Nervous System & Special Senses

Hemorrhagic stroke: management and blood pressure goals

Clinical Overview and When to Suspect Hemorrhagic Stroke

— ICH = bleeding into brain parenchyma, usually from small-vessel rupture

— SAH = bleeding into subarachnoid space, usually from saccular aneurysm rupture

— Sudden severe headache ("thunderclap," "worst of life") → SAH until proven otherwise

— Vomiting, decreased level of consciousness, or seizure at onset — far more common with hemorrhage

— Markedly elevated BP (>220/120) at presentation with focal deficits

— Rapid neurologic deterioration over minutes to hours (hematoma expansion)

— Anticoagulant use (warfarin, DOAC) with any new neuro symptom

— Chronic hypertension (deep ganglionic ICH: putamen, thalamus, pons, cerebellum)

— Cerebral amyloid angiopathy (elderly, recurrent lobar ICH, often on antiplatelets)

— Anticoagulation, thrombolytic therapy, cocaine/methamphetamine use

— AVM (younger patients), aneurysm, vasculitis, tumor with hemorrhage

— ABCs, fingerstick glucose, IV access ×2, NIHSS, last-known-well

— Stat non-contrast head CT — distinguishes ICH/SAH from ischemic

— Activate stroke team; do NOT give tPA, aspirin, or heparin until bleed excluded

Board pearl: Any patient on a DOAC presenting with new focal deficit or altered mental status gets a head CT before any antithrombotic decision — assume hemorrhage until imaging proves otherwise.

Definition: Acute neurologic deficit from non-traumatic intracranial bleeding — encompasses intracerebral hemorrhage (ICH, ~10–15% of strokes) and subarachnoid hemorrhage (SAH, ~3–5%).

Why it matters on Step 3: 30-day mortality 35–50% for ICH; aggressive ED-phase management (BP, reversal, airway, ICP) directly changes outcomes and is the testable lever.

When to suspect hemorrhagic over ischemic stroke at the bedside:

High-risk populations:

First 10 minutes in the ED — universal stroke workflow:

Presentation Patterns and Key History

— Putamen (most common): contralateral hemiplegia, hemisensory loss, gaze deviation toward the lesion, aphasia (dominant) or neglect (non-dominant)

— Thalamus: contralateral sensorimotor loss, "wrong-way eyes" (gaze deviates away from lesion, toward hemiparesis), upgaze palsy, miotic pupils

— Cerebellum: sudden occipital headache, vomiting, ataxia, inability to walk — surgical emergency if >3 cm or brainstem compression

— Pons: coma, pinpoint reactive pupils, quadriparesis, decerebrate posturing — usually devastating

— Lobar: focal cortical signs (aphasia, hemianopia, hemineglect) — suspect amyloid angiopathy in elderly, AVM in young

— Thunderclap headache peaking in seconds, often occipital ("hit by a bat")

— Neck stiffness, photophobia, brief LOC, vomiting

— Sentinel headache in days–weeks prior in ~30–50% (warning leak)

— May have subhyaloid (preretinal) hemorrhages on funduscopy (Terson syndrome)

— Exact time of symptom onset / last known well

— Anticoagulants, antiplatelets, thrombolytics — name, dose, last dose, indication

— Hypertension history and medication adherence

— Trauma, sympathomimetic use (cocaine, meth, MDMA, decongestants)

— Prior stroke, aneurysm, AVM, polycystic kidney disease, connective tissue disease

— Pregnancy status (eclampsia, RCVS, PRES)

— Family history of aneurysm or SAH (ADPKD, Ehlers-Danlos IV)

Key distinction: Ischemic stroke usually presents with focal deficits and normal level of consciousness early; hemorrhagic stroke more often features headache, vomiting, depressed consciousness, and markedly elevated BP from onset. Headache + vomiting + coma in <1 hour ≈ bleed.

Intracerebral hemorrhage (ICH) — classic anatomic syndromes:

Subarachnoid hemorrhage (SAH):

Key history to extract — every minute counts on CCS:

Physical Exam Findings and Hemodynamic Assessment

— Severe hypertension (often SBP 180–250) — reactive surge plus chronic baseline

— Cushing reflex (hypertension + bradycardia + irregular respirations) = elevated ICP, impending herniation

— Hyperthermia common; fever portends worse outcome

— Irregular respirations: Cheyne-Stokes (bihemispheric), apneustic (pontine), ataxic (medullary)

— GCS and NIHSS at baseline and serially (q1h initial)

— Pupils: unilateral fixed/dilated = uncal herniation (CN III compression); pinpoint = pons; mid-position fixed = midbrain

— Gaze: conjugate deviation toward lesion (cortical) vs. away (thalamic "wrong-way")

— Motor: asymmetric tone, posturing (decorticate = above red nucleus; decerebrate = below)

— Brainstem reflexes: corneal, gag, cough, oculocephalic (only if C-spine cleared)

— Meningismus: Kernig, Brudzinski — supports SAH (may take hours to develop)

— Papilledema if subacute ICP rise

— Subhyaloid hemorrhages = Terson syndrome, classic for SAH

— Needle marks (IVDU → endocarditis → mycotic aneurysm)

— Café-au-lait, skin angiomas (neurocutaneous syndromes)

— Stigmata of chronic liver disease (coagulopathy)

— Continuous arterial line once SBP >180 or active titration begins

— Two large-bore IVs; avoid hypotonic fluids (worsen edema) — use isotonic saline

— Avoid hypotension: cerebral perfusion pressure (CPP) = MAP − ICP; aim CPP ≥60

CCS pearl: Order "neuro checks q1h," continuous cardiac/pulse ox/BP monitoring, HOB 30°, NPO, and arterial line in the same order set — these are scoreable actions in an ICH CCS case.

