hypocalcemia
Introduction
Introduction to hypocalcemia The total calcium in adults is about 1000~1300g, 99% is in the form of bone salt in bones and teeth, and the rest is in various soft tissues. Extracellular liquid calcium accounts for only 0.1% of total calcium, about 1g. Adult blood calcium level is about 2.2 ~ 2.6mmol / L (8.8 ~ 10.4mg / dl), mainly in three forms: 1 free calcium (50%), also known as ionized calcium; 2 protein bound calcium (40%); 3 can diffusely bind calcium (10%). When the serum albumin concentration is in the normal range, the blood calcium is lower than 2.2mmol/Ll (8.8mg/l) and the normal value is 2.2~2.70mmol/L, which is called hypocalcemia. There are small differences in blood calcium test reference values in different hospitals. Blood calcium is lower than 2.1mmol/l (8.4mg/l), and normal value is 2.1~2.55mmol/L, which is determined to be hypocalcemia. In acidosis or hypoproteinemia, only protein-bound calcium is reduced. At this time, blood calcium is lower than normal, but ionized calcium is not low, and no clinical symptoms occur. Conversely, in case of alkalosis or hyperproteinemia, free calcium is reduced, but Protein-binding calcium is increased, so serum calcium can still be normal, and clinical symptoms of hypocalcemia can occur. In the case of hypoproteinemia, the calculated calcium concentration needs to be calculated to diagnose hypocalcemia. basic knowledge Sickness ratio: 0.1% Susceptible people: no special people Mode of infection: non-infectious Complications: sinus tachycardia atrioventricular block congestive heart failure
Cause
Cause of hypocalcemia
Disease factor (45%)
1, hypoparathyroidism: including primary, secondary and pseudo-hypoparathyroidism. 1 primary hypoparathyroidism is a group of multi-factor diseases, such as congenital hypoparathyroidism or non-development, DiGeorge syndrome, autoimmune polygland syndrome type I, neonatal hypocalcemia Caused by congenital hypoparathyroidism, or hypercalcemia due to hyperparathyroidism or familial benign hypercalciuria in the mother, resulting in temporary hypoparathyroidism in the newborn; 2 secondary hypoparathyroidism is more common, more common in thyroid or parathyroid surgery and neck malignant tumor surgery, after radiotherapy, invasive diseases such as hemochromatosis, hepatolenticular degeneration, metastatic tumors, etc.; Bone starvation syndrome is another cause of hypocalcemia after surgery. It is seen in patients with severe hyperparathyroidism after parathyroidectomy, resulting in relative hypoparathyroidism resulting in a large amount of Ca2+ entering the bone cells. . Severe magnesium deficiency is a common cause of functional hypoparathyroidism, which can lead to parathyroid hormone (PTH) secretion disorders and the resistance of effector tissues such as bone and kidney to PTH. 3 pseudohypoparathyroidism is similar to hypoparathyroidism, but the parathyroid itself has no lesions, low calcium stimulates parathyroid hyperplasia, and PTH secretion increases, so serum PTH is often elevated.
2, vitamin D metabolic disorders: 1 vitamin D deficiency: more common in malnutrition, especially when exposed to too little sunlight; in addition to chronic diarrhea, steatorrhea, chronic pancreatitis, cystic fibrosis and gastrectomy 2 vitamin D Hydroxylation disorders: found in kidney failure, liver disease, hereditary 1 hydroxylase deficiency, vitamin D-dependent osteomalacia type I and other diseases. Due to the hydroxylation of vitamin D, the body cannot effectively produce active vitamin D3. There is also vitamin D-dependent osteomalacia type II, which is caused by mutations in the vitamin D receptor. 3 Vitamin D catabolism acceleration: long-term application of anti-epileptic drug phenobarbital can effectively enhance the activity of liver microsomal enzymes, so that vitamin D and 25 (OH) D3 accelerate catabolism in the liver. Although phenytoin has no direct effect on vitamin D catabolism, it can reduce the release of calcium from the bone and reduce the reabsorption of calcium by the intestine, which can also lead to hypocalcemia. At the same time, the use of anti-epileptic drugs can enhance the demand for vitamin D.
