses cocaine presenting with presumed new onset migraine.

1. Reversible Cerebral Vasoconstriction Syndrome: This condition is associated with recurrent episodes of Thunderclap headache (TCH), which is characterized by sudden onset of severe headache. 10-25% of patients may have SAH. TCH is a diagnosis of exclusion and thus requires CT scan of the brain and/or Lumbar puncture to exclude SAH.

2. Glaucoma: Typically presents with headache, ocular pain and evidence of increase in intraocular pressure. No signs of meningeal irritation.

3. Complicated migraine: presents with headache, neurological deficits but no signs of meningeal irritation. Head Computed tomography (CT) scan shows no vascular pathology.

A therapeutic response to the use of Triptans does not exclude SAH.

4. Hypertensive encephalopathy, encephalitis, cerebral venous thrombosis, arterial dissection, pituitary apoplexy.

All of the above conditions may present with altered mental status and varying neurological deficits. The major distinguishing features are the absence of signs of meningeal irritation and their specific diagnostic findings on computed tomography (CT) scan and/or magnetic resonance imaging (MRI).

Clinical findings depend on the location of the culprit lesion(s) and extent of the hemorrhage. Minor cases are characterized by features of meningeal irritation and increase in intracranial pressure:

1. Nuchal rigidity, Kernig’s sign, papilloedema, subhyaloid hemorrhage.

2. Cranial neuropathies commonly seen involve the oculomotor and abducens nerves.

3. Hemiparesis and aphasia occur with middle cerebral artery aneurysms, and lower extremity paresis are seen with anterior cerebral artery aneurysms.

4. Massive bleeds may result in comatose patients, with or without evidence of seizure activity.

1. Non-contrast head CT scan: This detects SAH if done within 24 hours of onset of symptoms with a sensitivity of approximately 95%. Sensitivity of CT scan decreases to 75% in 3 days, and to 50% after 1 week of onset of symptoms (See Figure 1).

Figure 1.

Non-contrast CT scan of the brain showing evidence of SAH.

A normal CT angiogram following a normal head CT scan has about a 98% predictability of excluding SAH.

2. Lumbar puncture (LP): Looking for evidence of xanthochromia is the gold standard for diagnosing SAH. Xanthochromia is detected within 6-12 hours of SAH and may last for 2-3 weeks.

Attribution of all cases of reducing number of red cells in the CSF in subsequent tubes to a traumatic tap and thereby excluding SAH is unreliable and may result in a wrong diagnosis.

Diagnosis is mainly by history, clinical findings and radiological results.

Basic laboratory results needed for additional evaluation and management include:

  • Complete blood count (CBC)

  • Chemistry panel

  • Cardiac muscle markers: Troponin levels

  • Prothrombin time (PT)

  • Partial thromboplastin time (PTT)

  • Calcium, magnesium and albumin levels

  • Blood typing and screening

  • CSF specimen analysis.

Hyponatremia and Hyperglycemia are associated with adverse outcomes and need to be addressed early in the management of SAH.

4-Vessel catheter cerebral angiography is required to localize the ruptured aneurysm and to detect other vascular lesions. The renewed emphasis on early aneurysm management (within 3 days) has resulted in angiograms being done within days of diagnosing SAH (Figure 2).

1. Cerebral vasospasm associated with SAH may make smaller aneurysms undetectable in the first week. Normal cerebral angiograms in the acute-phase of SAH diagnosis should be repeated in 2-3 weeks before the diagnosis of non-aneurysmal SAH is made.

2. Although aneurysms larger than 10mm may be seen on CT scan, a 4-Vessel angiogram is still needed before planning surgical intervention because there may be multiple aneurysms.

3. CT angiogram and MRI are non-invasive imaging techniques being used increasingly in cases of SAH. Their sensitivity is lower (86%-95%) than that of the gold standard catheter cerebral angiography. They are highly sensitive for lesions 4mm or larger but may miss aneurysms that are smaller than 4mm.

4. Magnetic resonance angiography (MRA) is an option in patients with mild to moderate chronic kidney disease who are not on hemodialysis.

