Water-electrolyte balance - health mechanics. Body water balance: causes of disturbance and methods of restoration Electrolyte disturbances what

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

• With overhydration - excessive accumulation of water in the body and its slow release. The liquid 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 involves nerve cells, then convulsions occur and the nerve centers are excited.
• With dehydration - lack of moisture or dehydration, the blood begins to thicken, due to viscosity, blood clots form and blood flow to tissues and organs is disrupted. When its deficiency in the body exceeds 20% of body weight, death occurs.

Manifested by a decrease in body weight, dry skin and cornea. With a high level of deficiency, the skin can be gathered into folds, the subcutaneous fatty tissue has a dough-like consistency, and the eyes become sunken. The percentage of circulating blood also decreases, this is manifested in the following symptoms:

• facial features become sharper;
• cyanosis of lips and nail plates;
• hands and feet are cold;
• blood pressure decreases, pulse is weak and frequent;
• hypofunction of the kidneys, high levels of nitrogenous bases as a result of impaired protein metabolism;
• cardiac dysfunction, respiratory depression (Kussmaul), possible vomiting.

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 through vomiting and diarrhea.

ICD-10 code

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

Symptoms of water and electrolyte imbalance

The first symptoms of water-electrolyte imbalance depend on what pathological process occurs in the body (hydration, dehydration). This includes increased thirst, swelling, vomiting, and diarrhea. Often there is an altered acid-base balance, low blood pressure, and arrhythmic heartbeat. These signs cannot be ignored, as they lead to cardiac arrest and death if medical assistance is not provided on time.

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

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

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

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

Diagnosis of water-electrolyte imbalance

Diagnosis of water-electrolyte imbalance upon initial admission is carried out approximately; further treatment depends on the body’s reaction to the administration of electrolytes and anti-shock drugs (depending on the severity of the condition).

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

• According to the anamnesis. During the survey (if the patient is conscious), data on existing disorders of water-salt metabolism are clarified (peptic ulcer, diarrhea, narrowing of the pylorus, some forms of ulcerative colitis, severe intestinal infections, dehydration of other etiologies, ascites, low-salt diet).
• 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. Additional instrumental and laboratory tests are also prescribed to clarify the cause of the ailment.

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

Treatment of water-electrolyte imbalance

Treatment of water-electrolyte imbalance should be carried out 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. The following drugs are most often prescribed to normalize water-salt metabolism: NaCl 0.9%, glucose solution 5%, 10%, 20%, 40%, polyionic solutions (Ringer-Lock solution, lactasol, Hartman solution, etc. .), red blood cell mass, polyglucin, soda 4%, KCl 4%, CaCl2 10%, MgSO4 25%, etc.
• Prevent possible iatrogenic complications (epilepsy, heart failure, especially when administering sodium drugs).
• If necessary, carry out diet therapy in parallel with intravenous administration of medications.
• When administering saline solutions intravenously, it is necessary to monitor the level of VSO, CBS, monitor hemodynamics, and monitor renal function.

An important point is that before starting intravenous administration of saline components, you need to calculate the likely loss of fluid and draw up a plan for restoring normal VSO. Calculate the loss 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 true – true sodium concentration.

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

where 0.2 x Weight (kg) – volume of extracellular fluid

HtN = 40 for females, 43 for males.

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

Prevention of water-electrolyte imbalance

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

For preventive purposes, it is worth monitoring your health, monitoring the course of existing diseases that can provoke salt imbalance, not prescribing yourself medications that affect fluid transit, replenishing the required daily fluid intake under conditions close to dehydration, and eating a healthy and balanced diet.

Prevention of water-electrolyte imbalance also lies in a proper diet - eating oatmeal, bananas, chicken breast, carrots, nuts, dried apricots, figs, grape and orange juice is not only healthy in itself, but also helps 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 an electrolyte imbalance, 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 levels of these electrolytes in your body become 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 electrolyte levels are balanced, your blood contains 135-145 mmol/L sodium. You get the most sodium from salty foods. Therefore, when your body's sodium levels are low (called hyponatremia), you crave salty foods.

• Symptoms: You will crave salty foods. Other symptoms of hyponatremia include feeling very tired, muscle weakness, and increased urination.
• When sodium levels in your body become too low, you may experience a heart attack, be unable to breathe, and even fall 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. Loss of fluid 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 many salty foods.

   • 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 a decreased level of consciousness.

