Disorders Of Potassium,phosphorus And Magnesium In Critical Illness

Vol. 19, No. 1 January 1997

V

HEINZ SYMPOSIUM 1996

Continuing Education Article

FOCAL POINT ★Intensive management of critically ill animals can lead to severe electrolyte and acid–base abnormalities.

Disorders of Potassium, Phosphorus, and Magnesium in Critical Illness

KEY FACTS Auburn University ■ Hyperkalemia can cause lifethreatening cardiac arrhythmia.

Douglass K. Macintire, DVM, MS

■ Imbalances of potassium, phosphorus, and magnesium must be corrected cautiously to avoid severe side effects.

P

■ Hypophosphatemia can cause acute hemolysis in recovering diabetics and malnourished patients receiving nutritional support.

DISORDERS OF POTASSIUM BALANCE Potassium is the primary intracellular cation; 95% of total body potassium is within cells.1 Potassium maintains intracellular volume and normal membrane potential. If the ratio between intracellular and extracellular potassium is disturbed, the membrane potential of excitatory tissue (heart, nerve, and muscle) is affected; conduction disturbances result.2 In normal animals, daily potassium intake equals daily losses.

■ Unexplained decreases in serum phosphorus should prompt a search for infection, p. 44. ■ Until the magnesium deficit is corrected, concurrent hypokalemia may be refractory to aggressive potassium replacement.

otassium, phosphorus, and magnesium are primarily intracellular ions. Their serum concentrations are maintained within a narrow range by strict homeostatic mechanisms. When imbalances of these ions occur in critical illness, the results can be life threatening.

Hypokalemia Hypokalemia is probably the most common electrolyte abnormality recognized in critically ill veterinary patients. Clinical signs include muscle weakness, cramping, lethargy, myocardial depression, ileus, urine retention, inability to concentrate urine, and mild hyperglycemia from decreased insulin secretion.1,2 Severe potassium depletion can result in death from paralysis of respiratory muscles. Hypokalemia can result from decreased intake, excessive losses, or translocation of potassium to the intracellular space. Animals with anorexia, vomiting, and diarrhea are prone to hypokalemia, especially if they are given intravenous fluids deficient in potassium. Animals with pancreatitis, peritonitis, parvoviral enteritis, and other causes of vomiting generally require potassium supplementation to maintain normal serum levels.2 Fluids containing 14 to 20 mEq/L usually maintain serum potassium levels and prevent them from dropping precipitously in conditions in which

