Intracranial hemorrhage nursing: care plans, interventions, and NCLEX guide

Intracranial hemorrhage (ICH in the broad sense) is any bleeding inside the skull – within the brain parenchyma, between the protective membranes, or in the subarachnoid space. For nurses in the ED, ICU, or neuro unit, the priority is the same regardless of subtype: protect the airway, control intracranial pressure, reverse anticoagulation, and prevent secondary injury. This reference covers the priority nursing interventions, nursing diagnoses, assessment framework, and the four distinct subtypes (SAH, EDH, SDH, ICH) with NCLEX-style questions throughout.

Priority nursing interventions (snippet summary)

The priority nursing interventions for a patient with intracranial hemorrhage are:

1. Airway protection – intubate if GCS ≤8 or absent gag reflex
2. Neurological assessment every 1–2 hours – GCS, pupil size and reactivity, motor strength
3. Blood pressure control – SBP <140 mmHg in ICH; <140–160 mmHg in SAH before aneurysm secured
4. Anticoagulation reversal – immediate; agent depends on drug (see reversal table below)
5. ICP management – HOB elevated 30°, head midline, minimize stimulation, osmotherapy if signs of herniation
6. Seizure precautions and prophylaxis – levetiracetam common; padded side rails, suction at bedside
7. Fever, glucose, and oxygenation control – treat fever >38.3°C; maintain glucose 140–180 mg/dL; SpO₂ ≥94%
8. Notify provider for any 2-point GCS decline – do not wait for the next scheduled check

Each of these is expanded with rationale, drugs, and subtype-specific targets below.

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.

Nursing diagnoses for intracranial hemorrhage

The most common NANDA-I nursing diagnoses for a patient with intracranial hemorrhage, with associated interventions:

These diagnoses apply across all four hemorrhage subtypes, with the priority ordering shifting based on presentation. For an acutely deteriorating patient with EDH, ineffective airway clearance and risk for decreased intracranial adaptive capacity dominate. For a chronic SDH on the medical floor, risk for falls and impaired physical mobility move higher.

Nursing care plans with rationales

Below are the three highest-yield NANDA-I care plans for intracranial hemorrhage, formatted with related factors, defining characteristics, assessment cues, interventions with rationales, and expected outcomes. Use these as a template for clinical paperwork or NCLEX scenarios.

Care plan 1: Risk for ineffective cerebral tissue perfusion

Related to: hemorrhage, cerebral vasospasm, increased intracranial pressure, hematoma expansion, anticoagulation.

As evidenced by (risk factors – no signs/symptoms because it is a risk diagnosis): GCS decline, pupillary changes, motor weakness, hypertension or hypotension, hypoxia.

Expected outcomes:

• Patient maintains GCS at or above baseline throughout shift
• Pupils remain equal, round, and reactive to light
• MAP maintained within prescribed range; CPP 60–70 mmHg
• No new focal neurological deficit during the vasospasm window (days 4–14 in SAH)

Care plan 2: Risk for decreased intracranial adaptive capacity

Related to: cerebral edema, mass effect from hematoma, hydrocephalus, sustained ICP >15 mmHg.

Assessment cues: repeated ICP elevations above 20 mmHg lasting more than 5 minutes, disproportionate ICP rise to minor stimuli, declining CPP, Cushing’s triad.

Expected outcomes:

• ICP remains <20 mmHg
• CPP maintained 60–70 mmHg
• No signs of herniation (no pupillary changes, no Cushing’s triad)

Care plan 3: Ineffective airway clearance

Related to: decreased level of consciousness, absent gag or cough reflex, GCS ≤8, retained secretions.

As evidenced by: abnormal breath sounds, hypoxemia, ineffective cough, tachypnea or bradypnea, agonal respirations.

Expected outcomes:

• Airway remains patent; clear breath sounds
• SpO₂ ≥94%, end-tidal CO₂ within range
• No aspiration event during the shift

For broader airway protocols, see the airway management nursing reference and the mechanical ventilation nursing reference. For a full GCS scoring guide, see the Glasgow Coma Scale reference.

Cushing’s triad: the late sign of herniation

Cushing’s triad is the body’s reflex response to dangerously high intracranial pressure and is a late sign – often a pre-terminal one. All three components must be present to call it a true triad:

1. Hypertension with widening pulse pressure – the brain raises systemic BP to maintain cerebral perfusion against rising ICP
2. Bradycardia – baroreceptor reflex response to the hypertensive surge
3. Irregular respirations (Cheyne-Stokes, ataxic, or apneustic) – brainstem compression disrupts the respiratory center

If a nurse identifies Cushing’s triad, herniation is imminent or occurring. The response is immediate provider notification, osmotherapy (hypertonic saline or mannitol), and preparation for definitive surgical or ICP-lowering intervention. Do not delay for additional assessment.

