Hypocalcemia in the elderly

Introduction to hypocalcemia in the elderly The serum total calcium in normal people is quite constant, ranging from 2.25 to 2.75 mmol/L, and children are high. Calcium in plasma and body fluids mainly exists in the form of combined calcium and free calcium. The former is mainly combined with albumin and a small amount is combined with organic acids, such as calcium citrate, calcium lactate and calcium phosphate. The free exchange of free calcium and bound calcium is in a dynamic equilibrium, which is mainly affected by pH, and the increase of free calcium (Ca2+) in acidemia is opposite to that in alkalemia. In addition, a certain product is maintained between blood calcium and blood phosphorus concentration, that is, [Ca]×[P]=350-400 mg/L, and only free calcium actually has the physiological function of calcium. Those with serum calcium below 2.2mmol/L are called hypocalcemia. basic knowledge The proportion of illness: 0.052% Susceptible people: the elderly Mode of infection: non-infectious Complications: angina

Causes of hypocalcemia in the elderly

Vitamin D and calcium deficiency (20%):

It is the most common cause of hypocalcemia in the elderly. Other common causes of hypocalcemia are: 1 parathyroid hypofunction (hypothyroidism), 2 pseudohypoparathyroidism (pseudoparathyroidism), 3 chronic renal failure, 4 acute pancreatitis, 5 chronic diarrhea and intestinal malabsorption syndrome, etc., the cause of parathyroidism can also be attributed to the following three categories: hereditary, acquired and hypomagnesemia.

Hereditary parathyroid dysfunction (20%):

It is divided into the following three cases:

(1) Idiopathic hypoparathyroidism: due to PTH persistent secretion disorder, mainly caused by PTH gene mutation leading to inhibition of FTH synthesis and secretion or glandular destruction caused by autoimmunity.

(2) Congenital hypoplasia of the parathyroid gland: extremely rare, if accompanied by thymic developmental defects, it is called DiGeorge syndrome.

(3) Pseudohypoparathyroidism: due to PTH dysfunction, the target organ is resistant to PTH, there are at least two types: Ia and Ib, type Ia is autosomal dominant, and may encode Gs protein gene Mutation-related, limiting the normal response of cAMP to PTH, type Ib may be caused by PTH receptor defects, but has not been confirmed.

Acquired hypoparathyroidism (10%):

Mainly due to neck surgery or radiotherapy, it can also be caused by hemochromatosis, which can be manifested as temporary or permanent hypoparathyroidism.

Hypomagnesemia (10%):

Hypomagnesemia can not only inhibit PTH secretion, but also affect its function, so it can cause hypoparathyroidism. Magnesium replacement therapy can correct this defect, so this hypoparathyroidism is reversible.

Pathogenesis

1. PTH lack or resistance

The lack of PTH in the elderly is often caused by surgery, autoimmune or tumor infiltration and damage to the parathyroid glands. Pseudoparathyroidism caused by PTH resistance is rare in the elderly.

2. Vitamin D deficiency or resistance

Older people are often due to insufficient intake of vitamin-rich dairy products and/or insufficient sun exposure. Vitamin D metabolic disorders (such as chronic renal failure) may also be present, but not sensitive to active vitamin D, active vitamin D It promotes the reabsorption of calcium by intestinal mucosa, synergizes with PTH to promote bone resorption and increases the reabsorption of calcium and phosphorus by renal tubules.

3. Hypoproteinemia

Often lead to pseudohypocalcemia.

4. Other

For example, severe hypomagnesemia often leads to hypocalcemia by affecting the secretion of PTH and attenuating the effects of PTH. Hyperphosphatemia can be caused by a variety of causes, such as rhabdomyolysis, acute renal failure, tumor chemotherapy, etc. Excessive blood phosphorus leads to low calcium sputum, and acute pancreatitis is not common in the elderly.

Prevention of hypocalcemia in the elderly

The application of vitamin D preparations must pay attention to the full supplement of calcium, and monitor urinary calcium, blood calcium to avoid hypercalcemia caused by ectopic calcification, hypocalcemia with hyperphosphatemia, in principle oral aluminum hydroxide to reduce phosphorus Absorption.

