Violation of the ionic balance in the body. Water and electrolyte balance - health mechanics

What causes an imbalance in the water-salt balance in the body, and what consequences can this imbalance cause?

Two phenomena - one problem

The water-electrolyte (water-salt) balance can be disturbed in two directions:

1. Hyperhydration - excessive accumulation of fluid in the body, slowing down the excretion of the latter. It accumulates in the intercellular space, its level inside cells increases, the latter swell. When nerve cells are involved in the process, nerve centers are excited and convulsions occur;
2. Dehydration is the opposite of the previous one. The blood begins to thicken, the risk of blood clots increases, and blood flow in tissues and organs is disrupted. With a deficit of more than 20%, death occurs.

Violation of the water-salt balance is manifested by weight loss, dry skin and cornea. With a strong moisture deficit, the subcutaneous fatty tissue resembles dough in consistency, the eyes sink, the volume of circulating blood decreases.

Dehydration is accompanied by an exacerbation of facial features, cyanosis of the lips and nails, low blood pressure, weak and frequent pulse, kidney hypofunction, an increase in the concentration of nitrogenous bases due to impaired protein metabolism. Also, a person's upper and lower extremities are freezing.

There is such a diagnosis as isotonic dehydration - the loss of water and sodium in equal amounts. This happens in acute poisoning, when electrolytes and the volume of the liquid medium are lost during diarrhea and vomiting.

Why there is a lack or excess of water in the body

The main causes of pathology are external fluid loss and water redistribution in the body. The level of calcium in the blood decreases:

• with pathologies thyroid gland or after removing it;
• when radioactive iodine preparations are used (for treatment);
• with pseudohypoparathyroidism.

Sodium decreases with long-term ongoing diseases, accompanied by a decrease in urine output; in postoperative period; with self-medication and uncontrolled intake of diuretics.

1. Potassium decreases as a result of its intracellular movement;
2. With alkalosis;
3. Aldosteronism;
4. Corticosteroid therapy;
5. Alcoholism;
6. Liver pathologies;
7. After operations on the small intestine;
8. With insulin injections;
9. Hypofunction of the thyroid.

The reason for its increase is an increase in catitones and a delay in its compounds, damage to cells and the release of potassium from them.

Symptoms and signs of water-salt imbalance

The first warning signs depend on what is happening in the body - overhydration or dehydration. This includes:

• swelling;
• vomiting;
• diarrhea;
• intense thirst.

1. The acid-base balance often changes, decreases arterial pressure, there is an arrhythmic heartbeat... These symptoms cannot be ignored, as progressive pathology leads to cardiac arrest and death.
2. Calcium deficiency leads to smooth muscle cramps... Spasm of large vessels and larynx is especially dangerous. With an excess of this element, stomach pain, severe thirst, vomiting, frequent urination, poor blood circulation occur.
3. Potassium deficiency is accompanied by alkalosis, atony, chronic renal failure, intestinal obstruction, brain pathologies, ventricular fibrillation of the heart and other changes in its rhythm.
4. With an increase in its concentration in the body, ascending paralysis occurs, nausea, vomiting. This condition is very dangerous, since fibrillation of the heart ventricles develops very quickly, that is, the probability of atrial arrest is high.
5. Excess magnesium occurs with antacid abuse and kidney dysfunction. This condition is accompanied by nausea, up to vomiting, fever, slow heart rate.

The role of the kidneys and urinary system in the regulation of water-salt balance

The function of this paired organ is aimed at maintaining the constancy of various processes. They answer:

• for ion exchange that occurs on both sides of the tubular membrane;
• elimination of excess cations and anions from the body through adequate reabsorption and excretion of potassium, sodium and water.

The role of the kidneys is very important, since their functions allow maintaining a stable volume of intercellular fluid and the optimal level of substances dissolved in it.

A healthy person needs about 2.5 liters of liquid per day. He receives about 2 liters through food and drink, 1/2 liter is formed in the body itself as a result of metabolic processes. One and a half liters are excreted by the kidneys, 100 ml - by the intestines, 900 ml - by the skin and lungs.

The amount of fluid excreted by the kidneys depends on the condition and needs of the body itself. With maximum diuresis, this organ of the urinary system can remove up to 15 liters of fluid, and with antidiuresis - up to 250 ml.

Sharp fluctuations in these indicators depend on the intensity and nature of tubular reabsorption.

Diagnostics of violations of water-salt balance

At the initial examination, a presumptive conclusion is made, further therapy depends on the patient's response to the introduction of anti-shock agents and electrolytes.

The doctor makes a diagnosis based on the patient's complaints, history, research results:

1. Anamnesis. If the patient is conscious, he is interviewed, information on violations of the water-electrolyte balance (diarrhea, ascites, peptic ulcernarrowing of the gatekeeper, severe intestinal infections, some types of ulcerative colitis, dehydration of various etiologies, short-term low-salt diets on the menu);
2. Setting the degree of pathology, taking measures to eliminate and prevent complications;
3. General, bacteriological and serological blood teststo identify the cause of the rejection. Additional laboratory and instrumental studies may be prescribed.

Modern diagnostic methods make it possible to establish the cause of the pathology, its degree, as well as to promptly begin to relieve symptoms and restore human health.

How can you restore the water-salt balance in the body

Therapy involves the following activities:

• Conditions that can become life threatening are stopped;
• Bleeding and acute blood loss are eliminated;
• Hypovolemia is eliminated;
• Hyper- or hyperkalemia is eliminated;
• It is necessary to apply measures to regulate normal water-electrolyte metabolism. Most often, a glucose solution, polyionic solutions (Hartmann, lactasol, Ringer-Locke), erythrocyte mass, polyglucin, soda are prescribed;
• You also need to prevent the development of possible complications - epilepsy, heart failure, in particular during therapy with sodium preparations;
• During recovery with intravenous administration saline solutions it is necessary to control hemodynamics, renal function, the level of CBS, VCO.

Preparations that are used to restore water-salt balance

1. Potassium and magnesium asparaginate - required for myocardial infarction, heart failure, artimia, hypokalemia and hypomagnesemia. The drug is well absorbed when taken orally, excreted by the kidneys, transfers magnesium and potassium ions, and promotes their entry into the intercellular space.
2. Sodium bicarbonate - often used for peptic ulcer disease, gastritis with high acidity, acidosis (intoxication, infection, diabetes mellitus), as well as for kidney stones, inflammation of the respiratory system and oral cavity.
3. Sodium chloride - is used in case of a lack of intercellular fluid or its large loss, for example, with toxic dyspepsia, cholera, diarrhea, indomitable vomiting, severe burns. The drug has a rehydrating and detoxifying effect, allows you to restore water-electrolyte metabolism in various pathologies.
4. Sodium citrate - allows you to restore normal blood counts. This product increases sodium concentration.
5. Hydroxyethyl starch (ReoHES) - the product is used when surgical interventions, acute blood loss, burns, infections as prevention of shock and hypovolemia. It is also used for deviating microcirculation, as it promotes the diffusion of oxygen throughout the body, restores the walls of the capillaries.

Maintaining the natural water-salt balance

This parameter can be violated not only with serious pathologies, but also with profuse sweating, overheating, uncontrolled use of diuretics, long-term salt-free diet.

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 - lack of moisture or dehydration, the blood begins to thicken, blood clots form due to viscosity and blood flow to tissues and organs is disturbed. With its lack in the body over 20% of the body weight, death occurs.

Manifested by a decrease in body weight, dryness 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. This condition is common when 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 imbalance in 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, since they lead to cardiac arrest and death if medical assistance is not provided on time.

With a lack of calcium in the blood, convulsions appear smooth muscles, especially dangerous spasm of the larynx, large vessels. With an increase in Ca content - 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. There is nausea, vomiting, the temperature rises, the heart rate slows down.

Symptoms of imbalance in the 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:

• Anamnesis. 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, the following drugs are prescribed to normalize water-salt metabolism: 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 when sodium preparations are administered).
• If necessary, in parallel with the intravenous administration of medicines, carry out diet therapy.
• When intravenous administration saline solutions, it is necessary to control the level of VCO, CBS, control hemodynamics, monitor renal function.

