Intracranial hemorrhage nursing: complete reference guide

Intracranial hemorrhage (ICH in the broad sense) refers to any bleeding that occurs within the skull — whether inside the brain parenchyma, between the brain’s protective membranes, or in the subarachnoid space. There are four distinct subtypes, each with a different anatomy, mechanism, CT appearance, and treatment priority. For nurses working in emergency, critical care, or neuro settings, the ability to distinguish these subtypes rapidly — and act on the correct priorities — can be the difference between a good outcome and catastrophic neurological injury.

Quick reference: the four types at a glance

All four types share critical nursing priorities: airway protection, neurological assessment every 1–4 hours, ICP management, and seizure precautions. The differences lie in mechanism, timeline, and specific pharmacological targets. This reference covers each subtype in depth — including grading scales, CT findings, pharmacology, surgical options, anticoagulation reversal, and NCLEX-targeted content.

Subarachnoid hemorrhage (SAH)

Pathophysiology and causes

Subarachnoid hemorrhage occurs when blood fills the subarachnoid space — the layer between the arachnoid mater and pia mater through which cerebrospinal fluid (CSF) normally flows. The most common cause is rupture of a saccular (berry) aneurysm, typically located at bifurcation points of the circle of Willis. Berry aneurysms are thin-walled outpouchings of arterial wall where the tunica media is deficient; they are found in 2–5% of the general population and are most common at the junction of the posterior communicating and internal carotid arteries, the anterior communicating artery, and the middle cerebral artery bifurcation.

The second most common cause is arteriovenous malformation (AVM) rupture. Other etiologies include traumatic injury, cocaine use, and, rarely, mycotic aneurysm from infective endocarditis.

When an aneurysm ruptures, arterial blood under high pressure floods the subarachnoid space within seconds. This triggers a massive spike in ICP — sometimes transiently equaling mean arterial pressure — which produces the characteristic thunderclap onset. The blood irritates meningeal surfaces (causing nuchal rigidity and photophobia), obstructs CSF reabsorption (leading to communicating hydrocephalus), and sets the stage for delayed cerebral ischemia through vasospasm.

Clinical presentation

The hallmark is the thunderclap headache — a sudden, explosive headache the patient describes as “the worst headache of my life,” reaching peak intensity within seconds. Patients sometimes describe the exact moment of onset: “I was bending over to pick something up” or “I was straining at the toilet.” This differs from migraine, which builds over minutes to hours, and from tension headache. Any sudden severe headache warrants urgent CT head.

Associated features:

• Nuchal rigidity — meningeal irritation causes resistance to neck flexion (takes 3–4 hours to develop after SAH)
• Photophobia and phonophobia
• Loss of consciousness — brief LOC at onset occurs in up to 45% of patients; sustained LOC indicates severe injury
• Focal neurological deficits — present when the aneurysm is large or mass effect is significant
• Subhyaloid retinal hemorrhages — visible on fundoscopy; highly specific for SAH

For patients presenting with sudden severe headache but a normal CT scan, the next step is lumbar puncture. Xanthochromia — a yellow discoloration of the CSF from bilirubin degradation of lysed RBCs — confirms SAH when CT is negative. Xanthochromia typically develops 2–4 hours after bleed onset and persists for up to 2 weeks.

The differential for sudden severe headache is broad and includes cerebral venous sinus thrombosis, hypertensive crisis, cervical artery dissection, and meningitis — see the meningitis nursing reference for distinguishing features.

Grading scales

Hunt-Hess scale — grades clinical severity at presentation; predicts operative risk and 30-day mortality:

NCLEX tip 1: Hunt-Hess grades I–II are good surgical candidates; grades IV–V carry very high mortality regardless of intervention. Grade determines urgency and approach.

Fisher Scale — grades blood burden on CT; predicts vasospasm risk:

Fisher Grade 3 carries the highest vasospasm risk — NCLEX frequently tests this.

