Last reviewed: March 2026
Contents
MDM Templates
Intracerebral Hemorrhage
Patient presents with acute neurologic deficits and elevated blood pressure. CT head demonstrates intracerebral hemorrhage. No history of trauma. This is a neurosurgical emergency requiring immediate blood pressure control and reversal of any coagulopathy to limit hematoma expansion.
Most hematoma expansion occurs in the first 3–4 hours. Priorities are blood pressure reduction, anticoagulant reversal if applicable, and neurosurgical consultation. Not consistent with ischemic stroke given hemorrhage on CT. Workup directed at identifying contributing factors and preventing secondary injury.
If on anticoagulation: Anticoagulated patients have the highest risk of hematoma expansion. Reversal agents administered emergently. Coagulopathy correction confirmed with repeat labs.
If signs of elevated ICP: Clinical signs of herniation present. Hyperosmolar therapy initiated. Neurosurgery consulted emergently regarding operative intervention.
Plan: Blood pressure controlled with nicardipine infusion. Neurosurgery consulted. Admit to ICU.
Cerebellar Hemorrhage
Patient presents with acute onset headache, vomiting, gait ataxia, and inability to walk. CT head demonstrates cerebellar hemorrhage. This is a neurosurgical emergency — cerebellar hemorrhages can rapidly deteriorate from brainstem compression and obstructive hydrocephalus.
Cerebellar hemorrhage carries the highest risk of rapid deterioration among ICH locations due to posterior fossa anatomy. A patient who looks stable can herniate within hours. Neurosurgery consulted emergently regarding need for suboccipital decompression or EVD placement.
Plan: Blood pressure controlled. Neurosurgery consulted emergently. Admit to ICU with frequent neuro checks. Low threshold for intubation if declining.
Clinical Education
Blood Pressure Control
Blood pressure reduction limits hematoma expansion and must start immediately. Most expansion occurs in the first 3–4 hours. Don’t wait for the ICU to start a drip.[1]
Nicardipine is the preferred agent — pure arterial vasodilator with no effect on heart rate, easily titratable. Start at 5 mg/hr, titrate up by 2.5 mg/hr every 5–15 minutes to goal. Once at goal, decrease to 3 mg/hr and re-titrate up to find the maintenance dose (the initial titration is essentially a load).
Labetalol is the alternative: 20 mg IV push over 1–2 minutes, then 20 mg every 3–5 minutes until target BP, then start infusion at 1–8 mg/min. Avoid in patients with reactive airway disease, severe bradycardia, or heart block.
BP target: SBP <140 is reasonable for most patients presenting with SBP 150–220. The INTERACT II trial showed better functional outcomes with SBP <140 within 1 hour compared to <180.[2] However, ATACH-2 found no benefit to intensive reduction (110–139) vs standard (140–179) and higher rates of renal adverse events in the intensive group.[3] For patients presenting with SBP >220, a less aggressive initial reduction is reasonable — drop by 15–25% rather than targeting a specific number.
Cerebral perfusion pressure = MAP − ICP. Keep MAPs high enough to perfuse, keep ICP low. Perihematoma ischemia is not a validated concern for MAPs above 75.
Anticoagulant Reversal
Anticoagulated patients have the most hematoma expansion in the first hour. Reversal must happen simultaneously with BP control, not after.[4]
| Agent | Reversal |
| Warfarin | 4-factor PCC (KCentra) + Vitamin K 10 mg IV. Check INR 15 min post-PCC (goal <1.5). Recheck at 5 hours. PCC lasts 5–7 hours — vitamin K bridges the gap. FFP 15 mL/kg is the alternative if PCC unavailable. |
| Dabigatran | Idarucizumab (Praxbind) 5 g IV. If unavailable: PCC 25–50 U/kg. Consider activated charcoal if within 2 hours of ingestion. Hemodialysis if feasible. |
| Rivaroxaban, Apixaban, Edoxaban | Andexanet alfa if available. Otherwise 4-factor PCC (KCentra) 50 U/kg. Consider activated charcoal if within 2 hours of ingestion. |
| Heparin | Protamine 1 mg per 100 units of heparin (based on recent dose). |
| Enoxaparin (LMWH) | Protamine 1 mg per 1 mg of enoxaparin (only ~60% reversal). Timing matters — less effective >8 hours after last dose. |
| Antiplatelets (ASA, clopidogrel) | DDAVP 0.3 mcg/kg. Avoid platelet transfusion per the PATCH trial (worse outcomes).[5] |
| tPA | Cryoprecipitate (goal fibrinogen >200). Consider TXA but know the thrombosis risk. |
| Thrombocytopenia | Platelets <100K: consider transfusion. Platelets <50K: transfuse. |
Hyperosmolar Therapy
Only use with clinical signs of elevated ICP — blown pupil, declining GCS, or optic nerve sheath diameter >5 mm on ultrasound. Do not give prophylactically based on CT appearance alone.