An important point is that before the start of intravenous administration of salt 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) \u003d 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) \u003d (Htst - HtN): (100 - HtN) x 0.2 x Weight (kg),

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

HtN \u003d 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 is to maintain a normal water-salt balance. Salt metabolism can be disrupted not only in severe pathologies (3-4 degree burns, gastric ulcer, ulcerative colitis, acute blood loss, food intoxication, infectious diseases 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 preventive 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 necessary daily rate liquid under conditions close to dehydration, eat properly and in a balanced manner.

Prevention of imbalance in water and electrolyte balance also consists in the correct diet - use 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.

IN SURGICAL PATIENTSAND PRINCIPLES OF INFUSION THERAPY

Acute disorders of water and electrolyte balance are one of the most frequent complications of surgical pathology - peritonitis, intestinal obstruction, pancreatitis, trauma, shock, diseases accompanied by fever, vomiting and diarrhea.

9.1. The main causes of violations of water and electrolyte balance

The main reasons for violations include:

external losses of fluid and electrolytes and their pathological redistribution between the main fluid media due to pathological activation of natural processes in the body - with polyuria, diarrhea, excessive sweating, with profuse vomiting, through various drains and fistulas or from the surface of wounds and burns;

internal movement of fluids during edema of injured and infected tissues (fractures, crush syndrome); accumulation of fluid in the pleural (pleurisy) and abdominal (peritonitis) cavities;

changes in the osmolarity of fluids and the movement of excess water into or out of the cell.

Movement and accumulation of fluid in the gastrointestinal tract,reaching several liters (with intestinal obstruction, intestinal infarction, as well as with severe postoperative paresis), the severity of the pathological process corresponds to external lossesliquids, as both cases lose large volumes of liquid with high electrolyte and protein content. No less significant external losses of fluid identical to plasma from the surface of wounds and burns (into the pelvic cavity), as well as during extensive gynecological, proctological and thoracic (into the pleural cavity) operations.

Internal and external fluid loss determine the clinical picture of fluid deficiency and violations of water-electrolyte balance: hemoconcentration, plasma deficiency, protein loss and general dehydration. In all cases, these disorders require a targeted correction of the water-electrolyte balance. Being unrecognized and not eliminated, they worsen the results of treatment of patients.

The entire body water supply is located in two spaces - intracellular (30-40% of body weight) and extracellular (20-27% of body weight).

Extracellular volumedistributed between interstitial water (water of ligaments, cartilage, bones, connective tissue, lymph, plasma) and water that does not take an active part in metabolic processes (cerebrospinal, intraarticular fluid, gastrointestinal tract contents).

Intracellular sectorcontains water in three types (constitutional, protoplasm and colloidal micelles) and electrolytes dissolved in it. Cellular water is unevenly distributed in various tissues, and the more hydrophilic they are, the more vulnerable they are to disorders of water metabolism. Part of the cellular water is formed as a result of metabolic processes.

The daily volume of metabolic water during the "combustion" of 100 g of proteins, fats and carbohydrates is 200-300 ml.

The volume of extracellular fluid can increase with trauma, starvation, sepsis, severe infectious diseases, i.e., in those conditions that are accompanied by significant loss muscle mass... An increase in the volume of extracellular fluid occurs with edema (cardiac, protein-free, inflammatory, renal, etc.).

The volume of extracellular fluid decreases with all forms of dehydration, especially with the loss of salts. Significant disorders are observed in critical conditions in surgical patients - peritonitis, pancreatitis, hemorrhagic shock, intestinal obstruction, blood loss, severe trauma. The ultimate goal of the regulation of water and electrolyte balance in such patients is to maintain and normalize the vascular and interstitial volumes, their electrolyte and protein composition.

Maintenance and normalization of the volume and composition of extracellular fluid are the basis for the regulation of arterial and central venous pressure, cardiac output, organ blood flow, microcirculation and biochemical homeostasis.

Maintaining the body's water balance normally occurs through an adequate supply of water in accordance with its losses; the daily “turnover” is about 6% of all body water. An adult consumes about 2500 ml of water per day, including 300 ml of water formed as a result of metabolic processes. Water loss is about 2500 ml / day, of which 1500 ml is excreted in the urine, 800 ml evaporates (400 ml through the respiratory tract and 400 ml through the skin), 100 ml is excreted in sweat and 100 ml in feces. When carrying out corrective infusion-transfusion therapy and parenteral nutrition, the mechanisms regulating the intake and consumption of fluid, thirst are shunted. Therefore, to restore and maintain a normal state of hydration, careful monitoring of clinical and laboratory data, body weight and daily urine output is required. It should be noted that physiological fluctuations in water loss can be quite significant. With an increase in body temperature, the amount of endogenous water increases and the loss of water through the skin during respiration increases. Respiratory disorders, especially hyperventilation with low air humidity, increase the body's water requirements by 500-1000 ml. Fluid loss from extensive wound surfaces or during long-term surgical interventions on the abdominal and chest cavity organs for more than 3 hours increases the need for water to 2500 ml / day.

If the inflow of water prevails over its release, the water balance is considered positive;against the background of functional disorders on the part of the excretory organs, it is accompanied by the development of edema.

With the predominance of water release over input, the balance is considered negative- in this case, a feeling of thirst serves as a signal of dehydration.

Failure to correct dehydration can lead to collapse or dehydration shock.

The main organ regulating water and electrolyte balance is the kidneys. The volume of urine excreted is determined by the amount of substances that must be removed from the body and the ability of the kidneys to concentrate urine.

During the day, from 300 to 1500 mmol of metabolic end products are excreted in the urine. With a lack of water and electrolytes, oliguria and anuria are

viewed as a physiological response associated with the stimulation of ADH and aldosterone. Correction of water and electrolyte losses leads to the restoration of diuresis.

Normally, the regulation of the water balance is carried out by activating or inhibiting the osmoreceptors of the hypothalamus, which react to changes in the osmolarity of the plasma, the feeling of thirst arises or is inhibited, and the secretion of antidiuretic hormone (ADH) of the pituitary gland changes accordingly. ADH increases the reabsorption of water in the distal tubules and the collecting ducts of the kidneys and decreases urinary flow. On the contrary, with a decrease in the secretion of ADH, urination increases, and the osmolarity of urine decreases. The formation of ADH naturally increases with a decrease in fluid volumes in the interstitial and intravascular sectors. With an increase in BCC, the secretion of ADH decreases.

In pathological conditions, factors such as hypovolemia, pain, traumatic tissue damage, vomiting, and drugs that affect the central mechanisms of nervous regulation of water and electrolyte balance are of additional importance.

There is a close relationship between the amount of fluid in various sectors of the body, the state of peripheral circulation, capillary permeability and the ratio of colloidal osmotic and hydrostatic pressures.

Normally, the exchange of fluid between the vascular bed and the interstitial space is strictly balanced. In pathological processes associated primarily with the loss of the protein circulating in the plasma (acute blood loss, liver failure), the plasma COP decreases, as a result of which the fluid from the microcirculation system in excess passes into the interstitium. The blood thickens, its rheological properties are violated.

9.2. Electrolyte exchange

The state of water exchange in health and disease is closely interrelated with the exchange of electrolytes - Na +, K +, Ca 2+, Mg 2+, SG, HC0 3, H 2 P0 4 ~, SOf, as well as proteins and organic acids.

The concentration of electrolytes in the fluid spaces of the body is not the same; plasma and interstitial fluid differ significantly only in protein content.

The content of electrolytes in the extracellular and intracellular fluid spaces is not the same: the extracellular contains mainly Na +, SG, HCO ^; in the intracellular - K +, Mg + and H 2 PO 4; the concentration of S0 4 2 and proteins is also high. Differences in the concentration of some electrolytes form the resting bioelectric potential, which endows nerve, muscle and sector cells with excitability.

Conservation of electrochemical potential cellular and extracellularspaceensured by the operation of the Na + -, K + -ATPase pump, thanks to which Na + is constantly "pumped out" from the cell, and K + - is "driven" into it against the gradients of their concentration.