Vasospasm: the silent second injury

Vasospasm is delayed arterial narrowing that peaks at days 4–14 after the initial SAH and causes delayed cerebral ischemia (DCI) — effectively a secondary stroke on top of the hemorrhage. It is the leading cause of death and disability in SAH patients who survive the initial bleed.

Nimodipine (a calcium channel blocker) is the only proven pharmacological intervention. It does NOT treat blood pressure — it reduces vasospasm-mediated ischemia by protecting neurons from calcium-mediated injury. Standard dosing: 60 mg PO/NG every 4 hours for 21 days starting within 96 hours of SAH.

NCLEX tip 2: Nimodipine is given for vasospasm prevention, NOT blood pressure control. If you see a question where nimodipine drops BP, hold the dose and notify the provider — the drug is not a BP agent.

Monitoring for vasospasm includes daily transcranial Doppler (TCD) ultrasonography and frequent neuro checks. New focal deficits, worsening headache, or declining GCS in the Day 4–14 window should trigger urgent CT angiography to evaluate for vasospasm.

Surgical management

Two options exist for securing a ruptured aneurysm:

1. Endovascular coiling — a catheter is advanced from the femoral artery to the aneurysm sac; platinum coils are deployed to thrombose the aneurysm. Less invasive; preferred for posterior circulation aneurysms and older/higher-grade patients.
2. Surgical clipping — open craniotomy with a titanium clip placed across the aneurysm neck. More durable for certain aneurysm geometries; preferred for younger patients with anterior circulation aneurysms and accessible anatomy.

Nursing priorities for SAH

• Quiet environment: Dark room, low stimulation; any Valsalva-like activity (straining, coughing) risks rebleeding before the aneurysm is secured
• Continuous neuro checks: GCS, pupil size and reactivity, pronator drift, speech every 1–2 hours
• BP management: Target SBP <140–160 mmHg before aneurysm is secured; nimodipine 60 mg PO/NG q4h for 21 days
• Seizure precautions: Levetiracetam commonly used for first 7 days; side rails padded, suction at bedside — see the seizure nursing reference
• Avoid Valsalva: Stool softeners (docusate), avoid coughing, elevate HOB 30°, no nose-blowing
• ICP management: HOB 30°, head midline, avoid neck flexion — see the ICP nursing reference for full protocol
• Fever management: Treat aggressively; fever worsens cerebral ischemia in the vasospasm window
• Fluid balance: Euvolemia preferred; avoid aggressive fluid restriction (can worsen vasospasm/DCI)

NCLEX tip 3: The priority nursing intervention for a patient with SAH before aneurysm repair is maintaining a quiet, dark environment and preventing any activity that raises ICP or triggers rebleeding.

Epidural hematoma (EDH)

Pathophysiology

An epidural hematoma forms between the skull and the dura mater. Unlike subdural hematomas, EDH almost always results from arterial bleeding — most commonly from rupture of the middle meningeal artery, a branch of the external carotid artery that runs in a groove along the inner surface of the temporal bone. A temporal bone fracture, even a linear one without displacement, can lacerate this artery.

Because it is arterial, the bleed under high pressure rapidly strips the dura from the inner skull table, accumulating as a large clot. The dura is firmly attached at cranial sutures, which is why EDH does NOT cross suture lines on imaging.

EDH accounts for about 1–3% of all traumatic brain injuries. The mechanism is typically blunt trauma to the temporal region — a fall, motor vehicle collision, or strike to the head. The middle meningeal vein or dural venous sinus can occasionally be the source (venous EDH), which bleeds more slowly and may not present as acutely.

Classic presentation: the lucid interval

The lucid interval is one of the most tested concepts in emergency nursing. The sequence:

1. Initial LOC — brief loss of consciousness at the moment of impact (concussive mechanism)
2. Lucid interval — the patient regains consciousness and appears alert; they may walk, talk, and seem fine
3. Rapid deterioration — as the hematoma expands, ICP rises, and the patient deteriorates precipitously over minutes to hours

NCLEX tip 4: The lucid interval is NOT always present — it occurs in roughly 30–50% of EDH cases — but when it is present, it is PATHOGNOMONIC for EDH. A patient with head trauma who “talked and died” is the classic NCLEX scenario.

