Water and electrolyte balance is a health mechanic. Water balance of the body: causes of disturbance and methods of recovery Electrolyte disturbances that

Violation of the water-electrolyte balance in the body occurs in the following situations:

• With overhydration - excessive accumulation of water in the body and its slow release. The fluid medium begins to accumulate in the intercellular space and because of this, its level inside the cell begins to increase, and it swells. If overhydration activates nerve cells, then convulsions occur and nerve centers are excited.
• With dehydration - a lack of moisture or dehydration, the blood begins to thicken, due to viscosity, blood clots form and blood flow to tissues and organs is disturbed. With its lack in the body over 20% of the body weight, death occurs.

It is manifested by a decrease in body weight, dryness of the skin, cornea. With a high level of deficiency, the skin can be collected in folds, the subcutaneous fatty tissue is similar in consistency to the dough, the eyes sink. The percentage of circulating blood also decreases, this is manifested in the following symptoms:

• facial features are sharpened;
• cyanosis of the lips and nail plates;
• hands and feet are cold;
• pressure decreases, pulse is weak and frequent;
• hypofunction of the kidneys, a high level of nitrogenous bases as a result of impaired protein metabolism;
• disruption of the heart, respiratory depression (according to Kussmaul), vomiting is possible.

Isotonic dehydration is often recorded - water and sodium are lost in equal proportions. A similar condition is common in acute poisoning - the required volume of fluid and electrolytes is lost during vomiting and diarrhea.

ICD-10 code

E87 Other disorders of water-salt and acid-base balance

Symptoms of water-electrolyte imbalance

The first symptoms of a violation of the water-electrolyte balance depend on what pathological process occurs in the body (hydration, dehydration). This is increased thirst, and edema, vomiting, diarrhea. Altered acid-base balance, low blood pressure, irregular heartbeat are often noted. These signs cannot be neglected, as they lead to cardiac arrest and death if medical assistance is not provided on time.

With a lack of calcium in the blood, cramps of smooth muscles appear, a spasm of the larynx and large vessels is especially dangerous. With an increase in the content of Ca - pain in the stomach, thirst, vomiting, increased urination, inhibition of blood circulation.

Lack of K is manifested by atony, alkalosis, chronic renal failure, brain pathologies, intestinal obstruction, ventricular fibrillation and other changes in heart rhythm. An increase in potassium is manifested by ascending paralysis, nausea, and vomiting. The danger of this condition is that ventricular fibrillation and atrial arrest rapidly develop.

High Mg in the blood occurs with renal dysfunction, abuse of antacids. Nausea, vomiting appear, the temperature rises, the heart rate slows down.

Symptoms of imbalance in water and electrolyte balance indicate that the described conditions require immediate medical attention in order to avoid even more serious complications and death.

Diagnostics of the violation of water-electrolyte balance

Diagnosis of imbalance in water and electrolyte balance at the initial admission is carried out approximately, further treatment depends on the body's response to the introduction of electrolytes, anti-shock drugs (depending on the severity of the condition).

The necessary information about a person and his state of health upon hospitalization is established by:

• History. During the survey (if the patient is conscious), data on the existing disturbances in water-salt metabolism (peptic ulcer, diarrhea, narrowing of the pylorus, some forms of ulcerative colitis, severe intestinal infections, dehydration of a different etiology, ascites, a diet with a low salt content) are clarified.
• Establishing the degree of exacerbation of the current disease and further measures to eliminate complications.
• General, serological and bacteriological blood tests to identify and confirm the root cause of the current pathological condition. Also, additional instrumental and laboratory tests are prescribed to clarify the cause of the malaise.

Timely diagnosis of a violation of the water-electrolyte balance makes it possible to identify the severity of the violation as soon as possible and to organize the appropriate treatment in a timely manner.

Treatment of imbalance in water and electrolyte balance

Treatment of imbalance in water and electrolyte balance should take place according to the following scheme:

• Eliminate the likelihood of progressive development of a life-threatening condition:
  • bleeding, acute blood loss;
  • eliminate hypovolemia;
  • eliminate hyper- or hypokalemia.
• Resume normal water-salt metabolism. Most often, to normalize water-salt metabolism, the following drugs are prescribed: NaCl 0.9%, glucose solution 5%, 10%, 20%, 40%, polyionic solutions (Ringer-Locke solution, lactasol, Hartman's solution, etc. .), erythrocyte mass, polyglucin, soda 4%, KCl 4%, CaCl2 10%, MgSO4 25%, etc.
• To prevent possible complications of an iatrogenic nature (epilepsy, heart failure, especially with the administration of sodium preparations).
• If necessary, in parallel with the intravenous administration of medicines, carry out diet therapy.
• With the intravenous administration of saline solutions, it is necessary to control the level of VCO, CBS, control hemodynamics, and monitor renal function.

An important point is that before the start of the intravenous administration of saline components, it is necessary to calculate the probable loss of fluid and draw up a plan for restoring a normal VOS. The loss is calculated using the formulas:

Water (mmol) = 0.6 x Weight (kg) x (140 / Na true (mmol / L) + glucose / 2 (mmol / L)),

where 0.6 x Weight (kg) is the amount of water in the body

140 - average% Na (norm)

Na ist - true concentration of sodium.

Water deficit (l) = (Htst - HtN): (100 - HtN) x 0.2 x Weight (kg),

where 0.2 x Weight (kg) is the volume of extracellular fluid

HtN = 40 for females, 43 for males.

• Electrolyte content - 0.2 x Weight x (Norm (mmol / l) - true content (mmol / l).

Prevention of imbalance in water and electrolyte balance

Prevention of imbalance in the water-electrolyte balance consists in maintaining a normal water-salt balance. Salt metabolism can be disrupted not only in severe pathologies (grade 3-4 burns, gastric ulcer, ulcerative colitis, acute blood loss, food intoxication, infectious diseases of the gastrointestinal tract, mental disorders accompanied by malnutrition - bulimia, anorexia, etc.), but also with excessive sweating, accompanied by overheating, systematic uncontrolled use of diuretics, prolonged salt-free diet.

For prophylactic purposes, it is worth monitoring the state of health, controlling the course of existing diseases that can provoke a salt imbalance, not prescribing medications for yourself that affect the transit of fluid, replenishing the required daily fluid intake under conditions close to dehydration, and eating properly and in a balanced manner.

Prevention of imbalance in water and electrolyte balance also lies in the correct diet - the use of oatmeal, bananas, chicken breast, carrots, nuts, dried apricots, figs, grape and orange juice is not only useful in itself, but also helps to maintain the correct balance of salts and trace elements ...

Electrolytes are ions in the human body that contain electrical charges. The four most well-known electrolytes in the human body are sodium, potassium, calcium, and magnesium. They play a key role in ensuring the normal functioning of the body. If you think you may be suffering from electrolyte imbalances, read this article to learn about the symptoms of this disorder and how to treat it.

Steps

Assess electrolyte levels

The most common electrolytes are sodium, potassium, calcium, and magnesium. When the balance of the levels of these electrolytes in your body is imbalanced, it is called an electrolyte imbalance.

Note the symptoms of sodium deficiency in your body. Sodium is one of the most abundant electrolytes in the human body. When your electrolyte levels are in balance, your blood contains 135-145 mmol / L sodium. You get the most sodium from salty foods. Therefore, when sodium levels in your body are low (called hyponatremia), you crave salty foods.

• Symptoms: You will crave salty foods. Other symptoms of hyponatremia include extreme tiredness, muscle weakness, and increased urination.
• When your sodium levels get too low, you can experience a heart attack, inability to breathe, and even go into a coma. However, these symptoms occur only in extreme situations.

1. Be aware of the symptoms of excess sodium in your body. As already mentioned, the normal sodium content in the blood is 135-145 mmol / L. When the amount of sodium exceeds 145 mmol / L, it is called hypernatremia. Fluid loss through vomiting, diarrhea, and burns can lead to this condition. You can also get too much sodium if you don't drink enough water or eat too much salty food.

