Hydrocephalus after Subarachnoid Hemorrhage: Pathophysiology, Diagnosis, and Treatment

Abstract

Hydrocephalus (HCP) is a common complication in patients with subarachnoid hemorrhage. In this review, we summarize the advanced research on HCP and discuss the understanding of the molecular originators of HCP and the development of diagnoses and remedies of HCP after SAH. It has been reported that inflammation, apoptosis, autophagy, and oxidative stress are the important causes of HCP, and well-known molecules including transforming growth factor, matrix metalloproteinases, and iron terminally lead to fibrosis and blockage of HCP. Potential medicines for HCP are still in preclinical status, and surgery is the most prevalent and efficient therapy, despite respective risks of different surgical methods, including lamina terminalis fenestration, ventricle-peritoneal shunting, and lumbar-peritoneal shunting. HCP remains an ailment that cannot be ignored and even with various solutions the medical community is still trying to understand and settle why and how it develops and accordingly improve the prognosis of these patients with HCP.

Figure 1

After SAH, the subarachnoid space is filled with blood cells and products. Leptomeninx is detected thickened with hemosiderin deposits, which has also been confirmed histologically.

Figure 2

This picture shows the major pathological mechanisms in arachnoid granulations; the upper ones demonstrate the blood clots and corresponding products blocking the outflow tract of CSF and the inferior ones show the fibrosis of arachnoid membrane meanwhile.

Figure 3

This picture shows some broadly verified molecules or pathways that are involved in the pathophysiogenesis of hydrocephalus caused by SAH.

Figure 4

This picture shows a case of acute HCP induced by aneurysmal SAH, typically with an IVH. It happened as soon as the occurrence of SAH. (a) The CT scans above show widely hemorrhagic sulci and arachnoid cisterns with dilated lateral and third ventricles containing blood. (b), (c), and (d) Immediate CTA after admission locates the culprit aneurysm on the anterior communicating artery (marked by black arrows).

Figure 5

This picture simulates how to calculate the BCI, namely, the severity of HCP, the ratio. Segment “a” is the distance between caudate nuclei and “b” is at the same level the width of brain. The ratio “a/b” of respective group of age, that is, relative bilateral caudate index is also widely accepted among researchers.