Yesterday, our department admitted a patient with hypernatremia from the emergency room, no diabetes mellitus, blood sodium as high as 187mmol/l. The patient was irritable, had little urine, fever but no obvious foci of infection, and it turned out to be dehydration fever! The patient could not take care of herself because of senile dementia, and she could not speak, so she could only wait for others to give her water to drink, and she could not speak or help herself because she was living in a nursing home. So, elderly people, don’t forget to drink water often! So what are the causes of hypernatremia? How to identify and deal with it?
First, to clarify the concept of hypernatremia
Hypernatremia refers to a condition in which the blood sodium is too high (usually >145 mmol/L) and accompanied by high blood osmolarity. (The disease is mainly caused by water loss, sometimes also accompanied by sodium loss, but the degree of water loss is greater than the degree of sodium loss; very few patients due to the input of too much fluid containing too much sodium, etc.). The disease is often associated with a decrease in intracellular water, which is due to the high extracellular osmotic pressure that can draw out intracellular water to the outside of the cells, so that blood volume does not decrease at first, but can decrease in advanced stages of severe disease. The main clinical manifestations of hypernatremia are neuropsychiatric symptoms.
II. Etiology of hypernatremia
In normal people, the osmotic center is sensitive to high blood osmolality. Generally, a 2 mmol/L rise in blood osmolality can stimulate the secretion of antidiuretic hormone and promote water reabsorption from the kidneys; at the same time, high osmolality causes excitation of the thirst center, which can dilute blood by drinking water. Hypernatremia may result when water sources are lacking or unavailable, when ADH release or action is impaired, or when hypotonic body fluids are lost from the kidneys or other extrarenal routes. Common causes are as follows.
1. Inadequate water intake
Lack of water source, insufficient water intake, perhaps due to coma, refusal to eat, digestive tract pathology caused by water difficulties, traumatic brain injury, cerebrovascular accident, etc. resulting in thirst sensing center retardation or osmotic pressure receptor insensitivity, primary hyponatremia, etc. can cause insufficient water intake leading to hypernatremia.
2.Excessive water loss
(1) extra-renal loss such as high fever, high-temperature environment operations, strenuous exercise through the skin resulting in a large number of sweating water loss; wheezing state, hyperventilation, tracheotomy, etc. can make water through the exhaled
Excessive water loss through the respiratory tract; gastrointestinal osmotic watery diarrhea can also cause this disease, and if combined with eating disorders, the condition can be aggravated.
(2) Transrenal loss is mainly caused by central uremia and nephrogenic uremia or the application of large amounts of osmotic diuretics. Renal enuresis is a disease caused by abnormalities in the V2 receptor gene of AVP. In congenital enuresis, nearly 10% of patients are caused by variants in the AQP2 gene. Acquired nephrogenic uremia, such as those due to lithium toxicity, hypokalemia, hypercalcemia, and obstructive nephropathy, also has impaired regulation of AQP2 causing excessive water loss. Uncontrolled diabetic osmotic diuresis can lead to hypertonic dehydration1; solute diuresis due to long-term nasal feeding of high protein fluid diet, etc. (called nasal feeding syndrome); solute diuresis due to dehydration therapy using hypertonic glucose solution, mannitol, sorbitol, urea, etc.
3. Water transfer into the cells
It can be seen in strenuous exercise, convulsions, etc. Due to the above reasons, the increase of small molecules in the cells and the increase of osmotic pressure prompt the water to enter the cells, which usually does not last long. In lactic acidosis, a large amount of glycogen is decomposed into small molecules of lactic acid, which makes the intracellular osmotic pressure too high, and water is transferred into the cells, which also causes hypernatremia.
4.Excessive sodium input
It is common in the injection of NaHCO3, excessive input of hypertonic NaCl, etc. Patients are mostly accompanied by severe blood volume excess.
