Since phosphorus is abundant in many foods and readily absorbed, hypophosphatemia is relatively unusual. Mechanisms leading to hypophosphatemia are reduced oral intake, excessive loss, or shift from the ECF into cells. Significant hypophosphatemia is unlikely to be encountered in the ED, because it is most often associated with hyperalimentation. There may be a shift into cells seen with alkalosis (respiratory or metabolic). Alcoholics may be in a sufficiently poor nutritional state that hypophosphatemia becomes an issue. Other conditions that may on occasion present to the ED with complications related to phosphate depletion include hyperparathyroidism, malignancy with hypercalcemia (phosphaturia), renal tubular defects, and use of phosphate-binding antacids. As explained earlier, hypokalemia and hypomagnesemia are likely to be associated with hypophosphatemia. Conditions unlikely to be seen in ED practice but associated with hypophosphatemia include rapid healing, prolonged anabolic states, recovery from starvation or severe burns, and partial hepatectomy.
Redistribution phenomena also can occur with glucose infusion. Phosphorus is consumed during phosphorylation as glucose moves into cells. This is one of the theoretical reasons why potassium phosphate is advocated as part of K+ replacement regimens in the treatment for diabetic ketoacidosis. However, it should not be the initial form of K+ replacement in the ED, as significant hypophosphatemia is unlikely to occur for 12 to 24 h, and parenteral administration may cause precipitous falls in serum [Ca2+]. (Also see Chap,.203, "Diabetic Ketoacidosis.")
DIAGNOSIS Symptoms of hypophosphatemia are unlikely to appear until levels are quite low, usually less than 1 mg/dL. Patients with diabetic or alcoholic ketoacidosis or severe malnutrition may develop complications of hypophosphatemia. It should be particularly sought as a potential complication 12 to 24 h after initiating treatment for diabetic ketoacidosis and 24 to 96 h after treatment for alcoholic ketoacidosis. Detecting total body depletion cannot reliably be ascertained from blood phosphorus levels, as the ratio of intracellular to extracellular phosphorus is approximately 100:1.
PHYSIOLOGIC EFFECTS The most frequent consequences of hypophosphatemia are hematologic and neuromuscular. Hypophosphatemia may be associated with depletion of ATP in platelets, red blood cells, and white blood cells, reducing their survival time and function. Platelet membrane changes may result in a bleeding tendency due to impaired aggregation. Phosphate deficiency also causes a tendency for red blood cells to become rigid spherocytes, thereby impairing capillary perfusion. In addition, decreased 2,3-diphosphoglycerate (2,3-DPG) increases the affinity of hemoglobin for oxygen, thereby reducing the arterial P o2 and oxygen availability to tissues. Phosphate depletion in macrophages may impair chemotaxis, phagocytosis, and intracellular killing, resulting in decreased resistance to infection.
Progressive weakness and tremors may be noted as blood phosphate levels fall below 0.5 to 1.0 mg/dL. Circumoral and fingertip paresthesias may be present along with absent deep tendon reflexes. Mental obtundation, anorexia, and hyperventilation may also occur. Myocardial function, as measured by left ventricular stroke work, may also be impaired.
TREATMENT Fortunately, phosphate deficiency is easily reversible by correcting the underlying disorder and replacing phosphorus. Milk is an excellent source of phosphorus and contains 1000 mg/L. Tablets come in the form of sodium or potassium phosphate and must be given in divided doses.
For severe hypophosphatemia with blood levels less than 1.0 mg/dL (0.32 mmol/L) or symptoms, immediate IV replacement is required. Otherwise, oral preparations can be often used.
If the hypophosphatemia is recent and uncomplicated, the initial recommended daily dose is 2.5 mg/kg. Prolonged or multifactorial hypophosphatemia may require 5 mg/kg. Up to 25 to 50 percent more phosphorus is needed if a patient is symptomatic; however, less is required in the presence of hypercalcemia. Each dose is administered IV over 6 h, and serum phosphorus is checked after each dose. To minimize the risks of hyperphosphatemia, a total dose of no more than 7.5 mg/kg should be administered.
Risks of phosphate therapy include hypocalcemia, metastatic calcification, hypotension, and hyperkalemia from the potassium salts. One should switch to oral therapy as soon as possible.
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