key: cord-1053280-i9q1zvah
authors: Giannattasio, Antonietta; Maglione, Marco; Zenzeri, Letizia; Mauro, Angela; Di Mita, Onorina; Iodice, Raffaella M; Tipo, Vincenzo
title: A child with a severe multi‐system inflammatory syndrome following an asymptomatic COVID‐19 infection: a novel management for a new disease?
date: 2020-06-17
journal: J Med Virol
DOI: 10.1002/jmv.26189
sha: fa8d45fedf2d3a8cb40d585b0785f1062c307925
doc_id: 1053280
cord_uid: i9q1zvah

Clinical presentation of COVID‐19 disease is only in part due to viral infection itself, with the host response playing an important role.(1‐3) Despite the mild clinical course during the acute phase of infection in children, latest ongoing researches are pointing the attention towards a hyperinflammatory shock or a Kawasaki‐like disease as a possible consequence to COVID‐19 exposure.(4,5) This article is protected by copyright. All rights reserved.

2 nd day showed two small bilateral areas of atelectasis associated to minimal pleural effusion. Abdominal CT was unremarkable. Azythromycin and methylprednisolone (2 mg/kg/day) were started. Because of the high levels of BNP and troponin, subcutaneous heparin was added and methylprednisolone dosage was then increased to 5 mg/kg/day.

Due to an increase of the QT interval on electrocardiogram, azythromycin was replaced with doxycycline. The patient gradually recovered and fever disappeared after 48 hours.

Laboratory exams dramatically improved. He was discharged with oral steroid and heparin therapy and a close follow-up was planned.

This picture represents a new pediatric condition following an asymptomatic COVID-19 infection. A rise in the number of critically ill children presenting with an unusual clinical picture overlapping a Kawasaki disease (KD) has been reported. 4, 5 . Unlike these reported cases admitted to pediatric intensive care units for the severity of the clinical picture, our patient was clinically well. However, laboratory parameters strongly suggested a multiorgan involvement due to infection or inflammation. No pathological organism was identified in all cultured samples. The hypothesized link between COVID-19 infection and the hyperinflammatory syndrome was strongly supported by serological pattern (both qualitative and quantitative analysis), and by confirmed family exposure.

However, the infection at the time of clinical presentation was resolved as confirmed by repeated negativity of SARS-CoV2 on nasopharyngeal swabs. It is hypothesizable that virus persistence is not the cause of poor outcome in pediatric cases, but it is likely the subsequent inflammatory cascade plays a pivotal role in the development of the condition. The hypothesis of a cytokine storm was confirmed by high levels of IL6 and IL2 on admission, which decreased in association to all laboratory parameters after steroid therapy. Nevertheless, the inflammatory response observed in pediatric patients differs from what described in adults with COVID-19. In adults, acute respiratory 

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