If this pump malfunctions due to oxygen deficiency or as a result of metabolic disorders, the cell space becomes available for sodium and chlorine. The concomitant increase in osmotic pressure in the cell enhances the movement of water in it, causes swelling,

and in the subsequent violation of the integrity of the membrane, up to lysis. Thus, sodium is the dominant cation in the intercellular space, and potassium in the cell.

9.2.1. Sodium exchange

Sodium - the main extracellular cation; the most important cation of the interstitial space is the main osmotically active substance of the plasma; participates in the generation of action potential, affects the volume of extracellular and intracellular spaces.

With a decrease in the concentration of Na +, the osmotic pressure decreases with a simultaneous decrease in the volume of the interstitial space. An increase in sodium concentration causes the opposite process. The sodium deficiency cannot be filled with any other cation. The daily sodium requirement for an adult is 5-10 g.

Sodium is excreted from the body mainly by the kidneys; a small part - with sweat. Its blood level rises with prolonged treatment with corticosteroids, prolonged mechanical ventilation in the hyperventilation mode, diabetes insipidus, with hyperaldosteronism; decreases due to prolonged use of diuretics, against the background of prolonged heparin therapy, in the presence of chronic heart failure, hyperglycemia, liver cirrhosis. The sodium content in urine is normal 60 mmol / l. Surgical aggression associated with the activation of antidiuretic mechanisms leads to sodium retention at the kidney level, therefore, its content in urine may decrease.

Hypernatremia(plasma sodium more than 147 mmol / l) occurs with an increased sodium content in the interstitial space, as a result of dehydration with water depletion, salt overload of the body, diabetes insipidus. Hypernatremia is accompanied by the redistribution of fluid from the intracellular to the extracellular sector, which causes cell dehydration. In clinical practice, this condition occurs due to increased sweating, intravenous infusion of hypertonic sodium chloride solution, and also in connection with the development of acute renal failure.

Hyponatremia(plasma sodium less than 136 mmol / l) develops with excessive secretion of ADH in response to a pain factor, with pathological fluid losses through the gastrointestinal tract, excessive intravenous administration of salt-free solutions or glucose solutions, excessive water intake against a background of limited food intake; accompanied by cell hyperhydration with a simultaneous decrease in the BCC.

Sodium deficiency is determined by the formula:

Deficiency (mmol) \u003d (Na HOpMa - actual No.) body weight (kg) 0.2.

9.2.2. Potassium exchange

Potassium -the main intracellular cation. The daily requirement for potassium is 2.3-3.1 g. Potassium (together with sodium) takes an active part in all metabolic processes of the body. Potassium, like sodium, plays a leading role in the formation of membrane potentials; it affects pH and glucose utilization, and is essential for protein synthesis.

In the postoperative period, in critical conditions, potassium loss may exceed its intake; they are also characteristic for prolonged starvation, accompanied by the loss of the body's cell mass - the main "depot" of potassium. The metabolism of hepatic glycogen plays a role in increasing potassium loss. In seriously ill patients (without appropriate compensation), up to 300 mmol of potassium is transferred from the cellular space to the extracellular space in 1 week. In the early post-traumatic period, potassium leaves the cell along with metabolic nitrogen, the excess of which is formed as a result of cellular protein catabolism (on average, 1 g of nitrogen "carries away" 5-6 meq of potassium).

I monk.themia(plasma potassium less than 3.8 mmol / l) can develop with an excess of sodium, against the background of metabolic alkalosis, with hypoxia, severe protein catabolism, diarrhea, prolonged vomiting, etc. With intracellular potassium deficiency, Na + and H + are intensively entering the cell, which causes intracellular acidosis and hyperhydration against the background of extracellular metabolic alkalosis. Clinically, this condition is manifested by arrhythmia, arterial hypotension, decreased skeletal muscle tone, intestinal paresis, and mental disorders. Characteristic changes appear on the ECG: tachycardia, narrowing of the complex QRS, flattening and inversion of the prong T,increase in the amplitude of the wave U. Treatment of hypokalemia begins by eliminating the etiological factor and compensating for the potassium deficiency, using the formula:

Potassium deficiency (mmol / l) \u003d K + patient plasma, mmol / l 0.2 body weight, kg.

The rapid introduction of a large amount of potassium preparations can cause complications from the heart, up to cardiac arrest, so the total daily dose should not exceed 3 mmol / kg / day, and the infusion rate should not exceed 10 mmol / h.

The potassium preparations used should be diluted (up to 40 mmol per 1 liter of the injected solution); the optimal is their introduction in the form of a polarizing mixture (glucose + potassium + insulin). Treatment with potassium preparations is performed under daily laboratory supervision.

Hyperkalemia(plasma potassium more than 5.2 mmol / l) most often occurs when potassium excretion from the body is impaired (acute renal failure) or with its massive exit from damaged cells due to extensive trauma, hemolysis of erythrocytes, burns, positional compression syndrome, etc. In addition, hyperkalemia is characteristic of hyperthermia, convulsive syndrome and accompanies the use of a number medicines - heparin, aminocaproic acid, etc.

Diagnosticshyperkalemia is based on the presence of etiological factors (trauma, acute renal failure), the appearance of characteristic changes in cardiac activity: sinus bradycardia (up to cardiac arrest) in combination with ventricular extrasystole, pronounced slowing of intraventricular and atrioventricular conduction and characteristic laboratory data (plasma potassium more than 5, 5 mmol / L). A high pointed tooth is recorded on the ECG T,expansion of the complex QRS, decrease in wave amplitude R.

Treatmenthyperkalemia begins with the elimination of the etiological factor and the correction of acidosis. Prescribe calcium supplements; to transfer excess plasma potassium into the cell, a glucose solution (10-15%) with insulin (1 U for every 3-4 g of glucose) is injected intravenously. If these methods do not bring the desired effect, hemodialysis is indicated.

9.2.3. Calcium exchange

Calcium is about 2 % body weight, of which 99% are in a bound state in the bones and do not participate in electrolyte metabolism under normal conditions. The ionized form of calcium is actively involved in the neuromuscular transmission of excitation, blood coagulation processes, the work of the heart muscle, the formation of the electric potential of cell membranes and the production of a number of enzymes. The daily requirement is 700-800 mg. Calcium enters the body with food, is excreted through the digestive tract and in the urine. Calcium metabolism is closely related to phosphorus metabolism, plasma protein levels and blood pH.

Hypocalcemia(plasma calcium less than 2.1 mmol / l) develops with hypoalbuminemia, pancreatitis, transfusion of large amounts of citrated blood, long-standing biliary fistulas, vitamin D deficiency, malabsorption in the small intestine, after highly traumatic operations. Clinically manifested by increased neuromuscular excitability, paresthesias, paroxysmal tachycardia, tetany. Correction of hypocalcemia is carried out after laboratory determination of its level in blood plasma by intravenous administration of drugs containing ionized calcium (gluconate, lactate, chloride or calcium carbonate). The effectiveness of corrective therapy for hypocalcemia depends on the normalization of albumin levels.

Hypercalcemia(plasma calcium more than 2.6 mmol / l) occurs in all processes accompanied by increased destruction of bones (tumors, osteomyelitis), diseases of the parathyroid glands (adenoma or parathyroiditis), excessive administration of calcium preparations after citrated blood transfusion, etc. Clinical condition manifested by increased fatigue, lethargy, muscle weakness. With an increase in hypercalcemia, symptoms of gastrointestinal atony join: nausea, vomiting, constipation, flatulence. On the ECG, a characteristic shortening of the interval appears (2-7; rhythm and conduction disturbances, sinus bradycardia, slowing of antrioventricular conduction are possible; the G wave can become negative, biphasic, reduced, rounded.

Treatmentconsists in influencing the pathogenetic factor. With severe hypercalcemia (more than 3.75 mmol / l), targeted correction is required - 2 g of disodium salt of ethylenediamine tetraacetic acid (EDTA), diluted in 500 ml of 5% glucose solution, is administered intravenously slowly, drip 2-4 times a day, under control of calcium content in blood plasma.

