Hypocalcemia is a polytheological pathological condition, which is observed as a symptomatic complex of other nosological forms, which is based on a sharp or moderate decrease in the concentration of serum ionized calcium. Signs of hypocalcemia occur when various electrophysiological processes at the cellular level are disrupted.
Of course, the determination of the saturation index of ionized calcium in the blood serum does not belong to the routine screening algorithm of the patient's examination, however, the detection of latent hypocalcemia makes it possible to diagnose a number of pathological conditions requiring early treatment (oncopathology, renal failure, etc.).
Causes of hypocalcemia
The most common etiopathogenetic factor provoking the development of hypocalcemic syndrome is the complete absence or lack of parathycrinin, which occurs in pathologies such as hypoparathyroidism or parathycrinic insufficiency.
Another mechanism in the pathogenesis of hypocalcemia is parathycrinin resistance of the peripheral type, which consists in the ineffectiveness of parathycrinin exposure to target cells. A remarkable fact is that in this situation the normal or increased content of parathycrinin is most often observed.
The relative deficiency of parathycrinin activity occurs when a combination of rapid loss of calcium and simultaneous decompensation of the functional capabilities of the parathyroid glands, which are the main regulator of calcium metabolism. Thus, in the development of hypocalcemic syndrome, the fundamental link is a violation of parathyroid regulation in a direct or indirect way.
Inadequate production of parathyroid hormone sooner or later provokes the development of hyperphosphataemia and hypocalcemia. An auxiliary mechanism of provocation of hypocalcemic syndrome is the inadequate production of calcitriol (active vitamin D) by the kidneys. As a result of the above abnormal disorders, an acid-alkaline imbalance occurs, accompanied by an increase in the serum potassium level, an increase in convulsive readiness due to the increased tone of the muscle fibers. Thus, the basis of the convulsive syndrome, which is a classic variant of the course of hypocalcemia, is a sharp increase in the potassium content in the cells of the muscle tissue.
Acute hypocalcemic syndrome is observed at various urgent conditions, accompanied by a massive cytolytic process in the organs (severe polytrauma, prolonged crush syndrome, burn injury, shock, cytostatic therapy). In this situation, there is a rapid release of intracellular potassium and phosphate with a simultaneous decrease in the level of ionized calcium in the blood serum. In case of adherence of signs of renal insufficiency, critical hyperphosphatemic hypocalcemia is observed.
Also, an acute course of hypocalcemia is noted when using drugs that bind calcium in the blood and drugs that have a negative effect on the absorption of calcium in the small intestine and kidneys. The severe form of pancreatitis in the stage of pancreatic necrosis is also often accompanied by hypocalcemia, caused by the increased formation of soap-like compounds containing calcium.
A separate nosological form is hypocalcemia in newborns, the origin of which is due to the insufficient intake of ionized calcium with mother's milk and the increased need of a growing organism in this nutrient element.
A rare reason for the acute form of hypocalcemia is kidney transplantation, since the transplanted material does not metabolize citric acid for a long time and provokes hypercitrateemia.
The most rare and at the same time life-threatening form is postpartum hypocalcemia, which in 90% of cases ends in a fatal outcome due to the lightning course of the tetanic convulsive syndrome.
The chronic course of hypocalcemia occurs in hypoparathyroidism, chronic renal failure and rickets.
Symptoms of hypocalcemia
The earliest and pathognomonic clinical manifestation of hypocalcemia is a specific convulsive syndrome, manifested exclusively by cramps of a tonic type. Fortunately, unlike clonic convulsive readiness, tetany is not life threatening for the patient, but its constant presence significantly impairs the patient's quality of life. However, with prolonged course of tetany, serious consequences of hypocalcaemia develop, which in some situations can provoke the development of a lethal outcome (laryngotracheal stridor, convulsive contraction of the diaphragm and tetany of the heart, followed by the development of asphyxia in patients in the postoperative period after surgical treatment of hypoparathyroidism).
The long-term consequences of chronic hypocalcemia include cataract, generalized calcification , psychoneurological disorders, habitual miscarriage of the fetus and a secondary form of infertility, activation of chronic foci of infection.
The classical clinical course of tetany with hypocalcemia syndrome consists in the appearance of signs of widespread paresthesia, increased convulsive readiness and difficulty of the act of breathing. The primary localization of a sensitivity disorder is the skin of the lips, with the subsequent spread to the skin of the distal parts of the limbs. In a situation where the tonic convulsive syndrome occurs locally, a specific "carpopedal syndrome" or "sardonic mask" is formed.
