Stroke Hemoragik

01Pathophysiology

Hemorrhagic stroke results from the rupture of a blood vessel within or around the brain, leading to direct parenchymal damage and secondary injury from mass effect, raised intracranial pressure, and toxic effects of blood breakdown products.

Intracerebral hemorrhage (ICH) accounts for approximately 15 to 20% of all strokes. The most common mechanism is chronic hypertension, which causes lipohyalinosis and fibrinoid necrosis of small penetrating arteries supplying the basal ganglia, thalamus, pons, and cerebellum. These weakened vessels rupture under hemodynamic stress, producing a rapidly expanding hematoma. The hematoma itself causes immediate mechanical disruption of neural tissue, and surrounding edema develops over hours to days due to thrombin release, complement activation, and breakdown of the blood-brain barrier. Hematoma expansion, which occurs in roughly one-third of patients within the first few hours, is the primary driver of early neurological deterioration and is the key target of acute intervention.

In elderly patients, cerebral amyloid angiopathy (CAA) is the predominant cause of lobar ICH. Beta-amyloid deposits weaken cortical and leptomeningeal vessel walls, predisposing to recurrent lobar hemorrhages. Unlike hypertensive ICH, CAA-related hemorrhages tend to be superficial, multifocal, and associated with cortical microbleeds on MRI.

Subarachnoid hemorrhage (SAH) is most commonly caused by rupture of a saccular (berry) aneurysm, typically at arterial bifurcations in the Circle of Willis. The sudden release of arterial blood into the subarachnoid space causes an acute rise in intracranial pressure, often producing transient global cerebral hypoperfusion (explaining the sudden loss of consciousness seen in many patients). The blood in the subarachnoid space triggers an inflammatory cascade that, over the following days, leads to cerebral vasospasm (peak incidence days 3 to 14) and delayed cerebral ischemia (DCI), the leading cause of morbidity in patients who survive the initial bleed.

The connection between pathophysiology and clinical presentation is direct: the location of an ICH determines the neurological deficit (putaminal hemorrhage causes contralateral hemiplegia; thalamic hemorrhage causes contralateral sensory loss with gaze deviation; cerebellar hemorrhage causes ataxia, vomiting, and rapid obtundation from brainstem compression), while in SAH the diffuse irritation of meninges by blood explains the headache, neck stiffness, and photophobia.

02Classification and Clinical Manifestation

Clinical Grading Scales

Hunt-Hess Scale (SAH) per the PNPK Stroke 2026:

WFNS Scale and modified Fisher Scale are also recommended by the PNPK for risk stratification and prediction of vasospasm/DCI.

NIHSS is used for all stroke types to quantify neurological deficit severity, with the following interpretation:

ICH Score (for prognosis in intracerebral hemorrhage):

03Diagnostic Workup

Summary Table

The best initial test for any patient presenting with sudden neurological deficit is a non-contrast CT scan of the head. This is the single most important step: it immediately differentiates hemorrhagic from ischemic stroke, which dictates entirely different management pathways. On CT, acute ICH appears as a hyperdense (white) lesion within the brain parenchyma. SAH appears as hyperdensity within the basal cisterns, Sylvian fissures, or interhemispheric fissure. PNPK Stroke 2026 mandates that brain imaging (CT without contrast or MRI DWI) be completed within 20 minutes of arrival for patients who are candidates for reperfusion therapy.

For ICH, PNPK Stroke 2026 recommends CTA and/or venography to rule out macrovascular causes in the following scenarios: lobar ICH in patients younger than 70 years, posterior fossa or deep hemorrhage in patients younger than 45 years, or posterior fossa/deep hemorrhage in patients aged 45 to 70 without a history of hypertension. The "spot sign" on CTA (a focus of contrast enhancement within the hematoma) predicts hematoma expansion and worse outcomes.

For SAH, if the initial CT is negative but clinical suspicion remains high, a lumbar puncture should be performed to look for xanthochromia or red blood cells that do not clear across sequential tubes. If SAH is confirmed, CTA is performed to localize the aneurysm. DSA remains the gold standard for detecting and characterizing cerebral aneurysms, AVMs, and other vascular malformations, and is indicated when CTA/MRA results are inconclusive .

All ICH patients must undergo hemostasis testing (PT/INR, aPTT, platelet count), and any identified coagulopathy should be corrected as rapidly as possible.

04Management and Treatment

Summary Table: Intracerebral Hemorrhage

Summary Table: Subarachnoid Hemorrhage

Step-by-Step Management

Intracerebral Hemorrhage: Acute Phase

The immediate priorities upon confirming ICH on non-contrast CT are airway protection, blood pressure reduction, coagulopathy reversal, and assessment for surgical intervention.

Blood pressure is the single most actionable target in the first hour. PNPK Stroke 2026 states that an intensive systolic target of 140 mmHg achieved within 1 hour is safe and improves functional outcomes. For patients presenting with systolic BP >220 mmHg or mean arterial pressure >150 mmHg, aggressive IV antihypertensive therapy with monitoring every 5 to 15 minutes is indicated. The preferred agents are nicardipine (5 to 15 mg/hr IV infusion, titrated), labetalol (10 to 20 mg IV bolus, repeat as needed), or diltiazem. The key clinical caveat: maintain cerebral perfusion pressure (CPP) above 60 to 70 mmHg, especially in patients with raised intracranial pressure.