   • Symptoms: You will be thirsty and your mouth will be very dry. You may notice that your muscles begin to twitch, feel irritable, and may have difficulty breathing.
   • With extreme excess sodium, you may experience convulsions and decreased levels of consciousness.

2. Watch out for potassium deficiency. 98% of the body's potassium is contained within cells, and your blood contains 3.5-5 mmol / L potassium. Potassium contributes to healthy skeletal and muscle movement and normal heart function. Hypokalemia means a low amount of potassium in the body (less than 3.5 mmol / L). This can happen when you sweat too much during exercise or if you are taking laxatives.

   • Symptoms: You will feel tired and weak. You may also experience constipation, leg cramps, and decreased tendon reflexes.
   • If you are severely deficient in potassium, you may experience an irregular heartbeat, also known as arrhythmia.

3. Pay attention to muscle weakness, as this could be a sign of excess potassium. Usually, only some kind of disease such as kidney failure and diabetes mellitus can lead to an excess of potassium.

   • Symptoms: You will feel very weak because too much potassium leads to muscle weakness. You may also feel tingling and numbness in your muscles. In some cases, you may also experience clouding of consciousness.
   • Severely excessive potassium levels can cause an irregular heartbeat, which, in the most severe cases, can lead to a heart attack.

4. Watch for signs of calcium deficiency. Calcium may be the most well-known electrolyte. It is found in most dairy products and strengthens bones and teeth. The normal blood calcium level is 2.25-2.5 mmol / L. When your calcium levels fall below this level, you develop hypocalcemia.

   • Symptoms: Hypocalcemia can cause muscle cramps and tremors. Your bones can become brittle and weak.
   • You may experience irregular heartbeats or seizures if your calcium levels are too low for a long time.

5. Watch for symptoms of excess calcium in your body. When the blood calcium level exceeds 2.5 mmol / L, it is called hypercalcemia. Parathyroid hormone (parathyroid hormone) is responsible for the production of calcium in the body. When the parathyroid hormone becomes too active (in hyperparathyroidism), excess calcium is formed in the body. It can also happen due to long periods of immobilization.

   • Symptoms: Mild hypercalcemia (a slight excess of calcium in the blood) usually has no symptoms. However, if calcium levels continue to rise, you may experience weakness, bone pain, and constipation.
   • In severe cases, you may develop kidney stones if you leave the hypercalcemia untreated.

6. Watch out for low magnesium levels when you are in the hospital. Magnesium is the fourth most abundant electrolyte in your body. The average magnesium content in the human body is 24 g, and 53% of this amount is in the bones. Hypomagnesemia is commonly seen in people who have been hospitalized and very rarely in people who are not hospitalized.

   • Symptoms: Symptoms include slight tremors, confusion and difficulty swallowing.
   • Severe symptoms include difficulty breathing, anorexia, and convulsions.

7. Be aware that excess magnesium is also rare in non-hospitalized people. Hypermagnesemia is a condition in which an excess of magnesium is formed in the human body. This is a very rare condition and usually only occurs in people who are hospitalized. Dehydration, bone cancer, hormonal imbalances, and renal failure are the most common causes of hypermagnesemia.

   • Symptoms: Your skin may turn red and warm to touch. You may also experience decreased reflexes, weakness, and vomiting.
   • Severe symptoms include coma, paralysis, and hypoventilation syndrome. Slowing heart rate is also possible.

   Electrolyte imbalance treatment

   1. Increase your sodium levels. First of all: take a rest, normalize your breathing and relax. Chances are, you just need to eat something salty, so sit down and eat. Mild sodium deficiency symptoms usually begin because you haven't eaten anything salty for a long time. You can also drink an electrolyte-rich drink.

      Lower your sodium levels. Sit down and have a glass of water. Most of the symptoms associated with excess sodium are caused by eating too much salty food. Drink plenty of water until you are completely thirsty. Vomiting can also lead to dehydration, so if you feel nauseous, address the cause of the nausea and be careful with what you eat.

      • If you start having convulsions, call an ambulance.

   2. Increase your potassium levels. If your potassium deficiency is caused by excessive sweating or vomiting, drink plenty of fluids to rehydrate your body. If you experience symptoms of hypokalemia while exercising, stop, sit down and drink an electrolyte-rich drink. If you feel a muscle spasm, pull it. You can also restore normal blood potassium levels by eating foods high in potassium.

      Reduce the level of magnesium in your body. If you experience only mild symptoms of hypermagnesemia, drink plenty of water and stop eating magnesium-rich foods for a few days. However, high magnesium levels are most commonly seen as a symptom of kidney disease. You will need to heal your underlying medical condition in order to normalize your magnesium levels. Talk to your doctor about the best treatment.

      • If you have a history of heart disease and an irregular heartbeat, seek immediate medical attention.

   3. Strengthen bones by increasing your calcium levels. Mild to moderate symptoms of calcium deficiency can usually be alleviated by eating foods fortified with calcium. You can also increase your vitamin D intake, which improves the way your body uses calcium, by sun exposure for 30 minutes until 8am. Exposure to the sun after 8 a.m. can lead to individual health problems. You can also take vitamin D as a dietary supplement. If you feel muscle spasms, stretch and massage.

      Reduce the amount of calcium in your body. If you experience only mild symptoms of excess calcium, drink enough water and eat high fiber foods to help relieve constipation. You should refrain from eating foods high in calcium. Excess calcium is usually due to hyperparathyroidism, which you will have to get rid of before you can lower your calcium levels. Talk to your doctor about treatment options.

Violation of water-electrolyte metabolism is an extremely common pathology in seriously ill patients. The resulting disorders of the water content in various environments of the body and the associated changes in the content of electrolytes and CBS create the prerequisites for the emergence of dangerous disorders of vital functions and metabolism. This determines the importance of an objective assessment of the exchange of water and electrolytes both in the preoperative period and in the process of intensive therapy.

Water with substances dissolved in it is a functional unity both in biological and physicochemical terms and performs various functions. Metabolic processes in a cell take place in an aqueous medium. Water serves as a dispersion agent for organic colloids and as an indifferent basis for the transport of building and energetic substances to the cell and the evacuation of metabolic products to the excretory organs.

In newborns, water accounts for 80% of the body weight. With age, the water content in the tissues decreases. In a healthy man, water is on average 60%, and in women 50% of the body weight.

The total volume of water in the body can be divided into two main functional spaces: intracellular, the water of which is 40% of the body weight (28 liters in men with a weight of 70 kg), and extracellular - about 20% of the body weight.

The extracellular space is the fluid that surrounds cells, the volume and composition of which is maintained by regulatory mechanisms. The main cation of the extracellular fluid is sodium, the main anion is chlorine. Sodium and chlorine play a major role in maintaining the osmotic pressure and fluid volume of this space. The extracellular fluid volume consists of a rapidly moving volume (functional volume of extracellular fluid) and a slowly moving volume. The first of these includes plasma and interstitial fluid. The slowly moving volume of extracellular fluid includes the fluid in the bones, cartilage, connective tissue, subarachnoid space, synovial cavities.

The concept of "third water space" is used only for pathology: it includes the fluid accumulating in the serous cavities with ascites and pleurisy, in the subperitoneal layer during peritonitis, in the closed space of intestinal loops with obstruction, especially during volvulus, in the deep layers of the skin in the first 12 hours after the burn.

The extracellular space includes the following water sectors.

Intravascular water sector - plasma serves as a medium for erythrocytes, leukocytes and platelets. The protein content in it is about 70 g / l, which is much higher than in the interstitial fluid (20 g / l).

