syndrome of abnormal antidiuretic hormone secretion
Introduction
Introduction to antidiuretic hormone abnormal syndrome Syndromeofinappropriatesecretion of antidiuretichormone (SIADH) was first reported by Schwartz in 1957, due to excessive secretion of antidiuretic hormone (ADH) or similar antidiuretic hormone-like substances, resulting in impaired water excretion. The change was characterized by hyponatremia. SIADH is a syndrome in which a series of clinical manifestations such as antidiuretic hormone (ADH) are not regulated by plasma osmotic pressure, resulting in abnormal increase in secretion of water, increased urinary sodium excretion, and dilute hyponatremia. In addition to severe head injury, cervical spinal cord injury, severe intracranial infection and acute phase of cerebrovascular disease (10% to 14%), there are malignant tumors and lung tumors. basic knowledge The proportion of illness: the incidence rate is about 0.001% - 0.009% Susceptible people: no specific population Mode of infection: non-infectious Complications: swelling
Cause
Causes of urinary hormone secretion abnormal syndrome
Tumor (25%)
Many malignant tumors can produce ADH, which causes SIADH. Pulmonary oat cell carcinoma is the most common malignant tumor causing SIADH (data show that about 80% of SIADH is caused by lung oat cell cancer). Others such as pancreatic cancer, prostate cancer, thymoma, lymphoma, etc. can also cause SIADH to come. Say,
The performance of primary tumors in the presence of SIADH is already evident. But sometimes SIADH can be the first manifestation of the tumor, that is, the primary tumor of the tumor when SIADH appears is still unclear. For most tumor-like SIADHs, the underlying cause is that tumor tissue produces too much ADH to be released into the bloodstream. However, some studies have shown that ADH is sometimes not detected in the excised tumor tissue, indicating that part of the neoplastic SIADH is not caused by ADH produced by the tumor. Such SIADH is essentially an ectopic endocrine syndrome. The formation mechanism of this type of SIADH may be: 1 tumor tissue produces some ADH-like substances, which have ADH activity but no immunological cross-linking with ADH; 2 tumor tissue produces certain mediators to stimulate the secretion of pituitary ADH; 3 tumor through some mechanism The osmotic setting point of central ADH release is lowered such that normal (even below normal) extracellular fluid osmotic pressure also causes ADH release.
Drug factor (20%)
Drugs are another important cause of SIADH. The mechanism of SIADH caused by different drugs is different: vasopressin and its analogues cause SIADH through direct effects; clofibrate, vincristine, cyclophosphamide, tricyclic antibiotics Depressants and monoamine oxidase inhibitors mainly play a role in promoting the secretion of ADH; chlorpropamide and carbamazepine not only promote the secretion of ADH, but also enhance the kidney's response to ADH.
Lung disease (20%)
Many lung diseases can cause SIADH, such as acute respiratory failure (especially those with obvious hypoxemia and hypercapnia), pneumonia, tuberculosis, mechanical ventilation and so on. The detailed mechanism of SIADH caused by lung disease is unclear. ADH-like activity has been found in tuberculous lung tissue by bioassay, indicating that in some cases lung tissue can produce ADH or ADH-like substances.
Surgical factors (15%)
Various operations can cause SIADH, which often occurs 3 to 5 days after surgery, and the mechanism is unknown. During this period, hyponatremia can be caused by administration of a low-tensioning liquid such as dextran, and hyponatremia can be caused by administration of an isotonic fluid such as physiological saline.
Neuro-psychiatric disorders (15%)
Many neuro-psychiatric disorders can cause SIADH, such as stroke trauma, infection, and cancer mania. The mechanism of SIADH caused by the above diseases is still not clear, and it is speculated that it may affect the function of the hypothalamus and the secretion of ADH is not regulated by the normal mechanism. Mental illness with mental polydipsia combined with compulsive drinking water, so that body fluid dilution, more likely to cause SIADH.
Prevention
Prevention of abnormal urinary hormone secretion syndrome
1. Limit water intake to prevent recurrence of SIADH.
2. Children should not use melamine (demethyl chlortetracycline), because it affects bone development, can induce azotemia, renal function should be reviewed regularly.
