bubble_chart Overview

Post-traumatic ventriculitis is typically bacterial in nature, primarily seen in cases of penetrating brain injuries, especially in patients with inadequate early debridement of ventricular perforating wounds, or as a secondary condition following meningitis or brain abscess. Occasionally, it may even result from iatrogenic infections caused by prolonged external ventricular drainage or catheter shunt procedures. Common causative pathogens include staphylococci, gram-negative bacilli, Pseudomonas aeruginosa, or anaerobic bacteria.

bubble_chart Clinical Manifestations

Grade I ventriculitis may present with no specific clinical manifestations, resembling meningitis, and is often overlooked in the early stages. Therefore, if a patient with meningitis shows no improvement in clinical symptoms or laboratory findings after conventional treatment—especially in severe cases accompanied by significant intracranial hypertension—the possibility of ventriculitis and/or special infections should be considered. Severe ventriculitis has an acute onset, often presenting with high fever, delirium, impaired consciousness, and life-threatening signs, and may even lead to brain herniation. If a brain abscess ruptures suddenly, releasing a large amount of pus into the ventricular system, it can trigger intense autonomic reactions, including high fever, unconsciousness, dilated pupils, and a drop in blood pressure, rapidly progressing to respiratory and circulatory failure, with little hope of recovery. Occasionally, deep-seated abscesses near the ventricular wall may cause inflammatory infiltration of the local ventricular ependyma due to inflammatory reactions or minor pus leakage, leading to intraventricular adhesions and septation. This can result in hydrocephalus and the formation of infected compartments within the ventricles. In such cases, ventriculitis often follows a subacute or chronic course, with occasional acute exacerbations. The prolonged nature of the condition makes it difficult for antibiotics to reach the infected site, complicating treatment. Ultimately, the patient may succumb to systemic failure.

bubble_chart Diagnosis

The diagnosis of ventriculitis primarily relies on cerebrospinal fluid cytology. In addition to increased white blood cells and the presence of pus cells in the cerebrospinal fluid obtained via lumbar puncture, inflammatory changes in the ventricular fluid are also evident. Flocculent purulent secretions may even be observed, with elevated protein content and decreased glucose levels. Bacterial cultures may yield positive results. CT scans may reveal localized or diffuse thin linear enhancement of the ventricular ependymal membrane affected by inflammation, as well as septate enhancing lesions due to intraventricular adhesions, hydrocephalus, or ventricular deformation and enlargement. In the early stages of ventriculitis, MRI may show no positive findings. However, in severe cases, seasonal epidemic T₂-weighted scans may demonstrate band-like high-signal areas surrounding the periventricular white matter, and purulent foci within the ventricles may also appear as high-signal areas. Additionally, CT and MRI often reveal complications associated with ventriculitis, such as meningitis, brain abscess, cerebral edema, and softening lesions.

bubble_chart Treatment Measures

The treatment of bacterial ventriculitis is similar to that of meningitis. It is essential to identify the causative bacteria and conduct drug sensitivity tests as early as possible to select potent antibiotics and medications that can cross the blood-brain barrier, which should be administered promptly. At the same time, any previously placed ventricular drainage or shunt tubes should be removed immediately, as bacteria adhering to the tube walls exhibit greater medicinal resistance. If there is no obstruction in the ventricular system and the selected antimicrobial drugs are effective, the infection can often be controlled, leading to a reduction in cerebrospinal fluid cell counts and rapid clinical improvement. However, if there is an obstruction in the ventricular system or if the drugs identified as effective in sensitivity tests poorly penetrate the blood-brain barrier, systemic medication should be combined with repeated ventricular puncture and drainage, along with intraventricular drug administration. In cases where the obstruction has progressed to pyocephalus (pus accumulation in the ventricles), catheter drainage or double-tube irrigation and drainage should be employed. A solution of 40,000–80,000 units of gentamicin in 500 ml of saline should be slowly and continuously infused through one tube, while an equal amount is drained through another tube into a closed bottle or bag, maintaining a balance of 30–40 drops per minute until the drainage fluid clears, symptoms improve, bacterial cultures turn negative, and white blood cell counts normalize, after which the tubes can be removed.

For abscesses located deep in the brain near the ventricles, the abscess wall adjacent to the ependymal membrane is often thin due to slower fibrosis, posing a risk of sudden rupture into the ventricle and causing acute purulent ventriculitis. In such cases, the only hope for rescue lies in emergency craniotomy to remove the abscess, thorough irrigation of the ventricle with antibacterial saline, and placement of a tube for continuous external ventricular drainage, combined with intensive systemic antimicrobial therapy.