Page 1382 - Hall et al (2015) Principles of Critical Care-McGraw-Hill

CHAPTER 99: Electrolyte Disorders in Critical Care 955

stay, or central nervous system lesion such as stroke or Guillain-Barré published cases of hyperkalemic paralysis (excluding hereditary periodic
syndrome). The muscle damage causes upregulation of the nicotinic paralysis), the average potassium was 9 mmol/L. The use of potassium-
acetylcholine receptors so that subsequent exposure to succinylcholine sparing diuretics was the etiology of the hyperkalemia in over half of
causes massive rhabdomyolysis. Nearly all of the reported cases of rhab- the cases. Electromyograms showed the paralysis to be due to abnormal
domyolysis occurred in patients with a preexisting myopathy often a nerve depolarization rather than muscle pathology. 120
form of muscular dystrophy (Duchenne or Becker). 106
Diagnosis: The high intracellular potassium content results in frequent
Renal Dysfunction Increased intake and cellular redistribution cause only misdiagnosis of hyperkalemia. The most common cause is hemolysis
transient increases in serum potassium because the kidneys are so effi- following phlebotomy. The lab should report this, as it is easy to detect.
cient at excreting potassium. Persistent hyperkalemia is almost always Increased platelets or white cells can also release potassium, especially if
associated with a defect in renal potassium clearance. Renal potassium the specimen is allowed to clot. Thrombocytosis greater than 1,000,000
excretion is dependent on adequate tubular flow and adequate aldoste- platelets or leukocytosis over 100,000 increase the likelihood of pseu-
rone activity. Besides dramatic decreases in renal function, defects in dohyperkalemia. Rarely, counts as low as 600,000 platelets or 70,000
renal potassium clearance can always be traced back to one of these two leukocytes have been reported to cause the same phenomenon. The
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problems. other major cause of pseudohyperkalemia is fist pumping prior to phle-
Decreases in GFR from chronic renal insufficiency or prerenal azote- botomy. Forearm exercise in the presence of a tourniquet can falsely
mia reduce the flow through the distal tubule and can cause hyperkalemia. elevate potassium by 1.4 mmol/L. 122
Decreases in renal function not associated with oliguria do not typically In the diagnosis of hyperkalemia, urine chemistries have a limited
cause hyperkalemia. Examples of this include aminoglycoside toxicity role since they are primarily useful for differentiating decreased renal
(usually associated with hypokalemia) and chronic interstitial nephritis. excretion from increased potassium loads. Increased potassium loads,
Inadequate aldosterone activity can be due to pathology at any point whether endogenous or exogenous, rarely are an occult cause of persis-
in the aldosterone axis. Inadequate renin production causes hypoal- tent hyperkalemia, and so the urinary chemistries nearly always point to
dosteronism and subsequently type IV renal tubular acidosis (RTA). inappropriate renal handling of potassium.
Angiotensin-converting enzyme inhibitors and angiotensin-receptor
blockers prevent angiotensin II from stimulating the release of aldoste- Treatment: The decision of when and how to treat hyperkalemia should
rone. Since serum potassium itself can directly stimulate aldosterone be based on physical signs, the clinical situation, and serum potassium.
release, most patients can maintain potassium homeostasis despite the Individual tolerances of hyperkalemia can vary dramatically and are
loss of angiotensin II. However, patients with other defects in potas- influenced by pH, calcium concentration, rate of potassium rise, and
sium handling (eg, renal insufficiency or decreased insulin) can become underlying heart disease. Patients with rapid increases in serum potas-
hyperkalemic. 107 sium or hypocalcemia may have arrhythmias at serum potassium levels
Ketoconazole and heparin cause hyperkalemia by blocking aldo- as low as 7 mmol/L, while newborns regularly tolerate potassium con-
sterone synthesis. Spironolactone and eplerenone act as competitive centrations of that level. Patients with muscle weakness or ECG changes
inhibitors of aldosterone. Calcineurin inhibitors cause hyperkalemia consistent with hyperkalemia should be urgently treated. Modestly
in a subset of patients, possibly by inducing tubular insensitivity to elevated potassium in the absence of ECG or muscle weakness can be