Complication
Complications of dysfunctional urinary hormone secretion syndrome Complications swelling
The serum sodium concentration at 135mmol/L is called hyponatremia. The root cause of hyponatremia is that the intake of water exceeds the excretion of water by the kidneys, making the blood more water than sodium, hyponatremia and sodium. There is a certain difference in sodium depletion. Sodium deficiency refers to the reduction of total sodium in the body. It is one of the causes of hyponatremia. However, sodium deficiency is not necessarily accompanied by hyponatremia, but low sodium. There is also no need for sodium deficiency in blood.
Most hyponatremia is associated with a decrease in blood osmotic pressure (tension), but some hyponatremia blood osmotic pressure does not decrease or even increase, and the state of reduced blood osmotic pressure is called hypoosmolemia. Produces a series of manifestations called hypotonic syndrome.
The purpose of treatment for hyponatremia is to increase blood sodium concentration and blood tension to restore the volume of cells, especially nerve cells, and to relieve brain cell swelling caused by decreased blood tension.
Patients with serum sodium concentration below 120mmol/L should be actively treated. The goal of treatment is to increase blood sodium to 125mmol/L and plasma osmotic pressure to 250mOsm/L. Although this level is still lower than normal, it has not caused For nervous system damage, the method of treatment is to infuse a high-content NaC1 solution (concentration 3% to 5%), and the sodium replenishment can be calculated by the following formula (where 0.6 × body weight is the total liquid amount):
Need sodium amount (mmol) = (125-measured serum sodium concentration) × 0.6 × body weight (kg)
For example, if the measured serum sodium concentration is 115 mmol/L and the patient's body weight is 60 kg, it is necessary to supplement 360 mmol of sodium, which is equivalent to 21.06 g of NaCl.
Acute hyponatremia is advocated by high-tension NaC1 solution (such as 3% NaCl solution), which can effectively increase the blood sodium concentration, and the expansion of high-tension NaCl solution, which is for patients with congestive heart failure. It is unfavorable. Therefore, it is advisable to replenish saline in patients with congestive heart failure. SIADH patients also have a certain degree of volume expansion, and SIADH has significant sodium deficiency. Therefore, high-sodium NaCl solution can not effectively correct low sodium. In these patients, these patients often use a combination of saline (or high-sodium NaCl solution) and furosemide, because furosemide can cause salt loss, thereby reducing the amount of extracellular fluid. In addition, furosemide can also cause The urine is diluted, which contributes to the improvement of blood sodium. In recent years, angiotensin V2 receptor antagonist has been tried to treat SIADH, and good results have been obtained.
In general, when the blood sodium concentration reaches 125mmol/L, the symptoms associated with hyponatremia can be eliminated. Moreover, even if the blood sodium reaches this level, even if the hypertonic sodium chloride solution is not given, as long as the water intake is properly controlled. The blood sodium can gradually return to normal levels within a few days, so it is not necessary to quickly increase the blood sodium concentration to a normal level by infusion of a hypertonic sodium chloride solution.
The rate of correction for chronic hyponatremia is still controversial. It is reported that the mortality rate of rapid correction of severe hyponatremia is 33% to 86%, if the rate of increase of blood sodium is 0.6mmol/L per hour (every day 14mmol/L), there is a great chance of neurological complications. On the contrary, if the rate of increase of blood sodium is below 0.5mmol/L, neurological complications rarely occur, and the mortality rate does not increase. Animal experiments show that severe If hypokalemia rats are corrected too quickly, it can cause diffuse brain cell necrosis, and mild hyponatremia does not occur even if it is improved quickly. At present, it is advocated at a rate of 0.5mmol/(L·h). Increase the blood sodium concentration to 120 ~ 125mmol / L, the first 24h blood sodium increased not more than 12mmol / L, the first 48h blood sodium increased not more than 25mmol / L, young women's tolerance to hyponatremia Poor, in order to avoid serious low-sodium brain damage, the blood sodium can be appropriately increased, generally 1 ~ 2mmol / (L · h) is appropriate, according to the expected blood sodium lifting rate can be calculated sodium speed:
Sodium supplementation rate (mmol/h) = expected blood sodium elevation rate × 0.6 × body weight (kg) For example, if the patient's body weight is 70 kg and the blood sodium elevation rate is expected to be 0.5 mmol/(L·h), the sodium supplementation rate should be 21mmol / h, such as infusion of normal saline (sodium concentration of 154mmol / L), should be input 136ml per hour; if supplemented with 3% NaCl solution (sodium concentration of 513mmol / L), then enter 41ml per hour.
