Page 1381 - Hall et al (2015) Principles of Critical Care-McGraw-Hill

954 PART 8: Renal and Metabolic Disorders

ions with a proton-pump inhibitor or H blocker. Proton pump inhibi- function. One teaspoon of potassium chloride contains 50 to 65 mEq of
99
98
2
tors may have a similar role in ameliorating hypokalemia associated with potassium. Enteral nutrition supplements may be rich sources of potas-
gastric suction. sium. Ensure Plus at 100 mL/h provides 130 mEq of potassium per day.
Red blood cell transfusions can have extracellular potassium
■ HYPERKALEMIA concentrations as high as 70 mmol/L. The risk of hyperkalemia from
100
Etiologies: The ability of the kidney to excrete potassium is flexible and transfusions rises as the age of the transfusions increases (Table 99-6).
Use of “washed” packed red blood cells reduces the risk of transfusion-
adaptable. If dietary ingestion of potassium is increased over a number of associated hyperkalemia. 101
days, the kidney increases daily potassium excretion to match. Because Intracellular Redistribution of Potassium Increases in plasma osmolality, most
of this, dietary loads of potassium do not result in hyperkalemia unless often due to hyperglycemia, causes an osmotic movement of water from
they are sudden, or paired with a defect in renal potassium handling. the intracellular compartment. Potassium moves out of the cell with
Likewise, conditions associated with the movement of intracellular the water. Using mannitol to increase serum osmolality from 283 to
potassium to the extracellular space are associated with only transient 300 mmol/kg increased potassium from 4.4 to 5.2 mmol/L. 102
hyperkalemia because either the kidneys excrete or the cells reuptake the The Na-K-ATPase is critical in preventing intracellular potassium
excess potassium. Defective renal potassium handling increases suscep- from causing hyperkalemia. Any factor that decreases the activity of
tibility to hyperkalemia from increased potassium intake or transcellular this enzyme will cause potassium to leak from cells. A lack of insulin
shifts (Table 99-5). slows the Na-K-ATPase. In diabetic ketoacidosis hyperkalemia is typi-
Increased Potassium Intake Dietary potassium is typically in the range of cal despite total body potassium depletion, and in this setting is largely
40 to 80 mEq/d. Hyperkalemia has been reported to follow the use of related to the hyperglycemia.
potassium chloride salt substitutes, even in the presence of normal renal β-Blockers inhibit the Na-K-ATPase activity and are associated with a
mild increase in serum potassium. Uremia reduces Na-K-ATPase activity
so that renal failure patients are less able to use the intracellular compart-
TABLE 99-5 Causes of Hyperkalemia ment to buffer potassium loads. Digitalis is an Na-K-ATPase antagonist.
Digitalis toxicity can cause severe hyperkalemia. Removing digitalis with
Decreased Potassium binding antibodies allows rapid correction of the hyperkalemia. 103
Increased Potassium Intake Cellular Shift Excretion
Inorganic acids increase serum potassium. Attempts to predict the
Oral β-Blockers Decreased tubular flow change in potassium from changes of pH have shown tremendous vari-
Dietary Lack of insulin Renal insufficiency ability (0.3-1.1 mmol/L for a decrease in pH of 0.1) and are considered
unreliable. Decreases in pH due to respiratory or organic acidosis have
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K supplements Acidemia (inorganic) Prerenal azotemia
minimal effect on serum potassium.
Salt substitutes Digitalis toxicity Volume depletion Cell death results in release of intracellular potassium. Large-scale
Ingestion of red clay Succinylcholine Congestive heart failure cell death can cause fatal hyperkalemia. Tissue necrosis and hyperka-
lemia can be seen with rhabdomyolysis of any etiology. Likewise, tissue
Enteral feeding supplements Hyperkalemic periodic Cirrhosis ischemia can cause cell death and release large amounts of potassium.
paralysis NSAID use Bowel and limb ischemia are occult causes of hyperkalemia. Hemolysis
Parenteral Hypertonicity Decreased stimulation of causes hyperkalemia by releasing the intracellular potassium of red
aldosterone blood cells. Tumor destruction with chemotherapy results in release of
intracellular contents. Tumor lysis syndrome (TLS) is hyperphosphate-
Medical error Hyperglycemia Type IV RTA (hyporeninism)
mia, hyperuricemia, hyperkalemia, and hypocalcemia associated with
TPN Mannitol ACE inhibitor use acute renal failure (due to uric acid nephropathy). The use of hydration
CVVH replacement Cell destruction Angiotensin-receptor blocker and hypouricemic agents in prophylaxis regimens has substantially
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fluid Ischemia Decreased synthesis of aldosterone reduced the incidence of TLS. The syndrome most often occurs with
poorly differentiated neoplasms with large tumour burden and/or high
Peritoneal dialysis fluid Necrosis Adrenal insufficiency, primary proliferation rates such as Burkitt lymphoma and acute leukemias, but
Hemolysis Ketoconazole it has been reported with breast cancer, medulloblastoma, and ovarian
Old blood transfusions Rhabdomyolysis Heparin and lung cancer. In some rapidly growing tumors, spontaneous lysis
occurs prior to therapy. Hyperkalemia in tumor lysis syndrome is more
Treatment of hypokalemia Tumor lysis syndrome Congenital adrenal hyperplasia
common in patients with premorbid renal insufficiency. 105
Penicillin Chemotherapy Decreased aldosterone activity Succinylcholine is a depolarizing paralytic. It can cause hyperkale-
(K formulations) Radiation therapy Spironolactone mia by two unique mechanisms. The first occurs after muscle damage
Spontaneous Trimethoprim from burns, trauma, or disuse (often from denervation, prolonged ICU
Amiloride
Triamterene
TABLE 99-6 Potassium Concentration in Red Blood Cell Transfusions
Cyclosporine A Extracellular Potassium (mmol) per
Tacrolimus Age (Days) Plasma Potassium (mmol/L) a 250 mL of PRBC (Hematocrit 60%)
Type I RTA, hyperkalemic 0 1.6 0.2
variety
SLE, obstruction, sickle cell 7 17 1.7
14 27 2.7
Decreased GI excretion
35 44 4.4
Constipation in ESRD patients
42 46 4.6
ACE, angiotensin-converting enzyme; CVVH, continuous venovenous filtration; ESRD, end-stage renal
disease; NSAID, nonsteroidal anti-inflammatory drug; RTA, renal tubular acidosis; SLE, systemic lupus PRBC, packed red blood cells.
erythematosus; TPN, total parenteral nutrition. a Per Murthy. 318

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