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Resident PGY 2
Henry Ford Macomb
The novel SARS-CoV-2 which originated in Wuhan and has spread worldwide is well known to cause severe acute respiratory syndrome. The most common clinical presentations that patients exhibited are fevers, shortness of breath, cough, diarrhea, loss of smell/taste. However, this virus has also been observed to cause multi-organ failure. We present the case of a 44yo F with a PMHx of GERD, Hashimoto’s thyroiditis, obesity, HTN, and neuropathy who presented to the hospital with the chief complaint of worsening shortness of breath. The patient was saturating 92% on room air and with ambulation her pulse oximetry dropped to 80%. Remaining vital signs were stable. Chest x-ray displayed patchy bilateral interstitial and alveolar airspace opacities. Prior to coming to the hospital, the patient had indeed visited an urgent care center and tested positive for COVID-19. On arrival, significant labs included ALT/AST 588/321, NA 133, Ferritin 712, CRP 6.3, LDH 284, WBC 3.4, absolute lymphocytes 0.60, and D-dimer 1.27. It was determined to admit the patient for acute hypoxic respiratory failure secondary to covid-19 infection. GI was consulted for the elevated liver enzymes. The patient had no prior history of hepatitis, blood transfusions, recent travel, diarrhea, alcohol abuse, IV drug use or family history of liver disease. She also had no recent medication changes or over the counter supplemental use. Extensive work-up was initiated for the elevated transaminases and results revealed a negative acute hepatitis panel, ANA, autoimmune liver panel, and no evidence of thrombosis. Given the lack of explanation for the patient’s continually rising liver enzymes, it was decided that a liver biopsy would be performed to be able to provide a valid cause for the elevated enzymes. During the patient’s hospitalization, she was placed on high dose steroids for her acute respiratory failure due to the COVID infection. The liver pathology report results were received after 4 days and reported that the liver lobular parenchyma demonstrated mild lobular inflammation with occasional hepatocyte drop-out and mild sinusoidal congestion without steatosis, granuloma or necrosis. These findings may be due to the patient's SARS-CoV-2 infection. This virus has astonished the medical world and there is a great deal of medical knowledge that still needs to be learned about SARS-COV-2. Patients present with a spectrum of clinical presentations ranging from asymptomatic patients while others can develop grave complications such meningoencephalitis. In patients with elevated transaminases, it is essential to rule out acute hepatitis, autoimmune hepatitis, drug induced liver injury and thrombosis prior to proceeding with a liver biopsy to rule out other causes. In this patient, we had ruled out the above and the only explanation for the acute liver injury was in fact COVID-19.
Singh, Lovepreet; Siu, Jordan; Abbasi, Arsalan; and Bajwa, Ramanpreet, "Viral Hepatitis in COVID-Era" (2020). Case Reports. 18.