Hypocalcemia: what is it, symptoms, treatment, causes, signs. Hypocalcemia in children. Clinical observation

The normal concentration of calcium in the blood plasma is 2.2-2.5 mmol / l. Its content below 1.87 mmol/l is defined as hypocalcemia.

Hypocalcemia can be either acute or chronic. In any case, this syndrome is expressed by changes in electrophysiological processes.

Hypocalcemia: causes

The formation of hypocalcemia occurs for various reasons and can be caused by various factors.

A common cause of hypocalcemia is hypoparathyroidism - a disease expressed by a decrease in the content of parathyroid hormone in the blood as a result of long-term ischemia of the parathyroid glands. Parathyroid hormone is necessary in order for the level of calcium ions in the blood plasma to be maintained at the required vital level. A decrease in the level of the hormone leads to excessive excretion of calcium by the kidneys and a decrease in its release from bone tissue.

Magnesium deficiency also leads to a decrease in calcium levels, which also contributes to a decrease in the production of parathyroid hormone and vitamin D activity. A similar violation is observed with hypomagnesemia.

In addition, the parathyroid hormone antagonist, thyrocalcitonin, can also cause hypocalcemia if its secretion is increased.

No less rarely, hypocalcemia develops against the background of hypovitaminosis D, in which the mechanism of calcium absorption in the intestine and its exchange in bone tissue changes.

In violation of the absorption of calcium by the mucous membrane of the small intestine, resulting from diseases of the intestine, such as chronic enteritis, resection of the small intestine, malabsorption syndrome, the development of hypocalcemia is also possible.

Causes of hypocalcemia can be diseases such as acholia, and hypoalbuminemia.

A decrease in calcium concentration in acholia occurs as a result of the cessation of delivery of bile to the small intestine, which disrupts the process of cavitary and membrane digestion and vitamin D metabolism.

With hypoalbuminemia, a disease characterized by a decrease in protein in the blood, the level of serum calcium decreases due to the bonds of its fractions with albumins.

The concentration of calcium also decreases with uncompensated chronic alkalosis, when, as a result of an increase in the pH level of the blood, calcium ions actively bind to proteins.

The causes of hypocalcemia can be tumor neoplasms, hypodynamia, liver damage by toxic substances, taking certain medications - interleukins and corticosteroids.

Quite often the hypocalcemia develops at and shock states.

As a result of renal failure, due to a decrease in the resorption of phosphorus and calcium salts, the development of the syndrome is also possible.

Signs of hypocalcemia

The acute form of hypocalcemia is a rather serious disease in which there is a syndrome of massive destruction of special cells - zukaryotes. This situation occurs with traumatic shock, burns, hemolysis, and the use of cytostatics. At the same time, ionized calcium rapidly leaves the blood. The situation of the patient is even more complicated if cytolysis - the destruction of these cells, is combined with acute renal failure. But the acute form often proceeds with mild symptoms and ends quickly. Signs of hypocalcemia in this case are frequent convulsions.

The chronic form of the syndrome is expressed by titanium and increased neuromuscular excitability. Therefore, signs of hypocalcemia are expressed by paresthesia - numbness, tingling and goosebumps on the skin. In addition, there are laryngospasm (sudden contraction of the muscles of the larynx), bronchospasm (narrowing of the bronchi), convulsions.

Spasms also occur on the feet, hands, facial muscles. Patients have depression, psychoses, and short-term respiratory arrest often occurs.

Sometimes hypocalcemia is manifested by hypocoagulation and hemorrhagic syndromes. In this case, increased bleeding occurs, as a result of a decrease in blood clotting and permeability of the walls of blood vessels due to a lack of calcium in the body.

Calcium deficiency leads to brittle hair and nails, heart rhythm disturbance and the development of cataracts, diseases of the bones and teeth.

If hypocalcemia leads to impaired brain activity, then the symptoms are expressed by memory loss, delirium, confusion, hallucinations. If proper medical measures are taken quickly, these processes are reversible.

Treatment of hypocalcemia

Usually, a decrease in calcium concentration is detected during a blood test and most often even before the symptoms of the syndrome begin to be pronounced. For a more detailed diagnosis, the patient's blood and urine biochemistry is once again examined, and a general examination is carried out to determine the cause of the decrease in calcium levels.

