Subarachnoid hemorrhage: ED presentation, evaluation, and management

Authors: Mikalah Ward, MD (EM Resident Physician, University of Kentucky); Susan Owens, MD (EM Attending Physician, University of Kentucky) // Reviewed by: Jessica Pelletier, DO (EM Education Fellow, Washington University in St. Louis); Alex Koyfman, MD (@EMHighAK); Marina Boushra, MD (EM-CCM Attending, Cleveland Clinic Foundation)

Case

A 62-year-old male with past medical history of hypertension (HTN), hyperlipidemia (HLD), and prior cerebrovascular accident (CVA) presents to the emergency department (ED) via ambulance. The patient has baseline left-sided weakness, but his wife noticed that he developed dense left-sided paralysis and left facial droop a few hours ago. His last known normal was 5 hours prior to ED presentation. On arrival, the patient is taken directly to CT scan due to concerns for CVA. During their report, medics note that the patient had three episodes of emesis during transport and received antiemetics. National Institutes of Health Stroke Scale (NIHSS) is 13; vital signs include pulse 86 beats/minute (bpm), blood pressure 164/94 mmHg, and saturation of 98% on room air. The patient is in no acute distress. He is dysarthric but nods in agreement when asked if he is dizzy. Glasgow coma scale (GCS) is 12. The CT room is dark and the ED provider notes the patient’s pupils are 5 mm on the right and 3 mm on the left but briskly reactive bilaterally. As the CT is completed, the patient becomes more somnolent and the ED team electively intubates him due to concern for continued clinical deterioration. CT reveals subarachnoid hemorrhage (SAH) with midline shift.

What is the typical presentation of SAH in the ED?

What are the next steps in the management of this patient?

What other examination findings are expected?

What additional workup is necessary in the ED?

Introduction

SAH has the potential for rapid progression and devastating outcomes. SAH is broadly categorized into traumatic SAH versus spontaneous SAH. Traumatic brain injury (TBI) is the most common cause of SAH, and aneurysm rupture is the most common cause of spontaneous SAH.^1,2 The etiology of the SAH will lead to differences in patient presentation, evaluation, and management.

Presentation

Traumatic SAH occurs following a direct or indirect traumatic mechanism leading to TBI that allows for bleeding into the subarachnoid space.³ Common associated injuries may include skull fractures, intracerebral contusion, cervical spine injuries, and vascular injuries of the head and neck.³ Depending on GCS score and distracting injuries, patients may or may not complain of headache or exhibit gross neurological deficits. Vital signs may be abnormal in the setting of increased intracranial pressure (ICP) leading to the Cushing triad of bradycardia, hypertension, and irregular respirations. However, the presence of other traumatic injuries must be considered when assessing vitals.

Spontaneous SAH is classically taught as presenting with a “thunderclap headache,” a headache that is sudden onset and at maximal intensity at the time of onset.  Spontaneous SAH accounts for 2-3% of patients who present to the ED with headache.⁴ Patients who are significantly altered due to SAH may not be able to complain of headache.⁴ Common symptoms of SAH on presentation include vomiting, neck stiffness, altered mental status or decreased level of consciousness, hemiparesis, and seizure-like activity.⁴

Regardless of the underlying etiology, patients with SAH may experience increased ICP. This occurs because the calvarium is a fixed space with a limited ability to tolerate additional volume, and once the scant potential space is occupied by blood, any further bleeding causes the ICP to increase exponentially.^5,6  The Cushing triad is highly specific but not sensitive for increased ICP.^5,6   Because ICP can rapidly increase, changes in mental status and vital signs must be carefully monitored throughout evaluation and management.

Evaluation

History and Physical Exam

As with any presentation to the ED, history and physical exam are crucial to evaluating a patient with concern for SAH. Any personal or family history of intracranial aneurysm should be elicited. Other important pieces of clinical history when considering SAH are prior central neurological pathology such as TBI, CVA, or masses and any known coagulopathy or use of anticoagulant or antiplatelet medications. Patients on anticoagulants should be considered for emergent reversal as this is essential to reduce hematoma expansion.⁷ For patients with known coagulopathies, early factor replacement is critical. Particularly in hemophilia, recombinant activated factor VII (rFVIIa) or activated prothrombin complex concentrate (aPCC) can be lifesaving.⁸ In traumatic SAH, history and physical examination should also include mechanism of injury and associated traumatic injuries.

All patients with concern for SAH need a rapid primary survey to assess the airway, breathing, and circulation as well as a comprehensive neurologic exam to create a baseline for the patient. This neurological evaluation should include assessment and documentation of the GCS, the presence of any neurologic deficits, and an NIHSS. Baseline neurological deficits from prior pathology should be elicited from the patient or family members if possible. Identifying signs of increased ICP and impending herniation, such as progressive abnormalities in consciousness or vital sign abnormalities, is critically important when assessing clinical severity.