In cases where iodinated dye cannot be avoided, measures ought to be taken to reduce the incidence of contrast-induced nephropathy by using non-ionic low osmolar contrast agents,
body weight and serum creatinine-based formula for the volume of contrast used, ensuring adequate IV hydration.

1. Brain MRI does not provide a higher diagnostic yield if CT scan is negative in the first 72 hours on onset of symptoms. These patients require a lumbar puncture to exclude SAH. The sensitivity of MRI begins to exceed that of CT scan after day 5 of onset of symptoms.

2. Non-aneurysmal pretruncal SAH are due to venous hemorrhages and/or intramural hematoma. These are characterized by a focal clot in front of the brain stem. This type of SAH runs a benign cause. Patients with this type of SAH do not require a repeat cerebral angiogram if the initial study is normal.

3. Screening of family members for brain aneurysms after the index case is only recommended for those with autosomal dominant polycystic kidney disease since 8% of them have cerebral aneurysms. Screening may also be worthwhile only in individuals who have two or more first degree relatives who have experienced aneurysmal SAH.

Clinical grading scales for patients presenting with aneurysmal subarachnoid haemorrhage (See Table I).

Table I.
Hunt and Hess grading system WFNS grading system
I Asymptomatic or mild headache GCS sum score 15 without hemiparesis
II Moderate to severe headache, nuchal rigidity, no focal deficits other than cranial nerve palsy GCS sum score 14–13 without hemiparesis
III Confusion, lethargy or mild focal deficits other than cranial nerve palsy GCS sum score 14–13 with hemiparesis
IV Stupor or moderate to severe hemiparesis GCS sum score 12–7 with or without hemiparesis
V Coma, extensor posturing, moribund appearance GCS sum score 6–3 with or without hemiparesis

WFNS=World Federation of Neurological Surgeons. GCS=Glasgow coma scale.

The Ramsay sedation scale (See Table II).

Table II.
1 Anxious or agitated
2 Cooperative and tranquil
3 Arouses to voice and command
4 Briskly arouses to physical or loud auditory stimulus
5 Sluggish response to physical or loud auditory stimulus

No response to physical or loud auditory stimulus

1. Admit to neurointensive care unit or intensive care unit (ICU). In hospitals lacking the expertise to manage these patients, the goal should be to stabilize and transfer the patients to an appropriate tertiary health care center.

2. Airway protection through intubation and mechanical ventilation based on Glasgow coma score (GCS), and/or cardiopulmonary status. Elective intubation if GCS is less than 8.

3. Treat evidence of increased intracranial pressure and/or hydrocephalus promptly and aggressively. Measures used include intubation and hyperventilation, use of osmotic agents.

4. Intravenous fluids to maintain euvolemia. Avoid dextrose-containing and hypotonic solutions.

5. Aim for Systolic blood pressure between less than 160mmHg, and MAP <130mmHg.

6. Review of serum electrolytes, hematology panel, cardiac and hepatic enzymes, chest X-ray, electrocardiography (EKG), coagulation panel and cross-matching of blood.

7. Order Nimodipine, 60mg every 4 hours for 21 days.

8. Aim for normothermia and normoglycemia.

9. Sedation to reduce sympathetic surge using the Ramsay sedation scale as a guide. Patients should be kept between scale level 2 and 4. Avoid oversedation.

10. Analgesics, opt for less sedating narcotics. Avoid Non-steroidal anti-inflammatory medications. Do not use Tramadol if seizures have occurred.

11. Lorazepam and/or Levetiracetam (Keppra) if seizures have occurred. Seizure prophylaxis remains controversial.

12. Pneumatic compression stockings for Deep vein thrombosis prophylaxis.

13. Start stool softeners and plan on starting enteric nutrition on day 2 of admission.

14. Plan on securing and/or occluding aneurysm as soon as possible by consulting appropriate subspecialists or transferring to a high volume center for management.