As the hematoma expands and uncal herniation begins, compression of cranial nerve III produces the classic sign: ipsilateral fixed and dilated pupil (blown pupil). This is followed rapidly by contralateral hemiplegia (corticospinal tract compression), declining GCS, and Cushing’s triad — the late sign of herniation.

CT appearance

On non-contrast CT, EDH appears as a biconvex (lens-shaped or lenticular) hyperdense collection adjacent to the skull. Key features:

• Does NOT cross suture lines (dura anchors there)
• Usually overlies the temporal region
• May show a skull fracture on bone windows
• Hyperdense (bright white) acutely — blood is more dense than brain tissue on CT

NCLEX tip 5: EDH = lens-shaped (biconvex) = does NOT cross sutures. SDH = crescent-shaped = DOES cross sutures. This CT differentiation is high-yield.

Treatment and nursing priorities

EDH is a surgical emergency. Rapid evacuation via craniotomy dramatically reduces mortality — outcome is largely determined by the patient’s neurological status at the time of surgery. Patients who are operated on before herniation occurs have survival rates exceeding 95%.

Nursing priorities:

• Immediate physician notification if neuro status deteriorates — do not wait for scheduled check
• Prepare for emergent OR — NPO status, IV access, type and screen, consent if patient is capacitated
• Airway management: Intubate for GCS ≤8 or loss of airway reflexes — see the mechanical ventilation nursing reference
• Avoid hypotension: Unlike ICH, where BP reduction is the priority, EDH management requires preserving cerebral perfusion pressure. Target MAP ≥70–80 mmHg until the clot is evacuated
• Serial GCS and pupil checks every 15–30 minutes in acute phase
• No sedation unless airway-controlled — sedating a deteriorating EDH patient masks herniation signs

Traumatic EDH often co-exists with other injuries. In the context of significant mechanism, follow TBI nursing protocols for multi-system assessment.

Subdural hematoma (SDH)

Pathophysiology

Subdural hematoma forms between the dura mater and the arachnoid mater when bridging veins — thin-walled veins that span from the brain surface to the dural sinuses — are stretched and torn. This is a venous bleed, slower than arterial EDH, but can still be life-threatening when large or in patients with impaired reserve.

Because it is venous, the blood layers along the brain’s surface in a crescent shape, conforming to the brain’s contours. The arachnoid and dura are not attached at sutures the same way as the skull-dura interface, so SDH does cross suture lines — distinguishing it from EDH.

Three types of SDH

NCLEX tip 6: Chronic SDH can be missed on CT because the blood becomes isodense with brain tissue at 1–3 weeks. A patient on warfarin with slowly progressive confusion and a history of minor head trauma — even weeks ago — should trigger suspicion. Look for asymmetric sulci or midline shift on CT.

Populations at highest risk for chronic SDH:

• Elderly patients — brain atrophy increases the space between brain and skull, stretching bridging veins and allowing larger hematomas before symptoms develop
• Patients on anticoagulants (warfarin, DOACs) or antiplatelet agents
• Alcoholics — both brain atrophy and coagulopathy contribute
• Mechanism is often trivial — a minor bump, a fall from standing, occasionally no recalled trauma

Anticoagulation reversal (SDH and ICH)

Reversal of anticoagulation is urgent in both SDH and ICH. Know the agents:

NCLEX tip 7: Idarucizumab (Praxbind) reverses dabigatran. Andexanet alfa reverses factor Xa inhibitors (rivaroxaban, apixaban). Protamine reverses heparin. Vitamin K + 4F-PCC reverses warfarin.