Treatment of the syndrome involves not only replenishing calcium deficiency, but also eliminating the cause of its development.

Hypoparathyroidism is treated with hormone therapy. To stop an attack of titanium in an acute form of hypocalcemia, intravenous administration of calcium gluconate or calcium chloride solution is prescribed.

For the treatment of chronic hypocalcemia, ergocalciferol, calcitriol (vitamin D), as well as calcium tablets - calcium carbonate, calcium gluconate are prescribed.

Decompensated alkalosis is treated with drugs that correct the acid-base state of the blood.

An obligatory condition for the treatment of hypocalcemia is the normalization of the level of magnesium, potassium and protein in the blood plasma.

In diseases of the gastrointestinal tract that cause calcium deficiency, adequate therapy is prescribed to treat the underlying disease.

Hypocalcemia - total plasma calcium concentration less than 8.8 mg/dL (

Manifestations include paresthesia, tetany, and, in severe cases, epileptic seizures, encephalopathy, and heart failure. Diagnosis is based on determining the level of calcium in the plasma. Treatment of hypocalcemia involves the administration of calcium, sometimes in combination with vitamin D.

ICD-10 code

E83.5 Disorders of calcium metabolism

Causes of hypocalcemia

Hypocalcemia is due to a number of reasons. Some of them are listed below.

Hypoparathyroidism

Hypoparathyroidism is characterized by hypocalcemia and hyperphosphatemia, often causing chronic tetany. Hypoparathyroidism develops when parathyroid hormone (PTH) is deficient, often due to removal or damage to the parathyroid glands during thyroidectomy. Transient hypoparathyroidism is observed after subtotal thyroidectomy. Permanent hypoparathyroidism results from less than 3% of thyroidectomy performed by experienced surgeons. Symptoms of hypocalcemia usually develop 24 to 48 hours after surgery, but may take months or years to appear. PTH deficiency is more often observed after radical thyroidectomy for cancer or as a result of surgical interventions on the parathyroid glands themselves (subtotal or total parathyroidectomy). Risk factors for severe hypocalcemia after subtotal parathyroidectomy include severe preoperative hypercalcemia, removal of a large adenoma, and elevated alkaline phosphatase.

Idiopathic hypoparathyroidism is a rare sporadic or hereditary condition in which the parathyroid glands are absent or atrophied. It appears in childhood. The parathyroid glands are sometimes absent in aplasia of the thymus and in abnormalities of the arteries extending from the bronchial branches (Dee-George's syndrome). Other hereditary forms include the X-linked genetic syndrome of hypoparathyroidism, Addison's disease, and mucocutaneous candidiasis.

Pseudohypoparathyroidism

Pseudohypoparathyroidism combines a group of disorders characterized not by hormone deficiency, but by resistance of the target organ to PTH. There is a complex genetic transmission of these disorders.

Patients with type la pseudohypoparathyroidism (Albright's hereditary osteodystrophy) have a mutation in the Gsa1 stimulatory protein of the adenylate cyclase complex. As a result, a violation of the normal renal phosphaturic response or an increase in the level of urinary cAMP to PTH develops. Patients usually develop hypocalcemia as a result of hyperphosphatemia. Secondary hyperparathyroidism and bone damage may develop. Associated anomalies include short stature, round face, mental retardation with calcification of the basal ganglia, short metatarsal and metacarpal bones, mild hypothyroidism, and other less significant endocrine disorders. Since only the maternal allele of the mutated gene is expressed in the kidneys, patients who have an abnormal paternal gene, despite the presence of somatic signs of the disease, will not develop hypocalcemia, hyperphosphatemia, or secondary hyperparathyroidism; this condition is sometimes described as pseudopseudohypoparathyroidism.

Less information is available on type lb pseudohypoparathyroidism. These patients present with hypocalcemia, hyperphosphatemia, and secondary hyperparathyroidism, but no other associated abnormalities.

Type II pseudohypoparathyroidism is even rarer than type I. In these patients, exogenous PTH increases urinary cAMP but does not increase plasma calcium or urinary phosphate. Intracellular resistance to cAMP is suspected.

