Because J.P. has been unable to eat for the past few days, decreased oral intake
may have contributed to her hypokalemia. Because most foods are rich in potassium,
however, inadequate intake rarely is the sole cause of potassium depletion unless
inappropriate and continued renal or extrarenal losses occur, or potassium intake is
severely restricted to less than 10 to 15 mEq/day.
111 hypertonic solution administration, periodic paralysis,
125 and treatment of megaloblastic anemia with vitamin
126 all have been associated with increased cellular potassium uptake (Table 27-
2). Although the relationship between the degree of hypokalemia and increase in
118 J.P.’s metabolic alkalosis probably enhances the cellular
uptake of potassium. The transcellular shift of potassium should not result in total
body potassium depletion, however.
The GI tract is an important site of potassium loss, particularly through vomiting
and diarrhea. Because the potassium content of gastric secretion (5–10 mEq/L) is
much less than that of the intestinal secretion (up to 90 mEq/L),
volume of gastric secretion is needed to produce substantial potassium depletion.
Potassium deficit induced by vomiting, however, is commonly secondary to renal
potassium loss, especially within the initial 24 to 48 hours.
ion in gastric juice results in an elevated plasma bicarbonate concentration. The
increased amount of bicarbonate ion, as a nonresorbable anion, increases water
delivery to the distal nephron and enhances sodium reabsorption and potassium
secretion, resulting in hypokalemia. The potassium wasting is often transient, because
increased proximal reabsorption of sodium and bicarbonate will result in diminished
bicarbonate delivery to the distal site. Reduced potassium excretion will ensue,
commonly within 48 to 72 hours. Subsequent potassium loss will then be primarily
consequent to gastric secretion removal.
The absence of diarrhea in J.P. excludes the GI tract as the source of potassium
loss. Potassium loss through the skin is also unlikely in J.P. because the potassium
concentration of sweat is less than 10 mEq/L. Therefore, profuse sweating, such as
that induced by vigorous exercise in a hot, humid environment, or severe burns are
needed to cause substantial loss.
J.P.’s inappropriately high urinary potassium concentration indicates that the
kidney is the source of the potassium loss.
34,122 The urinary potassium concentration is
a good marker for differentiating various hypokalemic syndromes. A urinary
potassium excretion of less than 20 mEq/day suggests extrarenal potassium loss.
Renal potassium wastage cannot be excluded, however, unless the low urinary
potassium excretion is accompanied by a sodium intake of at least 100 mEq/day,
because a low-sodium diet can reduce renal potassium excretion.
metabolic alkalosis and hypovolemia promote renal potassium wastage.
distal delivery of a large sodium bicarbonate load and increased aldosterone activity
(from hypovolemia) enhance potassium secretion and severely impair the kidney’s
ability to conserve potassium. The hydrochlorothiazide, which J.P. had been taking
until 3 days before admission, could also have induced hypokalemia through volume
depletion, hypochloremic metabolic alkalosis, and renal potassium wastage. The
diuretic is unlikely, however, to be the cause for J.P.’s hypokalemia because she has
stopped taking the medication, and this is reflected by the low urinary chloride
15 Bartter syndrome, which presents as normotension, hypokalemia,
hypochloremic metabolic alkalosis, and renal potassium wastage, is characterized by
impaired renal sodium and chloride reabsorption. The low urinary chloride
concentration in J.P. can rule out Bartter syndrome. Other causes of hypokalemia are
In an asymptomatic hypokalemic patient with no apparent causes for potassium
depletion or transcellular redistribution, pseudohypokalemia should be excluded
before pursuing an intensive evaluation.
106 Spurious hypokalemia can occur in
leukemic patients whose leukocyte count ranges from 100,000 to 250,000 cells/μL.
The potassium in serum is taken up by the large number of leukemic cells when the
blood specimen is allowed to stand at room temperature.
CASE 27-8, QUESTION 2: What clinical manifestations of hypokalemia are evident in J.P.?
Drugs that Most Commonly Induce Hypokalemia
Drug Mechanism Predisposing Factors
Acetazolamide Marked ↑ in renal K+ loss Most profound with short-term therapy
Amphotericin Renal K+ loss (renal tubular acidosis) Concurrent piperacillin, ticarcillin
-Agonists Intracellular shift of K+
Cisplatin Renal K+ loss secondary to renal tubular
May be dose related but can occur after a
Corticosteroids Renal K+ loss. Enhanced Na+ reabsorption
at distal tubule and collecting ducts in
Supraphysiologic doses of agents with
moderate to strong mineralocorticoid
activity (e.g., prednisone, hydrocortisone)
Insulin with glucose Intracellular shift of K+ Predictable effect when insulin
administered to patients with diabetic
ketoacidosis’ combination used to treat
High Na+ load and nonresorbable anions
Was more common with carbenicillin when
it was available; newer penicillins are used
in lower doses; less likely to produce
Renal K+ loss. ↑ Na+ delivery to the late
distal tubule, resulting in Na+ resorption in
Patients with hyperaldosteronism (e.g.,
cirrhosis, HF) predisposed; may be dose
The clinical presentation of hypokalemia, which depends on the severity of
potassium depletion, is a result of changes in cell membrane polarization.