2. Watch for potassium deficiency. 98% of the body's potassium is found inside cells, and your blood contains 3.5-5 mmol/L of potassium. Potassium promotes healthy skeletal and muscle movement and normal heart function. Hypokalemia means low potassium levels in the body (less than 3.5 mmol/l). This can happen when you sweat too much during exercise or if you take laxatives.

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

3. Pay attention to muscle weakness, as this may be a sign of excess potassium. Typically, excess potassium can only be caused by a disease such as kidney failure and diabetes.

   • Symptoms: You will feel very weak because excess potassium leads to muscle weakness. You may also experience tingling and numbness in your muscles. In some cases, you may also experience confusion.
   • Extremely excess levels of potassium can cause irregular heartbeats, which, in the most severe cases, can lead to a heart attack.

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

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

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

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

6. Monitor low magnesium levels while 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 found in the bones. Hypomagnesemia is usually observed in people who have been hospitalized, and very rarely in non-hospitalized people.

   • Symptoms: Symptoms include mild shaking, confusion and difficulty swallowing.
   • Severe symptoms include difficulty breathing, anorexia and convulsions.

7. Know that excess magnesium is also rare in non-hospitalized people. Hypermagnesemia is a condition in which excess 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 imbalance and kidney failure are the most common causes of hypermagnesemia.

   • Symptoms: Your skin may become red and warm to the touch. You may also experience decreased reflexes, weakness, and vomiting.
   • Severe symptoms include coma, paralysis, and hypoventilation syndrome. It is also possible that your heart rate may slow down.

   Treatment of electrolyte imbalance

   1. Increase your sodium levels. First of all: rest, normalize your breathing and relax. Most likely, you just need to eat something salty, so sit down and eat. Mild symptoms of sodium deficiency usually begin because you haven't eaten anything salty in a while. You can also drink a drink fortified with electrolytes.

      Lower your sodium levels. Sit down and drink 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 thirst-free. Vomiting can also lead to dehydration, so if you feel sick, treat the cause of the nausea and be careful what you eat.

      • If you begin to convulse, 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 during exercise, stop, sit down, and drink an electrolyte-fortified drink. If you feel a muscle spasm, stretch it. You can also restore normal potassium levels in your blood by eating foods high in potassium.

      Lower magnesium levels 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 often observed as a symptom of kidney disease. You will need to treat the underlying condition to normalize the magnesium levels in your body. Talk to your doctor to determine the best treatment option.

      • If you have a history of heart disease and experience irregular heartbeats, seek medical attention immediately.

   3. Strengthen your bones by increasing your calcium levels. Mild to moderate symptoms of calcium deficiency can usually be relieved by eating foods fortified with calcium. You can also increase your intake of vitamin D, which improves how your body uses calcium, by spending 30 minutes in the sun before 8 am. Staying in the sun after 8 am can lead to certain health problems. You can also take vitamin D as a dietary supplement. If you feel muscle spasms, stretch and massage them.

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

Disturbance of water-electrolyte metabolism is an extremely common pathology in seriously ill patients. The resulting disturbances in the water content in various environments of the body and the associated changes in the content of electrolytes and CBS create the preconditions for the occurrence 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 during intensive care.

Water with the substances dissolved in it represents a functional unity both biologically and physicochemically and performs diverse functions. Metabolic processes in the cell take place in an aqueous environment. Water serves as a dispersion medium for organic colloids and an indifferent basis for the transport of building and energy substances to the cell and the evacuation of metabolic products to the excretory organs.

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

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

The extracellular space is the fluid surrounding 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 extracellular fluid volume) and a slowly moving volume. The first of these includes plasma and interstitial fluid. The slowly moving volume of extracellular fluid includes fluid located in bones, cartilage, connective tissue, subarachnoid space, and synovial cavities.

The concept of the “third water space” is used only in pathology: it includes fluid accumulating in the serous cavities with ascites and pleurisy, in the layer of subperitoneal tissue with peritonitis, in the closed space of intestinal loops with obstruction, especially with 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 aqueous sector - plasma serves as a medium for red blood cells, leukocytes and platelets. The protein content in it is about 70 g/l, which is significantly 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 freely moving fluid, but with a gel that holds water in a fixed state. The gel is based on glycosaminoglycans, mainly hyaluronic acid. Interstitial fluid is a transport medium that does not allow substrates to spread throughout the body, concentrating them in the right place. Through the interstitial sector, the transit of ions, oxygen, and nutrients into the cell and the reverse movement of waste 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 “container” containing? total body fluid (15% of body weight). Due to the fluid of the interstitial sector, compensation of plasma volume occurs during acute blood and plasma loss.

