Hypokalaemia and paralysis.
A patient with a severe degree of hypokalaemia (1.8 mmol/l) and paralysis was brought to the emergency department. Hypokalaemic periodic paralysis was an unlikely diagnosis, because an acid-base disorder (metabolic alkalosis) and a high rate of potassium (K(+)) excretion were present. During an imaginary consultation with Professor McCance, the combination of emphasis on principles of integrative physiology, a deductive analysis, common sense, and clinical skills led to an obvious diagnosis. Nevertheless, a surprise was in store, because renal K(+) wasting persisted for almost 2 weeks after removal of the causative agent. Possible explanations for the continued kaliuresis, as well as therapeutic strategies to avoid potential complications, were considered. This case illustrates the value of applying principles of physiology in a quantitative fashion at the bedside.
Lin
S-H
SH
Division of Nephrology, Department of Medicine, Tri-Service General Hospital, National Defense National Center, Taipei, Taiwan.
Davids
M R
MR
Halperin
M L
ML
D000368:Aged; D000450:Aldosterone / Q000378:metabolism; D000471:Alkalosis / Q000175:diagnosis / Q000378:metabolism; D003937:Diagnosis, Differential; D006034:Glycyrrhetinic Acid / Q000009:adverse effects*; D006035:Glycyrrhiza / Q000009:adverse effects / Q000737:chemistry; D006801:Humans; D007008:Hypokalemia / Q000175:diagnosis* / Q000209:etiology; D007668:Kidney / Q000378:metabolism; D008297:Male; D008564:Membrane Potentials; D010243:Paralysis / Q000209:etiology; D011188:Potassium / Q000378:metabolism*
D000450:Aldosterone; D006034:Glycyrrhetinic Acid; D011188:Potassium