are usually asymptomatic when the plasma potassium level is 3.0 to 3.5 mEq/L, but
they may complain of malaise, weakness, fatigue, and myalgia. J.P.’s muscle
weakness and ECG changes reflect the muscular and cardiac manifestations of
Potassium depletion can lead to hyperpolarization of myocardial cells and a
prolonged refractory period. When serum potassium concentrations fall below 3
mEq/L, T-wave flattening, straight tubule segment depression, and prominent U
Mild hypokalemia (potassium concentration of 3.0–3.5 mEq/L) is potentially
arrhythmogenic in patients with underlying coronary artery disease. The incidence of
ventricular arrhythmia increases with the degree of hypokalemia. Patients without
underlying heart disease may be susceptible to these myocardial effects during
exercise, especially if the patient’s pre-exercise potassium concentration is less than
3.5 mEq/L, because the potassium concentration may drop to less than 3.0 mEq/L as
-adrenergic receptor-mediated cellular potassium uptake.
depletion may also increase the BP,
123 which can be lowered with potassium
When the serum potassium concentration is less than 2.5 to 3.0 mEq/L, muscle
weakness, cramps, general malaise, fatigue, restless leg syndrome, and paresthesia
can occur, probably because potassium is necessary for vasodilation in skeletal
muscle. In addition, severe potassium depletion (<2.5 mEq/L) can result in elevation
of serum creatine phosphokinase, aldolase, and aspartate aminotransferase levels.
Rhabdomyolysis can ensue when the serum potassium concentration falls below 2.0
Chronic potassium depletion can alter renal function and structure, which can
manifest as decreased GFR and renal blood flow, disturbance in tubular sodium
handling, impaired urinary concentrating ability with polydipsia, and ADH-resistant
nephrogenic diabetes insipidus.
106,115 Reversible pathologic changes include renal
hypertrophy and epithelial vacuolization of the proximal convoluted tubule.
Interstitial scarring and tubular atrophy have been reported with prolonged potassium
Other effects of hypokalemia and potassium depletion include decreased insulin
secretion resulting in carbohydrate intolerance,
132 metabolic alkalosis, and increased
renal ammoniagenesis, which may play a role in the development of hepatic
CASE 27-8, QUESTION 3: How should J.P.’s hypokalemia be treated?
J.P.’s protracted vomiting should be corrected, and fluids and electrolytes
(sodium, potassium, and chloride) should be replaced to correct the volume deficit,
hypokalemia, and hypochloremic metabolic alkalosis. Hydrochlorothiazide should
The amount of potassium deficit and the rate of continued potassium loss should be
determined to guide replacement therapy. It has been estimated that a 1-mEq/L fall in
serum potassium from 4 to 3 mEq/L represents a total body deficit of approximately
200 mEq. When the serum potassium falls to less than 3 mEq/L, the total body deficit
increases by 200 to 400 mEq for each 1 mEq/L reduction in serum concentration.
Other data suggest that even greater degrees of potassium loss can occur—a deficit of
100 mEq per 0.27-mEq/L fall in the serum potassium concentration.
redistribution of potassium may, however, significantly alter the relationship between
serum concentration and total body deficit.
122 Therefore, potassium repletion should
be guided by close monitoring of serum concentrations and analysis of J.P.’s urine
for potassium content to help assess the need for additional replacement.
The route of potassium administration depends on the acuity and severity of
134 but oral supplementation is usually preferred. The parenteral route is
indicated for patients who cannot tolerate high dosages of oral potassium
supplements and for those with severe or symptomatic hypokalemia. J.P.’s potassium
deficit is estimated to be 300 to 500 mEq, but because she is only moderately
symptomatic, aggressive therapy is not indicated. Potassium chloride can be added to
her IV fluid in a concentration of 40 mEq/L and infused at a rate that does not exceed
10 mEq/hour. For patients with life-threatening, hypokalemia-induced arrhythmias or
those with a serum potassium level less than 2.0 mEq/L, a more concentrated
potassium solution (60 mEq/L) can be infused at a rate not exceeding 40 mEq/hour. A
solution that is too concentrated or a rate of infusion that is too rapid would likely
cause phlebitis in the peripheral veins and could cause arrhythmias, especially when
administered through a central line. The potassium concentration should be monitored
every 4 hours, more frequently in patients with severe potassium depletion or when a
135 ECG monitoring is mandatory to identify life-threatening
hyperkalemia that can result from over-correction.
Parenteral potassium can be given as chloride, acetate, or phosphate. The chloride
salt is preferred in J.P., who has concurrent hypochloremic metabolic alkalosis. The
acetate preparation is useful in cases of concomitant metabolic acidosis. Potassium
phosphate is indicated if hypophosphatemia coexists. In the latter condition, the
serum calcium concentration should also be monitored because hypocalcemia may
ensue. Glucose solution should be avoided as the vehicle because glucose-induced
insulin secretion will promote intracellular potassium uptake.
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