Intercellular water also includes transcellular fluid (0.5-1% of body weight): fluid of the 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 water movement between the body's environments are presented in Fig. 3.20.

The stability of the volumes of liquid spaces is ensured by the balance of gains and losses. Typically, the vascular bed is replenished directly from the gastrointestinal tract and lymphatic route, emptied through the kidneys and sweat glands, and exchanges 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 disturbances in water-electrolyte balance are external fluid losses and non-physiological redistribution between the main fluid sectors of the body. They can occur due to pathological activation of natural processes in the body, in particular with polyuria, diarrhea, excessive sweating, profuse vomiting, due to losses through various drainages and fistulas or from the surface of wounds and burns. Internal movements of fluids are possible with the development of edema in injured and infected areas, but are mainly due to changes in the osmolality of fluid environments. Specific examples of internal movements are the accumulation of fluids in the pleural and abdominal cavities during pleurisy and peritonitis, blood loss in tissue during extensive fractures, movement of plasma into injured tissue during crush syndrome, etc. A special type of internal movement of fluid is the formation of so-called transcellular pools in the gastrointestinal tract (with intestinal obstruction, volvulus, intestinal infarction, severe postoperative paresis).

Fig.3.20. General directions of water movement between body environments

An imbalance of water in the body is called dyshydria. Dyhydria is divided into two groups: dehydration and overhydration. Each of them has three forms: normoosmolal, hypoosmolal and hyperosmolal. The classification is based on the osmolality of the extracellular fluid, since it is the main factor determining the distribution of water between cells and the interstitial space.

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

Finding out the circumstances that led the patient to this or that dyshydria is of utmost importance. Indications of frequent vomiting, diarrhea, and taking diuretic and laxative medications suggest that the patient has a water-electroite imbalance.

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

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

The tone of the eyeballs may indicate, on the one hand, dehydration (decreased tone), and on the other, hyperhydration (strain of the eyeball).

Edema is often caused by excess interstitial fluid and sodium retention in the body. No less informative for interstitial hyperhydria are such signs as puffiness of the face, smoothness of the reliefs of the hands and feet, the predominance of transverse striations on the dorsum of the fingers, and the complete disappearance of longitudinal striations on their palmar surfaces. It must be taken into account 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 the high protein gradient between them.

Changes in the turgor of soft tissues of relief zones: the face, hands and feet are reliable signs of interstitial dyshydria. Interstitial dehydration is characterized by: retraction of the periocular tissue with the appearance of shadow circles around the eyes, sharpening of facial features, contrasting relief of the hands and feet, especially noticeable on the dorsal surfaces, accompanied by a predominance of longitudinal striations 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 during exhalation. Its appearance is due to the fact that excess water is quickly deposited in the interstitial tissue of the lungs and leaves it when the chest is elevated. Therefore, it should be looked for in those areas that occupied the lowest position for 2-3 hours before listening.

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

Body weight is a significant indicator of fluid loss or gain. 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 complement 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 content, total protein and albumin to globulin ratio; results of clinical and biochemical analysis of urine (quantity, specific gravity, pH values, sugar level, osmolality, protein content, potassium, sodium, acetone bodies, sediment examination; concentration of potassium, sodium, urea and creatinine).

Dehydration. Isotonic (normo-osmolal) dehydration develops due to the loss of extracellular fluid, which is similar in electrolyte composition to blood plasma: with acute blood loss, extensive burns, copious discharge from various parts of the gastrointestinal tract, with leakage of exudate from the surface of extensive superficial wounds, with polyuria, with excessively energetic therapy with diuretics, especially against the background of a salt-free diet.

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

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

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.

Characteristic signs of this dyshydria are a decrease in blood pressure when the patient is kept in bed, compensatory tachycardia, and orthostatic collapse is possible. With increasing isotonic fluid loss, both arterial and venous pressure decreases, peripheral veins collapse, slight thirst occurs, deep longitudinal folds appear on the tongue, the color of the mucous membranes is not changed, diuresis is reduced, urinary excretion of Na and Cl is reduced due to increased entry into the blood vasopressin and aldosterone in response to a decrease in blood plasma volume. At the same time, the osmolality of blood plasma remains almost unchanged.

