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Shoshin beriberi with severe lactic acidosis and haemodynamic collapse due to long-term diuretic therapy.

Shoshin beriberi with severe lactic acidosis and haemodynamic collapse due to long-term diuretic therapy.

期刊: BMJ case reports 日期: 2026-08-25 PMID: 42642096 DOI: 10.1136/bcr-2026-272300 浏览: 7
作者: C K A, Jacob J, C A, Devan J
A, C.K., J, J., A, C., & J, D. (2026). Shoshin beriberi with severe lactic acidosis and haemodynamic collapse due to long-term diuretic therapy.. BMJ case reports. https://doi.org/10.1136/bcr-2026-272300
A CK, J J, A C, J D. Shoshin beriberi with severe lactic acidosis and haemodynamic collapse due to long-term diuretic therapy.. BMJ case reports. 2026; doi: 10.1136/bcr-2026-272300
A CK, J J, A C, et al. Shoshin beriberi with severe lactic acidosis and haemodynamic collapse due to long-term diuretic therapy.[J]. BMJ case reports. 2026. DOI: 10.1136/bcr-2026-272300.
@article{a2026,
  author = {C K A and Jacob J and C A and Devan J},
  title = {Shoshin beriberi with severe lactic acidosis and haemodynamic collapse due to long-term diuretic therapy.},
  journal = {BMJ case reports},
  year = {2026},
  doi = {10.1136/bcr-2026-272300},
  note = {PMID: 42642096},
}
TY  - JOUR
AU  - C K A
AU  - Jacob J
AU  - C A
AU  - Devan J
TI  - Shoshin beriberi with severe lactic acidosis and haemodynamic collapse due to long-term diuretic therapy.
T2  - BMJ case reports
PY  - 2026
DO  - 10.1136/bcr-2026-272300
AN  - PMID:42642096
ER  - 

摘要

A patient on long-term diuretic treatment for pulmonary arterial hypertension presented with acute haemodynamic instability and profound high anion gap metabolic acidosis. Investigations showed severe lactic acidosis with no evidence of sepsis, hypoxia, diabetic ketoacidosis, acute pulmonary embolism or mesenteric ischaemia. Despite fluid resuscitation, vasopressor support and ventilatory support, the metabolic derangement persisted. Since she was on prolonged diuretic use and no other cause was identified, thiamine deficiency was suspected. Empirical intravenous thiamine administration led to rapid and sustained improvement in acid-base status and haemodynamics, allowing tapering of vasopressors. This case highlights thiamine deficiency as an under-recognised but readily reversible cause of severe lactic acidosis and cardiovascular collapse, particularly in patients receiving chronic diuretic therapy.

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