hyponatremia
Introduction
Introduction to hyponatremia Hyponatremia only indicates that the serum sodium ion concentration is lower than the normal level, and it is not necessarily true that the sodium content of the body is decreased. According to the rapid onset, it can be divided into acute hyponatremia and chronic hyponatremia. The former refers to serum sodium ion concentration below normal level within 48 hours, otherwise it is chronic hyponatremia. basic knowledge The proportion of illness: 0.021% Susceptible people: no special people Mode of infection: non-infectious Complications: headache, coma, cerebral edema
Cause
Cause of hyponatremia
(1) Causes of the disease
The causes of the three types of hyponatremia are different and are described below.
1. Total sodium reduction hyponatremia
This situation is seen in the loss of sodium is greater than the loss of water, seen in extra-renal loss and kidney loss of sodium, according to the urine sodium can be distinguished, urine sodium concentration [Na]> 20mmol / L for kidney loss of sodium increased; <20mmol / L for extrarenal Lost.
The causes of renal sodium loss are:
1 excessive diuretic use: the mechanism is that diuretics inhibit the reabsorption of Henle's thick ascending NaCl, low blood volume stimulates ADH release, interfere with urine dilution and potassium deficiency-mediated changes in osmotic receptors and thirst;
2 lack of mineralocorticoid, so that renal tubular reabsorption of sodium decreased;
3 salt-tolerant nephritis associated with renal tubular acidosis and metabolic alkalosis;
4 ketones and urine (including diabetic ketoacidosis, starvation, alcoholic ketonuria).
The causes of extrarenal sodium loss are:
1 loss of gastrointestinal tract, such as vomiting, diarrhea, fluid retention in the third cavity, burns, pancreatitis and pancreatic fistula and biliary fistula;
2 The brain salt loss caused by subarachnoid hemorrhage is a rare syndrome, and the blood volume is reduced. The mechanism is unknown. Some people suspect that it may be related to the increase of brain natriuretic peptide release.
2. The cause of total sodium hyponatremia
(1) Glucocorticoid deficiency: On the one hand, renal water excretion is impaired, ADH release can also be increased without blood volume reduction (non-osmotic ADH release); on the other hand, renal hemodynamics disorders, In the absence of increased release of ADH, the permeability of the manifold can be increased.
(2) hypothyroidism: due to decreased cardiac output and glomerular filtration rate, leading to ADH-mediated intrarenal mechanism disorder.
(3) Patients with acute schizophrenia have a tendency to develop hyponatremia. The mechanism is multifactorial, including increased thirst (drinking), osmotic pressure regulation of ADH release, and mild osmotic pressure. ADH release, increased reactivity of renal ADH and antipsychotic drugs; surgery is a kind of stress, postoperative patients can develop hyponatremia, which is characterized by elevated levels of ADH in the plasma and increased free water retention in the body. The input of electrolyte-free liquid is also a factor.
(4) Drug-induced hyponatremia: its mechanism is mediated by ADH, or increase the release of ADH, or enhance the role of ADH, drugs are: antipsychotic drugs, such as flexidine, containing trulin (sertraline) ), thiothixene, haloperidol, amitripine; amphetamine-related drug ecstasy; certain anticancer drugs, such as vinblastine, vincristine, high dose cyclophosphamide, carbamazepine, Bromocriptine, chlorpromazine, intravenous vasopressin and lorcainide.
(5) ADH hypersecretion syndrome (SIADH) and the like.
The overall water volume of these patients is increased, and the sodium concentration [Na] in urine is often >20 mmol/L.
3. The cause of hyponatremia with an increase in overall sodium
Although patients with hyponatremia have an overall increase in sodium, blood sodium is reduced due to water retention in the body. Common causes are: acute or chronic renal failure, nephrotic syndrome, cirrhosis and heart failure in heart failure. In the middle, the cardiac output decreased, the mean arterial pressure decreased, resulting in increased release of non-osmotic ADH. The expression of aquaporin (AQP-2) in renal tubular cells was up-regulated, and the renal tubular reabsorption of water increased. Sodium is reduced; heart failure is accompanied by activation of the renin-angiotensin-aldosterone system and increased release of catecholamines, which further aggravates hyponatremia. The mechanism of hyponatremia in patients with cirrhosis is similar to heart failure, except that The cardiac output of this patient is not reduced but increased; the reason for the increase is the presence of multiple arteriovenous fistulas in the gastrointestinal tract and skin, resulting in increased venous return. Others such as ADH, catecholamine and AQP-2 expression are up-regulated with heart failure. Similarly, patients with nephrotic syndrome can cause non-osmotic ADH release due to effective blood volume reduction, and water reabsorption increases, resulting in hyponatremia. In chronic renal failure, kidneys are often present. Increased sodium excretion of the components, combined with obstacles in the drainage of the kidneys, especially when the intake of water exceeds the ability of the kidney to drain, is more likely to occur hyponatremia, such as excessive intake of sodium can cause edema.
