Clinical manifestations of hypophosphatemia

Hypophosphatemia is a common disease, which is generally caused by the lower-than-normal phosphate concentration in the blood, resulting in phosphorus metabolism disorders. This disease is generally manifested by muscle pain, weakness, coma, etc. There are many clinical causes of hypophosphatemia. Hypophosphatemia must be taken seriously and treated actively. What are the clinical manifestations of hypophosphatemia?

Symptoms of hypophosphatemia are: central nervous system symptoms such as paresthesia, dysarthria, hyperreflexia, tremor, ataxia, and coma. Due to the decrease of erythrocyte 2,3-diphosphoglycerate, the life span of erythrocytes is shortened, and spherocytosis and hemolysis may occur. Fatigue, muscle weakness, muscle pain, and even paralysis. Bone pain (due to osteomalacia), false fractures may be seen on X-rays. White blood cell phagocytic function is impaired, making infection more likely to occur. Platelet dysfunction, reduced platelet aggregation ability.

Diagnosis The most common cause of hypophosphatemia is alkali poisoning (respiratory and metabolic). Usually hypophosphatemia can be identified by the following procedure: first exclude the cause of alkali poisoning and then measure the urine phosphate. If urine phosphate excretion is increased, measure plasma calcium. If plasma calcium increases, consider primary hyperparathyroidism, ectopic parathyroid glands, or malignant tumors. If plasma calcium is normal or decreased, consider secondary hyperparathyroidism, rickets or osteomalacia, Fanconi's syndrome, or hypophosphatemic rickets. If urinary phosphate excretion is reduced, consideration should be given to reducing dietary phosphate intake, taking antacids, and taking insulin.

Pay attention to distinguishing various causes of hypophosphatemia.

Treatment of hypophosphatemia can be corrected with intravenous fluid and phosphate replacement. Commonly used phosphates include a mixture of potassium dihydrogen phosphate (KH2PO4) and disodium hydrogen phosphate (Na2HPO4). If hypercalcemia is present, intravenous phosphate supplementation should be reduced to prevent the formation of displaced calcification. In addition, intravenous phosphate supplementation can cause the following complications: hypocalcemia. Displaced calcification formation. Iatrogenic hyperkalemia and hypernatremia (caused by phosphate supplementation). The cause of hypophosphatemia should also be treated.

What causes symptoms of hypophosphatemia? What diseases can cause symptoms of hypophosphatemia?

Pathogenesis The diet generally contains sufficient phosphate. However, hypophosphatemia can occur in the following situations: fasting, especially in patients receiving intravenous hypernutrition, because glucose can increase the cell's uptake of phosphate, leading to hypophosphatemia. Long-term use of binders such as aluminum hydroxide, magnesium hydroxide or aluminum carbonate inhibits the intestinal absorption of phosphate. Glycolysis and alkali poisoning can quickly consume the concentration of intracellular phosphate and increase the cell's uptake of phosphate, thus causing hypophosphatemia. When patients with diabetic acidosis receive insulin treatment, glycolysis increases and phosphates move into cells. Hyperparathyroidism increases the secretion of parathyroid hormone and increases the excretion of phosphate in urine. Vitamin D deficiency reduces the absorption of phosphate in the intestinal cavity. In certain renal tubular diseases, such as Fanconi's syndrome, urinary phosphate excretion is significantly increased. Alcoholism, reduced diet, increased glycolysis, and the use of antacid binders to treat gastritis can cause hypophosphatemia. Vitamin D-resistant rickets (familial hypophosphatemia) is a sex-linked dominant genetic disease, which causes impaired phosphate reabsorption in the proximal tubule and poor intestinal calcium absorption.