Lucan · Conditions

Headache red flags / SAH

Australian guidance: eTG Neurology — Headache + Stroke Foundation SAH

1. Definition and epidemiology

Subarachnoid haemorrhage (SAH) is the accumulation of blood in the subarachnoid space, most commonly from rupture of an intracranial saccular (berry) aneurysm. SAH accounts for approximately 5% of all strokes in Australia. The condition carries high mortality, with many patients dying before reaching hospital; survivors face significant rates of disability, delayed cerebral ischaemia, and rebleeding. Headache red flags are the clinical features that compel urgent investigation to exclude SAH and other life-threatening intracranial pathology.

2. Pathophysiology

Approximately 85% of non-traumatic SAHs arise from rupture of a saccular aneurysm at arterial branch points in the circle of Willis, most commonly at the anterior communicating artery, posterior communicating artery, or middle cerebral artery bifurcation. Aneurysms develop at sites of congenital medial deficiency in the arterial wall, exacerbated by haemodynamic stress from hypertension and turbulent flow. Rupture causes an abrupt and massive increase in intracranial pressure, precipitating the thunderclap headache as blood dissects into the subarachnoid space. Irritation of meningeal nociceptors by blood breakdown products produces meningism. Subsequent vasospasm, driven by spasmogenic substances released from haemolysed erythrocytes, leads to delayed cerebral ischaemia in up to 30% of patients from days 4 to 14. Secondary hydrocephalus arises from impaired cerebrospinal fluid (CSF) reabsorption at the arachnoid granulations. A minority of SAHs result from arteriovenous malformations, perimesencephalic non-aneurysmal haemorrhage, or cocaine-induced vasospasm (Robbins Ch 28).

3. Clinical presentation and diagnostic criteria

The hallmark of SAH is a thunderclap headache, defined as a severe headache reaching maximal intensity within 60 seconds of onset, classically described as "the worst headache of my life." Approximately 75% of patients with SAH present this way; the remainder present with sudden loss of consciousness. Around 20% report a sentinel headache in the days to weeks preceding the major bleed, representing a minor aneurysmal leak. Examination may reveal neck stiffness, photophobia, and a positive Kernig sign. Focal neurological deficits and third nerve palsy (posterior communicating artery aneurysm compressing CN III) may be present but are not required for the diagnosis. The Ottawa SAH Rule identifies patients for CT investigation: any of thunderclap onset, age 40 years or older, neck pain or stiffness, witnessed loss of consciousness, onset during exertion, or limited neck flexion on examination.

Additional headache red flags requiring urgent workup include new headache in a patient over 50 years (giant cell arteritis, space-occupying lesion), headache with fever and meningism (bacterial meningitis), headache with progressive neurological deficit, headache in an immunocompromised patient, headache associated with postural change, and new headache in a patient with known malignancy or HIV.

4. Investigations and AU-specific cutoffs

Investigation follows a sequential pathway anchored to time of headache onset.

First-line: non-contrast CT brain. Performed urgently on all patients with suspected SAH. A normal non-contrast CT performed within 6 hours of headache onset has sensitivity exceeding 98% for SAH and is sufficient to exclude the diagnosis when the clinical picture is not compelling. This 6-hour cutoff is the AU standard for CT-alone rule-out.

Second-line: lumbar puncture (LP). If CT is performed more than 6 hours after headache onset and is negative but clinical suspicion remains high, LP is required to assess for xanthochromia in the CSF. Xanthochromia (yellow discolouration from oxyhaemoglobin and bilirubin) develops within 2 to 4 hours of SAH and persists for up to 2 weeks. LP should be performed at least 12 hours after headache onset to allow xanthochromia to develop; spectrophotometry of CSF is the preferred method in Australian laboratories.

Third-line: CT angiography (CTA) or MR angiography (MRA). Once SAH is confirmed, vascular imaging identifies the causative aneurysm and guides neurosurgical or endovascular planning. Digital subtraction angiography (DSA) remains the gold standard for aneurysm characterisation when CTA is non-diagnostic.

Additional investigations include: full blood count, coagulation studies, urea, electrolytes and creatinine (hyponatraemia from cerebral salt-wasting or SIADH is common), troponin and ECG (neurogenic myocardial injury occurs in up to 30%), and blood glucose.