Microcirculation disorders that occur due to hypovolemia are accompanied by metabolic acidosis. As isotonic dehydration progresses, hemodynamic disturbances worsen: central venous pressure decreases, blood thickening and viscosity increase, which increases resistance to blood flow. Severe microcirculation disorders are noted: “marbled”, cold skin of the extremities, oliguria turns into anuria, and arterial hypotension increases.

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

Hypertonic (hyperosmolal) dehydration differs from the previous type in that, against the background of a general fluid deficiency in the body, a lack of water predominates.

This type of dehydration develops when there is a loss of electrolyte-free water (perspiration loss), or when the water loss exceeds the loss of electrolytes. The molal concentration of extracellular fluid increases, then the cells dehydrate. The causes of this condition may be an absolute lack of water in the diet, insufficient intake of water into the patient’s body due to defects in care, especially in patients with impaired consciousness, loss of thirst, and impaired swallowing. It can be caused by increased water loss during hyperventilation, fever, burns, the polyuric stage of acute renal failure, chronic pyelonephritis, diabetes mellitus and diabetes insipidus.

Along with water, potassium comes from the tissues, which, with preserved diuresis, is lost in the urine. With moderate dehydration, hemodynamics are slightly affected. With severe dehydration, blood volume decreases, resistance to blood flow increases due to increased blood viscosity, increased release of catecholamines, and increased afterload on the heart. Blood pressure and diuresis decrease, while urine is released with a high relative density and an increased concentration of urea. The Na concentration in the blood plasma becomes higher than 147 mmol/l, which accurately reflects the deficiency of free water.

The clinical picture of hypertensive dehydration is caused by dehydration of cells, especially brain cells: patients complain of weakness, thirst, apathy, drowsiness; as dehydration deepens, consciousness is impaired, hallucinations, convulsions, and hyperthermia appear.

Water deficit is calculated using the formula:

C (Nap.) – 142

X 0.6 (3.36),

Where: с (Napl.) is the concentration of Na in the patient’s blood plasma,

0.6 (60%) - the content of total 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 cellular fluid deficiency by infusion of a 5% glucose solution with the addition of up to 1/3 of the volume of an isotonic NaCl solution. If the patient's condition allows, rehydration is carried out at a moderate pace. Firstly, it is necessary to be wary of increased diuresis and additional fluid loss, and secondly, rapid and abundant administration of glucose can reduce the molal concentration of extracellular fluid and create conditions for the movement of water into brain cells.

In case of severe dehydration with symptoms of dehydration hypovolemic shock, impaired microcirculation and centralization of blood circulation, 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 entry into the blood vessels. brain. In these cases, infusion therapy begins with the infusion of a 5% glucose solution, adding to it up to 1/3 of the volume of rheopolyglucin, 5% albumin solution.

The blood serum ionogram is initially uninformative. Along with the increase in Na+ concentration, the concentration of other electrolytes also increases, and normal K+ concentrations always make one think about the presence of true hypocaligistia, which manifests itself after rehydration.

As diuresis is restored, intravenous infusion of K+ solutions must be prescribed. As rehydration progresses, 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, moistening of the mucous membranes, and reduction of Na+ concentration in the blood plasma. An important indicator of the adequacy of hemodynamics, especially venous flow to the heart, can be the measurement of central venous pressure, which is normally 5-10 cm of water. Art.

Hypotonic (hypoosmolal) dehydration is characterized by a predominant lack of electrolytes in the body, which causes a decrease in the osmolality of the extracellular fluid. True Na+ deficiency may be accompanied by a relative excess of “free” water while maintaining dehydration of the extracellular space. The molal concentration of extracellular fluid is reduced, creating conditions for fluid to enter the intracellular space, including into brain cells with the development of brain edema.

The volume of circulating plasma is reduced, blood pressure, central venous pressure, and pulse pressure are reduced. The patient is lethargic, drowsy, apathetic, has no feeling of thirst, and has a characteristic metallic taste.

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

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

The required amount of Na is calculated using the formula:

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

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

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

M - body weight (kg).

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

The identified Na deficiency is replenished with solutions of NaCl or NaHCO3. 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) - from the fact that an 8.4% solution of hydrogen carbonate in 1 ml contains 1 mmol. The calculated amount of one or another of these solutions is administered to the patient along with a transfused normosmolar saline solution.