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decreased intake or exPotassium depletion TABLE I cessive losses are expectcan worsen progressive Potassium Replacement ed. Excessive renal losses renal damage through Potassium Chloride can be seen in patients Serum decreased ability to auPotassium Added to Fluid Maximum Infusion Rate a toregulate glomerular with chronic renal fail(mEq/L) ml/lb/hr ml/kg/hr ure,3–5 during the recov- (mEq/L) filtration rate and inery or diuretic phase of creased ammoniagene20 11 25 acute renal failure, and 3.6–5.0 sis, which can be toxic 30 8 17 during the diuresis that 3.1–3.5 to tubule and interstitial 40 5.5 12 often follows relief of uri- 2.6–3.0 cells.14,15 Therefore, cats 60 4 8 with chronic renal failnary obstruction in male 2.1–2.5 80 3 6 ure and other condicats.2 Serum potassium <2.0 levels in these patients tions associated with inshould be checked fre- aSo as not to exceed 0.5 mEq/kg/hr. creased potassium losses quently. If hypokalemia should receive oral pooccurs, potassium suptassium gluconate (2 to plementation can be administered according to the slid4 mEq/day). ing scale6 in Table I. Cats accept potassium gluconate fairly readily, but Intravenous potassium supplementation must not exoral potassium chloride liquid is generally unpalatable ceed 0.5 mEq/kg/hr (Table I); otherwise, serious arto cats and may cause vomiting. Enteric-coated tablets rhythmia or asystole may occur. If the animal is eating, are poorly absorbed and may cause gastrointestinal irrioral potassium supplementation is safe and effective. tation. If the cat is eating, potassium gluconate powder Diabetic animals, particularly those with ketoacidocan be mixed in the food. Supplemental potassium can sis, are also prone to hypokalemia.7,8 The body stores of also be safely given in subcutaneous fluids at concentrapotassium in sick diabetic animals are often depleted tions of up to 30 mEq/L. Higher concentrations may through increased urinary and gastrointestinal losses cause skin sloughs. and decreased intake. Serum potassium levels appear Inappropriate loss of potassium via urine can be docfalsely elevated in animals with acidosis because potassiumented by measuring fractional excretion (FEK ) from a single urine sample and concurrent serum sample acum has moved out of cells. For each 0.1 change in cording to the following formula: blood pH, an inverse change in serum potassium of approximately 0.6 mEq/L can be expected because of translocation.9 U /S Serum potassium levels can drop precipitously after FEK = K K × 100 UCR /SCR insulin treatment and correction of acidosis. Potassium levels in sick diabetic patients must therefore be closely where U K = urine potassium (mEq/L), S K = serum monitored. If hypokalemia is present, potassium suppotassium (mEq/L), UCR = urine creatinine (mg/dl), plementation should be instituted before aggressive inand SCR = serum creatinine (mg/dl). Values over 4% to sulin treatment is begun.10 Feline hypokalemic polymopathy syndrome was first 6% are consistent with inappropriate loss of potassium. reported in 1984.11 Clinical signs include generalized Animals with increased losses, especially geriatric cats, muscle weakness, cervical ventroflexion (Figure 1), eleshould receive oral potassium supplementation daily. vated creatine kinase levels, and severe hypokalemia. Hyperkalemia These signs remit after potassium supplementation.12,13 Most affected cats were geriatric and had evidence of Elevated serum potassium levels can be a life-threatchronic renal disease. Many commercial feline diets ening emergency because of the effect on the myocardiwere found to provide inadequate potassium for cats um (Figure 2). Progressive abnormalities appear on the with increased losses resulting from chronic renal diselectrocardiogram.16 Mild hyperkalemia is associated with peaked T waves, decreased amplitude of the R ease. wave, and prolongation of the P–R interval. As serum Most diets today contain adequate amounts of potaspotassium levels increase, flattening of the P wave, sium (0.6% to 0.7% of dry weight), and the syndrome bradycardia, prolongation of the Q–T interval, and has become infrequent. Nevertheless, cats with chronic widening of the QRS complex can occur. Severe liferenal disease and other causes of increased losses or dethreatening hyperkalemia can cause a sinoventricular creased intake are at risk of hypokalemia.13 FELINE HYPOKALEMIC POLYMYOPATHY ■ FRACTIONAL EXCRETION ■ ELECTROCARDIOGRAM