In the process of sodium supplementation, the blood electrolyte concentration should be continuously checked (it is recommended to check every 2h in foreign countries) to monitor the blood sodium lifting rate. If the blood sodium lifting speed exceeds the expected speed, the drip rate should be slowed down when the blood sodium is elevated. When it reaches 120-125mmol/L, sodium can be stopped, because this level is still lower than normal, but it will not cause low-sodium brain damage.
Asymptomatic hyponatremia has a low degree of hyponatremia. Generally, the blood sodium can be restored to normal by treating the primary disease, and there is no need to replenish the hypertonic NaC1 solution.
Symptom
Symptoms of dysfunctional urinary hormone secretion syndrome Common symptoms Urinary persistent sodium hyponatremia antidiuretic hormone (A... Dehydration slumber coma antidiuretic hormone (A... lethargy edema convulsions
The clinical manifestations of SIADH include two aspects:
1. The performance of SIADH itself is mainly characterized by hyponatremia.
2. Causes the manifestation of primary disease of SIADH.
The hyponatremia of SIADH is mainly caused by excessive retention of free water by the kidneys and excessive intake of water. Therefore, it is a dilute hyponatremia, the water in the patient increases, and the body fluid capacity is often expanded. The body weight can be increased by 5% to 10%, and the patient generally has no edema, which is related to the discharge of urinary sodium.
Hyponatremia can reduce the osmotic pressure of extracellular fluid, causing brain cell edema, resulting in corresponding neurological symptoms. The clinical manifestations of patients are closely related to serum sodium concentration. Patients with mild disease can be asymptomatic, when serum sodium concentration is lower than At 120mmol/L, the patient may have anorexia, nausea, vomiting, weakness, muscle spasm, lethargy, severe cases may have mental abnormalities, convulsions, lethargy and even coma. If not treated properly in time, it may lead to death, SIADH performance also It is related to the rate of hyponatremia. Acute hyponatremia is prone to symptoms even if it is not heavy, while chronic hyponatremia is less prone to symptoms.
Most SIADH is caused by cancer. Patients often have the corresponding manifestations of cancer. Some SIADH are caused by lung diseases or brain diseases, and patients have corresponding clinical manifestations. A small number of SIADH are caused by drugs, and patients have used this drug. Medical history and the performance of the corresponding original disease.
Examine
Examination of dysfunctional urinary hormone secretion syndrome
Laboratory examination
The main findings are as follows:
(1) Serum sodium is generally less than 130 mmol/L.
(2) Plasma osmotic pressure <270mOsm/kgH2O.
(3) The urine osmotic pressure is inappropriately increased, and the urine osmotic pressure is greater than the blood osmotic pressure when the plasma osmotic pressure is decreased.
(4) Increased urinary sodium excretion >20mmol/L.
(5) The carbon dioxide binding force is normal or slightly low, and the serum chloride is low.
(6) serum urea nitrogen, creatinine, uric acid, albumin often decreased.
(7) AVP levels in plasma and urine increased, plasma AVP was greater than 1.5pg/ml (blood AVP value <0.5-1.5pg/ml when blood osmotic pressure <280mOsm/kgH2O).
(8) The thyroid, liver, kidney, heart and adrenal cortex function normally.
2. Water load test
(1) Principle: In the case of hypertonic urine, water load test can be used to identify, normal human water load can inhibit the release of neuropituitary AVP, generally when blood sodium >125mmol / L can be used for this test, otherwise induced The risk of water poisoning, when the blood sodium is lower than 125mmol / L, you can first limit the water to make the blood sodium rise before doing.
