0521779407-09 CUNY1086/Karliner 0 521 77940 7 June 13, 2007 7:54
Hypophosphatemia 795
tests
■Low serum phosphorus does not necessarily indicate total body
depletion as only 1% of body phosphorus is in blood.
■Basic blood tests: Serum phosphorus: (moderate=serum phosph
<2.5 mg/dl; severe <1.0 mg/dl)
■Basic urine tests: Diagnosis based on history, trend in phosphorus
values and blood pH (to distinguish acute shift), and urine phos-
phorus (<100 mg/day=GI loss or shift)
■Other tests: If urine phosphorus >100 mg/day, measure 24-h urine
for glucose, amino acids for Fanconi’s syndrome, and serum calcium
(high in primary hyperparathyroidism, low in vitamin D-resistant
rickets)
differential diagnosis
■Hypophosphatemia occurs because of 1) decreased intestinal
absorption, 2) increased urinary losses, and/or 3) extracellular to
intracellular shift. Severe hypophosphatemia is usually due to com-
bination of factors.
■Decreased intestinal absorption: antacid abuse, malabsorption,
chronic diarrhea, vitamin D deficiency, starvation, anorexia, alco-
holism
■Increased urinary losses: primary hyperparathyroidism, post renal
transplant, extracellular fluid volume expansion, glucosuria (after
treating DKA), post obstructive or resolving ATN diuresis, aceta-
zolamide, Fanconi’s syndrome, X-linked and vitamin D-dependent
rickets, oncogenic osteomalacia due to circulating phosphatonins
■Redistribution: respiratory alkalosis, alcohol withdrawal, severe
burns, TPN, recovery from malnutrition when inadequate phosph is
provided (post feeding syndrome), leukemic blast crisis
management
What to Do First
■Assess severity and symptoms so as not to overtreat hypophos-
phatemia due to cellular shifts.
General Measures
■If possible, treat orally to avoid metastatic calcification.
specific therapy
■Indications: Only treat symptomatic severe hypophosphatemia with
intravenous agents. Otherwise choose oral agent. Phosph comes as