9.2.4. Magnesium exchange

Magnesium is an intracellular cation; its concentration in plasma is 2.15 times less than inside erythrocytes. The trace element reduces neuromuscular excitability and myocardial contractility, causing depression of the central nervous system. Magnesium plays a huge role in the assimilation of oxygen by cells, energy production, etc. It enters the body with food and is excreted through the digestive tract and with urine.

Hypomagnesemia(plasma magnesium less than 0.8 mmol / l) is observed in liver cirrhosis, chronic alcoholism, acute pancreatitis, polyuric stage of acute renal failure, intestinal fistulas, unbalanced infusion therapy... Clinically, hypomagnesemia is manifested by increased nervous

muscle excitability, hyperreflexia, convulsive contractions of various muscle groups; the appearance of spastic pain in the digestive tract, vomiting, diarrhea is possible. Treatmentconsists in a targeted effect on the etiological factor and the appointment under laboratory control of magnesium salts.

Hypermagnesemia(plasma magnesium more than 1.2 mmol / l) develops in ketoacidosis, increased catabolism, acute renal failure. Clinically manifested by drowsiness and lethargy, hypotension and bradycardia, decreased breathing with the appearance of signs of hypoventilation. Treatment- targeted action on the etiological factor and the appointment of magnesium antagonist - calcium salts.

9.2.5. Chlorine exchange

Chlorine -the main anion of the extracellular space; is in equivalent relationships with sodium. It enters the body in the form of sodium chloride, which dissociates Na + and C1 in the stomach. "Coming in combination with hydrogen, chlorine forms hydrochloric acid.

Hypochloremia(plasma chlorine less than 95 mmol / l) develops with prolonged vomiting, peritonitis, pyloric stenosis, high intestinal obstruction, increased sweating. The development of hypochloremia is accompanied by an increase in the hydrocarbonate buffer and the appearance of alkalosis. Clinically manifested by dehydration, impaired respiration and cardiac activity. The occurrence of a convulsive or coma with a fatal outcome is possible. Treatmentconsists in a targeted effect on the pathogenetic factor and conducting infusion therapy with chlorides (primarily sodium chloride preparations) under laboratory control.

Hyperchloremia(plasma chlorine more than PO mmol / l) develops with general dehydration, impaired excretion of fluid from the interstitial space (for example, ARF), increased fluid transfer from the vascular bed to the interstitium (with hypoproteinemia), the introduction of large volumes of fluids containing an excessive amount of chlorine. The development of hyper-chloremia is accompanied by a decrease in the buffer capacity of the blood and the appearance of metabolic acidosis. Clinically, this is manifested by the development of edema. The basic principle treatment- impact on the pathogenetic factor in combination with syndromic therapy.

9.3. The main types of violations of water and electrolyte metabolism

▲ Isotonic dehydration(plasma sodium is within the normal range: 135-145 mmol / l) occurs due to the loss of fluid in the interstitial space. Since the electrolyte composition of the interstitial fluid is close to blood plasma, there is a uniform loss of fluid and sodium. Most often, isotonic dehydration develops with prolonged vomiting and diarrhea, acute and chronic diseases of the gastrointestinal tract, intestinal obstruction, peritonitis, pancreatitis, extensive burns, polyuria, uncontrolled administration of diuretics, polytrauma. Dehydration is accompanied by a loss of electrolytes without a significant change in plasma osmolarity; therefore, there is no significant redistribution of water between the sectors, but hypovolemia is formed. Clinically

there are violations of the central hemodynamics. Skin turgor is reduced, tongue dry, oliguria up to anuria. Treatmentpathogenetic; replacement therapy with isotonic sodium chloride solution (35-70 ml / kg / day). Infusion therapy should be carried out under the control of CVP and hourly urine output. If the correction of hypotonic dehydration is carried out against the background of metabolic acidosis, sodium is administered in the form of bicarbonate; with metabolic alkalosis - in the form of chloride.

▲ Dehydration hypotonic(plasma sodium less than 130 mmol / l) develops when sodium loss exceeds water loss. It occurs with massive losses of fluids containing a large amount of electrolytes - repeated vomiting, profuse diarrhea, profuse sweating, division, polyuria. A decrease in the sodium content in plasma is accompanied by a decrease in its osmolarity, as a result of which water from the plasma begins to redistribute into cells, causing their edema (intracellular hyperhydration) and creating a water deficit in the interstitial space.

Clinicallythis condition is manifested by a decrease in the turgor of the skin and eyeballs, impaired hemodynamics and volemia, azotemia, impaired renal and brain function, hemoconcentration. Treatmentconsists in a targeted effect on the pathogenetic factor and carrying out active rehydration with solutions containing sodium, potassium, magnesium (ace-salt). With hyperkalemia, disol is prescribed.

▲ Hypertensive dehydration(plasma sodium more than 150 mmol / l) arises due to the excess of water loss over sodium loss. It occurs during the polyuric stage of acute renal failure, prolonged forced diuresis without timely replenishment of water deficit, with fever, insufficient water intake during parenteral nutrition. An excess of water loss over sodium causes an increase in plasma osmolarity, as a result of which the intracellular fluid begins to pass into the vascular bed. Intracellular dehydration (cellular dehydration, exicosis) is formed.

Clinical symptoms- thirst, weakness, apathy, drowsiness, and with severe lesions - psychosis, hallucinations, dry tongue, fever, oliguria with a high relative density of urine, azotemia. Dehydration of brain cells causes the appearance of nonspecific neurological symptoms: psychomotor agitation, confusion, convulsions, and the development of a coma.

Treatmentconsists in a targeted effect on the pathogenetic factor and elimination of intracellular dehydration by prescribing infusions of glucose solution with insulin and potassium. The introduction of hypertonic solutions of salts, glucose, albumin, diuretics is contraindicated. Plasma sodium levels and osmolarity should be monitored.

▲ Isotonic hyperhydration(plasma sodium within the normal range of 135-145 mmol / l) most often occurs against the background of diseases accompanied by edematous syndrome (chronic heart failure, toxicosis of pregnancy), as a result of excessive administration of isotonic saline solutions. The occurrence of this syndrome is also possible against the background of liver cirrhosis, kidney diseases (nephrosis, glomerulonephritis). The main mechanism for the development of isotonic hyperhydration is an excess of water and salts with normal plasma osmolarity. Fluid retention occurs mainly in the interstitial space.

Clinicallythis form of overhydration is manifested by the appearance of arterial hypertension, a rapid increase in body weight, the development of edema syndrome, anasarca, and a decrease in blood concentration indices. Against the background of overhydration, there is a deficiency of free fluid.

Treatmentconsists in the use of diuretics aimed at reducing the volume of the interstitial space. In addition, 10% albumin is injected intravenously in order to increase the plasma oncotic pressure, as a result of which the interstitial fluid begins to pass into the vascular bed. If this treatment does not give the desired effect, they resort to hemodialysis with blood ultrafiltration.

Hyperhydration hypotonic(plasma sodium less than 130 mmol / l), or "water poisoning", can occur with a single intake of very large amounts of water, with prolonged intravenous administration of salt-free solutions, edema against the background of chronic heart failure, liver cirrhosis, Surge arrester,hyperproduction of ADH. The main mechanism is a decrease in plasma osmolarity and the transfer of fluid into cells.

Clinical picturemanifested by vomiting, frequent loose watery stools, polyuria. Signs of damage to the central nervous system join: weakness, weakness, fatigue, sleep disturbance, delirium, impaired consciousness, convulsions, coma.

Treatmentconsists in the fastest possible excretion of excess water from the body: diuretics are prescribed with simultaneous intravenous administration of sodium chloride and vitamins. A high-calorie diet is required. If necessary, hemodialysis with blood ultrafiltration is performed.

f Hyperhydration hypertensive(plasma sodium more 150 mmol / l) occurs when large amounts of hypertonic solutions are injected into the body against the background of preserved renal excretory function or isotonic solutions - to patients with impaired renal excretory function. The condition is accompanied by an increase in the osmolarity of the interstitial fluid, followed by dehydration of the cell sector and an increased release of potassium from it.