aldosterone. 108,109 Potassium-sparing diuretics such as amiloride and treated more conservatively (Table 99-7).
triamterene and the antibiotic trimethoprim all block collecting tubule First-line therapy for hyperkalemia includes stopping any and all
sodium channels, decreasing potassium secretion. Distal RTA usually potassium sources. Total parenteral nutrition, potassium supplements,
110
causes hypokalemia; however, one subtype causes hyperkalemia due transfusions, and medications containing potassium should be stopped.
to a defect in sodium resorption at the cortical collecting duct. This is Patients already on peritoneal dialysis with potassium added to the
different from type IV RTA and does not respond to supplemental min- peritoneal fluid should be switched to potassium-free fluid. Patients on
eralocorticoids. This defect has been reported in chronic urinary tract continuous renal replacement therapies need to have the replacement
obstruction, lupus, and sickle cell anemia. 111,112 fluid potassium verified and removed.
Calcium Calcium reverses the ECG changes seen in hyperkalemia and
Clinical Sequelae: The potassium concentrations inside and outside of decreases the risk of arrhythmia. Both calcium chloride and calcium
the cell are the primary determinants of the cellular resting membrane gluconate can be used, but the chloride formulation has three times
potential (E ). Changes in the extracellular concentration can have the elemental calcium (0.225 mmol/mL vs. 0.68 mmol/mL of a 10%
m
dramatic effects on the resting membrane potential and the cell’s ability solution). Since the cardioprotective effect of calcium has been shown
to depolarize. As extracellular potassium rises, the normally negative E to be dose dependent it is presumed that the chloride salt is more effec-
m
increases toward zero; this allows easier depolarization (ie, increased tive than the gluconate. The downside of calcium chloride is that it
123
excitability). However, this excitability is short-lived as chronic hyper- is more irritating to veins. Both compounds cause tissue necrosis if
kalemia ultimately inactivates the sodium channels critical to produc- extravasated. The onset of action is immediate and duration is approxi-
ing an action potential. Hyperkalemia shortens the refractory period mately 1 hour. If, following a dose of IV calcium, hyperkalemic ECG
following depolarization by facilitating faster potassium uptake. changes persist, the calcium should be repeated. In animal studies, cal-
In the myocardium, inactivated sodium channels slow conduction cium channel blockers ablate the cardioprotective effect of calcium. 123,124
velocity, and high serum potassium speeds repolarization. On ECG, Historically, calcium was considered to be contraindicated in hyper-
hyperkalemia causes widened QRS complexes (slowed conduction kalemia due to digitalis toxicity. Digitalis toxicity is associated
125
velocity) and shortened ST intervals with tented T waves (rapid repo- with intracellular hypercalcemia. Theoretically, additional calcium can
larization). The slowed conduction associated with rapid repolarization worsen the toxicity and precipitate arrhythmias. Clinical data to support
predisposes the myocardium to ventricular fibrillation. this are scant. Bower and Mengle reported two cases of cardiovascular
While animal models and experimental protocols document a step- collapse and death following the administration of calcium in digitalized
wise progression of ECG changes from peaked T waves to widened QRS patients, but no information on digitalis levels, serum calcium, or potas-
to disappearance of P waves, and ultimately a sinusoidal ECG, clinically sium concentrations was provided. Other case reports document
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patients may develop symptomatic arrhythmias without prior ECG no adverse effects after calcium administration for digoxin-induced
changes. 113,114 Rapid increases in potassium, hyponatremia, hypocalcemia, hyperkalemia. 127,128 A recent retrospective review of patients with digoxin
and metabolic acidosis all increase the likelihood of arrhythmia. 115-119 toxicity detected no adverse events for those treated with calcium.
129
Ascending paralysis mimicking Guillain-Barré syndrome has been Digitalis toxicity with hyperkalemia is best treated with digoxin FAB to
documented with a serum potassium of 7 mmol/L. In a review of all rapidly remove the drug (improvement within 2 hours).

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