Subarachnoid Hemorrhage – Treatment
Neurological
First 5 Minutes
Stabilization – Initial care for patients with SAH involves ABCs and treatment of seizures.3
Intubation:
- patients with GCS of ≤8,
- hemodynamic instability,
- increased ICP, or
- hypoventilation/poor oxygenation.
Intravascular volume resuscitation with isotonic fluids is recommended with a target for euvolemia (while monitoring for hyponatremia).
Acute seizures affect 6-18% of patients with SAH and are treated with levetiracetam or benzodiazepines.4 Avoid phenytoin as associated with worse cognitive outcomes in patients with aneurysmal SAH.5
Pain control with short-acting opiates.
Context
Majority of non-traumatic subarachnoid hemorrhage (SAH) cases are caused by rupture of an intracranial saccular aneurysm.
15-20% of SAH are non-aneurysmal:
- vascular malformations,
- perimesencephalic hemorrhage, and
- intracranial arterial dissection.
In the general population, the prevalence of unruptured intracranial aneurysms is approximately 3%. Aneurysmal subarachnoid hemorrhage occurs at an estimated rate of 6 to 16 per 100,000 population.1
The mean age of aneurysmal rupture is in the range of 50 to 55 years.2
Prognosis
One year mortality rate is 22%.
Long-term complications of SAH include neurocognitive dysfunction, focal neurologic deficits, and epilepsy, with 10% of patients being moderate to severely disabled long-term.
Recommended Treatment
Initial management of aneurysmal SAH
Includes patient stabilization, grading the severity of the SAH, and admitting the patient to an appropriate centre for SAH management.
Stabilization – Initial care for patients with SAH involves ABCs and treatment of seizures.3
Intubation:
- patients with GCS of ≤8,
- hemodynamic instability,
- increased ICP, or
- hypoventilation/poor oxygenation.
Intravascular volume resuscitation with isotonic fluids is recommended with a target for euvolemia (while monitoring for hyponatremia).
Acute seizures affect 6-18% of patients with SAH and are treated with levetiracetam or benzodiazepines.4 Avoid phenytoin as associated with worse cognitive outcomes in patients with aneurysmal SAH.5
Pain control with short-acting opiates.
Admit versus transfer to expert center – Improved outcomes, including lower mortality, are associated with treating patients in centres with neurosurgical and IR capabilities.
Specific management of aneurysmal SAH
SAH is associated with a variety of early complications such as rebleeding, hydrocephalus, cerebral edema, vasospasm, delayed cerebral ischemia, seizures, hyponatremia, cardiopulmonary abnormalities, and neuroendocrine dysfunction. Specific treatments are required to minimize the risk of these complications. These include:
- Blood pressure control
- CPP = MAP – ICP.
- Maintain systolic blood pressure (SBP) <160 mmHg or mean arterial pressure (MAP) <110 mmHg (American Heart & Stroke guidelines).6 In cases of elevated ICP, increases in MAP are needed to maintain adequate CPP to prevent cerebral infarction. For patients that are alert SBP <140mmHg is recommended. Intravenous agents such as labetalol, nicardipine, or enalapril are recommended for BP control.
- Correct coagulopathy – Discontinuation of all antithrombotic agents and reversal of anticoagulation is recommended until a definitive aneurysmal repair is undertaken:
- Platelet transfusion for patients on antiplatelet therapy (ASA, clopidogrel) or platelet count <100,000/microL.
- PCC and intravenous vitamin K for patients on warfarin.
- Idarucizumab for Dabigatran and PCC for other DOACs.
- Brain supportive care is targeted at preventing and managing increases in ICP.7
- Head-of-bed elevation to 30 degrees.
- Analgesia for pain control.
- Eucapneic ventilation.
- Glucose levels are recommended to be maintained at <300 mg/dL as hyperglycemia is a predictor of 28-day fatality in both diabetic and non-diabetic patients with intracranial hemorrhage. Antipyretics are recommended to prevent temperature >37C as fever is associated with increases in ICP and therefore worse outcomes for ICH patients.
- Treat suspected herniation – Osmotic agents such as mannitol and hypertonic saline if needed for rapid lowering of ICP if brain herniation is suspected, followed by emergent neurosurgical intervention.
- Antifibrinolytics – tranexamic acid has NOT been shown to reduce the risk of poor outcomes including death, vegetative state, or severe disability.8
- Seizure prophylaxis – NOT routinely performed. While seizures are associated with poor outcomes, there is some evidence that exposure to phenytoin may be associated with worse neurologic and cognitive outcomes after SAH.5
- Nimodipine (CCB) – Nimodipine 60mg PO or NG Q4H for all patients with aneurysmal SAH starting within 48 hours of symptom onset x 21 days is recommended, to decrease the risk of vasospasm and delayed cerebral ischemia. It has been shown to reduce the odds of deficit, mortality, or both attributed to vasospasm by 0.46.9 The number needed to treat (NNT) with Nimodipine to prevent one poor outcome is 13 (95% CI 8-30).10
- Treat hydrocephalus – Hydrocephalus affects 20-30% of patients with SAH and usually presents within the first few minutes to hours after SAH.11 Immediate CSF diversion using EVD for communicating hydrocephalus or LP for non-communicating hydrocephalus is recommended in patients with deteriorating LOC.
