CARDIOVASCULAR JOURNAL OF AFRICA • Volume 34, No 1, January–April 2023 40 AFRICA Case Reports Resurgence of Shoshin beriberi during the COVID-19 pandemic K Govind, GL Gaskin, DP Naidoo Abstract This report describes two patients who presented with severe type B lactic acidosis and shock, initially thought to be due to bowel ischaemia/myocardial infarction and pulmonary sepsis, respectively. This led to a delay in the diagnosis of thiamine deficiency. In both cases there was a dramatic response to intravenous thiamine, confirming the diagnosis of Shoshin beriberi. Both patients admitted to drinking home-brewed alcohol during the time of COVID-19 restrictions on alcohol consumption. These cases highlight the need for early diagnosis and immediate empirical treatment with intravenous thiamine in patients presenting with unexplained severe metabolic acidosis and circulatory shock. Keywords: Shoshin beriberi, thiamine deficiency, shock, lactic acidosis Submitted 31/8/21, accepted 9/10/21 Published online 5/12/22 Cardiovasc J Afr 2023; 34: 40–43 www.cvja.co.za DOI: 10.5830/CVJA-2021-051 Acute pernicious (Shoshin) beriberi is a rare, fulminant type of cardiovascular beriberi characterised by hypotension and/ or circulatory shock with severe lactic acidosis. Knowledge around the clinical characteristics, management and outcomes of patients with this condition is limited to isolated case reports and case series.1-3 It was last described in South Africa in the 1980s in patients with a history of excessive alcohol consumption. All patients responded to administration of intravenous thiamine.1 Here, we describe two cases of Shoshin beriberi that will alert the clinician to the pitfalls in the early diagnosis and management of this condition. Case report 1 A 54-year-old unemployed black female patient presented to the emergency department (ED) of a regional-level hospital in KwaZulu-Natal with a five-day history of right lower-quadrant abdominal pain associated with nausea, vomiting and loss of appetite. There was no accompanying fever, diarrhoea or constipation. She denied alcohol and herbal medication intake or substance abuse. The patient was hypotensive on admission (blood pressure 86/54 mmHg, pulse rate 88 beats/min). She had Kussmaul’s breathing with a respiratory rate of 25 breaths/min. Her oxygen saturation was 97% on room air. Finger-prick glucose was 8.9 mmol/l. Physical examination revealed mild bilateral parotidomegaly. The abdomen was soft and not distended. Tenderness was elicited in the right lower quadrant, but there were no features of peritonitism. No organomegaly was noted and normal bowel sounds were present. Other systems were normal. Blood gas analysis revealed a severe metabolic acidosis: pH 7.12, serum lactate 21 mmol/l, bicarbonate 3 mmol/l and PO2 157 mmHg. The full blood count was as follows: haemoglobin level 11.4 g/dl, white cell count 8.47 × 109 cells/l, platelets 126 × 109 cells/l and mean corpuscular volume 99.1 fl. Blood chemistrywas as follows: sodium124mmol/l, potassium 3.1 mmol/l, chloride 89 mmol/l, bicarbonate 3 mmol/l, urea 2.3 mmol/l and creatinine 100 μmol/l. Serum transaminases were mildly elevated: alanine aminotransferase 72 U/l (normal 7–35 U/l) and aspartate aminotransferase 105 U/l (normal 13–35 U/l). Initial imaging demonstrated mild cardiomegaly on chest X-ray and a distended loop of bowel with a ‘coffee-bean’ appearance on abdominal X-ray (Fig. 1). Because of the abdominal symptoms and the abdominal X-ray findings, a provisional diagnosis of lactic acidosis secondary to sigmoid volvulus or mesenteric ischaemia was made. The patient was reviewed by the general surgeon who felt that the abdominal X-ray showed excess gas in the descending colon with no features of sigmoid volvulus or bowel obstruction. The surgeon was of the opinion that the abdomen was ‘non-surgical’ and advised that other causes be considered. Non-ST-segment elevation myocardial infarction (NSTEMI) was also considered in the differential diagnosis when a troponin I estimation, taken two hours after arrival in the ED, returned a result of 1 358 ng/l. However, the patient experienced no chest pain symptoms and the admission electrocardiogram (ECG) showed no evidence of myocardial infarction. The troponin I elevation or ‘leak’ was attributed to the presenting problem of profound hypotension with severe acidosis. Department of Internal Medicine, University of KwaZuluNatal, Durban, South Africa K Govind, MB ChB, kamal.govind04@gmail.com GL Gaskin, MB ChB, FCP (SA), MMed (UKZN) Department of Cardiology, University of KwaZulu-Natal, Durban, South Africa DP Naidoo, FRCP, MD, naidood@ukzn.ac.za
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