Post-haemorrhagic hydrocephalus is associated with poorer surgical and neurodevelopmental sequelae than other causes of infant hydrocephalus

Malak Mohamed,Cristine Sortica Da Costa,William Dawes,Greg James,Saniya Mediratta,Kristian Aquilina,Aswin Chari

doi:10.1007/s00381-021-05226-4

Abstract

PurposeThis retrospective cohort study aimed to investigate the surgical and neurodevelopmental outcomes (NDO) of infant hydrocephalus. We also sought to determine whether these outcomes are disproportionately poorer in post-haemorrhagic hydrocephalus (PHH) compared to other causes of infant hydrocephalus.MethodsA review of all infants with hydrocephalus who had ventriculoperitoneal (VP) shunts inserted at Great Ormond Street Hospital (GOSH) from 2008 to 2018 was performed. Demographic, surgical, neurodevelopmental, and other clinical data extracted from electronic patient notes were analysed by aetiology. Shunt survival, NDO, cerebral palsy (CP), epilepsy, speech delay, education, behavioural disorders, endocrine dysfunction, and mortality were evaluated.ResultsA total of 323 infants with median gestational age of 37.0 (23.29–42.14) weeks and birthweight of 2640 g (525–4684 g) were evaluated. PHH was the most common aetiology (31.9%) and was associated with significantly higher 5-year shunt revision rates, revisions beyond a year, and median number of revisions than congenital or “other” hydrocephalus (all p < 0.02). Cox regression demonstrated poorest shunt survival in PHH, related to gestational age at birth and corrected age at shunt insertion. PHH also had the highest rate of severe disabilities, increasing with age to 65.0% at 10 years, as well as the highest CP rate; only genetic hydrocephalus had significantly higher endocrine dysfunction (p = 0.01) and mortality rates (p = 0.04).ConclusionsInfants with PHH have poorer surgical and NDO compared to all other aetiologies, except genetic hydrocephalus. Research into measures of reducing neurodisability following PHH is urgently required. Long-term follow-up is essential to optimise support and outcomes.

Highlights

Infant hydrocephalus is often associated with developmental delay and multiple comorbidities [1, 2]
In addition to the raised intracranial pressure (ICP) and distortion of developing neural tracts caused by hydrocephalus, pro-inflammatory cytokines and free radicals from iron due to haemoglobin breakdown cause toxicity and brain injury [10, 11]
Premature neonates with VP shunts have higher rates of shunt infection and obstruction secondary to immature immune systems and high cerebrospinal fluid (CSF) protein levels and red blood cells [14,15,16]

Summary

Introduction

Infant hydrocephalus is often associated with developmental delay and multiple comorbidities [1, 2]. Both surgical and neurodevelopmental outcomes (NDO) have been shown to vary depending on the aetiology of hydrocephalus, with mixed findings in the literature in terms of ventriculoperitoneal (VP) shunt failure rates [3,4,5,6,7]. As most studies are retrospective and not constrained to infant hydrocephalus alone, separating the effects of the hydrocephalus from the underlying pathology can be difficult. Prematurity is an independent risk factor for poor NDO and has been associated with high rates of cerebral palsy (CP), epilepsy, and visual impairment [12, 13]. Premature neonates with VP shunts have higher rates of shunt infection and obstruction secondary to immature immune systems and high cerebrospinal fluid (CSF) protein levels and red blood cells [14,15,16]

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Discussion

Conclusion