Encephalopathy and bilateral thalamic lesions in a child with MIS-C associated with COVID-19

The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) pandemic, characterized predominantly by respiratory symptoms, has affected a small subset of children.Neurologic manifestations have been described in adults, including encephalitis/meningitis, encephalopathy, strokes, seizures, and anosmia, 1,2 but there are few reports of neurologic manifestations in children with SARS-CoV-2. 3 Multisystem inflammatory syndrome in children (MIS-C) has been reported in children following infection with SARS-CoV-2.MIS-C is characterized by a Kawasaki-like illness with persistent fever, elevated inflammatory markers, and multisystem organ involvement.4 Although altered mental status has been described in the presence of MIS-C, 5 there are rare reports of severe encephalopathy or focal brain lesions in children with MIS-C.We report a case of a 2-year-old with MIS-C presenting with altered mental status, who was found to have abnormal EEG and MRI findings. CaseA previously healthy 33-month-old boy presented to the emergency department with 2 days of fever, emesis, and rash.Examination revealed a tachycardic, interactive toddler with erythematous macules on his thighs.Nasopharyngeal SARS-CoV-2 reverse transcription PCR testing was initially negative; the repeat test was indeterminate.SARS-CoV-2 antibody testing was positive.Laboratory findings were remarkable for normal white blood cell count with bandemia and elevated inflammatory markers.Chest radiograph was unremarkable.Cardiac markers were normal; echocardiogram showed trace pericardial effusion.Electrocardiogram demonstrated sinus tachycardia without improvement with fluid resuscitation.He was admitted to the hospital and treated with empiric antibiotic therapy for 48 hours, IV methylprednisolone, IV immunoglobulin (IVIG), anakinra, prophylactic anticoagulation, and supportive therapy for a presumed diagnosis of MIS-C.The figure depicts the patient's clinical course.The patient developed worsening respiratory status over the subsequent 24-48 hours, requiring noninvasive respiratory support and diuresis.He was irritable, but alert and active.Chest radiograph displayed bilateral pleural effusions.Echocardiogram revealed decreased left ventricular systolic function.Laboratory findings demonstrated uptrending inflammatory and cardiac markers and thrombocytopenia.On hospital day 6, he became increasingly somnolent in the absence of sedative medication.