ABSTRACT
Severe hypophosphatemia (i.e., serum phosphorus concentration below 1 mg/dl) occurs infrequently in veterinary patients. It is most often associated with diabetic ketoacidosis in small animals. Phosphate is necessary for the production of 2,3 diphosphoglycerate (2,3-DPG) and adenosine triphosphate (ATP); both are important for normal cellular metabolism. Consequences of severe hypophosphatemia may include hemolytic anemia, seizures, altered mentation, cardiomyopathy, and skeletal muscle weakness. Parenteral phosphate therapy is necessary in most cases of severe hypophosphatemia.
Subject(s)
Phosphates/blood , Phosphorus Metabolism Disorders/veterinary , Phosphorus/metabolism , 2,3-Diphosphoglycerate , Adenosine Triphosphate/biosynthesis , Animals , Cardiomyopathies/etiology , Cardiomyopathies/veterinary , Central Nervous System Diseases/etiology , Central Nervous System Diseases/veterinary , Diabetes Complications , Diabetes Mellitus/veterinary , Diphosphoglyceric Acids/biosynthesis , Hematologic Diseases/etiology , Hematologic Diseases/veterinary , Humans , Kidney Diseases/etiology , Kidney Diseases/veterinary , Muscular Diseases/etiology , Muscular Diseases/veterinary , Phosphates/administration & dosage , Phosphates/therapeutic use , Phosphorus/deficiency , Phosphorus Metabolism Disorders/complications , Phosphorus Metabolism Disorders/etiologyABSTRACT
Too often neglected, dosage of phosphatemia should yet be kept on mind. The role of phosphorus in bone mineralization and regulation of acid-base balance is well known. Phosphorus is also an energy purveyor during numerous biologic reactions, and deep deprivation may lead to a lot of pathologic situations, sometimes severe. Mild hypophosphatemia is not rare and occurs in various clinical or therapeutic circumstances; deep hypophosphatemia is rather uncommon, occuring chiefly during hyperalimentation or realimentation of starving patients, especially alcoholics. Deep hypophosphatemia (by depletion or transfer) mainly induces clinical and pathological manifestations; they are subsequent to alterations of glucose metabolism, leading to a failure in ATP and 2,3 DPG synthesis. These metabolic events particularly explain muscular and hematological manifestations of hypophosphatemia. Phosphorus loading per os, or in severe cases intravenously corrects the biological abnormalities and improves clinical manifestations.