The interstitial sector is the environment in which cells are located and actively function; it is the fluid of the extracellular and extravascular spaces (together with lymph). The interstitial sector is not filled with a freely moving fluid, but with a gel that holds water in a fixed state. The basis of the gel is made up of glycosaminoglycans, mainly hyaluronic acid. The interstitial fluid is a transport medium that does not allow the substrates to spread throughout the body, concentrating them in the right place. Through the interstitial sector, the transit of ions, oxygen, nutrients into the cell and the reverse movement of toxins into the vessels, through which they are delivered to the excretory organs, take place.

Lymph, which is an integral part of the interstitial fluid, is intended mainly for the transport of chemical large-molecular substrates (proteins), as well as fatty conglomerates and carbohydrates from the interstitium into the blood. The lymphatic system also has a concentration function, since it reabsorbs water in the area of ​​the venous end of the capillary.

The interstitial sector is a significant "reservoir" containing? all body fluid (15% of body weight). Due to the fluid in the interstitial sector, the plasma volume is compensated for in acute blood and plasma loss.

Intercellular water also includes transcellular fluid (0.5-1% of body weight): fluid of serous cavities, synovial fluid, fluid of the anterior chamber of the eye, primary urine in the kidney tubules, secretions of the lacrimal glands, secretions of the glands of the gastrointestinal tract.

The general directions of movement of water between the environments of the body are shown in Figure 3.20.

The stability of the volumes of liquid spaces is ensured by the balance of gains and losses. Usually, the vascular bed is replenished directly from the gastrointestinal tract and by the lymphatic pathway, emptied through the kidneys and sweat glands, and exchanged with the interstitial space and the gastrointestinal tract. In turn, the interstitial sector exchanges water with the cellular, as well as with the blood and lymphatic channels. Free (osmotically bound) water - with the interstitial sector and intracellular space.

The main causes of violations of the water-electrolyte balance are external fluid losses and their non-physiological redistribution between the main fluid sectors of the body. They can occur as a result of pathological activation of natural processes in the body, in particular with polyuria, diarrhea, excessive sweating, with profuse vomiting, due to losses through various drains and fistulas or from the surface of wounds and burns. Internal movement of fluids is possible with the development of edema in injured and infected areas, but mainly due to changes in the osmolality of fluid media. Specific examples of internal movements are the accumulation of fluids in the pleural and abdominal cavities in pleurisy and peritonitis, tissue blood loss in extensive fractures, plasma movement into injured tissues in crush syndrome, etc. A special type of internal fluid movement is the formation of so-called transcellular pools in the gastrointestinal tract (with intestinal obstruction, volvulus, intestinal infarction, severe postoperative paresis).

Figure 3.20. General directions of movement of water between body fluids

Water imbalance in the body is called dyshydria. Dyshydria is divided into two groups: dehydration and hyperhydration. In each of them, three forms are distinguished: normo-osmolar, hypo-osmolar and hyperosmol. The classification is based on the osmolality of the extracellular fluid, because it is the main factor that determines the distribution of water between cells and the interstitial space.

Differential diagnosis of various forms of dyshidria is carried out based on anamnestic, clinical and laboratory data.

Clarification of the circumstances that led the patient to this or that dyshidria is of paramount importance. Indications of frequent vomiting, diarrhea, taking diuretics and laxatives suggest that the patient has a water-electrolyte imbalance.

Thirst is one of the early signs of water scarcity. The presence of thirst indicates an increase in the osmolality of the extracellular fluid, followed by cellular dehydration.

Dryness of the tongue, mucous membranes and skin, especially in the axillary and groin areas, where sweat glands are constantly functioning, indicate significant dehydration. At the same time, the turgor of the skin and tissues is reduced. Dryness in the axillary and groin areas indicates a pronounced water deficit (up to 1500 ml).

The tone of the eyeballs may indicate, on the one hand, about dehydration (decreased tone), on the other, about overhydration (tension of the eyeball).

Edema is often caused by excess interstitial fluid and sodium retention in the body. No less informative in case of interstitial hyperhydria are such signs as puffiness of the face, smooth relief of the hands and feet, the predominance of transverse striation on the dorsum of the fingers, and the complete disappearance of longitudinal striation on their palmar surfaces. It should be borne in mind that edema is not a highly sensitive indicator of the balance of sodium and water in the body, since the redistribution of water between the vascular and interstitial sectors is due to a high protein gradient between them.

Changes in the turgor of the soft tissues of the relief zones: face, hands and feet are reliable signs of interstitial dyshidria. Interstitial dehydration is characterized by: retraction of the periocular tissue with the appearance of shadow circles around the eyes, sharpening of facial features, contrasting of the reliefs of the hands and feet, especially noticeable on the dorsal surfaces, accompanied by a predominance of longitudinal striation and folding of the skin, highlighting of the articular areas, which gives them the appearance of a bean pod, flattening of the fingertips.

The appearance of "hard breathing" during auscultation is due to increased sound conduction on exhalation. Its appearance is due to the fact that excess water is quickly deposited in the interstitial tissue of the lungs and leaves it with an elevated position of the chest. Therefore, it should be looked for in those areas that occupied the lowest position for 2-3 hours before listening.

Changes in the turgor and volume of parenchymal organs are a direct sign of cellular hydration. The most accessible for research are the tongue, skeletal muscles, liver (size). The size of the tongue, in particular, should correspond to its location, limited by the alveolar process of the lower jaw. With dehydration, the tongue noticeably decreases, often does not reach the front teeth, the skeletal muscles are flabby, foam or gutta-percha consistency, the liver is reduced in size. With hyperhydration, teeth imprints appear on the lateral surfaces of the tongue, skeletal muscles are tense, painful, the liver is also enlarged and painful.

Body weight is a significant indicator of fluid loss or increase. In young children, severe fluid deficiency is indicated by a rapid decrease in body weight of over 10%, in adults - over 15%.

Laboratory tests confirm the diagnosis and complete the clinical picture. Of particular importance are the following data: osmolality and concentration of electrolytes (sodium, potassium, chloride, bicarbonate, sometimes calcium, phosphorus, magnesium) in plasma; hematocrit and hemoglobin, blood urea, total protein and albumin to globulin ratio; results of the study of clinical and biochemical analysis of urine (amount, specific gravity, pH values, sugar level, osmolality, protein, potassium, sodium, acetone bodies, sediment study; concentration of potassium, sodium, urea and creatinine).

Dehydration. Isotonic (normo-osmolar) dehydration develops as a result of the loss of extracellular fluid, according to the electrolyte composition of a similar blood plasma: with acute blood loss, extensive burns, abundant discharge from various parts of the gastrointestinal tract, when exudate leaks from the surface of extensive superficial wounds, with polyuria, with excessively vigorous diuretic therapy, especially against the background of a salt-free diet.

This form is extracellular, because with its inherent normal osmolality of the extracellular fluid, cells are not dehydrated.

A decrease in the total content of Na in the body is accompanied by a decrease in the volume of the extracellular space, including its intravascular sector. Hypovolemia occurs, hemodynamics is disturbed early, and with severe isotonic losses, dehydration shock develops (example: cholera algid). Loss of 30% or more of blood plasma volume is directly life-threatening.

There are three degrees of isotonic dehydration: I degree - loss of up to 2 liters of isotonic fluid; II degree - loss of up to 4 liters; III degree - loss from 5 to 6 liters.

The characteristic signs of this dyshidria are a decrease in blood pressure when the patient is kept in bed, compensatory tachycardia, orthostatic collapse is possible. With an increase in isotonic fluid loss, both arterial and venous pressure decreases, peripheral veins collapse, slight thirst arises, deep longitudinal folds appear on the tongue, the color of the mucous membranes is not changed, urine output is reduced, urine excretion of Na and Cl is reduced due to increased blood flow vasopressin and aldosterone in response to a decrease in plasma volume. At the same time, the osmolality of blood plasma remains almost unchanged.

Microcirculation disorders arising from hypovolemia are accompanied by metabolic acidosis. With the progression of isotonic dehydration, hemodynamic disturbances are aggravated: CVP decreases, blood thickening and viscosity increase, which increases resistance to blood flow. There are marked disturbances of microcirculation: "marble", cold skin of the extremities, oliguria turns into anuria, arterial hypotension increases.

