Non-traumatic bleeding into brain parenchyma; higher mortality than ischemic stroke.
Also known as: ICH, intracerebral hemorrhage, intraparenchymal hemorrhage, hypertensive hemorrhage
Overview
Spontaneous (non-traumatic) bleeding into the brain parenchyma, with or without extension into the ventricles or subarachnoid space. Distinguished from subarachnoid hemorrhage and traumatic hemorrhage.
Epidemiology
~10-15% of all strokes but accounts for ~40% of stroke mortality. 30-day mortality 30-50%. More common in Black, Hispanic, and Asian populations.
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Question 1HematologyMedium
A 72-year-old female develops sudden onset severe headache and confusion while on warfarin for atrial fibrillation (AF) (INR 4.8). Non-contrast CT shows a large right parietal intracerebral hemorrhage with midline shift. Which of the following is the most appropriate immediate management?
ARecombinant activated factor VIIa plus IV tranexamic acid
BIdarucizumab infusion plus IV vitamin K administration
CPlatelet transfusion plus IV desmopressin and cryoprecipitate
D4-factor prothrombin complex concentrate plus IV vitamin K
EFresh frozen plasma transfusion plus IV vitamin K administration
Reveal answer & full explanation
Correct answer: D — 4-factor prothrombin complex concentrate plus IV vitamin K
ARecombinant activated factor VIIa plus IV tranexamic acid
BIdarucizumab infusion plus IV vitamin K administration
CPlatelet transfusion plus IV desmopressin and cryoprecipitate
D4-factor prothrombin complex concentrate plus IV vitamin K✓
EFresh frozen plasma transfusion plus IV vitamin K administration
Why 4-factor prothrombin complex concentrate plus IV vitamin K is correct
4-factor prothrombin complex concentrate (4-PCC) (Kcentra) contains factors II, VII, IX, X, protein C and S — reverses INR within 15-30 minutes.
Given weight-based: 25-50 units/kg depending on INR.
Superior to fresh frozen plasma (FFP): faster, smaller volume, no crossmatch, no thaw time required.
Vitamin K 10 mg IV ensures sustained reversal because PCC lasts only 6-12 hours.
Why the others are wrong
Fresh frozen plasma transfusion plus IV vitamin K administration — second-line if PCC unavailable; requires large volume (15-30 mL/kg), slow infusion, and carries risk of volume overload (right-concept-slower-agent).
Recombinant activated factor VIIa plus IV tranexamic acid — corrects only factor VII, carries thrombotic risk, and is not recommended for warfarin reversal (confused-with wrong agent).
Platelet transfusion plus IV desmopressin and cryoprecipitate — addresses platelet dysfunction and fibrinogen, not warfarin-mediated coagulopathy (confused-with wrong mechanism).
Idarucizumab infusion plus IV vitamin K administration — idarucizumab is the specific reversal agent for dabigatran, which many patients with atrial fibrillation take, but it is an antibody fragment that binds only dabigatran and does nothing for the warfarin-induced deficiency of factors II, VII, IX and X; the INR of 4.8 marks a warfarin coagulopathy that needs immediate factor replacement with 4-PCC (confused-with DOAC reversal)
Additional high-yield points
Direct oral anticoagulant (DOAC) reversal agents: idarucizumab (Praxbind) for dabigatran; 4-PCC for apixaban and rivaroxaban in the US, where andexanet alfa (Andexxa) was withdrawn from the market in December 2025.
INR targets post-reversal: full reversal preferred for life-threatening hemorrhage.
Question 2NeurologyEasy
A 74-year-old man with hypertension and atrial fibrillation treated with warfarin is brought to the emergency department 45 minutes after the abrupt onset of severe occipital headache with repeated vomiting. He is alert and fully oriented but cannot sit up or stand without toppling to the right. Blood pressure is 204/108 mm Hg. His speech is slurred, there is coarse nystagmus on rightward gaze, and his right hand overshoots the target on finger-to-nose testing. Strength and sensation are normal in all four limbs, and the pupils are 3 mm and briskly reactive. Noncontrast head CT confirms an acute intraparenchymal hematoma. On the basis of the neurologic examination, which of the following is the most likely location of the hematoma?