Treatment and nursing priorities for SDH

• Surgical options: Craniotomy (large/acute SDH) or burr hole drainage (chronic SDH). Asymptomatic small SDHs may be managed conservatively with serial imaging.
• Anticoagulation reversal: Initiate immediately on diagnosis (see table above)
• Avoid hypotension: Similar to EDH — brain compliance is already reduced; maintain MAP ≥70 mmHg
• Seizure precautions: SDH carries seizure risk; levetiracetam commonly prescribed
• Cognitive monitoring: Chronic SDH patients may present with confusion, personality change, or falls — distinguish from dementia baseline
• Discharge education: Patients recovering from chronic SDH should avoid anticoagulants and antiplatelet agents until cleared by neurosurgery; fall prevention is a priority

Intracerebral hemorrhage (ICH)

Pathophysiology and causes

Intracerebral hemorrhage — bleeding into the brain parenchyma itself — is the most lethal stroke type. Roughly 10–15% of all strokes are ICH, but the 30-day mortality approaches 40–50%. Hypertension is the most common cause, responsible for approximately 50–70% of cases. Chronic hypertension causes lipohyalinosis and formation of Charcot-Bouchard microaneurysms in the small penetrating arteries supplying the basal ganglia, thalamus, pons, and cerebellum — the classic locations for hypertensive ICH.

Other causes:

• Cerebral amyloid angiopathy (CAA): Amyloid deposits in cortical arterioles cause fragility and rupture; responsible for most lobar ICH (cortical and subcortical) in patients over 65; often recurrent
• AVM (arteriovenous malformation): Abnormal tangle of vessels without a capillary bed; higher risk of rupture in younger patients; typically presents in patients under 40
• Coagulopathy: Warfarin, DOACs, thrombocytopenia, liver failure — anticoagulant-related ICH tends to expand aggressively
• Cocaine and methamphetamine: Sympathomimetic surges cause severe hypertension and vasospasm; ICH risk is dramatically elevated in the hours after use, particularly in young patients

ICH score: predicting 30-day mortality

The ICH Score (0–6) is used to estimate 30-day mortality. Higher scores correspond to worse outcomes:

Approximate 30-day mortality by score: Score 0 = 0%; Score 1 = 13%; Score 2 = 26%; Score 3 = 72%; Score 4 = 97%; Score 5–6 = ~100%. The ICH Score guides early goals-of-care conversations.

NCLEX tip 8: ICH Score ≥4 is associated with near-universal 30-day mortality. This makes early, honest family communication — and goals of care discussions — a nursing priority, not a deferral.

Hematoma expansion

Approximately 30% of ICH patients experience hematoma expansion within the first 24 hours — defined as >33% or >6 mL growth on follow-up CT. Expansion is the strongest independent predictor of neurological deterioration and death. This is why aggressive blood pressure reduction is the top priority in the first 24 hours.

Per AHA/ASA 2022 guidelines, for patients with ICH and initial SBP 150–220 mmHg, acute lowering of SBP to 140 mmHg is safe and may improve functional outcomes. This represents a shift from earlier guidelines that targeted 160 mmHg; the goal is now 130–140 mmHg. Agents of choice:

• Labetalol IV (alpha- and beta-blocker): 10–20 mg IV bolus, repeat every 10 minutes to a total of 300 mg; or continuous infusion
• Nicardipine IV (calcium channel blocker): 5–15 mg/hr infusion, titrated; more controllable for sustained BP targets
• Clevidipine IV (ultra-short-acting CCB): 1–2 mg/hr, doubled every 90 seconds to target — highly titratable

For blood pressure management principles, see the hypertensive emergency nursing reference.

NCLEX tip 9: For ICH, the priority BP target per AHA/ASA 2022 is SBP <140 mmHg. The rationale is hematoma expansion prevention. Agents used include labetalol and nicardipine — NOT nitroprusside (can increase ICP).