Mannitol 20%: For adults, give the 500 mL bag wide open. Must place a Foley and match urine output with isotonic crystalloid to avoid hypovolemia and renal injury.
Hypertonic saline: 250 mL of 3% NaCl over 10–15 minutes. Can repeat. No Foley requirement. Preferred if the patient is hypotensive or hypovolemic (mannitol will make both worse).
Intubation Considerations
Pretreatment: Consider fentanyl 1–2 mcg/kg to blunt the ICP surge from laryngoscopy. Preoxygenate with NC under a non-rebreather. Have nicardipine push-dose and push-dose epinephrine at bedside for hemodynamic swings.
Induction: Etomidate 0.3 mg/kg is the most hemodynamically neutral. Ketamine is a reasonable alternative — the old concern about raising ICP has been largely debunked.
Paralysis: Succinylcholine is acceptable — the transient fasciculations have not been shown to meaningfully affect ICP. The advantage is a faster return of the neurologic exam.
Post-intubation sedation: Propofol is preferred — best evidence for decreasing ICP and is seizure-protective. Keep the patient adequately sedated to avoid ICP spikes from agitation.
Ventilation: Target normocapnia (EtCO2 35–40). Do not hyperventilate unless actively herniating — routine hyperventilation decreases cerebral blood flow. Sat goal ≥95%. Avoid high PEEP if possible (increases intrathoracic pressure, impairs venous return from the brain).
Seizure Prophylaxis
Traumatic ICH: yes, prophylax. Levetiracetam (Keppra) 1 g IV is the standard choice — fewer drug interactions than phenytoin and no need to monitor levels.
Spontaneous ICH: not routinely recommended. Per AHA/ASA guidelines, routine prophylactic AEDs are not indicated for spontaneous ICH. Treat seizures if they occur. Subcortical (lobar) hemorrhages have the highest seizure risk.[1]
Presentation by Lesion Location
| Location | Presentation |
| Putamen | Hemiplegia, hemisensory loss, homonymous hemianopsia, gaze palsy, stupor/coma |
| Thalamus | Hemiplegia, hemisensory loss, aphasia or neglect, upgaze palsy with miotic unreactive pupils |
| Cerebellum | Gait ataxia, vomiting, headache, neck stiffness, gaze palsy, facial weakness. Can rapidly deteriorate from brainstem compression. |
| Pons | Total paralysis, pinpoint reactive pupils, absent horizontal eye movements, deep coma within minutes of onset. Often fatal. |
| Lobar (subcortical) | Depends on lobe: parietal (contralateral hemiplegia), occipital (hemianopsia). Highest incidence of seizure. Consider amyloid angiopathy in elderly. |
Disposition
All ICH patients are admitted to the ICU. There is no discharge scenario for acute intracerebral hemorrhage. These patients need continuous blood pressure monitoring, frequent neuro checks, and neurosurgical availability.
Transfer if no neurosurgery available. Ensure 2 IV access sites, BP controlled on a drip, benzodiazepines available for seizure, and intubation meds drawn up if not already intubated. Do not delay transfer for additional imaging.
CTA head is important for prognostication — a contrast blush (spot sign) predicts ongoing hematoma expansion. Also identifies underlying aneurysm or vascular malformation as the bleeding source.
References
- Greenberg SM, Ziai WC, Cordonnier C, et al. 2022 Guideline for the management of patients with spontaneous intracerebral hemorrhage. Stroke. 2022;53(7):e282-e361. PubMed
- Anderson CS, Heeley E, Huang Y, et al. Rapid blood-pressure lowering in patients with acute intracerebral hemorrhage (INTERACT2). N Engl J Med. 2013;368(25):2355-2365. PubMed
- Qureshi AI, Palesch YY, Barsan WG, et al. Intensive blood-pressure lowering in patients with acute cerebral hemorrhage (ATACH-2). N Engl J Med. 2016;375(11):1033-1043. PubMed
- Kuramatsu JB, Gerner ST, Schellinger PD, et al. Anticoagulant reversal, blood pressure levels, and anticoagulant resumption in patients with anticoagulation-related intracerebral hemorrhage. JAMA. 2015;313(8):824-836. PubMed
- Baharoglu MI, Cordonnier C, Al-Shahi Salman R, et al. Platelet transfusion versus standard care after acute stroke due to spontaneous cerebral haemorrhage associated with antiplatelet therapy (PATCH). Lancet. 2016;387(10038):2605-2613. PubMed
tydotphrase.com 