Case studies · Medicine · 8 November 2026

Subarachnoid hemorrhage case study

The case

Patient: A 58‑year‑old right‑handed male, Mr R, presents to the emergency department (ED) with a sudden, severe headache.

Presenting complaint: “The worst headache of my life” that began 45 minutes ago while he was watching television. The pain is described as a “thunderclap” and is diffuse, radiating to the neck. He reports nausea, one episode of non‑bloody vomiting, and brief loss of consciousness (≈30 seconds) before regaining awareness. No focal weakness, seizures, or visual changes are reported.

Past medical history:

• Hypertension for 12 years, on amlodipine 5 mg daily (poor adherence).
• Smoker: 20 pack‑years, currently 1 pack/day.
• No known aneurysms, trauma, or coagulopathy.

Family history: Father died of myocardial infarction at 62 y; mother had a subarachnoid hemorrhage (SAH) at 55 y (unknown cause).

Medications: Amlodipine 5 mg daily, occasional ibuprofen for knee pain.

Allergies: None.

Social history: Works as a civil engineer; lives with spouse.

Examination (within 1 hour of arrival):

Initial investigations (drawn in the ED):

• Non‑contrast CT head (plain): Hyperdense (bright) fluid in the basal cisterns and sulci, especially in the Sylvian fissures – classic “star‑field” appearance suggestive of acute SAH. No mass effect or midline shift.
• Complete blood count (CBC): Hb 14.2 g/dL, WBC 9.8 × 10⁹/L, Platelets 240 × 10⁹/L.
• Basic metabolic panel: Na⁺ 138 mmol/L, K⁺ 4.1 mmol/L, Cl⁻ 102 mmol/L, HCO₃⁻ 24 mmol/L, BUN 18 mg/dL, Creatinine 0.9 mg/dL, Glucose 112 mg/dL.
• Coagulation profile: PT 12 s (INR 1.0), aPTT 30 s – within normal limits.
• Serum electrolytes, calcium, magnesium: All within normal range.
• ECG: Normal sinus rhythm, no ischemic changes.

The patient is placed on a cardiac monitor, given analgesia (IV fentanyl 50 µg), anti‑emetic (ondansetron 4 mg IV), and a stat dose of oral nimodipine 60 mg (to be continued). A lumbar puncture (LP) is deferred because the CT already shows SAH.

Questions

1. What is the most likely diagnosis?
2. Which clinical and radiological findings point toward this diagnosis, and why are they significant?
3. What further investigations are required to identify the source of bleeding and assess for complications?
4. Outline the acute management plan for this patient, including pharmacologic and non‑pharmacologic measures, with reference to current guidelines.
5. Discuss the major early and delayed complications of subarachnoid hemorrhage and their preventive strategies.

Answers

1. What is the most likely diagnosis?

Answer: Acute spontaneous subarachnoid hemorrhage (SAH), most commonly due to rupture of a saccular (berry) aneurysm.

Reasoning:

• The hallmark “thunderclap” headache reaching maximal intensity within seconds, accompanied by neck stiffness, is classic for SAH.
• The CT scan shows hyperdense blood in the basal cisterns and sulci, which is the most sensitive early imaging sign (sensitivity >95 % within 6 hours).
• Absence of trauma, anticoagulant use, or coagulopathy makes a spontaneous aneurysmal bleed the leading etiology.

2. Which clinical and radiological findings point toward this diagnosis, and why are they significant?

Clinical clues:

Radiological clues:

• Non‑contrast CT hyperdensity in basal cisterns: Blood is denser than brain tissue (≈60–70 HU vs 30–40 HU for parenchyma). This distribution is typical for aneurysmal SAH, especially when the Sylvian fissure and interhemispheric fissure are involved.
• Absence of intraparenchymal hematoma: Helps differentiate SAH from intracerebral hemorrhage (ICH).

These findings together confirm SAH and prompt urgent evaluation for the bleeding source.

3. What further investigations are required to identify the source of bleeding and assess for complications?

4. Outline the acute management plan for this patient, including pharmacologic and non‑pharmacologic measures, with reference to current guidelines.