Correction of the considered form of dehydration is achieved mainly by infusion of normo-osmolar fluid (Ringer's solution, lactasol, etc.). In case of hypovolemic shock, in order to stabilize hemodynamics, a 5% glucose solution (10 ml / kg), normo-osmolar electrolyte solutions are first injected, and only then a colloidal plasma substitute is transfused (at the rate of 5-8 ml / kg). The rate of infusion of solutions in the first hour of rehydration can reach 100-200 ml / min, then it is reduced to 20-30 ml / min. The completion of the stage of urgent rehydration is accompanied by an improvement in microcirculation: the marbling of the skin disappears, the limbs warm up, the mucous membranes turn pink, the peripheral veins fill, diuresis is restored, tachycardia decreases, and blood pressure normalizes. From this point on, the rate is reduced to 5 ml / min or less.

Hypertensive (hyperosmolar) dehydration differs from the previous type in that, against the background of a general lack of fluid in the body, a lack of water prevails.

This type of dehydration develops when electrolyte-free water is lost (perspiration loss), or when water losses exceed electrolyte losses. The molar concentration of the extracellular fluid increases, and then the cells are dehydrated. The reasons for this condition may be an absolute lack of water in the diet, insufficient water intake in the patient's body with defects in care, especially in patients with impaired consciousness, with a loss of thirst, and impaired swallowing. It can lead to increased water loss during hyperventilation, fever, burns, polyuric stage of acute renal failure, chronic pyelonephritis, diabetes mellitus and diabetes insipidus.

Together with water, potassium comes from the tissues, which is lost with urine with preserved diuresis. With moderate dehydration, hemodynamics is disturbed a little. With severe dehydration, the BCC decreases, blood flow resistance increases due to increased blood viscosity, increased release of catecholamines, and increased afterload on the heart. Blood pressure, diuresis decrease, while urine is excreted with a high relative density and an increased concentration of urea. The concentration of Na in the blood plasma rises above 147 mmol / L, which accurately reflects the lack of free water.

The clinic of hypertensive dehydration is caused by dehydration of cells, especially brain cells: patients complain of weakness, thirst, apathy, drowsiness, with deepening dehydration, consciousness is disturbed, hallucinations, convulsions, and hyperthermia appear.

Water deficit is calculated using the formula:

C (Napl.) - 142

X 0.6 (3.36),

Where: c (Napl.) - concentration of Na in the patient's blood plasma,

0.6 (60%) - the content of all water in the body in relation to body weight, l.

Therapy is aimed not only at eliminating the cause of hypertensive dehydration, but also at replenishing the cellular fluid deficit by infusing a 5% glucose solution with the addition of up to 1/3 of the volume of isotonic NaCl solution. If the patient's condition allows, rehydration is carried out at a moderate pace. Firstly, it is necessary to be afraid of increased diuresis and additional fluid loss, and secondly, the rapid and abundant administration of glucose can reduce the molal concentration of extracellular fluid and create conditions for the movement of water into the brain cells.

In severe dehydration with symptoms of dehydration hypovolemic shock, impaired microcirculation and centralization of blood circulation, an urgent restoration of hemodynamics is necessary, which is achieved by replenishing the volume of the intravascular bed not only with a glucose solution, which quickly leaves it, but also with colloidal solutions that retain water in the vessels, reducing the rate of fluid intake in brain. In these cases, infusion therapy begins with the infusion of 5% glucose solution, adding to it up to 1/3 of the volume of rheopolyglucin, 5% albumin solution.

At first, the blood serum ionogram is not very informative. Along with an increase in the concentration of Na +, the concentration of other electrolytes is also increased, and normal indicators of the concentration of K + always make one think about the presence of true hypokalygism, which manifests itself after rehydration.

As diuresis is restored, intravenous infusion of K + solutions should be prescribed. As the rehydration proceeds, a 5% glucose solution is poured in, periodically adding electrolyte solutions. The effectiveness of the rehydration process is monitored according to the following criteria: restoration of diuresis, improvement of the general condition of the patient, moisturizing of the mucous membranes, and a decrease in the concentration of Na + in the blood plasma. An important indicator of the adequacy of hemodynamics, especially venous flow to the heart, can be the measurement of CVP, which is normally 5-10 cm of water. Art.

Hypotonic (hypoosmolar) dehydration is characterized by a predominance of a lack of electrolytes in the body, which leads to a decrease in the osmolality of the extracellular fluid. A true Na + deficiency may be accompanied by a relative excess of "free" water while maintaining dehydration of the extracellular space. At the same time, the molar concentration of extracellular fluid is reduced, conditions are created for the flow of fluid into the intracellular space, including into the cells of the brain with the development of its edema.

The volume of circulating plasma is reduced, blood pressure, CVP, pulse pressure are reduced. The patient is inhibited, drowsy, apathetic, he has no feeling of thirst, there is a characteristic metallic taste.

There are three degrees of Na deficiency: I degree - deficiency up to 9 mmol / kg; II degree - deficiency of 10-12 mmol / kg; III degree - deficit up to 13-20 mmol / kg of body weight. With III degree of deficiency, the general condition of the patient is extremely difficult: coma, blood pressure is reduced to 90/40 mm Hg. Art.

With moderately severe disorders, it is enough to limit yourself to the infusion of 5% glucose solution with isotonic sodium chloride solution. With a significant Na + deficiency, half of the deficit is compensated for with hypertonic (molar or 5%) sodium chloride solution, and in the presence of acidosis, Na deficiency is corrected with a 4.2% sodium bicarbonate solution.

The required amount of Na is calculated according to the formula:

Na + deficiency (mmol / l) = x 0.2 x m (kg) (3.37),

Where: with (Na) pl. - concentration of Na in the patient's blood plasma, mmol / l;

142 - concentration of Na in blood plasma is normal, mmol / l,

M - body weight (kg).

Infusion of solutions containing sodium is carried out at a decreasing rate. During the first 24 hours, 600-800 mmol of Na + is injected, in the first 6-12 hours - about 50% solution. In the future, isotonic electrolyte solutions are prescribed: Ringer's solution, lactasol.

The revealed Na deficiency is replenished with NaCl or NaHCO3 solutions. In the first case, it is assumed that 1 ml of a 5.8% NaCl solution contains 1 mmol of Na, and in the second (used in the presence of acidosis), it is assumed that an 8.4% solution of bicarbonate in 1 ml contains 1 mmol. The estimated amount of one or another of these solutions is administered to the patient together with the transfused normo-osmolar saline solution.

Hyperhydration. It can also be normo-, hypo- and hyperosmolar. Anesthesiologists-resuscitators have to meet with her much less often.

Isotonic hyperhydration often develops as a result of excessive administration of isotonic saline solutions in the postoperative period, especially with impaired renal function. The reasons for this overhydration can also be heart disease with edema, cirrhosis of the liver with ascites, kidney disease (glomerulonephritis, nephrotic syndrome). The development of isotonic hyperhydration is based on an increase in the volume of extracellular fluid due to a proportional retention of sodium and water in the body. The clinic of this form of overhydration is characterized by generalized edema (edema syndrome), anasarca, a rapid increase in body weight, reduced blood concentration indices; tendency to arterial hypertension. Therapy for this dyshidria comes down to eliminating the causes of their occurrence, as well as correcting the protein deficiency by infusing native proteins with the simultaneous excretion of salts and water using diuretics. If the effect of dehydration therapy is insufficient, hemodialysis with blood ultrafiltration can be performed.

Hypotonic hyperhydration is caused by the same factors that cause an isotonic form, but the situation is aggravated by the redistribution of water from the intercellular to the intracellular space, transmineralization and increased cell destruction. With hypotonic overhydration, the water content in the body increases significantly, which is also facilitated by infusion therapy with electrolyte-free solutions.

