Cardiovascular Journal of Africa: Vol 25 No 6 (November/December 2014)

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CARDIOVASCULAR JOURNAL OF AFRICA • Volume 25, No 6, November/December 2014 AFRICA e1
Case Report
A case of shoshin beriberi presenting as cardiogenic
shock with diffuse ST-segment elevation, which
dramatically improved after a single dose of thiamine
Jihye Kim, Sooyoun Park, Jun-Hyun Kim, Sun Woong Kim, Won Chan Kang, Sun Jong Kim
Abstract
Shoshin beriberi is a fulminant form of cardiac beriberi
caused by thiamine deficiency. We report on a case of an
87-year-old man with shoshin beriberi presenting as cardio-
genic shock with diffuse ST-segment elevation, which dramat-
ically improved after thiamine administration. Because of the
rarity of the occurrence, lack of diagnostic test and atypical
presentation, diagnosing shoshin beriberi is challenging and
requires a high index of clinical suspicion. Shoshin beriberi
leads to rapid haemodynamic collapse and death. Therefore,
clinicians should consider shoshin beriberi (or cardiac beri-
beri) as one of the differential diagnoses in patients with heart
failure or cardiogenic shock.
Keywords: shoshin beriberi, thiamine deficiency, cardiogenic
shock
Submitted 18/4/14, accepted 21/8/14
Cardiovasc J Afr 2014; 25: e1–e5
DOI: 10.5830/CVJA-2014-053
Thiamine deficiency (beriberi) has two major clinical
manifestations: dry beriberi (peripheral neuropathy) and wet
beriberi (cardiovascular disease). Shoshin beriberi is a fulminant
form of wet beriberi and is characterised by hypotension,
tachycardia and lactic acidosis, rapidly progressing to death if
left untreated.1
Cardiac beriberi has repeatedly been reported for centuries
all over the world, although it is very rare in the modern era,
especially in developed countries.2 Cardiac beriberi is commonly
missed without a high index of suspicion. Considering the
severity of the potential outcome left untreated, it is essential for
clinicians to have an understanding of this disease.
We herein describe a case of shoshin beriberi presenting
as cardiogenic shock with diffuse ST-segment elevation. It
improved dramatically after thiamine administration.
Case report
An 87-year-old male in a general ward was transferred to the
medical intensive care unit (ICU) with sudden onset of shock.
He complained of chest discomfort. His vital signs revealed
blood pressure of 85/56 mmHg, respiration rate 30–40 per
minute, heart rate 128 beats per minute, temperature 36.5°C and
95% oxygen saturation in room air. An electrocardiogram (ECG)
demonstrated ST-segment elevation in lead I, II, III, aVF and
V2–V6 (Fig. 1). He was comatose.
He was admitted to our hospital for control of blood sugar
level 40 days before the event. During the hospitalisation period,
he fell into septic shock secondary to small bowel infarction;
small bowel resection surgery was undergone. Since then, he had
remained on total parenteral nutrition (TPN).
He had a history of diabetes mellitus, hypertension, asthma
and stable angina, and was on regular medication. He had had
right hemicolectomy surgery due to Burkitt lymphoma on the
terminal ileum 14 months earlier, and a burr hole trephination
due to traumatic subarachnoid haemorrhage 11 months before.
On auscultation of the chest, a coarse breathing sound
was heard without crackles on both lungs. On laboratory
investigation, haemoglobin level was 11.7 g/dl, white blood cell
count was 8.43 × 103 cells/ml (neutrophils 85.7%, lymphocytes
11.0%), and platelet count was 61 × 10 3 cells/μl.
The biochemical profile showed: total protein 6.2 g/dl,
albumin 3.1 g/dl, aspartate aminotransferase 12 IU/l, alanine
aminotransferase 10 IU/l, alkaline phosphatase 91 IU/l, total
bilirubin 1.7 mg/dl, prothrombin time 85%, blood urea nitrogen
55.7 mg/dl, creatinine 1.08 mg/dl, C-reactive protein 3.58 mg/
dl, CK-MB/troponin I 8.3/0.22 ng/ml, brain natriuretic peptide
454.2 pg/ml, D-dimer 1.00 μg/ml, sodium/potassium/chloride
128/5.3/93 mmol/l, anion gap 27 mmol/l and lactic acid 12.2
mmol/l. Arterial blood gas revealed a pH of 7.49, pCO2 of 22.7
mmHg, pO2 of 98.8 mmHg, HCO3 of 16.8 mEq/l, base excess of
–4.9 mEq/l and SaO2 98% on room air.
His chest X-ray showed cardiomegaly with mild pulmonary
congestion, both pleural effusion and consolidation in the right
upper lung field. This was not changed compared with the
previous X-ray (Fig. 2).
We initially suspected cardiogenic shock due to an acute
Department of Internal Medicine, Konkuk University Hospital,
School of Medicine, Konkuk University, Seoul, Korea
Jihye Kim, MD
Sooyoun Park, MD
Jun-Hyun Kim, MD
Sun Woong Kim, MD
Won Chan Kang, MD
Sun Jong Kim, MD,