Clinical picturecharacterized by thirst, skin redness, increased body temperature, blood pressure and CVP. With the progression of the process, signs of damage to the central nervous system join: mental disorder, convulsions, coma.

Treatment- infusion therapy with the inclusion of 5 % glucose and albumin solution against the background of stimulation of diuresis by osmodiuretics and saluretics. According to indications - hemodialysis.

9.4. Acid-base state

Acid-base state(CBS) is one of the most important components of the biochemical constancy of body fluids as the basis of normal metabolic processes, the activity of which depends on the chemical reaction of the electrolyte.

CBS are characterized by the concentration of hydrogen ions and are denoted by the pH symbol. Acidic solutions have a pH from 1.0 to 7.0, basic solutions - from 7.0 to 14.0. Acidosis- a shift in pH towards the acidic side occurs due to the accumulation of acids or a lack of bases. Alkalosis- the shift in pH to the alkaline side is due to an excess of bases or a decrease in the acid content. The constancy of pH is an indispensable condition for human life. pH is the final, total reflection of the equilibrium of the concentration of hydrogen ions (H +) and the buffer systems of the body. Keeping the balance of CBS

carried out by two systems that prevent a shift in blood pH. These include the buffer (physicochemical) and physiological systems for the regulation of CBS.

9.4.1. Physico-chemical buffer systems

There are four known physicochemical buffer systems of the body - bicarbonate, phosphate, the buffer system of blood proteins, and hemoglobin.

Bicarbonate system, constituting 10% of the entire buffer capacity of the blood, is the ratio of bicarbonates (HC0 3) and carbon dioxide (H 2 CO 3). Normally, it is 20: 1. The end product of the interaction of bicarbonates and acid is carbon dioxide (CO2), which is exhaled. The bicarbonate system is the fastest acting and works in both plasma and extracellular fluid.

Phosphate system occupies a small place in buffer tanks (1%), acts more slowly, and the final product - potassium sulfate - is excreted by the kidneys.

Plasma proteins depending on the pH level, they can act both as acids and as bases.

Hemoglobin buffer system takes the main place in maintaining the acid-base state (about 70% of the buffer capacity). Hemoglobin of erythrocytes binds 20% of the incoming blood, carbon dioxide (C0 2), as well as hydrogen ions formed as a result of the dissociation of carbon dioxide (H 2 C0 3).

The hydrocarbonate buffer is predominantly present in the blood and in all sections of the extracellular fluid; in plasma - bicarbonate, phosphate and protein buffers; in erythrocytes - bicarbonate, protein, phosphate, hemoglobin; in urine - phosphate.

9.4.2. Physiological buffer systems

Lungsregulate the content of CO 2, which is a decomposition product of carbonic acid. The accumulation of CO 2 leads to hyperventilation and shortness of breath, and thus the excess carbon dioxide is removed. In the presence of an excess of bases, the reverse process takes place - pulmonary ventilation decreases, bradypnea occurs. Along with CO2, blood pH and oxygen concentration are strong irritants of the respiratory center. A shift in pH and changes in oxygen concentration lead to increased pulmonary ventilation. Potassium salts act in a similar way, but with a rapid increase in the concentration of K + in the blood plasma, the activity of chemoreceptors is suppressed and pulmonary ventilation decreases. Respiratory regulation of KOS refers to a rapid response system.

Kidneysupport CBS in several ways. Under the influence of the enzyme carbonic anhydrase, which is contained in large quantities in the renal tissue, C0 2 and H 2 0 are combined to form carbonic acid. Carbonic acid dissociates into bicarbonate (HC0 3 ~) and H +, which combines with phosphate buffer and is excreted in the urine. Bicarbonates are reabsorbed in the tubules. However, with an excess of bases, reabsorption decreases, which leads to an increased excretion of bases in the urine and a decrease in alkalosis. Each millimole of H + excreted in the form of titratable acids or ammonium ions adds 1 mmol to the blood plasma

HC0 3. Thus, the excretion of H + is closely related to the synthesis of HCO 3. Renal regulation of CBS is slow and requires many hours or even days to fully compensate.

Liverregulates CBS, metabolizing under-oxidized metabolic products coming from the gastrointestinal tract, forming urea from nitrogenous waste products and removing acid radicals with bile.

Gastrointestinal tractoccupies an important place in maintaining the constancy of CBS due to the high intensity of the processes of intake and absorption of liquids, food and electrolytes. Violation of any link in digestion causes a violation of CBS.

Chemical and physiological buffering systems are powerful and effective mechanisms for compensating for CBS. In this regard, even the most insignificant changes in CBS indicate severe metabolic disorders and dictate the need for timely and targeted corrective therapy. The general directions of normalization of CBS include the elimination of the etiological factor (pathology of the respiratory and cardiovascular systems, organs abdominal and others), normalization of hemodynamics - correction of hypovolemia, restoration of microcirculation, improvement of rheological properties of blood, treatment of respiratory failure, up to transferring the patient to mechanical ventilation, correction of water-electrolyte and protein metabolism.

CBS indicators determined by the equalization micro-method Astra-pa (with interpolation calculation of pCO 2) or by methods with direct oxidation of CO 2. Modern microanalyzers automatically determine all KOS values \u200b\u200band partial voltage of blood gases. The main indicators of CBS are presented in table. 9.1.

Table 9.1.CBS indicators are normal

To assess the type of violation of CBS in normal practical work, use the indicators pH, PC0 2, P0 2, BE.

9.4.3. Types of acid-base disorders

There are 4 main types of CBS disorder: metabolic acidosis and alkalosis; respiratory acidosis and alkalosis; their combinations are also possible.

and Metabolic acidosis- deficiency of bases, leading to a decrease in pH. Causes: acute renal failure, uncompensated diabetes (ketoacidosis), shock, heart failure (lactic acidosis), poisoning (salicylates, ethylene glycol, methyl alcohol), small intestinal (duodenal, pancreatic) fistulas, diarrhea, adrenal insufficiency. Indicators of CBS: pH 7.4-7.29, PaCO 2 40-28 Hg. Art., BE 0-9 mmol / l.

Clinical symptoms- nausea, vomiting, weakness, impaired consciousness, tachypnea. Clinically mild acidosis (BE up to -10 mmol / L) may be asymptomatic. With a decrease in pH to 7.2 (state of subcompensation, then decompensation), shortness of breath increases. With a further decrease in pH, respiratory and heart failure increases, hypoxic encephalopathy develops up to coma.

Treatment for metabolic acidosis:

Strengthening the bicarbonate buffer system - the introduction of 4.2% sodium bicarbonate solution (contraindications- hypokalemia, metabolic alkalosis, hypernatremia) intravenously through a peripheral or central vein: undiluted, diluted 5% glucose solution in a 1: 1 ratio. The infusion rate of the solution is 200 ml in 30 minutes. The required amount of sodium bicarbonate can be calculated using the formula:

The amount of mmol of sodium bicarbonate \u003d BE body weight, kg 0.3.

Without laboratory control, use no more than 200 ml / day, drip, slowly. The solution should not be administered simultaneously with solutions containing calcium, magnesium and should not be mixed with phosphate-containing solutions. Transfusion of lactasol by the mechanism of action is similar to the use of sodium bicarbonate.

and Metabolic alkalosis- a state of deficiency of H + ions in the blood in combination with an excess of bases. Metabolic alkalosis is difficult to treat, as it is the result of both external electrolyte losses and disorders of cellular and extracellular ionic relationships. Such violations are characteristic of massive blood loss, refractory shock, sepsis, severe loss of water and electrolytes with intestinal obstruction, peritonitis, pancreatic necrosis, long-term intestinal fistulas. Quite often, it is metabolic alkalosis, as the final phase of metabolic disorders incompatible with life in this category of patients, that becomes the direct cause of death.