15. Discuss care plan with family and plan for frequent updates from management team as per patient’s clinical response.

1. Blood pressure, heart rate and volume status using Central venous pressure (CVP) or pulmonary capillary wedge pressure (PCWP) readings, have to be monitored and followed closely. These are critical in preventing rebleeds (rerupture) and in the managing cerebral vasospasm.

2. Heart and lung sounds to detect volume overload and/or focal areas of lung consolidation.

3. Abdominal exam and stool hemoccult tests due to risk of gastrointestinal (GI) bleed (Cushing’s ulcers).

4. Daily monitoring of mental status, motor and sensory functions is critical for the early detection of complications of SAH.

5. Ocular exam looking for subretinal hemorrhages: Its management requires input from ophthalmology to prevent permanent loss of vision. The presence of vitreous (preretinal) hemorrhage is due to abrupt significant increases in intraocular pressures and is associated with a poor prognosis.

The association of SAH with preretinal hemorrhages is Terson’s syndrome.

6. Transcranial Doppler studies to evaluate flow velocities in cerebral arteries.

7. Telemetry review, and review of latest blood gas analysis of patients.

8. Monitor the intracranial pressure daily in patients with ventricular drains.

Leukocytosis may be the only sign of an infection and needs to be followed daily, especially in intubated patients and those with ventricular drains. Hematocrit should be kept within normal limits.

The components of 3H or hyperdynamic fluid therapy are:

Hypervolemia, Hemodilution and Hypertension. Prophylactic 3H has been the main modality for preventing cerebral vasospasm for years. Crystalloids, colloids and/or Albumin infusions in conjunction with Vasopressin have been used to achieve hypervolemia.

The goal for hemodilution is to keep hematocrit at 30-35% in order to optimize the viscosity of blood and oxygen delivery.

Vasopressors and/or Inotropes have been used to initiate aggressive hypertensive therapy.

Increasing reports of adverse outcomes associated with the hypervolemic aspect of the 3H therapy has led to a switch to euvolemia.

The emphasis is now in hemodilution and hypertension (2H) but with euvolemia. Recommendation is now to maintain euvolemia but still maintain emphasis on hypertension and hemodilution components of the traditional 3H therapy to augment cerebral blood flow.

Should all be within normal limits to prevent worsening vasospasm, seizures and/or failure to wean off the ventilator. Hyponatremia is a common problem which requires attention. SAH may result in hypothalamic dysfunction and result in diabetes insipidus, so look out for non-iatrogenic hypernatremia.

This has to be monitored closely in conjunction with the hemoglobin due to the risk of bleeding from gastritis and/or Cushing’s ulcers with SAH.

Needs to be followed closely because of the need for invasive and non-invasive angiographic studies so that measures to reduce the risk of contrast-induced nephropathy can be instituted.

To help avoid hypoglycemia (serum glucose <80 mg/dL), which is associated with adverse outcomes, serum glucose levels should be targeted for a more permissive glucose level at <180 mg/dL and not for “tight control” of normoglycemia.

To ensure they are within therapeutic limits. This should be done 48 hours after initial dose and then weekly on stable patients.

To monitor for dysrhythmias. Patients require continuous telemetry monitoring in the acute phase of their diagnosis.

For patients on the ventilator. This should be done daily and 15 minutes after a change in the ventilator settings.

  • Repair of aneurysm

  • Management of factors associated with aneurysmal rupture

  • Management of complications

  • Management of causes of non-aneurysmal SAH.

Repair of aneurysms require early interventions by Neurosurgeons or Interventional Neuroradiologists using clips and/or coils. Endovascular therapy using coils is becoming the modality of choice for patients above older than 65 years and for lesions involving the posterior circulation. Its use though is limited in cases of giant aneurysms (>2.5cm) or aneurysms with a wide neck because of risk of coil mobilization. New endovascular modalities using balloon occlusion, angioplasty, new coil technologies and vascular reconstruction are being used successfully.

Traumatic, mycotic and neoplastic aneurysms usually have no neck and thus require trapping or excision of the diseased vessel. Additionally, these aneurysms tend to be located in peripheral arteries and pose additional management challenges.