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

Isotonic overhydration often develops as a result of excessive administration of isotonic saline solutions in the postoperative period, especially when renal function is impaired. The causes of this overhydration can also be heart disease with edema, liver cirrhosis with ascites, kidney disease (glomerulonephritis, nephrotic syndrome). The development of isotonic overhydration is based on an increase in the volume of extracellular fluid due to the proportional retention of sodium and water in the body. The clinical picture of this form of overhydration is characterized by generalized edema (edematous syndrome), anasarca, rapid increase in body weight, and decreased blood concentration parameters; tendency towards arterial hypertension. Therapy for this dyshydria comes down to eliminating the causes of their occurrence, as well as correcting protein deficiency with infusions of native proteins with the simultaneous removal 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 the isotonic form, but the situation is aggravated by the redistribution of water from the intercellular to 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 into the body in quantities exceeding the excretion capacity, if a) the bladder and prostate gland bed are washed with water (without salts) after transurethral resection, b) drowning occurs in fresh water, c) excessive infusion of glucose solutions is carried out in the oligoanuric stage of SNP. This dyshydria may also be caused by a decrease in glomerular filtration in the kidneys in acute and chronic kidney failure, congestive heart failure, liver cirrhosis, ascites, glucocorticoid deficiency, myxedema, Barter syndrome (congenital failure of the kidney tubules, a 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, tuberculosis, increased production of vasopressin with lesions of the hypothalamic region, meningoencephalitis, hematoma, congenital anomalies and brain abscess, prescription of medications drugs that increase the production of vasopressin (morphine, oxytocin, barbiturates, etc.).

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

The clinical picture of hyponatremia is varied: disorientation and stupor in elderly patients, convulsions and coma during 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 overhydration of brain cells and its edema.

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

The method of choice for the treatment of hypertensive overhydration is ultrafiltration.

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

Hypertonic overhydration occurs as a result of excessive administration of hypertonic solutions into the body by enteral and parenteral routes, as well as during infusions of isotonic solutions to patients with impaired renal excretory function. Both major water sectors are involved in the process. However, an increase in osmolality in the extracellular space causes cell dehydration and the release of potassium from them. The clinical picture of this form of hyperhydration is characterized by signs of edema syndrome, hypervolemia and damage to the central nervous system, as well as thirst, skin hyperemia, agitation, and decreased blood concentration parameters. Treatment consists of adjusting infusion therapy with replacing electrolyte solutions with native proteins and glucose solutions, using osmodiuretics or saluretics, and in severe cases, hemodialysis.

There is a close connection between the severity of deviations in water-electrolyte status and nervous activity. The peculiarities of the psyche and state of consciousness can help to navigate the direction of the tonic shift. With hyperosmia, compensatory mobilization of cellular water and replenishment of water reserves from the outside occurs. This is manifested by corresponding 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 brought into an inactive state, providing the cell mass with rest and the opportunity to assimilate part of the water unbalanced by sodium. More often there are: lethargy and physical inactivity; 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 functions of the body. Violation of the K+ content in cells and in extracellular fluid can lead to serious functional disorders and unfavorable metabolic changes.

The total potassium reserve in the adult human body ranges from 150 to 180 g, that is, approximately 1.2 g/kg. Its main part (98%) is located in cells, and only 2% is in the extracellular space. The largest amounts of potassium are concentrated in intensively metabolizing tissues - kidney, muscle, brain. In a muscle cell, some of the potassium is in a state of chemical bonding with the polymers of protoplasm. Significant amounts of potassium are found in protein deposits. It is present in phospholipids, lipoproteins and nucleoproteins. Potassium forms a covalent type of bond with phosphoric acid residues and carboxyl groups. The significance of these connections 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 ensure 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. By competing with calcium and magnesium, potassium facilitates the depolarizing effect of acetylcholine and the transition of the cell to an excited state. With hypokalemia, this translation is difficult, and with hyperkalemia, on the contrary, it is facilitated. In the cytoplasm, free potassium determines the mobility of the energy cellular substrate - glycogen. High concentrations of potassium facilitate the synthesis of this substance and at the same time make it difficult to mobilize it to supply energy to cellular functions; low concentrations, on the contrary, inhibit the renewal of glycogen, but contribute to its breakdown.

Regarding the influence 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, dosing should be individual - until the desired inotropism is achieved or until the first signs of glycoside intoxication.

Potassium is a companion of plastic processes. Thus, 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 refers to a lack of total potassium content in the body. Like any deficit, it is the result of losses that are not compensated by revenues. Its expression sometimes reaches 1/3 of the total content. The reasons may vary. A decrease in dietary intake may be a consequence of forced or deliberate fasting, loss of appetite, damage to the masticatory apparatus, stenosis of the esophagus or pylorus, consumption of potassium-poor foods, or infusion of potassium-depleted solutions during parenteral nutrition.

