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Q J Med 2002; 95: 695-704
© 2002 Association of Physicians


Masterclasses in medicine

Severe hypokalaemia in a Chinese male

Y.-F. LIN1, S.-H. LIN1, W.-S. TSAI1, M.R. DAVIDS2 and M.L. HALPERIN3,

From the 1 Renal Division, Tri-Service General Hospital, National Defense Medical Center, Taipei, Taiwan ROC, 2 Nephrology Unit and Department of Internal Medicine, Stellenbosch University, Cape Town, South Africa, and 3 Renal Division, St. Michael's Hospital, University of Toronto, Toronto, Canada

Summary

A 34-year-old Chinese man developed acute, severe, generalized muscle weakness while mountain climbing. In the Emergency Department that morning, the most striking abnormalities were flaccid paralysis of both upper and lower limbs and a plasma potassium (K+) concentration (PK) of 1.7 mmol/l. To explain the basis for this constellation of findings, an imaginary consultation was sought with Professor McCance, the legendary integrative physiologist. Using both a deductive and a quantitative analysis, he illustrated that a simple story of an acute shift of K+ into cells was not sufficient to explain the patient's hypokalaemia. The clue he used to suspect a large total body deficit of K+ was a higher than expected rate of K+ excretion on the initial spot urine (higher than expected ratio of K+: creatinine in the urine). This interpretation was supported by the fact that the patient needed a large supplement of K+ to raise his PK to just under 3 mmol/l. It was only after more detailed studies based on urine chemistry that an accurate diagnosis and effective treatment could be instituted. The final question was why one of the hallmarks of the diagnosis of hyperaldosteronism (hypertension) was absent, yet hypokalaemia was so severe.

Notes

Address correspondence to Professor M.L. Halperin, St. Michael's Hospital, Lab #1, Research Wing, 38 Shuter Street, Toronto, Ontario, M5B 1A6, Canada. e-mail: mitchell.halperin{at}utoronto.ca


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