(2) Method At 6 o'clock in the morning, the patient evacuates the bladder, and at 7:30, the first urine specimen is left, and the urine volume and urine osmotic pressure are measured. At the same time, the water is supplied with 1 L (or 20 ml/kg), and the drink is finished within 10 to 20 minutes. Lying for 5 hours, at 8:30, 9:30, 10:30, 11:30, each time to stay in the urine for 5 times, at 7:00, 8:00, 9:00, 10:00 during the urination interval At 11:00, each blood was taken for plasma osmotic pressure examination.
(3) Judgment of results: normal people have a diuretic effect on water load, 80% water is discharged within 5 hours, urine osmotic pressure is reduced to 100mOsm/kgH2O (specific gravity is about 1.003), lower than plasma osmotic pressure, and the patient's urine The amount is less than 40% of the intake water, and can not excrete hypotonic urine, urine osmotic pressure> plasma osmotic pressure. Occasionally, the urine osmotic pressure of SIAVP patients after strict sodium restriction can be lower than the plasma osmotic pressure, but the urine osmotic pressure can not be reduced to Ideal (still greater than 100mOsm/kgH2O).
3. Alcohol and phenytoin inhibition test
Slow intravenous injection of 95% alcohol 50ml or phenytoin 0.25g, before injection, plasma AVP after injection, normal person and hypothalamic dysfunction caused by SIAVP, AVP decreased after injection, tumor-induced SIAVP patients AVP did not decrease, improve The alcohol inhibition test is to urinate 3% of ethanol per kilogram of body weight within 30 minutes after urinating in the morning in the water stress test. If the water diuresis in the water load test is improved by alcohol test, it indicates excessive secretion of AVP. It is a pituitary.
Imaging examination: Papapostolou et al found that 8 cases (87.5%) of the patients with SIAVP had a high density signal of the pituitary gland disappeared by MRI, while 20 (87.5%) of the 23 non-SIAVP patients in the control group had this signal. MRI examination is considered to be important for the diagnosis of SIAVP.
Diagnosis
Diagnosis and differentiation of urinary hormone secretion abnormal syndrome
Diagnostic criteria
1. The classic diagnostic criteria were proposed by Schwartz and Bartter, who reported the first SIAVP, including:
1 hyponatremia, blood sodium plasma osmotic pressure;
2 urinary sodium L;
3 plasma osmotic pressure decreased with increased osmolality, plasma osmotic pressure <280mOsm> 20mmol / d;
4 clinically no dehydration, edema;
5 heart, kidney, liver, adrenal gland, normal thyroid function.
2. In addition, Zhang Tianxi (1991) proposed the diagnostic criteria for SIAVP, including:
1 blood sodium <130mmol / L (normal 135 ~ l45mmol / L);
2 plasma osmotic pressure <270mOsm / kgH2O (normal 270 ~ 290mOsm / kg H2O;
3 urinary sodium>80mmol/d (normal <20 mmol/d);
4 increased urine osmotic pressure, urine osmotic pressure / blood osmotic pressure > 1 (normal <1);
5 After the water intake is strictly restricted, the symptoms are alleviated;
6 no edema, heart, liver, kidney function is normal;
7 plasma AVP increased, greater than 1.5pg / ml (plasma osmotic pressure < 280mOsm / kg H2O, plasma AVP value <0.5 ~ l.5pg / ml).
Differential diagnosis
The causes of hyponatremia and hypoosmolaremia are diverse. Hyponatremia can be divided into "true" hyponatremia and "pseudo" hyponatremia, the so-called "pseudo" hyponatremia. , refers to hyperlipidemia and hyperplasminemia, the water content in the plasma is reduced, and blood sodium is actually only present in the aqueous part of the plasma, so the measured blood sodium concentration decreases, forming a "false" low sodium Blood, can be seen in hyperlipidemia, multiple myeloma, Sjogren's syndrome, macroglobulinemia or some patients with diabetes, hyperglycemia, hypertriglyceridemia or oral hypoglycemic treatment, "true" low sodium In addition to SIAVP, the cause of the disease is as follows:
1. Loss of digestive juice in the gastrointestinal tract
This is the most common cause of hyponatremia in the clinic. The sodium ion concentration in various digestive juices, except for slightly lower gastric juice, is similar to plasma sodium ion concentration, diarrhea, vomiting and gastrointestinal, biliary tract, pancreatic fistula or stomach. Intestinal decompression can lose a lot of digestive juice and cause hyponatremia.
