What are the management and monitoring recommendations for patients with subarachnoid hemorrhage (SAH) and hydrocephalus?

From the Guidelines

Management of patients with subarachnoid hemorrhage (SAH) and hydrocephalus requires prompt intervention with external ventricular drainage (EVD) placement, followed by careful monitoring and potential permanent CSF diversion, as recommended by the 2023 guideline for the management of patients with aneurysmal subarachnoid hemorrhage 1.

Key Recommendations

• An EVD should be placed immediately when hydrocephalus is diagnosed to relieve increased intracranial pressure, with the drain typically set at 15-20 cmH2O above the external auditory meatus.
• Continuous ICP monitoring through the EVD is essential, with targets below 20 mmHg, as stated in the guidelines for the management of aneurysmal subarachnoid hemorrhage 1.
• Daily CT scans should be performed to assess ventricular size and hemorrhage clearance.
• Weaning trials should begin after aneurysm securing and hemorrhage stabilization, typically after 48-72 hours, by gradually raising the drain height in 5 cmH2O increments while monitoring for clinical deterioration.
• If patients tolerate clamping for 24-48 hours with stable neurological status and ventricular size, the EVD can be removed, as suggested by the comment on the 2023 guidelines for the management of patients with aneurysmal subarachnoid hemorrhage 1.

Permanent CSF Diversion

• Approximately 20-30% of SAH patients will require permanent CSF diversion with a ventriculoperitoneal shunt, particularly those with high Hunt-Hess grades, significant intraventricular hemorrhage, or persistent symptoms after multiple weaning attempts.
• Permanent CSF diversion is recommended for chronic symptomatic hydrocephalus, as stated in the guidelines for the management of aneurysmal subarachnoid hemorrhage 1.

Infection Prevention

• Throughout management, meticulous attention to preventing EVD-related infections is crucial, including sterile technique during manipulation and prophylactic antibiotics according to institutional protocols, as emphasized in the canadian stroke best practice recommendations 1.

Additional Considerations

• Early initiation of enteral nimodipine is beneficial in preventing delayed cerebral ischemia and improving functional outcomes after aSAH, as recommended by the 2023 guideline for the management of patients with aneurysmal subarachnoid hemorrhage 1.
• Elevating blood pressure and maintaining euvolemia in patients with symptomatic delayed cerebral ischemia can be beneficial in reducing the progression and severity of delayed cerebral ischemia, as stated in the 2023 guideline for the management of patients with aneurysmal subarachnoid hemorrhage 1.

From the FDA Drug Label

In animal experiments, nimodipine had a greater effect on cerebral arteries than on arteries elsewhere in the body perhaps because it is highly lipophilic, allowing it to cross the blood-brain barrier; concentrations of nimodipine as high as 12. 5 ng/mL have been detected in the cerebrospinal fluid of nimodipine-treated subarachnoid hemorrhage (SAH) patients.

The FDA drug label does not answer the question about eye exam changes in subarachnoid hemorrhage with hydrocephalus. The management and monitoring recommendations for patients with subarachnoid hemorrhage (SAH) and hydrocephalus are not directly addressed in terms of eye exams. Key points for management include:

• Oral nimodipine therapy should commence as soon as possible within 96 hours of the onset of subarachnoid hemorrhage 2.
• The recommended oral dose is 60 mg (two 30 mg capsules) every 4 hours for 21 consecutive days 2. However, there is no information regarding eye exam changes or specific monitoring recommendations for eye exams in patients with SAH and hydrocephalus.

From the Research

Management and Monitoring of Subarachnoid Hemorrhage with Hydrocephalus

• The management of hydrocephalus associated with subarachnoid hemorrhage is tailor-made to the patient, and it is usually seen with an aneurysmal bleed, independent of the primary modality of treatment 3.
• Hydrocephalus occurs in 6% to 67% of subarachnoid hemorrhage (SAH) cases and may present as acute, subacute, or chronic at the time of presentation 3.
• Diagnosis is made with a plain computed tomography scan of the brain, and the treatment is observant, temporary, or permanent cerebrospinal fluid diversion 3.

Risk Factors and Predictive Scoring System

• Several factors associated with the severity of SAH, such as a high Hunt and Hess grade, intraventricular hemorrhage, and a ruptured aneurysm in the posterior circulation, also predict the development of shunt-dependent hydrocephalus 4.
• A predictive scoring system is available to identify patients at risk of developing shunt-dependent hydrocephalus 4.

Treatment Options

• Effective treatment of hydrocephalus still involves the use of CSF shunts, with no superiority between ventriculoperitoneal and lumboperitoneal shunts established 4.
• Curative shunt operation is possible with low frequency of hemorrhagic complications, even during oral, single antiplatelet treatment after coil embolization for ruptured aneurysms 4.
• Surgery is the most prevalent and efficient therapy for hydrocephalus, despite respective risks of different surgical methods, including lamina terminalis fenestration, ventricle-peritoneal shunting, and lumbar-peritoneal shunting 5.

Clinical Presentation and Treatment

• Acute hydrocephalus is present in 20% of patients with subarachnoid hemorrhage, and one third of them may be asymptomatic on admission 6.
• If a patient presents with subarachnoid hemorrhage accompanied by acute hydrocephalus and preserved level of consciousness, they should be carefully observed for the first 24 h, and ventriculostomy should be performed if deterioration of consciousness ensues 6.
• After ventriculostomy, intracranial pressure should be maintained above 15 mm Hg to prevent rebleeding, and prophylactic antibiotics and long subcutaneous catheters should be used to avoid shunt infections 6.

Pathophysiology and Molecular Originators

• Inflammation, apoptosis, autophagy, and oxidative stress are the important causes of hydrocephalus, and well-known molecules including transforming growth factor, matrix metalloproteinases, and iron terminally lead to fibrosis and blockage of HCP 5.
• The pathophysiology of hydrocephalus after SAH is complex and not fully understood, but it is thought to involve an inflammatory reaction and the ensuing fibrosis process that impedes continuous CSF flow outward to the sinus 4, 5.