3, renal failure: renal failure caused by various reasons, the formation of 1,25 (OH) 2 D3 decreased, reducing intestinal calcium absorption; phosphorus excretion during renal failure reduced phosphorus retention caused by intestinal absorption of calcium decreased Hyperphosphatemia and bone resistance to PTH cause mobilization that hinders intra-osseous calcium; acidosis accelerates calcium excretion from the kidneys and causes further reduction of blood calcium.
4, acute hemorrhagic necrotizing pancreatitis, fat necrosis can cause a large amount of calcium precipitation to form soap calcium; rhabdomyolysis can also produce similar symptoms.
Drug factor (35%)
1 for the treatment of hypercalcemia and excessive bone absorption drugs, such as bisphosphonates, pucamycin (light phosfomycin), calcitonin, phosphate and so on. 2 anticonvulsants: such as phenobarbital can cause hypocalcemia by changing vitamin D metabolism. 3 calcium chelating agents: commonly used are EDTA, citric acid and the like. 4 foscarnet: capable of sequestering calcium in extracellular fluid and causing hypomagnesemia.
Hypocalcemia associated with malignant tumors (10%)
Osteoblastic metastasis of prostate cancer or breast cancer can accelerate bone formation leading to hypocalcemia. In addition, lymphoma, leukemia chemotherapy, a large number of tissue destruction, phosphate release into the blood, blood calcium can be significantly reduced, known as tumor lysis syndrome.
Pathophysiology
Calcium is reduced by various causes, hypocalcemia stimulates the synthesis of parathyroid glands and releases PTH; and hypocalcemia and PTH can enhance the activity of 1 hydroxylase in proximal renal tubular epithelial cells, thereby promoting 1,25 (OH). ) 2 D3 synthesis. PTH can promote bone absorption, while PTH and 1,25(OH)2 D3 can increase the calcium absorption of distal renal tubules. 1,25(OH)2 D3 can also increase the absorption of intestinal calcium, thus Blood calcium is elevated. When parathyroid dysfunction, vitamin D metabolism disorder, renal failure, PTH, 1,25 (OH) 2 D3 synthesis disorders, so that the body's normal blood calcium balance regulation disorder, resulting in hypocalcemia, and caused a A series of clinical symptoms.
Prevention
Hypocalcemia prevention
1. Actively control the primary disease and regular physical examination. Hypocalcemia is prone to occur after thyroid or parathyroid surgery.
2. Increase sun exposure, proper nutrition, prevent weight loss, chronic diarrhea and other causes of dystrophic hypocalcemia.
Complication
Hypocalcemia complications Complications sinus tachycardia atrioventricular block congestive heart failure
Hypocalcemia can cause sinus tachycardia, arrhythmia, and can also cause atrioventricular block, and in rare cases can cause congestive heart failure. Hypocalcemia can increase the excitability of the vagus nerve and cause cardiac arrest.
Symptom
Symptoms of hypocalcemia Common symptoms Sleeping calf tendon softening hand sour convulsions facial sniper sign osteoporosis cartilage dysplasia with... bone pain apnea-like phenomenon irritability
Hypocalcemia often has no obvious clinical symptoms. The severity of clinical symptoms is not completely consistent with the degree of blood calcium reduction, but is related to the rate and duration of blood calcium reduction. Rapid decline in blood calcium, even if the blood calcium level is 2mmol / l, can cause clinical symptoms. The clinical manifestations of hypocalcemia are mainly related to the increased excitability of neuromuscular.