Management of hypertension after aneurysm repair and addressing other risk factors such as Alcohol dependence, tobacco use and abuse of sympathomimetics reduces risk of rebleeds. Estrogen deficiency is associated with SAH. Estrogen use in appropriate women may be beneficial in preventing recurrent episodes.

Individuals who develop seizures may require long-term use of anti-seizure medications and close follow-up with Neurology.

Non-aneurysmal SAH due to hematological issues have to be referred to a hematologist.

1. Rebleeding: This occurs mainly in patients with poor-grade aneurismal bleeds, and those with larger aneurysms. It is seen in 20-30% of patients who do not have their aneurysms repaired. The highest incidence in the first 2 weeks, and the peak occurrence is within 24 hours.

2. Hydrocephalus which may be acute or chronic is the result of obstruction of cerebrospinal fluid outflow or decreased CSF resorption by arachnoid granulations. It is the most common early neurologic complication after aneurysmal SAH.

3. Cerebral vasospasm is seen as early as day 3 and has a peak incidence between days 4 and 12. This is due to effect of blood products on the vasculature and reduced nitric oxide production. Its severity is worsened by increasing size of the bleed, age of patient (<50 years) and hyperglycemia. It is seen angiographically in about 70% of patients, however 50% of them are asymptomatic. Clinical features are due to reduced regional and global cerebral blood flow.

4. A number of severe cases of SAH are complicated by intracerebral bleeds and/or sub-dural hematoma.

5. Increase in intracranial pressure, seizures, hyponatremia and cardiac dysfunction are other common management challenges.

Control of blood pressure is critical in the management of SAH.

The acceptable range is SBP (Systolic blood pressure) of 120-140mmHg before ablation of aneurysm to prevent re-bleed, and SBP of 150-160mmHg after this intervention when cerebral vasospasm increases the risk of cerebral hypoperfusion and infarcts.

Nimodipine has been shown to reduce ischemic damage and has to be given PO or via Nasogastric tube, 60mg every 4 hours daily for 21 days. It should never be given IV, and its use should not compromise the blood pressure goals of noted above. Dose may be changed to 20mg and given every 2 hours if hypotension occurs.

Hydrocephalus occurs in about 20% of patients with SAH. Asymptomatic patients are managed conservatively, however in the setting of associated deterioration of mental status ventricular drainage is required. This procedure has 2 major complications, the risk of rebleed and infection. Mental status improvement is usually seen within 36-48 hours of CSF (cerebrospinal fluid) diversion. Rebleed which is most likely due to loss of “tamponade effect” is minimal when this intervention is done at moderate CSF pressures (<14 cmH2O).

Patients may have altered mental status on presentation because of the direct effect of the bleed and/or the associated hydrocephalus. The major therapeutic intervention that may be helpful in this setting is the placement of a ventricular drain although this may provoke rebleed.

The 2H therapy requires keeping systolic blood pressures 20-40mmHg over pre-treatment levels with or without inotropes, and maintaining hematocrit at 30-35%.

The original third component of what was the 3H therapy, the use of plasma volume expanders to achieve hypervolemia is no longer required. Emphasis is now on maintaining euvolemia.

The risks of this therapy include acute coronary syndrome, heart failure, hemorrhagic infarcts, rebleeding, hyponatremia and dysrhythmias.

Telemetry, Central venous pressure monitoring and transcranial Doppler monitoring are required to balance the risk and benefit of the therapy.

Rebleeding is associated with a high mortality so patients who are not due to have early surgical intervention or at risk of rebleeding may be given Aminocaproic acid (epsilon), an antifibrinolytic agent since the lysis of the perianeurysmal clot is thought to be harbinger of rebleeds. The use of Epsilon is however controversial because it does increase the risk of cerebral vasospasm and has to be used cautiously.

Hyponatremia is seen in about 30% of patients with SAH. Serum levels less than120mEq/L or rapid decrease in serum sodium levels can result in lethargy, cerebral vasospasm and trigger seizures. Cerebral salting wasting (CSW) due to increase in circulating natriuretic levels is the main etiology of the hyponatremia. Additional causes of hyponatremia include inadequate ADH secretion (SIADH) and iatrogenic volume expansion with IVF.