NCLEX tip: Hypertension + bradycardia + irregular breathing = Cushing’s triad = late herniation. The priority action is to notify the provider and prepare for emergent ICP-lowering interventions – not to administer antihypertensives, which would compromise the brain’s last attempt to maintain perfusion.

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.

Aneurysmal vs traumatic SAH: Aneurysmal SAH is the spontaneous medical emergency described above and is the focus of most NCLEX questions. Traumatic SAH results from blunt head injury and is the most common form of SAH overall when trauma is included in the denominator. Traumatic SAH is usually a marker of injury severity rather than a primary surgical target – the management overlap is significant (ICP control, BP control, seizure precautions), but vasospasm and nimodipine are reserved for aneurysmal SAH unless the trauma protocol specifically calls for it. Always confirm the cause on CT angiography before initiating SAH-specific therapy.

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)
• Kernig’s sign – with hip flexed at 90°, passive knee extension elicits pain and resistance; positive when meningeal irritation is present
• Brudzinski’s sign – passive neck flexion provokes involuntary flexion of the hips and knees; another meningeal-irritation indicator
• 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, target SBP of 140 mmHg (acceptable range 130–150 mmHg) within 1 hour of treatment initiation, started within 2 hours of symptom onset, and maintained for at least 24 hours. The guidelines emphasize smooth, sustained control – avoid large BP swings, which independently worsen outcomes and increase the risk of acute kidney injury. Continuous infusion is preferred over repeated bolus dosing for that reason. 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

Discharge teaching for intracranial hemorrhage survivors

For patients stable enough to discharge home or to acute rehab, the nursing teaching plan covers:

• Medication adherence: Antihypertensives, antiepileptics (if prescribed), and stool softeners. Emphasize that BP control is the single most important factor in preventing recurrence of hypertensive ICH.
• Warning signs requiring 911: Sudden severe headache, new weakness or numbness, facial droop, slurred speech, vision changes, new seizure, decreasing alertness, repeated vomiting.
• Anticoagulant guidance: Patients with prior intracranial bleed should not restart anticoagulation without explicit neurosurgical or stroke team approval. Document the plan in the discharge summary.
• Fall prevention: Remove throw rugs, install grab bars, use night lights, review medications for orthostatic risk. SDH survivors are at high risk for re-bleed from another fall.
• Activity restrictions: Avoid heavy lifting, Valsalva-inducing activity, contact sports, and driving until cleared. Specific clearance from neurosurgery for SAH or post-craniotomy patients.
• Follow-up appointments: Neurosurgery or neurology within 2–4 weeks; primary care for BP optimization within 1–2 weeks; rehabilitation therapy as indicated.
• Family education on cognitive/personality changes: Survivors may have lasting cognitive or behavioral changes that families should be prepared for; refer to stroke support groups and brain injury association resources.

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 right-sided hemiplegia C) Right-sided fixed dilated pupil and left hemiplegia D) Pinpoint pupils and absent gag reflex

Answer: B. EDH causes ipsilateral CN III compression and contralateral corticospinal tract findings. The hematoma is on the LEFT, so left uncal herniation compresses the LEFT CN III → LEFT pupil dilates. The corticospinal tract decussates, so left-hemisphere compression causes RIGHT hemiplegia. The combination of ipsilateral blown pupil and contralateral hemiplegia is the classic uncal herniation pattern.

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.

Frequently asked questions

What is the priority nursing intervention for a patient with intracranial hemorrhage?

The priority is airway protection. A Glasgow Coma Scale of 8 or below means the patient cannot reliably protect their own airway, and intubation is indicated before blood pressure control, imaging, or medications. Once the airway is secure, blood pressure control (SBP <140 mmHg for ICH), anticoagulation reversal, and ICP management follow in rapid sequence.

What are the most common nursing diagnoses for intracranial hemorrhage?

The most common NANDA-I nursing diagnoses are: risk for ineffective cerebral tissue perfusion, risk for decreased intracranial adaptive capacity, ineffective airway clearance, risk for injury related to seizure activity, risk for falls, acute pain, impaired physical mobility, and anxiety. Priority ordering depends on the patient’s acuity and the specific hemorrhage subtype.

What is the difference between SAH, SDH, EDH, and ICH?

These are the four subtypes of intracranial hemorrhage, distinguished by anatomy and mechanism. Subarachnoid hemorrhage (SAH) is bleeding into the subarachnoid space, usually from a ruptured berry aneurysm. Subdural hematoma (SDH) is venous bleeding between the dura and arachnoid mater, often from torn bridging veins. Epidural hematoma (EDH) is arterial bleeding between the skull and dura, usually from the middle meningeal artery after temporal trauma. Intracerebral hemorrhage (ICH) is bleeding within the brain parenchyma itself, most often from hypertension.

What blood pressure target should the nurse maintain for an intracerebral hemorrhage?

