An inaugural diabetic ketoacidosis with acute pancreatitis during COVID-19
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CASE REPORT
An inaugural diabetic ketoacidosis with acute pancreatitis during COVID‑19 Clémence Tollard1,2 · Vanessa Champenois3 · Brigitte Delemer2,4 · Aline Carsin‑Vu5 · Sara Barraud2,4 Received: 25 August 2020 / Accepted: 14 October 2020 © Springer-Verlag Italia S.r.l., part of Springer Nature 2020
Keywords Diabetes · COVID-19 · Ketoacidosis · Pancreas · SARS CoV-2 · Obesity
Introduction
Clinical case
A new viral infection (COVID-19) related to Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) provoked a major public health crisis all around the world at the end of 2019. Diabetes and obesity are described as risk factors for severe forms [1]. Besides the typical respiratory presentation, different organs impairments have been reported: digestive symptoms, multiple cases of neurological and/or cardiac manifestations. Accordingly, symptoms seem to be more diversified than initially expected. It is through Angiotensin—Converting Enzyme 2 (ACE2) that SARS-CoV-2 enter the host cells. This receptor is present in lungs, digestive tract, heart and brain. Additionally, ACE2 was also found in the pancreas, raising fears of pancreatic damages resulting from COVID-19 [2]. We aimed to describe the case of a French patient who developed an initial diabetic ketoacidosis followed by an acute pancreatitis with COVID-19.
A 32-year-old female patient was hospitalized in emergency at the Reims University hospital in March 2020 for acute shortness of breath associated with a polyuria, polydipsia for several weeks. She had morbid obesity (BMI 40.4 kg/ m2) and a first-degree family history of insulin-dependent diabetes. She presented tachycardia, abdominal pain, polypnea without desaturation and fever (Table 1). She was agitated with a 15 Glasgow score. A severe diabetic ketoacidosis was present, with hyperleukocytosis, normal liver function and normal lipase level, as detailed in Table 1. She was transferred to the intensive care unit for support with rehydration, IVSE insulin therapy (11 IU/h) and venous potassium supplementation. On day 2, fever at 39.1 °C appeared with a dry cough, and persisting epigastric abdominal pain, despite the disappearance of ketoacidosis. Leukocytes were increased at 27 G/L with normal procalcitonin level. No bacterial infection was found, but SARS-CoV-2 polymerase chain reaction (PCR) on a nasopharyngeal swab was positive without other virus found in the multiplex PCR. On day 4, she presented a brutal degradation with hypotension, enhanced epigastralgia and desaturation. Blood
Managed by Antonio Secchi. * Sara Barraud sbarraud@chu‑reims.fr
2
Centre Hospitalier Universitaire de Reims, Service dʼEndocrinologie - Diabète - Nutrition, Avenue du Général Koenig, 51092 Reims Cedex, France
3
Centre Hospitalier Universitaire de Reims, Service de Médecine Intensive et Réanimation Polyvalente, Avenue du Général Koenig, 51092 Reims Cedex, France
4
CRESTIC EA 3804, Université de Reims Champagne Ardenne, UFR Sciences Exactes et Naturelles, Moulin de La Housse, BP 1039, 51687 Reims
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