With an excess of "free" water, the molal concentration of body fluids decreases. "Free" water is evenly distributed in the fluid spaces of the body, primarily in the extracellular fluid, causing a decrease in the concentration of Na + in it. Hypotonic overhydration with hyponatriplasmia is observed when there is an excessive intake of "free" water in the body in quantities that exceed the capacity for excretion, if a) the bladder and the prostate bed are washed with water (without salts) after its transurethral resection, b) drowning occurs in fresh water, c) an excessive infusion of glucose solutions is carried out in the oligoanuric stage of the SNP. This dyshidria can also be caused by a decrease in glomerular filtration in the kidneys in acute and chronic kidney failure, congestive heart failure, cirrhosis of the liver, ascites, glucocorticoid deficiency, myxedema, Barter's syndrome (congenital failure of kidney tubules, violation of their ability to retain Na + and K + with increased production of renin and aldosterone, hypertrophy of the juxtaglomerular apparatus). It occurs with ectopic production of vasopressin by tumors: thymoma, oat-round cell lung cancer, adenocarcinoma of the duodenum and pancreas, with tuberculosis, increased production of vasopressin with lesions of the hypothalamic region, meningoencephalitis, drug-induced hematoma and congenital brain drugs that increase the production of vasopressin (morphine, oxytocin, barbiturates, etc.).

Hyponatremia is the most common violation of water-electrolyte metabolism, accounting for 30-60% of all electrolyte disturbances. Often this violation is of an iatrogenic nature - when an excess amount of 5% glucose solution is injected (glucose is metabolized and "free" water remains).

The clinical picture of hyponatremia is diverse: disorientation and deafness in elderly patients, convulsions and coma in the acute development of this condition.

Acute development of hyponatremia always manifests itself clinically. In 50% of cases, the prognosis is unfavorable. With hyponatremia up to 110 mmol / l and hypoosmolality up to 240-250 mosmol / kg, conditions are created for the hyperhydration of brain cells and its edema.

The diagnosis is based on an assessment of the symptoms of central nervous system damage (weakness, delirium, confusion, coma, convulsions) that occur during intensive infusion therapy. Clarifies its fact that the elimination of neurological or mental disorders as a result of the preventive administration of solutions containing sodium. Patients with an acute development of the syndrome, with pronounced clinical manifestations of the nervous system, primarily with the threat of the development of cerebral edema, require urgent therapy. In these cases, intravenous administration of 500 ml of 3% sodium chloride solution is recommended in the first 6-12 hours, followed by repeated administration of the same dose of this solution during the day. When natremia reaches 120 mmol / l, the administration of hypertonic sodium chloride solution is stopped. With possible decompensation of cardiac activity, it is necessary to prescribe furosemide with the simultaneous administration of hypertonic solutions to correct the loss of Na + and K + - 3% potassium chloride solution and 3% sodium chloride solution.

The method of choice for the therapy of hypertensive hyperhydration is ultrafiltration.

In hyperthyroidism with glucocorticoid deficiency, the administration of thyroidin and glucocorticoids is useful.

Hypertensive hyperhydration occurs as a result of excessive introduction into the body of hypertonic solutions by enteral and parenteral routes, as well as with infusion of isotonic solutions to patients with impaired renal excretory function. Both main water sectors are involved in the process. However, an increase in osmolality in the extracellular space causes dehydration of cells and the release of potassium from them. The clinical picture of this form of overhydration is characterized by signs of edematous syndrome, hypervolemia and damage to the central nervous system, as well as thirst, skin hyperemia, agitation, and a decrease in blood concentration indices. Treatment consists in adjusting infusion therapy with the replacement of electrolyte solutions with native proteins and glucose solutions, in the use of osmodiuretics or saluretics, in severe cases - hemodialysis.

There is a close connection between the severity of deviations in the water-electrolyte status and nervous activity. The peculiarity of the psyche and the state of consciousness can help to orientate in the direction of the tonic shift. With hyperosmia, there is a compensatory mobilization of cellular water and replenishment of water reserves from the outside. This is manifested by appropriate reactions: suspiciousness, irritability and aggressiveness up to hallucinosis, severe thirst, hyperthermia, hyperkinesis, arterial hypertension.

On the contrary, with a decrease in osmolality, the neurohumoral system is rendered inactive, which provides the cell mass with rest and the ability to assimilate part of the water unbalanced by sodium. More often there are: lethargy and lack of exercise; aversion to water with profuse losses in the form of vomiting and diarrhea, hypothermia, arterial and muscular hypotension.

Imbalance of K + ions. In addition to disorders related to water and sodium, a seriously ill patient often has an imbalance of K + ions, which plays a very important role in ensuring the vital activity of the body. Violation of the K + content in cells and in the extracellular fluid can lead to serious functional disorders and unfavorable metabolic changes.

The total potassium reserve in an adult's body is between 150 and 180 g, that is, approximately 1.2 g / kg. Its main part (98%) is in cells, and only 2% - in the extracellular space. The largest amounts of potassium are concentrated in intensively metabolizing tissues - renal, muscle, and cerebral. In the muscle cell, some of the potassium is in a state of chemical bond with protoplasmic polymers. Significant amounts of potassium are found in protein sediments. It is present in phospholipids, lipoproteins and nucleoproteins. Potassium forms a covalent bond with phosphoric acid residues, carboxyl groups. The significance of these bonds is that complexation is accompanied by a change in the physicochemical properties of the compound, including solubility, ionic charge, and redox properties. Potassium activates several dozen enzymes that provide metabolic cellular processes.

The complex-forming abilities of metals and the competition between them for a place in the complex itself fully manifest themselves in the cell membrane. Competing with calcium and magnesium, potassium facilitates the depolarizing action of acetylcholine and the transition of the cell into an excited state. With hypokalemia, this translation is difficult, but with hyperkalemia, on the contrary, it is facilitated. In the cytoplasm, free potassium determines the mobility of the cellular energy substrate - glycogen. High concentrations of potassium facilitate the synthesis of this substance and at the same time make it difficult to mobilize it for energy supply of cellular functions; low concentrations, on the contrary, inhibit the renewal of glycogen, but contribute to its breakdown.

Concerning the effect of potassium shifts on cardiac activity, it is customary to dwell on its interaction with cardiac glycosides. The result of the action of cardiac glycosides on Na + / K + - ATPase is an increase in the concentration of calcium, sodium in the cell and the tone of the heart muscle. A decrease in the concentration of potassium, a natural activator of this enzyme, is accompanied by an increase in the action of cardiac glycosides. Therefore, the dosage should be individual - until the desired inotropism is achieved or until the first signs of glycosidic intoxication.

Potassium is a companion of plastic processes. So, the renewal of 5 g of protein or glycogen needs to be provided with 1 unit of insulin, with the introduction of about 0.1 g of disubstituted potassium phosphate and 15 ml of water from the extracellular space.

Potassium deficiency is understood as a lack of its total content in the body. Like any deficit, it is the result of a loss that is not offset by revenue. Its severity sometimes reaches 1/3 of the total content. The reasons may vary. Decreased food intake may be due to involuntary or deliberate starvation, loss of appetite, damage to the masticatory apparatus, esophageal or pyloric stenosis, consumption of potassium-poor food, or infusion of potassium-depleted solutions during parenteral nutrition.

Excessive losses can be associated with hypercatabolism, increased excretory functions. Any profuse and uncompensated loss of body fluids leads to massive potassium deficiencies. It can be vomiting with stomach stenosis or with intestinal obstruction of any localization, loss of digestive juices in intestinal, biliary, pancreatic fistulas or diarrhea, polyuria (polyuric stage of acute renal failure, diabetes insipidus, saluretic abuse). Polyuria can be stimulated by osmotically active substances (high glucose concentration in diabetes mellitus or steroidal diabetes, the use of osmotic diuretics).

Potassium practically does not undergo active resorption in the kidneys. Accordingly, its losses with urine are proportional to the amount of diuresis.

