Subarachnoid Hemorrhage: ED Critical Care Management

Authors: Philip Jarrett, MD, MBA (EM Resident Physician, UT Southwestern Medical Center / Parkland Memorial Hospital) and Avi Ruderman, MD (EM Attending Physician, UT Southwestern Medical Center / Parkland Memorial Hospital) // Reviewed by: Anthony DeVivo, DO (EM-Critical Care, Icahn School of Medicine at Mount Sinai Hospital); Alex Koyfman, MD (@EMHighAK); Brit Long, MD (@long_brit)

Case

You are working in the emergency department (ED) of a regional medical center without advanced surgical services. A 48-year-old male arrives by EMS transport with a severe unilateral headache that started one hour prior to arrival. He is vomiting and complaining of neck pain but is otherwise neurologically intact. A non-contrast head computed tomography (CT) demonstrates a diffuse hyperdensity within the sylvian fissure and intraventricular space consistent with subarachnoid hemorrhage (SAH). His blood pressure is 200/120 mm Hg. How would you manage his blood pressure? What preparations would you take prior to transfer?

During your resuscitation, the patient loses consciousness and becomes unresponsive to sternal rub. How does this information affect your transfer preparations? What is your airway approach?

Family arrives and reports that the patient slipped and hit his head on the edge of a kitchen counter around the time of headache onset, but they aren’t entirely sure if the fall was before or after the headache started. The CT read also notes a contusion to the R parietal scalp without clear evidence of skull fracture. How does this information change your management?

Background

SAH is one of the most dangerous conditions we evaluate as emergency physicians, with all-cause mortality rates reported as high as 42% at 30 days.¹ SAH can result from three broad categories of disease, including traumatic vascular catastrophe, non-traumatic aneurysmal rupture and non-traumatic non-aneurysmal hemorrhage (arteriovenous malformations, arterial dissections, central nervous system tumors and others).^2-4 While the majority of SAH cases stem from head trauma, 80% of non-traumatic SAH results from aneurysmal rupture.^5,6 This subset of SAH is referred to in the literature as aneurysmal SAH (aSAH).

Diagnosis

This article will provide a brief summary of the current diagnostic approach for SAH in the ED and will focus most heavily on the ED management and disposition. The standard ED algorithm for the evaluation of SAH begins with a non-contrast head CT, which is most sensitive (98-100%) for patients who present within 6 hours of symptom onset.^7,8 Because the sensitivity of this imaging declines for patients with delayed presentation (>6 hours), a negative CT in the population of delayed presenters is classically followed by lumbar puncture (LP) to assess for xanthochromia.^9,10 Due to the inherent limitations and adverse effects of LP (coagulopathy, patient positioning, time requirement, post-LP headache, etc.), more recent literature has explored CT angiography (CTA) of the brain as an alternative.^11,12

One study found that CT followed by LP was more cost effective than CT followed by CTA or CT followed by observation.¹³ The ACEP clinical policy for acute, non-traumatic headaches lists a level C recommendation for using either a lumbar puncture or a CTA to rule out SAH after a negative CT brain, endorsing the use of shared decision making to address the pros and cons of each modality.¹⁴ However, the AHA/ASA guidelines for the management of aSAH still endorse the use of LP following a negative CT (Class I, Level of Evidence B).¹⁵ CTA can be used to evaluated

The ACEP clinical policy also includes a Level B recommendation for the use of the Ottawa Subarachnoid Hemorrhage Rule for ruling out SAH without a CT scan.¹⁴

Management

Unfortunately, there is no clear benefit for any medical intervention with regards to patient-centered outcomes (as opposed to surgical interventions) based on current data. Most of the following management strategies are based on expert consensus and physiologic theory.

As with most emergent ED presentations, management begins with an assessment of airway safety and the potential need for endotracheal intubation. When possible, an effort should be made to utilize short-acting sedation and paralytics to retain the neurological exam for consultants. However, institutional norms and provider experience should be considered to ensure that the safest and most efficient approach is utilized, thereby minimizing secondary brain injury from apneic time and hypoxia. When hospital transfer is necessary to obtain neurosurgical consultation, the decision to intubate should be tailored to the patient’s current condition, the capabilities of the transfer team and the transfer route/duration. This decision may be made in conjunction with the receiving center.