Vitamin D deficiency

Vitamin D deficiency may develop due to insufficient dietary intake or reduced absorption due to hepatobiliary disorders or intestinal malabsorption. It may also develop as a result of altered vitamin D metabolism, as seen with certain drugs (eg, phenytoin, phenobarbital, rifampin), or as a result of insufficient sun exposure. The latter is a common cause of acquired vitamin D deficiency in institutionalized elderly people and in people living in countries with a northern climate and wearing closed clothes (for example, Muslim women in England). In type I vitamin D-dependent rickets (pseudo-vitamin D-deficient rickets), which is an autosomal recessive disease, a mutation occurs in the gene encoding the enzyme 1 hydroxylase. Normally, this enzyme in the kidneys is involved in the conversion of the inactive form of 25hydroxycholecalciferol into the active form of 1,25dihydroxycholecalciferol (calcitriol). In type II vitamin D dependent rickets, the target organs are resistant to the active form of the enzyme. Vitamin D deficiency, hypocalcemia, and severe hypophosphatemia are observed. Muscle weakness, pain, and typical bone deformities develop.

kidney disease

Tubular renal disease, including proximal tubular acidosis due to nephrotoxins (eg, heavy metals) and distal renal tubular acidosis, can cause severe hypocalcemia due to abnormal renal calcium loss and reduced renal formation of calcitriol. Cadmium specifically causes hypocalcemia by damaging proximal tubular cells and disrupting vitamin D conversion.

Renal failure can lead to hypocalcemia by reducing the formation of calcitriol due to direct damage to the kidney cells and suppression of 1-hydroxylase in hyperphosphatemia.

Other causes of hypocalcemia

Decreased magnesium levels, as seen with intestinal malabsorption or inadequate dietary intake, can cause hypocalcemia. There is a relative deficiency of PTH and resistance of target organs to the action of PTH, resulting in a plasma magnesium concentration of less than 1.0 mg/dL (

Acute pancreatitis causes hypocalcemia because lipolytic substances released by the inflamed pancreas chelate with calcium.

Hypoproteinemia can reduce the protein-bound plasma calcium fraction. Hypocalcemia due to reduced protein binding is asymptomatic. Since the level of ionized calcium remains unchanged, this condition is called artificial hypocalcemia.

Increased bone formation with impaired calcium uptake is observed after surgical correction of hyperparathyroidism in patients with generalized fibrous osteodystrophy. This condition is called the hungry bone syndrome.

Septic shock can cause hypocalcemia by suppressing the release of PTH and reducing the conversion of the inactive form of the vitamin to calcitriol.

Hyperphosphatemia causes hypocalcemia by mechanisms that are not fully understood. Patients with renal insufficiency and subsequent phosphate retention are usually in the supine position.

The drugs that cause hypocalcemia are mainly those used to treat hypercalcemia: anticonvulsants (phenytoin, phenobarbital) and rifampin; transfusion of more than 10 units of citrated blood; radiocontrast agents containing the bivalent chelating agent ethylenediaminetetraacetate.

Although excessive secretion of calcitonin should theoretically cause hypocalcemia, low plasma calcium levels are rarely observed in patients with large amounts of calcitonin circulating in the blood due to medullary thyroid cancer.

Symptoms of hypocalcemia

Hypocalcemia is often asymptomatic. The presence of hypoparathyroidism is often suggested by clinical manifestations (eg, cataracts, calcification of the basal ganglia, chronic candidiasis in idiopathic hypoparathyroidism).

Symptoms of hypocalcemia are due to a violation of the membrane potential, which leads to neuromuscular irritability. Spasms of muscles of a back and legs are more often observed. Gradually developing hypocalcemia can cause mild diffuse encephalopathy and should be suspected in patients with unexplained dementia, depression, or psychosis. Sometimes there is swelling of the optic nerve, with prolonged hypocalcemia, cataracts may develop. Severe hypocalcemia with plasma calcium levels less than 7 mg/dL (

Tetany develops with severe hypocalcemia, but may develop as a result of a decrease in the ionized fraction of plasma calcium without significant hypocalcemia, which is observed in severe alkalosis. Tetany is characterized by sensory symptoms, including paresthesias of the lips, tongue, fingers, feet; carpopedal spasm, which can be long and painful; generalized muscle pain, spasm of the facial muscles. Tetany can be severe with spontaneous symptoms or latent, requiring provocative tests to detect. Latent tetany is more common at plasma calcium levels of 7–8 mg/dl (1.75–2.20 mmol/l).

