Author: Molly Piccione, DO
The Case:
An older woman with PMH of ESRD is found unresponsive by her home health aide. On arrival to the Emergency Department (ED), the patient’s BP is 173/111 mm Hg, HR 109/min, RR 30/min, and SpO2 92% on room air. She is responsive only to painful stimuli and has a right gaze deviation. A fingerstick shows glucose of 106 mg/dL. The patient is intubated for respiratory failure and obtundation, and a stroke code is activated.
The non-contrast CT:
The Diagnosis: Spontaneous Intracranial Hemorrhage
Spontaneous intracranial hemorrhage (ICH) is the second most common cause of stroke behind infarction, representing up to ~20% of all strokes and accounting for ~50% of all stroke-related deaths.[1,2] Of these, approximately one-quarter of all spontaneous ICH occur in the setting of oral anticoagulant use.[3] The biggest risk factor for spontaneous ICH is hypertensive vasculopathy, but it may also be seen in the setting of cerebral amyloid, arteriovenous malformation (AVM), ruptured berry aneurysm, ischemic stroke conversion, tumors, and others. Magnetic resonance imaging suggests that the underlying hyalinosis/amyloidosis leads to microscopic pseudoaneurysms that both rupture and compress other fragile pseudoaneurysms, leading to clinically significant bleeding. Classically, these patients present with headache, vomiting, and decreased mental status, but because ICH may be clinically indistinguishable from an ischemic stroke, CT is required to differentiate the two.
The Goals in the ED: Prevent hematoma expansion, edema, and herniation
In 2015, the American Heart Association and American Stroke Association (AHA/ASA) jointly released a set of guidelines for the management of spontaneous ICH.[4] If you’re thinking to yourself, did we even have DOACS then? The answer is “Yes.” But your head-scratching is apt because a lot has changed in our understanding of how to manage these intracranial bleeds since 2015 (including the invention of specific DOAC reversal agents).
Blood Pressure Goals
These are based on a few landmark trials
- 1. ATACH I showed no safety differences in lowering systolic blood pressure (SBP) to <140 compared to 140-179 mm Hg[5]
- 2. INTERACT2 demonstrated that lowering SBP to < 140 mm Hg, compared to <180 mm Hg did not reduce the risk of death or severe disability but improved the modified Rankin Score at 90 days[6]
- 3. ATACH II evaluated patients with spontaneous ICH with volume < 60 cc and GCS > 4 and demonstrated no mortality benefit in lowering SBP to <140 with nicardipine when compared to 140-179 mm Hg
Based on these, the AHA/ASA recommends the following:
- 1. If presenting SBP 150 – 220 mm Hg, lowering to < 140 mm Hg is safe
- 2. If presenting SBP > 220 mm Hg, it may be reasonable to consider aggressive reduction of BP with IV infusion
Seizure Prophylaxis
The AHA/ASA recommends against the routine use of seizure prophylaxis, citing that it is not associated with improved neurologic function during long-term follow-up.[4] However, the 2019 Meta-Analysis that informed this recommendation included eight studies, only one of which was an RCT and only two of which used levetiracetam as its antiepileptic agent.[8] Given the 15% risk of seizure after ICH and its safety profile, levetiracetam should be considered for patients in lobar hemorrhage – seizure seems to be more common in ICH with lobar involvement than those with a true, lacunar bleed.
Takeaway: Routine seizure prophylaxis is not recommended but may be considered in patients with lobar hemorrhage.
Hemostatic Agents
ED management of ICH is aimed heavily at decreasing the hematoma expansion. Logically, Tranexamic acid (TXA), an agent that shows decreased hematoma expansion in spontaneous ICH, is often considered. However, the TXA for hyperacute primary IntraCerebral Haemorrhage (TICH-2) Trial showed no functional benefit or mortality benefit at 90 days. Of note, this study excluded patients who were on anticoagulants.[9]
Takeaway: TXA has not shown benefit for the treatment of spontaneous ICH.
Antiplatelet Use
The PATCH Trial, an RCT published in the Lancet in 2016, recommends against the use of platelet transfusion for the treatment of spontaneous ICH in the setting of antiplatelet use. This study found that those receiving platelet transfusion to counteract baseline anti-platelet therapy were twice as likely to die or becoming functionally dependent.[10]
Takeaway: Platelets are not indicated for the treatment of antiplatelet use in spontaneous ICH (but may be indicated for associated thrombocytopenia)
Osmotic Therapy
A 2011 meta-analysis of RCTs comparing equimolar doses of hypertonic saline to mannitol for treatment of elevated ICP (with quantitative measurement) showed a relative risk of 1.16 (95% Cl, 1.00–1.33) for pressure control when using hypertonic saline compared to mannitol and an average pressure decrease of 2 mm Hg more with hypertonic saline.[11]
Takeaway: Hypertonic Saline may be more effective than mannitol for lowering ICP.
Prognostication
The last part of the AHA/ASA Guidelines includes a recommendation against prognostication in the first 24 hours. Specifically, they warn against a new DNR order for patients whose goals of care don’t preclude aggressive treatment. Although this Class III recommendation is informed by low-quality evidence (Level of Evidence C), it is suggested that de-escalation of care may be its own predictor of poor outcomes.
Takeaways
- 1. Lowering SBP < 140 is safe and may improve outcomes but is not recommended for presenting SBP > 220
- 2. Hypertonic saline may be slightly better for lowering ICP compared to mannitol
- 3. Seizure prophylaxis is not routinely recommended except in lobar involvement
- 4. Platelets should not be used for reversal of antiplatelet agent
- 5. Consider aggressive care in the first 24 hours
- 6. Treatment should be personalized for each patient
References
[3] Schols AM, Schreuder FH, van Raak EP, et al. Incidence of oral anticoagulant–associated intracerebral hemorrhage in the Netherlands. Stroke. 2014;45(1):268-270. doi:10.1161/STROKEAHA.113.003003
[5] Antihypertensive Treatment of Acute Cerebral Hemorrhage (ATACH) investigators. Antihypertensive treatment of acute cerebral hemorrhage. Crit Care Med. 2010;38(2):637-648. doi:10.1097/CCM.0b013e3181b9e1a5
[6] Anderson CS, Heeley E, Huang Y, et al. Rapid Blood-Pressure Lowering in Patients with Acute Intracerebral Hemorrhage. N Engl J Med. 2013;368(25):2355-2365. doi:10.1056/nejmoa1214609
[7] Qureshi AI, Palesch YY, Barsan WG, et al. Intensive Blood-Pressure Lowering in Patients with Acute Cerebral Hemorrhage. N Engl J Med. 2016;375(11):1033-1043. doi:10.1056/nejmoa1603460
[8] Angriman F, Tirupakuzhi Vijayaraghavan BK, Dragoi L, Lopez Soto C, Chapman M, Scales DC. Antiepileptic Drugs to Prevent Seizures After Spontaneous Intracerebral Hemorrhage. Stroke. 2019;50(5):1095-1099. doi:10.1161/strokeaha.118.024380
[9] Sprigg N, Flaherty K, Appleton JP, et al. Tranexamic acide for hyperacute primary IntraCerebral Haemorrhage (TICH-2): an international, randomised, placebo-controlled, phase 3 superiority trial. Lancet. 2018 doi:10.1016/S0140-6736(18)31033-X
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