Hemodynamics should also be monitored closely in the ED, not only in the context of traumatic SAH for which additional bodily injuries may be identified but also for the potential development of the Cushing triad (hypertension, bradycardia and irregular respirations) indicative of rapidly rising intracranial pressure (ICP) with imminent brainstem compression.¹⁶ Importantly, patients with hypertension and bradycardia, regardless of respiratory status, have a two-fold risk of death from intracranial hemorrhage compared to patients who present with stable vital signs.¹⁶ The definitive treatment for subarachnoid hemorrhage ultimately requires neurosurgical consultation and this should be prioritized as a core component of early management.

When any intracranial hemorrhage (ICH) is suspected, reversal of coagulopathy, in combination with blood pressure (BP) management discussed below, has been shown to provide significant mortality benefit. In a large retrospective cohort study of patients with anticoagulation-associated intracranial hemorrhage, rapid reversal of warfarin anticoagulation to a goal INR < 1.3 within 4 hours of presentation combined with reduction of systolic BP to less than 160 mm Hg resulted in an absolute mortality risk reduction of 7.2%.¹⁷  To this end, any coagulopathy, whether acquired or innate, should be reversed. Specific reversal strategies have been detailed for each class of anticoagulant and coagulopathy in the context of intracranial hemorrhage by multiple sources and is amalgamated by an UpToDate article on the topic.⁶ To review, anticoagulant medications should be held. Warfarin should be reversed with functional coagulation factors via 4-factor prothrombin complex concentrate (PCC) or fresh frozen plasma (FFP), dependent upon institutional availability. Due to the short half-life of these products, vitamin K should also be administered to promote endogenous production of functional coagulation factors. Unfractionated heparin and low molecular weight heparin should be reversed with protamine sulfate. The preferred reversal agent for factor Xa inhibitors and fondaparinux is PCC or andexanet alfa. Lastly, reversal of dabigatran requires the targeted monoclonal antibody idarucizumab or PCC. Regarding antifibrinolytic therapy, at least two large multicenter studies do not support the use of antifibrinolytic agents such as tranexamic acid (TXA) or aminocaproic acid for this purpose.^18,19  While the CRASH-3 trial suggested mild mortality benefit among patients with mild to moderate traumatic brain injury with evidence of ICH on initial CT who received TXA within 3 hours of injury, there were several issues with study design.²⁰  Though the trial also demonstrated pharmacologic safety of TXA, recommendations for the standardized use of TXA within a SAH subgroup are not yet available, and at the time of publication of this article, TXA for SAH is not recommended.

The goal of BP management remains a point of contention in the literature. Numerous studies demonstrate the benefit of aggressive BP reduction for prevention of hematoma expansion and rebleed.^21,22 However, such an approach significantly increases the risk of subsequent cerebral ischemia associated with cerebral vasospasm.^21,22 As a result, there has not yet been convincing evidence to support mortality benefit with specific BP goals. Nonetheless, current recommendations by the Neurocritical Care Society endorse BP reduction to a goal systolic less than 160 mm Hg.²² This is commonly achieved at our center with titratable agents, such as labetalol, nicardipine, or clevidipine.

SAH can result in increased intracranial pressure (ICP) through two mechanisms: hemorrhage into the intracranial cavity and hydrocephalus through obstruction of the ventricular system. As ICP rises, the patient’s cerebral perfusion pressure can become compromised, leading to loss of consciousness.  Unfortunately, most emergency physicians currently lack the capacity to obtain objective, quantitative measurements of ICP in this cohort. Although ultrasound measurement of optic nerve sheath diameter (US-ONSD) is developing traction as a proxy for ICP measurement, the utility of US-ONSD specifically for SAH has been challenged in the literature. Although additional studies are needed, multiple small human studies have shown that US-ONSD is an inconsistent predictor of ICP in patients with SAH and may, in some circumstances, relate inversely to ICP.^23-25 Lumbar puncture opening pressure (LPOP) also has not been extensively evaluated as a method of ICP measurement, but limited data suggests that it is an unreliable modality for ICP measurement.^26,27