Labs  

Laboratory evaluation should be broad to assess for other contributing medical conditions and to complete the patient’s clinical picture. There are no specific guidelines for labs that should be collected in SAH. However, evaluating for underlying intrinsic (thrombocytopenia, liver or renal disease, factor deficiencies) or extrinsic (anticoagulant or antiplatelet use) coagulopathy can help guide management.

Imaging  

Non-contrast head computed tomography (NCHCT) may be obtained rapidly and is sensitive for the detection of SAH within 6 hours of symptom onset.⁹ Delayed NCHCT is less sensitive due to decreased visibility of blood collection secondary to red blood cell (RBC) degradation. CT angiography (CTA) is growing in favor for SAH assessment as the arterial-timed contrast highlights abnormalities such as aneurysm and active extravasation. Negative CTA in the setting of a negative non-contrast head CT has a post-test probability of SAH of <1%; however, there have not been large prospective studies examining the use of CTA for the diagnosis of SAH to date.^10,11

Magnetic resonance imaging (MRI) is not recommended as a primary imaging modality for the diagnosis of SAH due to test duration (which can delay life-saving interventions), as well as the fact that the mixing of blood with cerebrospinal fluid (CSF) may delay the transition of hemoglobin to its deoxyhemoglobin state that is best imaged on MRI.¹⁰ Additionally, discussion with radiology and neurology is advisable prior to obtaining an MRI, as data is not available to guide the specific timing of the test following symptom onset.¹⁰ The most recent SAH guidelines, published in 2012, still recommend NCHCT and lumbar puncture (LP) for the diagnosis of SAH; CTA and MRI may be considered on a case-by-case basis according to local institutional protocols.^11,12

Lumbar puncture  

Historically, a negative NCHCT in the setting of high suspicion for SAH or a negative NCHCT after 6 hours of symptom onset would be followed by lumbar puncture (LP).⁷  The utility of LP is increased when the NCHCT is obtained after 6 hours of symptom onset and LP can be completed prior to 12 hours after symptom onset.¹⁰ Xanthochromia – yellowing of the CSF due to the presence of bilirubin from RBC breakdown – is pathognomonic for SAH and can be identified on visual inspection or spectrophotometry in the setting of high clinical suspicion and insufficient RBC in CSF to be diagnostic of SAH.^10,13 A limitation of LP is the risk of a traumatic tap, in which RBCs are introduced into the CSF via direct vessel injury by the LP needle; unfortunately, there has been no specific data or process produced to reliably differentiate a traumatic tap from the presence of subarachnoid blood and the presence of RBCs can obscure xanthochromia.¹⁰ LP is also an invasive procedure that may not be appropriate for all patients, particularly those with coagulopathy; in such cases, other diagnostic testing like CTA should be considered.¹⁰

Management

Initial management of suspected SAH in the first few minutes of presentation to the ED needs to be directed at addressing immediate life threats on primary survey. Once SAH has been identified, management should be focused on preventing hematoma expansion, preventing re-bleed, limiting delayed ischemia, reducing intracranial pressure, and preparing for definitive management.² These patients also warrant early consultation by neurology and neurosurgery for definitive intervention and management.

Hematoma expansion  

Reducing blood pressure to a level that limits bleeding but maintains perfusion is critical to limit hematoma expansion, especially in spontaneous SAH. Regarding hemorrhagic stroke, older studies recommended an SBP goal of <140 mmHg, but the recent ATACH2 trial identified no statistically significant difference in outcomes with SBP goals significantly under 140 mmHg.¹⁴ The American Stroke Association (ASA) and American Heart Association (AHA) recommend SBP <160 mmHg until definitive management of the bleed is completed.¹² Nicardipine is the antihypertensive agent of choice for blood pressure control in SAH.¹² Initial dosing of nicardipine is 5 mg/h, increasing by 2.5mg/h every 15 minutes with a max of 15mg/h.¹⁵ Institutional titration protocols may differ. Reversal of anticoagulation must also be completed if applicable.⁷

Delayed Cerebral Ischemia (DCI)

DCI is unlikely to be a complicating factor in the ED setting, as its presentation is delayed, occurring between day 3 and 21 post-spontaneous SAH.¹⁶ Oral nimodipine should be prophylactically administered to all spontaneous SAH.¹² It is the only medication recommended by ASA guidelines for spontaneous SAH and supported by data from randomized controlled trials to improve morbidity.^11,12,17 Recommended nimodipine dosing is 60 mg orally every 4 hours for SAH.¹⁸