Excessive losses may be associated with hypercatabolism and increased excretory functions. Any heavy and uncompensated loss of body fluids leads to massive potassium deficiency. This can be vomiting due to gastric stenosis or intestinal obstruction of any location, loss of digestive juices due to intestinal, biliary, pancreatic fistulas or diarrhea, polyuria (polyuric stage of acute renal failure, diabetes insipidus, abuse of saluretics). Polyuria can be stimulated by osmotically active substances (high concentrations of glucose in diabetes mellitus or steroid diabetes, the use of osmotic diuretics).

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

A 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 increased, there is no acidosis or alkalosis and no pronounced stress reaction. Under such conditions, a K+ level in plasma of 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 products). A decrease in potassium excretion to 25 mmol per day or less indicates a severe potassium deficiency. With potassium deficiency, resulting from its large losses through the kidneys, the potassium content in daily urine is above 50 mmol; with potassium deficiency as a result of insufficient intake into the body, it is below 50 mmol.

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

The severity of clinical manifestations of hypokalemia and potassium deficiency depends on the speed 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 of the central and peripheral nervous system, the tone of striated skeletal muscles, smooth muscles of the gastrointestinal tract and bladder muscles. When examining patients, hypotension or atony of the stomach, paralytic intestinal obstruction, gastric congestion, nausea, vomiting, flatulence, bloating, hypotension or atony of the bladder are revealed. From the cardiovascular system, 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 widening, PQ shortening. Typically, weakening of tendon reflexes up to their complete disappearance and the development of flaccid paralysis, decreased 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 that potassium enters the body in the amount of physiological need, to compensate for the existing deficiency of intracellular and extracellular potassium.

K+ deficiency (mmol) = (4.5 - K+ sq.), mmol/l * body weight, kg * 0.4 (3.38).

Eliminating potassium deficiency requires eliminating any stress factors (strong emotions, pain, hypoxia of any origin).

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

To ensure the required rate of restoration of potassium levels in glycogen or protein, every 2.2 - 3.0 g of potassium chloride or disubstituted potassium phosphate should be administered along 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.

To correct hypocaligistia, it is best to use dibasic potassium phosphate, since glycogen synthesis is impossible in the absence of phosphates.

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

When eliminating K+ deficiency intravenously, its calculated dose in the form of a KCl solution is infused 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, so the concentration of infused K+ solutions should not exceed 0.5 mmol/l, and the infusion rate should not exceed 30-40 mmol/h. 1 g of KCl, from which a solution for intravenous administration is prepared, contains 13.6 mmol K+.

If the K+ deficiency is large, it is replenished within 2-3 days, given that the maximum daily dose of intravenously administered K+ is 3 mmol/kg.

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

Where: 0.33 – maximum permissible safe infusion rate, mmol/min;

20 is the number of drops in 1 ml of crystalloid solution.

The maximum rate of potassium administration 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 K+ content in plasma, can be determined by the ratio of its intake and release 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 deficiency is eliminated.

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

Hyperkalemia may be a consequence of acute and chronic renal failure in the stage of oliguria and anuria; massive release of potassium from tissues due to insufficient diuresis (deep or extensive burns, injuries); long-term positional or tourniquet compression of the arteries, late restoration of blood flow in the arteries during thrombosis; massive hemolysis; decompensated metabolic acidosis; rapid administration of large doses of relaxants of a depolarizing type of action, diencephalic syndrome in traumatic brain injury and stroke with convulsions and fever; excess intake of potassium into the body against the background of insufficient diuresis and metabolic acidosis; the use of excess potassium in 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 clearly defined, characteristic clinical symptoms. The most common complaints are weakness, confusion, various types of parasthesia, constant fatigue with a feeling of heaviness in the limbs, muscle twitching. In contrast to hypokalemia, hyperreflexia are recorded. Possible intestinal spasms, nausea, vomiting, diarrhea. From the cardiovascular system, bradycardia or tachycardia, decreased blood pressure, and extrasystoles may be detected. The most typical changes are in the ECG. In contrast to hypokalemia, with hyperkalemia there is a certain parallelism between ECG changes and the level of hyperkalemia. The appearance of a tall, narrow, pointed positive T wave, the onset of the ST interval below the isoelectric line, and shortening of the QT interval (ventricular electrical systole) are the first and most characteristic ECG changes in hyperkalemia. These signs are especially pronounced with hyperkalemia close to a critical level (6.5-7 mmol/l). With a further increase in hyperkalemia above a critical level, the QRS complex expands (especially the S wave), then the P wave disappears, an independent ventricular rhythm occurs, ventricular fibrillation occurs, 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 a threatening condition.

