P 2.3 - 4.0 LOW
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HYPOPHOSPHATEMIA, a serum phosphorus level less than 3.0 mEq/L. Phosphorpus is a mineral that is involved n many organ systems to inluce cellular membrane sturctures, the clotting cascade, bone mineralization, immune function and others. Symptoms include rhabdomyolysis, metabolic acidosis, respiratory failure, weakness, paresthesias, myalgias, osteomalacia, respiratory failure (may be a reason in patients who have difficulty being weened from ventilator support), hemolysis, dysarthria, confusion, stupor, seizure, and coma. Symptoms usually manifest at levels less than 1mEq/L as depletion of intracellular ATP and erythrocyte 2, 3-DPG result. A reduction of intracellular ATP results in end organ dysfunction, and hypoxia is the result of a reduced level of erythrocyte 2, 3-DPG.
Hypophosphatemia can occur in the presence of low, normal or high total body phophorous, and conversely, total body phophorous depletion can exist in the presence of low, normal or high serum phosphorous values. The three major mechanisms resulting in hypophophatemia include decreased intestinal absorption, internal redistribution, and increased renal phosphate wasting. Intestinal phosphorous absorption occurs in the duodenum and jejunum. Elevated 1, 25-dihydroxyvitamin D and parathyroid hormone levels serve to increase intestinal absorption. Serum phosphorous levels are regulated mainly by moderating renal excretion.
Severe malmutrition, excessive ingestion of phosphate binders, vitamin D deficiency/resistence, malabsorption, and prolonged secretory diarrhea all are associated with decreased intestinal absorption. Cellular redistribution, which is the most frequent cause of hypophosphatemia, results during intavenous glucose or insulin administration, the refeeding period after malnutrition, recovery from DKA, respiratory alkalosis, certain medications (insulin, glucagon, epinephrine, dopamine, beta 2 agonists, steroids, and xanthine derivatives), and conditions associated with increased cellular proliferation (hungry bone syndrome, acute leukemia, Burkitt lymphoma, Epogen therapy). Increased urinary loss results from hyperparathyroidism (both primary and secondary), paraneoplastic hypercalcemia (PTH rP driven), hypomagnesemia, hypokalemia, alkalosis, and Fanconi's syndrome, and may also be seen in patients who have had a renal transplant. A 24-hour urinary phosphorus level greater than 100 mg/dayor a fractional excreation of phophate greater than 5% in the face of hypophosphatemia are indicative of excessive renal phosphorus excretion.
Phosphorous should be followed closely when refeeding patients with anorexia nervosa or bulimics and when giving hospital care to chronic alcoholics. Hypophophatemia associated with bone pain and a low 1,25-dihydroxyvitamin D level should raise suspicion for underlying tunor-induced osteomalacia (oncogenic osteomalacia).
Hypophosphatemia in a patient with DKA usually requires no specific treatment other than correcting the DKA. Therapy for moderate hypophosphatemia (1. 0-2. 5 mg/dL) includes oral supplementation with either Neutra-Phos, Neutra-Phos K, or Phospho-Soda. Therapy for severe hypophosphatemia (less than 1. 0 mg/dL) entails intravenous phosphorus replacement with either potassium phosphate or sodium phosphate. An infusion of 0.08-0.16 mmol/kg phosphate (2. 5-5.0 mg elemental phosphorus/kg) in 500 ml of 0.45% saline should be given over 6-12 hours. During intravenous replacement therapy, serum levels of calcium, phosphorus, and potassium should be measured every 6 hours.