5.Decreased renal sodium excretion
See in right heart failure, nephrotic syndrome, cirrhotic ascites and other prerenal oliguria; acute and chronic renal failure and other renal oliguria; metabolic acidosis, cardiopulmonary resuscitation and other excessive alkaline supplementation; poor renal function in the elderly or infants; Cushing’s syndrome, primary aldosteronism and other potassium- and sodium-repelling diseases; the use of deoxycorticosterone, glycopyrrolide-type potassium- and sodium-repelling drugs.
6.Idiopathic hypernatremia
Caused by central thirst disorder or abnormal AVP regulation, the exact etiology is unknown. A few cases may have a history of brain tumor, sarcoidosis and other lesions or trauma, cerebrovascular accident, etc.
III. Identification of hypernatremia
1. The clinical manifestations of patients depend on the speed and degree of elevated blood sodium concentration.
The main clinical manifestations are water loss and neuropsychiatric symptoms. In the early stage, the main symptoms include thirst, decreased urine output, weakness, nausea and vomiting, and elevated body temperature; physical examination suggests signs of water loss, blood pressure and pulse rate, mental changes, increased muscle tone and hyperreflexia. In the late stage, the clinical manifestations of water loss in brain cells appear, with irritability, irritability, gradually changing to apathy, lethargy, convulsions or seizures and coma; accompanied by increased muscle tone and hyperreflexia, which can lead to death in severe cases.
Patients with idiopathic familial hypernatremia (Liddle disease) mainly present with hypertension and hypokalemia, similar to aldosteronism. Idiopathic hypernatremia due to an upregulation of the osmotic pressure threshold in the thirst center usually has no obvious clinical manifestations. Hypernatremia due to excessive water loss is often more water loss than sodium loss, and its clinical manifestations are often masked by water loss. These include signs of water loss, blood pressure and pulse rate, altered mental status, increased muscle tone and hyperreflexia.
2. Blood sodium, blood and urine osmolality can be identified by laboratory tests.
If blood sodium > 150 mmol/L, plasma osmolality > 295 mmol/L and urinary osmolality partner, it suggests ADH release or defect in its target organ of action; if urinary osmolality > 800 mmol/L, it indicates normal renal tubular concentration function, suggesting hypernatremia is due to impaired sodium excretion (or retention hypernatremia). If the blood osmolality is higher than the urine osmolality, it is more likely to be central or nephrogenic uremia. Finding the cause facilitates the next step of treatment.
IV. Treatment
The first step is to remove the cause or treat the cause as much as possible. If water deficiency should be immediately let patients drink water, you can correct hypernatremia. For those caused by excessive water loss and sodium excretion disorder, different treatment methods are adopted.
1.Hypernatremia due to water loss
In addition to the etiological treatment, the main thing is to correct the water loss. The preferred type of rehydration fluid is isotonic saline and 5% glucose solution, prepared by mixing 1/4:3/4 or 1:1 ratio. Glucose is quickly metabolized after entering the body, so the mixed solution is equivalent to hypotonic solution. 0.45% saline or 5% glucose solution can also be used. In general, patients can drink by mouth, and those who cannot drink by themselves can be injected by nasogastric tube, which is generally used for mild patients and is safe and reliable. For patients with severe symptoms, especially those with central nervous system symptoms, intravenous rehydration is required. When taking intravenous rehydration, attention should be paid to the speed of rehydration should not be too fast and the blood sodium concentration should be closely monitored, so that the decrease of blood sodium concentration per hour does not exceed 0.5mmol/L is appropriate, otherwise it will lead to cerebral edema caused by the imbalance of osmotic pressure of brain cells.
2.Sodium excretion disorder hypernatremia
The main purpose is to remove excessive sodium from the body. 5% glucose solution can be infused, and sodium-removing diuretics can be used to increase sodium excretion, such as furosemide or sodium etanercept. These diuretics have a stronger drainage effect than sodium removal, so they must be used with fluid replacement. If the patient is in renal failure, hemodialysis or peritoneal dialysis may be used. Dialysis fluid containing hypertonic glucose is appropriate. Again, the rate of decline of blood sodium should be monitored to avoid too rapid a decline that could cause cerebral edema.