Hand-foot-and-mouth disease and enterovirus infection — branching viva

Branching structured-oral viva on HFMD and enterovirus infection: the causative enteroviruses and faecal-oral, droplet and vesicle-fluid transmission, the classic and atypical (CVA6) clinical phenotypes, the EV71 neurological spectrum from brainstem encephalitis to neurogenic pulmonary oedema, PCR sample selection, the fluid-restriction and milrinone critical-care strategy, the absence of a proven antiviral, childcare exclusion and outbreak management, and the inactivated EV71 vaccines licensed in China with the WHO SAGE 2016 position.

branching clinical structured oral5 min readVerification in progress

Prompt

You are the general paediatric registrar in the emergency department. A 22-month-old boy is brought on day three of a febrile vesicular illness consistent with hand-foot-and-mouth disease; overnight the parents have noticed brief limb jerks during sleep and this morning he is unsteady on walking. The examiner asks you to take the candidate through the recognition, investigation, stepwise management and prevention of this presentation.

Opening question

Examiner: Take me through this child. What is going on, and what is your frame? [2]

Candidate: This is enterovirus 71 brainstem encephalitis complicating hand-foot-and-mouth disease. The classic vesicular rash on day three, plus sleep myoclonus and ataxia, is the textbook early presentation of EV71 reaching the brainstem. My frame is two-layered: confirm the diagnosis and grade the neurological severity, and get this child into a monitored bed with PICU alerted, because the interval between a tremor and neurogenic pulmonary oedema can be short. I would admit, send PCR and imaging, and observe continuously. [2] [5]

Examiner: Why is this child at particular risk? [1]

Candidate: The burden and the mortality of EV71 fall on children under five, and especially under two, because of immature immunity, small physiological reserve and close-contact behaviours that maximise transmission. In this age group the same brainstem injury that produces myoclonus and ataxia progresses more readily to autonomic dysregulation and pulmonary oedema. The host turns a neurotropic virus into a lethal one. [1] [2]

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References5Show ledger

[1]Solomon T; Lewthwaite P; Perera D; Cardosa MJ; Ooi MH; et al Virology, epidemiology, pathogenesis, and control of enterovirus 71. Lancet Infect Dis, 2010.PMID 20961813
[2]Ooi MH; Wong SC; Lewthwaite P; Cardosa MJ; Solomon T Clinical features, diagnosis, and management of enterovirus 71. Lancet Neurol, 2010.PMID 20965438
[5]Ooi MH; Wong SC; Mohan A; Podin Y; et al Identification and validation of clinical predictors for the risk of neurological involvement in children with hand, foot, and mouth disease in Sarawak. BMC Infect Dis, 2009.PMID 19152683
[7]Griffiths MJ; Ooi MH; Wong SC; Mohan A; et al In enterovirus 71 encephalitis with cardio-respiratory compromise, elevated interleukin 1β, interleukin 1 receptor antagonist, and granulocyte colony-stimulating factor levels are markers of poor prognosis. J Infect Dis, 2012.PMID 22829643
[8]Cox JA; Hiscox JA; Solomon T; Ooi MH; et al Immunopathogenesis and Virus-Host Interactions of Enterovirus 71 in Patients with Hand, Foot and Mouth Disease. Front Microbiol, 2017.PMID 29238324