Subarachnoid haemorrhage

01OverviewDefinition, clinical context and the essential points that orientate the chapter.

Spontaneous SAH is most often caused by rupture of an intracranial aneurysm, releasing blood into the basal cisterns and provoking abrupt meningeal pain. Non-aneurysmal perimesencephalic bleeding has a different prognosis, while trauma, arteriovenous malformation, dissection and reversible cerebral vasoconstriction are alternative causes. Initial severity ranges from isolated headache to coma. The history should establish exact onset, time to peak, exertion or sex, syncope, seizure, neck pain, family history, polycystic kidney disease, smoking, hypertension and antithrombotic exposure.

Diagnosis is time dependent. Modern non-contrast CT is very sensitive soon after onset when imaging and reporting quality are appropriate, but sensitivity falls as blood clears. NICE uses the 6-hour boundary to guide whether lumbar puncture is routinely needed after a negative CT. LP performed for this question should be at least 12 hours after symptom onset so bilirubin can form, and local laboratory requirements for spectrophotometry and paired samples must be followed. Visible SAH leads to CTA; a negative vascular study does not always end investigation.

Management has three overlapping aims: prevent rebleeding by securing the aneurysm, maintain physiological stability and prevent or treat secondary brain injury. Neurovascular specialists choose coiling or clipping from aneurysm anatomy, patient factors and procedural risk. Nimodipine reduces the impact of delayed cerebral ischaemia but does not replace neurological monitoring and vascular investigation. New focal deficit or consciousness change after initial stabilisation should trigger assessment for rebleeding, hydrocephalus, delayed ischaemia, seizure, infection and metabolic disturbance.

Key points

Suspect subarachnoid haemorrhage when a new severe headache reaches peak intensity within minutes, especially with neck stiffness, vomiting, photophobia, collapse, seizure or focal deficit.
A normal neurological examination does not exclude SAH; many alert patients have only headache at presentation, and a sentinel headache may precede a larger aneurysmal bleed.
Obtain urgent non-contrast CT brain, document the interval from onset and ensure expert interpretation because sensitivity is highest in the first 6 hours and decreases thereafter.
If a high-quality CT performed within 6 hours is reported negative by an appropriate radiologist, NICE advises not routinely performing lumbar puncture; if CT occurs after 6 hours and is negative, consider LP after at least 12 hours from onset.
When CT confirms SAH, perform CTA without delay to identify an aneurysm and involve a specialist neurosurgical or neurointerventional centre immediately; catheter angiography may be required when CTA is negative or treatment planning needs it.
Secure a ruptured aneurysm as early as feasible by endovascular coiling or neurosurgical clipping through multidisciplinary assessment; rebleeding risk is greatest before definitive treatment.
Offer enteral nimodipine unless contraindicated to reduce poor outcome from delayed cerebral ischaemia, and monitor pressure because hypotension can compromise cerebral perfusion.
Watch for hydrocephalus, delayed cerebral ischaemia, seizures, hyponatraemia, fever, cardiac injury, pulmonary oedema and venous thrombosis throughout neurocritical care.

02AetiologyUnderlying causes, associations and risk factors, with why each one matters.

Ruptured saccular aneurysm

Most spontaneous clinically important SAH arises when an intracranial arterial aneurysm ruptures into basal cisterns or adjacent brain.

Non-aneurysmal perimesencephalic bleeding

A characteristic limited venous-pattern haemorrhage around the midbrain can occur without an aneurysm and generally follows a different risk course.

Dissection and vascular malformation

Intracranial dissection, arteriovenous malformation and other vascular lesions cause less common subarachnoid bleeding, particularly with atypical distribution.

Traumatic haemorrhage

Head injury commonly produces sulcal subarachnoid blood but requires a trauma pathway distinct from spontaneous thunderclap aneurysmal disease.

03PathophysiologyThe causal sequence from the underlying abnormality to symptoms and harm.

1
Arterial rupture
A vessel wall fails and releases high-pressure blood into the subarachnoid space, abruptly raising intracranial pressure.
2
Global perfusion disturbance
The pressure surge and acute vasoconstriction reduce cerebral blood flow, causing collapse, transient deficit or early brain injury.
3
Clot and cerebrospinal-fluid obstruction
Subarachnoid blood blocks arachnoid absorption and ventricular pathways, producing hydrocephalus and pressure-related deterioration after acute haemorrhage.
4
Delayed vascular dysfunction
Blood breakdown products trigger vasoconstriction, inflammation and microcirculatory failure, causing delayed cerebral ischaemia after the initial bleed.

