Ventriculitis

Last revised by Liz Silverstone on 20 Oct 2024

Ventriculitis refers to inflammation of the ependymal lining of the cerebral ventricles and is most commonly due to infection as a complication of meningitis, cerebral abscess, neurosurgical procedures or hematogenous spread. Mortality and neurological sequelae are common 7.

The entity or closely related variants have also been variously referred to as ependymitis, ventricular empyema, intraventricular abscess, and pyocephalus 5.

Its epidemiology is varied and depends on the underlying cause. 

In the case of infection CSF analysis demonstrates high white cell count, high protein, low glucose and positive culture.

Patients may present with 7:

  • fever

  • headache

  • neck stiffness

  • photophobia

  • phonophobia

  • impaired level of consciousness

  • altered mental statue

  • focal neurology

  • seizures

Meningitis is the most common underlying condition responsible for ventriculitis. It is directly related to lower host immunity and higher virulence of the causative organism. The occurrence of direct hematogenous spread to the choroid plexus has also been suggested. In long-standing cases (>2 months) ventricular septations develop which result in compartmentalisation and multiloculated hydrocephalus and makes prognosis worse.

Common organisms are 7:

  • Streptococcus pneumoniae or millerii

  • Staphylococcus aureus

  • gram negative organisms (Pseudomonas aeroginosa, Enterobacteriaceae)

In neonates with ventriculitis, neonatal cranial ultrasound can show increased periventricular echogenicity and irregularity of the ventricular surface. Choroid plexus irregularity, thought to be due to hematogenous spread via the choroid plexus, can also be seen. Additionally, echogenic intraventricular debris may be present. When present, intraventricular septations may be well delineated on ultrasound 3,4.

Non-contrast CT of the brain usually demonstrates non-specific features, most frequently dependent hyperdense layering material, particularly in the occipital horns of the lateral ventricles 1.

Hydrocephalus and periventricular low density (which probably represents reactive edema rather than transependymal edema related to hydrocephalus 1) are also frequently present, as may also be the features of the underlying abnormality (e.g. meningitis, shunt/EVD, trauma) 

Following administration of contrast, thin uniform enhancement of the ependymal lining of the ventricles may be seen. 

MRI may also show layering debris in the occipital horns as well as intraventricular pus, loculations, ependymal enhancement and associated meningitis, abscess, thrombophlebitis or empyema.

There is often intense restricted diffusion of intraventricular debris, as seen in the center of a brain abscess. Additionally, the periventricular region may also demonstrate restricted diffusion on DWI and ADC.

MRI is also more sensitive to the often subtle periventricular abnormal signal (high T2) and thin contrast enhancement.

For infective etiology:

  • antibiotics (mean 21 days 7)

  • external ventricular drain insertion

  • surgical drainage

  • ventriculostomy

  • removal of infected device

For infective ventriculitis death or neurological sequelae are common outcomes 7:

  • in-hospital mortality 30.6%

  • 1-year mortality 38.8§

  • 61.8% of survivors suffer long-term neurological sequelae

Low Glasgow coma score at presentation, epilepsy, hydrocephalus and age >65 are poor prognostic factors.

The main differential diagnosis is that of ependymal lining enhancement, which includes ependymal spreading of glioblastoma or primary CNS lymphoma. In these cases, the enhancement is usually bumpy or nodular. Metastases and germinoma may also be responsible for similar findings.

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