ABSTRACT
INTRODUCTION: There are increasing reports of a pediatric multisystem inflammatory syndrome associated with coronavirus disease 2019 (COVID-19) that presents with varying clinical features, but includes features of Kawasaki disease or toxic shock syndrome. Symptoms include fever, rash, abdominal pain, vomiting, and diarrhea. Many patients present without any respiratory symptoms and testing for SARS-CoV-2 is often negative. METHODS: A retrospective chart review was performed. RESULTS: A 7-year-old previously healthy male presented with 3 days of fevers up to 102.4F, headaches, abdominal pain, and intractable vomiting. Both parents had tested positive for SARS-CoV-2 four weeks prior. Nasopharyngeal swab tested positive for SARS-CoV-2 RNA. Echocardiogram was normal. CT venogram of his head was negative for any pathology. He developed severe neck pain and persistent headache during his hospitalization. Soon after receiving hydroxychloroquine, he developed a facial rash and altered mental status with episodes of aphasia, agitation, and pinpoint pupils. He then became unresponsive with left gaze deviation. A non-contrast head CT and CT angiography were negative. He was given levetiracetam and cefazolin and transferred to the pediatric intensive care unit. An electroencephalogram (EEG) showed no epileptiform activity. Over the following 7 hours, the EEG demonstrated left frontotemporal slowing, which progressed into a loss of fast activity over the right hemisphere with increased delta activity in the left hemisphere, then abruptly changed to generalized voltage attenuation.He rapidly lost brainstem reflexes, developing fixed and dilated pupils. Repeat CT scan revealed diffuse cerebral edema with loss of gray-white differentiation. Lab results then were consistent with severe inflammation. An intracranial pressure monitor revealed pressures greater than 76 mmHg. His exam soon became consistent with brain death. Pathologic evaluation showed diffuse cerebral edema with perivascular mononuclear infiltrates. CONCLUSION: The cause of this pediatric multi-system inflammatory syndrome is unclear and the mechanism by which SARS-CoV-2 affects the nervous system is unknown. Pediatric patients with COVID-19 and neurologic symptoms should be closely monitored as they can rapidly decline due to fulminant cerebral edema.
ABSTRACT
BACKGROUND AND PURPOSE: Severe Acute Respiratory Syndrome coronavirus 2 (SARS-CoV-2) infection is associated with hypercoagulability. We sought to evaluate the demographic and clinical characteristics of cerebral venous thrombosis among patients hospitalized for coronavirus disease 2019 (COVID-19) at 6 tertiary care centers in the New York City metropolitan area. MATERIALS AND METHODS: We conducted a retrospective multicenter cohort study of 13,500 consecutive patients with COVID-19 who were hospitalized between March 1 and May 30, 2020. RESULTS: Of 13,500 patients with COVID-19, twelve had imaging-proved cerebral venous thrombosis with an incidence of 8.8 per 10,000 during 3 months, which is considerably higher than the reported incidence of cerebral venous thrombosis in the general population of 5 per million annually. There was a male preponderance (8 men, 4 women) and an average age of 49 years (95% CI, 36-62 years; range, 17-95 years). Only 1 patient (8%) had a history of thromboembolic disease. Neurologic symptoms secondary to cerebral venous thrombosis occurred within 24 hours of the onset of the respiratory and constitutional symptoms in 58% of cases, and 75% had venous infarction, hemorrhage, or both on brain imaging. Management consisted of anticoagulation, endovascular thrombectomy, and surgical hematoma evacuation. The mortality rate was 25%. CONCLUSIONS: Early evidence suggests a higher-than-expected frequency of cerebral venous thrombosis among patients hospitalized for COVID-19. Cerebral venous thrombosis should be included in the differential diagnosis of neurologic syndromes associated with SARS-CoV-2 infection.