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rhythm, ventricular fibrillato 0.5 U/kg) combined with tion, asystole, and cardiac glucose (2 g/U) diluted to a arrest. 10% solution. Dextrose Causes of hyperkalemia in (2.5% to 5%) should be veterinary patients include added to subsequent fluids hypoadrenocorticism (Addito prevent hypoglycemia. son’s disease), acute oliguric The third option for treatrenal failure, ruptured blading animals with life-threatder or urethral tear, urethral ening hyperkalemia is 10% obstruction, severe crushing calcium gluconate (50 to injuries, heatstroke, massive 100 mg/kg; 0.5 to 1.5 ml/kg) cellular destruction (snakegiven by slow intravenous bite, tumor lysis syndrome, bolus while monitoring overwhelming infection, heart rate and the electrothromboembolism), Tri- Figure 1—This cat has cervical ventroflexion secondary to cardiogram. Calcium prochuris vulpis infection, and hypokalemia (serum potassium 2.0 mEq/L), which result- tects the myocardium from body cavity effusion. Hyper- ed from extreme polyuria after exposure to a toxin. Clini- the arrhythmogenic effects kalemia can also be iatro- cal signs resolved after potassium supplementation. of hyperkalemia. genic (overdose of potassiAfter the underlying cause um-sparing diuretics or of hyperkalemia is removed, overzealous potassium supcontinued diuresis is generplementation). ally required to enhance reWhen the hyperkalemia is nal potassium excretion. not life-threatening, the aniAnimals with acute oliguric mal generally requires no renal failure may require specific therapy for reducing peritoneal dialysis or hemohyperkalemia, other than redialysis if urine flow cannot moval of the underlying be initiated by pharmacocause and dilutional fluid logic means. therapy. Life-threatening The choice of fluid for hyperkalemia is treated by hyperkalemic animals is removing the underlying somewhat controversial. cause and taking immediate Potassium-free fluids are ofsteps to stabilize cell memten recommended (5% dexbranes and promote intra- Figure 2—Electrocardiographic tracings from a male cat trose in water, 0.9% sodium cellular translocation of with urethral obstruction (lead 2, 50 mm/sec). Ventricular chloride), but these fluids potassium. This can be ac- tachycardia (top) was associated with a serum potassium may worsen sodium imballevel of 9.2 mEq/L. Normal sinus rhythm (bottom) was recomplished through three ance. Also, because they are stored by a slow intravenous bolus of sodium bicarbonate 2 different mechanisms. Some (2.2 mEq/kg). not buffered, they do not animals require all three help correct acidosis. treatments to stabilize the If the hyperkalemia is semyocardium. vere (>10 mEq/L), a potassium-free fluid should be First, a slow intravenous bolus of sodium bicarbonate chosen for initial fluid therapy. Otherwise, lactated (1 to 2 mEq/kg) can be administered. This is the treatRinger’s solution (which has a potassium content of 4 ment of choice for animals with Addison’s disease. It is mEq/L) appears to be the most physiologic choice for also effective in most feline cases of urinary obstrucanimals with normal renal function once the underlytion, but it may promote hypocalcemia in some cases. ing cause of hyperkalemia is removed. The hyperCats with urinary obstruction often have low serum kalemia usually resolves with dilution, restoration of calcium levels secondary to high phosphorus levels.17 Inperfusion, and enhanced renal excretion. travenous sodium bicarbonate lowers ionized calcium DISORDERS OF PHOSPHORUS BALANCE levels and may cause tetany or muscle tremors. The preLike magnesium and potassium, phosphorus is priferred method for lowering serum potassium in these marily an intracellular ion.18 It is important for energy patients is an intravenous bolus of regular insulin (0.25 BICARBONATE ■ INSULIN AND GLUCOSE ■ CALCIUM GLUCONATE

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production (it is a cofactor for glycolysis and is needed to form ATP) and cell membrane maintenance (it is a component of phospholipid membrane and is required to form 2,3-diphosphoglycerate). Serum phosphorus concentration is regulated by dietary intake, renal excretion, factors that promote ion translocation into or out of cells (e.g., insulin, glucose, blood pH), and interactions of the regulatory hormones vitamin D and Figure 3—An unexplained drop in hematocrit accompanied by hemolysis in recovering diabetics or malnourished aniparathyroid hormone. mals receiving nutritional phatemia.

Hypophosphatemia Until recently, clinically significant decreases in serum phosphorus levels were considered uncommon. Now hypophosphatemia is increasingly being recognized as a problem in critically ill humans and animals. Clinical sequelae of hypophosphatemia include hemolysis (Figure 3), skeletal muscle weakness, leukocyte dysfunction, and poor oxygenation of tissue as a result of reduced 2,3-diphosphoglycerate levels.19 Nutritional recovery syndrome was first recognized in prisoners of war after World War II.20 Aggressive feeding after prolonged malnutrition resulted in a syndrome of lethargy, depression, diarrhea, and multiple electrolyte abnormalities. It was later found that malnourished patients are prone to hypophosphatemia upon refeeding. Glucose and phosphorus are transported into cells as a result of insulin secretion. Phosphorus is a cofactor for glycolysis and is rapidly consumed, sometimes dropping to dangerously low levels. The same syndrome can be seen in veterinary patients that receive enteral nutrition or intravenous dextrose solutions after a period of malnutrition. 21 Hypophosphatemia can be prevented by gradually increasing feeding to the full caloric requirements over several days and avoiding overzealous feeding of highcarbohydrate diets. Another cause of clinically significant hypophosphatemia is insulin therapy in patients with diabetic ketoacidosis.22,23 The problem usually manifests as acute hemolysis, lethargy, and weakness several days after insulin and fluid therapy begin. Hypophosphatemia may be caused or enhanced by aluminum hydroxide products that bind phosphorus in the gut, thereby decreasing its absorption.24 Sucralfate