CVP and/or PCWP monitoring, serum and urine osmolality, and urine sodium values are used to distinguish between CSW which is associated with hypovolemia, Syndrome of Inappropriate Antidiuretic hormone secretion which is associated with euvolemia and iatrogenic hypervolemia. Salt and fluid replacements using isotonic or hypertonic solutions and use of fludrocortisone are therapeutic options used. SIADH is managed with fluid restriction.

Sedation is necessary to reduce the sympathetic which accompanies SAH, this however does decrease the ability to mobilize secretions increasing the risk of pneumonia.

Dexamethasone is used in non-diabetics with SAH with significant cerebral edema. 10mg loading dose and then 4-6mg every 6 hours. Insulin is needed to manage associated hyperglycemia which is associated with poor outcomes. Mannitol and hyperventilation are other modalities for management of intracranial pressure secondary to cerebral edema.

Patients who develop seizure are treated with preferentially with Levetiracetam (Keppra) after an initial dose of Lorazepam, although a few centers still use Phenytoin.

  • Nimodipine: Calcium channel blocker. Usual dose is 60mg every 4 hours for 21 days. Never give it IV!

  • Keppra (Levetiracetam): Anti-convulsant – loading dose of 2gms –IV and then usual dose is 500mg twice daily.

  • Dilantin (Phenytoin): Anticonvulsant – loading dose is 1gm, then 300mg daily maintenance dose.

    More recent reports indicate its use is associated increased incidence of cerebral vasospasm and with worse cognitive outcomes.

  • Epsilon (Aminocaproic acid): A fibrinolysis Inhibitor – Its use is controversial but it used early in some patients to reduce the risk of re-bleed. The usual dose is 1gm over 10 minutes and then 1gm every 6hours for 24 hours.

  • Labetalol: Antihypertensive (alpha and beta-blocker) – maximum daily IV dose is 300mg and for the oral dose is 2400mg.

  • Hydralazine: Antihypertensive (peripheral vasodilator) – initial IV dose should not exceed 20mg.

  • Nicardipine: Calcium Channel blocker.- IV: 5mg/hr by slow infusion. Dose may be increased by 2.5mg/hr every 15 minutes but not to exceed 15mg/hr.

  • In transitioning to PO dosing, an oral dose should be given an hour before discontinuing IV.

  • Codeine and morphine: Narcotic analgesics for pain management.

  • Tramadol: Non-narcotic centrally-acting synthetic analgesic which binds to opioid receptors. Usual dose 50-100mg every 6-8 hours.

  • Lorazepam: (Benzodiazepine): An anxiolytic and a sedative. Usual dose is 0.5-2mg IV/PO.

  • Other IV medications include hypertensive crisis, including IV Nitroprusside and Esmolol.

  • Stool softeners used include senna, lactulose is preferred in patients with cirrhosis. Anti-emetics – Phenergan or Zofran. Avoid Reglan (metoclopramide) in those with seizures.


1. The need of invasive and non-invasive angiographic studies which require the use of iodinated dyes poses a risk for contrast-induced nephropathy. IV Hydration, avoidance of potential nephrotoxins and episodes of hypotension are steps that are taken to reduce this potential complication. The routine prophylactic use of N-acetylcysteine (NAC) to prevent contrast-induced nephropathy is debatable. Although it is not strictly evidence-based, use NAC is recommended by some Nephrologists in patients with significant baseline renal dysfunction (glomerular filtration rate < 45 mL/min/1.73 m2), multiple concurrent risk factors such as hypotension, diabetes, preexisting kidney injury, or congestive heart failure that limits the use of intravenous fluids, or who need a high volume of contrast dye.

2. Adequate hydration and blood pressure control are required for the prevention of cerebral vasospasm. In patients with renal failure closer monitoring is needed to avoid pulmonary edema. Patients on dialysis may require a change in their regimen in order to avoid hypotension.