Principles of metabolic alkalosis correction.Metabolic alkalosis is easier to prevent than to cure. TO preventive measures include adequate administration of potassium during blood transfusion therapy and replenishment of cellular potassium deficiency, timely and complete correction of volemic and hemodynamic disorders. In the treatment of developed metabolic alkalosis, of paramount importance is

elimination of the main pathological factor of this condition. Purposeful normalization of all types of exchange is carried out. The relief of alkalosis is achieved by intravenous administration of protein preparations, glucose solutions in combination with potassium chloride, and a large amount of vitamins. Isotonic sodium chloride solution is used to reduce the osmolarity of the extracellular fluid and eliminate cellular dehydration.

▲ Respiratory (respiratory) acidosischaracterized by an increase in the concentration of H + ions in the blood (pH< 7,38), рС0 2 (> 40 mmHg Art.), BE (\u003d 3.5 + 12 mmol / L).

The causes of respiratory acidosis can be hypoventilation as a result of obstructive pulmonary emphysema, bronchial asthma, impaired ventilation in debilitated patients, extensive atelectasis, pneumonia, acute pulmonary injury syndrome.

The main compensation of respiratory acidosis is carried out by the kidneys by the forced excretion of H + and SG, increasing the reabsorption of HCO 3.

IN clinical picturerespiratory acidosis is dominated by symptoms of intracranial hypertension, which arise from cerebral vasodilation caused by excess CO2. Progressive respiratory acidosis leads to cerebral edema, the severity of which corresponds to the degree of hypercapnia. Stupor often develops with a transition to a coma. The first signs of hypercapnia and increasing hypoxia are the patient's anxiety, motor agitation, arterial hypertension, tachycardia, followed by a transition to hypotension and tachyarrhythmia.

Respiratory acidosis treatmentfirst of all, it consists in improving alveolar ventilation, eliminating atelectasis, pneumo- or hydrothorax, sanitizing the tracheobronchial tree and transferring the patient to mechanical ventilation. Treatment must be carried out urgently, before hypoxia develops as a result of hypoventilation.

f Respiratory (respiratory) alkalosischaracterized by a decrease in the pCO 2 level below 38 mm Hg. Art. and a rise in pH above 7.45-7.50 as a result of increased ventilation of the lungs both in frequency and depth (alveolar hyperventilation).

The leading pathogenetic link in respiratory alkalosis is a decrease in cerebral volumetric blood flow as a result of an increase in the tone of cerebral vessels, which is a consequence of a CO2 deficiency in the blood. At the initial stages, the patient may have paresthesias of the skin of the extremities and around the mouth, muscle spasms in the extremities, mild or severe drowsiness, headache, sometimes deeper disturbances of consciousness, up to coma.

Prevention and treatmentrespiratory alkalosis is primarily aimed at normalizing external respiration and the effect on the pathogenetic factor that caused hyperventilation and hypocapnia. Indications for transferring the patient to mechanical ventilation are oppression or absence of spontaneous breathing, as well as shortness of breath and hyperventilation.

9.5. Infusion therapy of water-electrolyte disorders and acid-base state

Infusion therapyis one of the main methods in the treatment and prevention of dysfunctions of vital organs and systems in surgical patients. Infusion efficiency

noah therapy depends on the validity of its program, the characteristics of the infusion media, pharmacological properties and pharmacokinetics of the drug.

For diagnostics volemic violations and building infusion therapy programsin the pre- and postoperative period, the turgor of the skin, the moisture of the mucous membranes, the filling of the pulse in the peripheral artery, heart rate and blood pressure are important. During surgical intervention the filling of the peripheral pulse, hourly urine output, and blood pressure dynamics are most often assessed.

Manifestations of hypervolemiaare tachycardia, shortness of breath, moist wheezing in the lungs, cyanosis, frothy sputum. The degree of volemic disorders is reflected by laboratory data - hematocrit, arterial blood pH, relative density and osmolarity of urine, concentration of sodium and chlorine in urine, sodium in plasma.

To laboratory signs dehydrationinclude an increase in hematocrit, progressive metabolic acidosis, a relative urine density of more than 1010, a decrease in the concentration of Na + in urine less than 20 meq / l, and urine hyperosmolarity. There are no laboratory signs characteristic of hypervolemia. Hypervolemia can be diagnosed on the basis of lung X-ray data - increased vascular pulmonary pattern, interstitial and alveolar pulmonary edema. CVP is assessed according to the specific clinical situation. The most indicative is the volumetric load test. A slight increase (1-2 mm Hg) of CVP after a rapid infusion of crystalloid solution (250-300 ml) indicates hypovolemia and the need to increase the volume of infusion therapy. Conversely, if after the test, the increase in CVP exceeds 5 mm Hg. Art., it is necessary to reduce the rate of infusion therapy and limit its volume. Infusion therapy involves intravenous administration of colloidal and crystalloid solutions.

and Crystalloid solutions - aqueous solutions of low molecular weight ions (salts) quickly penetrate the vascular wall and are distributed in the extracellular space. The choice of solution depends on the nature of the loss of fluid, which must be replaced. The loss of water is compensated for with hypotonic solutions, which are called maintenance solutions. Water and electrolyte deficiencies are replenished with isotonic electrolyte solutions, which are called replacement type solutions.

▲ Colloidal solutions based on gelatin, dextran, hydroxyethyl starch and polyethylene glycol, they maintain the colloidal osmotic pressure of the plasma and circulate in the vascular bed, providing a vollemic, hemodynamic and rheological effect.

In the perioperative period, with the help of infusion therapy, the physiological needs for fluid (maintenance therapy), concomitant fluid deficiency, and losses through the surgical wound are replenished. The choice of the infusion solution depends on the composition and nature of the fluid lost - sweat, the contents of the gastrointestinal tract. Intraoperative loss of water and electrolytes is due to evaporation from the surface of the surgical wound during extensive surgical interventions and depends on the area of \u200b\u200bthe wound surface and the duration of the operation. Accordingly, intraoperative fluid therapy includes replenishment of basic physiological fluid requirements, elimination of preoperative deficit and operational losses.

Table 9.2.The content of electrolytes in the media of the gastrointestinal tract

Need for wateris determined on the basis of an accurate assessment of the resulting fluid deficit, taking into account renal and extrarenal losses.

For this purpose, the volume of daily urine output is summed up: V, - the proper value of 1 ml / kg / h; V 2 - losses with vomiting, stool and gastrointestinal contents; V 3 - discharge by drainage; P - losses by perspiration through the skin and lungs (10-15 ml / kg / day), taking into account the constant T - losses during fever (with an increase in body temperature by 1 ° C above 37 °, the loss is 500 ml per day). Thus, the total daily water deficit is calculated by the formula:

E \u003d V, + V 2 + V 3 + P + T (ml).

To prevent hypo- or overhydration, it is necessary to control the amount of fluid in the body, in particular, in the extracellular space:

OBJ \u003d body weight, kg 0.2, conversion factor Hematocrit - Hematocrit

Deficiency \u003d true due body weight, kg Hematocrit due 5

Calculation of essential electrolyte deficiency(K +, Na +) is produced taking into account the volume of their losses with urine, contents of the gastrointestinal tract (GIT) and drainage media; determination of concentration indicators - according to generally accepted biochemical methods. If it is impossible to determine potassium, sodium, chlorine in the gastric contents, losses can be estimated mainly taking into account fluctuations in the concentration of indicators in the following ranges: Na + 75-90 mmol / l; K + 15-25 mmol / L, SG up to 130 mmol / L, total nitrogen 3-5.5 g / L.

Thus, the total loss of electrolytes per day is:

E \u003d V, C, + V 2 C 2 + V 3 C 3 g,

where V] - daily diuresis; V 2 - the volume of the discharge of the gastrointestinal tract during vomiting, with stool, by probe, as well as fistulous losses; V 3 - discharge from the abdominal drainage; C, C 2, C 3 - concentration indicators in these media, respectively. When calculating, you can refer to the data in Table. 9.2.

When converting the value of losses from mmol / l (SI system) to grams, the following conversions must be performed:

K +, g \u003d mmol / L 0.0391.

Na +, g \u003d mmol / L 0.0223.