General and vital signs:

Neurologic exam — structured and time-stamped:

Funduscopy:

Skin and systemic clues:

Hemodynamic assessment:

Diagnostic Workup — Initial Labs and Imaging

— Sensitivity for acute blood ~100% within first 6 hours

— ICH: hyperdense parenchymal collection; measure volume by ABC/2 method (A×B×C/2 cm³); volume >30 mL portends poor outcome

— SAH: hyperdensity in basal cisterns, sylvian fissures, interhemispheric fissure; Fisher grade predicts vasospasm risk

— "Spot sign" on CTA = active contrast extravasation → high risk of hematoma expansion

— Indicated in nearly all spontaneous ICH and all SAH to identify aneurysm, AVM, dural fistula, or active bleeding

— Especially urgent if lobar location, young patient, no HTN history, or SAH pattern

— CBC, BMP, PT/INR, aPTT — coagulopathy assessment

— Type and screen / crossmatch

— Fingerstick glucose immediately (hypoglycemia mimics stroke)

— Troponin, ECG — neurogenic stress cardiomyopathy, especially SAH (deep T-wave inversions, QT prolongation, "cerebral T waves")

— Urine toxicology (cocaine, amphetamines)

— β-hCG in women of reproductive age (before contrast/radiation decisions)

— Lipid panel, A1c, LFTs — vascular risk profile and baseline

— DOAC-specific assays if available: anti-Xa for apixaban/rivaroxaban; dilute thrombin time or ecarin for dabigatran

— Not first-line acutely; useful subacutely to look for microbleeds (GRE/SWI) suggesting amyloid angiopathy or chronic HTN, or underlying tumor/cavernoma

Board pearl: If NCHCT is negative but SAH is strongly suspected (thunderclap headache), proceed to lumbar puncture looking for xanthochromia (>6–12 hours after onset) — CT sensitivity drops to ~85% by 24 hours and ~50% by day 5.

Stat non-contrast head CT (NCHCT) — the cornerstone:

CT angiography (CTA) head and neck:

Labs to order simultaneously (CCS-style bundle):

MRI:

Diagnostic Workup — Advanced and Confirmatory Studies

— Gold standard for aneurysm, AVM, dural AV fistula, vasculitis

— Mandatory in SAH when CTA negative but clinical suspicion remains

— Allows simultaneous endovascular coiling of culprit aneurysm

— GRE or susceptibility-weighted imaging (SWI): detects microbleeds — lobar microbleeds + superficial siderosis = cerebral amyloid angiopathy (Boston criteria)

— Identifies underlying tumor, cavernous malformation, or hemorrhagic transformation of infarct

— MRA non-invasive aneurysm screen for at-risk relatives (ADPKD, ≥2 first-degree relatives with SAH)

— Repeat NCHCT at 6 and 24 hours (or sooner if neuro decline) to detect hematoma expansion — occurs in ~30% within first 24 hours

— Perfusion imaging assesses delayed cerebral ischemia (DCI) risk in SAH days 4–14

— Daily monitoring in SAH ICU course to detect vasospasm; rising mean flow velocities (especially MCA >120 cm/s, Lindegaard ratio >3) trigger CTA/CT perfusion and intervention

— Indicated when CT negative and suspicion persists

— Xanthochromia (yellow CSF supernatant from bilirubin) is the definitive finding, present from ~6–12 hours up to 2 weeks

— Distinguish traumatic tap: consistent RBC counts across tubes 1 and 4, plus xanthochromia, support true SAH

— Indicated for unexplained altered mental status, suspected non-convulsive status epilepticus (especially lobar ICH or SAH with fluctuating exam)

Step 3 management: In a patient with suspected SAH and a negative CT done >6 hours after onset, the next best step is lumbar puncture for xanthochromia, not immediate CTA — confirms hemorrhage before committing to vascular workup. If LP positive → CTA/DSA next.