Surgical options

Surgical intervention for ICH is nuanced:

• Cerebellar ICH >3 cm compressing the brainstem or causing obstructive hydrocephalus: surgical evacuation is strongly recommended — this is the clearest surgical indication
• Supratentorial ICH: Multiple randomized trials have failed to show consistent mortality benefit from open craniotomy; conservative management is standard unless herniation is imminent
• Minimally invasive surgery (MIS): Stereotactic aspiration and endoscopic evacuation are under active investigation; emerging evidence suggests benefit for select patients with superficial lobar hematomas

External ventricular drain (EVD) placement is indicated for obstructive hydrocephalus from intraventricular extension of ICH.

Nursing priorities for ICH

Immediate priorities (first hour):

1. Airway: Intubate if GCS ≤8 or airway reflexes absent — refer to mechanical ventilation nursing
2. BP management: Labetalol or nicardipine to SBP <140 mmHg; continuous arterial line monitoring preferred
3. Anticoagulation reversal: Do not wait — begin reversal as soon as hemorrhagic stroke is confirmed on CT (see reversal table above)
4. Glucose management: Both hypoglycemia and hyperglycemia worsen neurological outcomes; target glucose 140–180 mg/dL in critically ill patients
5. Temperature: Treat fever aggressively with acetaminophen; fever worsens cerebral metabolism and outcomes

Ongoing ICU priorities:

• Neuro checks every 1–2 hours (GCS, pupils, pronator drift, speech)
• ICP monitoring with EVD or parenchymal bolt if GCS ≤8 and volume warrants; target ICP <20 mmHg, CPP 60–70 mmHg
• HOB 30°, head midline — see ICP nursing for full protocol
• DVT prophylaxis timing: Sequential compression devices (SCDs) acutely; pharmacologic prophylaxis (low-dose heparin or LMWH) typically started after 24–48 hours for stable ICH once hematoma expansion risk is reduced
• Seizure monitoring: EEG if clinical suspicion; levetiracetam prophylaxis for cortical ICH (especially lobar)
• Family communication and early goals of care — ICH Score guides prognosis discussion

NCLEX tip 10: For ICH, withhold pharmacologic DVT prophylaxis acutely (rebleed risk) and start SCDs immediately. Restart anticoagulation — if the patient had atrial fibrillation, for example — is typically deferred for weeks and is a physician/multidisciplinary decision.

Neurological assessment priorities across all subtypes

GCS monitoring

The Glasgow Coma Scale (GCS) is the primary neurological monitoring tool. Score 15 = fully intact; GCS ≤8 = coma-level, intubation typically indicated. Any decline of 2 or more points from baseline is clinically significant and requires immediate provider notification.

Components: Eye opening (4 points) + Verbal response (5 points) + Motor response (6 points) = Total 3–15.

NCLEX tip 11: A GCS of 8 or below means the patient cannot protect their airway reliably. Airway management is the immediate priority — not blood pressure, not imaging, not medications.

Pupil assessment

• Unilateral fixed and dilated pupil (blown pupil): CN III compression from uncal herniation; ipsilateral to the lesion in EDH/SDH — act immediately
• Bilateral fixed and dilated pupils: Bilateral herniation, massive brainstem compression, or pharmacological (atropine, epinephrine in arrest) — extremely poor prognostic sign
• Pinpoint pupils (1–2 mm, bilateral): Pontine lesion or opioid toxicity
• Unequal pupils (anisocoria) — new onset: Asymmetric pressure or CN III involvement; warrants CT

ICP management fundamentals

Applicable to all subtypes causing mass effect:

• HOB 30° — reduces venous engorgement; do NOT use Trendelenburg
• Head midline — neck rotation impedes venous drainage and elevates ICP
• Minimize noxious stimuli — suction, painful procedures trigger ICP spikes; pre-medicate when possible
• Osmotherapy: Mannitol 0.25–1 g/kg IV bolus (monitor serum osmolarity <320 mOsm/L); or hypertonic saline (3% NaCl, 23.4% for emergent herniation)
• Avoid hypercapnia: Maintain PaCO₂ 35–40 mmHg; hyperventilation (PaCO₂ 30–35) is a bridge measure for acute herniation only

NCLEX tip 12: Hypertonic saline draws water out of brain cells osmotically, reducing cerebral edema. It is preferred over mannitol in patients who are hypovolemic or hypotensive because it also expands intravascular volume.