Elderly hypocalcemia complications Complications

Complicated with low calcium convulsions, difficulty breathing, asphyxia, circulatory system involvement tachycardia, angina pectoris, severe hypocalcemia crisis.

Symptoms of hypocalcemia in the elderly Common symptoms Nail streaks or spots on limbs twitching Intelligence reduction Vitamin D deficiency Visual impairment Calcified metacarpal and humerus short neck

Mild hypocalcemia can be asymptomatic or manifest as non-specific central nervous system symptoms. Long-term hypocalcemia can lead to cataract formation and mild diffuse encephalopathy, while severe hypocalcemia or alkalosis is neuromuscular. Increased irritability and mental abnormalities, typical cases of hand and foot sputum, or Chvostek sign positive (finger hitting the front nerve of the ear, causing the ipsilateral mouth or nose wing) and Trousseau sign positive (wrap the sphygmomanometer cuff around the upper arm, Keep blood pressure between systolic and diastolic blood pressure for at least 3 min, causing local finger and arm spasm). In addition, there is a characteristic change in parathyroidism. For example, autoimmune may be accompanied by other endocrine defects. The most common Addison's disease, due to T cell deficiency, prone to skin mucosal candidiasis, pseudo-parathyroidism Ib type appearance is normal, while type Ia shows interrelated signs, including obesity, short stature, round Short face, short neck, short metacarpal and humerus (often occurring in 4th and 5th), short, wide and subcutaneous calcification of the distal phalanx, may be associated with mental retardation and certain endocrine abnormalities (especially thyroid and sex) gland).

If the serum calcium level is lower than 8.8mg/dl (2.2mmol/L) or the ionized calcium is lower than 4.4mg/dl (1.1mmol/L), hypocalcemia can be diagnosed, and the total calcium level or ionized calcium level should be correctly evaluated. To reduce, it is necessary to simultaneously measure phosphorus, magnesium, potassium, bicarbonate concentration and renal function. Serum calcium reduction is often accompanied by elevated serum phosphorus, especially in patients with hypoparathyroidism or severe vitamin D deficiency, and vitamin D deficiency or magnesium phosphate. Depletion can be manifested as mild hypocalcemia and hypophosphatemia.

Examination of hypocalcemia in the elderly

In the elderly who are sick all the year round, their serum calcium levels are often lowered. If the adjusted serum calcium level is still lower than 8.8 mg/dl (2.2 mmol/L) or the ionized calcium is lower than 4.4 mg/dl (1.1 mmol/L), Diagnosis of hypocalcemia.

Imaging can reveal calcification of the base nodules, ST segment extension of ECG, QT interval prolongation and T wave abnormalities, and even EEG abnormalities may occur.

Diagnosis and diagnosis of hypocalcemia in the elderly

Differential diagnosis

Diagnosis is not difficult with hypocalcemia caused by vitamin D deficiency, pancreatic disease or renal failure, but the distinction between primary hypoparathyroidism and pseudohypoparathyroidism requires measurement of blood PTH levels and PTH stimulation. Trial, the following appendix diagnostic criteria for hypoparathyroidism:

1, primary hypoparathyroidism

(1) Blood calcium is lowered.

(2) Increased blood phosphorus, increased blood phosphorus is not caused by renal insufficiency.

(3) Skeletal X-ray films must be normal to exclude rickets and rickets.

(4) Has a history of chronic hand and foot.

2, pseudohypoparathyroidism

In addition to meeting the diagnostic criteria for primary hypoparathyroidism, it is necessary to have:

(1) Short finger syndrome.

(2) Round face, short and short.

(3) It is highly resistant to PTH.

(4) The normal presence of the parathyroid gland.

3. Idiopathic hypoparathyroidism

(1) Chronic hand, foot and ankle.

(2) serum calcium decreased, inorganic phosphorus increased, alkaline phosphatase was normal, and urinary calcium was rare.

(3) No rickets, X-ray signs of rickets, no renal tubular acidosis or renal failure, no vitamin D deficiency or metabolic alkalosis.

(4) After intravenous injection of exogenous PTH, urinary cAMP increased, renal TPR decreased, and urinary phosphorus excretion increased.

(5) There is no history of neck surgery or other injuries to the parathyroid glands, and no history of taking 131I.

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