Per AHA/ASA 2022 guidelines, for patients with intracerebral hemorrhage and initial SBP 150–220 mmHg, acute lowering of SBP to 140 mmHg is safe and may improve functional outcomes. The agents of choice are IV labetalol or nicardipine. Nitroprusside is avoided because it can raise intracranial pressure.

Why is nimodipine given in subarachnoid hemorrhage?

Nimodipine is a calcium channel blocker given to prevent cerebral vasospasm and delayed cerebral ischemia after subarachnoid hemorrhage. It is not given to control blood pressure. Standard dosing is 60 mg PO or NG every 4 hours for 21 days, starting within 96 hours of the bleed. If a dose drops the patient’s blood pressure significantly, hold and notify the provider rather than treating it as a BP medication.

What is the lucid interval in epidural hematoma?

The lucid interval is a transient period of normal consciousness between the initial loss of consciousness at the time of injury and a rapid neurological decline as the hematoma expands. It occurs in roughly 30–50% of epidural hematoma cases and is pathognomonic when present. A head trauma patient who “talked and died” is the classic lucid interval presentation.

How is anticoagulation reversed in intracranial hemorrhage?

Reversal depends on the anticoagulant. Warfarin is reversed with vitamin K plus 4-factor prothrombin complex concentrate (Kcentra). Heparin is reversed with protamine sulfate. Dabigatran (Pradaxa) is reversed with idarucizumab (Praxbind). Rivaroxaban and apixaban (factor Xa inhibitors) are reversed with andexanet alfa (Andexxa), or 4F-PCC when Andexxa is not available. Reversal should begin as soon as hemorrhage is confirmed.

When is surgery indicated for intracerebral hemorrhage?

Surgical evacuation is clearly indicated for cerebellar ICH greater than 3 cm that is compressing the brainstem or causing obstructive hydrocephalus. For supratentorial ICH, randomized trials have not shown consistent mortality benefit from open craniotomy, so conservative management is standard unless herniation is imminent. Minimally invasive evacuation is under active investigation for select superficial lobar hematomas.

What is Cushing’s triad and what does it indicate?

Cushing’s triad is hypertension with widening pulse pressure, bradycardia, and irregular respirations. It is a late sign of severely elevated intracranial pressure and indicates that brainstem compression or imminent herniation is occurring. The triad is the brain’s reflex attempt to maintain cerebral perfusion against rising ICP. When a nurse identifies all three components, the priority is immediate provider notification and preparation for emergent ICP-lowering interventions such as osmotic therapy, ventriculostomy, or surgical decompression.

How often should neurological assessments be performed in intracranial hemorrhage?

In the acute phase, neurological assessments – including Glasgow Coma Scale, pupil size and reactivity, motor strength, and speech – should be performed every 1 to 2 hours. During the first hour after a deteriorating event, or in patients with an evolving EDH or impending herniation, frequency increases to every 15 to 30 minutes. Any 2-point decline in GCS from baseline, a new pupillary asymmetry, or a new focal deficit warrants immediate provider notification – do not wait for the next scheduled check.

What is the right fixed dilated pupil with decerebrate posturing pointing to?

A right fixed and dilated pupil with decerebrate posturing indicates uncal herniation from a right-sided mass lesion compressing the right cranial nerve III, with brainstem compression now reaching the level of the red nucleus or below. The right pupil dilates because the parasympathetic fibers of CN III run on the surface of the nerve and are compressed first. Decerebrate posturing – arms extended and pronated, legs extended – is more ominous than decorticate posturing and carries mortality up to 90% in TBI populations. This is a neurosurgical emergency: notify the provider immediately, prepare for emergent imaging, osmotherapy, and possible surgical decompression.

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.

Nurses drawn to neurological care can explore the neuroscience nurse career path and the neurology nurse practitioner path for information on specializing in this area. Salary data for both roles is available at the neuroscience nurse salary guide and neurology NP salary guide.

Clinical sources

• American Heart Association / American Stroke Association. 2022 Guideline for the Management of Patients With Spontaneous Intracerebral Hemorrhage. Stroke 2022.
• Connolly ES et al. Guidelines for the Management of Aneurysmal Subarachnoid Hemorrhage. AHA/ASA Guideline. Stroke.
• Hemphill JC et al. The ICH Score: A Simple, Reliable Grading Scale for Intracerebral Hemorrhage. Stroke 2001.
• Hunt WE, Hess RM. Surgical risk as related to time of intervention in the repair of intracranial aneurysms. Journal of Neurosurgery.
• Fisher CM et al. Relation of cerebral vasospasm to subarachnoid hemorrhage visualized by computerized tomographic scanning. Neurosurgery.
• Frontera JA et al. Guideline for Reversal of Antithrombotics in Intracranial Hemorrhage. Neurocritical Care Society and Society of Critical Care Medicine.