Hyponatremia

Introduction

Introduction Hyponatremia is serum sodium <135mmol / L, only reflects the decrease in sodium concentration in plasma, does not necessarily mean the loss of total sodium in the body, the overall sodium can be normal or even slightly increased. Clinically very common, especially in the elderly. Clinical manifestations include convulsions, stupor, coma, and elevated intracranial pressure, which can lead to severe cerebral palsy. If hyponatremia occurs within 48 hours, there is a high risk of causing permanent neurological damage. In patients with chronic hyponatremia, there is a risk of osmotic demyelination, especially when correcting hyponatremia is excessive or too fast. In addition to brain cell edema and clinical manifestations of intracranial hypertension, due to reduced blood volume, low blood pressure, fine pulse rate and circulatory failure may occur, as well as signs of dehydration. The overall sodium hyponatremia was normal without cerebral edema.

Cause

Cause

1. Total sodium reduction hyponatremia

When body fluids are lost, the loss of solute exceeds the loss of water, that is, hypotonic dehydration. This condition is seen in the loss of sodium greater than the loss of water, seen in extra-renal loss and kidney loss of sodium. According to the situation of urinary sodium excretion, the sodium concentration of Na+>20mmol/L is increased by sodium loss in the kidney, and <20mmol/L is extrarenal loss.

(1) The cause of renal sodium loss is the excessive use of diuretics: the mechanism is that diuretics inhibit the reabsorption of Henle's thick ascending NaCl, low blood volume stimulates ADH release, interferes with urine dilution and potassium deficiency-mediated penetration. Pressure receptors and changes in thirst. 2 mineralocorticoid deficiency: reduce renal tubular reabsorption of sodium. 3 salt-tolerant nephritis: accompanied by renal tubular acidosis and metabolic alkalosis. 4 ketones and urine (including diabetic ketoacidosis, starvation, alcoholic ketonuria).

(2) The cause of extrarenal sodium loss is 1 gastrointestinal loss, such as vomiting, diarrhea, third cavity fluid retention, burns, pancreatitis and pancreatic fistula and biliary fistula. 2 brain salt loss caused by subarachnoid hemorrhage.

2. Overall sodium normal hyponatremia

(1) Glucocorticoid deficiency: On the one hand, renal water excretion disorder, 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, can increase the permeability of the collecting duct.

(2) Hypothyroidism: It is due to a decrease in cardiac output and glomerular filtration rate, leading to a disorder of the intrarenal mechanism mediated by ADH.

(3) patients with acute schizophrenia: there is a tendency to hyponatremia, the mechanism is multi-factor, including increased thirst (drinking), osmotic pressure regulation of ADH release, mild defects, in the case of low plasma osmotic pressure There are also ADH release, increased reactivity of the kidney ADH and antipsychotics. Surgery is a kind of stress. Postoperative patients may develop hyponatremia, which is characterized by elevated levels of ADH in the plasma and increased free water retention in the body. Intraoperative input of electrolyte-free fluid is also a factor.

(4) Drug-induced hyponatremia: The mechanism is that ADH mediates, or increases ADH release, or enhances ADH.

(5) ADH hypersecretion syndrome (SIADH), etc.: The total water volume of these patients is increased, and the sodium concentration in urine is usually +20 mmol/L.

3. Overall sodium increased hyponatremia

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

Examine

an examination

(1) medical history

Should understand the patient's water, sodium intake and discharge, if there is vomiting, diarrhea, intestinal disease and drainage, water intake and salt supplementation; patients with heart, liver, kidney disease, lung cancer, brain trauma, brain Tumor, brain inflammation, history of stress irritation or diabetes; use of diuretics, and taking chlorfenapyr, vincristine, and carbamazepine.

(2) Physical examination

Those with mild hyponatremia may have no obvious symptoms, or only fatigue, weakness, anorexia, nausea, and lethargy. In severe cases, there may be unconsciousness, sputum, jet vomiting, convulsions, and coma. Physical examination should pay attention to changes in body weight and skin, such as skin elasticity. Various symptoms of edema or dehydration. If there is a change in heart rate, jugular vein filling and blood pressure, it indicates that there is a disorder of circulatory function, indicating that the condition has progressed to a serious stage.

(3) Laboratory inspection

Patients with sodium sodium concentration <135mmol / L are hyponatremia. It is best to make multiple measurements to rule out experimental errors and follow up. Blood tests should also include serum potassium and chloride. Blood sugar, plasma protein, muscle research urea nitrogen, etc., in addition to red blood cell count. Hemoglobin measurement and hematocrit, Russian blood dilution and changes in blood volume. Hyponatremia is often accompanied by hypotonicity and plasma osmotic pressure <275mmol / L. Urine sodium determination can help identify, answer and extrarenal sodium loss, the former urinary sodium is often >20mmol / L, the latter urinary sodium often <20mmol / L. Urine routine examination helps to understand whether the kidney has lesions. For those with more urine and higher urine density, urine sugar and ketone bodies must be examined. Patients with suspected renal tubular acidosis should be tested for chlorinated amine load.

Diagnosis

Differential diagnosis

The prominent symptom in the early stage of hypernatremia is thirst. In severe cases, the brain cells are dehydrated and mainly manifest symptoms of the nervous system such as irritability, lethargy, hyperreflexia, increased muscle tone, and later convulsions, convulsions, and coma.

Hyperkalemia: serum potassium is higher than 5.5mmol / L. Muscle weakness can occur in the early stage, severe abdominal reflexes disappear, muscle paralysis, and even respiratory muscles are paralyzed. The early circulatory rate of the circulatory system is slow, severe arrhythmia, and even ventricular fibrillation leads to cardiac arrest.

Patients with mild hypokalemia often have no obvious clinical signs, and may have weak body weakness, soft limbs, weakened or disappeared biliary reflexes, severe respiratory paralysis and cardiac dysfunction, heart rhythm disorder, heart enlargement, and even heart. Stopping in.

Hypercalcemia: When serum protein is normal, serum calcium is increased by > 2.75 mmol / L. In addition to the signs of the primary disease, the main signs of hypercalcemia are mood changes, depression, increased reflexes, decreased pain, weakness of the proximal muscles, and gait instability. In addition, attention should be paid to the symptoms of impaired renal function and changes in cardiac function.

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