Author: Martin Crook
Phosphate is a predominately intracellular anion with numerous physiological functions. It acts as a buffer, plays a central role in metabolic processes such as oxidative phosphorylation and glycolysis, as well as nucleotide pathways and nervous system conduction. Classification of plasma phosphate concentration is given in Box 89.1.
Causes of hyperphosphataemia are given in Table 89.1. Pseudohyperphosphataemia can be due to phosphate leakage out of cells if the sample is haemolysed or delivery to the laboratory is delayed.
Symptomatic severe hyperphosphataemia
Treat the underlying cause.
The major clinical consequence of severe hyperphosphataemia is hypocalcaemia (Chapter 87). The reason for this is that calcium phosphate precipitation into the tissues occurs when the phosphate and calcium plasma concentrations exceed their solubility product ([calcium]×[phosphate]).
In the presence of renal dysfunction and/or symptoms, a nephrologist's opinion and possible dialysis may be necessary. Consider oral phosphate-binding agents.
Mild to Moderate Hyperphosphataemia
Treat with oral phosphate-binding agents, for example magnesium hydroxide or calcium carbonate.
Causes of hypophosphataemia are given in Table 89.2.
Severe hypophosphataemia can cause numerous clinical features. These may include rhabdomyolysis, impaired skeletal muscle function, weakness and myopathy, impaired diaphragmatic contractility and difficulty weaning patients off mechanical ventilators and cardiomyopathy. Severe hypophosphataemia can provoke seizures, paraesthesiae, and renal tubular impairment and osteomalacia.
Other effects of severe hypophosphataemia include thrombocytopenia and haemolysis, as well as erythrocyte 2,3-DPG depletion, resulting in a shift in the haemoglobin/oxygen dissociation curve to the left (increasing its oxygen affinity).
Hypophosphataemia can be associated with hypomagnesaemia and hypokalaemia. A urine phosphate determination may help see if there is a renal cause of phosphate loss, for example Fanconi syndrome.
Symptomatic severe hypophosphataemia
Treat the underlying cause.
Give IV phosphate replacement:
- 9 mmol of monobasic potassium phosphate in half-normal saline by continuous IV infusion over 12h or
- Phosphate Polyfusor® up to 50 mmol by continuous IV infusion over 24h. This should not be given to patients with hypercalcaemia, because of the risk of metastatic calcification, or to patients with hyperkalaemia or hypernatraemia. Each 500 mL Polyfusor® contains: phosphate 50 mmol, potassium 9.5 mmol and sodium 81 mmol. In severe hypophosphataemia 20 mmol phosphate up to 0.5 mmol/kg of body weight may be given in up to a maximum of 50 mmol over 6–12hours.
In addition to phosphate, measure plasma electrolytes, calcium, magnesium and renal function including eGFR, which must be monitored during therapy.
Mild to moderate hypophosphataemia
Treat the underlying cause.
Give oral phosphate (although gastrointestinal side-effects such as diarrhoea can be a problem and phosphate correction may be delayed), for example Phosphate-Sandoz® one tablet (containing phosphate 16.1 mmol, sodium 20.4 mmol, potassium 3.1 mmol) 8-hourly PO, which can be increased to maximum of 6 tablets daily, in divided doses, if tolerated.