Definition

1. Post-SAH hydrocephalus is staged acute (within 72 h), subacute or chronic; the chronic form most often needs a shunt.

Hydrocephalus after aSAH: ventricular enlargement relative to the patient's own premorbid state.
- Ventricular enlargement weeks to months after SAH must be distinguished from ex vacuo dilatation (infarction, atrophy).
The enlargement comes from haemorrhage-related obstruction or impaired absorption of CSF.
The cause is the haemorrhage rather than parenchymal loss.

Timing classification of post-SAH hydrocephalus (Vale 1997 convention)

Acute	0–3 days, i.e. within 72 h of ictus
Subacute	4–13 days (days 4 to 13)
Chronic	≥14 days
Alternative published thresholds	acute ≤48 h or ≤72 h; chronic >7 days or ≥14 days

⚡ Contested: Staging: acute (0–3 days, within 72 h of ictus), subacute (4–13 days), chronic (≥14 days). Chronic hydrocephalus is a communicating, absorptive form. Chronic hydrocephalus most often needs a permanent shunt.

Convention of Vale and colleagues (1997), used in most subsequent series.

Subacute hydrocephalus is the least common form, approximately 2–3% of patients.

Subacute hydrocephalus typically presents as a communicating pattern with insidious decline rather than abrupt coma.

Published definitions of post-SAH hydrocephalus are not uniform. Acute has been set at ≤48 h or ≤72 h, chronic at >7 days or ≥14 days.

The team must define both interval since ictus and block site before choosing ventricular or lumbar drainage.
Timing classification and the communicating versus non-communicating distinction are independent.

Sources 1, 2, 3, 4, 5, 6, 7

Epidemiology and risk factors

2. Acute ventriculomegaly occurs in roughly 20–30% of aneurysmal SAH; about one fifth of survivors become shunt-dependent.

Acute ventriculomegaly is seen on early CT in roughly 20–30% of aSAH patients.
The spread reflects differing radiological and clinical definitions.
About one fifth of aSAH survivors become shunt-dependent.
Approximately 30% of patients with acute hydrocephalus after aSAH ultimately need a permanent shunt.
Acute hydrocephalus is itself one of the strongest predictors of later shunt dependence.

Modified Fisher grade (home: NS-05-01-01-01)

High (modified) Fisher grade: thick cisternal and ventricular blood

Intraventricular haemorrhage and a high (modified) Fisher grade are consistently associated with acute hydrocephalus and later shunt dependence.
Intraventricular haemorrhage accompanies 30–70% of aSAH.
A high (modified) Fisher grade means thick cisternal and ventricular blood.

Hunt and Hess grade (home: NS-05-01-01-01)

Poor clinical grade on admission	high Hunt and Hess grade or Glasgow Coma Scale ≤8
Poor-grade	Hunt and Hess IV–V

Older age (commonly ≥50 years) is an independent risk factor for shunt dependence after aSAH.
- Rebleeding before the aneurysm is secured is an independent risk factor for shunt dependence after aSAH.
- A posterior-circulation aneurysm approximately doubles the likelihood of needing CSF diversion.
- Ventriculitis or meningitis during the acute admission is associated with over two-fold shunt-dependent hydrocephalus risk.
Poor clinical grade on admission: high Hunt and Hess grade or GCS ≤8.
Poor grade and need for mechanical ventilation are each associated with over two-fold shunt-dependence risk.
Meta-analytical data do not show a difference in shunt dependence between coiling and clipping.
- Treatment modality should therefore not be chosen on the basis of hydrocephalus risk.

Sources 3, 7, 8, 9, 10, 11

Pathophysiology

3. Acute hydrocephalus is mainly obstructive from ventricular clot; chronic hydrocephalus reflects impaired CSF absorption through fibrosed arachnoid granulations.

