Hyperphosphatemia in Emergency Medicine Clinical Presentation

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

History

Patients with hyperphosphatemia most commonly complain of muscle cramping secondary to low calcium levels. This may progress to tetany, delirium, and seizures. A search for the following historical clues may help identify those patients at risk for increased phosphorus levels.

  • Renal disease
    • Past or present hemodialysis
    • Adherence to renal (low phosphorus) diet
    • Use of oral phosphate binders
  • Cancer
    • Leukemia
    • Lymphoma
    • Bone tumors
    • Other cancers
    • Chemotherapy treatment
  • Endocrinopathies
  • Trauma
  • Burns or heat-related illnesses
  • Prolonged immobilization
  • Metabolic or hematologic disorders including genetic predisposition
  • Medications
    • Oral phosphate binders
    • Potassium phosphate
    • Antacid use
    • Bisphosphonate therapy
  • Use of laxatives (oral/rectal) and enemas
  • Use of nutritional supplements or hyperalimentation
  • Ischemic bowel (possible phosphorus elevations)
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Physical

The nervous and cardiovascular systems are most commonly affected.

  • CNS
    • Altered mental status
    • Delirium
    • Obtundation
    • Coma
    • Convulsions and seizures
    • Muscle cramping or tetany
    • Neuromuscular hyperexcitability (ie, Chvostek and Trousseau signs)
    • Paresthesias (particularly perioral and distal extremities)
  • Cardiovascular system
    • Hypotension and heart failure
    • Prolongation of the QT interval
  • Ocular - Cataracts
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Causes

Phosphorus balance between intracellular and extracellular compartments and between bone and other tissues may be influenced by many factors. The most common cause of hyperphosphatemia is decreased renal excretion due to renal insufficiency from any cause. All marked elevations of phosphorus involve significant addition of phosphorus to the extracellular compartment, usually with some impairment of renal function.

  • Renal insufficiency (acute or chronic)
  • Medications - Liposomal amphotericin B
  • Increased catabolism or cellular injury
    • Rhabdomyolysis
    • Trauma, burns, crush injuries, shock
    • Exhaustive exercise
    • Prolonged immobilization
    • Heat-related illnesses
    • Malignant hyperthermia
    • Hypothermia
    • Massive hemolysis
    • Severe infections
    • Ischemic bowel
  • Endocrinopathies
    • Hypoparathyroidism
    • Pseudohypoparathyroidism
    • Abnormal parathyroid hormone
    • Acromegaly and other causes of growth hormone excess
    • Thyrotoxicosis
    • Glucocorticoid withdrawal or deficiency
  • Poisoning, excessive intake or administration
    • Bisphosphonate therapy
    • Vitamin D intoxication or other causes of increased vitamin D (sarcoidosis)
    • Ingestion or administration of phosphate salts (eg, oral/rectal laxatives, enemas, intravenous phosphate)
    • Hyperalimentation (including lipid administration)
    • White phosphorous burns
    • Milk-alkali syndrome
    • Transfusion of outdated blood
  • Neoplasms
    • Leukemia
    • Lymphoma
    • Bone tumors
    • Tumor lysis after chemotherapy
  • Acidosis
  • Alkalosis
  • Miscellaneous
    • Tumoral calcinosis
    • Cortical hyperostosis
    • Syndrome of familial intermittent hyperphosphatemia
    • Hyperbilirubinemia (controversial as cause)
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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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