eMedicine Specialties > Emergency Medicine > Endocrine & Metabolic

Hypophosphatemia: Treatment & Medication

Author: Devon J Moore, MD, Resident Physician, Department of Emergency Medicine, Wayne State University Detroit Medical Center, Detroit Receiving Hospital
Coauthor(s): Adam J Rosh, MD, MS, Assistant Professor, Department of Emergency Medicine, Wayne State University/Detroit Receiving Hospital
Contributor Information and Disclosures

Updated: Sep 22, 2009

Treatment

Emergency Department Care

  • Treatment of hypophosphatemia is twofold.
    • Correct any precipitating causes of hypophosphatemia.
    • Replace total body phosphates.
  • Depending on the clinical situation, replacement options include dietary phosphate, oral phosphate preparations, and IV phosphate.
  • Hypophosphatemia and hypokalemia can coexist in certain disorders like diabetic ketoacidosis and alcoholism, so replacement with the potassium salt is most appropriate.
  • The most important consideration in choosing replacement therapy is whether the patient has signs or symptoms of phosphate depletion.
  • Mild to moderately severe, asymptomatic hypophosphatemia
    • Mild to moderately severe, asymptomatic hypophosphatemia may require oral phosphate replacement; however, correcting factors that led to the hypophosphatemia usually is sufficient.
    • In most asymptomatic patients, the serum phosphate level spontaneously normalizes over several days when factors inducing hypophosphatemia are corrected.
    • In patients with minimal symptoms or moderate hypophosphatemia (serum phosphate 1-2 mg/dL), providing oral phosphate replacement may be desirable.
    • The average adult consumes 1 gram of phosphorus daily. A quart of cow's milk provides this amount of phosphorus (1 mg phosphorus/mL). Dairy products have an additional advantage of supplying absorbable calcium, which can help avoid the hypocalcemia that may result with more aggressive replacement regimens.
    • Phosphorus preparations with sodium and potassium are available, but they have disadvantages, including causing osmotic diarrhea, volume overload, or hyperkalemia.
    • Usual starting doses are 2-3 grams of elemental phosphorus in divided doses.
  • Severe/symptomatic hypophosphatemia
    • Patients with symptoms of hypophosphatemia or with serum phosphate levels less than 1 mg/dL require IV phosphate replacement.
    • The intracellular nature of phosphate makes interpreting a low serum phosphate level difficult and predicting the amount required to replenish cellular stores nearly impossible.
    • Accordingly, recommendations for IV phosphate in the literature are varied and based on therapeutic experiences with limited numbers of patients.
    • Avoid hyperphosphatemia when replacing phosphorus intravenously, as this can lead to hypocalcemia (leading to tetany) and calcium-phosphate deposition in tissues (eye, heart, kidney, lung).

Medication

Treatment depends on the symptoms and severity of the condition.

Electrolyte supplements

These agents are used to increase serum phosphorus to normal physiologic levels.


Phosphate salt

IV preparations are available as sodium phosphate (Na2 HPO4 and NAH2 PO4) or potassium phosphate (K2 HPO4 and KH2 PO4).
Response to IV phosphorus supplementation varies widely and may be associated with hyperphosphatemia and hypocalcemia. Rate of infusion and choice of initial dosage should be based on severity of hypophosphatemia and presence of symptoms.
When treating hypophosphatemia with potassium phosphate, potassium level may limit amount of phosphate that can be given safely.
One Canadian group recently reported administering 30 mmol of potassium phosphate via central line over 3 h for severe hypophosphatemia and 15 mmol of potassium phosphate via central line over 3 h for moderate hypophosphatemia.
Another study reported safely administering IV phosphate at a rate of 14.5 mmol of phosphate ions over 1 h.

Adult

8 mmol of potassium phosphate IV q6h initially (32 mmol/24 h)
Aggressive IV replacement: 15 mmol of potassium phosphate over 6 h

Pediatric

0.25-0.5 mmol/kg IV over 4-6 h; repeat if symptomatic hypophosphatemia persists

Magnesium- and aluminum-containing antacids or sucralfate can act as phosphate binders and decrease serum phosphate levels; potassium-sparing diuretics, ACE inhibitors, and salt substitutes may increase serum phosphate levels

Hyperphosphatemia; hypocalcemia; hypomagnesemia; hyperkalemia; renal failure

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Caution in patients with renal insufficiency or metabolic alkalosis; admixture of phosphate and calcium in IV fluids can result in calcium-phosphate precipitation

More on Hypophosphatemia

Overview: Hypophosphatemia
Differential Diagnoses & Workup: Hypophosphatemia
Treatment & Medication: Hypophosphatemia
Follow-up: Hypophosphatemia
References
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References

  1. Shaikh A, Berndt T, Kumar R. Regulation of phosphate homeostasis by the phosphatonins and other novel mediators. Pediatr Nephrol. Aug 2008;23(8):1203-10. [Medline].