Acute hydrocephalus within 72 h of aSAH is predominantly obstructive (non-communicating).
- Acute hydrocephalus is caused by clot in the lateral, third and fourth ventricles.
Clot also sits at the foramina of Monro, the aqueduct and the outlets of Magendie and Luschka.
Acute ventriculomegaly can also occur without intraventricular clot.
- Most patients in fact have a mixed obstructive and communicating mechanism.
Then blood in the basal cisterns obstructs CSF flow in the subarachnoid space.
Ruptured posterior-circulation and AComm aneurysms bleed directly into the basal cisterns and ventricular system.
Chronic hydrocephalus after SAH is typically communicating.
- Chronic hydrocephalus reflects impaired CSF absorption.
- Blood degradation products mechanically block, then fibrose, the arachnoid granulations.
- Acute hydrocephalus is therefore usually reversible with temporary EVD.
- A subgroup with established leptomeningeal and arachnoid fibrosis becomes permanently shunt-dependent.
Blood degradation products thicken the leptomeninges with haemosiderin deposition.
Obstructive mechanisms resolve as intraventricular clot lyses and clears; absorptive failure persists.
Blood and its breakdown products injure the ependyma.
The injury causes loss of ciliated ependymal cells, disrupted cell junctions and altered ion-transporter function.
Untreated acute hydrocephalus raises ICP and lowers CPP.

Sources 2, 4, 5, 12

Clinical presentation

4. Acute hydrocephalus presents as depressed or fluctuating consciousness, sometimes within hours, and an apparently poor grade may reverse after drainage.

Acute hydrocephalus after aSAH presents as depressed or fluctuating consciousness.
- The depressed consciousness may develop within hours of the ictus.
- Acute hydrocephalus may instead show as failure to improve after the initial haemorrhage.
Ventriculomegaly on the admission CT is often clinically silent.
Acute hydrocephalus after SAH may cause impaired upgaze with downward gaze preference and small poorly reactive pupils.
The gaze and pupil signs come from dorsal midbrain compression by the dilated third ventricle.
Acute hydrocephalus may also cause abducens palsy, a non-localising sign of raised ICP.
An apparently poor clinical grade may be caused by hydrocephalus.
- An apparently poor grade from hydrocephalus is therefore potentially reversible.
Consciousness improved after ventricular drainage in 25 of 32 drained patients (78%) (Rotterdam cohort).
Definitive clinical grading should be made only after neurological resuscitation, including CSF diversion for hydrocephalus.
- Any decision about withholding aneurysm treatment should likewise be made only after neurological resuscitation.
Grades assigned before drainage overestimate brain-injury severity.
Poor-grade (Hunt and Hess IV–V) patients who improve at least one grade after drainage have long-term outcomes like patients presenting in that lower grade.
Sedation and ventilation mask the clinical presentation of hydrocephalus.
- Deterioration may show only as rising ICP or new ventricular enlargement on surveillance imaging, rather than examination change.

Sources 2, 13, 14, 15, 16, 17

Diagnosis

5. Diagnosis combines clinical deterioration with ventricular enlargement on CT relative to the patient's earlier scan, aided by ventricular indices.

Diagnosis of hydrocephalus after aSAH is clinico-radiological.
- Clinical part: deterioration or failure of recovery of consciousness with no other detectable cause.
- Radiological part: ventricular enlargement on CT relative to the patient's own earlier scan.
Non-contrast head CT is the first-line and usually sufficient imaging test.
- CT shows enlarged temporal horns and third ventricle, intraventricular clot and effaced cortical sulci.
CT also shows periventricular hypodensity from transependymal CSF flow.

Bicaudate index

Bicaudate index	width of the frontal horns at the level of the caudate nuclei and foramen of Monro divided by the diameter of the brain at that same level
Acute hydrocephalus	bicaudate index above the 95th percentile for age on CT within 72 hours of ictus, i.e. relative bicaudate index (measured index divided by the age-specific upper limit) >1
Age-specific 95th-percentile upper limit (one SAH-derived series): 0.12 at age ≤45 years, 0.14 at 55, 0.16 at 65, 0.17 thereafter
Caution	the upper limit rises with age and published tables differ, so the same absolute value may be normal in an older and abnormal in a younger patient

Evans index

Evans index	maximal width of the frontal horns divided by the maximal internal diameter of the skull on the same axial slice
Value above 0.3 taken as ventriculomegaly

Sources 2, 7, 18, 19

Procedure: indications

6. CSF diversion is indicated for symptomatic hydrocephalus, usually an external ventricular drain; obstruction, mass effect or coagulopathy contraindicate lumbar drainage.