3. Frequent monitoring of electrolytes is needed to prevent CNS side-effects of electrolyte abnormalities, notably hyponatremia.

4. Dose adjustments of a number of medications is required in the setting of renal failure.

1. Liver diseases may be associated with coagulopathy and intravascular volume depletion and delayed metabolism of medication.

2. Vitamin K and blood products are used to correct coagulopathy to decrease risk of rebleed.

3. Lower doses of sedatives and analgesics are required to prevent excessive sedation.

4. Use for albumin is helpful in addressing volume depletion associated with hypoalbuminemia.

The sympathetic surge associated SAH can result in neurocardiogenic injury resulting in takotsubo cardiomyopathy.

This may be seen within 48 hours and resolves spontaneously in 2-3 weeks. Neurogenic pulmonary edema due to sympathetic surge also occurs early in poor grade cases of SAH.

Management of heart failure in patients with SAH therefore requires adjustments of the permissive hypervolemia as part of the therapy for management of cerebral vasospasm. Angioplasty is used for managing cerebral vasospasm in those who do not respond to conservative measures.

Neurogenic pulmonary edema responds well to ventilatory support and use of high levels of PEEP (Positive end-expiratory pressure). Medication regimen need to be adjusted based on the clinical course and echocardiographic findings.

All anti-platelet agents have to be discontinued when SAH is diagnosed.

Acute EKG changes are seen in over 50% of patients with SAH. Deep T-wave inversions (cerebral T waves) have been described but all manner of EKG changes may be seen and may last for 2 weeks. The significance of these changes which are also due to sympathetic surge is limited although dysrhythmias resulting in sudden death have been reported. Bradyarrhythmias may require temporary pacemaker placement.

Patients are managed medically without compromising cerebral blood flow but keeping SBP between 120-140mmHg to avoid rebleed and then at above 160mmHg after securing the aneurysm to prevent cerebral vasospasm. Angioplasty of culprit vessels in cases of cerebral vasospasm is offered to patients who are not ideal candidates for or do not respond to conservative measures to address cerebral vasospasm.

1. Insulin is used in the acute – phase of SAH to maintain normoglycemia and thereby decrease the incidence of cerebral vasospasm and secondary infections.

2. Stress dose steroids are required for patients with Addison’s disease and the ensuing hyperglycemia needs to be managed as noted above.

3. Hypothyroid patients have to continue on their current medications. Low levels of TSH may be due to sick euthyroid status and does not require adjustments in doses of medications.

No major changes in management except in cases where coagulopathy and/or electrolyte abnormalities associated with the malignancies have to be addressed in managing SAH. Recurrent bleeding due to refractory thrombocytopenia poses major challenges.

SAH may precipitate Addisonian crises in patients who are chronically on steroids.

Stress dose steroids may be required in steroid-dependent patients and doses need to be adjusted based on hemodynamic response.

This has a high risk of worsening pulmonary function, resulting in hypoxia and worsening outcomes.

In many centers prophylactic intubations are performed, however current coma support selective intubation for patients with Glasgow Coma Score (GCS) less than 8 are to avoid aspiration. During intubation, Lidocaine is used to depress the cough reflex and short-acting anesthetic agents that do not impair cerebral blood flow such as Propofol are used during intubation.

Appropriate antibiotic coverage should be based on likely pathogens and available antibiogram data.

SAH is associated with a high incidence of gastric ulcers (Cushing’s ulcers). These ulcers are prevented or treated with use of Proton pump inhibitors or H2 blockers. Sucralfate has been used as an adjunct medication in a number of cases.

Venous thromboembolism is prevented with the use of stockings and intermittent pneumatic compression in patients with SAH. Enoxaparin is avoided due to the bleeding risk.

Subcutaneous (SC) Heparin has not been tested to access its safety in cases of SAH.

Recent studies indicate that in patients who have had their ruptured aneurysms repaired, pharmacologic thromboprophylaxis with heparinoids can be used 12-14 hours after repair of the ruptured aneurysm.