Digital subtraction angiography (DSA):

MRI/MRA — subacute and outpatient roles:

CT perfusion / repeat NCHCT:

Transcranial Doppler (TCD):

Lumbar puncture for SAH:

EEG:

Risk Stratification and First-Line Management Logic

— ICH Score (0–6): GCS, ICH volume, IVH presence, infratentorial location, age ≥80 — predicts 30-day mortality (score 0 ≈ 0%; score 5 ≈ 100%)

— Use for prognostic discussion, NOT to withhold early aggressive care

— Avoid early DNR orders in first 24–48 hours — premature withdrawal is a self-fulfilling prophecy and a tested patient-safety point

— Hunt and Hess (clinical, I–V) and WFNS (GCS-based) grade severity

— Modified Fisher scale (CT blood burden) predicts vasospasm and DCI

— 1. Airway: intubate if GCS ≤8, loss of protective reflexes, or impending herniation

— 2. Blood pressure control (see chunk 7)

— 3. Reverse coagulopathy immediately (see chunk 7)

— 4. ICP management: HOB 30°, midline neck, normothermia, normocapnia, mannitol or 3% saline if herniation signs

— 5. Seizure prophylaxis only if clinical/electrographic seizures — not routine in ICH (AHA: routine prophylactic AEDs not recommended); reasonable short-course in lobar ICH or SAH per local practice

— 6. Glucose 140–180 mg/dL; avoid hypo- and hyperglycemia

— 7. Temperature <37.5°C; treat fever aggressively

— 8. DVT prophylaxis: intermittent pneumatic compression on admission; pharmacologic (LMWH/UFH) can be started 24–48 hours after bleeding stable

— All hemorrhagic strokes → neuro ICU with neurosurgery consult

— Transfer to comprehensive stroke center if local capabilities lack neurosurgery/endovascular

CCS pearl: On the CCS interface, your initial ICH order set should include: NCHCT → BP control → coagulation reversal → neurosurgery consult → ICU admit → q1h neuro checks → HOB 30° → SCDs → glucose and temp control. Missing any of these costs points.

ICH severity scores:

SAH grading:

First-line ED/ICU priorities (memorize order):

Disposition:

Pharmacotherapy — Blood Pressure Control and Coagulation Reversal

— Spontaneous ICH with SBP 150–220 and no contraindication: target SBP 140 mm Hg (range 130–150). INTERACT-2 and ATACH-2 show safety; aggressive lowering to <130 offers no benefit and may harm.

— ICH with SBP >220: aggressive lowering with continuous IV infusion and arterial line; avoid abrupt drops >25% of MAP in the first hour

— SAH (unsecured aneurysm): keep SBP <160 (some guidelines <140) until aneurysm secured, then permissive higher BP to prevent vasospasm-related ischemia

— Post-thrombolytic hemorrhage: SBP <180/105

— Nicardipine infusion 5 mg/h, titrate by 2.5 mg/h q5–15min (max 15 mg/h) — first-line, smooth titration

— Clevidipine — ultra-short acting, useful in volume-restricted patients

— Labetalol 10–20 mg IV bolus, then infusion — caution in bradycardia, asthma, decompensated heart failure

— Avoid nitroprusside and nitroglycerin — increase ICP via cerebral vasodilation

— Warfarin (INR ≥1.4): 4-factor PCC (e.g., Kcentra) 25–50 units/kg IV + IV vitamin K 10 mg — PCC preferred over FFP (faster, lower volume)

— Dabigatran: idarucizumab 5 g IV

— Apixaban/rivaroxaban: andexanet alfa (per dose/timing algorithm) or 4-factor PCC 50 units/kg if andexanet unavailable

— Heparin/LMWH: protamine (1 mg per 100 units heparin; partial reversal for LMWH)

— tPA-related ICH: cryoprecipitate 10 units ± tranexamic acid 10–15 mg/kg; stop tPA infusion

— Antiplatelets: routine platelet transfusion not recommended (PATCH trial showed harm) unless neurosurgical procedure planned

— Nimodipine 60 mg PO q4h ×21 days for SAH — reduces DCI/poor outcome (cornerstone therapy)

Board pearl: ICH on apixaban → give andexanet alfa or 4F-PCC 50 U/kg; ICH on dabigatran → idarucizumab; ICH on warfarin with INR 3.0 → 4F-PCC + IV vitamin K, not FFP first.

Blood pressure targets (the most testable point):

Preferred IV agents:

Coagulopathy reversal — act within minutes:

Other:

Procedures and Neurosurgical Management

— Cerebellar hemorrhage >3 cm, brainstem compression, or hydrocephalus → emergent suboccipital craniectomy (life-saving, strong AHA recommendation)

— Supratentorial ICH: routine surgical evacuation not shown to improve outcomes (STICH I/II); consider in deteriorating patients with lobar clots within 1 cm of cortical surface

— Minimally invasive surgery + thrombolysis (MISTIE III): trend toward benefit when residual clot <15 mL; emerging option

— Place for obstructive hydrocephalus, IVH with intraventricular extension, or GCS ≤8 with elevated ICP

— Allows ICP monitoring and CSF diversion; target ICP <22, CPP 60–70

— Intraventricular tPA (CLEAR III) may speed clot clearance but no mortality benefit

— Endovascular coiling preferred over clipping when anatomically feasible (ISAT: better 1-year functional outcome)

— Surgical clipping preferred for wide-necked, MCA bifurcation, or large MCA aneurysms with mass effect

— Flow diverters/stents for selected complex aneurysms

— Nimodipine PO continued for 21 days

— Euvolemia (older "triple-H" abandoned — avoid hypervolemia)

— Symptomatic vasospasm → induced hypertension (SBP up to 200 with aneurysm secured) + endovascular intra-arterial vasodilators (verapamil, nicardipine) or balloon angioplasty

— HOB 30° → sedation/analgesia → osmotherapy (3% saline bolus or mannitol 1 g/kg) → brief hyperventilation to PaCO₂ 30–35 → EVD drainage → decompressive craniectomy

Step 3 management: Cerebellar ICH >3 cm with declining GCS = call neurosurgery for emergent posterior fossa decompression now — do not delay for further imaging. This is a classic high-yield decision point.

