A. Does patient have any acute symptoms related to hypophosphatemia? Patients with moderate to severe hypophosphatemia (< 1 mg/dL) may have many systemic manifestations and need to be promptly treated. Symptoms can include cardiomyopathy with heart failure; muscle weakness that can lead to rhabdomyolysis; hemolysis; and encephalopathy, seizures, and coma.
B. Are there acute factors that have resulted in severe hypophosphatemia? Most cases of hypophosphatemia result from a shift of phosphate from extracellular to intracellular fluid. Factors causing this shift can be severe and life threatening and include refeeding syndromes and treatment of diabetic ketoacidosis (DKA).
C. Pertinent Historical Information. Ask about diet, medications, underlying conditions, and relevant family history.
III. Differential Diagnosis. Hypophosphatemia usually results from one of the following processes: shift of phosphate into the intracellular compartment, renal losses, or GI losses. Changes can be acute, chronic, or a combination.
A. Transcellular Shift From Extracellular to Intracellular Compartment
1. Nutritional repletion or refeeding syndrome. Can occur with enteral or parenteral nutrition in patients who are malnourished or those with anorexia nervosa or AIDS.
2. DKA and insulin therapy. Renal losses are also involved.
3. Respiratory alkalosis. Increased renal losses are also present.
4. Sepsis. Especially gram-negative and toxic shock syndrome.
5. Leukemia with blast crisis.
B. Increased Urinary Losses
1. Renal tubular defects. Fanconi syndrome (may be primary or acquired), X-linked hypophosphatemic (XLH) rickets, post-renal transplantation status.
2. Hyperparathyroidism. Primary (rare in children) or secondary to vitamin D deficiency or other nonrenal causes.
3. Diuretic phase of acute tubular necrosis (ATN).
4. Postobstructive diuresis.
5. Post-renal transplantation status.
C. Increased GI Losses
2. Decreased intake. Starvation, anorexia nervosa, protein-calorie malnutrition. At high risk for refeeding syndrome (see III, A, 1, earlier). Premature infants require phosphate supplementation.
3. Malabsorption syndromes.
4. Vitamin D deficiency. Low levels of vitamin D due to dietary deficiency or lack of sunshine, malabsorption, or liver disease.
5. Vitamin D-dependent rickets. Block in 1,25-dihydroxyvita-min D formation (type 1) or abnormal receptor (type 2).
1. Vital signs and general appearance a. Temperature. Severe hyperthermia can cause hypophos-phatemia through transcellular shift. Fever may be a sign of sepsis or toxic shock.
b. Respiratory rate. May be a sign of respiratory alkalosis.
c. Body mass. Look for evidence of malnutrition or short stature, as well as cystinosis or congenital Fanconi syndrome.
2. Heart. Look for evidence of heart failure as result of severe depletion.
3. Neuromuscular. Assess for confusion, coma, and muscle weakness. Muscle tenderness may be a sign of rhabdomy-olysis.
4. Skeletal. Look for bowing, rachitic rosary, and flared growth plates at wrists and knees as sign of rickets.
5. Skin. Large café au lait spots may point to McCune-Albright syndrome.
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