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ventriculitis

Ventriculitis

Ventriculitis is inflammation of the ependymal lining of the ventricular system.

Epidemiology

It is a rare but serious intracranial infection.

Uncommonly, ventriculitis is a complication of meningitis or occurs spontaneously in immunocompromised patients 1).

Etiology

Pyogenic ventriculitis is an uncommon manifestation of severe intracranial infection that might be clinically obscure.

Most cases are caused by intraventricular rupture of cerebral abscess and direct implantation of pathogens following head injury and neurosurgical procedures, e.g., ventricular drain insertion 2).

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).

Acinetobacter baumannii is an important cause of nosocomial ventriculitis associated with external ventricular drainage (EVD) and have substantially increased over recent years 6).

see Acinetobacter baumannii ventriculitis.

see Iatrogenic ventriculitis

Clinical features

The clinical course of ventriculitis is typically indolent and non-specific, and early diagnosis and treatment are important to improve prognosis.

Diagnosis

Treatment

Outcome

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 7).

Case series

2016

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 8).

2001

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 9).

Case report

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 10).

1)
Nakayasu H, Sawada H, Doi M, Hayashi M, Murakami T, Nakashima K (2005) Spontaneous Haemophilus influenzae Type B meningoventriculitis with intraventricular debris. Intern Med 44(4): 332–334
2)
Humphreys H, Jenks P (2015) Surveillance and management of ventriculitis following neurosurgery. J Hosp Infect 89(4):281–286
3)
Fujikawa A, Tsuchiya K, Honya K, Nitatori T (2006) Comparison of MRI sequences to detect ventriculitis. AJR Am J Roentgenol 187(4): 1048–1053
4)
Fukui MB, Williams RL, Mudigonda S (2001) CT and MR imaging features of pyogenic ventriculitis. AJNR Am J Neuroradiol 22:1510– 1516
5) , 7)
Wang JH, Lin PC, Chou CH, Ho CM, Lin KH, Tsai CT, Wang JH, Chi CY, Ho MW. Intraventricular antimicrobial therapy in postneurosurgical Gram-negative bacillary meningitis or ventriculitis: a hospital-based retrospective study. J Microbiol Immunol Infect. 2014 Jun;47(3):204-10. doi: 10.1016/j.jmii.2012.08.028. Epub 2012 Nov 30. PubMed PMID: 23201321.
6)
Hoenigl M, Drescher M, Feierl G, Valentin T, Zarfel G, Seeber K, Krause R, Grisold A. Successful management of nosocomial ventriculitis and meningitis caused by extensively drug-resistant Acinetobacter baumannii in Austria. Can J Infect Dis Med Microbiol. 2013 Fall;24(3):e88-90. PubMed PMID: 24421838.
8)
Srihawan C, Castelblanco RL, Salazar L, Wootton SH, Aguilera E, Ostrosky-Zeichner L, Sandberg DI, Choi HA, Lee K, Kitigawa R, Tandon N, Hasbun R. Clinical Characteristics and Predictors of Adverse Outcome in Adult and Pediatric Patients With Healthcare-Associated Ventriculitis and Meningitis. Open Forum Infect Dis. 2016 Apr 13;3(2):ofw077. doi: 10.1093/ofid/ofw077. eCollection 2016 Apr. PubMed PMID: 27419154.
9)
Fukui MB, Williams RL, Mudigonda S. CT and MR imaging features of pyogenic ventriculitis. AJNR Am J Neuroradiol. 2001 Sep;22(8):1510-6. PubMed PMID: 11559498.
10)
Lo WB, Mitra R, Cadwgan A, Albanese E. Pyogenic ventriculitis and the 'lodge sign'. Acta Neurochir (Wien). 2016 Oct;158(10):1849-50. doi: 10.1007/s00701-016-2914-1. Epub 2016 Aug 19. PubMed PMID: 27541492.
ventriculitis.txt · Last modified: 2018/09/03 08:45 by administrador