also binds to phosphorus. These agents should be discontinued if the patient has hypophosphatemia and should not be used in animals prone to hypophosphatemia. For example, male cats with postobstructive diuresis may initially exhibit hyperphosphatemia and azotemia; however, hypophosphatemia may develop later as a result of excessive renal losses. Therefore, the use of phosphate binders in these animals should be avoided. support suggests hypophosAlthough the mechanism is unclear, hypophosphatemia can be an early sign of sepsis. Unexplained decreases in serum phosphorus should therefore prompt a search for infection.24 The decline in phosphorus may be secondary to the hypermetabolic state or respiratory alkalosis, both of which occur early in sepsis. When hypophosphatemia is causing clinical signs or when serum phosphorus levels drop below 1.0 mg/dl, the hypophosphatemia should be treated with intravenous replacement. Complications of intravenous replacement can include hyperphosphatemia, hypocalcemia, tetanic seizures, soft tissue mineralization, and hypotension secondary to rapid infusion.24 Phosphorus must be administered slowly and cautiously, and serum levels should be monitored every 6 hours. Replacement can be discontinued when serum levels reach 2.0 to 2.5 mg/dl. Potassium phosphate is available in a solution containing 3 mmol of phosphate (93 mg) and 4.3 mEq of potassium per milliliter. Most veterinary references recommend a dosage of 0.01 to 0.03 mmol/kg/hr to be given for 6 hours and continued for another 6 hours if the phosphorus levels remain low.21–24 This dosage is safe but may be inadequate for animals with severe depletion. A recommended dose for humans is 7.7 mg/kg/hr (0.025 mmol/kg/hr) administered over 4 hours.25 Potassium phosphate must be administered in calcium-free solutions, such as 0.9% saline instead of lactated Ringer’s solution. Although some texts recommend giving half of the potassium requirement as potassium phosphate, this protocol can result in phosphorus overdose because the potassium deficit greatly exceeds the phosphorus deficit in most patients.22 Phosphorus replacement (0.5 to 2 mmol/kg/day) can

NUTRITIONAL RECOVERY SYNDROME ■ SEPSIS ■ POTASSIUM PHOSPHATE

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safely be accomplished by the oral route if the patient is not exhibiting severe clinical signs. The phosphorus content of cow’s milk is 0.029 mmol/ml.20 Calcium phosphate tablets containing 580 mg of calcium, 450 mg of phosphorus, and 400 IU of vitamin D3 are also available.

ATPase, and proton pumps. It is essential for many metabolic functions, including ATP production and synthesis of nucleic acids and proteins. It helps regulate smooth muscle vascular tone and may influence lymphocyte activation and cytokine production.

Hyperphosphatemia Increases in serum phosphorus levels are most commonly seen in veterinary patients with renal failure.18 Decreased glomerular filtration rate results in phosphorus retention. Other causes include massive cellular damage (tumor lysis syndrome, rhabdomyolysis, snakebite, thromboembolism), hypoparathyroidism, and poisoning from hypertonic sodium phosphate enemas26 or vitamin D toxicity. Iatrogenic causes include overzealous phosphorus replacement or overdose of phosphorus-containing urine acidifiers. Mild elevations of phosphorus are considered normal in young, growing dogs. Clinical findings include diarrhea, hypocalcemia, tetany, hyperosmolality, hypernatremia, and an increased tendency toward metastatic calcification of soft tissues when the calcium–phosphorus product exceeds 58.18 Hyperphosphatemia also contributes to the progression of renal disease by stimulating renal secondary hyperparathyroidism.19 Hyperphosphatemia is treated with intravenous fluids to correct acidosis and promote phosphorus excretion. Fluids containing dextrose promote translocation of phosphorus into cells. Animals with renal failure should receive a low-phosphorus diet, and intestinal phosphate binders should be given with food to decrease absorption.