NCLEX differentiation: SAH vs EDH vs SDH vs ICH

NCLEX tip 13: When the NCLEX describes a patient with temporal bone fracture and a brief lucid interval followed by rapid deterioration — that is EDH until proven otherwise. The CT showing a biconvex lesion confirms it. The answer is emergency surgical evacuation.

NCLEX tip 14: When the NCLEX describes an elderly patient on warfarin with weeks of progressive confusion after a minor bump to the head — that is chronic SDH. The CT may show an isodense or hypodense crescent. The answer involves reversing the warfarin AND consulting neurosurgery.

Clinical priorities: head-to-toe nursing assessment

Every patient with intracranial hemorrhage requires a systematic assessment. The following framework applies regardless of subtype:

Airway and breathing:

• GCS ≤8 → intubation and mechanical ventilation
• Assess gag and cough reflex; if absent, airway is unprotected
• Monitor SpO₂ continuously; target ≥94%; hypoxia worsens cerebral injury

Circulation:

• Continuous cardiac monitoring — SAH is associated with cardiac arrhythmias (repolarization changes, Q-T prolongation, T-wave inversions from catecholamine surge)
• Arterial line preferred for continuous BP monitoring in ICH and SAH
• Establish large-bore IV access; type and screen for potential surgery

Disability (neuro):

• GCS every 1–2 hours; notify for any 2-point decline
• Pupil size, symmetry, and reactivity every 1–2 hours
• Pronator drift: patient extends arms palms up with eyes closed — downward drift of one arm suggests contralateral cortical motor deficit
• Speech: assess for aphasia (dominant hemisphere) vs. dysarthria (motor control)
• Grip strength bilateral comparison

Exposure and environment:

• Temperature: treat fever ≥38.3°C (101°F) aggressively; fever directly worsens neurological outcomes
• Glucose: check q4–6h; treat <140 and >180 mg/dL per protocol
• Skin: turn every 2 hours; pressure injury prevention in patients with decreased mobility or LOC

Goals-of-care and family communication

Intracranial hemorrhage carries high mortality and frequent long-term disability. Early, honest family communication is a nursing and physician responsibility — not a deferral for “after we see how they do.”

Key communication points for families:

• Prognosis is often guarded in the first 24–72 hours — early imaging findings and GCS guide but do not definitively predict long-term outcome
• Early self-fulfilling prophecy of poor outcomes: Studies show that early withdrawal of life support (before 72 hours) is a major driver of poor outcomes in ICH — families and teams should be cautious about too-early withdrawal decisions unless clinical decline is unambiguous
• Rehabilitation potential: Many ICH survivors have significant recovery potential with neurorehabilitation; early PT/OT/SLP involvement matters
• Goals of care documentation: Ensure advance directives are documented; if none exist, identify healthcare proxy immediately

NCLEX-style practice questions

Question 1

A 52-year-old woman presents to the ED with a sudden-onset headache she describes as “the worst headache of my life.” She reports nausea, neck stiffness, and sensitivity to light. Non-contrast CT of the head is negative for blood. What is the nurse’s priority next action?

A) Administer sumatriptan for probable migraine
B) Prepare the patient for lumbar puncture to assess for xanthochromia
C) Obtain an MRI of the brain with and without contrast
D) Discharge with neurology follow-up in 48 hours

Answer: B. A negative CT in a patient with thunderclap headache does NOT rule out SAH. Xanthochromia on lumbar puncture — present when CSF turns yellow due to bilirubin from lysed RBCs — is required to exclude SAH. This is a time-sensitive diagnosis; LP should not be delayed. Sumatriptan is contraindicated if SAH is suspected.