04Clinical features and red flagsSymptoms, examination findings, patterns of presentation and time-critical warnings.

Thunderclap headache

Pain reaches maximum intensity almost immediately or within a few minutes and is often described as unlike previous headache, although wording such as worst-ever is not mandatory.

Meningeal syndrome

Neck stiffness, photophobia, nausea and vomiting can evolve after the initial headache; their absence early does not reassure.

Collapse or seizure

Brief loss of consciousness or generalised seizure at onset suggests an abrupt rise in intracranial pressure and may accompany a high-grade bleed.

Focal aneurysm clues

A painful third-nerve palsy with a dilated pupil can indicate a posterior communicating artery aneurysm, while focal weakness may reflect intraparenchymal extension or ischaemia.

Sentinel presentation

A sudden unexplained severe headache in preceding days may represent a small leak, but retrospective labels must not replace investigation of the current event.

Delayed cerebral ischaemia

New focal deficit, reduced consciousness or cognitive change typically several days after SAH may develop gradually or fluctuate and requires urgent exclusion of other causes.

Red flags requiring action

Reduced consciousness, airway compromise, recurrent seizure or cardiorespiratory instability requires immediate resuscitation and neurocritical-care involvement.
A new painful oculomotor palsy with pupillary dilation may signal an enlarging or recently ruptured posterior communicating aneurysm and warrants emergency vascular imaging.
Sudden recurrent headache or decline before aneurysm treatment suggests rebleeding and needs immediate CT and neurovascular escalation.
Progressive drowsiness, downward gaze or worsening headache with ventricular enlargement indicates acute hydrocephalus and a possible urgent CSF-diversion requirement.
New neurological deficit days after securing the aneurysm may be delayed cerebral ischaemia and must not be attributed automatically to fatigue or sedating medicines.

05InvestigationsWhat to request, why it matters and how to interpret it.

Investigation order

Read from the initial assessment onwards. Tests may run in parallel in urgent care; first-line, preferred, confirmatory, definitive and gold-standard labels appear only when the chapter explicitly states them.

01
Non-contrast CT brainFirst step
Why
Detect subarachnoid blood, hydrocephalus, intraventricular or intracerebral extension and early mass effect.
Interpretation and limitations
Record onset-to-scan time; an appropriately acquired and reported negative scan within 6 hours changes the need for LP, whereas later negative imaging is less reassuring.
02
Lumbar puncture for bilirubin
Why
Investigate persisting SAH suspicion after a negative CT performed more than 6 hours after onset.
Interpretation and limitations
Wait at least 12 hours from onset and follow the laboratory protocol for spectrophotometric bilirubin; traumatic red cells alone do not supply a reliable simple cut-off.
03
CT angiography
Why
Identify a ruptured aneurysm or other vascular lesion once SAH is diagnosed on CT or LP.
Interpretation and limitations
Aneurysm location and morphology guide treatment, but incidental aneurysms occur and the bleeding pattern must be matched; negative CTA may need catheter angiography.
04
Digital subtraction angiography
Why
Provide high-resolution vascular definition when CTA is inconclusive, negative despite suspicious bleeding, or endovascular treatment is planned.
Interpretation and limitations
It is invasive and specialist-led; repeat angiography may be needed for a non-perimesencephalic angiogram-negative haemorrhage.
05
Serial CT and transcranial or vascular assessment
Why
Investigate deterioration for rebleeding, hydrocephalus, infarction or delayed arterial narrowing.
Interpretation and limitations
No single vasospasm test replaces clinical assessment; interpret vessel narrowing and perfusion alongside examination, sedation, seizures and metabolic variables.
06
Electrolytes, ECG and cardiac biomarkers when indicated
Why
Detect hyponatraemia, potassium disturbance, arrhythmia and neurogenic myocardial injury complicating SAH.
Interpretation and limitations
ECG and troponin changes can be neurogenic but still require cardiac assessment; sodium loss and fluid status need careful differentiation before treatment.
07
Pregnancy test where relevant
Why
Inform imaging, anaesthetic and medicine planning without delaying life-saving diagnosis.
Interpretation and limitations
Necessary CT and CTA should not be withheld in a neurological emergency; coordinate radiation and treatment decisions with specialist teams.

