Abstract
The clinical presentation of coronavirus disease 2019 (COVID-19) has a wide spectrum, ranging from asymptomatic patients to severe presentations with acute respiratory distress syndrome (ARDS), kidney injury, stroke, electrolyte imbalance, and multi-organ failure. Encephalopathy and encephalitis are devastating severe acute respiratory syndrome coronavirus‐2 (SARS‐CoV‐2) virus‐associated central nervous system complications.We reported a case of a 67-year-old male who was admitted to the hospital for the management of COVID-19 pneumonia. Due to worsening hypoxia, the patient was transferred to ICU and was intubated. On examination, he was aphasic and noted to have right-sided hemiplegia with left-sided hemiparesis on day 4. CT scan of the head without contrast and MRI findings were suggestive of acute necrotizing encephalopathy secondary to intracranial cytokine storm caused by viral infection. The patient was treated with intravenous immunoglobulin (IVIG), and high dose corticosteroids, with clinical improvement in the right-sided hemiparesis on day 5. A repeat MRI brain revealed decreased edema.The pathogenesis of encephalopathy associated with COVID-19 may be multifactorial. Postulated mechanisms include hypoxic/metabolic changes produced by the intense inflammatory response due to cytokine storm and neurotropism. Cytokine storm causes hypoxia and metabolic insults that result in global dysfunction of the brain. Altered consciousness, ranging from mild confusion, delirium, to deep coma, are some of the cardinal clinical features. The most common imaging finding on MRI T2-weighted fluid-attenuated inversion recovery (MRI T2/FLAIR) includes symmetric, multifocal lesions with invariable thalamic involvement. Other commonly involved locations include the brainstem, cerebral white matter, cortical and subcortical white matter, and cerebellum. In a few case reports, cerebrospinal fluid (CSF) analysis has shown the presence of the virus. Management of encephalopathy in COVID-19 patients involves supportive care including supplemental oxygen therapy and immune modulators. Immune modulation therapy including high-dose corticosteroids and IVIG have been shown to improve outcomes in these patients.
Highlights
The pathogenesis of encephalopathy associated with COVID-19 may be multifactorial
An outbreak of the coronavirus disease 2019 (COVID-19) caused by severe acute respiratory distress syndrome coronavirus 2 (SARS-CoV-2) began in the Hubei province of China resulting in a global health emergency
angiotensin-converting enzyme 2 (ACE2) is expressed in multiple cell types including endothelium, lungs, kidney, and central nervous system (CNS) [9]
Summary
An outbreak of the coronavirus disease 2019 (COVID-19) caused by severe acute respiratory distress syndrome coronavirus 2 (SARS-CoV-2) began in the Hubei province of China resulting in a global health emergency. We describe a patient here who developed encephalopathy, a neurological complication secondary to COVID-19 infection. We aim to present the clinical features, pathophysiology, and management options for COVID-19 patients with encephalopathy. A 67-year-old male with a past medical history of hypertension presented to the emergency department (ED) with new-onset dyspnea He is a physician who was recently exposed to COVID-19 patients. The diagnosis of COVID-19 was confirmed by reverse transcription-polymerase chain reaction (RT-PCR) He was discharged with instructions to self-quarantine at home for 14 days, as he was hemodynamically stable and saturating well on room air. Repeat CT chest revealed interval worsening of multilobar pneumonia with worsening consolidation bilaterally On admission, he was hypoxic with oxygen saturation of 78% on room air which improved to 96% with 6 L of oxygen by nasal cannula. He was discharged to a long-term acute care facility for further management and rehabilitation
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