Hemorrhagic Stroke and SAH

Subarachnoid hemorrhage — by mechanism

• Trauma: the most common cause of subarachnoid blood overall; the stem must specify spontaneous/nontraumatic before aneurysm becomes the answer
• Ruptured saccular aneurysm: the large majority of spontaneous SAH; degeneration of the tunica media at bifurcation apices where wall shear stress is highest
• Non-aneurysmal perimesencephalic SAH: presumed venous or perforator bleeding; angiogram-negative, benign course
• Arteriovenous malformation, dural AV fistula, arterial dissection
• Mycotic (infective) aneurysm: septic emboli from infective endocarditis seed distal MCA branches — a distal, peripheral aneurysm is the tell
• Reversible cerebral vasoconstriction syndrome: recurrent thunderclap headaches, "sausage-on-a-string" vessels, often postpartum or after serotonergic/sympathomimetic drugs

Intracerebral hemorrhage — by mechanism

• Hypertensive small-vessel disease: deep bleeds (putamen > thalamus > pons > cerebellum) from lipohyalinotic penetrators and Charcot-Bouchard microaneurysms
• Cerebral amyloid angiopathy: lobar, recurrent, elderly; cortical microbleeds and superficial siderosis on gradient-echo/SWI
• Anticoagulant- or antithrombotic-associated bleeding, thrombocytopenia, hepatic coagulopathy
• Vascular malformations: AVM and cavernous malformation — the leading structural cause in patients under 45
• Hemorrhage into tumor (melanoma, renal cell, choriocarcinoma, thyroid, lung), hemorrhagic transformation of infarct, cerebral venous sinus thrombosis, vasculitis, moyamoya

Subarachnoid Hemorrhage (SAH)

• Aneurysm rupture mechanism: Saccular ("berry") aneurysms located at arterial bifurcations in the Circle of Willis (particularly anterior communicating artery and middle cerebral artery) rupture due to wall weakness and hemodynamic stress, causing sudden accumulation of blood in the subarachnoid space
• Acute intracranial hypertension: Blood in the subarachnoid space impairs cerebrospinal fluid reabsorption at arachnoid granulations, causing rapid elevation of intracranial pressure and global cerebral hypoperfusion
• Vasospasm cascade: Oxidative stress from hemoglobin breakdown products (especially oxyhemoglobin) triggers endothelial dysfunction, smooth muscle contraction, and delayed cerebral vasospasm (typically days 4-14 post-hemorrhage), leading to secondary ischemic injury independent of initial hemorrhage volume
• Meningeal inflammation: Blood triggers sterile meningeal inflammation with release of pro-inflammatory cytokines (IL-1, IL-6, TNF-α) and free radical production, contributing to neuronal damage and blood-brain barrier disruption
• Rebleeding risk: Hemostatic plug at rupture site is fragile; untreated aneurysms have 4% rebleeding risk in first 24 hours and cumulative 50% risk by 6 months

Intracerebral Hemorrhage (ICH)

• Hypertensive ICH: Chronic hypertension causes lipohyalinosis of penetrating vessels (particularly lenticulostriate arteries supplying basal ganglia), leading to vessel rupture and hemorrhage expansion over minutes to hours
• Amyloid angiopathy: Amyloid-β deposition in cortical arteries of elderly patients causes vessel fragility and lobar ICH (cortical and subcortical white matter), often with recurrent bleeding
• Hematoma expansion: Active bleeding and coagulopathy cause hematoma growth in first 24-48 hours; early hemostasis and reversal of anticoagulation reduce expansion and improve outcomes
• Perihematomal edema: Inflammatory response to blood products (thrombin, hemoglobin) causes vasogenic edema surrounding the hematoma, contributing to mass effect and neurological deterioration
• Herniation risk: Large hematomas cause increased intracranial pressure, uncal herniation, and brainstem compression