Deficiency of K + in the body may be indicated by a decrease in its content in the blood plasma (normally about 4.5 mmol / l), but provided that catabolism is not enhanced, there is no acidosis or alkalosis and a pronounced stress reaction. Under such conditions, the level of K + in plasma 3.5-3.0 mmol / l indicates its deficiency in the amount of 100-200 mmol, in the range of 3.0-2.0 - from 200 to 400 mmol and with a content of less than 2, 0 mmol / L - 500 mmol or more. To some extent, the lack of K + in the body can be judged by its excretion in the urine. The daily urine of a healthy person contains 70-100 mmol of potassium (equal to the daily release of potassium from tissues and consumption from food). A decrease in potassium excretion to 25 mmol per day or less indicates a deep potassium deficiency. With a deficiency of potassium, resulting from its large losses through the kidneys, the potassium content in daily urine is above 50 mmol, with a deficiency of potassium as a result of insufficient intake of it into the body - below 50 mmol.

Potassium deficiency becomes noticeable if it exceeds 10% of the normal content of this cation, and threatening - when the deficit reaches 30% or more.

The severity of the clinical manifestations of hypokalemia and potassium deficiency depends on the rate of their development and the depth of the disorders.

Disorders of neuromuscular activity are leading in the clinical symptoms of hypokalemia and potassium deficiency and are manifested by changes in the functional state, the central and peripheral nervous system, the tone of the striated skeletal muscles, smooth muscles of the gastrointestinal tract and the muscles of the bladder. Examination of patients reveals hypotension or atony of the stomach, paralytic intestinal obstruction, congestion in the stomach, nausea, vomiting, flatulence, bloating, hypotension or atony of the bladder. From the side of the cardiovascular system, a systolic murmur at the apex and expansion of the heart, a decrease in blood pressure, mainly diastolic, bradycardia or tachycardia are recorded. With acutely developing deep hypokalemia (up to 2 mmol / l and below), atrial and ventricular extrasystoles often occur, myocardial fibrillation and circulatory arrest are possible. The immediate danger of hypokalemia lies in the disinhibition of the effects of antagonistic cations - sodium and calcium, with the possibility of cardiac arrest in systole. ECG signs of hypokalemia: low biphasic or negative T, the appearance of a V wave, QT expansion, PQ shortening. Typically, the weakening of tendon reflexes up to their complete disappearance and the development of flaccid paralysis, a decrease in muscle tone.

With the rapid development of deep hypokalemia (up to 2 mmol / L and below), generalized weakness of skeletal muscles comes to the fore and can result in paralysis of the respiratory muscles and respiratory arrest.

When correcting potassium deficiency, it is necessary to ensure the intake of potassium in the body in the amount of physiological need, to compensate for the existing deficiency of intracellular and extracellular potassium.

Deficiency K + (mmol) = (4.5 - K + pl.), Mmol / L * body weight, kg * 0.4 (3.38).

Elimination of potassium deficiency requires the elimination of any stress factors (strong emotions, pain, hypoxia of any origin).

The amount of nutrients, electrolytes and vitamins prescribed in these conditions should exceed the usual daily requirements so as to cover both losses to the environment (during pregnancy - to the needs of the fetus) and a certain proportion of the deficit.

To ensure the desired rate of restoration of the level of potassium in the composition of glycogen or protein, every 2.2 - 3.0 g of chloride or disubstituted potassium phosphate should be injected together with 100 g of glucose or pure amino acids, 20 - 30 units of insulin, 0.6 g of calcium chloride, 30 g of sodium chloride and 0.6 g of magnesium sulfate.

For the correction of hypokalygism, it is best to use disubstituted potassium phosphate, since glycogen synthesis is impossible in the absence of phosphates.

Complete elimination of cellular potassium deficiency is equivalent to complete restoration of proper muscle mass, which is rarely achievable in a short time. We can assume that a deficit of 10 kg of muscle mass corresponds to a potassium deficiency of 1600 meq, that is, 62.56 g K + or 119 g KCI.

With intravenous elimination of K + deficiency, its calculated dose in the form of a KCl solution is poured in together with a glucose solution, based on the fact that 1 ml of a 7.45% solution contains 1 mmol K., 1 meq of potassium = 39 mg, 1 gram of potassium = 25 meq. , 1 gram of KCl contains 13.4 meq of potassium, 1 ml of 5% KCl solution contains 25 mg of potassium or 0.64 meq of potassium.

It must be remembered that the entry of potassium into the cell takes some time, therefore the concentration of the infused K + solutions should not exceed 0.5 mmol / l, and the infusion rate should be 30-40 mmol / h. 1 g of KCl, from which a solution for intravenous administration is prepared, contains 13.6 mmol K +.

If the deficit of K + is large, its replenishment is carried out within 2-3 days, given that the maximum daily dose of intravenous K + is 3 mmol / kg.

The following formula can be used to determine the safe infusion rate:

Where: 0.33 is the maximum allowable safe infusion rate, mmol / min;

20 - number of drops in 1 ml of crystalloid solution.

The maximum potassium introduction rate is 20 meq / h or 0.8 g / h. For children, the maximum rate of potassium administration is 1.1 meq / h or 43 mg / h. The adequacy of the correction, in addition to determining the content of K + in the plasma, can be determined by the ratio of its intake and excretion into the body. The amount of K + excreted in the urine in the absence of aldesteronism remains reduced in relation to the administered dose until the deficit is eliminated.

Both K + deficiency and excessive K + content in plasma pose a serious danger to the body in case of renal failure and very intensive intravenous administration of it, especially against the background of acidosis, increased catabolism and cellular dehydration.

Hyperkalemia can be a consequence of acute and chronic renal failure in the stage of oliguria and anuria; massive release of potassium from tissues against the background of insufficient diuresis (deep or extensive burns, trauma); prolonged positional or tourniquet compression of the arteries, late restoration of blood flow in the arteries with their thrombosis; massive hemolysis; decompensated metabolic acidosis; rapid administration of large doses of depolarizing relaxants, diencephalic syndrome in traumatic brain injury and stroke with convulsions and fever; excessive intake of potassium in the body against the background of insufficient diuresis and metabolic acidosis; using excess potassium for heart failure; hypoaldosteronism of any origin (interstitial nephritis; diabetes; chronic adrenal insufficiency - Addison's disease, etc.). Hyperkalemia can occur with rapid (within 2-4 hours or less) transfusion of massive doses (2-2.5 liters or more) of donor erythrocyte-containing media with long preservation periods (more than 7 days).

Clinical manifestations of potassium intoxication are determined by the level and rate of increase in plasma potassium concentration. Hyperkalemia does not have well-defined, characteristic clinical symptoms. The most common complaints are weakness, confusion, various kinds of parasthesias, constant fatigue with a feeling of heaviness in the limbs, muscle twitching. In contrast to hypokalemia, hyperreflexia is recorded. Intestinal cramps, nausea, vomiting, diarrhea are possible. From the side of the cardiovascular system, bradycardia or tachycardia, a decrease in blood pressure, extrasystoles can be detected. The most common ECG changes. In contrast to hypokalemia, with hyperkalemia there is a certain parallelism of ECG changes and the level of hyperkalemia. The appearance of a high, narrow, pointed positive T wave, the onset of the ST interval below the isoelectric line, and a shortening of the QT interval (electrical ventricular systole) are the first and most characteristic ECG changes in hyperkalemia. These signs are especially pronounced with hyperkalemia, close to the critical level (6.5-7 mmol / l). With a further increase in hyperkalemia above the critical level, the QRS complex expands (especially the S wave), then the P wave disappears, an independent ventricular rhythm occurs, ventricular fibrillation and circulatory arrest occurs. With hyperkalemia, a slowdown in atrioventricular conduction (an increase in the PQ interval) and the development of sinus bradycardia are often observed. Cardiac arrest with high hyperglycemia, as already indicated, can occur suddenly, without any clinical symptoms of the threatening condition.

