It is a rare but serious intracranial infection.
Pyogenic ventriculitis is an uncommon manifestation of severe intracranial infection that might be clinically obscure.
The commonest organisms causing pyogenic ventriculitis are Staphylococcus aureus, other Gram-positive cocci, Enterobacter and Klebsiella species, in association with nosocomial infection or immunosuppression 3) 4).
In the series of Wang et al., the most frequently isolated pathogen from cerebrospinal fluid (CSF) was Acinetobacter baumannii, followed by Pseudomonas aeruginosa, Escherichia coli, Klebsiella pneumoniae, and Serratia marcescens 5).
The clinical course of ventriculitis is typically indolent and non-specific, and early diagnosis and treatment are important to improve prognosis.
Endoscopic washout for medically refractory cerebral ventriculitis 7).
The cure rate was 73.3%. Of note, the mean period to sterilize the CSF after appropriate IVT antibiotic treatment was 6.6 days. There were no incidents of seizure or chemical ventriculitis during this IVT therapy.
The findings of this study suggest that IVT antibiotic therapy is a useful option in the treatment of postneurosurgical GNBM or ventriculitis, especially for those with a treatment-refractory state 8).
Srihawan et al performed a retrospective study of adults and children with the diagnosis of healthcare associated meningitis or ventriculitis, as defined by the 2015 Centers of Disease Control and Prevention case definition, at 2 large tertiary care hospitals in Houston, Texas from July 2003 to November 2014. Patients were identified by infection control practitioners and by screening cerebrospinal fluid samples sent to the central laboratory. We collected data on demographics, clinical presentations, laboratory results, imaging studies, treatments, and outcomes. Results. A total of 215 patients were included (166 adults and 49 children). A positive cerebrospinal fluid culture was seen in 106 (49%) patients, with the majority of the etiologies being Staphylococcus and Gram-negative rods. An adverse clinical outcome was seen in 167 patients (77.7%) and was defined as death in 20 patients (9.3%), persistent vegetative state in 31 patients (14.4%), severe disability in 77 patients (35.8%), or moderate disability in 39 patients (18.1%). On logistic regression analysis, age >45 years (adjusted odds ratio [OR], 6.47; 95% confidence interval [CI], 2.31-18.11; P ≤ .001), abnormal neurological exam (adjusted OR, 3.04; 95% CI, 1.27-7.29; P = .013), and mechanical ventilation (adjusted OR, 5.34; 95% CI, 1.51-18.92; P = .01) were associated with an adverse outcome. Conclusions. Healthcare-associated meningitis or ventriculitis is associated with significant morbidity and mortality 9).
Review of the medical records from 1990 to 2000 revealed 17 cases (12 men, five women) that satisfied inclusion criteria of abscess (n = 3) and/or positive cultures or increased white cells and protein in ventricular (n = 12) or cisternal (n = 1) cerebrospinal fluid. In one case, the diagnosis of ventriculitis was based on the combination of bacterial growth in lumbar cerebrospinal fluid and follow-up imaging. Staphylococcus species and Enterobacter species were the most common organisms. Two neuroradiologists independently evaluated imaging studies for hydrocephalus, ventricular debris, periventricular attenuation or signal abnormality, ependymal enhancement, and signs of meningitis or abscess. Sixteen studies in 11 patients were performed after the intravenous administration of contrast material.
Ventricular debris was detected in 16 (94%) of 17 cases and was irregular in 13 (81%) of 16 cases. Hydrocephalus was present in 13 (76%) of 17 cases. Periventricular hyperintense signal was present in most (seven [78%] of nine) cases with MR imaging and was most conspicuous on fluid-attenuated inversion recovery sequences. Ependymal enhancement was detected in seven (64%) of 11 cases in which contrast material was administered. Signs of meningitis (eg, pial or duraarachnoid signal abnormality or enhancement) were present in 13 (76%) of 17 cases. Three cases had imaging signs of abscess.
Ventricular debris was the most frequent sign of ventriculitis in this series. An irregular level was characteristic of debris in ventriculitis. Hydrocephalus and ependymal enhancement were less frequent signs. Detection of ventricular debris might facilitate diagnosis of pyogenic ventriculitis, a potentially fatal infection, and thus permit appropriate therapy 10).
A 53-year-old previously well man who presented with a collapse after a 4-day history of severe non-specific headache and vomiting. His initial Glasgow Coma Score (GCS) was 7/15 (E1V1M5), temperature was 38.2 °C, and he was intubated. Empirical ceftriaxone and acyclovir were commenced for suspected encephalitis. Cranial CT revealed intraventricular hyperdense areas in bilateral occipital horns and hydrocephalus, suggestive of spontaneous hemorrhage (39–48 Hounsfield units) (Fig. 1). He was transferred to our Neurosurgery Unit. CT angiogram excluded intracranial vascular abnormalities. Blood tests showed neutrophilia (26.5 × 109 /l) and raised C-reactive protein (260.5 mg/l). Following extubation 4 h later, the patient’s GCS improved to E4V1M6. Cerebrospinal fluid (CSF) from a lumbar puncture was turbid; opening pressure was low; glucose was 2.2 mmol (serum glucose 5.9 mmol); microscopy showed pleocytosis (4105 × 106 /l, polymorphs 92 %), and presence of Gram-negative diplococci. Nuclei acid test and polymerase chain reaction test confirmed Neisseria meningitides serogroup B. In retrospect, the intraventricular materials were suppurative substance. On day 2, the patient’s GCS returned to 15. Tests for immunodeficiency, including HIV test, were negative. He completed a 10-day course of ceftriaxone. On day 10, a repeat scan showed complete resolution of the intraventricular purulent material. On day 12, his inflammatory markers normalized, and he was discharged with a full neurological recovery and returned to work 6 weeks later 11).