Yesterday, our department admitted a patient with hypernatremia from the emergency department, without diabetes, with blood sodium as high as 187 mmol/l. The patient was irritable, urinated little, and was feverish but had no obvious foci of infection, which turned out to be dehydration fever! The patient due to senile dementia, life can not take care of themselves, can not speak, can only wait for others to give her water to drink, because of living in a nursing home can not tell, and can not help themselves, and ultimately due to dehydration and irritability, was pulled into the hospital! Therefore, elderly friends, do not forget to drink water often! So what are the causes of hypernatremia? How to recognize and deal with it? First, to clarify the concept of hypernatremia Hypernatremia refers to the condition of high blood sodium (usually >145mmol/L) accompanied by high blood osmolality. (The disease is mainly caused by water loss, sometimes 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.). There is often a decrease in intracellular water, which is due to the high extracellular osmolarity that allows intracellular water to be drawn out of the cell into the extracellular space, so that blood volume does not decrease to begin with, but it can decrease in advanced and severe cases. The main clinical manifestations of hypernatremia are neuropsychiatric symptoms. Second, the etiology of hypernatremia Normal human osmotic center is very sensitive to the response of high blood osmolality, general blood osmolality can be stimulated when the blood osmolality rises by 2mmol/L antidiuretic hormone secretion, prompting the water reabsorption from the kidneys; at the same time, high osmolality causes the excitement of the thirst center, which can be diluted by drinking water and blood. Hypernatremia may result when there is a lack of or inability to drink water from water sources, impaired release or action of ADH, or loss of hypotonic body fluids from the kidneys or other extrarenal routes. Common causes are as follows: 1, insufficient water intake Lack of water sources, insufficient water intake, perhaps due to coma, refusal to eat, gastrointestinal tract pathology caused by water difficulties, traumatic brain injury, cerebrovascular accidents, etc., resulting in the thirst center retardation or osmolality receptors insensitive, primary hypernatremia, etc. can cause insufficient water intake leading to hypernatremia. (1) Extra-renal loss, such as hyperthermia, high-temperature environment work, strenuous exercise through the skin caused by a large number of sweat water loss; wheezing state, hyperventilation, tracheotomy, etc. can make the water through the respiratory tract loss of water; the gastrointestinal osmotic watery diarrhea can also cause this disease, and if at the same time combined with the dietary disorders, the condition can be aggravated. (2) Transrenal loss is mainly caused by central and renal diabetes insipidus or the application of large amounts of osmotic diuretics. Renal dysuria is a disease caused by an abnormality in the V2 receptor gene for AVP, and in congenital renal dysuria, nearly 10% of patients are caused by mutations in the AQP2 gene. Excessive water loss due to impaired AQP2 regulation is also found in acquired renal dysuria, such as lithium toxicity, hypokalemia, hypercalcemia, and those due to obstructive nephropathy. Uncontrolled diabetes mellitus osmotic diuresis can lead to hypertonic dehydration1; solute diuresis due to prolonged nasal feeding of high-protein fluid diets, etc. (called nasal feeding syndrome); use of hypertonic glucose solution, mannitol, sorbitol, urea, and other dehydration therapies lead to solute diuresis. 3, water transfer into the cell can be seen in strenuous exercise, convulsions, etc., due to the above reasons for the increase in small molecules in the cell, the osmotic pressure increases, prompting water into the cell, generally does not last long. Lactic acidosis, glycogen decomposition of large amounts of small molecules of lactic acid, so that the intracellular osmotic pressure is too high, the water transferred to the cell, also causing hypernatremia. 4.Excessive sodium input is commonly seen in injection of NaHCO3, excessive input of hypertonic NaCl, etc., and patients are mostly accompanied by severe hypervolemia. 5.Renal sodium excretion is reduced in right heart failure, nephrotic syndrome, cirrhosis ascites and other pre-renal oliguria; acute and chronic renal failure and other renal oliguria; metabolic acidosis, cardiopulmonary resuscitation, such as too much alkali supplementation; the elderly or infants and young children with poor renal function; Cushing’s syndrome, primary aldosteronism and other disorders such as potassium excretion and sodium preservation diseases; the use of desoxycorticosterone, licorice potassium excretion and preservation of sodium drugs, and so on. 6.Idiopathic hypernatremia is caused by the disorder of thirst center or abnormal regulation of AVP, and the exact etiology is unknown. A small number of cases may have brain tumor, granuloma and other lesions or trauma, cerebrovascular accident and other medical history. Recognition of hypernatremia 1. The clinical manifestations of the patient depend on the rate and degree of elevation of blood sodium concentration. The main clinical manifestations are water loss and neuropsychiatric symptoms. Early 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, altered mental status, increased muscle tone, and hyperreflexia. In the late stage, the clinical manifestations of cerebral water loss appear, and the patient is irritable and agitated, gradually changing to apathy, lethargy, convulsions or epileptic seizures and coma; accompanied by increased muscle tone and hyperreflexia, etc., and the severe cases will die as a result. Patients with idiopathic familial hypernatremia (Liddle disease) present mainly with hypertension and hypokalemia, similar to aldosteronism. Idiopathic hypernatremia due to upregulation of the osmolality threshold in the thirst-sensing center is usually not clinically significant. Hypernatremia due to excessive water loss is often more water loss than sodium loss, and its clinical manifestations are often masked by water loss. They include signs of water loss, blood pressure and pulse rate, altered mental status, increased muscle tone and hyperreflexia. 2, through the laboratory examination of blood sodium, blood and urine osmolality can be identified: if the blood sodium > 150mmol / L, plasma osmolality > 295mmol / L, while the urine osmolality partner, it suggests that the ADH release or its role in the target organ defects; if the urine osmolality > 800mmol / L, indicating that the renal tubular concentrative function, suggesting that the 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 renal dysuria. Finding the cause of the disease will facilitate the next step of treatment. The first step is to remove or treat the cause as much as possible. If the water shortage should immediately let the patient drink water, can correct the hypernatremia. For those caused by excessive water loss and sodium excretion disorders, different methods of treatment are adopted. In addition to the treatment of the cause of the hypernatremia, the main thing is to correct the water loss. The type of rehydration fluid is preferred isotonic saline and 5% glucose solution, mixed and prepared in the ratio of 1/4:3/4 or 1:1. 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. General patient rehydration pathway can be orally drink, can not drink the person can be injected through the nasogastric tube, generally used for mildly ill patients, this pathway is safe and reliable. For more severe symptoms, especially those with central nervous system symptoms, intravenous rehydration is required. When taking intravenous rehydration, attention should be paid to the rehydration rate should not be too fast, and closely monitor the blood sodium concentration, in order to the hourly drop in blood sodium concentration of no more than 0.5 mmol / L is appropriate, otherwise it will lead to osmotic pressure imbalance in brain cells and cause cerebral edema. Sodium excretion disorders of hypernatremia is mainly to eliminate excessive sodium in the body, can be transfused with 5% dextrose solution, and at the same time with sodium drainage diuretic to increase sodium drainage, available furosemide or sodium etanercept. These diuretics have a stronger effect on drainage than on sodium removal, so they must be used together with rehydration. If the patient has renal failure, hemodialysis or peritoneal dialysis can be used. Dialysis fluids containing hypertonic glucose are preferred. Again, the rate of decline of blood sodium should be monitored to avoid too rapid a decline and cerebral edema.