ICH — surgical evacuation indications:

External ventricular drain (EVD):

SAH — aneurysm securing (within 24 hours ideal, <72 hours mandatory):

SAH — vasospasm and DCI management (days 4–14):

ICP crisis ladder:

Special Populations — Elderly and Renal/Hepatic Impairment

— Cerebral amyloid angiopathy (CAA) is the leading cause of spontaneous lobar ICH; recurrence risk ~10%/year

— Avoid resuming anticoagulation in CAA-related ICH when possible — recurrent ICH risk often exceeds embolic risk

— Consider left atrial appendage occlusion (Watchman) in AF patients with prior ICH who cannot tolerate anticoagulation

— Polypharmacy: review antihypertensives, antiplatelets, SSRIs (mildly raise bleeding risk), and frailty before aggressive interventions

— Goals of care discussion early — but resist withdrawal in first 24–48 hours

— Dabigatran is 80% renally cleared — accumulates in CKD/AKI, prolonging bleeding; idarucizumab still works

— Adjust nicardipine and labetalol less for renal function but watch for accumulation in hepatic dysfunction

— Avoid contrast nephropathy: hydrate before CTA if eGFR <45, but do not delay life-saving imaging

— Uremic platelet dysfunction worsens bleeding — give DDAVP 0.3 mcg/kg IV and consider cryoprecipitate; dialysis if severe uremia

— Coagulopathy from impaired factor synthesis: vitamin K + 4F-PCC (FFP if PCC unavailable); avoid volume overload

— Thrombocytopenia from hypersplenism — transfuse platelets to >50–100 k/μL if neurosurgery planned

— Avoid hepatotoxic AEDs (valproate); levetiracetam safer

— Use Clinical Frailty Scale to guide intensity of care

— Pre-existing severe dementia + large ICH: emphasize comfort-focused care after structured family meeting

Key distinction: Recurrent lobar ICH in an elderly normotensive patient = amyloid angiopathy until proven otherwise; recurrent deep ganglionic ICH = uncontrolled hypertension. The location drives the secondary prevention plan.

Elderly (>75–80 years):

Renal impairment:

Hepatic impairment:

Frailty and dementia:

Special Populations — Pregnancy and Younger Patients

— Increased risk of hemorrhagic stroke, especially third trimester and first 6 weeks postpartum

— Etiologies: eclampsia/preeclampsia, reversible cerebral vasoconstriction syndrome (RCVS), PRES, ruptured aneurysm/AVM, cerebral venous sinus thrombosis with hemorrhagic conversion, choriocarcinoma metastases

— Eclampsia management: IV magnesium sulfate (load 4–6 g, then 1–2 g/h), labetalol or hydralazine for BP, deliver the fetus once stabilized; target SBP <160 / DBP <110

— Imaging: NCHCT acceptable (low fetal dose with abdominal shielding); MRI without gadolinium preferred when time allows

— Aneurysm rupture → secure aneurysm regardless of trimester; mode of delivery determined obstetrically (vaginal often acceptable post-coiling)

— Spontaneous ICH most often from AVM, cavernoma, moyamoya, sickle cell disease, or coagulopathy (hemophilia, ITP, leukemia)

— Always image vasculature (MRA or CTA) and screen for bleeding disorder

— Sickle cell with stroke → exchange transfusion to HbS <30%

— Workup: CTA/MRA for AVM/aneurysm, toxicology (cocaine, amphetamines, sympathomimetics), vasculitis labs (ESR, CRP, ANCA), thrombophilia screen if venous infarct with hemorrhage, echocardiogram for endocarditis (mycotic aneurysm)

— Counsel on substance cessation and reproductive planning

— ADPKD: screen with MRA if family history of SAH or ≥2 affected relatives

— Ehlers-Danlos type IV, Marfan, fibromuscular dysplasia, Osler-Weber-Rendu

Board pearl: Postpartum woman with thunderclap headache, recurrent over days, normal initial CT, and "string-of-beads" arterial narrowing on CTA = RCVS, not SAH — treat with nimodipine and remove triggers (SSRIs, sympathomimetics); steroids are harmful.