APutaminal intraparenchymal hemorrhage
BThalamic intraparenchymal hemorrhage
CPontine intraparenchymal hemorrhage
DOccipital lobar intraparenchymal hemorrhage
ECerebellar intraparenchymal hemorrhage
Reveal answer & full explanation
Correct answer: E — Cerebellar intraparenchymal hemorrhage
APutaminal intraparenchymal hemorrhage
BThalamic intraparenchymal hemorrhage
CPontine intraparenchymal hemorrhage
DOccipital lobar intraparenchymal hemorrhage
ECerebellar intraparenchymal hemorrhage✓
Why Cerebellar intraparenchymal hemorrhage is correct
Abrupt occipital headache, repeated vomiting, and truncal ataxia severe enough that the patient cannot sit unsupported is the classic cerebellar hemorrhage syndrome
Cerebellar hemispheric signs are ipsilateral because the cerebellar outflow crosses twice before it reaches the limb, so toppling to the right, coarse gaze-evoked nystagmus on right gaze, and right-hand dysmetria place the hematoma in the right cerebellar hemisphere
Cerebellar hemorrhage spares the corticospinal and sensory tracts, which is why strength and sensation are intact while coordination and truncal balance are destroyed; dysarthria here is the scanning speech of a cerebellar lesion, not a corticobulbar sign
Chronic hypertension is the leading cause of spontaneous cerebellar hemorrhage, which typically arises from small penetrating branches near the dentate nucleus; warfarin multiplies the risk of intracerebral hemorrhage severalfold and drives hematoma expansion over the first hours, which is why reversal cannot wait on the surgical decision
The posterior fossa has no room to absorb a mass, so a patient who looks well can deteriorate abruptly from fourth-ventricle compression with obstructive hydrocephalus or direct brainstem compression, which is why these patients are watched in an ICU with serial examinations
Reverse the anticoagulation immediately; the AHA/ASA 2022 spontaneous intracerebral hemorrhage guideline gives a Class 1 recommendation for immediate surgical evacuation, with or without an external ventricular drain, when a cerebellar hemorrhage causes neurologic deterioration, brainstem compression, or hydrocephalus from ventricular obstruction, or when the hematoma volume is 15 mL or greater, and it recommends against an external ventricular drain alone in place of evacuation; the 15 mL volume criterion is new in 2022, so an alert patient with a large clot can meet the operative threshold before any deterioration and the older deterioration-only or 3 cm teaching is superseded
Why the others are wrong
Putaminal intraparenchymal hemorrhage - the single most common hypertensive site, but it sits against the internal capsule and announces itself with contralateral hemiparesis and hemisensory loss and conjugate eye deviation toward the side of the bleed; ataxia of the trunk with intact strength does not fit a capsular lesion (the trap is reaching for the most common location instead of the one the findings name)
Thalamic intraparenchymal hemorrhage - the strongest competitor here, because thalamic astasia is a genuine inability to stand or sit unsupported that is out of proportion to any weakness; what separates it is the rest of the thalamic syndrome, contralateral hemisensory loss out of proportion to weakness plus forced downward and inward gaze with small poorly reactive pupils and impaired upgaze, while this patient has full sensation, briskly reactive 3 mm pupils, and coarse gaze-evoked nystagmus on gaze toward the side of the limb findings; a thalamic bleed can in fact produce limb dysmetria when it involves the ventral lateral nucleus that relays cerebellar outflow, but that thalamic ataxia is contralateral to the clot, and horizontal gaze-evoked nystagmus is a cerebellar and vestibular gaze-holding sign rather than a thalamic one (a thalamic clot large enough to press on the dorsal midbrain gives convergence-retraction nystagmus with impaired upgaze instead), so the posterior fossa findings settle this case
Pontine intraparenchymal hemorrhage - gives early coma, pinpoint (about 1 mm) reactive pupils, and quadriparesis with posturing because the bleed destroys the reticular activating system and both corticospinal tracts, so the deficits are bilateral rather than crossed (crossed cranial-nerve-plus-long-tract findings come from small unilateral brainstem lesions, paramedian ones such as Millard-Gubler as well as lateral ones, not from a large central pontine hematoma); appendicular dysmetria with truncal ataxia in an awake, conversant patient localizes dorsal to the pons, across the fourth ventricle, in the cerebellar hemisphere
Occipital lobar intraparenchymal hemorrhage - the headache is occipital and a lobar clot is a real pattern in an older anticoagulated patient, so this is tempting, but occipital headache locates the pain rather than the hematoma; an occipital lobar bleed declares itself with a contralateral homonymous hemianopia and leaves no truncal ataxia, limb dysmetria, or gaze-evoked nystagmus.