All of the above three hyponatremias have a decrease in blood sodium [Na], but the overall sodium does not necessarily decrease. It can be seen that the blood [Na] is low and does not often reflect the overall sodium condition, which is different in terms of overall water. The cause of hyponatremia, the overall water can be increased, can also be reduced, for plasma osmotic pressure, three different types of hyponatremia are reduced, the degree of reduction is not the same, it should be noted that: clinical The hyponatremia seen above is often not singular, but complex, and should be comprehensively analyzed for diagnosis and treatment.
(two) pathogenesis
Hyponatremia is caused by the loss and loss of sodium, or the relative increase of total water. The total effect is the decrease of plasma osmotic pressure (blood sodium concentration is the main component of plasma osmotic pressure maintenance), and sodium loss Often accompanied by dehydration, regardless of the cause of hyponatremia, the effective blood volume is reduced, resulting in the release of non-osmotic ADH, in order to increase the reabsorption of renal tubules to avoid further reduction in blood volume, however The protective mechanism is more serious about the reduction of blood sodium and plasma osmotic pressure. This compensation mechanism occurs in the early stage of effective blood volume reduction. When blood [Na] drops to <135mmol/L, ADH release is inhibited. The internal osmotic pressure maintains a steady state equilibrium. When the plasma sodium concentration decreases, the extracellular fluid osmotic pressure decreases, and the extracellular water bleeds into the cells, causing the cells to swell, resulting in impaired or even disrupted cell function, in which brain cells are swollen, which may lead to hyponatremia. The most serious clinical manifestations, if the blood volume reduction is not corrected, can lower blood pressure, reduce renal blood flow, and reduce glomerular filtration rate, which can lead to pre-renal azotemia.
Prevention
Hyponatremia prevention
Acute severe sodium deficiency can be supplemented by 2/3 of the calculated amount, increasing the concentration of 1-2mmol/L blood sodium per hour, 24h uniform filling, chronic sodium loss can be supplemented for 48h, for the circulation stability, taboo Quickly correct hyponatremia, otherwise it may lead to osmotic demyelinating syndrome, paraplegia, quadriplegia, aphasia, congestive heart failure and cerebral edema.
Complication
Hyponatremia complications Complications, headache, coma, brain edema
When the serum sodium concentration is lower than 115 ~ 120mmol / L, there will be headache, lethargy, and eventually coma, hyponatremia encephalopathy is often reversible, chronic hyponatremia, neurological symptoms and cerebral edema are far from serious Below the acute hyponatremia, if symptoms of chronic hyponatremia occur, the serum sodium concentration is often lower than 110mmol / L, and there is often a sharp deterioration of hyponatremia.
Symptom
Symptoms of hyponatremia common symptoms convulsions, polydipsia, fatigue, coma, diuretic, hyponatremia, nausea
1. Classification of hyponatremia
According to the changes in blood volume at the time of hyponatremia, it can be divided into:
(1) hypovolemic hyponatremia, in which case sodium loss is more than loss of water.
(2) Normal hypoxemia of blood volume, in which case the overall water increases and the total sodium does not change.
(3) Hyponatremia with high blood volume. At this time, the overall water increase is higher than the increase of blood sodium. According to the degree of blood sodium reduction, it can be divided into mild and severe hyponatremia, and the blood sodium level is 125-135mmol/ L and less than 125mmol / L, in addition to pseudohyponatremia, seen in the obvious hyperlipidemia and hyperproteinemia, pseudohyponatremia is also artificial, modern determination of plasma sodium by direct potentiometry False hyponatremia with low false readings when using the flame photometer method can be eliminated.
In addition to the above classification, there are also divided into: sodium loss, diluted and inflated; some people are divided into sodium loss hypotonic, dilute hypotonic and asymptomatic hypotonic syndrome or consumptive, dilute and lacking Patients with sodium hyponatremia.
2. Clinical manifestations of hyponatremia
The severity depends on the rate of blood [Na] and blood sodium decline. When blood [Na] is above 125 mmol/L, it rarely causes symptoms; when [Na] is between 125 and 130 mmol/L, only gastrointestinal symptoms are present. At this time, the main symptoms are weakness, nausea and vomiting, headache, sleepiness, muscle cramps, neuropsychiatric symptoms and reversible ataxia. In the early stage of hyponatremia, brain cells have imbalance of intracellular and extracellular osmotic pressure. Adaptive regulation, within 1 ~ 3h, the extracellular fluid in the brain is transferred into the cerebrospinal fluid, and then returned to the systemic circulation; if hyponatremia persists, the adaptive regulation of brain cells is the intracellular organic osmotic solutes including phosphoric acid, creatine Inositol and amino acids (such as alanine, aminoethanesulfonic acid) are discarded to reduce cell edema. If brain cells adapt to this regulation, brain cell edema will follow, and clinical manifestations include convulsions, stupor, coma and cranial Symptoms of elevated internal pressure, severe tenterium paralysis, if hyponatremia occurs within 48h, there is a great risk, which can lead to permanent neurological damage, chronic hyponatremia, Permeability demyelination The danger, especially in correcting hyponatremia too easy or too fast.
