Hyperphosphatemia in Emergency Medicine Treatment & Management

  • Author: Leigh A Patterson, MD; Chief Editor: Erik D Schraga, MD   more...
 
Updated: Jun 7, 2010
 

Prehospital Care

  • The diagnosis of hyperphosphatemia is rarely evident in the prehospital setting. No specific disease-directed prehospital management is indicated.
  • In patients without a history of renal failure or evidence of cardiac compromise, volume repletion may be initiated.
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Emergency Department Care

Most symptoms and sequelae are due to secondary hypocalcemia. Initial care is aimed at management and correction of the hypocalcemia and its sequelae. Endpoints of therapy include resolution of symptoms and a serum calcium level within the low reference range.

  • A secondary goal is to decrease the incidence of sequelae, which requires reducing serum phosphate to nearly normal levels, less than 5.5 mg/dL, and maintaining the calcium phosphate product less than 60.
  • The ultimate goal is resolution of the underlying disease state responsible for the hyperphosphatemia.
  • Saline diuresis and treatment of the primary cause usually lead to improvement.
  • Hypocalcemia is treated directly when symptoms arise.
  • Patients with symptomatic hypocalcemia and those with a corrected serum level of 1.875 mmol/L or less should be treated with parenteral calcium. The rate and extent of calcium replacement is determined clinically, based on the severity of the symptoms.
  • Calcium replacement carries a theoretical risk of acceleration of metastatic calcification, but the clinical significance of this risk is not known.
  • Oral binders are given to decrease GI absorption of phosphorus. Binders containing calcium may cause hypercalcemia and promote vascular calcium deposition by increasing the calcium-phosphate product. Resin binders like sevelamer (Renagel) promote phosphorus excretion without affecting calcium. Sevelamer has been shown to decrease incidence of vascular calcium deposition in patients with renal failure. Phosphate binders containing aluminum should be avoided in patients with renal failure due to a heightened potential for aluminum toxicity. Diuretics that act on the proximal renal tubules, such as acetazolamide, may be considered to increase urinary excretion.
  • Hemodialysis or peritoneal dialysis is indicated for severe refractory cases and for patients with renal failure. As with hyperkalemia, glucose and insulin may force translocation of intracellular phosphorus, and this can be a useful temporizing measure.
  • For toxic ingestions, gastric lavage and oral phosphate binders are given to prevent further absorption.
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Consultations

  • Nephrology consultation is necessary for patients with renal failure.
  • Poison control consultation is helpful for poisonings involving phosphorus.
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Contributor Information and Disclosures
Author

Leigh A Patterson, MD  Assistant Professor, Residency Director, Department of Emergency Medicine, Brody School of Medicine at East Carolina University

Leigh A Patterson, MD is a member of the following medical societies: American College of Emergency Physicians, American Institute of Ultrasound in Medicine, American Medical Association, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Coauthor(s)

Peter MC DeBlieux, MD  Professor of Clinical Medicine and Pediatrics, Section of Pulmonary and Critical Care Medicine, Program Director, Department of Emergency Medicine, Louisiana State University School of Medicine in New Orleans

Peter MC DeBlieux, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Emergency Medicine, American College of Emergency Physicians, American Medical Association, Radiological Society of North America, and Society of Critical Care Medicine

Disclosure: Nothing to disclose.

Specialty Editor Board

Robin R Hemphill, MD, MPH  Associate Professor, Director, Quality and Safety, Department of Emergency Medicine, Emory University

Robin R Hemphill, MD, MPH is a member of the following medical societies: American College of Emergency Physicians and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD  Senior Pharmacy Editor, eMedicine

Disclosure: eMedicine Salary Employment

Jeffrey L Arnold, MD, FACEP  Chairman, Department of Emergency Medicine, Santa Clara Valley Medical Center

Jeffrey L Arnold, MD, FACEP is a member of the following medical societies: American Academy of Emergency Medicine and American College of Physicians

Disclosure: Nothing to disclose.

John D Halamka, MD, MS  Associate Professor of Medicine, Harvard Medical School, Beth Israel Deaconess Medical Center; Chief Information Officer, CareGroup Healthcare System and Harvard Medical School; Attending Physician, Division of Emergency Medicine, Beth Israel Deaconess Medical Center

John D Halamka, MD, MS is a member of the following medical societies: American College of Emergency Physicians, American Medical Informatics Association, Phi Beta Kappa, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Chief Editor

Erik D Schraga, MD  Staff Physician, Department of Emergency Medicine, Mills-Peninsula Emergency Medical Associates

Disclosure: Nothing to disclose.

References

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Approximately 60-70% of dietary phosphate, 1000-1500 mg/d, is absorbed in the small intestine. Although vitamin D can enhance the absorption, especially under conditions of dietary phosphate depletion, intestinal phosphate absorption is generally unregulated. Specifically, high serum phosphate and high dietary phosphate intake do not significantly impair intestinal uptake. The movement of phosphate in and out of bone, the reservoir containing most of the total body phosphate, is generally balanced. Renal excretion of excess dietary phosphate intake ensures maintenance of phosphate homeostasis, maintaining serum phosphate at a level of approximately 4.5 mg/dL in the serum.
The vast majority of filtered phosphate is reabsorbed by type 2a sodium phosphate cotransporters located on the apical membrane of the renal proximal tubule. The expression of these cotransporters is increased by low dietary phosphate intake and several growth factors to enhance phosphate absorption. The expression is decreased by high dietary phosphate intake, parathyroid hormone, and dopamine. Phosphate absorption in the remainder of the nephron is generally mediated by type 1 or 3 sodium phosphate cotransporters. No direct evidence related to regulation of these transporters in renal cells under physiologic conditions has been found. The absorption in the proximal tubule is regulated such that the final excretion matches the dietary excess in order to maintain homeostasis.
Hyperphosphatemia inhibits 1-alpha hydroxylase in the proximal tubule, thus inhibiting the conversion of 25-hydroxy vitamin D3 to the active metabolite, 1,25 dihydroxyvitamin D3. The decrease in active vitamin D production is somewhat offset by the ability of hyperphosphatemia to stimulate the secretion of parathyroid hormone (PTH), which increases the activity of 1-alpha hydroxylase. The result is generally a neutral effect on intestinal phosphate absorption. Hyperphosphatemia-stimulated PTH secretion is mediated through an as yet unidentified pathway. With normal renal function, the transient increase in PTH and decrease in vitamin D serve to inhibit renal and intestinal absorption of phosphate, resulting in resolution of the hyperphosphatemia. In contrast, under conditions of renal failure, sustained hyperphosphatemia results in sustained hyperparathyroidism.The hyperparathyroidism enhances renal phosphate excretion but also enhances bone resorption, releasing more phosphate into the serum. As renal failure progresses and the ability of the kidney to excrete phosphate continues to diminish, the action of PTH on the bone can exacerbate the already present hyperphosphatemia.
 
 
 
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