5. Management

Transfer all patients with suspected SAH by ambulance to a hospital with neurosurgical and interventional neuroradiology capability. SAH is a medical emergency. Management is led by a neurosurgeon in collaboration with an interventional neuroradiologist.

Aneurysm securing: the ruptured aneurysm should be treated as early as possible to prevent rebleeding, which carries mortality of approximately 40 to 80%. Endovascular coiling is preferred over surgical clipping for most aneurysms where both options are feasible, based on the ISAT trial. Surgical clipping is favoured for middle cerebral artery aneurysms and those with a wide neck unsuitable for coiling.

Vasospasm prevention: nimodipine 60 mg orally every 4 hours for 21 days is standard AU practice to reduce the severity of delayed cerebral ischaemia. For refractory vasospasm, intra-arterial verapamil may be considered. Adequate volume resuscitation with isotonic saline maintains cerebral perfusion; hypertensive hypervolaemic haemodilution (triple-H therapy) is no longer routinely recommended.

Supportive measures: bed rest with analgesia (paracetamol, short-course opioids as needed), strict blood pressure management to reduce rebleeding risk before aneurysm securing (target systolic below 160 mmHg), seizure prophylaxis in selected patients, and venous thromboembolism prevention once haemostasis is secured.

Hydrocephalus: external ventricular drain (EVD) or lumbar drain for acute obstructive hydrocephalus; ventriculoperitoneal (VP) shunt for chronic communicating hydrocephalus.

6. Pharmacology and AU PBS notes

Nimodipine (Nimotop): 60 mg orally every 4 hours for 21 days. This is the only intervention with established mortality benefit in SAH via vasospasm attenuation. Available on the PBS under Section 100 (Highly Specialised Drugs) for SAH. Caution with hypotension; dose reduction to 30 mg every 2 hours may be required if systolic blood pressure falls below 100 mmHg. Intravenous nimodipine is available but carries greater hypotension risk and is reserved for patients unable to tolerate oral administration.

Analgesia: paracetamol 1 g orally or intravenously every 6 hours is first-line for headache. NSAIDs are avoided due to antiplatelet effects prior to aneurysm securing. Short-acting opioids (morphine or oxycodone) may be required for severe pain but should be used cautiously as they can confound neurological assessment.

Antiepileptics: phenytoin is no longer routinely recommended given evidence of worse cognitive outcomes. Levetiracetam is preferred when prophylaxis is indicated (e.g. intracerebral extension of haematoma, cortical involvement) but is not universally given.

Stool softeners: docusate sodium or lactulose to prevent Valsalva-induced rebleeding before aneurysm securing.

7. Complications and monitoring

Rebleeding: highest risk within the first 24 hours (up to 15% on day 1). Secured aneurysm eliminates this risk. Clinical surveillance with serial neurological observations.

Delayed cerebral ischaemia (DCI) from vasospasm: peaks days 4 to 14 post-bleed. Transcranial Doppler ultrasound monitoring for middle cerebral artery mean velocity greater than 120 cm/s indicates significant vasospasm. CT perfusion or DSA confirms ischaemia. Managed with induced hypertension and intra-arterial vasodilators.

Hydrocephalus: acute obstructive hydrocephalus in approximately 20% of patients within 72 hours. Monitored by serial CT brain. EVD placement when clinically indicated.

Hyponatraemia: cerebral salt-wasting or SIADH occurs in approximately 30% of patients. Daily electrolyte monitoring; isotonic saline replacement for cerebral salt-wasting; fluid restriction for SIADH (with caution given vasospasm risk).

Neurogenic cardiac injury: ECG changes (QT prolongation, T-wave inversion, ST elevation), elevated troponin, and regional wall motion abnormalities. Daily ECG for the first 72 hours; echocardiography if haemodynamically significant cardiac dysfunction is suspected.

Seizures: occur in 5 to 10% acutely; long-term epilepsy in 7%. EEG monitoring if clinical status does not improve as expected. Long-term antiepileptic therapy determined by clinical and EEG findings at 6 months.

Functional outcome and driving: patients with SAH are unfit to drive for a minimum of 3 months regardless of neurological deficit; reassessment by a neurologist is required before return to driving under Austroads standards.

Written for Australian practice and grounded in the guidance named above. Study material only — not medical advice. Always check against current guidelines.