Pregnancy and postpartum:

Pediatrics:

Young adults (<50):

Genetic considerations:

Complications and Adverse Outcomes

— Hematoma expansion in ~30% — risk factors: large initial volume, spot sign, anticoagulation, early presentation; mitigated by BP control and reversal

— Intraventricular hemorrhage extension → obstructive hydrocephalus → need EVD

— Cerebral edema and elevated ICP → herniation syndromes (uncal, central, tonsillar)

— Seizures (~5–15%, higher in lobar ICH) — treat with levetiracetam, IV lorazepam for status

— Neurogenic stunned myocardium / Takotsubo (SAH > ICH): troponin rise, apical ballooning, transient LV dysfunction — supportive care

— Neurogenic pulmonary edema — bilateral infiltrates, hypoxemia within hours of SAH

— Cerebral vasospasm and delayed cerebral ischemia (DCI) in SAH — peak day 7; monitor with TCD and neuro exam; treat with nimodipine, euvolemia, induced HTN, endovascular vasodilators

— Hyponatremia: cerebral salt wasting (hypovolemic, treat with salt and volume) vs. SIADH (euvolemic, fluid restrict) — distinction matters because fluid restriction in SAH worsens vasospasm

— Fever — often central; aggressive cooling improves outcome

— VTE/PE — start pharmacologic prophylaxis 24–48 hours after bleeding stable

— Hospital-acquired infections: pneumonia (aspiration), UTI, central-line infections

— Communicating hydrocephalus after SAH — may need permanent VP shunt

— Post-stroke depression in 30–40%; screen with PHQ-9 at follow-up

— Cognitive impairment, dementia — especially after multiple bleeds or CAA

— Recurrent hemorrhage — annual rate ~2% (hypertensive) to ~10% (CAA)

— Post-stroke epilepsy — late seizures (>7 days) warrant long-term AED

CCS pearl: In an SAH patient on day 6 with new aphasia and rising MCA velocities on TCD, the next step is CT angiography/perfusion to confirm vasospasm, then induce hypertension and arrange intra-arterial verapamil if symptoms persist.

Early (first 24–72 hours):

Subacute (days 3–14):

Late:

When to Escalate Care — ICU, Consult, and Triage

— Continuous BP monitoring, neuro checks q1h initially

— Specialized airway and ICP management

— Lower mortality in dedicated neuro ICUs (level B evidence)

— Any cerebellar hemorrhage (especially >3 cm)

— Hydrocephalus or IVH

— GCS ≤8 or rapid decline

— Surgical lobar ICH candidate

— All SAH (for aneurysm securing)

— SAH with aneurysm amenable to coiling

— Symptomatic vasospasm refractory to medical therapy

— Dural AV fistula or AVM management

— 24/7 neurosurgery, neurointerventional, neuro ICU

— Use EMTALA-compliant transfer: accept hospital agreement, stabilize first (BP control, reversal initiated), send imaging electronically

— Continue nicardipine drip during transport; ensure airway secured if GCS borderline

— Large devastating ICH (ICH score 4–5), brainstem hemorrhage with coma

— Goals-of-care discussion, but delay DNR/withdrawal decisions ≥24–48 hours when feasible

— Involve family early; provide prognostic data without nihilism

— Cardiology for neurogenic stress cardiomyopathy or new AF

— Hematology for refractory coagulopathy or thrombophilia workup

— Genetics for ADPKD, connective tissue disease, familial cavernoma

— PM&R early for rehab planning

Step 3 management: A community ED with a GCS-7 ICH patient on warfarin (INR 3.5) → intubate, start nicardipine drip targeting SBP 140, give 4F-PCC + IV vitamin K, call accepting comprehensive stroke center, transfer with neuro and BP monitoring — all initiated before transfer departure.

Automatic neuro ICU admission for all hemorrhagic strokes:

Immediate neurosurgery consult triggers:

Endovascular/neurointerventional consult:

Transfer to comprehensive stroke center if local hospital lacks:

Palliative care consult:

Other consults:

Key Differentials — Same-Category (Other Hemorrhagic Causes)

— Deep locations: putamen, thalamus, pons, cerebellum, deep cerebellar nuclei

— History of poorly controlled HTN; common in middle-aged to elderly

— Charcot-Bouchard microaneurysms of lenticulostriate vessels

— Lobar location, elderly, often on antiplatelets

— Multiple cortical microbleeds and superficial siderosis on SWI

— High recurrence risk; avoid antithrombotics when possible

— AVM: young patients, prior seizures, headache; high-flow nidus on angiography; risk of bleeding ~2–4%/year

— Cavernous malformation (cavernoma): "popcorn" on MRI with hemosiderin rim, low-pressure bleeds

— Dural arteriovenous fistula: pulsatile tinnitus, cortical venous drainage = high rebleed risk

— Saccular aneurysm at circle of Willis bifurcations (Acom > Pcom > MCA)

— Thunderclap headache, basal cistern blood on CT

— Usually large cardioembolic infarcts, especially after tPA or thrombectomy

— Petechial (HI1/HI2) vs. parenchymal hematoma (PH1/PH2 — clinical decline, mass effect)

— Distal cortical aneurysm in patient with endocarditis; obtain echocardiogram and blood cultures

— Hemorrhagic venous infarct in non-arterial territory; headache + seizure + papilledema

— Treat with anticoagulation even in presence of hemorrhage

— Melanoma, RCC, choriocarcinoma, thyroid, lung metastases bleed most often; primary GBM also

Key distinction: Lobar ICH in an 82-year-old normotensive woman on aspirin = amyloid angiopathy; deep putaminal ICH in a 58-year-old with SBP 220 = hypertensive; thunderclap headache + basal cistern blood = aneurysmal SAH. Location and demographics drive the differential.

