The most likely cause of this patient's elevated serum potassium level is heparin. Hypoaldosteronism caused by heparin, inhibitors of the renin-angiotensin system, type 4 renal tubular acidosis, or primary adrenal disease can cause hyperkalemia. Both unfractionated and low-molecular-weight heparin use is associated with a decrease in aldosterone synthesis. This occurs more frequently in patients with chronic kidney disease or diabetes mellitus, or in those taking an ACE inhibitor or angiotensin receptor blocker.
Major underlying causes of persistent hyperkalemia are disorders in which urine potassium excretion is impaired. This can be due to a marked decrease in glomerular filtration rate, decreased sodium delivery to the distal potassium secretory sites, and hypoaldosteronism. The most common cause is chronic kidney disease with a glomerular filtration rate <20 mL/min/1.73 m2 or acute oliguric kidney injury. Except in these cases, the kidney is able to maintain potassium homeostasis. The patient is not oliguric, and the slight increase in serum creatinine postoperatively is not sufficient to cause hyperkalemia.
Extreme elevations in glucose by increasing serum osmolality can directly cause hyperkalemia by pulling water from the intracellular space into the extracellular space, dragging potassium with it. This patient's glucose is only mildly elevated and would have little effect on osmolality and hyperkalemia.
In patients with metabolic acidosis caused by mineral acids (such as hydrochloric acid), buffering of intracellular hydrogen ions leads to potassium movement into the extracellular fluid to maintain electroneutrality. This does not occur with organic acids such as lactate or ketoacids. In most cases of hyperchloremic metabolic acidosis, hyperkalemia typically does not develop because there is concomitant urinary and/or gastrointestinal potassium loss. This is the case in patients with hyperchloremic metabolic acidosis with losses of potassium in the stool as the result of diarrhea or in the urine in patients with renal tubular acidosis.
Topiramate is a carbonic anhydrase inhibitor. Carbonic anhydrase inhibition results in proximal bicarbonate, sodium, and chloride urinary loss. The increased sodium loss causes hypovolemia and triggers secondary hyperaldosteronism, promoting potassium loss and hypokalemia.
Initial evaluation of hyperkalemia requires a history and physical examination, review of all medications, assessment of kidney function, and an ECG. Initial ECG manifestations include peaked precordial T waves and a shortened QT interval. With progression of hyperkalemia, lengthening of the PR interval, loss of the P wave, widening of the QRS complex, a sine wave pattern, and asystole may occur (Figure 8). However, ECG findings do not always correlate with the serum potassium level and do not necessarily progress in an orderly fashion.
During the clotting process, cells are disrupted with the release of intracellular potassium, and pseudohyperkalemia may occur in serum specimens when there are extreme elevations of leukocytes or platelets. In these cases, repeating a plasma specimen will be normal. A tight tourniquet or excessively clenched fist during blood draw can also cause local potassium release.
Hyperkalemia may be caused by transcellular shifts, as occur in states of insulin deficiency or hypertonicity or with the use of β2-adrenergic blockers. Rapid breakdown of cells such as that seen in rhabdomyolysis or in tumor lysis from treatment of leukemias and lymphomas can acutely raise serum potassium levels.
Hyperkalemia usually results from increased intake with decreased renal excretion. Hyperkalemia frequently occurs with oliguric acute or chronic kidney disease with a glomerular filtration rate (GFR) <20 mL/min/1.73 m2. Potassium-sparing diuretics (amiloride, triamterene, spironolactone) also commonly cause hyperkalemia through decreased excretion. Other medications that decrease potassium excretion include trimethoprim and pentamidine (by blocking the epithelial sodium channel) and NSAIDs (by decreasing renin). Hypoaldosteronism caused by inhibitors of the renin-angiotensin system, heparin, type 4 renal tubular acidosis (often seen in early diabetic nephropathy), or primary adrenal insufficiency also cause hyperkalemia, especially in the presence of excess potassium intake.