A 45–year–old white female with a remote history of bulimia, chronic mild hypokalemia, and a recent upper respiratory infection presented with two 2 days of ascending muscle weakness and paralysis. Physical exam showed normal vital signs and was significant for lower extremity paralysis, moderate upper extremity weakness, and diminished lower extremity reflexes. Initial serum potassium was 1.3 mEq/L. Acid/base status, magnesium, and creatinine were normal. Transtubular potassium gradient was not physiologically valid to calculate as the urine osmolality of 236 mOs/kg was less than the serum osmolality of 287mOs/kg. Thus, a 24–hour urine potassium was obtained and was 43 mmol/24 hr indicating renal losses. Electrocardiogram showed U waves, ST depression, and premature ventricular complexes. Electromyogram and nerve conduction studies were normal. Diuretic screen was negative; laxative screen was positive for Bisacodyl, but stool studies and acid/base status were inconsistent with laxative abuse. Aggressive replacement with enteral and parenteral potassium resulted in complete resolution of paralysis. Upon additional interview, a dietary history revealed a daily intake of 6–8.5L of caffeinated beverages. Post–hospitalization, normal serum potassium in relation to significant reduction in caffeine intake was documented with continued follow–up over a several month period.
Severe hypokalemia can lead to urgent medical situations such as paralysis as well as emergencies such as cardiac arrhythmias and respiratory failure. Hypokalemic paralysis is potentially reversible if correct identification of the underlying etiology is made. When the cause is unconventional, thorough history–taking in the hospital setting can be critical to prevent both worsening of symptoms and possible recurrence. Etiologies include renal and extrarenal losses as well as transcellular shifts. The two major players involved in the regulation of potassium are skeletal muscle, which regulates potassium at the cellular level, and the kidney, which regulates whole body potassium in the long term setting. Although an unusual cause, excessive caffeine use in the setting of chronic potassium deficiency can push one into the range of severe complications. Caffeine and its metabolites increase mobilization of endogenous catecholamines and affect the dynamics of sodium–potassium pumps and potassium channels, resulting in net movement of potassium into cells. Also, caffeine is a diuretic and increases renin secretion, promoting sodium reabsorption and potassium excretion. Thus, chronic excessive caffeine consumption can adversely affect potassium homeostasis and result in hypokalemic myopathy.
Thorough history taking, including a dietary history, can be critical for accurate diagnosis. Excessive caffeine intake, while an unusual cause of hypokalemia, may be sufficient in a patient with potassium deficiency to result in hypokalemic paralysis.