Signs and symptoms of hypophosphatemia
- Alan S L Yu, MB, BChir
Alan S L Yu, MB, BChir
- Harry Statland and Solon Summerfield Professor of Medicine
- University of Kansas Medical Center
- Jason R Stubbs, MD
Jason R Stubbs, MD
- Associate Professor of Medicine
- Division of Nephrology & Hypertension
- University of Kansas Medical Center
When combined with phosphate depletion (that is, when not due solely to phosphate movement into the cells), hypophosphatemia can cause a variety of signs and symptoms [1,2]. The manifestations depend, in large part, upon the severity and chronicity of the phosphate depletion, with the plasma phosphate concentration usually being below 1 mg/dL (0.32 mmol/L) in symptomatic patients.
The major conditions associated with symptomatic hypophosphatemia are chronic alcoholism, intravenous hyperalimentation without phosphate supplementation, urinary phosphate-wasting syndromes (such as Fanconi syndrome or tumor-induced osteomalacia), and the chronic ingestion of antacids or other phosphate binders. Significant hypophosphatemia is also observed in patients receiving continuous renal replacement therapies, yet the clinical relevance of this finding remains uncertain. (See "Causes of hypophosphatemia" and "Hypophosphatemia in the alcoholic patient".)
Severe hypophosphatemia can also be seen during treatment of diabetic ketoacidosis and with prolonged hyperventilation; however, symptoms are unusual in these settings since the hypophosphatemia is acute and there is no preexisting chronic phosphate depletion . (See "Diabetic ketoacidosis and hyperosmolar hyperglycemic state in adults: Treatment", section on 'Phosphate depletion'.)
Except for the effects on calcium and magnesium metabolism, the clinical manifestations of hypophosphatemia are primarily due to the consequences of intracellular phosphate depletion, which can affect many organ systems. The signs and symptoms of hypophosphatemia will be reviewed here. The diagnostic approach to and treatment of hypophosphatemia are discussed separately. (See "Evaluation and treatment of hypophosphatemia".)
EFFECTS OF HYPOPHOSPHATEMIA ON MINERAL METABOLISM
Prolonged hypophosphatemia produces a number of effects on both the kidney and bone. Distal tubular reabsorption of calcium and magnesium are inhibited, and striking hypercalciuria ensues. This response to phosphate depletion is dramatic, but the mechanism is unknown. A number of patients with idiopathic hypercalciuria have mild hypophosphatemia, and it has been suggested that impaired phosphate balance may be the primary abnormality, with enhanced calcium excretion representing a secondary effect.
Subscribers log in hereLiterature review current through: Jul 2017. | This topic last updated: Jul 25, 2016.References
- Knochel JP. The pathophysiology and clinical characteristics of severe hypophosphatemia. Arch Intern Med 1977; 137:203.
- Weisinger JR, Bellorín-Font E. Magnesium and phosphorus. Lancet 1998; 352:391.
- Liu PY, Jeng CY. Severe hypophosphatemia in a patient with diabetic ketoacidosis and acute respiratory failure. J Chin Med Assoc 2004; 67:355.
- Travis SF, Sugerman HJ, Ruberg RL, et al. Alterations of red-cell glycolytic intermediates and oxygen transport as a consequence of hypophosphatemia in patients receiving intravenous hyperalimentation. N Engl J Med 1971; 285:763.
- Silvis SE, DiBartolomeo AG, Aaker HM. Hypophosphatemia and neurological changes secondary to oral caloric intake: a variant of hyperalimentation syndrome. Am J Gastroenterol 1980; 73:215.
- Subramanian R, Khardori R. Severe hypophosphatemia. Pathophysiologic implications, clinical presentations, and treatment. Medicine (Baltimore) 2000; 79:1.
- Turnbull J, Lumsden D, Siddiqui A, et al. Osmotic demyelination syndrome associated with hypophosphataemia: 2 cases and a review of literature. Acta Paediatr 2013; 102:e164.
- Falcone N, Compagnoni A, Meschini C, et al. Central pontine myelinolysis induced by hypophosphatemia following Wernicke's encephalopathy. Neurol Sci 2004; 24:407.
- Michell AW, Burn DJ, Reading PJ. Central pontine myelinolysis temporally related to hypophosphataemia. J Neurol Neurosurg Psychiatry 2003; 74:820.
- O'Connor LR, Wheeler WS, Bethune JE. Effect of hypophosphatemia on myocardial performance in man. N Engl J Med 1977; 297:901.
- Davis SV, Olichwier KK, Chakko SC. Reversible depression of myocardial performance in hypophosphatemia. Am J Med Sci 1988; 295:183.
- Zazzo JF, Troché G, Ruel P, Maintenant J. High incidence of hypophosphatemia in surgical intensive care patients: efficacy of phosphorus therapy on myocardial function. Intensive Care Med 1995; 21:826.
- Ognibene A, Ciniglio R, Greifenstein A, et al. Ventricular tachycardia in acute myocardial infarction: the role of hypophosphatemia. South Med J 1994; 87:65.
- Heames RM, Cope RA. Hypophosphataemia causing profound cardiac failure after cardiac surgery. Anaesthesia 2006; 61:1211.
- Aubier M, Murciano D, Lecocguic Y, et al. Effect of hypophosphatemia on diaphragmatic contractility in patients with acute respiratory failure. N Engl J Med 1985; 313:420.
- Cohen J, Kogan A, Sahar G, et al. Hypophosphatemia following open heart surgery: incidence and consequences. Eur J Cardiothorac Surg 2004; 26:306.
- Alsumrain MH, Jawad SA, Imran NB, et al. Association of hypophosphatemia with failure-to-wean from mechanical ventilation. Ann Clin Lab Sci 2010; 40:144.
- Ravid M, Robson M. Proximal myopathy caused by latrogenic phosphate depletion. JAMA 1976; 236:1380.
- Knochel JP. Hypophosphatemia and rhabdomyolysis. Am J Med 1992; 92:455.
- Singhal PC, Kumar A, Desroches L, et al. Prevalence and predictors of rhabdomyolysis in patients with hypophosphatemia. Am J Med 1992; 92:458.
- Jacob HS, Amsden T. Acute hemolytic anemia with rigid red cells in hypophosphatemia. N Engl J Med 1971; 285:1446.
- Klock JC, Williams HE, Mentzer WC. Hemolytic anemia and somatic cell dysfunction in severe hypophosphatemia. Arch Intern Med 1974; 134:360.
- Craddock PR, Yawata Y, VanSanten L, et al. Acquired phagocyte dysfunction. A complication of the hypophosphatemia of parenteral hyperalimentation. N Engl J Med 1974; 290:1403.