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Author: Christina Behrend, Duke University
School of Medicine, Class of 2016
Introduction: Excessive caffeine intake, while
an unusual cause of hypokalemia, may be sufficient in a patient
with potassium deficiency to result in hypokalemic paralysis.
Thorough history taking, including a dietary history, can be
critical for accurate diagnosis.
Case Presentation: A 45-year-old white female
with a remote history of bulimia, chronic mild hypokalemia, and a
recent upper respiratory infection presented with two 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 1.3mEq/L. Acid/base
status, magnesium, and creatinine were normal. Transtubular
potassium gradient was not physiologically valid to calculate as
the urine osmolality of 236mOs/kg was less than the serum
osmolality of 287mOs/kg. Thus, a 24-hour urine potassium was
obtained and was 43mmol/24hr 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.
Discussion: 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 acutely 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
March 2013 Issue of IMpact