  2. Datta BN, Stone MD. Hyperventilation and hypophosphataemia. Ann Clin Biochem. Mar 2009;46:170-1. [Medline].

  3. Mehanna H, Nankivell PC, Moledina J, Travis J. Refeeding syndrome - awareness, prevention and management. Head Neck Oncol. Jan 26 2009;1(1):4. [Medline].

  4. Nowik M, Picard N, Stange G, Capuano P, Tenenhouse HS, Biber J, et al. Renal phosphaturia during metabolic acidosis revisited: molecular mechanisms for decreased renal phosphate reabsorption. Pflugers Arch. Nov 2008;457(2):539-49. [Medline].

  5. Rastegar A. New concepts in pathogenesis of renal hypophosphatemic syndromes. Iran J Kidney Dis. Jan 2009;3(1):1-6. [Medline].

  6. Faroqui S, Levi M, Soleimani M, Amlal H. Estrogen downregulates the proximal tubule type IIa sodium phosphate cotransporter causing phosphate wasting and hypophosphatemia. Kidney Int. May 2008;73(10):1141-50. [Medline].

  7. Bates JA. Phosphorus: a quick reference. Vet Clin North Am Small Anim Pract. May 2008;38(3):471-5, viii. [Medline].

  8. Sebastian S, Clarence D, Newson C. Severe hypophosphataemia mimicking Guillain-Barré syndrome. Anaesthesia. Aug 2008;63(8):873-5. [Medline].

  9. Bastepe M, Juppner H. Inherited hypophosphatemic disorders in children and the evolving mechanisms of phosphate regulation. Rev Endocr Metab Disord. Jun 2008;9(2):171-80. [Medline].

  10. Crook MA. Management of severe hypophosphatemia. Nutrition. Mar 2009;25(3):368-9. [Medline].

  11. Domrongkitchaiporn S, Disthabanchong S, Cheawchanthanakij R, Niticharoenpong K, Stitchantrakul W, Charoenphandhu N, et al. Oral Phosphate Supplementation Corrects Hypophosphatemia and Normalizes Plasma FGF23 and 25-Hydroxyvitamin D3 Levels in Women with Chronic Metabolic Acidosis. Exp Clin Endocrinol Diabetes. May 15 2009;[Medline].

  12. Fukumoto S. Physiological regulation and disorders of phosphate metabolism--pivotal role of fibroblast growth factor 23. Intern Med. 2008;47(5):337-43. [Medline].

  13. Ghosh AK, Joshi SR. Disorders of calcium, phosphorus and magnesium metabolism. J Assoc Physicians India. Aug 2008;56:613-21. [Medline].

  14. Juppner H. Novel regulators of phosphate homeostasis and bone metabolism. Ther Apher Dial. Oct 2007;11 Suppl 1:S3-22. [Medline].

  15. Moe SM. Disorders involving calcium, phosphorus, and magnesium. Prim Care. Jun 2008;35(2):215-37, v-vi. [Medline].

  16. Oud L. Transient hypoxic respiratory failure in a patient with severe hypophosphatemia. Med Sci Monit. Mar 2009;15(3):CS49-53. [Medline].

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Further Reading

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Keywords

hypophosphatemia, hypophosphatemia symptoms, hypophosphatemia treatment, phosphate, low phosphate level, low phosphorus level, 2, 3-diphosphoglycerate, 2, 3-DPG, serum phosphate, phosphorus, refeeding syndrome

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Contributor Information and Disclosures

Author

Devon J Moore, MD, Resident Physician, Department of Emergency Medicine, Wayne State University Detroit Medical Center, Detroit Receiving Hospital
Devon J Moore, MD is a member of the following medical societies: American Medical Student Association/Foundation, Emergency Medicine Residents Association, and Wayne State School of Medicine Black Medical Association
Disclosure: Nothing to disclose.

Coauthor(s)

Adam J Rosh, MD, MS, Assistant Professor, Department of Emergency Medicine, Wayne State University/Detroit Receiving Hospital
Adam J Rosh, MD, MS is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Medical Editor

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.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment

Managing Editor

Howard A Bessen, MD, Professor of Medicine, Department of Emergency Medicine, UCLA School of Medicine; Program Director, Harbor-UCLA Medical Center
Howard A Bessen, MD is a member of the following medical societies: American College of Emergency Physicians
Disclosure: Nothing to disclose.

CME Editor

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, Consulting Staff, Department of Emergency Medicine, Mills-Peninsula Emergency Medical Associates; Consulting Staff, Permanente Medical Group, Kaiser Permanente, Santa Clara Medical Center
Disclosure: Nothing to disclose.

 
 
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