9.5.1. Characterization of crystalloid solutions

Means that regulate water-electrolyte and acid-base homeostasis include electrolyte solutions and osmodiuretics. Electrolyte solutionsused to correct disorders of water metabolism, electrolyte metabolism, water-electrolyte metabolism, acid-base state (metabolic acidosis), water-electrolyte metabolism and acid-base state (metabolic acidosis). The composition of electrolyte solutions determines their properties - osmolarity, isotonicity, ionicity, reserve alkalinity. In relation to the osmolarity of electrolyte solutions to blood, they show an iso-, hypo- or hyperosmolar effect.

Isoosmolar effect -water introduced with iso-osmolar solution (Ringer's solution, Ringer's acetate) is distributed between the intravascular and extravascular spaces as 25%: 75% (the volemic effect will be 25% and will last about 30 minutes). These solutions are indicated for isotonic dehydration.

Hypoosmolar effect -more than 75% of water injected with an electrolyte solution (disol, acesol, 5% glucose solution) will pass into the extravascular space. These solutions are indicated for hypertensive dehydration.

Hyperosmolar effect -water from the extravascular space will flow into the vascular bed until the hyperosmolarity of the solution is brought to the osmolarity of the blood. These solutions are indicated for hypotonic dehydration (10% sodium chloride solution) and overhydration (10% and 20% mannitol).

Depending on the electrolyte content in the solution, they can be isotonic (0.9% sodium chloride solution, 5% glucose solution), hypotonic (disol, acesol) and hypertonic (4% potassium chloride solution, 10% sodium chloride, 4.2% and 8.4% sodium bicarbonate solution). The latter are called electrolyte concentrates and are used as an additive to infusion solutions (5% glucose solution, Ringer's acetate solution) immediately before administration.

Depending on the number of ions in the solution, monoionic (sodium chloride solution) and polyionic (Ringer's solution, etc.) are distinguished.

The introduction of carriers of reserve basicity (bicarbonate, acetate, lactate and fumarate) into electrolyte solutions makes it possible to correct disorders of CBS - metabolic acidosis.

▲ Sodium chloride solution 0.9 % administered intravenously through a peripheral or central vein. The rate of administration is 180 drops / min, or about 550 ml / 70 kg / h. The average dose for an adult patient is 1000 ml / day.

Indications:hypotonic dehydration; meeting the need for Na + and O; hypochloremic metabolic alkalosis; hypercalcemia.

Contraindications:hypertensive dehydration; hypernatremia; hyperchloremia; hypokalemia; hypoglycemia; hyperchloremic metabolic acidosis.

Possible complications:

hypernatremia;

hyperchloremia (hyperchloremic metabolic acidosis);

hyperhydration (pulmonary edema).

g Ringer's acetate solution- isotonic and isionic solution, administered intravenously. The rate of administration is 70-80 drops / min or 30 ml / kg / h;

if necessary up to 35 ml / min. The average dose for an adult patient is 500-1000 ml / day; if necessary, up to 3000 ml / day.

Indications:loss of water and electrolytes from the gastrointestinal tract (vomiting, diarrhea, fistulas, drains, intestinal obstruction, peritonitis, pancreatitis, etc.); with urine (polyuria, isostenuria, forced diuresis);

Isotonic dehydration with metabolic acidosis - delayed correction of acidosis (blood loss, burns).

Contraindications:

hypertensive hyperhydration;

• hypernatremia;

  hyperchloremia;

  hypercalcemia.

Complications:

overhydration;

• hypernatremia;

  hyperchloremia.

and Yonosteril- isotonic and isoionic electrolyte solution is administered intravenously through a peripheral or central vein. The rate of administration is 3 ml / kg of body weight or 60 drops / min or 210 ml / 70 kg / h; if necessary up to 500 ml / 15 min. The average dose for an adult is 500-1000 ml / day. In severe or urgent cases, up to 500 ml in 15 minutes.

Indications:

extracellular (isotonic) dehydration of various origins (vomiting, diarrhea, fistulas, drains, intestinal obstruction, peritonitis, pancreatitis, etc.); polyuria, isostenuria, forced diuresis;

Primary plasma replacement for plasma loss and burns. Contraindications:hypertensive hyperhydration; swelling; heavy

renal failure.

Complications:hyperhydration.

▲ Lactosol- isotonic and isoionic electrolyte solution is administered intravenously through a peripheral or central vein. The rate of administration is 70-80 drops / min, or about 210 ml / 70 kg / h; if necessary up to 500 ml / 15 min. The average dose for an adult is 500-1000 ml / day; if necessary, up to 3000 ml / day.

Indications:

loss of water and electrolytes from the gastrointestinal tract (vomiting, diarrhea, fistulas, drains, intestinal obstruction, peritonitis, pancreatitis, etc.); with urine (polyuria, isostenuria, forced diuresis);

isotonic dehydration with metabolic acidosis (fast and delayed correction of acidosis) - blood loss, burns.

Contraindications:hypertensive hyperhydration; alkalosis; hypernatremia; hyperchloremia; hypercalcemia; hyperlactatemia.

Complications:overhydration; alkalosis; hypernatremia; hyperchloremia; hyperlactatemia.

▲ Acesol- hypo-osmolar solution contains ions Na +, C1 "and acetate. Injected intravenously through a peripheral or central vein (jet

or drip). The daily dose for an adult is equal to the daily requirement for water and electrolytes plus 1/2 water deficit plus continuing pathological losses.

Indications:hypertensive dehydration in combination with hyperkalemia and metabolic acidosis (delayed correction of acidosis).

Contraindications:hypotonic dehydration; hypokalemia; hyperhydration.

Complication:hyperkalemia.

and Sodium hydrogen carbonate solution 4.2% for the rapid correction of metabolic acidosis. Administered intravenously undiluted or diluted 5 % glucose solution in a ratio of 1: 1, the dosage depends on the data of the ionogram and CBS. In the absence of laboratory control, no more than 200 ml / day is slowly injected drip. A solution of sodium bicarbonate 4.2% should not be administered simultaneously with solutions containing calcium, magnesium, and should not be mixed with phosphate-containing solutions. The dose of the drug can be calculated using the formula:

1 ml of a 4.2% solution (0.5 molar) \u003d BE body weight (kg) 0.6.

Indications -metabolic acidosis.

Contraindications- hypokalemia, metabolic alkalosis, hypernatremia.

▲ Osmodiuretics(mannitol). Inject 75-100 ml of 20% mannitol intravenously over 5 minutes. If the amount of urine is less than 50 ml / h, then the next 50 ml is injected intravenously.

9.5.2. The main directions of infusion therapy for hypo- and hyperhydration

1. Infusion therapy for dehydrationshould take into account its type (hypertonic, isotonic, hypotonic), as well as:

the volume of the "third space"; forcing diuresis; hyperthermia; hyperventilation, open wounds; hypovolemia.

2. Infusion therapy for overhydrationshould take into account its type (hypertensive, isotonic, hypotonic), as well as:

physiological daily requirement for water and electrolytes;

prior water and electrolyte deficiency;

continuing pathological loss of fluid with secretions;

the volume of the "third space"; forcing diuresis; hyperthermia, hyperventilation; open wounds; hypovolemia.

Intracellular water (70%) is associated with potassium and phosphate, basic cation and anion. Extracellular water makes up about 30% of the total amount in the body. The main cation of the extracellular fluid is sodium, and the anions are bicarbonates and chlorides. The distribution of sodium, potassium and water is presented in table. five.

According to AU Wilkinson (1974), the volume of plasma is 1/3 of the interstitial fluid. 1100 liters of water are exchanged daily between blood and intercellular fluid, 8 liters of fluid are secreted into the intestinal lumen and reabsorbed from it.

• Disorders of sodium metabolism

  In the blood sodium contains 143 meq / l, in the intercellular space 147, in cells 35 meq / l. Disorders of sodium balance can manifest themselves in the form of a decrease (hyponatremia), its excess (hypernatremia), or a change in the distribution in various environments of the body with a normal or altered total amount in the body.