Hypertensive ICH:

Cerebral amyloid angiopathy (CAA):

Vascular malformations:

Aneurysmal SAH:

Hemorrhagic transformation of ischemic stroke:

Mycotic aneurysm:

Cerebral venous sinus thrombosis (CVST):

Tumor-related hemorrhage:

Key Differentials — Other-Category Mimics

— Distinguishable only by NCHCT; clinical features overlap

— Time-sensitive — must exclude bleed before tPA/thrombectomy

— Younger, family history, gradual march of symptoms, headache follows aura

— Diagnosis of exclusion after imaging

— Postictal focal weakness resolves over hours

— Witnessed convulsion, tongue bite, incontinence support seizure

— Mimics any stroke syndrome — always fingerstick glucose before imaging decisions

— Treat with IV dextrose (D50 25–50 mL)

— Headache, confusion, seizures, cortical blindness; bilateral parieto-occipital edema on MRI

— Treat by lowering BP carefully (15–25% in first hour), withdraw triggers

— Fever, meningismus, altered mental status; LP after imaging

— HSV encephalitis can cause hemorrhagic temporal lobe lesions — treat empiric acyclovir

— Diffuse, no focal deficits; infection source elsewhere

— Alcohol/benzo withdrawal, opioid intoxication, lithium toxicity, hepatic encephalopathy

— Drug-induced (cocaine, amphetamines) — can cause real hemorrhage, not just mimic

— Inconsistent exam, Hoover sign, no imaging correlate — diagnosis of exclusion in young patients

— Considered only after thorough organic workup

— Trauma history; subdural in elderly/alcoholics on anticoagulants; epidural with lucid interval after temporal trauma — surgical decisions differ from ICH/SAH

Board pearl: In any stroke-like presentation, the two reversible mimics to rule out within minutes are hypoglycemia (fingerstick) and seizure with postictal deficit (history, witnessed event) — missing these is a tested safety failure.

Ischemic stroke:

Migraine with aura (hemiplegic migraine):

Seizure with Todd's paralysis:

Hypoglycemia:

Hypertensive emergency with encephalopathy / PRES:

Meningitis/encephalitis:

Sepsis-associated encephalopathy:

Toxic/metabolic:

Functional neurologic disorder:

Conversion / malingering:

Subdural and epidural hematomas:

Secondary Prevention and Discharge Planning

— Target <130/80 for all ICH survivors (AHA Class I) — reduces recurrence ~50%

— Lifelong therapy; preferred agents: ACE inhibitor or ARB + thiazide or CCB

— Home BP monitoring with twice-daily logs; teach correct technique

— Antiplatelets: generally safe to resume for clear secondary prevention indications (e.g., recent MI, prior ischemic stroke) after 1–4 weeks, shared decision

— Anticoagulation in AF after ICH: controversial; weigh CHA₂DS₂-VASc vs. ICH recurrence risk

— Deep hypertensive ICH with BP now controlled → resume cautiously after 4–8 weeks

— Lobar/CAA-related ICH: generally avoid anticoagulation; consider left atrial appendage occlusion (Watchman)

— DOACs preferred over warfarin when resumed (lower ICH risk)

— Continue if patient has clear ASCVD indication; benefits outweigh small ICH risk signal

— Do not start solely to prevent ICH

— Smoking cessation (especially after SAH — major recurrence risk factor)

— Alcohol ≤1–2 drinks/day; heavy use raises ICH risk

— Stop cocaine, amphetamines, MDMA; refer to addiction services

— Mediterranean or DASH diet, regular aerobic exercise

— Surveillance imaging (MRA or DSA) at 6 months, then per neurosurgery

— Screen first-degree relatives if ≥2 affected family members or ADPKD

— Continue AED only if seizure occurred or high-risk lobar ICH per local protocol; trial taper at 3–6 months if seizure-free

Step 3 management: In a patient with AF and recent lobar ICH from amyloid angiopathy, do not restart anticoagulation; refer for left atrial appendage occlusion and use aspirin short-term per shared decision — this is the modern answer.

Blood pressure — the single highest-yield long-term intervention:

Antithrombotic decisions (high-yield decision tree):

Statin therapy:

Lifestyle:

Aneurysm follow-up after SAH:

Seizure management:

Vaccinations: annual influenza, pneumococcal, COVID boosters

Follow-Up, Monitoring, and Rehabilitation

— From neuro ICU → step-down → acute rehab when medically stable, BP controlled, no surgical interventions pending

— Acute inpatient rehab for patients who tolerate ≥3 hours/day therapy and have rehab potential

— Subacute rehab/SNF for those with lower tolerance

— BP medications reconciled with target documented

— Antithrombotic plan explicit and communicated to PCP and patient

— Outpatient neurology follow-up within 1–2 weeks

— Neurosurgery follow-up at 2–4 weeks if procedure performed

— PCP follow-up within 1 week for BP titration

— Therapy services (PT/OT/speech) arranged at discharge

— Driving restriction counseling (state-specific; typically no driving until cleared by neurology, often 3–6 months)