Severe thrombocytopenia should be corrected to prevent rebleeds and also reduce bleeding associated with the invasive procedures required in the management of SAH. Platelet counts should be maintained above 50,000.

Non-aneurysmal SAH due to hematological pathology form a very small percentage of cases of SAH. In these rare instances the underlying condition has to be addressed with the help of a hematologist.

  • Mental status evaluation is a critical part of SAH management. Altered baseline mental status requires more diligent evaluation and medication adjustments.

  • Patients with SAH have to be sedated in the acute-phase of their management. In the setting of underlying psychiatric disorder or dementia early intubation is recommended for surgical candidates due to the need for better airway protection.

  • Cognitive deficits occur in about 40% of patients. The inability to execute high executive functions, fatigue and sleep disturbances result in reactive depression in many patients for which anti-depressants and psychotherapy are useful therapeutic interventions.

  • Input from psychiatry is required as part of discharge planning.

1. Urgent head CT scan needs to be obtained when there is a decline in mental status.

  • Neurosurgeon and/or Interventional Neuroradiologist on-call needs to be called if there is evidence of a hydrocephalus or a re-bleed.

  • Maintenance of euvolemia, induction of hypertension and/or cerebral angiogram and angioplasty may be required if delayed neurologic deterioration is thought to be due to cerebral vasospasm.

  • Mental status decline in the absence of new CT scan findings should lead to work-up for seizures and starting of anti-seizure medications after excluding a an infectious etiology

2. Blood pressure control: systolic blood pressure should be kept less than 140-150mmHg to reduce incidence of rebleed, and >160mmHg to reduce incidence of vasospasm after treatment of the aneurysm.

  • Labetalol is a choice agent because it also narrows the pulse pressure blunting the adrenergic surge seen with SAH.

  • In patients who are bradycardic, Hydralazine, ACE (Angiotensin converting enzyme) inhibitors or Nicardipine may be used.

  • CNS venodilators such as nitroprusside and nitroglycerin should be avoided if possible in patients with SAH.

3. Electrolytes: sodium level should be within normal limits. Low serum sodium levels lead to cerebral vasospasm. Immediate work-up to distinguish between SIADH and CSW is required to ensure appropriate management.

4. Dyspnea with hypoxia: evaluate patients for aspiration pneumonia or pulmonary edema which may be due to neurogenic pulmonary edema.

1. Length of stay depends on grade of SAH upon presentation, associated complications, pre-existing co-morbidities, and post-operative complications.

2. The average length of stay is 10-14 days.

1. Stable and/or improving mental status and neurological signs.

2. Well controlled blood pressure.

3. Stable medical co-morbidities such as diabetes mellitus, chronic obstructive airway disease, heart failure.

4. Acceptable range for basic metabolic profile and CBC indices.

5. Absence of severe secondary psychosomatic disorders that will stifle rehabilitation efforts.

1. The follow-up appointments should be made prior to discharge and must be included as part of the discharge summary with copies to appropriate consultants in order to avoid lapses in follow-up with appropriate consultants.

2. This a much higher compliance rate in regards to follow-up appointments especially for patients in rehabilitation facilities.

3. Discharge summaries must accompany the patients on the day of discharge to rehabilitation facilities.

4. Pre-appointment calls should be undertaken to confirm scheduled appointments.

1. Neurosurgeon and/or interventional radiologist in 4 weeks.

2. Neurology in 4-6 weeks: depending on associated seizure disorder and/or other neurological deficits.

3. Nephrology and/or Primary Care Physician in 4-6 weeks: depending upon on-going need for adequate blood pressure management.

1. A post-operative cerebral angiogram is done to access the adequacy of the clip and/or coil placement in the affected vessels.

2. A repeat cerebral angiogram needs to be in cases of pretruncal hemorrhage before discharge. The radiologic features of nonaneurysmal pretruncal SAH may be due to a posterior circulation aneurysm in about 15% of cases.

3. A major side-effect after successful intervention is cerebral vasospasm. Transcranial Doppler study is a non-invasive study used to detect and monitor this condition.