Additional high-yield points
Location signatures of spontaneous intracerebral hemorrhage: putamen gives contralateral hemiparesis with gaze deviation toward the lesion, thalamus gives hemisensory loss with forced downward gaze, pons gives coma with pinpoint pupils, cerebellum gives headache, vomiting, and ataxia with no hemiparesis
Lobar hemorrhage in an older patient, especially a recurrent one, points to cerebral amyloid angiopathy rather than hypertensive vasculopathy
Abrupt severe headache with vomiting also fits aneurysmal subarachnoid hemorrhage, and it stays on the differential until imaging is read: an alert patient with a supple neck does not exclude it, since nuchal rigidity needs hours of blood breakdown to develop and Hunt-Hess grade 1 patients are fully alert; what settles it here is the CT showing an intraparenchymal clot plus focal cerebellar localization, since subarachnoid blood is extra-axial and does not produce lateralized limb dysmetria
Cerebellar infarction produces a nearly identical bedside syndrome, which is why noncontrast CT precedes any treatment decision: blood is hyperdense immediately, while an early infarct is usually invisible on CT and needs MRI with diffusion-weighted imaging
The HINTS examination (head impulse, nystagmus, test of skew) is more sensitive than early MRI with diffusion-weighted imaging for a central cause, since DWI misses roughly 15 to 20 percent of posterior-circulation strokes in the first 24 to 48 hours, but it is validated only in a continuous acute vestibular syndrome with nystagmus, never in episodic or positional vertigo; headache, dysarthria, or limb ataxia sends the patient to imaging regardless
Reverse warfarin-associated intracranial hemorrhage with 4-factor prothrombin complex concentrate plus IV vitamin K; use idarucizumab for dabigatran and 4-factor PCC for apixaban or rivaroxaban (andexanet alfa was withdrawn from the US market in late 2025)
For spontaneous intracerebral hemorrhage of mild to moderate severity presenting with a systolic pressure of 150-220 mm Hg, lower it smoothly to a target near 140 mm Hg and keep it in the 130-150 range; avoid large rapid drops and wide variability
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Tumor (primary or metastatic — melanoma, RCC, choriocarcinoma, thyroid, lung)
Sympathomimetic drugs (cocaine, methamphetamine)
Coagulopathy, thrombocytopenia, vasculitis
Pathophysiology
Rupture of small perforating arteries such as the lenticulostriate branches of the MCA (lipohyalinosis and Charcot-Bouchard microaneurysms from chronic HTN) or amyloid-laden cortical vessels causes blood to dissect into surrounding brain tissue. Mass effect, perihematomal edema, and toxic effects of blood breakdown products drive secondary injury. Hematoma expansion in the first 6 hours is the strongest predictor of poor outcome.
Clinical presentation
Symptoms
Sudden focal neurologic deficit (similar to ischemic stroke)
Headache (more common and severe than ischemic stroke)
Nausea/vomiting
Decreased level of consciousness, often progressive over minutes-hours
Hypertensive ICH classically in basal ganglia (putamen most common), thalamus, pons, or cerebellum. ICH score predicts 30-day mortality.
Differential diagnosis
Ischemic stroke — Indistinguishable clinically — CT differentiates; ICH more often presents with headache, vomiting, depressed consciousness, and very high BP
Subarachnoid hemorrhage — Thunderclap headache, meningismus, blood in basal cisterns rather than parenchyma
Traumatic ICH / contusion — History of trauma; coup-contrecoup pattern; often frontal or temporal poles
Brain tumor with hemorrhage — Surrounding edema disproportionate to hematoma size; heterogeneous enhancement; metastatic primaries above
Hemorrhagic transformation — Recent ischemic stroke, classic arterial territory of hypodensity with petechial or confluent hemorrhage
Cerebral venous sinus thrombosis — Lobar hemorrhage in non-arterial territory; risk factors (OCPs, pregnancy, thrombophilia); empty delta sign on CTV/MRV
Diagnostic workup
Labs
CBC, platelets, PT/INR, PTT — assess coagulopathy
BMP, glucose, troponin
Toxicology screen (cocaine, methamphetamine in young patients)
Type and screen
Imaging
Non-contrast head CT — high-density acute hematoma; immediately diagnostic
Educational use only. This outline is a study aid for PA students and is not medical advice or a substitute for clinical judgment. FirstPassPA is an independent study tool and is not affiliated with, endorsed by, or sponsored by NCCPA or PAEA. PANCE® and PANRE® are registered trademarks of the National Commission on Certification of Physician Assistants; End of Rotation™ is a program of the Physician Assistant Education Association.