CSF diversion is indicated in aSAH with acute symptomatic hydrocephalus.
- Acute symptomatic hydrocephalus: ventriculomegaly with depressed or deteriorating consciousness.
- Drainage to reduce vasospasm or DCI, rather than to treat hydrocephalus, is a separate indication (NS-05-01-02).
Class 1 recommendation on non-randomised evidence (AHA/ASA SAH guideline 2023).
An EVD is the first-choice diversion in the acute phase.
- Ventriculoperitoneal shunting is not the primary treatment of acute SAH-related hydrocephalus.
An EVD treats both hydrocephalus and raised ICP.
An EVD permits ICP measurement and drainage of ventricular blood.
An EVD works whether the hydrocephalus is communicating or obstructive.
High CSF protein and blood content and patient instability increase shunt malfunction and infection.
EVD or lumbar drainage is preferred until CSF clears.
An awake patient with mild ventriculomegaly and intact consciousness may be managed without immediate drainage.
- Observation without drainage requires close serial neurological observation and repeat CT.
Acute ventricular enlargement after SAH improves spontaneously in a substantial proportion within the first 24 hours.

Lumbar drainage or serial LP is an acceptable alternative only when the hydrocephalus is communicating.
- A small fourth ventricle alone does not separate obstructive from communicating hydrocephalus after aSAH.
- A small fourth ventricle is therefore not by itself a contraindication to lumbar drainage.
In an aSAH cohort treated first by LP, 69 of 93 (74%) avoided external drainage.
22 later deteriorated and needed an EVD.
A small fourth ventricle is conventionally taken as a sign of intraventricular obstruction.

Sources 2, 13, 18, 20, 21, 22, 23, 24, 25, 26

Procedure: technique

7. The catheter passes from Kocher's point into the frontal horn after coagulation checks and is tunnelled to a closed system.

The standard entry site for ventriculostomy after aSAH is Kocher's point.
- Kocher's point lies approximately 11 cm posterior to the nasion.
- Kocher's point lies 2–3 cm lateral to the midline (mid-pupillary line) and 1–2 cm anterior to the coronal suture.
- The right (usually non-dominant) side is the default.
- The side is chosen for the larger or more accessible ventricle, avoiding the ventricle most packed with clot.
The side also matches any planned craniotomy for clipping.
The catheter is passed perpendicular to the skull surface.
- The catheter is aligned with the ipsilateral medial canthus (coronal) and the tragus/external auditory meatus (sagittal).
- The catheter is advanced 5–7 cm (about 6 cm in adults).
- The tip then lies in the ipsilateral frontal horn just anterior to the foramen of Monro.

The catheter is tunnelled subgaleally for at least about 5 cm, exiting the skin remote from the burr hole.
- The catheter is secured and connected to a closed, sealed drainage and monitoring system.
The drainage burette is levelled and zeroed to a fixed reference (external auditory meatus or foramen of Monro).
A bolt-fixed non-tunnelled system is an accepted alternative to a tunnelled catheter.
The cohort found no significant difference in infection, haemorrhage, obstruction, malposition or accidental pull-out.

Sources 21, 27, 28, 29, 30, 31

management

8. Until the aneurysm is secured CSF is drained cautiously because excessive drainage could precipitate rebleeding.

The EVD is levelled and zeroed to the foramen of Monro.
- The external auditory meatus or tragus is the surface reference.
- Chamber height above that reference: commonly 10–20 cm H2O, most often 10–15 cm H2O.

⚡ Evidence and practice diverge: Until the aneurysm is secured, CSF should be drained cautiously. The chamber is kept relatively high. Only enough CSF is removed to control ICP and restore consciousness. Rapid or excessive drainage could thus dislodge the sealing clot and precipitate rebleeding before the aneurysm is secured (proposed mechanism).

CSF is drained cautiously rather than by unrestricted low-level or free drainage.

Ventricular CSF drainage lowers ICP.

Lowering ICP raises the transmural pressure gradient across the aneurysm wall.

Current evidence therefore does not establish that pre-treatment drainage increases rebleeding.