If hyperkalemia occurs, it is necessary to intensify the removal of potassium from the body in natural ways (stimulating diuresis, overcoming oligo- and anuria), and if this way is not possible, carry out artificial removal of potassium from the body (hemodialysis, etc.).

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

If high hyperkalemia (more than 6 mmol/l) is detected, the first treatment measure is the prescription of calcium supplements. Calcium is a functional potassium antagonist and blocks the extremely dangerous effects of high hyperkalemia on the myocardium, 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 reduces hyperkalemia by increasing the movement of potassium from the extracellular space into the cells: intravenous administration of a 5% sodium bicarbonate solution in a dose of 100-200 ml; administration of concentrated (10-20-30-40%) glucose solutions in a dose of 200-300 ml with simple insulin (1 unit per 4 g of administered glucose).

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

In case of hyperkalemia uncorrectable by therapeutic measures (6.0-6.5 mmol/l and higher in acute renal failure and 7.0 mmol/l and higher in chronic renal failure) with simultaneously detected ECG changes, hemodialysis is indicated. Timely hemodialysis is the only effective method of directly removing 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 are associated with the usual causes of water-electrolyte disturbances (WED) - inadequate fluid intake by a person, excessive or insufficient infusion therapy, the use of diuretics, the composition of the drugs used for enteral and parenteral nutrition, etc.

Doctors should try to eliminate the problems that have arisen by adjusting the patient’s infusion therapy, medications, and diet. If the actions taken do not bring the expected result, and disturbances in water and electrolyte balance are still observed, doctors can assume that they are based on central neurogenic disorders.

Water and 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 will focus on the three most significant disorders for clinical practice and outcomes: central diabetes insipidus (CDI), syndrome of increased secretion of antidiuretic hormone (SIADH), and cerebral salt wasting 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 occurrence of this syndrome is associated with poor overall outcome and brain death. Its occurrence suggests that deep structures of the brain are involved in the pathological process - the hypothalamus, pituitary stalks or neurohypophysis.

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

Treatment of diabetes insipidus

It is necessary to control hourly diuresis and replace fluid losses with 0.45% sodium chloride solution, 5% glucose, and enteral water administration. Enter ( Minirin ):

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

In the absence of desmopressin or its insufficient effect, doctors prescribe hypothiazide. It paradoxically reduces diuresis (the mechanism of action is unclear). Take 25-50 mg 3 times a day. Carbamazepine reduces diuresis and reduces the patient's feeling of thirst. 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.

Antidiuretic hormone oversecretion syndrome

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

In this condition, the kidneys are able to excrete significantly less water. Urine osmolarity usually exceeds plasma osmolarity. The severity of these manifestations may vary. In the absence of restrictions on fluid intake, in some cases, hyponatremia and overhydration can progress rapidly. The result may be increased cerebral edema and worsening neurological symptoms. With severe hyponatremia (110-120 mmol/l), the patient may develop convulsive syndrome.

Treatment

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

It is worth noting 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 increase the sodium concentration in the blood;
• Loop diuretics are prescribed for minor fluid retention. sometimes prescribed orally 80-120 mg or intravenously at a dose of 40-60 mg;
• In case of severe hyponatremia, deterioration of neurological status, convulsions, intravenous administration (in 20-30 minutes) of 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, gradual correction of hyponatremia is carried out over 2-3 days by infusion of 3% sodium chloride at a rate of 0.25-0.5 ml/kg/hour.

It is necessary to frequently monitor the level of sodium in the blood to avoid neurological complications. Rapid correction of hyponatremia can lead to the development of focal demyelination of the brain. When carrying out treatment, you need to ensure that the daily increase in sodium level 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 start of sodium chloride infusion serves to prevent this complication. The effect of administering a hypertonic sodium chloride solution does not last too long; the infusion must be repeated periodically. The introduction of less concentrated solutions of sodium chloride does not reliably eliminate hyponatremia and increases fluid retention.

Cerebral salt wasting 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 diuresis and signs of BCC deficiency. Also typical are high urine specific gravity, increased urinary sodium levels greater than 50–80 mmol/L, hyponatremia, and elevated or normal serum uric acid levels. This syndrome often occurs in patients with subarachnoid hemorrhage. Develops during the first week after cerebral damage. Lasts up to 4 weeks (average 2 weeks). The severity can range from minimal to very strong.