Hypomagnesemia Magnesium deficiency may result from decreased intake, increased losses, or alteration of distribution. Critically ill animals may be predisposed to hypomagnesemia because of stress, catabolic illness, nasogastric suctioning, peritoneal dialysis, total parenteral nutrition, diuretics, massive blood transfusion, or aggressive intravenous fluid therapy with magnesium-deficient fluids.31 Because similar conditions cause hypokalemia and/or hypophosphatemia, magnesium deficiency may be unrecognized and overlooked. In fact, concurrent hypokalemia may be refractory to aggressive potassium replacement until the magnesium deficit is corrected.28 Clinical signs of hypomagnesemia include cardiac arrhythmia, muscle weakness, tremors, seizures, altered mentation, esophageal motility disorders, and respiratory muscle paralysis.31 Normal serum magnesium concentrations range from 1.89 to 2.51 mg/dl.29 If an animal exhibits clinical signs (cardiac arrhythmia, muscle tremors, refractory hypokalemia) and serum magnesium levels are 1.2 mg/dl or lower, magnesium supplementation can be considered. Mild deficits can be corrected by intravenous fluids that contain magnesium. In cases of severe magnesium depletion, magnesium chloride or magnesium sulfate can be added to 5% dextrose in water at an initial dose of 0.75 to 1.0 mEq/kg/day and continued at half of the initial dose for 3 to 5 days.31 For life-threatening ventricular arrhythmia, digitalis-induced arrhythmia, or cardiac arrest, a dose of 0.15 to 0.3 mEq/kg (50 to 100 mg/kg) can be diluted in 5% dextrose or 0.9% saline and administered slowly intravenously over 5 to 15 minutes to raise the ventricular fibrillation threshold. Even when serum magnesium levels are normal, magnesium infusion should be considered for some animals with refractory tachyarrhythmia, especially when conventional therapy has failed.32 The lack of a reliable measure of total body magnesium tends to make therapy somewhat empirical. Potential side effects of intravenous magnesium therapy include hypocalcemia, hypotension, and cardiac conduction abnormalities (atrioventricular and bundle-branch blocks). Overdoses can be treated with calcium gluconate (10 to 50 mg/kg intravenously).31 Fortunately, it is difficult to cause prolonged hypermagnesemia because the kidneys can eliminate most of the excess magnesium.27

DISORDERS OF MAGNESIUM BALANCE Recent reports in human critical care medicine indicate a high incidence (>50%) of hypomagnesemia.27,28 Although serum magnesium in veterinary patients is seldom measured, certain critically ill animals are probably also at risk for magnesium imbalance. A recent report documented that magnesium imbalance was the most common electrolyte abnormality in 101 critically ill dogs admitted to the intensive care unit at Colorado State University: 30% had hypermagnesemia and 20% had hypomagnesemia.29 Magnesium is the second most abundant intracellular cation. Most of the total body magnesium is present in bone and skeletal muscle. Only 1% is in the serum. Unfortunately, because of the dynamic nature of magnesium homeostasis, serum magnesium measurements may not accurately reflect total body stores.30 In fact, serum levels can be normal despite magnesium depletion or excess. Magnesium is a coenzyme for Na+,K+-ATPase, Ca++-

GLOMERULAR FILTRATION RATE ■ ARRHYTHMIA ■ REFRACTORY TACHYARRHYTHMIA

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Magnesium (1 to 2 mEq/kg/day) can also be given orally. It is available as oxide or hydroxide.

Hypermagnesemia At present, hypermagnesemia is not considered to be clinically significant in critically ill animals unless there are associated signs of hypocalcemia. The most common cause is renal failure combined with overuse of magnesium-containing antacids. CONCLUSION Intensive management of critically ill animals, including such interventions as total parenteral nutrition, enteral nutrition, intravenous insulin, aggressive fluid therapy, nasogastric suctioning, massive blood transfusion, and peritoneal dialysis, can lead to severe electrolyte and acid–base abnormalities. Veterinarians must closely monitor potassium, phosphorus, and magnesium levels to detect and correct any life-threatening imbalances in these patients. About the Author Dr. Macintire is affiliated with the Department of Small Animal Surgery and Medicine, College of Veterinary Medicine, Auburn University, Alabama, and is a Diplomate of the American College of Veterinary Internal Medicine and the American College of Veterinary Emergency and Critical Care.

