Hypophosphatemia
Hypophosphatemia has many causes and is severe when serum phosphorus
levels fall below 1.0 mg/dL. Conditions causing such low phosphate levels include
prolonged respiratory alkalosis and rapid cellular uptake. Severe hypophosphatemia
with total-body deficiency usually reflects poor dietary intake or consumption of
phosphate-binding antacids, or both.
Hypophosphatemia occurs in alcoholism (50% of hospitalized alcoholics),
ketoacidosis, osmotic diuresis, acidosis, and catabolic states. Depressed intake
or absorption and increased urinary losses are common causes. In chronic alcoholics,
reduction of the phosphorus content of skeletal muscle occurs as a result of renal
phosphate loss. The hypophosphatemic syndrome includes phosphate trapping, rhabdomyolysis,
cardiomyopathy, respiratory insufficiency from profound muscle weakness, erythrocyte
and leukocyte dysfunction, skeletal demineralization, metabolic acidosis, and nervous
system dysfunction ( Table 46-15
).
Before initiating treatment, the cause of hypophosphatemia should
be clearly identified with measurement
TABLE 46-14 -- Major causes of hyperphosphatemia
Causes |
Mechanisms |
Binding to serum proteins |
Including plasma cell dyscrasias |
Decreased renal excretion |
Renal insufficiency; hypoparathyroidism; pseudohypoparathyroidism,
types I and II; tumoral calcinosis; pseudoxanthoma elasticum; infantile hypophosphatasia;
hyperostosis; hyperthyroidism; adrenal insufficiency; bisphosphonate therapy |
Increased intestinal absorption |
Phosphorus-containing cathartics; medication with vitamin D compounds;
granulomatous disease producing vitamin D, including sarcoidosis and tuberculosis |
Internal redistribution |
Acute metabolic or respiratory acidosis; reduced insulin level;
clonidine administration |
Cellular release |
Rhabdomyolysis; organ infarction; tumor lysis as in Burkitt's
or lymphoblastic lymphomas or metastatic small cell carcinoma |
Parenteral administration |
Intravenous phosphate salts; lipid (phospholipid) infusion |
Adapted from Potts JT: Diseases of the parathyroid
gland and other hyper- and hypocalcemic disorders. In
Isselbacher KJ, Braunwald E, Wilson JD, et al (eds): Harrison's Principles of Internal
Medicine, 13th ed. New York, McGraw-Hill, 1995, p 2186. |
of arterial blood gases and the concentrations of ionized calcium, magnesium, potassium,
and serum and urinary phosphorus. Phosphate salts such as sodium or potassium phosphate
are available for oral or intravenous administration. Multiplying the volume of
distribution (400 mL/kg) by the desired change in inorganic phosphate provides the
total amount to be administered. The rate of intravenous administration should not
exceed 0.25 mmol/kg over 4 to 6 hours to avoid hypocalcemia and tissue damage. Oral
supplementation is often limited to 30 mmol/day (1 g/day) because of the induction
of diarrhea. Hyperphosphatemia should be avoided because it can cause hypocalcemia
and crystal deposition in the eyes, heart, lung, blood vessels, and kidneys. Most
hypophosphatemic patients, such as those with diabetic ketoacidosis or recovering
from exercise, are not severely phosphorus depleted unless they have been sick for
an extended time. They may typically be treated with a glass of milk (100 mg/dL
or 33 mmol/L of phosphorus). After achieving normal serum phosphate levels, the
TABLE 46-15 -- Major causes of hypophosphatemia
Chronic alcoholism and alcohol withdrawal |
Dietary deficiency and phosphate-binding antacids |
Severe thermal burns |
Recovery from diabetic ketoacidosis |
Hyperalimentation |
Nutritional recovery syndrome |
Respiratory alkalosis |
Therapeutic hyperthermia |
Neuroleptic malignant syndrome |
Recovery from exhaustive exercise |
Renal transplantation |
Acute renal failure |
Adapted from Potts JT: Diseases of the parathyroid gland
and other hyper- and hypocalcemic disorders. In
Isselbacher KJ, Braunwald E, Wilson JD, et al (eds): Harrison's Principles of Internal
Medicine, 13th ed. New York, McGraw-Hill, 1995, p 2185. |
concentrations of serum inorganic phosphate and ionized calcium and a 24-hour urine
sample should be monitored to ensure that balance has been achieved.