2. Sweating a lot
The content of sodium chloride in sweat is about 0.25%. The amount of sodium is related to the "amount" of sweating. In the case of dominant sweating, the amount of sodium in sweat can be increased to near the concentration of sodium in plasma. High fever patients or labor in high temperature areas. When there is a lot of sweating in the homework, such as only adding water and not replenishing the electrolyte, water loss due to sodium deficiency can occur.
3. Renal sodium loss
In patients with renal failure, urinary sodium excretion can be increased. At this time, the reaction of the kidney to low sodium is active. When uremia causes vomiting and diarrhea causes sodium deficiency in the body, the renal tubules do not respond to aldosterone. Continue to discharge sodium, resulting in hyponatremia, salt-loss nephropathy, aldosterone reduction, Fanconi syndrome, distal renal tubular acidosis, hyperparathyroidism, Bartter syndrome, etc. can lead to renal tubular reabsorption Sodium is reduced, and sodium sulphate is increased to cause hyponatremia. At this time, there is a corresponding history of kidney disease that can be identified.
4. Hypothyroidism
Hyponatremia occurs when A is low due to excessive release of AVP or the kidneys cannot discharge diluted urine. However, this disease often has low metabolic symptoms such as cold, drowsiness, bloating, constipation, pulse mitigation, weight gain, and typical mucus. Edema, serum T3, T4 decreased, TSH increased, can be identified.
5. Adrenal insufficiency, renal tubular lesions often associated with effective circulating blood volume reduction, hypoosmotic pressure, hypotension, hypotonic dehydration and azotemia, easy to identify.
6. Chronic congestive heart failure, cirrhosis, ascites, nephrotic syndrome
More obvious edema, ascites, urinary sodium decreased, at this time water retention more than sodium retention, dilute hyponatremia, positive sodium balance, increased plasma renin activity, aldosterone also increased.
7. Diabetic ketoacidosis
High blood sugar, hyponatremia can occur when the plasma osmotic pressure is high, and low blood sodium in hyperglycemia may be due to extracellular fluid hypertonicity, so that the intracellular water is moved to the outside of the cell, so that the blood sodium is diluted, and at this time the renal tubular filtrate The sugar content is high, the osmotic pressure is high, the reabsorption of sodium by the renal tubule is inhibited, and the sodium excretion in the urine is increased. At this time, the history of diabetes and blood, urine ketone positive, and elevated blood sugar can be identified.
8. Ascites and extensive burns
The concentration of sodium ions in ascites is similar to that of plasma. Therefore, a large amount of ascites, especially repeated ascites or 1 case of ascites, can cause hyponatremia, and large area burns cause loss of sodium and water by plasma extravasation, but Sodium deficiency is more obvious than water shortage and easy to identify.
9. Chronic disease cell syndrome
Seen in those who are chronically ill, such as tuberculosis, lung cancer, advanced cirrhosis, malnutrition and frail elderly, long-term malnutrition, cachexia, loss of organic matter in cells, extracellular sodium ions into cells; or re-regulation of patient osmotic pressure threshold , leading to hyponatremia.
10. Mental polydipsia
Patients with hyponatremia due to excessive drinking water, plasma osmotic pressure can be reduced, but urine osmotic pressure is significantly reduced, easy to identify with SIADH.
In addition, the symptoms of SIADH are sometimes similar or identical to the symptoms of the primary disease, and are confusing. For example, if the central nervous system is aggravated, the neuropsychiatric symptoms associated with SIADH may also be present. Depressive symptoms in depression are easily associated with antidepressants. The SIADH condition caused by fluoxetine and the like is confused. At this time, it relies on laboratory tests such as regular blood sodium, plasma osmotic pressure, and urinary sodium excretion to identify.