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tion of hydrogen ions with varying degrees of metabolic acidosis. J Clin Invest 36:373–382, 1957. Macintire DK: Emergency therapy of diabetic crises: Insulin overdose, diabetic ketoacidosis, and hyperosmolar coma. Vet Clin North Am Small Anim Pract 25:639–650, 1995. Schunk KL: Feline polymyopathy. Proc ACVIM:197–200, 1984. Dow SW, Le Couteur RA, Fettman MJ, et al: Potassium depletion in cats: Hypokalemic polymyopathy. JAVMA 191:1563–1568, 1987. Dow SW, Le Couteur RA, Fettman MJ, et al: Hypokalemia in cats: 186 cases (1984–1987). JAVMA 194:1604–1608, 1989. Tannen RL: Relationship of renal ammonia production and potassium homeostasis. Kidney Int 11:453–465, 1977. Tolins JP, Hostetter MK, Hostetter TH: Hypokalemic nephropathy in the rat: Role of ammonia in chronic tubular injury. J Clin Invest 79:1447–1458, 1987. Tilley LP: Essentials of Canine and Feline Electrocardiography, ed 2. Philadelphia, Lea & Febiger, 1985, pp 82, 86. Drobatz KJ: Serum electrolytes in cats with urethral obstruction. Proc 5th Annu Int Vet Emerg Crit Care Symp:24–27, 1996. Chew DJ, Meuten DJ: Disorders of calcium and phosphorus metabolism. Vet Clin North Am Small Anim Pract 12: 411–438, 1982. Berner VN, Shike M: Consequences of phosphate imbalance. Annu Rev Nutr 8:121–148, 1988. Solomon SM, Kirby DF: The refeeding syndrome: A review. J Parenter Enteral Nutr 14:90–97, 1990. Justin RB, Hohenhaus AE: Hypophosphatemia associated with enteral alimentation in cats. J Vet Intern Med 9: 228–233, 1995. Adams LG, Hardy RM, Weiss DJ, Bartges JW: Hypophosphatemia and hemolytic anemia associated with diabetes mellitus and hepatic lipidosis in cats. J Vet Intern Med 7:266–271, 1993. Willard MD, Zerbe CA, Schale WD, et al: Severe hypophosphatemia associated with diabetes mellitus in six dogs and one cat. JAVMA 190:1007–1010, 1987. Forrester SD, Moreland KJ: Hypophosphatemia: Causes and clinical consequences. J Vet Intern Med 3:149–159, 1989. Kingston M, Badawi AM: Treatment of severe hypophosphatemia. Crit Care Med 13:16–18, 1985. Atkins CE, Tyler R, Greenlee P: Clinical biochemical, acid–base, and electrolyte abnormalities in cats after hypertonic sodium phosphate enema administration. Am J Vet Res 46:980–988, 1985. Sachter JJ: Magnesium in the 1990’s: Implications for acute care. Top Emerg Med 14:23–29, 1992. Salem M: Hypomagnesemia in critical illness: A common and clinically important problem. Crit Care Clin 7:225–238, 1991. Wingfield W: Magnesium in critically ill animals. Proc 5th Int Vet Emerg Crit Care Symp:501, 1996. Martin LG, Van Pelt DR, Wingfield WE: Magnesium and the critically ill patient, in Kirk RW (ed): Current Veterinary Therapy. XII. Philadelphia, WB Saunders Co, 1995, pp 128–131. Dhupa N: Magnesium therapy, in Kirk RW (ed): Current Veterinary Therapy. XII. Philadelphia, WB Saunders Co, 1995, pp 132–133. Arsenian MA: Magnesium and cardiovascular disease. Prog Cardiovasc Dis 35:271–279, 1993.

HYPERMAGNESEMIA ■ HYPOCALCEMIA ■ MONITORING