Hypercalcemia is a severe emergency condition characterized by a sharp increase in the level of calcium in the blood. It is manifested by symptoms of intoxication: increasing weakness, intense thirst, decreased appetite, nausea, indomitable vomiting, spastic abdominal pain, apathy, absent-mindedness, forgetfulness, arthralgias and myalgias. As a result of calcification, the work of internal organs is disrupted. Key diagnostic methods are laboratory determination of hypercalcemia, bone and kidney x-ray, ECG. Treatment includes procedures that normalize the concentration of calcium – diuresis, hemodialysis, surgical removal of the source of hypersecretion of PTH.
ICD 10
E83.5 E21
Meaning
Synonyms of hypercalcemia caused by hyperparathyroidism are hyperparathyroid crisis, acute hyperparathyroid intoxication. The condition develops in cases when the amount of calcium entering the bloodstream exceeds the functional capabilities of the kidneys for its excretion. The value of the critical concentration of calcium is individual, but in most people its toxic effect is manifested at indicators of 3.49-4.19 mmol / l and higher. There are no reliable epidemiological data on the prevalence of hypercalcemia. Among women, the incidence is 4 times higher than among men. About 80% of patients belong to the age group from 40 to 70 years. People over the age of 60 are most susceptible to the crisis.
Causes
The risk group for the development of a crisis condition includes patients with hypercalcemia. The pathology is based on a violation of calcium metabolism: increased absorption of trace elements from the intestine, intensive leaching from bones, insufficient excretion by the kidneys, reduced absorption by bone tissue. Common causes of the crisis include:
- Hyperparathyroidism. Acute hypercalcemia is characteristic of severe primary, secondary or tertiary hyperparathyroidism. An exacerbation of the disease, rough palpation of the parathyroid glands, rapid dehydration, pregnancy, infection, fracture, immobility, treatment with absorbable antacids can provoke a crisis.
- Oncological diseases. Often, a hypercalcemic condition results from the formation of a bone tumor or the spread of metastases into the bone tissue. In addition, an increase in the amount of calcium is observed in myeloma due to osteolysis and in hormone-secreting neoplasms that exhibit activity similar to parathyroid hormone.
- Taking medications. The most likely cause is hypervitaminosis D, in which the absorption of calcium through the intestine and its reabsorption in the kidneys increases. Less often, a crisis occurs when using thiazide diuretics, hormonal agents, drugs with lithium, magnesium.
- Acute renal failure. With acute renal failure, all renal functions are disrupted, including excretory and filtration. Calcium is not excreted from the body, its plasma level is continuously increasing.
There are also less likely factors for the development of a hypercalcemia. They are Burnett’s syndrome, thyrotoxicosis, hypothyroidism, adrenal insufficiency, acromegaly, familial benign hypercalcemia, Paget’s disease, granulomatous diseases (sarcoidosis, tuberculosis, histoplasmosis), immobilization.
Pathogenesis
Hypercalcemia is the result of a rapid and sudden increase in the concentration of calcium in the plasma, provoking a state of acute intoxication. Opinions on the critical level of the trace element differ, the approximate range is 3.5–4.2 mmol/L. Normally, the indicators range from 2.4 to 2.9 mmol/l. Excess calcium is caused by its excessive intake from the outside and / or active excretion from the bone, intensive renal reabsorption. The most common cause of hypercalcemia is primary hyperparathyroidism. In this disease, excessive secretion of parathyroid hormone occurs by adenoma or hyperplastic tissues of the parathyroid glands. Under the influence of PTH, the content of serum calcium increases.
Parathyroid hormone, acting directly on the bones, increases the activity of osteoclasts, as a result of which citric acid is intensively released. Acidosis develops, which mobilizes the transport of calcium, phosphorus from bone tissues to plasma. The effect of PTH on the kidneys is to stimulate the reabsorption of calcium and inhibit the reabsorption of phosphorus, chlorides, sodium, potassium. Developing hypercalcemia suppresses the activity of vasopressin, which leads to polyuria and polydipsia, and also reduces neuromuscular excitability with the formation of muscular hypotension. In addition to an excess of parathyroid hormone, acute hypercalcemia can provoke an imbalance of ACTH, glucocorticoids, somatotropin, thyroxine, androgens, estrogens.
Symptoms
A rapid and sudden increase in signs of acute hypercalcemia is characteristic. At first, patients note causeless weakness, decreased muscle tone, nausea, joint and muscle pain, increased blood pressure. As intoxication increases, indomitable vomiting, constipation, and pain in the epigastric region appear, which may be of a shingling nature. Urination becomes frequent and abundant, the feeling of thirst increases, appetite disappears. Due to dehydration, patients feel dry mouth, itchy skin, headaches and dizziness. After a while, polyuria is replaced by oliguria, and then anuria.
Vomiting provokes dehydration, water-electrolyte imbalance. Abdominal pains are spastic in nature, sometimes similar to those with acute appendicitis, which makes diagnosis much more difficult. In the presence of diseases of the gastrointestinal tract or complications of this type against the background of hyperparathyroidism, perforation of a peptic ulcer, gastric or intestinal bleeding, acute pancreatitis is possible. Calcium salts are deposited in the parenchyma of various organs. Depending on the localization of calcifications, the symptoms of the crisis may resemble pneumonia, acute pulmonary, cardiac or renal failure. Sometimes intravascular thrombosis and DIC syndrome develop.
