01Core principlesThe concepts and mechanisms needed to understand the subject.
Rebleeding is renewed haemorrhage from an unsecured or incompletely secured culprit aneurysm. It often causes sudden headache, acute neurological decline and increased blood on CT and can be rapidly fatal. The risk is greatest in the first 24 hours, which is why diagnosis, transfer and aneurysm securing form one urgent pathway. A treated aneurysm greatly reduces this source but residual filling, procedural rupture and a different untreated aneurysm remain possible explanations for later new blood.
Angiographic vasospasm is arterial narrowing after SAH; delayed cerebral ischaemia is the clinical consequence of inadequate brain perfusion and is broader than visible spasm alone. It often emerges several days after haemorrhage as a new focal deficit or falling consciousness, but diagnosis requires exclusion of rebleeding, hydrocephalus, seizures and systemic causes. Nimodipine reduces poor neurological outcome through mechanisms not reliably captured by vessel calibre, and NICE does not support TCD-guided management outside research. For established DCI, restore euvolaemia and consider vasopressors for persistent symptoms under specialist monitoring.
Blood can obstruct ventricular pathways acutely or impair arachnoid CSF absorption over time. Acute hydrocephalus presents with worsening consciousness, headache, vomiting or raised-pressure signs and enlarging ventricles; CSF drainage may be lifesaving. Chronic hydrocephalus may produce cognitive slowing, gait decline and continence symptoms during recovery. Imaging must be compared over time because ventriculomegaly can reflect atrophy, and treatment depends on clinical concordance and likely benefit from temporary or permanent diversion.
Key points
- Rebleeding is most dangerous early, particularly while the culprit aneurysm is unsecured; prevention depends on securing the lesion at the earliest opportunity.
- Delayed cerebral ischaemia is a clinical syndrome of new deficit or reduced consciousness after excluding rebleeding, hydrocephalus, seizures and systemic or metabolic causes; angiographic vasospasm may be present without clinical ischaemia.
- Hydrocephalus may be acute or chronic and is diagnosed from symptoms and signs plus comparison of current with previous brain imaging, not ventricular size alone.
- For unexplained deterioration after SAH, NICE recommends non-contrast CT first; do not use transcranial Doppler to guide clinical management outside research.
- Consider CSF drainage or diversion for deterioration caused by acute hydrocephalus; persistent or progressive chronic symptoms may justify permanent diversion or a temporary drainage trial.
- For delayed cerebral ischaemia, ensure euvolaemia and consider vasopressor treatment if symptoms persist, recognising that improvement can be temporary and specialist rescue options require individual assessment.
- Enteral nimodipine is considered after confirmed SAH; intravenous use is confined to specialist care when enteral treatment is unsuitable and hypotension may constrain delivery.
02Mechanisms and patternsImportant relationships and how to distinguish them.
A sudden return of maximal headache, collapse, abrupt GCS fall or new blood burden on CT is recurrent haemorrhage until the specialist team proves another cause.
New focal neurology or a sustained consciousness decline days after SAH, unexplained by CT, seizures, sodium, fever, oxygenation or sedation, supports the clinical DCI syndrome.
Drowsiness, headache, vomiting, gaze or abducens change and progressive ventricular enlargement suggest impaired CSF flow requiring urgent drainage assessment.
Persistent gait, cognition or bladder deterioration during recovery with compatible ventricular change raises shunt-responsive hydrocephalus but overlaps with diffuse brain injury and deconditioning.
Non-convulsive seizure, hyponatraemia, infection, hypoxaemia, hypotension, medication and new infarction may resemble DCI and often coexist, so structured exclusion is essential.
03Interpreting evidenceInformation, measurements and their limitations.
Consider the information, its meaning and its limitations before deciding what follows.
- 01
Urgent non-contrast CT head - Why
- Identify rebleeding, acute hydrocephalus, haematoma, swelling and established infarction when neurology worsens.
- Interpretation and limitations
- New blood or enlarging ventricles directs immediate source control or CSF diversion; a scan without either preserves DCI, seizure and systemic causes.
- 02
CTA or catheter angiography - Why
- Assess aneurysm occlusion, recurrent filling and arterial narrowing when vascular pathology remains suspected.
- Interpretation and limitations
- Narrowing supports vasospasm but does not alone prove tissue ischaemia; residual culprit filling after new bleeding requires urgent treatment planning.
- 03
CT or MR perfusion imaging - Why
- Evaluate threatened tissue when delayed cerebral ischaemia is suspected and non-contrast CT is non-diagnostic.
- Interpretation and limitations
- A perfusion deficit supports haemodynamic compromise, while artifacts and systemic pressure must be considered before escalating endovascular rescue.
- 04
Serial neurological examination - Why
- Detect a sustained focal or consciousness change and define response to fluid, pressure or CSF interventions.
- Interpretation and limitations
- Trend is central to DCI diagnosis; temporary improvement after vasopressor treatment does not prove durable reversal or exclude another cause.
- 05
Electrolytes, glucose, oxygenation and infection studies - Why
- Find metabolic and systemic causes that mimic or worsen post-SAH neurological decline.
- Interpretation and limitations
- Correcting an abnormality does not end investigation if focal signs or impaired consciousness persist, because more than one complication may coexist.
- 06
EEG - Why
- Detect non-convulsive seizures when consciousness fluctuates or imaging does not explain decline.
- Interpretation and limitations
- Ictal activity requires treatment, but a seizure may also be provoked by rebleeding or ischaemia and should not close the structural investigation.
04Applied reasoningWorked examples connecting principles to decisions.