Rebleeding occurred in 11.04% (106/960) of drained patients versus 9.22% (250/2711) of controls.

The authors attributed this association to clustering of other rebleeding risk factors in drained patients rather than to drainage itself.

Fear of rebleeding is no reason to withhold or delay ventricular drainage when acute hydrocephalus impairs consciousness.
- Delay risks secondary injury from intracranial hypertension.
ICP cannot be measured validly while the drain is open.
A continuously open drain permits only intermittent pressure readings after the system is closed.
Intermittent drainage allows continuous pressure monitoring and detection of pressure crises.
Intermittent drainage was associated with fewer drain-related infections than continuous drainage (RR 0.20, 95% CI 0.05–0.72).
Intermittent drainage was associated with fewer drain blockages (RR 0.45, 95% CI 0.27–0.74).
Continuous drainage caused more complications (52.9% versus 23.1%; OR 3.75, 95% CI 1.21–11.66, p = 0.022).
There was no difference in vasospasm (OR 0.44, 95% CI 0.13–1.45, p = 0.177).

Sources 2, 21, 32, 33, 34, 35, 36, 37, 38

9. Drains are weaned by a clamp trial or graduated elevation once the aneurysm is secured and the patient stable.

Two weaning strategies are in use.
- In rapid weaning the drain is simply closed (a clamp trial) once the patient is stable.
- In gradual weaning the chamber is raised stepwise over several days before final closure.

Clamp trial

Drain closed for about 24 hours with serial neurological examination, intracranial pressure monitoring and follow-up CT
Failed if consciousness falls, headache or vomiting appear, intracranial pressure rises persistently, or the ventricles enlarge
Reopen immediately for any new neurological deterioration or sustained intracranial pressure above roughly 20 mmHg
Not run in a sedated or comatose patient without continuous intracranial pressure monitoring

Weaning is generally attempted only after the aneurysm has been secured.
- Weaning is attempted once the patient is neurologically stable with clearing CSF and low drainage volumes.
Drainage continued specifically to influence DCI is covered in NS-05-01-02.

⚡ Contested: Shunt implantation rates were essentially identical after rapid and gradual weaning (63.4% versus 62.5%). The early clamp-trial approach gave a lower VP shunt rate, shorter stay and fewer drain-related complications.

Gradually weaned patients spent a mean 2.8 more days in intensive care (p = 0.0002).

Gradually weaned patients spent 2.4 more days in hospital (p = 0.0314).

Cohort evidence contradicts the randomised trial. The pooled analysis found lower shunt-dependency risk with gradual weaning at the cost of longer treatment. The evidence base for either policy is therefore small and of low certainty.

Sources 21, 39, 40, 41, 42, 43

Procedure: complications

10. Ventriculostomy-related infection is the commonest drain complication; dual antiplatelet therapy after stent-assisted treatment raises tract haemorrhage.

Ventriculostomy-related infection is the commonest complication of EVD after aSAH.
- Drain-associated ventriculitis risk rises with duration of drainage.
- The risk rises with the number of catheter manipulations and CSF samplings.
- The risk rises with CSF leakage around the catheter.
Ventriculostomy-related infection is reported in approximately 9–20% of EVD patients.
The risk is higher in SAH with intraventricular blood than in most other indications.
In blood-stained CSF after SAH no single CSF, blood or microbiological variable reliably separates infection from sterile chemical inflammation.
- CSF culture remains the diagnostic gold standard.

Antibiotic-impregnated (rifampicin-based) ventricular catheters reduce CSF infection.
- A single antibiotic dose before insertion is recommended.
- Continuing systemic prophylactic antibiotics for the life of the drain has not been shown to reduce infection.
- Subcutaneous tunnelling away from the burr hole, a sealed dressing and a closed drainage system are standard infection-prevention measures.
- Routine scheduled catheter exchange should not be practised.
In the randomised trial, positive CSF cultures occurred in 1.3% versus 9.4% with impregnated versus standard catheters.
Insertion is done under full sterile barrier precautions with hair clipping and antiseptic skin preparation.
Continued prophylaxis selects resistant organisms.
Silver-impregnated catheters have given conflicting results.
Routine scheduled catheter exchange at fixed intervals does not reduce infection.
Established ventriculostomy-related infection is treated by removing or exchanging the catheter.
- Empirical vancomycin plus an anti-pseudomonal beta-lactam is given, de-escalated by culture.
Intraventricular administration is reserved for refractory or resistant Gram-negative ventriculitis.

