Hypernatremia

Introduction Hypernatremia refers to conditions in which blood sodium is too high (usually >145 mmol/L) with high blood osmotic pressure. Except in a few cases (input too much liquid containing too much sodium salt), this disease is mainly caused by dehydration, and sometimes with sodium loss, but the degree of water loss is greater than the loss of sodium. This disease often has a decrease in intracellular water. This is because extracellular extra-osmotic pressure can pump intracellular water out of the cell, so blood volume does not begin to decrease, but it can be reduced in the late stage. The main clinical manifestations of hypernatremia are neuropsychiatric symptoms.

Cause

The normal osmotic center is very sensitive to the reaction of hyperosmolarity. When the osmotic pressure rises by 2 mmol/L H2O, the secretion of antidiuretic hormone can be stimulated, and the water is reabsorbed from the kidney. At the same time, high osmotic pressure causes the thirst center to be excited, and the blood can be diluted by drinking water. Hypernatremia can result when water is scarce or unable to drink water, ADH release or dysfunction, or hypotonic body fluids are lost from the kidney or other routes. Common in the following situations.

1. Insufficient water intake

Lack of water in the voyage or desert, coma, refusal to eat, digestive tract lesions cause drinking water difficulties, brain trauma, cerebrovascular accidents, etc., causing thirst center bluntness or osmotic receptors are not sensitive, primary drinking water can cause water Insufficient intake leads to hypernatremia.

2. Too much water loss

(1) Loss of extra-renal: A large amount of sweat caused by intense exercise in high-heat and high-temperature environments can cause a large loss of water from the skin. Wheezing, hyperventilation, tracheotomy, etc. can cause excessive loss of water from the respiratory tract. Gastrointestinal osmotic watery diarrhea can also cause this disease, and if combined with eating disorders, the situation can be seriously deteriorated.

(2) Kidney loss: mainly caused by central diabetes insipidus and renal diabetes insipidus or the application of a large number of osmotic diuretics. Renal diabetes insipidus is a disease caused by abnormal V2 receptor gene of AVP. In congenital renal diabetes insipidus, nearly 10% of patients are caused by AQP2 gene mutation. Recent studies have confirmed that many acquired renal diabetes insipidus, including lithium poisoning, hypokalemia, hypercalcemia, and obstructive nephropathy, also have AQP2 dysregulation. Uncontrolled diabetes causes a large amount of excess solute particles to pass through the renal tubules to cause osmotic diuresis, long-term nasal feeding of high-protein liquid diet and other solute diuretic (called nasal feeding syndrome); use hypertonic glucose solution, mannitol, Yamanashi Dehydration therapy such as alcohol and urea causes solute diuresis.

3. Water is transferred into the cell

It can be seen in strenuous exercise, convulsions, etc. Due to the above reasons, the number of small molecules in the cells increases, and the osmotic pressure increases, which promotes the entry of water into the cells, which generally does not last long. In the case of lactic acidosis, glycogen is largely decomposed into small molecules of lactic acid, so that the intracellular osmotic pressure is too high, and water is transferred to the cells, which also causes hypernatremia.

4. Excessive sodium input

Commonly used in the injection of NaHCO3, excessive input of hypertonic NaCl, etc., patients with more severe blood volume.

5. Kidney sodium reduction

Found in right heart failure, nephrotic syndrome, cirrhosis, ascites and other pre-renal oliguria. Kidney oliguria such as acute and chronic renal failure. Metabolic acidosis, cardiopulmonary resuscitation and other supplemental alkali. Kidney dysfunction in the elderly or infants. Cushing's syndrome, primary aldosteronism and other potassium-sparing diseases. Use deoxycorticosterone, licorice potassium and sodium retention drugs.

6. Idiopathic hypernatremia

Caused by a thirst central disorder or abnormal regulation of AVP, the exact cause is unknown. A small number of cases may have brain tumors, granuloma and other diseases, or trauma, cerebrovascular accidents and other medical history.

an examination

Related inspection

Urine sodium serum (Cl-, Cl)

(1) medical history

Should pay attention to the history of a large amount of fluid loss, such as diarrhea and vomiting, high temperature sweating, tracheotomy combined with hyperthermia, etc., should pay special attention to the water supplement. Patients with polydipsia, polydipsia, and polyuria are manifestations of diabetes insipidus. Patients with diabetes insipidus with headache, vomiting, visual impairment, and traumatic brain injury should consider secondary diabetes insipidus. In addition, attention should be paid to the case of intravenous infusion of fluids, the use of dehydrating agents, diuretics, steroids and other drugs.

