Hydrocephalus after aSAH can be classified based on **timing** and **pathophysiology**:

This condition can present in acute, subacute, or chronic forms:

[[Acute hydrocephalus]] (within 72 hours of hemorrhage) results from obstruction of CSF pathways by blood clots or impaired absorption at the arachnoid granulations.
----

[[Subacute hydrocephalus]] (occurs within days to weeks) is often due to persistent inflammation and clot organization.
----

[[Chronic hydrocephalus]] (develops weeks to months later) is usually a communicating hydrocephalus caused by scarring and fibrosis affecting CSF resorption.

1. **Acute Hydrocephalus (within 3 days of aSAH)**  
   - Caused by obstruction of CSF flow due to **blood clots in the basal cisterns or ventricles**.
   - Can be **communicating** (impaired absorption at the arachnoid granulations) or **non-communicating** (obstructed CSF pathways, e.g., at the Sylvian aqueduct or fourth ventricle outlets).
   - Often manifests as **altered consciousness, headache, vomiting, and pupillary abnormalities**.
   - Treatment: External ventricular drainage (EVD) to relieve pressure and allow for CSF diversion.

2. **Subacute Hydrocephalus (4–14 days post-aSAH)**  
   - Thought to result from ongoing inflammation and dysfunction of CSF absorption.
   - Patients may develop **progressive confusion, gait disturbances, and urinary incontinence**.
   - Treatment: Persistent hydrocephalus after EVD removal may require **lumbar drainage or shunt placement**.

3. **Chronic Hydrocephalus (>14 days post-aSAH)**  
   - Typically **communicating hydrocephalus**, caused by scarring and fibrosis at the arachnoid granulations.
   - Presents insidiously with **cognitive decline, gait ataxia, and urinary urgency/incontinence**, resembling **normal pressure hydrocephalus (NPH)**.
   - Treatment: **Permanent CSF diversion** with a ventriculoperitoneal (VP) or ventriculoatrial (VA) shunt.

## **Risk Factors for Hydrocephalus After aSAH**
Several factors increase the likelihood of hydrocephalus after aSAH:

- **Higher Fisher grade (thick cisternal blood and IVH)** → greater inflammatory response and CSF obstruction.
- **Intraventricular hemorrhage (IVH)** → direct obstruction of CSF flow.
- **Older age** → reduced CSF resorption capacity.
- **Female sex** → associated with a higher risk in some studies.
- **Poor clinical grade (Hunt-Hess or WFNS score)** → higher initial brain injury burden.
- **Aneurysm location (e.g., anterior communicating artery aneurysm)** → increased risk of basal cistern blood clotting.

## **Diagnosis**
- **CT Scan (Initial Modality)**: Enlarged **temporal horns**, **third ventricle**, and **sylvian fissures** with periventricular lucency (suggesting transependymal CSF flow).
- **MRI with FLAIR and Cine Flow Studies**: Useful in chronic cases.
- **Lumbar Puncture (Caution Required)**: Can confirm communicating hydrocephalus but should be avoided in **high-pressure states** to prevent herniation.



## **Prognosis and Outcomes**
- Hydrocephalus after aSAH is associated with **worse functional outcomes**.
- Persistent hydrocephalus requiring shunting occurs in **~10-20% of cases**.
- **Early recognition and intervention improve functional recovery**.

## **Conclusion**
Hydrocephalus is a significant complication of aSAH, requiring **timely diagnosis and appropriate management**. Understanding the risk factors and clinical course is essential to improving **neurological outcomes and quality of life** for these patients.
----