In addition to brain cell edema and clinical manifestations of intracranial hypertension, due to reduced blood volume, low blood pressure, rapid pulse and circulatory failure, and signs of dehydration, total sodium hyponatremia without clinical manifestations of cerebral edema.
Examine
Hyponatremia check
All three types of hyponatremia have decreased plasma osmotic pressure, decreased blood sodium, and normal sodium hyponatremia. The reduction of both is not obvious. In addition, hyponatremia with total sodium loss is also potassium. Plasma protein and hematocrit and blood urea nitrogen increase, suggesting that there is insufficient blood volume; urine volume, urine sodium and chloride are reduced, urine specific gravity is elevated, blood pH is often low, and hypervolemic hyponatremia ( That is, dilute hyponatremia), except for blood sodium and plasma osmotic pressure and sodium hyponatremia (hypovolemia, hyponatremia), the other laboratory results are the opposite, blood volume is normal. The aforementioned laboratory tests for hyponatremia were more variable, and blood sodium was only slightly below normal.
According to the clinical manifestations, choose ECG, B-ultrasound, brain CT and so on.
Diagnosis
Diagnosis and diagnosis of hyponatremia
Diagnostic criteria
1. Determine if there is really hyponatremia
Patients with hyponatremia need to measure blood osmotic pressure. If the osmotic pressure is normal, it may be severe hypolipidemia caused by severe hyperlipidemia or rare abnormal hyperproteinemia. Hyperosmolarity is hyperosmolar. Hyponatremia.
2. Estimated extracellular fluid volume status
Low-sodium hyponatremia is mainly caused by absolute or relative deficiency of body fluids, low or decreased blood pressure, poor skin elasticity, laboratory blood tests, increased blood urea nitrogen, and mild increase in creatinine, all of which support the diagnosis. Gastrointestinal fluid loss, excessive sweating, urinary sodium <10mmol / L, suggesting extra-renal loss; urine sodium > 20mmol / L, with a history of diuretics or examination of diabetes or adrenal insufficiency can be identified as Determination of urinary potassium is also important through renal loss. High patients often suggest Na-reabsorption of proximal tubules or medullary sputum, or vomiting, diuretics, etc.; low suggestive of aldosterone is too low.
There are many extracellular fluids and there are edema or third interstitial fluid accumulation. Most of the hyponatremia is caused by edema caused by heart, liver and kidney, such as edema, normal blood pressure, and no signs of too little fluid. Hyponatremia is mainly caused by excessive secretion of ADH. At this time, if there is severe oliguria, blood urea nitrogen and creatinine are significantly increased, and urinary sodium excretion is still >20mmol/L, which is caused by renal failure; if urinary osmotic pressure Significantly reduced (<80mOsm/kgH2O), accompanied by significant polydipsia, the disease may be caused by polydipsia, a common cause is mental illness or taking certain drugs that cause severe thirst (such as tricyclic antidepressants).
Clinical Diagnostic Criteria for Antidiuretic Hormone Secretion Syndrome (SIADH): Persistent Hyponatremia with the following four items:
1 no kidney, heart, lung, adrenal gland, pituitary dysfunction;
2 The extracellular fluid is in a low osmotic state;
3 Urine can not be diluted normally, after the liquid load (including injection of physiological saline), the water is still stored in the body, Na is still discharged from the urine, and hyponatremia continues to increase;
4 limiting water intake can improve hyponatremia.
Pay attention to the diagnosis of this disease:
1 blood uric acid level is usually low in SIADH, if it is high, it should be excluded from the effective extracellular fluid volume;
2 blood potassium is usually normal, accompanied by hypokalemia is often caused by other causes of hyponatremia, especially vomiting and high aldosteronism; high potassium should pay attention to the presence of low aldosteronism;
3HCO3-: usually normal, caused by diuretics can be high; those with low aldosterone can be low;
4 blood urea nitrogen: mostly low.
There are four subtypes of SIADH in clinical practice:
1 sustained high levels of ADH release, mostly caused by lung cancer, accounting for 38% of SIADH;
2 osmotic value re-adjustment, showing that the regulation of ADH secretion is still normal, but the threshold is at a lower osmotic concentration, accounting for about 38%;
3 hypotonicemia has no inhibitory effect on ADH, accounting for about 16%. This type of patient has normal secretion when osmotic pressure is too high, but cannot be reduced to zero level when hypotonicemia occurs;
4 The kidney is allergic to ADH reaction. The level of ADH and secretion regulation are normal, and there is no ADH-like substance in the blood.
Judging hyponatremia is due to sodium loss, excessive water and normal blood volume can be identified according to the total water, total sodium, the total amount can be calculated according to body weight and measured serum sodium, but must know the body weight before the patient .
The total amount of existing body fluid = (normal serum sodium value / measured serum sodium value) × total amount of normal body fluid.
The total amount of normal body fluid = patient's pre-disease weight (kg) × 0.6.
Overall sodium = total fluid volume x blood sodium concentration (mmol/L).