4. Basic labs: CBC, Metabolic profile should be within normal limits. For patients on anti-seizure medications, drug levels ought to be within normal limits.

Basic labs: Basic metabolic profile, CBC and serum level of anti-seizure medication.

  • Patients with SAH invariably require placement at Inpatient acute rehabilitation facilities or subacute rehabilitation facilities. In a few cases where the diagnosis is made promptly and there are no major neurological deficits, outpatient rehabilitation programs may be sufficient.

  • Physical/occupational/speech therapy assessments are used as the basis for recommendations for placement.

  • Associated medical co-morbidities and the home environment are additional factors that determine the need for placement and the proposed duration.

1. SAH is associated with poor outcomes due to delay in diagnosis and associated side-effects of the bleed, such as hydrocephalus and cerebral vasospasm.

2. 25% of admitted patients die within 24 hours, and there is a 40-45% mortality within 3 months.

3. Coma at the time of diagnosis is associated with the worse outcome.

4. Patients above the age of 65 and smokers tend to have worse outcomes.

5. A major cause of death is rebleeding which occurs in 5% to 22% of patients in the first 72 hours. “Ultra-early” rebleeding (within 24 hours) has been reported with an incidence of about 15% and a fatality rate of about 70%.

6. Early surgical intervention (within 3 days) in appropriate cases and measures to address cerebral vasospasm are of utmost importance.

7. Aneurysms in posterior circulation have a worse prognosis compared to those in the anterior circulation.

8. In long-term survivors re-bleeds occur in about 3% annually. Medication compliance to ensure adequate blood pressure control in critical in reducing re-bleeds in survivors.

9. Human factors such as ETOH abuse, smoking and cocaine use are associated with high risk of rupture of aneurysms and thus re-bleeds.

There are no specific core indicators for SAH. The current measures used are those applicable to patients in critical care units such as Deep vein thrombosis (DVT) prophylaxis, ventilator-associated pneumonia, skin care protocol and glycemic control.

1. Nimodipine reduces risk of delayed ischemic damage and its use is associated with better functional outcomes. The usual dose is 60mg every 4 hours for 21 days. Its use should not compromise systemic blood pressure; therefore, the dose should be adjusted to prevent hypotension.

2. Patients with documented seizure activity should be maintained with appropriate anti-convulsants.

3. Use of PPIs or H2 blockers prevents associated GI bleed due to stress ulcers (Cushing’s ulcers).

4. DVT prophylaxis requires the use of compression stockings in conjunction with early mobilization. In patients who undergo aneurysmal repair, pharmacologic thromboprophylaxis can be started 12-24 hours after the procedure if done successfully and there is no evidence of recurrence of bleeding.

5. Maintaining normothermia and normoglycemia is necessary to prevent worsening of ischemic neuronal damage.

6. Placement in an inpatient or subacute rehab facility for physical/occupational/speech therapy improves outcomes in post-surgical patients.

7. Measures to prevent the development of pressure ulcers.

8. Post-operative wound care to prevent secondary infections.

9. Use of prophylactic antibiotics in patients with ventriculostomies and other CNS drains have decreased incidence of meningitis.

10. The role of HMG-CoA reductase inhibitors (statins), magnesium and albumin in outcomes of patients with SAH are inconclusive and are still being studied.

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Hillman, J, Fridriksson, S, Nilsson, O, Yu, Z, Saveland, H, Jakobsson, KE. “Immediate administration of tranexamic acid and reduced incidence of early rebleeding after aneurysmal subarachnoid hemorrhage: a prospective randomized study”. J Neurosurg. vol. 97. 2002. pp. 771-778. The routine use of Tranexamic acid is controversial is requires additional studies.

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de Oliveira Manoel, AL, Turkel-Parrella, D, Germans, M. “Safety of early pharmacological thromboprophylaxis after subarachnoid hemorrhage”. Can J Neurol Sci. vol. 41. 2014. pp. 554-561. There is a role for pharmacologic thromboprophylaxis in the management of SAH.

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