1. Neuromuscular system: Since calcium ions can reduce the excitability of neuromuscular, the excitability of neuromuscular muscles increases during hypocalcemia. Tendons may appear, and the peripheral nervous system is initially numb to the fingers. Mild patients can induce typical convulsions by a facial nerve slamming test (Chvostek sign) or a beam arm press test (Trousseau sign). Severe hypocalcemia can cause paralysis of the larynx, brachiopod, bronchi, etc., seizures and even apnea. Psychiatric symptoms such as irritability, depression, and cognitive decline can also occur.
2. Cardiovascular system: mainly arrhythmia such as conduction block, ventricular fibrillation in severe cases, and poor response to digitalis in heart failure. The ECG typically shows a significant extension of the QT interval and ST segment.
3. Bone and skin, soft tissue: Chronic hypocalcemia can be manifested as bone pain, pathological fractures, skeletal deformities, etc. Skeletal lesions may be osteomalacia, osteoporosis, rickets, fibrocystic osteitis, etc. according to the underlying cause. Patients with chronic hypocalcemia often have dry skin, inelasticity, dull color and itching; they are also prone to sparse hair, fragile nails, and crunchy teeth; cataracts caused by hypocalcemia are more common.
4. Hypocalcemia crisis: When blood calcium is lower than 0.88mmol/L (3.5mg/dl), severe voluntary muscles and smooth muscle spasm can occur, leading to convulsions, seizures, severe asthma, and severe throat. Tendon caused by tendon, cardiac insufficiency, cardiac arrest.
Examine
Hypocalcemia examination
Physical examination
Increased neuromuscular excitability during hypocalcemia, may occur in hand and foot convulsions, tendons, throat, convulsions, as well as irritability, emotional instability, hallucinations and other mental symptoms. Patients with hypocalcemia can show positive signs of Chvostek and Trousseau, but about one-third of patients can be negative.
Auxiliary inspection
Laboratory tests: blood calcium, blood phosphorus, PTH, liver function, kidney function, albumin, urinary calcium, 1,25 (OH) 2 D3, blood magnesium and so on.
Electrocardiogram: The electrocardiogram of patients with hypocalcemia often has prolonged QT interval, and sometimes tachycardia can occur.
Imaging examination: 20% of patients with idiopathic hypoparathyroidism have intracranial calcification (mainly basal nucleus), and patients with hypoparathyroidism or pseudohypoparathyroidism after surgery generally do not appear. Intracranial calcification. Bone radiographs can understand the nature and extent of bone disease, as well as determine whether there are metastatic tumors.
Diagnosis
Diagnosis and diagnosis of hypocalcemia
Diagnostic criteria
Medical history
Should pay attention to the presence or absence of chronic renal insufficiency, hyperthyroidism after surgery or radiation therapy, other thyroid and neck surgery, liver disease, intestinal malabsorption, inadequate intake, lack of light, multiple pregnancy, long-term breastfeeding history. Long-term use of anti-epileptic drugs (such as epilepsy, phenytoin, phenobarbital, carbamazepine) or protamine, heparin, repeated infusion of sodium-containing sodium can cause hypocalcemia. In addition, you should ask about the history of hand and foot episodes and paresthesia, as well as bone calcification disorders.
The total calcium concentration at the time of diagnosis of hypocalcemia must be the corrected calcium concentration after serum albumin correction, and the free calcium concentration can be determined if necessary. Corrected calcium concentration (mg/dl) = total calcium (mg/dl) - 0.8 x [4.0 - serum albumin concentration (g/dl)].
According to medical history, physical examination and laboratory tests (such as blood phosphorus, PTH, liver and kidney function, albumin, etc.), the cause of the disease can often be clarified. For example, most patients with low calcium, high phosphorus and normal renal function often have primary or secondary hypoparathyroidism; the parathyroid gland should be suspected in the history of neck surgery; magnesium content, nutritional status, and insufficient sunshine A large number of blood transfusions, chemotherapy, acute pancreatitis, gastrointestinal lesions, medication history, vitamin D deficiency, and other endocrine abnormalities are helpful for diagnosis.