Guideline reference: 2023 American Heart Association/American Stroke Association (AHA/ASA) Guideline for the Management of Aneurysmal Subarachnoid Hemorrhage; 2022 European Stroke Organization (ESO) guideline.

a. Initial stabilization

1. Airway, Breathing, Circulation (ABCs): Ensure airway protection; intubate only if Glasgow Coma Scale (GCS) ≤8 or airway compromise.
2. Blood pressure control: Target SBP <160 mmHg (or MAP <110 mmHg) to reduce re‑bleeding risk while maintaining cerebral perfusion.
   • Preferred agents: Intravenous nicardipine infusion 5 mg/h titrated up to 15 mg/h (or clevidipine).
   • Avoid nitroprusside (may increase ICP).
3. Analgesia & anti‑emesis: Fentanyl 25–50 µg IV bolus; ondansetron 4 mg IV.

b. Specific pharmacologic therapy

c. Definitive aneurysm treatment

• Timing: Secure the aneurysm within 24 h of admission if feasible (early clipping or endovascular coiling). Early treatment reduces re‑bleeding risk (mortality 30 % vs 60 % without).
• Choice of modality:
  • Endovascular coiling preferred for most posterior circulation aneurysms and those with favorable dome‑to‑neck ratio.
  • Microsurgical clipping considered for wide‑necked aneurysms, MCA bifurcation lesions, or when coiling not feasible.

d. Management of complications

1. Hydrocephalus:
   • External ventricular drain (EVD) placement if acute obstructive hydrocephalus (ventricular enlargement with decreased consciousness).
2. Cerebral vasospasm / DCI:
   • Maintain euvolemia (euvolemic fluid therapy: 2–3 L/day isotonic saline; avoid prophylactic hypervolemia).
   • Triple‑H therapy (Hypertension, Hypervolemia, Hemodilution) is no longer routine; induced hypertension (SBP 160–180 mmHg) may be used for symptomatic vasospasm.
   • Endovascular rescue: Intra‑arterial vasodilators (verapamil, nicardipine) or balloon angioplasty if refractory.
3. Electrolyte disturbances:
   • Monitor serum sodium every 6 h; treat hyponatremia with hypertonic saline (3 % NaCl) or fludrocortisone 0.1 mg PO daily.
4. Neurogenic cardiac injury:
   • Serial troponins, echocardiography; treat with standard heart‑failure therapy if needed.

e. Disposition

• Admit to a dedicated neuro‑intensive care unit (NICU).
• Continuous neurologic monitoring (hourly GCS, pupillary checks).
• Daily TCD screening for vasospasm (days 3–14).

5. Discuss the major early and delayed complications of subarachnoid hemorrhage and their preventive strategies.

Key learning points

• Thunderclap headache with meningeal signs is the classic presentation of spontaneous SAH; CT within 6 h has >95 % sensitivity.
• Early blood pressure control (SBP <160 mmHg) reduces re‑bleeding risk without compromising cerebral perfusion.
• Nimodipine for 21 days is the only medication with proven benefit in preventing delayed cerebral ischemia.
• Definitive aneurysm occlusion (coiling or clipping) should be performed as soon as feasible, ideally within 24 h.
• Cerebral vasospasm peaks between days 3–14; daily TCD monitoring and vigilant neurologic exams are essential.
• Hydrocephalus is common; an external ventricular drain relieves acute obstructive hydrocephalus and can be weaned later.
• Electrolyte disturbances, especially hyponatremia, are frequent and must be corrected promptly to avoid secondary brain injury.
• Multidisciplinary care in a neuro‑ICU, involving neurosurgery, interventional radiology, critical care, and rehabilitation, improves outcomes.

Practice MCQs

1. A 58‑year‑old man presents with a thunderclap headache. Non‑contrast CT shows blood in the basal cisterns. Which of the following is the most appropriate next step to prevent delayed cerebral ischemia?

A. Start intravenous labetalol to keep SBP < 140 mmHg.
B. Administer oral nimodipine 60 mg every 4 h for 21 days.
C. Begin high‑dose steroids to reduce cerebral edema.
D. Initiate prophylactic phenytoin for 14 days.

Answer: B — Nimodipine is the only therapy with Level I evidence (AHA/ASA 2023) for reducing the incidence of delayed cerebral ischemia after SAH.

2. Which imaging modality is considered the gold standard for characterizing a cerebral aneurysm prior to endovascular treatment?

A. Non‑contrast CT head.
B. CT‑angiography (CTA).
C. Magnetic resonance angiography (MRA).
D. Digital subtraction angiography (DSA).

Answer: D — DSA provides the highest spatial resolution and dynamic flow information, making it the gold standard for

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