— Return precautions: new headache, weakness, confusion, seizure

— BP log review at every visit; titrate to <130/80

— Cognitive screen (MoCA) at 3 and 12 months

— PHQ-9 for post-stroke depression at each follow-up; treat with SSRI (recognize small bleed-risk increase; benefits usually outweigh)

— Repeat MRI with SWI at 6–12 months for microbleed/CAA staging when relevant

— Motor: task-specific training, constraint-induced therapy when appropriate

— Speech therapy for aphasia/dysarthria/dysphagia (modified barium swallow before advancing diet)

— Spasticity: stretching, oral baclofen, botulinum toxin

— Bowel/bladder retraining, fall prevention, home safety eval

— Sexual activity generally safe after BP controlled (4–6 weeks)

— Air travel typically safe after 2 weeks if stable

— Work return individualized; cognitive demands considered

Board pearl: Post-stroke depression occurs in 30–40% — screen with PHQ-9 at every visit; first-line treatment is an SSRI (e.g., sertraline), which improves both mood and functional recovery. Do not withhold over modest bleed concerns.

Inpatient transitions:

Discharge checklist (CCS-style):

Long-term monitoring:

Rehabilitation focus:

Counseling:

Ethical, Legal, and Patient Safety Considerations

— Avoid early DNR / withdrawal of care in the first 24–48 hours of severe ICH — early limitation is associated with self-fulfilling worse outcomes (AHA Class III: harm)

— Use structured family meetings with realistic prognostic data; document decision-making capacity

— Aphasic, obtunded, or intubated patient → identify surrogate decision-maker per state hierarchy (spouse → adult children → parents → siblings)

— Emergency exception applies for life-saving interventions (aneurysm coiling, EVD, decompressive craniectomy) when no surrogate immediately available

— For elective long-term decisions (PEG, tracheostomy, LAA occlusion), ensure surrogate has time and information; document substituted judgment vs. best-interest standard

— Honor existing POLST/MOLST and durable power of attorney for healthcare

— Conflicts between family and prior directive → ethics consult; document conversations carefully

— Many states require physician reporting of new seizures or loss of consciousness to DMV; counsel patient and document

— Provide written driving restriction

— Medication reconciliation at every transition: stopping anticoagulants requires explicit plan and communication to PCP

— Closed-loop handoff to receiving hospital, rehab, or PCP — written summary with BP targets, antithrombotic plan, follow-up appointments

— Use teach-back for patient/family understanding of red-flag symptoms

— Black, Hispanic, and lower-SES patients have higher ICH incidence and worse BP control — address insurance/medication access at discharge

— Ensure post-discharge BP cuff, medication coverage, transportation to follow-up

— Wrong-side imaging or surgery in confused/aphasic patients — confirm laterality with imaging label and time-out

— Falls in hemiparetic patients — bed alarms, scheduled toileting

— VTE prophylaxis omission is a common harm event — automatic order set with SCDs

Step 3 management: A patient with severe ICH whose family requests withdrawal at hour 6 — do not comply immediately; provide updated prognosis, recommend reassessment at 48–72 hours, document the conversation, and offer palliative care consultation. This avoids premature limitation while respecting autonomy.

Goals of care and prognostic timing:

Informed consent edge cases:

Advance directives:

Mandatory reporting and driving:

Transition-of-care safety (high-yield Step 3 theme):

Health equity and access:

Patient safety events:

High-Yield Associations and Rapid-Fire Clinical Facts

— Putamen/thalamus/pons/cerebellum ICH → chronic hypertension

— Lobar ICH in elderly → cerebral amyloid angiopathy

— SAH at circle of Willis → saccular aneurysm (Acom most common overall; Pcom causes CN III palsy)

— Hemorrhagic temporal lobe → HSV encephalitis or contusion

— Pinpoint reactive → pons

— Fixed mid-position → midbrain

— Unilateral blown → uncal herniation, CN III

— ADPKD, Ehlers-Danlos IV, fibromuscular dysplasia, coarctation of aorta → aneurysms

— Familial cavernous malformations (KRIT1/CCM1)

— HHT (Osler-Weber-Rendu) → cerebral AVMs

Board pearl: Of all SAH interventions, only three are proven outcome-improvers: early aneurysm securing, oral nimodipine ×21 days, and avoidance of hypovolemia. Memorize these.