Chvostek's and Trousseau's symptoms are easily performed at the bedside to detect latent tetany. Chvostek's symptom is an involuntary contraction of the muscles of the face in response to a light blow with a hammer in the area of ​​​​the passage of the facial nerve in front of the external auditory canal. Positive at

Patients with severe hypocalcemia sometimes experience arrhythmias or heart blocks. With hypocalcemia on the ECG, lengthening of the QT and ST nerves is usually observed. There are also changes in repolarization in the form of a pointed T wave.

With chronic hypocalcemia, many other disorders can be observed, such as dry and flaky skin, brittle nails, and coarse hair. With hypocalcemia, candidiasis is sometimes observed, but more often in patients with idiopathic hypoparathyroidism. Prolonged hypocalcemia leads to the development of cataracts.

Diagnosis of hypocalcemia

Hypocalcemia - diagnosis is based on determining the level of total plasma calcium

If the cause of hypocalcemia is not obvious (eg, alkalosis, renal failure, massive blood transfusion), further investigations are necessary. Since hypocalcemia is the main stimulus for PTH secretion, PTH levels should be elevated during hypocalcemia. Low or normal PTH levels suggest hypoparathyroidism. Hypoparathyroidism is characterized by low plasma calcium, high plasma phosphate, and normal alkaline phosphatase. Hypocalcemia with high plasma phosphate levels is indicative of renal failure.

Type I pseudohypoparathyroidism can be distinguished by the presence of hypocalcemia despite normal or elevated circulating PTH levels. Despite the presence of high levels of circulating PTH, cAMP and phosphate are absent in the urine. Provocation tests with injections of parathyroid extracts or recombinant human PTH do not cause an increase in plasma or urinary cAMP levels. Patients with type la pseudohypoparathyroidism often also have skeletal abnormalities, including short stature, shortening of the first, fourth, and fifth metacarpals. Type lb patients have renal manifestations without skeletal abnormalities.

In type II pseudohypoparathyroidism, exogenous PTH increases urinary cAMP but does not cause phosphaturia or an increase in plasma calcium. Before diagnosing pseudohypoparathyroidism type II, vitamin D deficiency must be ruled out.

With osteomalacia or rickets, typical skeletal changes are visible on the x-ray. Plasma phosphate levels are often slightly low and alkaline phosphatase levels are elevated, reflecting increased mobilization of calcium from bone. Determination of plasma levels of active and inactive forms of vitamin D can help differentiate vitamin D deficiency from vitamin D-dependent conditions. Familial hypophosphatemic rickets is identified by associated renal phosphate loss.

Treatment of hypocalcemia

With tetany, 10 ml of a 10% solution of calcium gluconate is administered intravenously. The answer may be complete, but it only lasts a few hours. Repeated infusions of 20-30 ml of 10% calcium gluconate solution in 1 L of 5% dextrose solution or the addition of a continuous infusion may be required over the next 12-24 hours. Calcium infusions are dangerous in patients receiving digoxin and should be administered slowly with constant ECG monitoring. If tetany is associated with hypomagnesemia, a transient response to calcium or potassium administration may develop, but full recovery can only occur when magnesium deficiency is corrected.

In transient hypoparathyroidism after thyroidectomy and partial parathyroidectomy, oral calcium may be sufficient. However, hypocalcemia can be especially severe and prolonged after subtotal parathyroidectomy in patients with chronic renal failure or end-stage renal disease. After surgery, prolonged parenteral administration of calcium may be required; within 5-10 days, the introduction of 1 g per day of calcium may be required. An increase in the level of plasma alkaline phosphatase under such conditions may be evidence of a rapid uptake of calcium by bone tissue. The need for large amounts of parenteral calcium usually persists until the level of alkaline phosphatase decreases.