Seizure  

Seizure is common in the setting of acute SAH, especially spontaneous SAH, due to cerebral and meningeal irritation. Unfortunately, seizures in patients with SAH increase the risk of rebleeding.¹⁹ Prophylactic antiepileptic drugs (AEDs) are only loosely recommended in the most recent ASA guidelines, as there is limited data with often conflicting outcomes.¹² A few studies have shown that phenytoin with a loading dose of 1 g decreases seizure incidence in spontaneous SAH.¹⁹ Unfortunately, phenytoin has many potential side effects and drug-drug interactions, rendering it unfavorable in many clinical scenarios.¹⁹ There is poor data to guide the duration of AED use following spontaneous SAH.¹⁹ Studies comparing levetiracetam and phenytoin for seizure prophylaxis in patients with spontaneous SAH showed an increased incidence of seizure in the levetiracetam group.¹⁹ The levetiracetam group did demonstrate a lower rate of death and discharge to nursing homes, but levetiracetam as seizure prophylaxis in spontaneous SAH  has not been studied adequately to be recommended in current guidelines.¹⁹

AEDs are more commonly used as needed in traumatic SAH.¹⁹ In post-traumatic seizure (broadly, not only traumatic SAH), phenytoin with a loading dose of 20 mg/kg demonstrated a lower incidence of seizure compared to placebo.¹⁹ Levetiracetam use in TBI patients has been demonstrated to have increased epileptiform activity on EEG compared to phenytoin, but no increase in seizures.¹⁹ Its improved side effect profile over phenytoin is favorable, but there is not enough evidence to support its use over phenytoin according to the Brain Trauma Foundation Guidelines.²⁰

Intracerebral pressure management  

Clinical picture and progress will determine if an ICP monitor is necessary. This can be placed surgically and pressure goals are managed by neurology and neurosurgery. There are interventions that can be taken to clinically lower the ICP in the ED. Raising the head of the bed angle to more than 30 degrees reduces ICP by facilitating cerebral venous drainage, but decreases brain oxygenation and circulation; there are currently no guidelines regarding this practice for SAH.²¹  Mannitol and hypertonic saline are known to reduce ICP in TBI patients but there is less evidence for use in SAH.²² Hypertonic saline (HTS) has been shown to improve cerebral blood flow (CBF) and is recommended for ICP reduction in the most recent ASA guidelines.¹² A 2020 neurocritical care review of cerebral edema management recommends the use of HTS in SAH patients without specific sodium level goals, simply recommending symptom-based bolus dosing. They cite studies using 23.4% HTS at 30-60 mL per dose and 23.5% HTS at 2 mL/kg per dose.²² While hyperventilation is known to objectively decrease ICP, it has become increasingly controversial and there is no consistent society-supported guideline on its use in SAH currently. It is a strategy to reduce CBF and therefore decrease ICP, however, it can increase DCI and therefore is no longer recommended therapy for ICP management in spontaneous SAH.²³ Conflicting results exist for the use of hyperventilation in TBI, but if used should be temporary and with close monitoring of perfusion and oxygenation.²³

Surgical intervention 

The decision for surgical intervention needs to be made with the interventionalist performing the procedure. The patient may require clipping or coiling if an aneurysm is identified.²⁴ Craniotomy may be necessary for hematoma evacuation and cerebral decompression. Additionally, external ventricular drain (EVD) may be necessary to reduce ICP, specifically if there are signs of clinical deterioration or progressive ventricular enlargement.²⁵ Aneurysm coiling is cited in the most recent ASA guidelines and the 2020 review of those guidelines as a critically important, morbidity and mortality-improving intervention in spontaneous SAH where aneurysm is identified.^11,12

Traumatic SAH

The brain injury guidelines (BIG) were designed to assist level 1 trauma centers in stratifying TBI management and include guidelines on traumatic SAH. If any criteria within a risk stratification category are met, the patient should be managed based on the recommendations of that level.²⁶ Figure 1 demonstrates that trace, localized, and scattered SAH carry different levels of recommended therapeutic plans, with other factors also influencing management. There have been studies to extrapolate this data to smaller centers which demonstrates that the BIG can be used to guide transfer necessity in traumatic SAH.²⁷ Prudent transfer of patients to a center with neurosurgical capabilities should be considered in any SAH, though this is not well studied.

Pearl and Pitfalls 

• Sudden-onset headaches (particularly in the presence of other neurological abnormalities) should raise concern for SAH; however, not all SAH present with headaches. 
• LP can be difficult to interpret due to the potential for traumatic tap, so CTA is growing in favor as a diagnostic modality for SAH. However, there is no significant prospective data to support use at this time and this is an area of controversy with differing expert opinions.
• Blood pressure control with SBP goal <160 mmHg and prevention of hematoma expansion should be a priority.  Nicardipine is the preferred agent.
• Symptomatically-directed bolus dosing of 23.5% HTS can improve CBF. 
• Traumatic SAH should be managed following the BIG guidelines until more data becomes available.

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