In the event of hyperkalemia, it is necessary to intensify the excretion of potassium from the body by natural means (stimulation of diuresis, overcoming oligo- and anuria), and if this path is impossible, artificial excretion of potassium from the body (hemodialysis, etc.) must be carried out.

If hyperkalemia is detected, any oral and parenteral potassium administration is immediately stopped, drugs that promote potassium retention in the body (capoten, indomethacin, verospiron, etc.) are canceled.

When high hyperkalemia (more than 6 mmol / l) is detected, the first therapeutic measure is the appointment of calcium supplements. Calcium is a functional potassium antagonist and blocks the extremely harmful effects of high hyperkalemia on the myocardium, thereby eliminating the risk of sudden cardiac arrest. Calcium is prescribed in the form of a 10% solution of calcium chloride or calcium gluconate, 10-20 ml intravenously.

In addition, it is necessary to carry out therapy that provides a decrease in hyperkalemia by increasing the movement of potassium from the extracellular space into the cells: intravenous administration of 5% sodium bicarbonate solution at a dose of 100-200 ml; the appointment of concentrated (10-20-30-40%) glucose solutions in a dose of 200-300 ml with simple insulin (1 unit per 4 g of injected glucose).

Alkalinization of the blood promotes the movement of potassium into cells. Concentrated solutions of glucose with insulin reduce protein catabolism and thereby the release of potassium, help to reduce hyperkalemia by increasing the flow of potassium into cells.

With uncorrected therapeutic measures of hyperkalemia (6.0-6.5 mmol / l and higher with acute renal failure and 7.0 mmol / l and higher with chronic renal failure) with simultaneously detected ECG changes, hemodialysis is indicated. Timely hemodialysis is the only effective method for the direct excretion of potassium and toxic products of nitrogen metabolism from the body, ensuring the survival of the patient.

Oliguria and polyuria, hypernatremia and hyponatremia - these disorders are recorded in more than 30% of patients with severe cerebral lesions. They have different origins.

A significant part of these disorders is associated with the usual causes of water-electrolyte disturbances (WES) - inadequate fluid intake by a person, excessive or insufficient infusion therapy, the use of diuretics, the composition of the agents used for enteral and parenteral nutrition, etc.

Doctors should try to eliminate the violations that have arisen by adjusting the infusion therapy, medication, and the patient's diet. If the actions taken did not bring the expected result, and violations of the water-electrolyte balance are still noted, doctors may assume that they are based on central neurogenic disorders.

Water-electrolyte disturbances, as a manifestation of central nervous system dysfunction, can occur with brain lesions of various etiologies: trauma, stroke, hypoxic and toxic brain damage, inflammatory diseases of the central nervous system, etc. In this article, we focus on three disorders that are most relevant to clinical practice and outcomes: central diabetes insipidus (CDI), syndrome of increased secretion of antidiuretic hormone (SIADH), and cerebral salt loss syndrome (CSWS).

Central diabetes insipidus

(CDI, cranial diabetes insipidus) is a syndrome that occurs as a consequence of a decrease in the level of antidiuretic hormone (ADH) in plasma. The appearance of this syndrome is associated with poor overall outcome and brain death. Its occurrence suggests that the deep structures of the brain are involved in the pathological process - the hypothalamus, the legs of the pituitary gland or the neurohypophysis.

As for the symptoms, polyuria is more than 200 ml / h, and hypernatremia is more than 145 mmol / l, signs of hypovolemia. Urine has a low specific gravity (<1010), низкую осмолярность (< 200 мосм/л) и низкое содержание натрия (< 50 ммоль/л).

Diabetes insipidus treatment

It is necessary to control the hourly urine output and replace fluid losses with a 0.45% sodium chloride solution, 5% glucose, and enteral administration of water. Introduce ( Minirin ):

• intranasally, 2-4 drops (10-20 μg) 2 times a day;
• inside, 100-200 mcg 2 times a day;
• intravenously slowly (15-30 min), after dilution in saline, at a dose of 0.3 μg / kg 2 times a day.

In the absence of desmopressin or its insufficient effect, doctors prescribe hypothiazide... It paradoxically reduces urine output (the mechanism of action is unclear). Take 25-50 mg 3 times a day. Carbamazepine reduces urine output and reduces the feeling of thirst in the patient. The average dose of carbamazepine for adults is 200 mg 2-3 times a day. It is also necessary to monitor and correct plasma electrolytes.

Syndrome of increased secretion of antidiuretic hormone

Syndrome of increased secretion of antidiuretic hormone (SIADH-syndrome of inappropriate secretion of antidiuretic hormone). This disease is based on excessive secretion of antidiuretic hormone (ADH).

In this condition, the kidneys are able to excrete significantly less water. Osmolarity of urine, as a rule, exceeds the osmolarity of plasma. The severity of these manifestations can be different. In the absence of restrictions on fluid intake, in some cases, hyponatremia and overhydration can progress rapidly. The result can be an increase in cerebral edema, deepening of neurological symptoms. With severe hyponatremia (110-120 mmol / L), the patient may develop convulsive syndrome.

Treatment

V2-vasopressin receptor blockers conivaptan, tolvaptan effectively eliminate fluid retention and lead to a rapid recovery of sodium levels in the blood. Conivaptan: loading dose of 20 mg for 30 minutes, then continuous infusion at a rate of 20 mg / day for 4 days. Tolvaptan is given to the patient by mouth 1 time a day in the morning, 15-30 mg. Patients receiving these drugs must stop any previous fluid restriction. If necessary, treatment with vaptans can be carried out indefinitely.

It should be noted that the cost of these drugs is high, which makes them inaccessible for widespread use. If vaptans are not available, carry out "Traditional" treatment:

• Limit fluid intake to 800-1200 ml / day. A negative fluid balance will lead to an increase in the concentration of sodium in the blood;
• Loop diuretics are prescribed for mild fluid retention. sometimes 80-120 mg orally or 40-60 mg IV is prescribed;
• With severe hyponatremia, deterioration of neurological status, seizures, intravenous administration (in 20-30 minutes) 1-2 ml / kg 3% (or 0.5-1 ml / kg 7.5%) solution is indicated sodium chloride;
• If the patient's condition is sufficiently stable, a gradual correction of hyponatremia is carried out within 2-3 days. by infusion of 3% sodium chloride at a rate of 0.25-0.5 ml / kg / hour.

Blood sodium levels need to be monitored frequently to avoid neurological complications. Rapid correction of hyponatremia can lead to the development of focal demyelination of the brain. During treatment, it is necessary to ensure that the daily increase in the level of sodium in the blood does not exceed 10-12 mmol.

When using hypertonic sodium chloride solutions, as a result of the redistribution of fluid into the vascular bed, there is a possibility of developing pulmonary edema. Intravenous administration of furosemide 1 mg / kg immediately after the initiation of sodium chloride infusion serves to prevent this complication. The effect of the introduction of a hypertonic sodium chloride solution does not last too long, the infusion has to be repeated periodically. The introduction of less concentrated solutions of sodium chloride does not reliably eliminate hyponatremia and increases fluid retention.

Cerebral salt loss syndrome

Cerebral salt wasting syndrome (CSWS). The pathophysiology of this syndrome is associated with impaired secretion of atrial natriuretic peptide and cerebral natriuretic factor.

A person exhibits high urine output and signs of BCC deficiency. Also typical are high urine specific gravity, increased urinary sodium levels greater than 50-80 mmol / L, hyponatremia, and increased or normal serum uric acid levels. This syndrome is common in patients with subarachnoid hemorrhage. It develops during the first week after cerebral injury. Lasts up to 4 weeks (average 2 weeks). The severity can be minimal to very strong.