In chronic hypocalcemia, oral calcium and sometimes vitamin D are usually adequate. Calcium can be taken as calcium gluconate (90 g elemental calcium/1 g) or calcium carbonate (400 mg elemental calcium/1 g) to provide one to two grams of elemental calcium per day. Although any form of vitamin D can be used, analogues of the active form of the vitamin have the best effect: 1-hydroxylated compounds, as well as synthetic calcitriol and pseudo-hydroxylated analogues (dihydrotachysterol). These drugs have a more active effect and are quickly excreted from the body. Calcitriol is especially useful in renal insufficiency, as it does not require metabolic changes. Patients with hypoparathyroidism usually respond to doses of 0.5-2 mcg/day orally. In pseudohypoparathyroidism, only oral calcium intake can sometimes be used. The result of the action of calcitriol is achieved when taking 1-3 mcg / day.

Vitamin D supplementation is not effective without an adequate intake of calcium (1-2 g of elemental calcium per day) and phosphate. Vitamin D toxicity with severe symptomatic hypercalcemia can be a serious complication of treatment with vitamin D analogs. After stabilization of calcium levels, plasma calcium concentrations should be monitored daily for the first month and then at 1-3 monthly intervals. The maintenance dose of calcitriol or dihydrotachysterol is usually reduced over time.

For vitamin D deficiency rickets, the usual dose is 400 IU per day of vitamin D (as vitamin D2 or D3); in the presence of osteomalacia for 6-12 weeks, a dose of 5000 IU per day of vitamin D is prescribed, and then reduced to 400 IU per day. At the initial stages of treatment, an additional appointment of 2 g of calcium per day is desirable. In patients with rickets or osteomalacia due to insufficient sun exposure, sun exposure or the use of ultraviolet lamps may be sufficient.

With vitamin D-dependent type I rickets, the use of 0.25-1.0 micrograms of calcitriol per day is effective. In patients with vitamin D-dependent type II rickets, vitamin D is not effective for treatment [a more understandable term is proposed - hereditary resistance to 1,25(OH)2D].

Hypocalcemia is treated depending on the severity of bone damage. In severe cases, up to 6 mcg/kg of body weight or 30-60 mcg/day of calcitriol with the addition of up to 3 g of elemental calcium per day is necessary. When treating with vitamin D, control of plasma calcium levels is necessary; hypercalcemia, which sometimes develops, usually responds quickly to a change in the dose of vitamin D.

Hypocalcemia can occur in children of all ages. There is a high probability of calcium deficiency in babies who were born prematurely, as well as in children who experienced hypoxia at birth. In an older child, this condition is often caused by accelerated growth and excessive stress (both physical and mental). The main causes of hypocalcemia include:

  • lack of magnesium;
  • reduced protein levels;
  • vitamin D deficiency;
  • diseases of the gastrointestinal tract;
  • kidney failure;
  • acute pancreatitis;
  • poisoning;
  • taking certain medicines.

Hypocalcemia can develop due to an unbalanced diet. The diet of the child should contain foods rich in calcium and magnesium, this is especially important during the growth period of the baby. Improper nutrition often leads to a lack of calcium in adolescence: excessive consumption of salt, sugar, caffeine, as well as carbonated drinks high in phosphorus, beloved by many teenagers, leads to calcium leaching from the body.

Symptoms

Often, hypocalcemia in children is asymptomatic, in this case, a lack of calcium is detected only according to the results of the tests. However, a deficiency of an important trace element can also be manifested by one or more signs:

  • aching muscle pain;
  • numbness of the limbs;
  • muscle spasms;
  • violation of the heart rhythm;
  • dryness and peeling of the skin;
  • brittle nails;
  • hair loss;
  • lack of appetite.

In young children, often calcium deficiency is manifested by convulsions, in which the hand assumes a characteristic position. Due to spasm of the glottis, some have stridor. Hypocalcemia leads to a deterioration in blood clotting: even a small cut in a child bleeds for a long time. Lack of calcium affects the nervous system: the child becomes irritable, he is tormented by insomnia.

Diagnosis of hypocalcemia in a child

It is important to diagnose hypocalcemia in a child in a timely manner, because this is the only way to avoid the negative consequences that such a condition leads to. If signs characteristic of hypocalcemia appear, you need to make an appointment with a pediatrician, if necessary, he will give a referral to an endocrinologist. First, the doctor examines the child, interviews a small patient and / or parents. You can diagnose a pathological condition using:

  • general blood test;
  • blood biochemistry;
  • urinalysis;
  • x-ray.