Sources 21, 44, 45, 46, 47, 48, 49, 50, 51

prognosis

11. Failed weaning defines shunt-dependent hydrocephalus, which leads to ventriculoperitoneal shunting and is associated with worse functional outcome.

⚡ Contested: The pooled analysis showed no reduction in shunt dependency (RR 0.93, 95% CI 0.70–1.22) and no difference in 3-month functional outcome.

The pooled analysis showed lower mortality (RR 0.58, 95% CI 0.47–0.72).

The pooled analysis showed fewer EVD obstructions (RR 0.41, 95% CI 0.22–0.74).

Intraventricular fibrinolysis in aSAH means instilling a plasminogen activator through an EVD. The technique therefore remains investigational and is not standard care.

The agent is most often alteplase, alternatively urokinase.

The aim is faster clearance of intraventricular clot, a patent drain and less later shunt dependence.

Cohort studies of endovascularly treated patients found that intraventricular fibrinolysis neither reduced permanent shunt dependency nor improved functional outcome.

Meta-analyses of intrathecal fibrinolysis report a protective effect against chronic hydrocephalus.

⚡ Contested: The evidence on lamina terminalis fenestration is directly contradictory. No completed randomised trial resolves the question. Lamina terminalis fenestration is a microsurgical opening of the membrane posterosuperior to the optic chiasm into the third ventricle.

A 2009 systematic review found no significant reduction in shunt-dependent hydrocephalus (RR 0.88, 95% CI 0.62–1.24).

The fenestration is midline and typically 5–6 mm wide, made during clipping of anterior circulation aneurysms.

The fenestration is intended to create an internal CSF pathway from the third ventricle to the basal cisterns.

Chronic shunt-dependent hydrocephalus after aSAH is defined by persistent clinical or radiological deterioration on EVD closure.
- Persistent deterioration on closure means a failed clamp trial or failed graduated weaning.
- Chronic shunt-dependent hydrocephalus mandates permanent CSF diversion, usually a VP shunt.
- Shunt-dependent hydrocephalus is not defined by any time threshold alone.
- The shunt decision is normally made after one or two failed weaning attempts rather than by an arbitrary drainage duration.
After clearly failed weaning, prolonging drainage to avoid a shunt increases cumulative ventriculostomy-related infection risk and length of stay.
Prolonged drainage does not reduce shunt dependence.

Hydrocephalus can also appear or recur weeks to months after discharge.
- The delayed form typically presents as failure to make expected progress or deterioration after initial improvement.
- The delayed form shows a normal-pressure-hydrocephalus picture: gait disturbance, psychomotor slowing or abulia, urinary incontinence.
- Delayed deterioration after aSAH therefore warrants repeat imaging.
Subacute and chronic post-haemorrhagic hydrocephalus presents days to weeks after the ictus.
Shunting can reverse the deficit.
Shunt-dependent hydrocephalus is independently associated with worse functional outcome, cognitive impairment and greater dependence at 6–12 months after aSAH.
- Part of this association reflects the severity of the initial bleed rather than the hydrocephalus itself.

Shunt-dependence prediction scores (CHESS, SDASH)

Built on poor clinical grade, acute hydrocephalus and intraventricular blood
Discrimination modest	area under the curve typically about 0.7

Prediction scores for shunt dependence include CHESS (Chronic Hydrocephalus Ensuing from SAH Score) and SDASH.
- The scores should inform counselling and surveillance rather than pre-emptive shunting.
The scores are built on poor clinical grade, acute hydrocephalus and intraventricular blood.
The scores achieve only modest discrimination (AUC typically about 0.7).

Sources 2, 7, 10, 15, 21, 40, 52, 53, 54, 55, 56, 57, 58

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Provisional list normalised from the author's source recall; replaced by grounded sources after step 5.4g.

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