People have substantial variations in serum phosphorus concentrations throughout the day. One millimole of phosphate contains 31 mg of elemental phosphorus. Currently, it seems safest to administer phosphate by constant-rate infusion at rates that have been used successfully in dogs and cats and to monitor the serum phosphorus concentration every 6 to 8 hours. Phosphorus plays an essential role in cellular structure and function. Check the full list of possible causes and conditions now! All animals absorb potassium through the gastrointestinal tract and then excrete it through the kidneys. In many ways, they may not be as robust as their wild ancestors”. bran or “big head” disease in horses ). Hypomagnesemia frequently is found in hypophosphatemic people, but the reasons for this association are not clear.32. At a pH of 7.4, the HPO42−:H2PO41− ratio is 4.0, and the average valence of phosphate in serum reflects this ratio. J Am Vet Med Assoc 234(8):1041-1048 ↑ Dhupa N & Proulx J (1998) Hypocalcemia and hypomagnesemia. Administering phosphate intravenously is potentially dangerous because it may cause hypocalcemia, tetany, soft tissue mineralization, renal failure, or hyperphosphatemia.88 Therefore, phosphorus administration typically has consisted of injecting small amounts slowly over hours to days and monitoring the patient repeatedly (e.g., 0.01 to 0.06 mmol/kg/hr in dogs and cats with measurement of serum phosphorus concentration every 6 to 8 hours).80,173 Although such caution is wise, it is noteworthy that more aggressive phosphorus administration has been used in people (i.e., 0.16 to 0.64 mmol/kg over 4 to 12 hours in patients receiving total parenteral nutrition).32 Other groups have used similarly large doses over even shorter times (e.g., 0.4 to 0.8 mmol/kg depending on the degree of hypophosphatemia over 30 minutes in patients with cardiac disease), also without problems.180 Sodium phosphate and potassium phosphate are commonly used, but administration of glucose phosphate also has been reported.180 Selection of the particular form of phosphorus to administer is based on the patient’s serum electrolyte concentrations. Mild to moderate phosphorus depletion can effectively be treated by oral phosphorus supplementation, either by adding dairy products to the diet or by providing solutions of sodium-phosphate salts for oral consumption. Intestinal phosphate absorption occurs via two mechanisms. Symptoms are generally consistent with the primary disease that is responsible for the hypophosphatemia, rather than any that would be related to the phosphate concentration itself. Prophylactic parenteral phosphate therapy (such as may be used for patients with diabetic ketoacidosis) may be reasonably estimated by giving one fourth to one half of the supplemented potassium as potassium phosphate and the rest as potassium chloride. They did not become hypophosphatemic, their CPK remained normal, and derangements of cellular Na, Cl, and H(2)O were rapidly corrected. However, decreased urinary phosphate excretion that develops during hypophosphatemia may persist during treatment and predispose to hyperphosphatemia. Although believed to be important in some pathologic conditions, their impact in normal phosphorus homeostasis is currently uncertain. Hypophosphatemia is often associated with: Acute mild hypophosphatemia if often subclinical in effect, but severe hypophosphatemia can result in muscle weakness, myalgia, seizures, rhabdomyolysis, intravascular hemolysis and death. Dogs and cats need to ingest 0.5 to 3.0 g of phosphorus per day, depending on their body size and energy requirements. * If 2.5 mg/dL is considered the lower limit of normal, serum phosphorus concentration was decreased in approximately one third of reported cases associated with parathyroid adenoma, but in six of six cases associated with parathyroid hyperplasia. The clinician should keep in mind that oversupplementation (especially but not exclusively parenteral) can cause morbidity (e.g., hypocalcemia, soft tissue calcification, renal failure). In fact, hypophosphatemia in people with hepatic damage has been suggested to reflect healing and regeneration of the liver.144 Hypophosphatemia has been seen in dogs experimentally intoxicated with xylitol,176 but it is uncertain whether hypophosphatemia is due to hepatic damage or to other metabolic effects of xylitol. The source of dietary phosphorus markedly affects absorption and excretion of phosphorus in cats. During phosphate deprivation, the kidneys dramatically reduce phosphate excretion to negligible amounts in fewer than 3 days. Normal serum phosphorus concentrations in adult dogs range from 2.5 to 6.0 mg/dL, but they are higher in dogs younger than 1 year.17,77,131,175 Serum phosphorus concentrations are highest in puppies less than 8 weeks of age (up to 10.8 mg/dL may be considered normal) and gradually decrease into the adult range after 1 year of age.73 Sex-related changes are not reported.134 The effect of age is less pronounced in cats, but immature cats have a tendency for higher serum concentrations.32 Bone growth and an increase in renal tubular reabsorption of phosphorus mediated by growth hormone presumably contribute to this age effect. However, as these patients frequently require nutritional supplementation (either enteral or parenteral), the need to avoid the refeeding syndrome was noted. Bones are a safe source of dietary calcium and if dogs eat enough of them, the diet will be balanced without a lot of difficult calculations. Even though phosphorus circulates in