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Hypophosphatemia

ISSN 2398-2950

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Synonym(s): Hypophosphataemia

Introduction

  • Definition: serum inorganic phosphorus <0.92 mmol/l.
  • Phosphate is a major intracellular anion. It has a structural role in cell membranes, hydroxyapatite of bone, nucleic acids and phosphoproteins including adenosine triphosphate (ATP). Important in oxygen transports (2,3-diphosphoglycerate), second messenger systems (cyclic adenosine monophosphate), coenzyme systems (nicotinamide adenine dinucleotide phosphate). Important in the regulation of protein, fat and carbohydrate metabolism. Involved in the activation of vitamin D and calcium homeostasis.
  • Phosphorus exists as organic (phospholipids, phosphate esters) and inorganic (orthophosphoric acid, pyrophosphoric acid) forms. 80-85% of total body phosphate is inorganic in bone as hydroxyapatite. 15% is organic and in soft tissues. Most serum phosphorus is inorganic orthophosphoric acid. 10-20% of inorganic is protein bound. 80-90% is free or bound to magnesium, sodium and calcium.
  • <1% of Total Body Phosphate found as extracellular active forms with only 33% of this being ionized.
  • Total Body Phosphate levels closely regulated in conjunction with calcium.

Presenting signs

  • Weakness.
  • Ileus.
  • Respiratory failure.
  • Joint or muscle pain.
  • Arrhythmias.
  • Hemolysis.

Acute presentation

  • Collapse.
  • Seizures.
  • Hemolysis.
  • Respiratory failure.
  • Hemoglobinuria.

Geographic incidence

  • Worldwide.

Age predisposition

  • None.

Breed/Species predisposition

  • None.

Public health considerations

  • None.

Cost considerations

  • None.

Special risks

  • General anesthesia.
  • Patients with hypophosphatemia are predisposed to arrhythmias (especially ventricular tachycardia) and muscular weakness potentially leading to respiratory muscle failure. Decreased oxygen delivery to tissues with consequent tissue hypoxia may result.
  • Severe hypophosphatemia leads to reduced ATP production in erythrocytes leading to decreased cell wall integrity and consequent hemolytic anemia Anemia: blood loss.

Pathogenesis

Etiology

  • Redistribution into intracellular compartment:
  • Cellular energy alteration:
    • Acute liver injury increases cellular ATP demand.
    • Increased metabolic demand in sepsis (not proven).
  • Reduced intestinal absorption:
    • Vitamin D deficiency.
    • Reduced intake.
    • Administration of phosphate binders.
    • Severe malabsorptive disorders.
  • Increased renal loss:
    • Primary hyperparathyroidism Primary hyperparathyroidism.
    • Paraneoplastic effect of parathyroid hormone-related protein.
    • Renal tubular dysfunction (eg Fanconis syndrome).
    • Hyperadrenocorticism Hyperadrenocorticism.
    • Central diabetes insipidus Diabetes insipidu (potentially seen after head trauma).
    • Diuresis (particularly with mannitol Mannitol and carbonic anhydrase inhibitors).

Predisposing factors

General

  • See Etiology.

Specific

  • Hypophosphatemia may be seen in association with hypocalcemia in eclampsia.

Pathophysiology

  • 60-70% of ingested phosphate is hydrolyzed to an inorganic form that is absorbed actively and passively. Active transport is increased by the presence of calcitriol primarily in the presence of hypophosphatemia. Passive absorption is largely dependent on the phosphorus content of the diet as well as the type of protein.
  • Phosphorus is excreted in the urine and primarily reabsorbed in the proximal tubules as a result of the effects of PTH. Increases in PTH PTH assay decreases reabsorption in the proximal tubules.
  • Other hormones that can increase reabsorption of phosphorus in the proximal tubules include growth hormone, insulin and thyroxine. ACTH, glucocorticoids and calcitonin decrease proximal tubular reabsorption of phosphorus.
  • Decreased RBC phosphorus decreases RBC, ATP and increases RBC fragility    →   hemolysis. Decreases RBC 2,3 DPG so impaired oxygen delivery to tissues.

Diagnosis

Presenting problems

  • See Acute Presentation.

Client history

  • Neurological signs weakness.
  • Cardiopulmonary signs arrhythmias, respiratory depression.
  • Iatrogenic DKA stabilization, TPN administration.
  • Dependent upon underlying condition (see Etiology).

Clinical signs

  • See Presenting Signs.

Diagnostic investigation

  • Blood work:
  • Urinalysis (see Etiology).
  • Diagnostic imaging evidence of poor bone mineralization or pathologic fractures.

Gross autopsy findings

  • Dependent upon underlying condition (see Etiology).

Histopathology findings

  • Dependent upon underlying condition (see Etiology)

Treatment

Initial symptomatic treatment

  • Therapy should be started once serum hypophosphatemia has been noted; however, it has been suggested that prophylactic supplementation should be administered in cases liable to become hypophosphatemic, eg diabetic ketoacidosis.
  • Intravenous fluid therapy with 0.9% sodium chloride supplemented with potassium phosphate (NaCl recommended as Hartmanns and Ringers type solutions contain calcium). Administer phosphate Phosphate at 0.010.06 mmol/kg/hr.
  • Supplement intravenous fluids with potassium chloride Potassium chloride / gluconate if concurrent hypokalemia. Ensure maximum rate of 0.5mEq/kg/hr potassium not exceeded.
  • Monitor for potential side effects of intravenous phosphate administration such as hypocalcemia, tetany, soft tissue mineralization or renal failure.
  • Consider ventilation if profound respiratory depression.
  • Consider administration of Fresh Whole Blood (or Packed Red Cell) transfusion Blood transfusion if anemia severe. 

Standard treatment

  • Oral phosphate supplementation. Starting dosage of 0.5-2.0 mmol/kg/day recommended although titration of dose according to response is essential.

Monitoring

  • Frequent evaluation of:
    • Phosphate.
    • Calcium.
    • Renal parameters.
    • Potassium and glucose (in select cases).

Subsequent management

Treatment

  • Dependent upon underlying disease (see Etiology).

Monitoring

  • Phosphate.
  • Calcium.
  • Potassium and other electrolytes.
  • Other parameters dependent upon underlying disease (see Etiology).

Prevention

Outcomes

Further Reading

Publications

Refereed papers

  • Recent references from PubMed and VetMedResource.
  • Schropp D M, Kovacic J (2007) Phosphorus and phosphate metabolism in veterinary patients. J Vet Emerg Crit Care 17 (2), 127-134 VetMedResource.

Other sources of information

  • Marino P (2007) Renal and Electrolyte Disorders: Calcium and Phosphorus. In: The ICU Book pp 639-655. Lippincott, Williams & Wilkins.
  • DiBartola S P, Willard M D (2006) Disorders of Phosphorus: Hypophosphataemia and Hyperphosphataemia. In: Fluid, Electrolyte, and Acid-Base Disorders in Small Animal Practice pp 195-209. Ed. S DiBartola, Saunders Elsevier.
  • Macintire D K, Drobatz K J, Haskins S C, Saxon W D (2005) Endocrine and Metabolic Emergencies. In: Manual of Small Animal Emergency and Critical Care Medicine pp 331-333. Lippincott, Williams & Wilkins.