(2) Physical examination

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. When examining the body, you should pay attention to the patient's mental performance, the symptoms of skin dehydration, and whether there is circulatory failure.

(3) Laboratory inspection

The blood sodium concentration is increased, generally more than 150 mmol / L, and the plasma osmotic pressure is also increased. Daily urine volume, urine routine, and urine relative density are measured. Renal function tests include urea nitrogen, muscle complex, PSP, and urine concentration and dilution tests. For patients with suspected diabetes, primary aldosteronism, and Cushing syndrome, endocrine function tests are also performed.

Differential diagnosis

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 m heart rhythm disorder, heart enlargement, and even heart Stopping in.

Hypocalcemia: serum calcium is less than 2.2mmol / L. Increased neuromuscular excitability during hypocalcemia, may occur in hand and foot convulsions, tendons, throat, convulsions, as well as irritability, emotional instability, hallucinations and other mental symptoms. Patients with hypocalcemia can show positive signs of Chvostek and Trousseau, but about one-third of patients can be negative. Hypocalcemia with calcium deficiency in the body can cause bone calcification disorders, rickets, hysteresis, skeletal deformities in children, and osteoporosis, fibrotic osteitis, osteoporosis, etc. in adults.

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.

Hyponatremia: normal blood sodium is 142 mmol/L (135-145 mmol/L), and blood sodium is lower than 135 mmol/L. 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.

During the follicular phase of the normal menstrual cycle, the serum testosterone concentration averages 0.43 ng/ml, and the upper limit is 0.68 ng/ml. If it exceeds 0.7 ng/ml (=2.44 nmol/L), it is hyperandrogenemia, also known as high testosterone. Blood. It is a common gynecological endocrine disease. More common are menstrual changes such as menstrual thinning, amenorrhea or dysfunctional uterine bleeding, no ovulation, infertility. Some have masculine changes, such as hairy, enlarged throat, and low pitch. Some obesity, hemorrhoids, breast dysplasia, poor uterine development, ovarian enlargement, a few cases of clitoris hypertrophy.

Phosphorus metabolism disorder caused by lower than normal phosphate concentration in circulating blood. Also known as hypophosphatemia. The table is currently hemolysis, burnout, weakness and convulsions.

Hyperuricemia, also known as gout, is a group of diseases caused by dysbial metabolic disorders. Its clinical features are hyperuricemia and the resulting recurrent attacks of gouty acute arthritis and tophi deposits. Chronic arthritis and joint deformity, often involving the kidney caused by chronic interstitial nephritis and uric acid kidney stones. The disease can be divided into two major categories: primary and secondary. The cause of primary disease is mostly unclear due to a small number of enzyme defects. It is often accompanied by hyperlipidemia, obesity, diabetes, hypertension, arteriosclerosis and crown. Heart disease, etc., is a hereditary disease. Secondary people can be caused by a variety of causes such as kidney disease, blood diseases and drugs.

Systemic atherosclerosis and thrombosis can occur early in patients with homocystinuria and cystathione.

Hyperviscosity (or hyperviscosity) is a clinical pathological syndrome characterized by elevated blood viscosity factors, excessive blood viscosity, slow blood flow, and abnormal blood rheology parameters. .

Galactosemia is a toxic clinical metabolic syndrome with increased blood galactose. Most children have lactation, vomiting, nausea, diarrhea, weight loss, hepatomegaly, jaundice, bloating, hypoglycemia, proteinuria, etc., due to galactose in breastfeeding or artificial feeding. The performer should consider the possibility of galactosemia, and the relevant laboratory tests should be carried out. If the measures can be detected and taken in time, cataracts and mental retardation can occur rapidly.

Hypoxemia refers to insufficient oxygen in the blood. The arterial partial pressure of oxygen (pao2) is lower than the normal lower limit of the same age, and the main manifestation is the decrease of blood oxygen partial pressure and blood oxygen saturation. Adult normal arterial oxygen partial pressure (PaO2): 83-108 mmHg. A variety of causes, such as central nervous system disorders, bronchial, pulmonary lesions, etc. caused by ventilation and / or ventilation dysfunction can lead to hypoxia. Due to the degree of hypoxemia, the speed and duration of hypoxia, the impact on the body is also different. Hypoxemia is one of the most common critical illnesses in respiratory diseases and one of the important clinical manifestations of respiratory failure.

