Hypophosphatemia is a pathological condition characterized by a decrease in the concentration of inorganic phosphorus in the blood plasma below 0.9 mmol / l. There can be many reasons for hypophosphatemia: insufficient intake from food, diseases of the kidneys, parathyroid glands, etc. The main clinical manifestations include muscle weakness, up to paralysis, and disorders of higher nervous activity in the form of lethargy, drowsiness. The diagnosis is established on the basis of determining the level of phosphates in the blood. As a treatment, phosphate deficiency is replenished and the underlying disease is treated.
Phosphorus (P) is an intracellular anion. Along with calcium, P forms the mineral basis of bone tissue, is necessary for the synthesis of ATP molecules (the main "energy carrier"), and also plays an important role in maintaining the acid-base balance of the blood. Phosphorus enters the human body with food. His daily requirement is 1000-120 mg. Hypophosphatemia is noted in 2% of patients who are in the hospital. Among hospitalized patients suffering from alcoholism, this condition is more common (in 10%).
Hypophosphatemia, especially clinically significant, in most cases develops due to the influence of many factors, i.e. is polyethological. Below are the causes of hyperphosphatemia, grouped according to the mechanism of action at various stages of phosphorus metabolism:
Rarer causes of hypophosphatemia include:
A drop in the concentration of inorganic phosphates leads to a decrease in the formation of ATP molecules, resulting in a hypoenergetic state. This has the most adverse effect on organs with a high energy demand - the central nervous system, skeletal muscles and myocardium. Hypophosphatemia causes rapid bone demineralization and osteoblast dysfunction.
With a low content of P, the reserves of 2,3-diphosphoglycerate in erythrocytes are depleted, which increases the affinity of hemoglobin for oxygen and makes it difficult to transfer it to cells and tissues. Also, due to a deficiency of intracellular ATP, the plasticity of erythrocytes worsens, they become more sensitive to damage in the capillary bed and may undergo hemolysis. With extremely pronounced hypophosphatemia, dysfunction of platelets and leukocytes occurs.
According to the severity, 2 types of hypophosphatemia are distinguished:
According to the rate of development, acute and chronic hypophosphatemia are distinguished. The severity and severity of the condition are important for the differential diagnosis of the etiological factor.
Hypophosphatemic rickets
The clinical picture depends on the time of onset and the severity of P depletion in the body. Slowly developing chronic hypophosphatemia is often completely asymptomatic. Sometimes such patients may be disturbed by a slight muscle weakness that manifests itself when performing physical exertion.
With a long course, aching pains in the bones may join. Vivid symptoms are inherent in acute severe hypophosphatemia. Muscle weakness is more pronounced, even normal movements such as walking are difficult. Due to the weakness of the diaphragm, hyperventilation (shortness of breath) occurs, and auxiliary muscles begin to participate in breathing.
There are disorders of the central nervous system - lethargy, drowsiness, deterioration in concentration. Some patients have motor dysfunctions - impaired coordination of movement, gait, hand tremor. Acute mental episodes in patients with chronic alcoholism (delusions, auditory, visual hallucinations) resemble those in alcohol withdrawal syndrome.
Severe acute hypophosphatemia causes a large number of adverse effects. The pronounced weakening of the skeletal muscles has a particularly detrimental effect on breathing, in some patients acute respiratory failure develops. Also, due to myopathy, swallowing is difficult, which increases the risk of aspiration pneumonia. The convulsive activity of the brain increases, epileptic-like seizures are possible.
The disturbance of consciousness is aggravated, up to supor and falling into a coma. A significant decrease in myocardial contractility leads to acute or congestive heart failure. In rare cases, rhabdomyolysis is possible. In chronic hypophosphatemia, osteomalacia occurs, which often causes bone curvature, deformities of the limbs and spine, and pathological fractures occur.
Since hypophosphatemia has a wide range of etiological factors, doctors of various specialties are involved in the supervision of patients with this disorder. More often such patients are under supervision of nephrologists, endocrinologists, resuscitators. The concentration of phosphorus is examined in the serum by biochemical analysis.
This condition can be suspected during a general examination of the patient (O- or X-shaped curvature of the limbs, hyperventilation, weakened muscle tone). Also, on the basis of physical data, it is sometimes possible to suggest the cause of the development of hypophosphatemia (hyperemia and telangiectasia on the face, yellowness of the skin, mucous membranes, an increase in the size of the liver in chronic alcoholism; cachexic appearance in hyperparathyroidism, especially ectopic).
Help in establishing the cause is provided by anamnestic data: taking medications (diuretics, antacids), undergone surgical operations. To confirm the diagnosis and determine the etiological factor, the following examination is prescribed:
Foods rich in phosphorus
Patients with a moderate asymptomatic form of this condition or with minor clinical signs can be treated on an outpatient basis. Patients with severe acute hypophosphatemia are subject to mandatory hospitalization in a hospital. Drugs that cause a decrease in blood phosphate levels should be immediately canceled and replaced with alternative drugs.
In the treatment of this disorder, 2 main goals are pursued: treatment of the underlying disease, against which hypophosphatemia developed (removal of parathyroid glands in hyperparathyroidism, correction of alkalosis, administration of bicarbonates and Fanconi syndrome, etc.) and replenishment of phosphate deficiency. For the latter, there are the following measures:
Moderate hypophosphatemia has a favorable prognosis and does not affect a person's life expectancy in any way. Severe and acute hypophosphatemia can often lead to death. Often it determines the outcome in patients who are in critical condition. The most common causes of death are respiratory failure due to paralysis of the diaphragm, heart failure, cardiac arrhythmias, and coma.
Primary prevention is reduced to the timely diagnosis and treatment of those diseases and conditions that can serve as a background for the development of hypophosphatemia. Also, to prevent this disorder, regular monitoring of P concentration is recommended in patients with chronic renal failure who are on renal replacement therapy (hemodialysis) and who take phosphate binders.