Neuropsychiatric disorders in crisis are represented by drowsiness, partial memory loss, psychasthenia, depression. With increased hypercalcemia, patients become inhibited or, conversely, excessively excitable. In critical cases, delusions with visual hallucinations, epileptic seizures, psychotic states, comas are formed.
Complications
A severe course of the crisis is observed with an increase in the calcium content to 5 mmol / l. The activity of the central nervous system is suppressed, the functions of the respiratory and vasomotor centers in the brain are inhibited, irreversible shock develops. Cardiovascular insufficiency with collapse, severe respiratory disorders (pulmonary edema) are formed. Inhibition, slowness of movement is progressing, the risk of stupor and coma with a fatal outcome is increasing. The overall mortality rate is 60%, among patients aged 60-65 it reaches 80-90%. The immediate cause of mortality is often thrombosis of large vessels, infarctions of vital organs (kidneys, lungs, heart).
Diagnostics
The diagnosis of a hypercalcemia is established by an endocrinologist on the basis of anamnesis data, assessment of clinical manifestations, results of instrumental studies of the state of bone tissue and laboratory tests that detect hypercalcemia. In the anamnesis of patients, hyperparathyroidism, bone tumors or bone metastases, treatment with easily absorbed antacids, impaired renal function is often determined. Objective diagnostic methods include:
- Blood test. In the initial stages of the crisis, moderate leukocytosis, increased ESR and moderate normochromic anemia are noted. With kidney dysfunction – an increase in protein, creatinine, urea.
- The study of calcium. In the initial emergency diagnosis of hypercalcemia, a Sulkovich test is performed (the sample is cloudy, the result is positive). The indicators of the blood test for calcium are more than 2.39 mmol/l. According to additional tests, hypokalemia, hypomagnesemia and hypophosphatemia are determined.
- Radiography. Densitometry reveals a decrease in bone density, subperiosteal resorption on the terminal, middle and main phalanges of the hands. The terminal phalanges are often scalloped, lacy. Radiography of the kidneys reveals signs of nephrocalcinosis (calcifications).
- Electrocardiography. ECG allows you to assess the effect of hypercalcemia on the heart. Tachycardia is characteristic, the QT interval is shortened, the RR interval is elongated.
Differential diagnosis is carried out to determine the cause of the crisis – primary, secondary or tertiary hyperparathyroidism, cancer, kidney pathology. The establishment of the underlying disease is necessary for the selection of adequate therapy. In a serious condition with organ damage, a crisis is differentiated with an acute attack of kidney stones, exacerbation of pancreatitis or stomach ulcers, acute psychosis, pneumonia, pulmonary edema, hypertensive crisis.
Treatment
Patients are hospitalized in the intensive care and intensive care unit. In an emergency, measures are taken to restore the volume of circulating blood. The next stage of treatment is normalization of calcium levels. The following methods are used to eliminate hypercalcemia:
- Forced diuresis. The procedures allow to increase the renal excretion of calcium. An isotonic sodium chloride solution is injected intravenously, followed by a furosemide solution. During the course of treatment, the potassium level is monitored.
- Plasma calcium binding. With the preservation of kidney function, the method of intravenous administration of sodium citrate solution or sodium-potassium-phosphate buffer is used. Phosphates bind calcium ions, reducing their concentration.
- Bone fixation of calcium. Calcitonin therapy is carried out – a thyroid hormone that stimulates the transfer of calcium from the blood into bone tissue. This method of treatment is safe for patients with renal insufficiency.
- Reduction of intestinal absorption of calcium. To reduce the exogenous absorption of calcium and enhance its excretion through the kidneys, glucocorticoids are prescribed. They are especially effective in vitamin D overdose, multiple myeloma, sarcoidosis.
- Therapy with PTH antagonists. An example of a parathyroid hormone antagonist is the antibiotic mitramycin. The drug is toxic, so its use in endocrinology is limited.
- Dialysis. Hemodialysis procedures with calcium-free dialysis are common. A special indication for this method is a hypercalcemia complicated by oligo– or anuria.
- NSAID therapy. In the case when hypercalcemia is caused by bone resorption, leaching of calcium from them, therapy with nonsteroidal anti-inflammatory drugs is recommended. They block the production of prostaglandins – mediators of bone destruction.
- Surgical operation. With adenoma, carcinoma or hyperplasia of the parathyroid glands, surgery is an effective treatment option. Tumor removal or resection of hyperplastic glandular tissue is performed.
Prognosis and prevention
Hypercalcemia is prognostically favorable in the absence of progressive renal dysfunction, azotemia and phosphatemia. The main preventive measures are timely diagnosis and adequate treatment of hyperparathyroidism, oncological diseases, kidney failure. People from risk groups need to monitor the intake of calcium – do not use absorbable antacids, only take vitamin D, thiazide diuretics, magnesium and lithium preparations as prescribed by a doctor.