Management of Intracerebral Hemorrhage

Please refer to the 2022 Guideline for the Management of Patients With Spontaneous Intracerebral Hemorrhage for complete recommendations.

• What follows are some helpful considerations for clinicians from that review; this information is not exhaustive and is simply designed for efficient review.

Noncontrast Head CT (or Brain MRI) is gold standard for the detection for intracranial hemorrhage and is critical to distinguish ischemic from hemorrhagic stroke. Perform complete blood count, coagulation studies (PT/PTT/INR), and screen for anticoagulant use, liver dysfunction, malignancy, and thrombocytopenia.

• The 2022 AHA guidelines make special note of the deleterious effects of renal failure and hyperglycemia, and make note of the negative associated functional outcome with elevated admission troponin.

Advanced imaging modalities can be useful to help determine risk for hematoma expansion (especially CTA and contrast-enhanced CT) and evaluate for underlying structural lesions, including vascular malformations and brain tumors (CTA, CT venography, contrast-enhanced CT, contrast-enhanced MRI, MRA, and MR venography). According to the 2022 AHA guidelines, the following patient populations should undergo at least noninvasive CTA or MRA. Note that catheter intra-arterial DSA (digital subtraction angiography) is still the gold standard for detection of arteriopathy.

• Patients <70 with lobar ICH
• Patients <45 with deep/posterior fossa ICH
• 45–70-year-olds with deep/posterior fossa ICH without hypertension or signs of small vessel disease
• Any patient with radiologic evidence of macrovascular lesions
• Any patient with primary IVH

Consider MRI for suspected cerebral amyloid angiopathy (CAA), cavernoma, or malignancy. For SBP between 150–220 mmHg, target SBP 130–140 mmHg as soon as possible.

• INTERACT2 and ATACH-2 demonstrated evidence for early, intense BP lowering that established this guideline.

Avoid lowering SBP to <130 mmHg acutely—it may worsen outcomes. Ensure smooth, sustained BP reduction rather than abrupt fluctuations. For warfarin: use 4-factor PCC + IV vitamin K. For direct thrombin inhibitors (dagibatran): use idarucizumab. For factor Xa inhibitors (apixaban, rivaroxaban): use andexanet alfa, or if unavailable, consider aPCC (activated prothrombin complex concentrate) or 4F-PCC (4-factor prothrombin complex concentrate). For heparin: use protamine sulfate. Don't delay treatment while awaiting labs if timing/dose indicates clinical anticoagulation. Platelet transfusions, desmopressin, and TXA have proven effective in reducing bleeding in many clinical scenarios but not in spontaneous ICH. In spontaneous ICH, platelet transfusions are deemed harmful and should not be administered unless emergency craniotomy for hematoma removal. The other treatments are not of proven benefit in spontaneous ICH. TXA (tranexamic acid) and recombinant factor VIIa have limited efficacy in improving outcomes. No definitive benefit shown even in patients with CTA spot sign. ICH expansion occurs very early after onset. Monitor and manage: dysphagia, immobility, hemodynamic instability, infection, delirium, and respiratory failure with loss of consciousness. Use intermittent pneumatic compression (IPC) devices from day 1. Initiate heparin or LMWH 48–96 hrs after onset if no hematoma expansion. Graduated compression stockings are ineffective. IVC filters may be used in select high-bleed-risk patients with VTE. Although hyperglycemia on admissions is associated with worse outcome, avoid overly tight glycemic control because of the potential harms of hypoglycemia. Fever is common and associated with worse outcomes, but aggressive treatment has uncertain benefit. Seizures occur in ~ 20% of patients, mostly within the first 24 hrs. Prophylactic antiseizure drugs have unclear benefit. Continuous EEG for ≥24 hrs is reasonable, especially for comatose patients. "The relationship among seizures, functional outcomes, and mortality is complex and not well defined." International League Against Epilepsy definition: “a transient occurrence of signs and/or symptoms due to abnormal excessive or synchronous neuronal activity in the brain.” American Clinical Neurophysiology Society: “epileptiform discharges averaging >2.5 Hz for ≥10 s (>25 discharges in 10 s) or any pattern with definite evolution and lasting ≥10 s.” Patients with IVH, hydrocephalus, or infratentorial hemorrhage require neurocritical care. Facilities without in-house neurosurgery should stabilize and transfer appropriately. Initiate life-sustaining therapy prior to transfer; a DNAR order does not preclude emergency intervention. Insert EVD for patients with hydrocephalus and reduced consciousness. Consider ICP monitoring if GCS ≤8. Hyperosmolar therapy may help transiently but has unclear long-term benefit. Avoid corticosteroids for ICP management. MIS (e.g., endoscopic or stereotactic aspiration) is safe and may reduce mortality and may improve function but evidence is limited. It requires experienced surgical teams; not superior to craniotomy for all patients.

• The 2022 AHA guidelines primarily rely on data from the largest RCT of MIS (MISTIE III),381 meta-analyses of trials comparing MIS with conventional craniotomy and standard medical care and smaller RCTs (randomized control trials).
• The majority of clinical trials have used ICH volume thresholds of >20 or >30 mL as an inclusion criterion.

Occurs in at least a third of ICH patients and 50% of those will develop hydrocephalus. EVD (external ventricular drainage) is used to treat intracranial hypertension and remove blood products. Thrombolytic irrigation with alteplase or urokinase enhances clot clearance and further reduces mortality. EVD + IVT (intraventricular thrombolysis) is safe and improves survival, but functional outcome benefit is less clear.  

• Perform a baseline severity score.
• Perform non-contrast CT or MRI (to distinguish ischemic stroke from ICH).
• Advanced imaging modalities can be useful to help determine risk for hematoma expansion (especially CTA and contrast-enhanced CT) and evaluate for underlying structural lesions, including vascular malformations and brain tumors (CTA, CT venography, contrast-enhanced CT, contrast-enhanced MRI, MRA, and MR venography).
• Reverse coagulopathies
• See above for details.
• Provide intermittent pneumatic compression for prevention of venous thromboembolism.
• Graduated compression stockings are not beneficial to reduce DVT or improve outcome.
• After 1 to 4 days from onset of bleeding and when bleeding has clearly ceased, low-dose subcutaneous low-molecular-weight heparin or unfractionated heparin may be considered for prevention of venous thromboembolism in patients with lack of mobility.
• In ICH patients with symptomatic DVT or PE, provide either systemic anticoagulation or IVC filter placement.
• Time from hemorrhage onset, hematoma stability, cause of hemorrhage, and overall patient condition are all factors that can help in deciding between anticoagulation and IVC filter.

• For SBP between 150–220 mmHg, target SBP 130–140 mmHg. Do not over-treat. Aim for smooth BP control.

• Monitor and treat hyperglycemia
• Monitor and treat fever
• Monitor for dysphagia
• Monitor for myocardial ischemia
• Monitor and treat seizures
• Consider continuous EEG monitoring in patients with reduced level of arousal out of proportion to the degree of brain injury.
• Prophylactic antiseizure medication is not recommended.

• Ventricular drainage for hydrocephalus when clinically indicated.
• Do NOT administer corticosteroids routinely for elevated ICP from ICH.

• Cerebellar hemorrhage with progressive deterioration OR with either:
• Brainstem compression
• Hydrocephalus from ventricular obstruction
• Supratentorial evacuation is typically reserved for deteriorating patients.