A specific symptom of tetany with hypocalcemia is the presence of harbingers in the form of dysarthria, dysphagia, paresis of the cranial nerves, stem neurological disorders and spastic paresis of the extremities. Also, in most cases, seizures are accompanied by severe disorders of vegetative genesis (functional dyspepsia, profuse sweating, nonspecific abdominal pain syndrome, bronchospasm).
In some situations, hypocalcemic convulsive syndrome can occur atypically in the form of tonic-clonic seizures like epilepsy with a brief period of loss of consciousness and even the development of hallucinatory psychosis.
To rare manifestations of hypocalcemia, simulating the clinical picture of other diseases, include stomach and heart tetanias, as well as laryngospasm. In this situation, good support is provided by conducting specific samples for spasmophilia, the skills of which must be possessed by a specialist of any medical profile.
Hypocalcemia in children
Symptoms of hypocalcemic syndrome can manifest in a child in any age, but the risk group for this pathology is newborn babies born before the due date, as well as children born to a woman suffering from severe diabetes . A characteristic manifestation of hypocalcemia in children born before the term is the complete absence of dependence of the severity of the course of hypocalcemia on the level of laboratory indicators, that is, in many situations severe "laboratory hypocalcemia" is asymptomatic.
The main etiopathogenetic factor provoking the development of hypocalcaemia in children of any age is alimentary, that is, the lack of sufficient intake of vitamin D and calcium in the baby's body. Auxiliary provoking risk factors are the lack of protein in the child's blood, mainly albumin fraction and to a lesser extent the parathyroid gland insufficiency.
Clinical manifestations of hypocalcemia in children are similar to adult patients only with the difference that the intensity of their manifestations is more pronounced and the risk of complications in this state is quite high. The appearance in the child of signs of laryngospasm development in the form of impossibility to perform a full inspiration, noisy breathing and loud cough requires immediate medication and subsequent hospitalization in the hospital in order to determine the level of calcium in the blood serum and further correction of hypocalcemia.
To acute care drugs with acute hypocalcemia in children, Calcium gluconate 10% solution at a calculated dose of 1 ml / 1 kg of the child's weight by the method of intravenous injection in combination with 200 mg of elemental calcium.
Treatment of hypocalcemia
The primary direction in the treatment of hypocalcemic syndrome is substitution therapy with the use of drugs containing high calcium concentration, however, the key to successful correction of this pathological condition is the elimination of the underlying cause of hypocalcemia. The control of the effectiveness of the substitution therapy is carried out by the method of laboratory assessment of the serum calcium content and the target value in this situation is 2.4 mmol / l with the excretory calcium index less than 10 mmol / l.
The most favorable treatment option for hypocalcemia is the development of a low level of calcium in the blood serum on the background of an unchanged calcium absorption process in the small intestine, as in this situation the positive effect of the substitution therapy is rapid and stable. This variant of therapy is prescribed by a short course without additional prescription of vitamin D.
In most cases, calcium supplementation therapy is reinforced by the appointment of vitamin D, and the dose of the drug is selected individually, depending on the underlying cause of hypocalcemia. For example, in a situation where hypocalcemia was a complication of pronounced demineralization of bone tissue, it is advisable to use vitamin D in the maximum saturating daily dose (Calcium D3 nikomed 1 tablet 3 r. / Day, Akvadetrim 2 drops per day orally), subject to mandatory monitoring of laboratory of calcium in order to prevent the development of hypercalcemic syndrome. Calcitriol therapy at a dose of 0.25 μg or Alfacalcidol at a dose of 1 μg does not require additional prescription of calcium preparations and is supported only by correction of the patient's eating behavior (eating foods containing high calcium concentration, which is used as an active prophylaxis for hypocalcemia).
In a situation where the patient has a developed clinical symptom complex of hypocalcemia attack of tetany, it is necessary to provide the patient with a full complex of urgent measures, the first step of which is the immediate administration of 10% calcium chloride solution intravenously in a dose of 10 ml, paying special attention to the place of injection, drug in surrounding soft tissues is fraught with the development of necrotic changes. An analogue of this drug, devoid of side effects is Calcium Gluconate 10% rr in a dose of 40 ml.
The absence of an expressed effect from the use of calcium chloride indicates the development of the patient's alkalosis or hypomagnesemia, which is quickly eliminated by intravenous injection of 5% of Ascorbic acid in a dose of 10 ml. After arresting the attack of tetanic convulsive syndrome, the following intake of vitamin D and calcium preparations in the form of combined drugs is recommended.