A blood test allows you to determine what level of potassium ions is in the serum. With the help of biochemistry, the concentration of magnesium, phosphate, vitamin D in the blood is detected. X-rays are needed to evaluate bone structures. Sometimes an MRI of the internal organs is additionally prescribed.

Complications

If hypocalcemia in a child is not treated, then there is a high likelihood of complications. Calcium is important for the normal functioning of all organs, so when it is deficient in the body, failures occur. If calcium deficiency occurs during the growth of a child, then this leads to improper development of bone tissue, entails various problems with internal organs and systems. Against the background of hypocalcemia may develop:

  • neuritis;
  • osteoporosis;
  • cataract;
  • heart failure;
  • bone deformity;
  • kidney failure.

Only timely diagnosis and treatment of hypocalcemia will help to avoid consequences. Therefore, at the first manifestations indicating calcium deficiency in a child, it is important to consult a doctor.

Treatment

What can you do

Parents need to promptly respond to the manifestations of hypocalcemia in a child and consult a doctor at the first characteristic signs. In the future, it is necessary to ensure that the child adheres to the recommendations that the doctor will give. Some foods will help increase the level of calcium, magnesium and vitamin D in the body: dried fruits, dairy products, legumes, seafood. Foods high in calcium should be included in a child's diet, especially during the growth period. However, it should be remembered that nutrition must be balanced, because excessive calcium in the body is also dangerous. Recommendations for adjusting nutrition in case of hypocalcemia should be given by a doctor.

It is not necessary to give the child preparations containing calcium without prior consultation with a specialist, because it is impossible to choose supplements and vitamin complexes on your own. With hypocalcemia, it is recommended to walk more with the child in sunny weather. Sunlight stimulates the synthesis of vitamin D.

What does a doctor do

The doctor prescribes treatment based on the cause of the development of hypocalcemia in the child, the age of the patient, the form of the disease. In acute hypocalcemia, hospitalization is required, treatment is carried out in a hospital. Therapy consists in the introduction of sterile solutions of calcium gluconate, glucose, sodium chloride.

In chronic hypocalcemia, therapy is carried out at home. Treatment consists of:

  • taking calcium-containing drugs;
  • a course of multivitamins;
  • diet therapy;
  • mode correction.

If hypocalcemia occurs against the background of any disease, in parallel with the restoration of calcium levels in the body, the underlying cause is treated. In the presence of various complications, the course of treatment is selected individually.

Prevention

Prevention of hypocalcemia in children comes down to simple measures. Preventing calcium deficiency is the task of parents. Necessary:

  • provide the child with a balanced diet;
  • monitor the child's eating habits (limit salt and sugar intake; make sure that the child does not drink sugary carbonated drinks; explain to the teenager the consequences of coffee abuse);
  • encourage sports;
  • long walks with the child in sunny weather;
  • set mode;
  • make sure that mental and physical stress is not excessive;
  • timely respond to various diseases and treat them.

Comments 2

Hypocalcemia is a pathological condition that develops as a result of a violation of the electrophysiological process, and is characterized by a decrease in the level of calcium in the body. This pathology can be both acute and chronic. It is important to timely establish the cause of the progression of the disease and begin adequate treatment in order to avoid the development of health-threatening consequences. Hypocalcemia can occur in people of various age groups, including young children.

The reasons

  • hypoparathyroidism. This is the most common cause of the progression of pathology in humans;
  • increased production of thyrocalcitonin;
  • hypovitaminosis D. In the case of the progression of this pathology, the processes of calcium absorption in the human intestine and its metabolism in bone structures are disrupted. This cause most often leads to the development of pathology in children;
  • hypomagnesemia;
  • acholia;
  • diseases of the gastrointestinal tract;
  • uncompensated chronic alkalosis;
  • hypoalbuminemia;
  • inflammatory diseases of the pancreas. In the case of their progression, the deposition of calcium salts is observed in the area of ​​fat necrosis;
  • toxic shock;
  • metastasis of malignant tumors;
  • bone pathology;
  • taking certain groups of drugs;
  • hypocalcemia in newborns can develop due to prematurity or if the mother has diabetes mellitus. Also, the reason for the decrease in the concentration of calcium in the body may be that the baby is fed with special mixtures, which contain phosphorus.