Question 2

A 34-year-old male is brought to the ED after a motor vehicle collision with blunt trauma to the left temporal region. He was unconscious briefly at the scene, then became alert and conversational during transport. En route, he becomes increasingly drowsy, begins vomiting, and his GCS drops from 14 to 9. CT reveals a biconvex hyperdense collection over the left temporal lobe that does not cross suture lines. Which assessment finding would the nurse anticipate next?

A) Bilateral Babinski signs
B) Left-sided pupil dilation and hemiplegia
C) Right-sided fixed dilated pupil and left hemiplegia
D) Pinpoint pupils and absent gag reflex

Answer: C. EDH causes ipsilateral CN III compression → ipsilateral fixed dilated pupil. The hematoma is on the LEFT, so the left uncus herniates through the tentorium, compressing the left CN III → LEFT pupil is dilated. The corticospinal tract decussates, so left-hemisphere compression causes RIGHT hemiplegia. Answer C is correct: right fixed dilated pupil (ipsilateral CN III) and left hemiplegia (contralateral corticospinal).

Wait — the hematoma is over the LEFT temporal lobe. Left uncal herniation compresses LEFT CN III → LEFT (ipsilateral) pupil dilates. Left corticospinal compression → right hemiplegia. Answer B is the physiologically correct answer: LEFT pupil dilation and right-sided deficits. On the NCLEX, carefully track which side the lesion is on. This is a classic trap.

Corrected answer: B — ipsilateral (left) pupil dilation from CN III compression; hemiplegia would be contralateral (right side).

Question 3

An 81-year-old man on warfarin for atrial fibrillation is brought to the ED by his daughter, who reports 3 weeks of progressive confusion, increasing falls, and personality change. He denies headache. CT head shows a hypodense crescent-shaped collection over the right hemisphere that crosses suture lines. INR is 3.2. Which intervention is the nurse’s immediate priority?

A) Administer vitamin K 10 mg IV and prepare 4-factor PCC for infusion
B) Place the patient in a quiet room and initiate seizure precautions
C) Prepare the patient for emergent endovascular coiling
D) Administer dexamethasone 10 mg IV for cerebral edema

Answer: A. This presentation — elderly, anticoagulated, progressive symptoms, hypodense crescent SDH — is chronic subdural hematoma. The INR of 3.2 is supratherapeutic and must be reversed immediately. Vitamin K provides sustained reversal (hours); 4-factor PCC (Kcentra) provides immediate factor replacement. Seizure precautions (B) are appropriate but secondary. Endovascular coiling (C) is for aneurysm — not SDH. Dexamethasone (D) has limited evidence in SDH and is not a first priority.

Key nursing takeaways

1. All four types of intracranial hemorrhage share the priorities of airway, neuro assessment, ICP management, and seizure precautions — the subtype determines the BP target, surgical urgency, and pharmacological approach.
2. Nimodipine in SAH is for vasospasm prevention — it is not a blood pressure medication. Do not hold it because it lowers BP unless hypotension is causing harm.
3. The lucid interval in EDH is a surgical emergency in waiting. Any temporal trauma patient who “woke up fine” but is now declining needs immediate CT and neurosurgical consultation.
4. Chronic SDH is a diagnosis of exclusion in elderly patients with progressive cognitive decline — especially those on anticoagulants. CT is required; the hematoma can be isodense and subtle.
5. ICH hematoma expansion drives mortality — BP control to SBP <140 mmHg in the first hour is the highest-impact intervention available.
6. Anticoagulation reversal is urgent in both SDH and ICH — know which agent reverses which drug.
7. Fever, hyperglycemia, and hypoxia worsen outcomes across all subtypes. These are modifiable variables under nursing control.
8. Early goals-of-care conversations should begin within the first 24 hours — not deferred until the patient “declares.”

For deeper content on related clinical priorities, see the stroke nursing reference for ischemic vs. hemorrhagic stroke differentiation, the ICP nursing reference for comprehensive ICP monitoring and management, and the TBI nursing reference for polytrauma assessment in patients with EDH or SDH.