Subarachnoid Hemorrhage

• "Thunderclap headache": Sudden, severe, maximal-at-onset occipital or diffuse headache (worst headache of life) is pathognomonic; patients often describe being "hit on back of head" or "explosion in head"
• Meningeal signs: Neck stiffness, photophobia, and phonophobia occur within hours as blood irritates meninges; Kernig and Brudzinski signs may be present but are insensitive
• Loss of consciousness: Altered mental status or coma occurs in 25-50% of cases due to elevated intracranial pressure; Glasgow Coma Scale score correlates with outcome
• Focal neurological deficits: Aneurysm location determines focal signs (e.g., CN III palsy from posterior communicating artery aneurysm suggesting mass effect); deficits may be from vasospasm, mass effect, or seizure
• Seizures: Occur in 10-15% at presentation; increased risk with middle cerebral artery aneurysms, cortical involvement, and higher-grade hemorrhages
• Sentinel headaches: 10-20% report "warning" headaches days to weeks prior from small "warning leaks" before catastrophic rupture
• Subtype: Non-aneurysmal SAH: Perimesencephalic nonaneurysmal SAH (blood around brainstem without aneurysm on angiography) has benign course with excellent prognosis

Intracerebral Hemorrhage

• Sudden focal neurological deficit: Hemiparesis, hemianopia, aphasia, or ataxia developing over minutes to hours reflects location; basal ganglia (putaminal/thalamic) and lobar hemorrhages are most common
• Headache: Present in 40-50% but less severe than SAH; may be absent in small hemorrhages
• Vomiting: Common, particularly with posterior fossa hemorrhage (cerebellar or pontine) suggesting increased intracranial pressure
• Altered consciousness: Coma indicates large hemorrhage, brainstem involvement, or ventricular extension causing obstructive hydrocephalus
• Cerebellar hemorrhage specific signs: Ataxia, vertigo, headache, and vomiting with preserved consciousness initially; rapid deterioration if swelling causes fourth-ventricle compression and brainstem herniation

Neuroimaging - Gold Standard

• Non-contrast CT head (STAT): First-line imaging showing acute blood as hyperdense (Hounsfield units 50-90); detects SAH with >95% sensitivity in first 6 hours, but sensitivity decreases with time as blood becomes isodense; also identifies hematoma location, volume, ventricular extension, and midline shift in ICH
• CT angiography (CTA) of head/neck: Performed for all SAH patients; demonstrates aneurysm location, size, and neck characteristics in 85-95% of cases; now often preferred over digital subtraction angiography as first-pass imaging
• Lumbar puncture (LP) with xanthochromia: Indicated if SAH suspected but CT negative (may occur >6 hours after onset); shows xanthochromia (yellow/amber discoloration from bilirubin) developing 2-12 hours post-hemorrhage and persisting 2 weeks—differentiates SAH from traumatic tap (RBCs increase then decrease progressively with sequential tubes; xanthochromia present throughout)
• Conventional digital subtraction angiography: Gold standard for definitive aneurysm diagnosis and endovascular intervention; sensitivity >98%; used when CTA inconclusive or for treatment planning
• MRI: Sensitivity for acute blood depends on sequence; less useful acutely but helpful for chronic bleeds and amyloid angiopathy evaluation

Grading/Risk Stratification

• Hunt and Hess Scale (SAH): Grade 0-5 based on consciousness level and neurological deficits; Grade 0 (unruptured), Grade 1 (asymptomatic/mild headache), Grade 5 (deep coma/moribund); higher grades predict worse outcome
• WFNS Scale: Uses Glasgow Coma Scale and focal neurological deficit; better interrater reliability than Hunt and Hess
• Modified Rankin Scale and FUNC Score: Predict 90-day functional outcome and guide treatment intensity

Ancillary Tests

• EEG: Detects subclinical seizures in 5-10% of SAH patients, particularly those with altered mental status
• Cardiac biomarkers (troponin): Elevated in 20-30% of SAH due to stress cardiomyopathy; associated with worse outcomes
• Coagulation studies and CBC: Assess for anticoagulation, thrombocytopenia, and fibrinogen consumption driving hematoma expansion

Subarachnoid Hemorrhage - Acute Management

• Blood pressure management (critical): Maintain SBP <160 mmHg in hyperacute phase (first 6 hours) to prevent rebleeding, but avoid excessive lowering that reduces cerebral perfusion pressure; use nicardipine or labetalol infusion titrated to goal; less aggressive targets (SBP <180

