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Up Acid-base Hyponatraemia Lactate Magnesium Phosphate Potassium

Phosphate metabolism




- rhabdomyolysis
- renal failure
- vit D toxicity
- acidosis
- tumour lysis
- hypoparathyroidism
- pseudohypoparathyroidism
- diphosphonate therapy
- excess IV administration

Clinical features

- include nephrocalcinosis, nephrolithiasis, band keratopathy


- may require haemodialysis
- aluminium hydroxide and hypertonic dextrose solutions can be used to shift ECF phosphate into cells



  • normal serum range: 0.84-1.58 mmol/l
  • hypophosphataemia: < 0.8; severe: < 0.32


- decreased intake, increased excretion or redistribution
- hyperparathyroidism
- vit D deficiency
- vit D resistant rickets
- renal tubular acidosis
- alkalosis
- parenteral nutrition
- refeeding after starvation
- alcoholism

Clinical features

- may be asymptomatic


- ¯ cardiac contractility
- respiratory muscle weakness: may lead to difficult weaning
- skeletal muscle weakness
- rhabdomyolysis


- hyperinsulinaemia
- decreased glucose metabolism, glycosuria


- parasthesia
- anorexia, irritability, confusion
- seizures
- coma


- decreased 2,3 DPG
- red cell haemolysis, spherocytosis and decreased life span
- impaired WBC chemotaxis and phagocytosis: decreased bactericidal activity
- thrombocytopaenia (due to increased destruction) and megakaryocytosis

Skeletal abnormalities

- rickets and osteomalacia
- radiolucent areas and pseudofractures
- bone pain


- treat underlying cause
- severe: IV sodium or potassium phosphate 0.08-0.16 mmol/kg over 6h. Stop when phosphate >0.65
- moderate: oral phosphate 1-4 g/day
- maintenance: 0.5 g/day in enteral feed, 0.4 mmol/kg/day in TPN

Further reading

Worthley LIG. Fluid and electrolyte therapy. In Oh TE. Intensive Care Manual, 4th ed

© Charles Gomersall December 1999


©Charles Gomersall, April, 2014 unless otherwise stated. The author, editor and The Chinese University of Hong Kong take no responsibility for any adverse event resulting from the use of this webpage.
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