01Worked case: post-SAH deteriorationNew deficit or falling consciousness after SAHA patient develops new focal neurology, reduced alertness, severe recurrent headache or another unexplained neurological change.+
- 1Reassess airway, breathing, circulation, glucose, temperature, oxygenation, blood pressure, pupils, GCS components and focal findings, and activate the specialist neurovascular team.
- 2Obtain urgent non-contrast CT as the first diagnostic investigation to look for new blood, hydrocephalus, haematoma, swelling or infarction while checking sodium, infection, medicines and seizure clues.
- 3If rebleeding is present, resuscitate and reassess culprit occlusion for immediate source control; if symptomatic acute hydrocephalus is present, obtain urgent neurosurgical CSF-drainage or diversion assessment.
- 4If CT does not explain the decline, investigate DCI with specialist vascular or perfusion imaging and seizure with EEG as indicated, then treat confirmed or strongly suspected causes without waiting for irreversible infarction.
- 5Document neurological response to every intervention and repeat imaging or escalation when improvement is absent, transient or discordant with the proposed diagnosis.
02DCI pathwaySuspected delayed cerebral ischaemiaA sustained neurological decline remains unexplained after immediate structural, seizure and systemic assessment.+
- 1Ensure normal circulating volume and correct hypoxia, hypotension, fever, glucose and sodium disturbances that reduce cerebral oxygen delivery.
- 2Consider vasopressor treatment when symptoms persist under specialist care, monitoring heart, lungs and neurological response and recognising that improvement may be temporary.
- 3Use CTA, DSA or perfusion evidence and clinical trajectory to decide on further specialist rescue; do not let an isolated Doppler velocity dictate management.
03Hydrocephalus pathwayAcute or chronic ventricular enlargementSymptoms and signs suggest impaired CSF circulation and imaging shows new or progressive ventriculomegaly.+
- 1Compare current and prior imaging and decide whether the neurological syndrome is acute pressure deterioration or a persistent chronic recovery problem.
- 2For acute decline, consider urgent temporary drainage or diversion; follow the authorised drain protocol and continue investigation for rebleeding or other causes.
- 3For chronic persistent or progressive symptoms, consider permanent diversion, using a temporary drainage trial when benefit remains uncertain and measuring functional response.
05Relevant medicines and safetySpecific regimens and precautions where medicines are relevant.
Nimodipine
Use the specialist subarachnoid-haemorrhage protocol and current product information; NICE recommends considering enteral administration and reserving intravenous treatment for specialist settings when enteral use is unsuitable.Monitor arterial pressure and cerebral perfusion, review missed or reduced doses with the specialist team, and do not describe it as a treatment that simply dilates every spastic artery.
Vasopressor therapy
Titrate in a neurocritical-care setting to clinical response and safe haemodynamic endpoints after euvolaemia is established; NICE does not specify one universal drug or pressure target.Benefit may be temporary; monitor cardiac ischaemia, arrhythmia, pulmonary oedema and the risk from unsecured aneurysm or other bleeding, and avoid prophylactic hypertension.
06Checking understandingVerify the reasoning, revisit uncertainties and apply feedback.
- Perform repeated GCS-component, pupil, language and limb examinations, recording the exact onset and duration of every change and its relationship to procedures or medicines.
- Maintain continuous arterial pressure, oxygenation, rhythm and temperature monitoring in unstable patients and track fluid balance to preserve euvolaemia rather than inducing routine hypervolaemia.
- Follow sodium, glucose, renal function and infection markers because systemic derangement can mimic, precipitate or compound delayed cerebral ischaemia.
- After CSF drainage, document device prescription, output, intracranial pressure where measured and neurological response; only authorised staff adjust the system.
- After aneurysm treatment, preserve the occlusion result and follow-up plan and reassess urgently if sudden headache or new blood suggests residual or recurrent rupture.
- Judge vasopressor or endovascular rescue by time-linked neurological and perfusion response, and escalate if improvement is absent or short lived.
07Special situationsVariants, exceptions and circumstances that change the usual approach.
Spasm is not ischaemia
Angiographic narrowing is a vessel finding, whereas DCI is a clinical tissue-perfusion syndrome; either can occur without the other.
CT comes first
The first urgent scan after unexplained decline can expose rebleeding or hydrocephalus that would be missed by a narrow vasospasm assumption.
Euvolaemia is the goal
Replacing deficit supports perfusion, while routine prophylactic hypervolaemia can cause pulmonary and cardiac harm without reliably preventing DCI.
Ventricles need context
A large ventricle can reflect hydrocephalus or loss of brain volume; symptoms, temporal change and response to drainage determine clinical relevance.
Aneurysm securing changes one risk
Definitive occlusion sharply reduces culprit rebleeding but leaves early brain injury and downstream complications requiring coordinated surveillance.
08Common pitfallsFrequent interpretation and management errors.
- 01
Calling every delayed deficit vasospasm before excluding rebleeding, hydrocephalus, seizure and metabolic or systemic disturbance.
- 02
Using transcranial Doppler velocities alone to guide treatment despite NICE's research-only recommendation for management guidance.
- 03
Diagnosing hydrocephalus from ventricular size without symptoms, signs or comparison with earlier imaging.
- 04
Providing routine hypervolaemia or prophylactic vasopressors instead of maintaining euvolaemia and treating clinically suspected DCI selectively.
- 05
Assuming that coiling or clipping eliminates the possibility of rebleeding from residual filling or another aneurysm.
- 06
Interpreting temporary neurological improvement after drainage or induced pressure as definitive proof that no competing pathology remains.