Treatment

Treatment consists of adequate replenishment of water and sodium losses. Restriction in the introduction of fluid is not applied. To compensate for losses, in most cases, a 0.9% solution is used. Sometimes very large volumes of infusion are required, reaching 30 liters or more per day. If hyponatremia is not eliminated by the introduction of 0.9% sodium chloride, which indicates a large sodium deficiency, doctors use an infusion of 1.5% sodium chloride solution.

Reducing the volume of infusion therapy and accelerating the stabilization of the BCC, allows the appointment of mineralocorticoids - the patient is given fludrocortisone(Kortineff), 0.1-0.2 mg orally 2 times a day. Hydrocortisone effective in doses of 800-1200 mg / day. Large volumes of infusion, the use of mineralocorticoid drugs, polyuria can lead to hypokalemia, which also requires timely correction.

It is understood that electrolyte balance is generally closely related to water balance (see above). Below we briefly consider the pathophysiological aspects of metabolic disorders of sodium, potassium and calcium.

Sodium. Let me remind you that this is the main cation of the extracellular fluid (135–155 mmol / L of blood plasma, on average - 142 mmol / L) practically does not enter the cells and, therefore, determines the osmotic pressure of plasma and interstitial fluid.

Hyponatremia is either asymptomatic or manifested by increased fatigue. This is caused by abundant glucose infusions, large water retention in certain kidney diseases (nephritis, tubular nephrosis), or excessive vasopressin secretion in acute and chronic brain diseases.

It must be remembered that hyponatremia is most often relative and associated with hyperhydration of the extracellular space, less often with true sodium deficiency. Therefore, it is necessary to carefully assess the patient's condition, on the basis of anamnestic, clinical and biochemical data, to determine the nature of sodium metabolic disorders and to decide whether it is advisable to correct it.

total Na deficiency (mmol) = (142 mmol / L - plasma Na concentration, mmol / L) the weight of the patient 0,2.

For information, 10 ml of 3% sodium chloride solution used to compensate for sodium deficiency contains 5.1 mmol of sodium.

Potassium. It is a cation, the main part of which is inside the cells - up to 98%. Despite this, the serum potassium content (3.6–5.0 mmol / l) is an important physiological constant, a change in which is poorly tolerated by the body.

Hyperkalemia is manifested by nausea, vomiting, metabolic acidosis, bradycardia, and cardiac arrhythmias.

The causes of hyperkalemia can be: 1) decreased excretion of potassium in the urine in renal failure; 2) intravenous administration of potassium-containing solutions (with weakened renal function); 3) increased protein catabolism; 4) cell necrosis (with burns, crash syndrome, hemolysis); 5) metabolic acidosis, leading to the redistribution of potassium: its release from the cells with a constant total content; 6) primary or secondary adrenal insufficiency, leading to sodium loss and compensatory potassium retention.

The concentration of potassium above 6.5 mmol / L of plasma is threatening, above 7.5 to 10.5 is toxic, and above 10.5 mmol / L is fatal.

In addition to determining the concentration of potassium in the blood plasma, electrolyte imbalance can be judged by ECG changes.

ECG in hyperkalemia: high pointed T wave, QT shortening, QRS complex expansion, sinus bradycardia, often atrioventricular block, extrasystoles.

Hypokalemia is accompanied by adynamia, asthenia, muscle hypotension, apathy, dry skin, and decreased skin sensitivity. There is flatulence and vomiting, simulating obstruction. Expansion of the borders of the heart, deafness of the 1st tone, tachycardia, a decrease in arterial and an increase in venous pressure are found.

On the ECG: a decrease in the ST interval below the isoline, widening of the QT interval, flat biphasic or negative T wave, tachycardia, frequent ventricular extrasystoles.

Hypokalemia can be caused by:

1. Loss of potassium through the gastrointestinal tract (vomiting, diarrhea, etc.).

2. Increased excretion of potassium in the intestinal mucosa with adenoma of the colon, pancreatic tumors.

3. Loss of potassium through the kidneys: a) under the influence of drugs (prescription of diuretics, antihypertensive drugs); b) with kidney disease (chronic pyelo- and glomerulonephritis, tubulopathy).

4. Endocrine diseases: a) primary or secondary hyperaldosteronism (Cohn's syndrome or bilateral adrenal hyperplasia); b) stimulation of aldosterone production in diseases of the liver, kidneys, heart, diabetes insipidus, stress situations, etc.).

5. Violation of potassium distribution in metabolic alkalosis, insulin therapy (due to excessive binding of potassium in cells, due to increased synthesis of glycogen and proteins).

6. Insufficient intake of potassium.

Treatment... Apply 0.5-0.7% solution of potassium chloride with 5% or 10% glucose solution at a rate of no more than 20 mmol / h (1 g of potassium chloride used for intravenous administration contains 13.4 mmol of pure potassium). When transfusing a solution of glucose with potassium, it is also necessary to inject insulin at the rate of 1 U per 3-4 g of dry matter. This promotes the penetration of potassium into cells, the movement of sodium ions from them into the extracellular space and the elimination of intracellular acidosis.

The daily requirement for potassium ranges from 60 to 100 mmol. An additional dose of potassium is administered at the rate of:

deficiency K / mmol= 5 (detectable level of potassium in blood plasma, mmol / l) ( body weight) 0,2.

To correct potassium deficiency, a 3% solution of potassium chloride is used, 10 ml of which contains 4 mmol of pure potassium. Thus, if 40 ml of a 3% solution of potassium chloride is added to 200 ml of a 5% glucose solution, then its concentration is 0.5%, and the potassium content is 16 mmol. The resulting solution is poured at a rate of no more than 80 drops per minute, which is 16 mmol / h.

In hyperkalemia, a 10% solution of glucose with insulin (1 U per 3-4 g of glucose) is injected intravenously in order to improve the penetration of extracellular potassium into the cell for its participation in the processes of glycogen synthesis. Since hyperkalemia is accompanied by metabolic acidosis, its correction with sodium bicarbonate is indicated. In addition, diuretic drugs (intravenous furosemide) are used.

Calcium... Calcium almost does not participate in maintaining osmotic pressure, since its content in the extracellular sector is small and a significant part of the ion is associated with proteins. The total content in blood serum is 2.12-2.60 mmol / l, ionized calcium in plasma is 1.03-1.27. Ionized calcium has a regulatory effect on the endocrine secretion of the parathyroid gland and thyroid C-cells. The content of ionized calcium in the blood is maintained according to the principle of negative feedback through parathyroid hormone and calcitonin, as well as vitamins D.

Hypercalcemia... An increase in the concentration of ionized calcium leads to pathological conditions manifested by polyuria, vomiting, asthenia, adynamia, hyporeflexia, depression, heart rhythm disturbances, bone pain, vascular calcification, and a shortening of the QT distance on the ECG. Outcomes - death from renal failure due to nephrocalcinosis or cardiac arrest.

Hypocalcemia manifested by increased neuromuscular excitability, tetanic convulsions, blood hypocoagulation, weakening of cardiac activity, arterial hypotension. ECG - lengthening of the QT interval. With prolonged hypocalcemia, rickets occur in children, various trophic disorders, including cataracts, impaired dentin calcification of the teeth.

Elimination of hypercalcemia can be achieved primarily by treating a disease that caused a violation of calcium metabolism. For example, with hyperparathyroidism, a hormonally active tumor or hyperplastic tissue of the parathyroid glands is surgically removed.

In children with hypercalcemia, when signs of calcium metabolism disorders are detected, the intake of vitamin D into the body is limited. In severe hypercalcemia, intravenous administration of disodium salt of ethyldiaminetetraacetic acid (Na 2 EDTA), which can form complex compounds with calcium ions, is used.

Elimination of hypocalcemia... Due to the fact that most often hypocalcemia is a consequence of weakening or loss of function of the parathyroid glands, hormone replacement therapy is of paramount importance. For this purpose, the drug parathyroidin is widely used. To stop the attacks of tetany in patients with severe hypocalcemia, intravenous administration of solutions of calcium chloride, gluconate or calcium lactate is used, and vitamin D preparations are also used.