06Differential diagnosisRealistic alternatives and the features that help distinguish them.

Migraine or primary thunderclap

A familiar gradual migraine pattern is reassuring, but first maximal-at-onset pain requires haemorrhage investigation before a primary label.

Meningitis

Fever, progressive headache and cerebrospinal-fluid inflammation support infection; neck stiffness and photophobia occur in both at presentation.

Cervical dissection or RCVS

Neck pain, Horner syndrome or repeated thunderclaps with arterial narrowing suggests dissection or reversible vasoconstriction, which may also bleed.

Cerebral venous thrombosis

Progressive headache, papilloedema, seizure and venous infarction with thrombosis risk supports a venous cause as an alternative.

07ManagementImmediate care, first-line treatment, alternatives and escalation.

01HEADACHEAcute thunderclap presentationFirst stepA patient has a new severe headache reaching maximum intensity within minutes.

1Assess airway, consciousness, focal neurology, pupils, meningism, seizure, pressure and antithrombotic exposure and treat immediate instability.
2Arrange urgent non-contrast CT and record exact onset and scan times, providing the radiologist with the suspected SAH diagnosis.
3If CT is positive, contact the neurovascular centre and obtain CTA; if negative, apply the 6-hour NICE pathway and the continuing clinical level of suspicion.
4AlternativeKeep safety advice and alternative thunderclap diagnoses active even if SAH is excluded, including dissection, venous thrombosis, RCVS and pituitary apoplexy.

02LPNegative later CTCT is negative but was performed more than 6 hours after onset and suspicion of SAH remains.

1Confirm that CT quality and interpretation are adequate and reassess for contraindications to lumbar puncture such as mass effect or severe coagulopathy.
2Wait until at least 12 hours after headache onset and collect samples using the local laboratory's spectrophotometry and light-protection instructions.
3Interpret bilirubin with the laboratory report and clinical timing rather than relying only on the red-cell count or visual appearance.
4If SAH is supported, arrange urgent CTA and neurovascular transfer; if not, investigate the remaining thunderclap differential and provide explicit safety-netting.

03SECUREAneurysmal SAH confirmedImaging demonstrates SAH and a vascular study identifies a likely ruptured aneurysm.

1Admit or transfer to a specialist neuroscience centre, control pain and nausea, avoid pressure extremes and start enteral nimodipine when suitable.
2Use multidisciplinary review to choose early endovascular coiling or neurosurgical clipping from aneurysm anatomy, age, bleed pattern and procedural risk.
3DefinitiveManage antithrombotic reversal, hydrocephalus, seizures and cardiorespiratory instability without delaying definitive aneurysm treatment.
4After securing the aneurysm, continue neurocritical monitoring and explain that delayed cerebral ischaemia remains a risk for days.

04DELAYEDNew deficit after SAHSeveral days after haemorrhage, the patient develops focal deficit, confusion or reduced consciousness.

1Perform immediate ABC, glucose, temperature and neurological assessment and review sedation, infection, sodium and seizure possibilities.
2Arrange urgent brain and vascular imaging to assess infarction, rebleeding, hydrocephalus and arterial narrowing or perfusion disturbance.
3Maintain euvolaemia and implement the neurovascular service's haemodynamic and endovascular rescue plan when delayed cerebral ischaemia is diagnosed.
4Continue nimodipine if tolerated and reassess pressure and neurological response closely in neurocritical care.

Key medicines and prescribing safety3 treatments · regimens, roles and cautions

Reduces poor neurological outcome associated with delayed cerebral ischaemia after aneurysmal subarachnoid haemorrhage.

Nimodipine

Give 60 mg orally or through an enteral tube every 4 hours, usually for 21 days from haemorrhage, following the neuroscience protocol; modify dosing if hypotension limits treatment.

Monitor blood pressure and interactions, use enteral rather than unsafe intravenous oral formulation administration, and coordinate reduced or interrupted dosing with the neurovascular team.

