What Are the Most Common Hyponatremia Causes?

Serum sodium <135mmol / L is called hyponatremia. Serum sodium only reflects a decrease in the concentration of sodium in the plasma, and does not necessarily indicate a loss of total sodium in the body. The overall sodium may be normal or even slightly increased. It is more common clinically, especially in the elderly. The main symptoms are weakness, nausea and vomiting, headache and drowsiness, muscle pain and spasm, neuropsychiatric symptoms and reversible ataxia.

Basic Information

English name

hyponatremia

Visiting department

Nephrology, Cardiovascular, Gastroenterology

Common locations

kidney

Common causes

Due to the use of diuretics, dehydrating agents, or caused by vomiting, diarrhea

Common symptoms

Cerebral edema, respiratory failure, convulsions, coma, etc.

Causes of Hyponatremia

The causes of the three types of hyponatremia are different, as described below:

1. Hyponatremia with reduced overall sodium

When body fluids are lost, solute loss exceeds water loss, which is hypotonic dehydration. This condition is seen when sodium loss is greater than water loss, as seen in extrarenal and renal loss of sodium. It can be distinguished according to urinary sodium excretion. Na ⁺ > 20mmol / L is an increase in renal loss of sodium and <20mmol / L is an extrarenal loss.

(1) Causes of renal sodium loss The use of diuretics and dehydrating agents; Deficiency of mineralocorticoids reduces the reabsorption of sodium in renal tubules; tubulo-interstitial disease, acute renal injury when polyuria, urinary tract obstruction Early after remission, aldosteronism, etc .; markedly increased blood sugar, ketonuria (including diabetic ketoacidosis, starvation, alcoholic keturia).

(2) Causes of extrarenal sodium loss Gastrointestinal loss, such as vomiting, diarrhea, retention of fluid in the third cavity, burns, pancreatitis, pancreatic fistula and bile fistula, etc .; Cerebral salt loss syndrome: cranial Hyponatremia due to internal nervous system damage such as internal tumors, bleeding, and trauma.

2. Hyponatremia with normal sodium

(1) Glucocorticoid deficiency When adrenocortical insufficiency occurs, reduced aldosterone secretion causes increased water and sodium excretion, and reduced cortisol can promote the secretion of antidiuretic hormone (ADH) and cause reduced water excretion.

(2) Decreased thyroid function Due to decreased cardiac output and glomerular filtration rate, disorders of the intrarenal mechanism mediated by ADH have occurred. On the one hand, cardiac output and glomerular filtration rate decrease, causing a decrease in urine output, on the other hand, effective blood volume decreases, and ADH release is stimulated by the effect of baroreceptors.

(3) Acute schizophrenia has a tendency to develop hyponatremia, the mechanism of which is multifactorial, including increased thirst (multiple drinking), mild deficiency in osmotic pressure regulation of ADH release, and ADH release under low plasma osmotic pressure Increased renal ADH responsiveness and antipsychotic drugs.

(4) The mechanism of drug-induced hyponatremia is ADH-mediated, or increase the release of ADH, or enhance the effect of ADH.

(5) The concentration of Na ^{+ in} urine of ADH hypersecretion syndrome (SIADH) is often> 20mmol / L.

3. Hyponatremia with increased overall sodium

Although patients with this type of hyponatremia have an increase in overall sodium, blood sodium is reduced due to water retention in the body.

Clinical manifestations of hyponatremia

The severity of the clinical manifestations of hyponatremia depends on the rate of decrease in blood sodium. Symptoms rarely occur when the blood Na ^{+ is} above 130 mmol / L. When Na ^{+ is} between 125 and 130 mmol / L, it shows gastrointestinal symptoms. When blood sodium drops below 125mmol / L, cerebral edema is easy to occur. At this time, the main symptoms are headache drowsiness, muscle pain spasm, neuropsychiatric symptoms and reversible ataxia. If brain edema is further exacerbated, cerebral hernia, respiratory failure, and even death may occur.

If hyponatremia occurs within 48 hours, it is very dangerous, and convulsions, coma, apnea, or death can quickly occur, which can lead to permanent neurological damage. Patients with chronic hyponatremia are at risk of osmotic demyelinating, especially if they are too fast to correct hyponatremia. In addition to the clinical manifestations of brain cell edema and intracranial hypertension, due to reduced blood volume, low blood pressure, pulse rate, and circulatory failure may occur, as well as signs of fluid loss. Hyponatremia with general sodium normal has no clinical manifestations of cerebral edema.

Hyponatremia test

All three types of hyponatremia have reduced plasma osmotic pressure, decreased blood sodium, and hyponatremia with normal sodium in general. In addition, hyponatremia with overall sodium loss also includes elevated potassium, plasma proteins, hematocrit, and blood urea nitrogen, suggesting hypovolemia, decreased urine output, sodium and chloride, and increased urine specific gravity. Blood pH often decreases. Hypervolemic hyponatremia (ie, dilute hyponatremia) except for blood sodium and plasma osmotic pressure are the same as those of sodium loss hyponatremia (hypovolemia and hyponatremia). In contrast, the laboratory tests of hyponatremia with normal blood volume have changed greatly, and the blood sodium is only slightly lower than normal.