Symptoms

Hypocalcemia can be asymptomatic for a long time. Symptoms may not appear, even if the calcium concentration is not lower than 2.0–2.2 mmol per liter. If this indicator decreases, then the symptoms of the pathology become more and more pronounced.

In the case of progression of hypocalcemia, the following symptoms are observed:

  • since the disease is often combined with hyperkalemia, the first symptom that manifests itself in a person is increased excitability of nerve and muscle structures;
  • paresis of the limbs;
  • bone pain;
  • memory impairment;
  • convulsions;
  • bronchospasm;
  • insomnia;
  • dizziness;
  • Chvostek's symptom;
  • Trousseau's symptom;
  • against the background of the progression of hypocalcemia, trophic disorders are observed;
  • vomit;
  • laryngospasm.

It is important, when the first signs of pathology appear, to immediately contact a medical institution for diagnosis, identification of the main cause of the progression of hypocalcemia, and also for the treatment of this condition.

Hypocalcemia in children

Hypocalcemia in children can develop due to malnutrition. Often the pathology affects young children. If there is an accelerated growth of the child, increased loads, then usually the symptoms are more pronounced:

  • tetany. It is usually atypical. The baby may have numb legs, twitch certain muscles, and so on;
  • mild muscle spasm;
  • diarrhea;
  • carpopedal spasm;
  • laryngospasm;
  • increased intracranial pressure.

Diagnostics

Hypocalcemia is diagnosed by a pediatrician or endocrinologist. The standard diagnostic program for this pathological condition includes:

  • . Needed to assess the level of calcium ions in the serum;
  • x-ray. This instrumental method is necessary to assess the state of bone structures in the body;
  • . It makes it possible to find out the concentration of bilirubin in the blood, magnesium, vitamin D, creatinine, phosphate, and so on.

Treatment

Treatment of hypocalcemia should be started as soon as test results are available. The treatment plan is developed by the attending physician, taking into account the general condition of the patient, as well as the severity of the course of his disease:

  • diet therapy. The doctor is developing a special diet that will be enriched with calcium salts - up to 2000 mg per day;
  • the patient is recommended to spend as much time as possible in the sun, but not to sunbathe, but simply to take walks;
  • do not use sunscreen cosmetics, as they block the ultraviolet light necessary for the full synthesis of vitamin D;
  • drug treatment is based on taking drugs containing calcium and vitamin D;
  • it is also important to treat diseases that could provoke the progression of hypocalcemia.

In the case of acutely developing hypocalcemia, urgent measures must be taken, since this condition threatens not only the health, but also the life of the patient:

  • it is shown to carry out slow intravenous administration of sterile solutions of sodium chloride, glucose, calcium gluconate. This therapy is mandatory to reduce the manifestations of the disease, as well as the risk of complications;
  • if hypomagnesemia is observed against the background of acute hypocalcemia, it is indicated to inject magnesium sulfate into a vein.

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Hypocalcemia occurs when the level of required calcium decreases. This is due to the fact that the electrophysiological process is disturbed. Hypocalcemia can be acute or chronic. It is very important to establish the cause of this disease in time and start timely treatment, because due to a lack of calcium, system organs do not work properly, a person feels bad and looks bad. it is especially important to pay attention to hypocalcemia that occurs in children, it is very dangerous and can lead to further pathologies.

Causes of hypocalcemia

Many factors can provoke hypocalcemia:

1. Due to hypoparathyroidism - autoimmune, postoperative, familial and idiopathic.

2. Pseudohypoparathyroidism, when extracellular calcium is lost very quickly.

3. Due to hypoalbuminemia, Albright's disease, in which there is not enough vitamin D.

4. Due to renal failure, in cases of reduced resorption of calcium and phosphorus salts.

5. Due to the fact that the pancreas is affected, when inflammation occurs in this organ, calcium salts begin to debug in the area of ​​fat necrosis.

