Hydrocephalus after aneurysmal subarachnoid hemorrhage (aSAH) is a well-known complication that can develop in both the acute and chronic phases. The etiology is multifactorial and involves disturbances in cerebrospinal fluid (CSF) dynamics due to hemorrhage-related pathophysiology.

### Etiology of Hydrocephalus Post-aSAH Hydrocephalus after aSAH results from impaired CSF circulation, absorption, or excessive CSF production. The underlying mechanisms include:

#### 1. Obstruction of CSF Pathways (Non-Communicating Hydrocephalus) - Intraventricular hemorrhage (IVH) can block the cerebral aqueduct or foramina of Luschka and Magendie, preventing normal CSF outflow. - Clot formation in the fourth ventricle or at the level of the aqueduct of Sylvius can cause trapping of CSF. - Aneurysm location matters: Aneurysms of the posterior circulation, especially at the basilar tip, are more likely to cause obstructive hydrocephalus due to proximity to the ventricular system.

#### 2. Impaired CSF Absorption (Communicating Hydrocephalus) - Arachnoid granulations dysfunction: The subarachnoid blood products and inflammatory response impair CSF reabsorption at the level of the arachnoid villi. - Fibrosis and scarring in the subarachnoid space and basal cisterns (especially if hydrocephalus develops in a delayed manner). - Inflammatory response triggered by blood breakdown products (e.g., bilirubin, hemosiderin) leads to meningeal fibrosis.

#### 3. CSF Overproduction (Rare) - Choroid plexus hypersecretion: Some studies suggest that blood components may stimulate the choroid plexus to produce more CSF, but this mechanism is less significant compared to obstruction or absorption failure.

### Types of Hydrocephalus in aSAH 1. Acute Hydrocephalus (within 72 hours)

1. Commonly occurs due to ventricular clot formation or acute dysfunction of arachnoid granulations.
2. Frequently associated with worse clinical outcomes.
3. High intraventricular pressure may require external ventricular drainage (EVD).

2. Subacute/Delayed Hydrocephalus (Days to Weeks)

1. Occurs as blood products break down, leading to fibrosis and scarring of the subarachnoid space.
2. Can present with progressive ventriculomegaly and worsening neurological function.

3. Chronic Hydrocephalus (Weeks to Months)

1. Gradual onset of ventricular enlargement.
2. Can mimic normal pressure hydrocephalus (NPH) with symptoms of gait disturbance, cognitive impairment, and urinary incontinence.
3. Often requires ventriculoperitoneal (VP) shunting.

### Risk Factors for Developing Hydrocephalus After aSAH - Presence of Intraventricular Hemorrhage (IVH) - High-volume SAH (Fisher grade 3 or 4) - Aneurysm location (posterior circulation > anterior circulation) - Older age - Delayed cerebral ischemia or vasospasm - Previous head trauma or pre-existing brain atrophy

### Clinical Implications - Early recognition of hydrocephalus is crucial, as it worsens neurological outcomes. - EVD placement is the primary intervention for acute hydrocephalus. - Permanent CSF diversion (VP shunt) may be required in cases of chronic hydrocephalus.

Would you like me to provide more details on management strategies for hydrocephalus post-aSAH?

The etiology of hydrocephalus following aSAH has yet to be fully elucidated, but is likely to include the following: obstruction of CSF flow within the basal cisterns and/or ventricles by clotted blood, diminished absorption at the arachnoid granulations, and inflammation ^{1) 2) 3) 4)}.

Na et al. found that higher sodium, lower potassium, and higher glucose levels were predictive values for shunt-dependent hydrocephalus from postoperative day (POD) 1 to POD 12-16 after subarachnoid hemorrhage. Strict correction of electrolyte imbalance seems necessary to reduce shunt-dependent hydrocephalus. Further large studies are warranted to confirm the findings ⁵⁾.

Data suggest that the volume of the third ventricle in the initial CT is a strong predictor for shunt dependency after aSAH ⁶⁾.