Nonetheless, there are several strategies for modulating the intracranial pressure to improve CPP, mostly aimed at reducing ICP. The first is hyperosmolar therapy. Hypertonic saline (HTS) and mannitol pull fluid from the brain parenchyma into blood vessels by increasing the intravascular oncotic pressure.²⁸ However, recent evidence suggests that HTS has a more sustained effect on ICP and a more dramatic improvement of CPP when compared to mannitol.^28-30 A significant complication of aSAH during the following two weeks after injury is cerebral vasospasm and delayed cerebral ischemia. It is believed that avoidance of hypovolemia may be protective. For this reason, we further recommend HTS over mannitol.^29,30 No clear guidelines are available for the dosing strategy but one approach is to give 3.2 mL/kg of 5% hypertonic saline over 10-15 minutes. Concentrations higher than 5% need to be infused via central line. Sodium bicarbonate is an alternative to hypertonic saline with a sodium concentration of 8.4%.³¹  To convert to a different concentration, multiply the sodium dose in mL by 5, then divide by the new concentration [for example, 320 mL of 5% saline would be 533 mL of 3% saline (320 * 5 / 3), or 190 mL of sodium bicarbonate (320 * 5 / 8.4)]. Additional doses can be administered every four hours so long as the serum sodium remains less than 155 mEq/L.

In addition to maintaining euvolemia, oral nimodipine at a dose of 60 mg PO every 4 hours should be administered to prevent vasospasm and delayed cerebral ischemia.¹⁵ Nimodipine should be held in the setting of hypotension or when there is concern for inadequate CPP (such as with altered mental status in the absence of an intracranial pressure monitor), given the lack of evidence nimodipine’s CPP effects. Furthermore, patients who develop decreasing levels of consciousness may be experiencing reduced CPP or cerebral vasospasm.^15,32 In this scenario, antihypertensive medications should be held. Interestingly, this population has shown mortality benefit with vasopressor support using norepinephrine or phenylephrine that bolsters CPP, though this decision is best made in collaboration with consultants.³²

Adjunctive strategies to decrease the ICP include elevating the head of the bed to 30-45 degrees.^33,34 Raising the head of the bed decreases hydrostatic pressure and is a reasonable adjunct. Hyperventilation can significantly decrease ICP in the acute setting but must be used judiciously given evidence that prolonged hypocarbia reduces CPP.¹⁵  Hyperventilation induces cerebral vasoconstriction which may be deleterious to the goal of preventing vasospasm and should be avoided unless herniation appears imminent.

The definitive treatment for aSAH is aneurysm coiling or clipping, given that 30% of patients with untreated aSAH will rebleed in the first month following initial hemorrhage.³⁵  Coiling is accomplished through endovascular means and boasts superior outcomes, while clipping is a surgical procedure available to patients that do not qualify for coiling.^{15, 35} Patients with SAH should be transferred to facilities capable of providing these therapies even if an aneurysm isn’t initially found, as repeat angiography will often be performed several days later. All patients should be admitted to a neurological intensive care unit for frequent neurological examination, close hemodynamic monitoring and titration of any infused agents.¹⁵

While several grading scales for aSAH have been published, they have limited utility in predicting clinical outcomes and do not change management in the ED.³⁶ The most important clinical predictors of poor outcome include patient age, volume of blood seen on CT scan and GCS score.^36,37 The formal scoring systems are largely designed to predict post-surgical complications. As a result, it is our opinion that there is little role for these grading scales in the ED and are not discussed here.

There are scenarios in which it is unclear whether the patient’s SAH represents an aneurysmal or post-traumatic etiology. While no specific blood pressure targets or hyperosmolar therapies have been recommended for traumatic SAH, it is our practice that all SAH be treated as aneurysmal until proven otherwise, so as not to deny benefit to the aSAH cohort.

Case Conclusion

When our case begins, the patient is hypertensive with an intact mental status. Titratable IV blood pressure agents such as labetalol, nicardipine or clevidipine should be started with a goal of lowering the systolic blood pressure to less than 160 mm Hg so long as the patient maintains consciousness. Additionally, 60 mg of nimodipine should be administered orally every 4 hours.

When the patient loses consciousness, we should be concerned that his cerebral perfusion pressure is compromised. At this point, we need to stop any antihypertensives and, if needed, use vasopressors to support his CPP. IV HTS can be administered while raising the head of the bed to 45 degrees. A repeat head CT should be obtained to evaluate for hydrocephalus and the patient will need either an external ventricular drain or a bolt to monitor his intracranial pressure.

So long as the story is unclear whether the patient had a traumatic injury prior to the headache, it is safest to treat the patient as if he presented with an aneurysmal SAH with the therapies described above.

Takeaway points

• Maintaining cerebral perfusion pressure is the priority in subarachnoid hemorrhage.
• In conscious patients, target a systolic blood pressure of 140 – 160 mm Hg and administer nimodipine.
• In unconscious patients, support CPP with vasopressors in consultation with neurosurgery.
• To treat elevated ICP, use hypertonic saline. The dose is 3.2 mL/kg of 5% hypertonic saline.

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