Five-year survival and outcome of treatment for postinfectious hydrocephalus in Ugandan infants

Clinical article

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Neonatal infection is the most common cause of infant hydrocephalus in Uganda. Postinfectious hydrocephalus (PIH) is often accompanied by primary brain injury from the original infection. Since 2001, ETV (with or without choroid plexus cauterization) has been our primary treatment for PIH. The long-term outcome in these children is unknown.


We studied the 5-year outcome in a cohort of 149 infants treated for PIH from 2001 to 2005 and who lived in 4 districts close to the hospital. Survival analysis was performed using the Kaplan-Meier method. Statistical significance was determined using the Fisher, Breslow, and log-rank tests.


The patients' mean age at presentation was 9.5 months (median 3.0 months). Eighty-four patients (56.4%) were successfully treated without a shunt. Operative mortality was 1.2% for ETV and 4.4% for shunt placement (p = 0.3). Five-year survival was 72.8% in the non–shunt-treated group and 67.6% in the shunt-treated group, with no difference in survival (log rank p = 0.43, Breslow p = 0.46). Of 43 survivors assessed at 5–11 years, those with shunts had significantly worse functional outcomes (p = 0.003–0.035), probably reflecting treatment selection bias since those with the worst sequelae of ventriculitis were more likely to be treated with shunt placement.


Nearly one-third of treated infants died within 5 years, and at least one-third of the survivors were severely disabled. There was no survival advantage for non–shunt-treated patients at 5 years. A randomized trial of endoscopic third ventriculostomy versus shunt placement for treating PIH may be indicated. Public health measures that prevent these infections are urgently needed.

Abbreviations used in this paper: CCHU = CURE Children's Hospital of Uganda; CPC = choroid plexus cauterization; ETV = endoscopic third ventriculostomy; PIH = postinfectious hydrocephalus; VP = ventriculoperitoneal.

Article Information

Address correspondence to: Benjamin C. Warf, M.D., Department of Neurosurgery, Children's Hospital Boston, 300 Longwood Avenue, Boston, Massachusetts 02115. email:

© AANS, except where prohibited by US copyright law.



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    Endoscopic view of the cerebral aqueduct in a child with PIH. The posterior commissure is seen in the upper third of the image. Note diffuse punctate inflammatory deposits and obstructing membrane over the aqueduct with only a pinhole-sized opening.

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    Flowchart demonstrating the treatment path for 149 patients in the study cohort.

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    Kaplan-Meier survival curves. Left: Graph showing survival curves for ETV with or without CPC and shunt treatment. The time points at which patients were lost to follow-up (without known subsequent death) are shown as censored (short vertical marks). For those patients known to have died but for whom the date of death was not known, the time of last encounter was considered the length of survival. Patients who reached 60 months' survival and who might have subsequently died were also censored for statistical calculations (but not marked). Note that there is a trend toward early and late shunt failures, but global statistical comparisons of the curves show that there is no overall statistical difference between the survival groups (p > 0.4 for both log-rank and Breslow generalized Wilcoxon tests). Right: Graph showing 95% CIs (broken lines, blue for ETV and green for shunt treatment) for the cumulative survival functions using Greenwood's formula (Mathworks implementation), demonstrating that the survival curves at all survival times remain within each others' CIs with the solitary exception of the shunt curve at 12 months.

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    Noncontrast axial CT scan of the brain obtained in a 5-month-old girl with a history of fever and seizures at 1 month of age and rapid development of macrocephaly. Note the severe, diffuse parenchymal destruction. A tapping reservoir was placed to externally drain CSF for 2 weeks until it was sufficiently clear. Ventriculoscopy revealed severe, diffuse ependymal scar, yellow intraventricular inflammatory deposits, and an occluded aqueduct. Endoscopic third ventriculostomy revealed arachnoid scarring within the prepontine cistern. Treatment with ETV/CPC failed and a VP shunt was placed 1 month later.



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