Coagulopathy reversal must be initiated immediately upon diagnosis. For patients on vitamin K antagonists with INR >=2, 4-factor PCC is recommended alongside IV vitamin K 5 to 10 mg infused at less than 1 mg/min. FFP may be used if PCC is unavailable. For patients on DOACs, idarucizumab is the reversal agent for dabigatran; for factor Xa inhibitors (rivaroxaban, apixaban, edoxaban), FEIBA or PCC can be considered, and activated charcoal may be given if the last dose was within 2 hours. For heparin-related hemorrhage, protamine sulfate 10 to 50 mg IV over 1 to 3 minutes is indicated with close monitoring for hypersensitivity.

Surgical intervention is indicated for cerebellar hemorrhage >=15 mL with neurological deterioration, brainstem compression, or obstructive hydrocephalus; emergent evacuation with or without EVD is recommended over medical management alone. For supratentorial ICH >20 to 30 mL with GCS in the moderate range (5 to 12), minimally invasive hematoma evacuation (stereotactic aspiration or endoscopic approach, with or without thrombolytics) can reduce mortality compared to medical therapy alone. Decompressive craniectomy may be considered in patients with supratentorial ICH who are comatose, have large hematomas with significant midline shift, or have ICP refractory to medical therapy.

VTE prophylaxis begins with intermittent pneumatic compression from day 1. Compression stockings are explicitly not recommended . After 1 to 4 days, once the hemorrhage is stable, subcutaneous heparin or LMWH may be started.

Subarachnoid Hemorrhage: Acute Phase

For SAH patients with Hunt-Hess grade 1 or 2 (good grade), PNPK Stroke 2026 recommends bed rest with the head elevated to 30 degrees, IV access, close neurological monitoring, and early referral for definitive treatment (coiling or clipping) ideally within 24 hours. For Hunt-Hess grade 3, 4, or 5 (poor grade), ABC stabilization is the priority, with intubation for airway protection if consciousness is impaired, and initiation of ICP management if herniation signs are present.

Nimodipine 60 mg orally every 4 hours for 21 days is the cornerstone of vasospasm prophylaxis and is the only calcium channel blocker proven to improve neurological outcomes in SAH. Other CCBs have not shown benefit and are not recommended.

Aneurysm securing should occur as early as possible. For posterior circulation aneurysms, endovascular coiling is preferred over clipping. For anterior circulation aneurysms with good clinical grade where both approaches are feasible, coiling is recommended as the first option to improve 1-year outcomes. Wide-neck aneurysms may benefit from stent-assisted coiling or flow diverters.

Long-term Prevention of Recurrence (ICH)

PNPK Stroke 2026 emphasizes that long-term blood pressure control with a target of <130/80 mmHg is the most important step to prevent recurrent ICH. Smoking cessation, avoiding excessive alcohol (>2 drinks/day), and abstinence from illicit drugs are recommended. Long-term warfarin should be avoided in patients with spontaneous lobar ICH due to high recurrence risk. Anticoagulant therapy, if indicated, should be delayed at least 4 weeks in patients without mechanical heart valves.

05Differential Diagnosis and Distractors

06Traps and High-Yield Pearls

The most common way students lose points on hemorrhagic stroke questions is by failing to distinguish between the two subtypes (ICH vs. SAH) and applying the wrong management algorithm. A vignette describing a 55-year-old hypertensive patient with sudden hemiplegia and a CT showing a hyperdense putaminal lesion is ICH, and the next best step is IV antihypertensive therapy targeting systolic <140 mmHg. A vignette describing a 45-year-old with the "worst headache of my life," neck stiffness, and diffuse subarachnoid blood on CT is SAH, and the next best step is CTA to identify the aneurysm, followed by early securing (coiling or clipping) and nimodipine.

Another frequent trap involves coagulopathy reversal. When a patient on warfarin presents with ICH and an elevated INR, the answer is 4F-PCC plus IV vitamin K, not FFP alone. FFP is slower to administer, requires large volumes, and takes longer to normalize INR. PCC provides rapid, concentrated factor replacement. Students must also remember that vitamin K alone takes hours to work and does not provide immediate reversal; it is given alongside PCC to prevent rebound INR elevation after the PCC effect wears off.

For SAH, students commonly select antifibrinolytics (such as tranexamic acid) to prevent rebleeding. PNPK Stroke 2026 explicitly states that routine antifibrinolytic use does not improve clinical outcomes and is not recommended. The correct answer for preventing rebleeding is early aneurysm securing (coiling or clipping), ideally within 24 hours.

Students should also remember that nimodipine is the only calcium channel blocker recommended for SAH vasospasm prophylaxis. It works by improving neurological outcomes (likely through neuroprotective effects rather than vasodilation per se), and other CCBs have not shown the same benefit. The dose, 60 mg orally every 4 hours for 21 days, is frequently tested.

For surgical indications, the highest-yield fact is that cerebellar hemorrhage >=15 mL with brainstem compression or hydrocephalus is an indication for emergent surgical evacuation. This is one of the few surgical emergencies in hemorrhagic stroke where there is strong evidence of mortality benefit. Supratentorial ICH surgery remains more nuanced, with minimally invasive approaches showing the most promise.

Finally, compression stockings are a classic distractor. PNPK Stroke 2026 explicitly states they have no benefit for DVT prevention or outcome improvement in ICH. The correct DVT prophylaxis is intermittent pneumatic compression starting from day 1.

The core competency being tested across hemorrhagic stroke questions is the ability to rapidly identify the hemorrhage type, initiate the correct acute stabilization sequence (BP control for ICH, aneurysm securing for SAH), select the appropriate reversal agent when coagulopathy is involved, and recognize the surgical indications that separate candidates who benefit from intervention from those who do not.