Emergencies after SAH

• Rebleeding: fragile clot at the rupture site; abrupt worsening of headache, new coma, or a fresh hyperdensity on repeat CT. Highest risk in the first 24 hours — the AHA/ASA 2023 aSAH guideline recommends securing the aneurysm by clipping or coiling as early as feasible
• Acute hydrocephalus: intraventricular blood or impaired arachnoid granulation reabsorption; declining arousal, small sluggish pupils, impaired upgaze. Treat with external ventricular drain, not lumbar puncture
• Delayed cerebral ischemia (days 4-14): hemoglobin breakdown products drive vasospasm and microvascular failure; new focal deficit or unexplained drop in mental status. Oral nimodipine is given prophylactically to all patients; established DCI is managed with euvolemia and induced hypertension, and refractory cases with endovascular angioplasty or intra-arterial vasodilator
• Neurogenic complications of catecholamine surge: stunned myocardium/Takotsubo with troponin rise and deep symmetric T-wave inversions or QT prolongation, and neurogenic pulmonary edema
• Hyponatremia: common (roughly 30-50% of patients); both SIADH and cerebral salt wasting occur and their relative frequency is debated. Volume status distinguishes them — euvolemic or hypervolemic in SIADH, hypovolemic with natriuresis in CSW. Regardless of mechanism, avoid aggressive fluid restriction and hypovolemia in aSAH because they worsen delayed cerebral ischemia; treat with isotonic or hypertonic saline
• Late complications: seizures and communicating hydrocephalus requiring ventriculoperitoneal shunt

Emergencies after ICH

• Hematoma expansion: active extravasation in the first hours; the CTA spot sign predicts it, and deterioration is the clinical signal. Reverse anticoagulation immediately — vitamin K plus four-factor PCC for warfarin, idarucizumab for dabigatran, andexanet alfa (or PCC) for factor Xa inhibitors, per the AHA/ASA 2022 ICH guideline
• Herniation: uncal herniation gives an ipsilateral blown pupil and contralateral hemiparesis; posterior fossa hematoma compresses the fourth ventricle. A cerebellar hemorrhage with brainstem compression or hydrocephalus requires suboccipital decompression, not medical management
• Intraventricular extension with obstructive hydrocephalus, perihematomal edema, and seizures

• Thunderclap headache with a normal non-contrast CT: the single best next step is lumbar puncture for xanthochromia (or, in some centers within the first 6 hours of onset, CTA). MRI is the classic distractor and is not the answer
• Nimodipine 60 mg PO every 4 hours for 21 days in all aneurysmal SAH patients per the AHA/ASA 2023 guideline. It improves functional outcome from delayed cerebral ischemia largely through neuroprotection — it does not reliably reverse angiographic vasospasm. Give it enterally; the IV route is not used in the US because of profound hypotension
• ADPKD or vascular Ehlers-Danlos plus worst-headache-of-life is the association examiners plant most often; flank masses, hematuria, and hypertension in the stem point at the aneurysm
• Pupil-involving CN III palsy = compressive posterior communicating artery aneurysm, because parasympathetic fibers run superficially in the nerve. Pupil-sparing painless CN III palsy is the microvascular/diabetic distractor
• Deep versus lobar decides etiology: putamen, thalamus, pons, or cerebellum = hypertensive vasculopathy; lobar and recurrent in an elderly normotensive patient = cerebral amyloid angiopathy
• Never give thrombolytics or start antiplatelets acutely — confirming hemorrhage on CT before tPA is precisely why the non-contrast head CT comes first in every acute stroke pathway
• Sequential-tube RBC counts that fall with xanthochromia absent = traumatic tap; a persistent RBC count with xanthochromia = SAH
• Hyponatremia after SAH: both SIADH and cerebral salt wasting occur, and which predominates is debated — sort them by volume status (euvolemic/hypervolemic vs. hypovolemic with natriuresis). Either way, treat with isotonic or hypertonic saline; reflexive fluid restriction is the trap because hypovolemia precipitates delayed cerebral ischemia
• Cerebellar hemorrhage: per the AHA/ASA 2022 ICH guideline, cerebellar hemorrhage with neurologic deterioration, brainstem compression, or hydrocephalus requires immediate surgical evacuation/decompression — EVD alone is not sufficient, and "observe in the ICU" is the wrong answer. A diameter >3 cm is long-standing exam teaching that predicts these events but is not itself the guideline threshold