Phosphate plays a vital role forming the high-energy band within ATP. The pathophysiological results of phosphate deficiency are inadequate supplies of energy-rich phosphates and, in particular, inhibition of glyceraldehyde-3- phosphate dehydrogenase, which occupies a key position in glycolysis. The effect of this on the central nervous system, muscle and erythrocyte energy metabolism is to reduce ATP and 2,3-diphosphoglycerate levels, leading to left-hand displacement of the oxygen-hemoglobin dissociation curve with decreased peripheral oxygen uptake and transport. Therefore, detection and treatment of acute hypophosphatemia is important in many hospitalized patients particularly in ICU patients. Severe hypophosphatemia is also associated with a number of neuromuscular and cardiovascular sequelae, in which phosphate supplementation leads to improved symptoms and clinical parameters. In clinical practice it is common on administering 0.4 mmol (12 mg) phosphate/kg per day, and to adjust this on the basis of the serum phosphate analysis.