6. In cases of hypomagnesemia.

7. If large tumors begin to metastasize, because of this, the calcium salt in the bones is adjusted and hypocalcemia develops.

9. In cases of bone disease.

10. Due to some critical conditions of the body.

11. Due to the intake of many drugs, due to phosphates, anticonvulsants, diuretics, certain antibiotics, antitumor drugs, calcitonin, diphosphonates.

12. In newborns, this disease can occur due to prematurity and if the mother has diabetes.

13. In newborns, calcium levels may temporarily decrease due to the fact that they are fed or mixtures that include phosphorus.

Symptoms of hypocalcemia

The most dangerous form of hypocalcemia is acute, because it has its own characteristics. The first symptom is massive cytolysis. This can happen if the patient has hepatosis, hemolysis, in cases of the use of cytostatics, severe traumatic shock and crush syndrome. Because of this, calcium begins to quickly be excreted from the blood. Hypocalcemia quickly begins to develop if there is still renal failure during cytolysis.

The symptoms of hypocalcemia are very different, they lead to various complications - the appearance and seizures, when the disease is severe. The acute form does not have many symptoms, if it is treated in time, it will pass.

The chronic form of hypocalcemia is considered pronounced, because it develops due to rickets, hypomagnesemia, chronic renal failure, and hypoparathyroidism. The main symptom is increased excitability in the neuromuscular system and tetany, which is characterized by peripheral and perioral paresthesia, carpo-pedal spasm.

Mild symptoms of hypocalcemia can develop into bronchospasm, convulsions, and laryngospasm.

Often chronic hypocalcemia is characterized by neuromuscular and neurological symptoms, patients experience spasms in the muscles of the hands, feet, face, larynx, psychosis may appear, the patient is constantly in, very irritable, his breathing stops.

Features of hypocalcemia in children

This disease very often appears in children, especially young children, who are malnourished and lack calcium. In cases of accelerated growth of the child and increased physical and mental stress, the symptoms of hypocalcemia are pronounced.

Children are characterized by the following symptoms:

1. Tetany of an atypical nature, the child is clumsy when moving, his legs go numb and his muscles are supported.

2. Mild muscle spasm - colic in the gallbladder, abdominal pain, short breathing, in which it seems that the child is suffocating.

3. Often there is a spasm in the calf muscle, it appears, because the child falls.

4. Increased intracranial pressure.

5. Carpopedal spasm may occur.

6. Diarrhea.

7. Tetany.

8. Laryngospasm.

For children, these are very dangerous symptoms, because they cause many complications. Therefore, it is urgent to treat this disease.

Hypocalcemia after childbirth

This disease proceeds in an acute form, the level of calcium in the blood and tissues decreases sharply, and paresis of smooth and striated muscles occurs, paralysis of the pharynx, intestines, tongue, stomach can occur, in a difficult condition a woman falls into a coma.

Postpartum hypocalcemia is classified as an endocrine disease. This form of the disease is very rare.

Diagnosis of hypocalcemia

He speaks of a lack of calcium, therefore, they can often diagnose the disease first, and therefore pronounced symptoms already appear. In cases of detection of hypocalcemia, it is imperative to find out the cause of its occurrence. To do this, you need to be fully examined and additionally donate blood and urine, biochemistry of urine and blood will be required.

Treatment of hypocalcemia

Be sure to take vitamin D and preparations that contain calcium. If hypocalcemia has developed due to hypoparathyroidism, it must be urgently treated.

If the patient has no problems with the absorption of calcium by the small intestine, then with the help of calcium preparations, the disease can be cured in a short time. In cases of acute disease, intravenous administration of chloride, calcium gluconate and gluceptate may be required. For this, up to 200 mg of calcium is administered over several minutes. It must be remembered that calcium can irritate the venous walls, so it is best to inject it through a central venous catheter or into a large vein. Treatment must be prescribed by an endocrinologist after a thorough examination.

So, hypocalcemia is diagnosed when the blood level is less than 2.2 mmol / l. Most often, this disease occurs due to metabolic disorders, due to diseases when a person loses calcium along with urine. Symptoms may not develop immediately, therefore it is very important to identify hypocalcemia at an early stage and begin timely treatment.

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