- Secure the aneurysm – most important goal of SAH management is the prevention of rebleeding (4-14% in the first 24 hours) as it is associated with a high mortality of 70%. Early repair of the unsecured aneurysm with surgical clipping or endovascular coiling is recommended within 24 hours.4 Endovascular coiling is preferred to clipping as it is associated with less cognitive impairment at 12 months (controversial ISAT trial).12
Criteria For Transfer To Another Facility
- Admit to high volume centers with neurosurgical and IR services.
- ICU – if intubated.
- Operating room – if urgent EVD placement is required and for aneurysm repair (coiling vs clipping).
Quality Of Evidence?
High
We are highly confident that the true effect lies close to that of the estimate of the effect. There is a wide range of studies included in the analyses with no major limitations, there is little variation between studies, and the summary estimate has a narrow confidence interval.
Moderate
We consider that the true effect is likely to be close to the estimate of the effect, but there is a possibility that it is substantially different. There are only a few studies and some have limitations but not major flaws, there are some variations between studies, or the confidence interval of the summary estimate is wide.
Low
When the true effect may be substantially different from the estimate of the effect. The studies have major flaws, there is important variations between studies, of the confidence interval of the summary estimate is very wide.
Justification
Evidence ranges from Level B (data derived from a single randomized trial or nonrandomized studies) to Level C (consensus opinion of experts, case studies, or standard of care) as summarized in the 2012 American Heart / Stroke Association guidelines.
Related Information
OTHER RELEVANT INFORMATION
Subarachnoid hemorrhage diagnosis
https://www.bcemergencynetwork.ca/clinical_resource/subarachnoid-hemorrhage-diagnosis/Hunt and Hess SAH grading scale
https://www.mdcalc.com/hunt-hess-classification-subarachnoid-hemorrhageWorld Federation of Neurological Surgeons SAH grading scale
https://qxmd.com/calculate/calculator_225/wfns-sah-scale
Reference List
Sarti C, Tuomilehto J, Salomaa V, et al. Epidemiology of subarachnoid hemorrhage in Finland from 1983 to 1985. Stroke 1991; 22:848.
Shea AM, Reed SD, Curtis LH, et al. Characteristics of nontraumatic subarachnoid hemorrhage in the United States in 2003. Neurosurgery 2007; 61:1131.
Suarez JI. Diagnosis and Management of Subarachnoid Hemorrhage. Continuum (Minneap Minn) 2015; 21:1263.
Connolly ES Jr, Rabinstein AA, Carhuapoma JR, et al. Guidelines for the management of aneurysmal subarachnoid hemorrhage: a guideline for healthcare professionals from the American Heart Association/american Stroke Association. Stroke 2012; 43:1711.
Naidech AM, Kreiter KT, Janjua N, et al. Phenytoin exposure is associated with functional and cognitive disability after subarachnoid hemorrhage. Stroke 2005; 36:583.
Connolly ES Jr, Rabinstein AA, Carhuapoma JR, et al. Guidelines for the management of aneurysmal subarachnoid hemorrhage: a guideline for healthcare professionals from the American Heart Association/american Stroke Association. Stroke 2012; 43:1711.
Broderick J, Connolly S, Feldmann E, Hanley D, Kase C, Krieger D, et al. Guidelines for the Management of Spontaneous Intracerebral Hemorrhage in Adults: 2007 Update: A Guideline from the American Heart Association/American Stroke Association Stroke Council, High Blood Pressure Research Council, and the Quality of Care and Outcomes in Research Interdisciplinary Working Group: The American Academy of Neurology affirms the value of this guideline as an educational tool for neurologists. Stroke. 2007 Jun 1;38(6):2001-23.
Baharoglu MI, Germans MR, Rinkel GJ, et al. Antifibrinolytic therapy for aneurysmal subarachnoid haemorrhage. Cochrane Database Syst Rev 2013; :CD001245.
Barker FG 2nd, Ogilvy CS. Efficacy of prophylactic nimodipine for delayed ischemic deficit after subarachnoid hemorrhage: a metaanalysis. J Neurosurg 1996; 84:405.
Feigin VL, Rinkel GJ, Algra A, et al. Calcium antagonists in patients with aneurysmal subarachnoid hemorrhage: a systematic review. Neurology 1998; 50:876.
Muehlschlegel S. Subarachnoid Hemorrhage. Continuum (Minneap Minn) 2018; 24:1623.
Molyneux AJ, Kerr RS, Birks J, et al. Risk of recurrent subarachnoid haemorrhage, death, or dependence and standardised mortality ratios after clipping or coiling of an intracranial aneurysm in the International Subarachnoid Aneurysm Trial (ISAT): long-term follow-up. Lancet Neurol 2009; 8:427.
RESOURCE AUTHOR(S)
DISCLAIMER
The purpose of this document is to provide health care professionals with key facts and recommendations for the diagnosis and treatment of patients in the emergency department. This summary was produced by Emergency Care BC (formerly the BC Emergency Medicine Network) and uses the best available knowledge at the time of publication. However, healthcare professionals should continue to use their own judgment and take into consideration context, resources and other relevant factors. Emergency Care BC is not liable for any damages, claims, liabilities, costs or obligations arising from the use of this document including loss or damages arising from any claims made by a third party. Emergency Care BC also assumes no responsibility or liability for changes made to this document without its consent.
Last Updated Dec 17, 2021
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