Locations and causes:

Pupils localize:

ECG findings in SAH: deep symmetric T-wave inversions, QT prolongation, U waves ("cerebral T waves"); troponin may rise → neurogenic stunned myocardium

Genetic associations:

Drugs that cause ICH: cocaine, methamphetamine, MDMA, phenylpropanolamine (historic), warfarin, DOACs, tPA, heparin

Hyponatremia in SAH: cerebral salt wasting (hypovolemic) > SIADH (euvolemic); never fluid-restrict an SAH patient

Nimodipine is the only SAH drug proven to improve outcomes — PO/NG only, never IV (causes hypotension)

Vasospasm peaks day 4–14; clinical exam + TCD = monitoring

ICH Score components: GCS, age ≥80, infratentorial, ICH volume, IVH

ABC/2 for ICH volume; >30 mL = poor prognosis

Spot sign on CTA = hematoma expansion risk

Cushing reflex: HTN + bradycardia + irregular respirations = herniation

Reversal pairings: warfarin→4F-PCC + vit K; dabigatran→idarucizumab; apixaban/rivaroxaban→andexanet or 4F-PCC; heparin→protamine; tPA→cryoprecipitate ± TXA

BP targets: ICH SBP ~140 (130–150); SAH SBP <160 until secured; post-tPA <180/105

Cerebellar ICH >3 cm with decline = surgical emergency

Board Question Stem Patterns

— 72-year-old on apixaban for AF, sudden hemiparesis, NCHCT shows 25-mL putaminal hemorrhage, SBP 210

— Answer: Start IV nicardipine to SBP 140, give andexanet alfa (or 4F-PCC 50 U/kg), neurosurgery consult, ICU admit

— 45-year-old, sudden worst-headache, exam normal, CT at 10 hours negative

— Answer: Lumbar puncture for xanthochromia; if positive → CTA for aneurysm

— 65-year-old hypertensive, vomiting, ataxia, declining GCS; NCHCT shows 4-cm cerebellar hematoma with 4th ventricle effacement

— Answer: Emergent posterior fossa decompression and EVD

— Aphasia and right hemiparesis return after improvement; TCD MCA velocity 180 cm/s

— Answer: CT angiography/perfusion, induce hypertension (aneurysm secured), prepare intra-arterial verapamil; ensure nimodipine continued

— 84-year-old normotensive woman, third lobar ICH, microbleeds on SWI

— Diagnosis: Cerebral amyloid angiopathy; do not restart anticoagulation; consider LAA occlusion if AF

— ICH with SBP 200 — target SBP 140, not 110 (ATACH-2 showed no benefit and harm at lower targets)

— Recurrent headaches, "string-of-beads" on CTA, normal LP

— Diagnosis: RCVS — nimodipine, remove triggers, NOT steroids

— Day 5, Na 128, hypovolemic on exam

— Diagnosis: Cerebral salt wasting — give hypertonic saline + fludrocortisone, NOT fluid restriction

— Severe ICH, intubated

— Answer: Continue aggressive care, schedule formal meeting at 48–72 hours, palliative consult, document

— ICH survivor, AF, deep hypertensive bleed, BP now controlled

— Answer: Restart DOAC at 4–8 weeks, target BP <130/80, neuro follow-up 2 weeks, PCP 1 week

Key distinction: Every hemorrhagic stroke stem rewards picking the specific reversal agent, the specific BP target, and the specific consultant in the right order. Anchor on these three.

Stem 1 — Anticoagulated ICH:

Stem 2 — Thunderclap headache with normal CT:

Stem 3 — Cerebellar hemorrhage:

Stem 4 — Day 7 of SAH:

Stem 5 — Elderly lobar bleed:

Stem 6 — BP target choice:

Stem 7 — Postpartum thunderclap:

Stem 8 — Hyponatremia in SAH:

Stem 9 — Family asks for withdrawal at hour 8:

Stem 10 — Discharge planning:

One-Line Recap

Hemorrhagic stroke is a time-critical neuroemergency where outcomes are determined in the first hour by rapid CT diagnosis, aggressive but smooth BP control to SBP ~140 in ICH (and <160 in unsecured SAH), immediate anticoagulant reversal with the agent matched to the offending drug, and prompt neurosurgical/endovascular engagement for cerebellar bleeds, hydrocephalus, and ruptured aneurysms.

Board pearl: When unsure on any hemorrhagic stroke vignette, the highest-yield reflexive answers are — CT first, BP to 140, reverse the anticoagulant, call neurosurgery, ICU admit, nimodipine if SAH. These six moves are right far more often than they are wrong on Step 3.

The hemodynamic rule: ICH with SBP 150–220 → target SBP 140 with nicardipine drip; SAH (unsecured aneurysm) → SBP <160; avoid nitroprusside/nitroglycerin (raise ICP).

The reversal rule: Match the drug — warfarin → 4F-PCC + IV vitamin K; dabigatran → idarucizumab; apixaban/rivaroxaban → andexanet alfa or 4F-PCC 50 U/kg; tPA → cryoprecipitate ± TXA; do not transfuse platelets routinely for antiplatelet-associated ICH (PATCH).

The surgical rule: Cerebellar ICH >3 cm or deteriorating → emergent posterior fossa decompression; SAH → secure aneurysm within 24 hours by coiling > clipping when feasible; EVD for IVH/hydrocephalus or ICP control.

The prevention rule: Lifelong BP <130/80; in CAA-related lobar ICH, avoid anticoagulation and consider LAA occlusion; in deep hypertensive ICH, DOAC may be cautiously resumed after 4–8 weeks; nimodipine ×21 days for every SAH; treat depression with SSRI; rehab early; counsel on driving, substance use, and red-flag symptoms.