Insulin/potassium/sodium-bicarbonate

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Acute respiratory distress syndrome: case report A 24-year-old man developed fatal acute respiratory distress syndrome (ARDS) during treatment insulin for diabetic ketoacidosis (DKA), potassium for electrolyte replacement therapy and sodium-bicarbonate for myocardial protection from hyperkalaemia [not all routes and dosages stated]. The man who had history of mild obesity, diabetes mellitus type 1 and hyperlipidaemia, presented to the emergency Department (ED) for vomiting, nausea, and an episode of haematemesis. He was noncompliant with his medications. On physical examination, showed he had mild distress, lethargy, and had delayed responses to questioning. Various examinations were performed. He was admitted to the ICU and received unspecified fluids along with vancomycin, cefepime, infusion of sodium bicarbonate 150 mEq, potassium repletion 100mL, and IV infusion of insulin 6 units/hour. Based on the clinical findings, he was diagnosed with DKA and acute kidney injury. On day 2 of admission, he developed signs of respiratory distress. Subsequently, his nasopharyngeal swab result was positive for COVID-19. The decision was made to intubate and mechanically ventilate, given his worsening respiratory status. Respiratory improvement was demonstrated postintubation. A chest X-ray indicated probable COVID-19 pneumonia. Thus, on day 3 of admission, he received off label treatment with azithromycin and hydroxychloroquine for COVID-19. On day 4, his oxygen saturation again dropped and continued to desaturate on day 7. On day 8, a sputum culture returned with yeast isolates. At this time, cefepime and vancomycin were withdrawn and replaced with meropenem for a wider antibiotic coverage along with voriconazole for fungal infection. A chest X-ray revealed worsening of his bilateral infiltrates. He remained intermittently febrile on day 9 and had multiple desaturations. Arterial blood gasses showed worsening hypercapnia. Chest X-ray revealed diffuse fluffy infiltrates throughout bilateral lungs, consistent with ARDS. Later that day, despite full PEEP and FiO2, he desaturated to 50%. Subsequently, he developed severe hypotension, bradycardia and eventually became pulseless. An advanced cardiovascular life support was initiated. Unfortunately, he could not be resuscitated and died due to hypoxic respiratory failure secondary to COVID-19 complicated by ARDS. The development of ARDS was attributed to the use of insulin, potassium and sodiumbicarbonate [duration of treatments to reaction onset not stated]. Singh S, et al. COVID-19-Induced Diabetic Ketoacidosis and Acute Respiratory Distress Syndrome in an Obese 24-Year-Old Type I Diabetic. American Journal of Case 803518250 Reports 21: 26 Oct 2020. Available from: URL: http://doi.org/10.12659/AJCR.925586

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Reactions 28 Nov 2020 No. 1832

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