A 28-month old boy presented with a 24-h history of lethargy, pyrexia, mottled peripheries and decreased responsiveness. Past history was notable for antenatal left middle cerebral artery (MCA) infarct, cerebral palsy with right hemiplegia, global developmental delay and West syndrome (infantile spasms). He was up-to-date with vaccinations. Epilepsy was poorly controlled with up to 30 seizures per day despite maintenance clobazam, lacosamide, sodium valproate and levetiracetam treatment.
On examination he had neck stiffness and was haemodynamically unstable with persistent tachycardia and hypotension. He was coagulopathic (platelets 94 × 10 [6]/L, INR 2.5, fibrinogen 4.03 g/L, prothrombin time 16.8 s), with elevated white cell count (WCC) 28.9 × 10 [6]/L, neutrophilia (25.8 × 10 [6]/L), normal lymphocyte count (8.5 × 10 [6]/L) and c-reactive protein (CRP) 276 mg/L. He was transferred to the intensive care unit (day 0) where he required intubation, ventilation, fluid resuscitation and inotropic support. He was treated with intravenous (IV) ceftriaxone, vancomycin and aciclovir. Polymerase chain reaction (PCR) identified human metapneumovirus, parainfluenza type-3 and adenovirus in a nasal swab. Lumbar puncture demonstrated a macroscopic yellow appearance: WCC 142 (predominantly polymorphonuclear); glucose, 1.6 mmol/L; and protein, 5.46 g/L. No organisms were seen on Gram stain. Blood and cerebrospinal fluid (CSF) were culture negative (taken on antimicrobials) but PCR positive for N. meningitidis serogroup B. Antimicrobial treatment was rationalised to cefotaxime monotherapy. He subsequently became more encephalopathic with persistent pyrexia associated with rising blood WCC and CRP. Brain computed tomogram (CT) and magnetic resonance imaging (MRI) demonstrated multiple abscesses in the left MCA territory, cystic encephalomalacia of posterior left frontal, left parietal and left temporal lobes, and left hemispheric pial enhancement (Fig. 1a). Empiric treatment for cerebral abscess with IV meropenem, vancomycin and fluconazole was commenced.
A frameless stereotactic-guided endoscopic fenestration, drainage and washout of the cerebral abscesses was performed and a left external ventricular drain was sited (day 10). Further deterioration in neurological status necessitated an extensive fronto-temporal-parietal craniotomy with evacuation and debridement of residual collections and infected encephalomalacial tissue (day 16). Intraoperative fluid and parenchymal tissue was culture negative but PCR positive for N. meningitidis serogroup B and antimicrobial therapy was rationalised to meropenem monotherapy. A second craniotomy was performed for evacuation of a left frontal lobe abscess in the context of persistent swinging pyrexia (day 18). Intravenous linezolid was added for the treatment of a surgical site infection in the left parietal region, associated with a toxic shock-like syndrome. Intra-operative specimens were culture negative. The patient returned to theatre for repeat burrhole drainage of an intracerebral collection (day 20; Fig. 1b demonstrates clinical status post-operatively day 21). Intraoperative specimens were culture-negative again and were not sent for PCR analysis. He was discharged from ICU for extensive multidisciplinary rehabilitation (day 23). The patient was discharged home on day 40 to complete a further 6-weeks IV ceftriaxone. On outpatient follow-up, he is back to his baseline functioning status with no evidence of new neurological or auditory sequelae. Unfortunately, his seizures, which had disappeared in the immediate post-operative period, have since returned to their usual frequency.