Controls severe meningeal headache and limits pain-related pressure surges before and after aneurysm treatment.

Analgesia

Use regular paracetamol within the individual maximum and carefully titrated additional analgesia from the neuroscience protocol while preserving reliable neurological assessment.

Avoid excessive sedation, respiratory depression and routine NSAIDs before haemostasis; account for low body weight, liver disease and duplicate paracetamol products.

Treats vomiting that worsens distress, aspiration risk and intracranial pressure during acute SAH care.

Antiemetic therapy

Give an intravenous or enteral antiemetic at the adult formulary dose, selected for QT interval, sedation and interaction profile, and repeat only within product limits.

Monitor consciousness, QT-prolonging combinations and extrapyramidal effects; recurrent vomiting may signal rebleeding or hydrocephalus and requires reassessment.

08ComplicationsImportant consequences, why they occur and why they matter clinically.

Early rebleeding

An unsecured aneurysm can rupture again before it is secured, causing a larger haemorrhage, herniation and high mortality.

Hydrocephalus

Blood obstructs cerebrospinal-fluid flow or absorption, causing headache, reduced consciousness and an urgent need for ventricular drainage.

Delayed cerebral ischaemia

Vasoconstriction and microvascular dysfunction can infarct previously viable brain during the days following definitive aneurysm treatment.

Seizure and systemic organ injury

Cortical blood, sympathetic activation and electrolyte disturbance can cause seizures, hyponatraemia, cardiac injury and acute pulmonary oedema.

09Monitoring and follow-upTreatment response, safety checks and longer-term review.

Perform frequent GCS, pupil and focal neurological observations with immediate imaging for any decline or recurrent thunderclap pain.
Monitor blood pressure closely before aneurysm securing and during nimodipine, avoiding both severe hypertension and perfusion-limiting hypotension.
Track fluid balance, weight, sodium, potassium, renal function and urine output; maintain euvolaemia and investigate rather than reflexively fluid-restricting hyponatraemia.
Use ECG monitoring and assess chest pain, pulmonary oedema, arrhythmia or troponin rise in the context of possible neurogenic cardiac injury.
Review for delayed cerebral ischaemia daily through the vulnerable period, adapting examination to sedation or impaired consciousness with imaging and physiological data.
Assess swallowing, VTE risk, pressure areas, nutrition, cognition and rehabilitation needs while neurovascular surveillance continues.

10Special situationsVariants, exceptions and circumstances that change the usual approach.

Timing changes the test

A negative expert CT soon after onset carries different meaning from the same result the next day because subarachnoid blood becomes progressively less conspicuous.

Wait for bilirubin

Lumbar puncture performed too early can miss bilirubin formation, which is why the NICE diagnostic pathway waits at least 12 hours from onset.

Angiogram-negative is not one entity

A classic perimesencephalic blood pattern has different recurrence and repeat-imaging implications from diffuse aneurysmal-pattern bleeding with no first source found.

Nimodipine is not angioplasty

Its clinical benefit relates to delayed ischaemic outcome and it should not be judged only by whether angiographic vasospasm disappears.

Hyponatraemia needs volume context

Both inappropriate antidiuresis and renal salt loss can occur; uncritical fluid restriction may worsen cerebral perfusion in a volume-depleted patient.

Cardiac changes can be neurogenic

Catecholamine-mediated ECG, troponin and ventricular abnormalities may follow SAH, but acute coronary disease must still be considered clinically.

11Common pitfallsFrequent interpretation and management errors.

01
Do not dismiss a thunderclap headache because the patient is alert, has no neck stiffness or describes pain that has partially improved.
02
Do not interpret all negative CT scans identically without documenting time from onset, acquisition quality and reporting expertise.
03
Do not perform lumbar puncture immediately after onset for bilirubin or when CT shows mass effect or another contraindication.
04
Do not delay CTA and neurovascular referral once CT or CSF supports SAH.
05
Do not treat a newly deteriorating patient as routine vasospasm without urgently excluding rebleeding, hydrocephalus and seizure.
06
Do not allow nimodipine-induced hypotension to persist without specialist dose review or assume the drug replaces aneurysm securing.
07
Do not fluid-restrict every hyponatraemic SAH patient before assessing volume status and the neurocritical care plan.