organic and inorganic forms, clinical laboratories typically measure inorganic phosphate. To examine this possibility, a subclinical muscle cell injury was induced in 23 dogs by feeding them a phosphorus- and calorie-deficient diet until they lost 30% of their original weight. Interestingly, infusion of a higher concentration (e.g., 10% dextrose) for a shorter time seems to be less detrimental than infusing 4% glucose continuously.99 Malnourished patients receiving total parenteral nutrition are particularly susceptible to hypophosphatemia because of the accelerated rate of tissue repair as phosphate is incorporated into new cells and phosphate use during glycolysis.88,136 Hypophosphatemia as part of the “refeeding syndrome” (i.e., severe electrolyte changes in malnourished patients that are being fed parenterally or enterally) was more likely in patients that were more severely emaciated, had lower initial serum phosphate concentrations, and experienced more aggressive initial infusion of parenteral nutrition.107 Respiratory alkalosis likewise causes translocation because it stimulates glycolysis by activating phosphofructokinase.88 This effect has been demonstrated in experimental dogs but was marked only when hyperventilation was combined with glucose administration.19 Increased intracellular pH may be more important than increased extracellular pH for causing hypophosphatemia in respiratory alkalosis, which could explain why severe hypophosphatemia may occur in people with severe respiratory failure who are mechanically ventilated.99, Diabetic patients are especially at risk for hypophosphatemia. Dr Billinghurst explains: Approximate biological balance is achieved so long as meat alone is not the principal dietary component. Adult … Intestinal alkaline phosphatases may facilitate absorption by freeing inorganic phosphate for transport. The volume of distribution for administered phosphate varies tremendously among hypophosphatemic people, and redistribution of phosphate can occur rapidly. Cats with decreased serum concentrations of cobalamin and folate have been found to be at increased risk for hypophosphatemia. Hypophosphatemia can occur even when total body phosphorus is normal. At a pH of 7.4, 1 mmol of phosphate equals 1.8 mEq, and conversion from millimoles per liter to milliequivalents per liter requires multiplication by 1.8. Passive absorption is largely dependent on the phosphorus content of the diet as well as the type of protein. Normally, 80% to 90% of the filtered phosphate load is reabsorbed by the renal tubules, and renal dysfunction is the most common cause of hyperphosphatemia beside that found in young dogs. It is more common and can be particularly severe after hepatic surgery, especially major resection and transplantation. The average phosphorus content of commercial pet foods is approximately 1% on a dry matter basis. The products available for oral and parenteral use are summarized in Tables 7-1 through 7-3. However, stratification of the cats into ketoacidotic and nonketoacidotic groups revealed that 5 of 38 ketoacidotic cats were hypophosphatemic and only 2 of 66 nonketotic cats were hypophosphatemic.39 Interestingly, serum phosphorus concentrations are often normal to increased at presentation in diabetic people, perhaps because of metabolic acidosis by organic acids (e.g., β-hydroxybutyrate), insulin deficiency, osmotic effects of hyperglycemia, or renal insufficiency.86,119, Administration of large doses of insulin makes hypophosphatemia even more likely in diabetic ketoacidotic patients. If oral supplementation is suitable (which is uncommon in patients with severe hypophosphatemia), it may be safer and therefore preferable to parenteral supplementation. Active mucosal phosphate transport is a sodium-dependent, saturable carrier-mediated process. Approximately 80% to 85% of total body phosphate is inorganic hydroxyapatite in bone, whereas 15% is in soft tissues such as muscle.59,88 Most soft tissue phosphorus is organic and can be readily converted to the inorganic form as needed. Changing the diet from a phosphorus-restricted diet to a maintenance diet plus supplementing sodium phosphate orally corrected the problem. Intravenous administration of saccharated ferric oxide to treat iron deficiency has caused hypophosphatemia in people. See if there is a diet that can improve the quality of life of people with Hypophosphatasia, recommended and to avoid food when having Hypophosphatasia Postsurgical hypophosphatemia is a well-established problem in people. More than one has been identified. Disorders of renal tubular phosphate transport associated with hypophosphatemia in humans include X-linked hypophosphatemia, autosomal dominant hypophosphatemic rickets, oncogenic hypophosphatemic osteomalacia, and hereditary hypophosphatemic rickets with hypercalciuria. Although vomiting and malabsorptive diseases potentially can cause phosphate loss, these disorders rarely cause hypophosphatemia in dogs or cats.31 Canine malabsorptive intestinal disorders often are characterized by hypocalcemia related to hypoalbuminemia, but serum phosphorus concentrations typically are normal.20,55. Active transport is increased by the presence of calcitriol primarily in the presence of hypophosphatemia. Platelet-associated abnormalities include shortened survival time, impaired clot retraction, megakaryocytosis in the bone marrow, and thrombocytopenia. To convert milligrams per deciliter to millimoles per liter, divide milligrams per deciliter by 3.1. 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