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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

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.

Clinical features

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

Diagnosis

In a febrile patient with a ventriculostomy, diagnosing or excluding bacterial or microbial ventriculitis is difficult, as conventional markers in analysis of cerebrospinal fluid (CSF) are not applicable due to presence of blood and inflammation.

Data from a large sample of CSF studies in patients with ventriculostomy indicate that no single value of cerebrospinal fluid lactate provided both sensitivity and specificity high enough to be regarded as reliable test 7).

Radiological studies have demonstrated the diagnostic ability of magnetic resonance (MR) imaging, including diffusion-weighted imaging 8) 9) 10).

Characteristic findings include: ventricular debris, periventricular hyperintensity, and diffusion restriction in the debris. However, in patients who are unstable to undergo MR scans, CT scans can still be informative. The irregular debris morphology is highly specific for purulent material 11).

The ventricular debris sinks towards the occipital horns with the patient supine in the scanner. The surface of the viscous debris is often round or irregular, in contrast to the straight level of acute intraventricular blood.

The ‘lodge sign’ is observed, a radiological phenomenon not previously described: in the right lateral ventricle, where the debris diameter exceeds the occipital horn, the debris is ‘lodged’, separating the CSF anteroposteriorly. On the left, CSF is also seen isolated at the tip of the occipital horn, by the overlying debris. The ‘lodge sign’ is likely to be underreported previously, as the shape of the small purulent material was not studied in details.

In patients whose clinical history is unclear and who are unsafe to undergo MRI scan, such as this case, the ‘lodge sign’ can differenitate pyogenic ventriculitis from acute intraventricular hemorrhage, both of which require prompt and specific investigations and treatments 12).

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 13).

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 14).

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 15).

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) , 8)
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) , 9) , 11)
Fukui MB, Williams RL, Mudigonda S (2001) CT and MR imaging features of pyogenic ventriculitis. AJNR Am J Neuroradiol 22:1510– 1516
5) , 13)
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.
7)
Hill E, Bleck TP, Singh K, Ouyang B, Busl KM. CSF lactate alone is not a reliable indicator of bacterial ventriculitis in patients with ventriculostomies. Clin Neurol Neurosurg. 2017 Jun;157:95-98. doi: 10.1016/j.clineuro.2017.03.021. Epub 2017 Mar 22. PubMed PMID: 28458153.
10)
Kim HS, Hong JT, Lee SW, Son BC, Sung JH, Kim MC (2005) Apparent diffusion coefficient maps for the evaluation of pyogenic ventriculitis. J Korean Neurosurg Soc 38:23–27
12) , 15)
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.
14)
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.
ventriculitis.txt · Last modified: 2017/06/24 17:15 by administrador