Treatment

Treatment consists of adequate replacement of water and sodium losses. There is no restriction on fluid administration. To make up for losses, in most cases a 0.9% solution is used. Sometimes very large volumes of infusion are required, reaching 30 or more liters per day. If hyponatremia is not corrected by the administration of 0.9% sodium chloride, indicating a severe sodium deficiency, doctors use an infusion of 1.5% sodium chloride solution.

The administration of mineralocorticoids allows the patient to be given fludrocortisone(Cortineff), 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, and polyuria can lead to hypokalemia, which also requires timely correction.

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

Sodium. Let me remind you that this 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 manifests itself as increased fatigue. This is caused by heavy infusions of glucose, large water retention in certain kidney diseases (nephritis, tubular nephrosis) or excessively increased secretion of vasopressin in acute and chronic brain diseases.

It must be remembered that hyponatremia is most often relative and is associated with overhydration of the extracellular space, less often with true sodium deficiency. Therefore, it is necessary to carefully assess the patient’s condition, based on anamnestic, clinical and biochemical data, determine the nature of sodium metabolism disorders and decide on the advisability of its correction.

total Na deficiency (mmol) = (142 mmol/l – indicator of plasma Na concentration, mmol/l) patient's weight 0,2.

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

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

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

The causes of hyperkalemia may be: 1) decreased excretion of potassium in the urine in renal failure; 2) intravenous administration of potassium-containing solutions (with weakened kidney function); 3) increased protein catabolism; 4) cell necrosis (in case of 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.

A potassium concentration above 6.5 mmol/l of plasma is dangerous, 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 for hyperkalemia: high pointed T wave, shortening of the QT, widening of the QRS complex, sinus bradycardia, atrioventricular block, and extrasystoles are not uncommon.

Hypokalemia is accompanied by adynamia, asthenia, muscle hypotonia, apathy, dry skin, and decreased skin sensitivity. Flatulence and vomiting are observed, simulating obstruction. An expansion of the borders of the heart, deafness of the first tone, tachycardia, a decrease in arterial pressure and an increase in venous pressure are detected.

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

The causes of hypokalemia can be:

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

2. Increased release of potassium from the intestinal mucosa in cases of colon adenoma and pancreatic tumor.

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

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

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

6. Insufficient potassium intake.

Treatment. Apply a 0.5–0.7% solution of potassium chloride with a 5% or 10% glucose solution at a rate of no more than 20 mmol/hour (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 administer insulin at the rate of 1 unit 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 varies, ranging from 60 to 100 mmol. An additional dose of potassium is administered at the rate of:

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

To correct potassium deficiency, use a 3% solution of potassium chloride, 10 ml of which contains 4 mmol of pure potassium. Thus, if 40 ml of 3% potassium chloride solution 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/hour.

For hyperkalemia, a 10% solution of glucose with insulin is administered intravenously (1 unit per 3–4 g of glucose) 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, diuretics (furosemide intravenously) are used.

Calcium. Calcium is almost not involved 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 regulating effect on the endocrine secretion of the parathyroid gland and the C-cells of the thyroid gland. 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 shortening of the QT distance on the ECG. Outcomes are death from renal failure due to nephrocalcinosis or cardiac arrest.

Hypocalcemia manifested by increased neuromuscular excitability, tetanic convulsions, blood hypocoagulation, weakening of cardiac activity, and arterial hypotension. The ECG shows prolongation of the QT interval. With prolonged hypocalcemia, rickets occurs in children, various trophic disorders, including cataracts, and impaired calcification of dental dentin.

Elimination of hypercalcemia can be achieved primarily by treating the disease that caused calcium metabolism disorders. For example, in case of hyperparathyroidism, surgical removal of a hormonally active tumor or hyperplastic tissue of the parathyroid glands is performed.

In children with hypercalcemia, when signs of calcium metabolism disorders are detected, the intake of vitamin D is limited. In case of severe hypercalcemia, intravenous administration of the disodium salt of ethyldiaminetetraacetic acid (Na2EDTA), which is capable of forming complex compounds with calcium ions, is used.

Elimination of hypocalcemia. Due to the fact that hypocalcemia is most often 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 relieve attacks of tetany in patients with severe hypocalcemia, intravenous solutions of calcium chloride, gluconate or calcium lactate are used, and vitamin D preparations are also used.