Cryoglobulinemia: 1. Purpura is the most common skin condition, such as cold urticaria, Raynaud phenomenon, acral cyanosis and reticular bluish, skin necrosis and ulceration. 2. Arthralgia is a common symptom in patients with mixed cryoglobulinemia. It often occurs in the hands and knee joints. It is polyarticular pain, symmetrical or asymmetrical, and occasionally joint swelling. 3. Renal damage can be manifested as acute and chronic nephritis, but also nephrotic syndrome, renal failure. 4. The nervous system is mainly peripheral neuropathy. Others such as hepatosplenomegaly, severe abdominal pain, pericarditis and generalized lymphadenopathy. 5. Laboratory examination of more than 90% of type I and more than 80% of patients with type II cold blood globulin content > 1mg / ml, more than 80% of patients with type III carotenoidemia is a high blood carotene content Caused by yellowing of skin color. Carotene is a lipid pigment that gives normal skin a yellow color.

Toxemia in pregnancy is a syndrome of ketosis, acidosis, hypoglycemia and liver failure. Most occur in the middle and late pregnancy. The symptoms of the milder are not obvious. In severe cases, the spirit is depressed, the breathing is difficult, the urine volume is severely reduced, and the exhaled gas has a ketone smell. Abortion, ataxia, convulsions and coma can occur before death. Hematological examination showed an increase in non-protein nitrogen, decreased calcium, increased phosphorus, and positive acetone test.

There is no hypoxemia during hypercapnia. Although PaCO2 has a lower pH value, there is only a temporary neurological inhibition in the clinic, which is characterized by slow response or coma.

Hypoproteinemia: mainly manifests malnutrition. The proteins in the blood are mainly plasma proteins and hemoglobin contained in red blood cells. Plasma proteins include plasma albumin, various globulins, fibrinogen and a small amount of binding proteins such as glycoproteins, lipoproteins, etc., in a total amount of 6.5 to 7.8 g%. If the total plasma protein is less than 6.0 g%, it can be diagnosed as hypoproteinemia.

Primary hypergastrinemia: CT cells proliferate due to genetic or chronic inflammation and Helicobacter pylori infection, which in turn increases the secretion of gastrin and absorbs blood into the blood, producing hypergastrinemia.

Endotoxemia is a pathophysiological manifestation caused by bacteria in the blood or bacteria in the lesion releasing a large amount of endotoxin to the blood, or by injecting a large amount of liquid contaminated by endotoxin. Clinical manifestations of chills, chills, hyperthermia, white blood cells and neutrophils increased. There is no restriction on a system that tends to or find multiple systems with migratory inflammation and multiple organ dysfunction. There is often a history of infection before the disease. In particular, those who have a basic disease that seriously affects the body's defense function, and who cannot control fever and other signs of systemic infection with general antibacterial drugs, should consider the possibility of endotoxemia. If there are defects or ecchymoses in the skin and mucous membranes, or complicated with septic shock, the clinical diagnosis of endotoxemia is basically established.

Hypermagnesemia: plasma magnesium is higher than 0.85mmol / L for hypermagnesemia, clinically less common, except for renal failure, most of which are iatrogenic, and related to the use of magnesium-containing drugs. This disease is most common in patients with renal dysfunction who have progressed to uremia. Hypermagnesemia mainly causes neuromuscular synaptic block. The early manifestations of neuromuscular disorders are similar to uremia and are easily overlooked. Hypermagnesemia should be considered in the presence of postural pus and blood pressure, bradycardia, weakening of deep reflexes, disappearance, muscle weakness, muscle paralysis, cardiac blockade, cardiac arrest, lethargy, and coma.

Magnesium deficiency: early magnesium deficiency often has nausea, vomiting, anorexia, and weakness. Abnormal magnesium deficiency often causes neuromuscular and behavioral abnormalities, such as fibrillation, tremor, ataxia, convulsions and rigidity, nystagmus, hyperreflexia, and are easily induced by sound, light, and mechanical stimulation. Patients often have significant painful brachiopods, Trousseau or Chvostek. Sometimes the mental disorder is abnormal and the orientation is lost.

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