According to clinical manifestations, ECG, B-ultrasound, and brain CT were selected.

Diagnosis of hyponatremia

1. Determine if you really have hyponatremia

Patients with hyponatremia need to measure blood osmotic pressure. If the osmotic pressure is normal, it may be pseudohyponatremia caused by severe hyperlipidemia or rare abnormal hyperproteinemia, and hyperosmolarity is hypertonic. Hyponatremia.

2.Estimating extracellular fluid capacity

Hyponatremia in low-volume subjects is mainly caused by absolute or relative inadequate body fluids, low or decreased blood pressure, poor skin elasticity, and laboratory tests showing blood urea nitrogen and a slight rise in creatinine all support this diagnosis. A history of gastrointestinal fluid loss, excessive sweating, and urine sodium L suggest extrarenal loss. Urine sodium> 20mmol / L, history of diuretics or examination of diabetes or adrenal insufficiency can be determined as renal loss. Urinary potassium determination is also very important, and the higher one often prompts Na ⁺ reabsorption disorder of the proximal tubule or myelin, or it is caused by vomiting, diuretics, etc. The lower one indicates that the aldosterone is too low.

Hyponatremia Treatment

The treatment of hyponatremia should adopt different treatment methods according to the etiology, the type of hyponatremia, the speed of the occurrence of hyponatremia and the accompanying symptoms. Therefore, the treatment of hyponatremia should emphasize individualization, but the total treatment Measures include: Eliminate the cause. Correct hyponatremia. Treat symptomatically. treatment of complications.

1. Treatment of acute hyponatremia

Acute hyponatremia refers to hyponatremia that occurs within 48 hours. Serum sodium <110 115mmol / L, accompanied by obvious central nervous system symptoms, should be treated quickly, otherwise it will cause cerebral edema or even death. Treatment target: Raise blood sodium by nearly 10mmol / L or 120-125mmol / L within a short time (4-6 hours). Over the next 24 to 48 hours or longer, the serum sodium concentration gradually returned to normal. Intravenous infusion of 3% sodium chloride solution, while injecting diuretics to accelerate the excretion of free water, make blood Na ⁺ recover faster, and avoid excessive volume.

2. Treatment of chronic hyponatremia

Different approaches should be taken depending on the presence or absence of symptoms. Chronic asymptomatic hyponatremia should first find the cause of hyponatremia, and then treat the cause. After the cause has been eliminated, some patients with hyponatremia also disappear. For patients whose cause cannot be eliminated temporarily, measures can be taken to limit water intake and inhibit ADH release, and increase solute intake or excretion. The treatment for chronic symptomatic hyponatremia is sodium supplementation and diuretics to increase the excretion of free water.

3.Treatment of hyponatremia

It is common in the gastrointestinal tract and kidneys to lose sodium. In this case, there is water loss at the same time, but sodium loss is more than water loss, so it causes a hypotonic state of sodium loss, resulting in insufficient blood volume and peripheral circulation failure. In this case, because water and sodium are lost, it will not cause imbalance in osmotic pressure inside and outside the brain cells, so there is no nerve damage and intracranial hypertension. Treatment is mainly supplemented with sodium. Mild patients can only take saline or sodium chloride tablets orally while drinking water to restore blood volume. In severe cases, saline or high-concentration saline is given intravenously. It should be noted that such patients should not be infused with glucose water, otherwise it will worsen hyponatremia.

4. Treatment of diluted hyponatremia

The main cause of this disease is renal excretion dysfunction and impaired heart, liver, and kidney function, which causes water and sodium to be retained in the body. Therefore, the main treatment measures are to limit water intake and diuresis to exclude free water. Those with mild symptoms need only appropriately limit water intake. The pathogenesis of dilute hyponatremia in patients with impaired heart, liver, and kidney function is multifactorial. The patient's overall sodium does not decrease, often too much, and the patient's overall water is too much, often with edema, pleural effusion or Ascites, but overall water is greater than overall sodium. Such patients are difficult to treat. Correct hyponatremia, giving sodium salt can aggravate edema; correcting too much water, diuretics can aggravate hyponatremia, and patients with excessive water restriction are not easy to accept. In principle, the daily intake of water should be less than the sum of daily urine output and insignificant water loss. Diuretics can be used appropriately to increase the excretion of water, because diuretics can inhibit the effect of ADH on the collecting tube and reduce water reabsorption; but too much diuretics can increase sodium loss. In addition to limiting water, these patients also need to limit their sodium intake.

The treatment of psychiatric polydipsia and antidiuretic hormone secretion disorder syndrome (SIADH syndrome) is mainly to strictly restrict water intake and use of diuretics, and treatments for acute hyponatremia can be used.