  The decrease in sodium can be true or relative. True hyponatremia is associated with sodium and water loss. This is observed with insufficient intake of table salt, profuse sweating, with extensive burns, polyuria (for example, in chronic renal failure), intestinal obstruction and other processes. Relative hyponatremia occurs with excessive introduction of aqueous solutions at a rate exceeding the excretion of water by the kidneys.

  According to A. U. Wilkinson (1974), the clinical manifestations of sodium deficiency are determined primarily by the rate, and then by the magnitude of its loss. The slow loss of 250 meq of sodium only causes a decrease in performance and appetite. Rapid loss of 250-500 and especially 1500 meq of sodium (vomiting, diarrhea, gastrointestinal fistula) leads to severe circulatory disorders. Deficiency of sodium, and with it water, reduces the volume of extracellular fluid.

  A true excess of sodium is observed with the administration of saline solutions to the patient, increased consumption of table salt, delayed excretion of sodium by the kidneys, excessive production or prolonged administration of gluco- and mineralocorticoids from the outside.

  A relative increase in sodium in blood plasma is observed with dehydration.

  True hypernatremia leads to overhydration and the development of edema.

• Potassium metabolism disorders

  98% of potassium is in the intracellular and only 2% in the extracellular fluid. The human blood plasma normally contains 3.8-5.1 meq / l of potassium.

  The daily potassium balance in humans was compiled by A.W. Wilkinson (1974). Changes in potassium concentration below 3.5 and above 7 meq / l are considered pathological and are referred to as hypo- and hyperkalemia.

  The kidneys play an important role in regulating the amount of potassium in the body. This process is controlled by aldosterone and partially glucocorticoids. There is an inverse relationship between blood pH and plasma potassium content, i.e., during acidosis, potassium ions leave the cells in exchange for hydrogen and sodium ions. Reverse changes are observed with alkalosis. It was found that when three potassium ions leave the cell, two sodium ions and one hydrogen ion enter the cell. With a loss of 25% potassium and water, cell function is impaired. It is known that under any extreme influences, for example, during starvation, potassium is released from the cells into the interstitial space. In addition, large amounts of potassium are released during protein catabolism. Therefore, due to the effects of aldosterone and cortisol, the renal mechanism is activated, and potassium is intensively secreted into the lumen of the distal tubules and excreted in large quantities in the urine.

  Hypokalemia is observed with excessive production or introduction from the outside of aldosterone, glucocorticoids, causing excessive secretion of potassium in the kidneys. A decrease in potassium was also noted with intravenous administration of solutions, insufficient intake of potassium into the body with food. Since the excretion of potassium occurs constantly, hypokalemia is formed under these conditions. Potassium loss also occurs with gastrointestinal secretions during vomiting or diarrhea.

  With a deficiency of potassium, the function of the nervous system is impaired, which manifests itself in drowsiness, rapid fatigue, and delayed slurred speech. The excitability of muscles decreases, the motility of the gastrointestinal tract worsens, systemic arterial pressure decreases, and the pulse decreases. The ECG reveals a slowdown in conduction, a decrease in the voltage of all teeth, an increase in the QT interval, a shift of the ST segment below the isoelectric line. An important compensatory reaction aimed at maintaining the constancy of potassium in blood plasma and cells is limiting its excretion in the urine.

  The main causes of gnperkalemia are protein breakdown during starvation, trauma, a decrease in circulating blood volume (dehydration and especially impaired K + secretion under conditions of oligo- and anuria (acute renal failure)), excessive administration of potassium in the form of solutions.

  Hyperkalemia is characterized by muscle weakness, hypotension, and bradycardia, which can lead to cardiac arrest. The ECG shows a high and sharp T wave, widening complex QRS, flattening and disappearance of the P wave.

• Magnesium metabolism disorders

  Magnesium plays an important role in the activation of many enzymatic processes, in the conduct of excitation in nerve fibers, in muscle contraction. According to A. W. Wilkinson (1974), an adult weighing 70 kg contains about 2000 meq of magnesium, while potassium 3400 meq, and sodium 3900 meq. About 50% of magnesium is found in bones, and the same amount in cells of other tissues. In the extracellular fluid, it is less than 1%.

  In adults, plasma contains 1.7-2.8 mg% magnesium. Its bulk (about 60%) is in ionized form.

  Magnesium, like potassium, is the most important intracellular element. The kidneys and intestines take part in the exchange of magnesium. Absorption is carried out in the intestine, and its constant secretion in the kidneys. There is a very close relationship between the exchange of magnesium, potassium and calcium.

  It is believed that bone tissue serves as a source of magnesium, which is easily mobilized in the event of its deficiency in soft tissue cells, and the process of magnesium mobilization from bones occurs faster than its replenishment from the outside. With a magnesium deficiency, calcium balance is also disturbed.

  Magnesium deficiency is observed during fasting and a decrease in its absorption, with a loss with secretions of the gastrointestinal tract as a result of fistulas, diarrhea, resections, as well as its increased secretion after the introduction of sodium lactate into the body.

  Determining the symptoms of magnesium deficiency is very difficult, but it is known that the combination of magnesium, potassium and calcium deficiencies is characterized by weakness and apathy.

  An increase in magnesium in the body is observed as a result of a violation of its secretion in the kidneys and increased cell decay in chronic renal failure, diabetes, hypothyroidism. An increase in magnesium concentration above 3-8 meq / l is accompanied by hypotension, drowsiness, respiratory depression, and the absence of tendon reflexes.

• Water imbalance

  The water balance in the body depends on the intake and excretion of water from the body. Water loss, especially under pathological conditions, can fluctuate significantly. Water metabolism disorders are closely interrelated with electrolyte balance and manifest themselves in dehydration (dehydration) and hydration (increased amount of water in the body), the extreme expression of which is edema.

Edema (oedema) characterized by excessive accumulation of fluid in body tissues and serous cavities... Thus, it is accompanied by hyperhydration of intercellular spaces with simultaneous disturbance of electrolyte balance in cells and their hyper- or hypohydration (BME, vol. 18, p. 150). Water retention is due to the accumulation of the main osmotic cation in the body of sodium.

The main general mechanisms of edema formation

With edema as a result of disturbances in water and electrolyte metabolism, a huge amount of fluid can accumulate in the tissues. A number of mechanisms are involved in this process.

Dehydration is a pathological process characterized by a lack of water in the body. There are two types of dehydration (Kerpel - Fronius):

1. Loss of water without an equivalent amount of cations. This is accompanied by thirst and the redistribution of water from cells to the interstitial space.
2. Loss of sodium. The compensation of water and sodium occurs from the extracellular fluid. Disturbance of blood circulation without the development of thirst is characteristic.

With dehydration caused by complete starvation, people lose weight, diuresis decreases to 600 ml / day, and the specific gravity of urine rises to 1.036. The sodium concentration and the volume of red blood cells do not change. At the same time, there is dryness of the oral mucosa, thirst, and residual nitrogen builds up in the blood (A. W. Wilkinson, 1974).

A.U. Wilkinson proposes to classify dehydration into aqueous and saline. True "water depletion, primary, or simple, dehydration" is due to a lack of water and potassium, as a result of which the volume of intracellular fluid changes; characterized by thirst and oliguria. In this case, the osmotic pressure of the interstitial fluid initially increases, and therefore water passes from the cells into the extracellular space. In connection with the developing oliguria, the amount of sodium is maintained at a stable level, and potassium continues to be secreted in the distal tubules and excreted in the urine.

True "salt depletion", secondary, or extracellular, dehydration is associated mainly with a lack of sodium and water. In this case, the volume of plasma and interstitial fluid decreases and the hematocrit increases. Therefore, its main manifestation is impaired blood circulation.

The most serious sodium losses occur in surgical practice and are caused by the secretion of gastrointestinal secretions through extensive wound surfaces. Table 6 shows the amount of electrolytes in plasma and various secretions of the digestive tract.

The main causes of salt dehydration are sodium loss with secretions sucked from the stomach (for example, in operated patients), vomiting, gastrointestinal fistula, intestinal obstruction. Loss of sodium can lead to a critical decrease in the volume of extracellular fluid and plasma and circulatory disorders, accompanied by hypotension and decreased glomerular filtration.

With dehydration caused by both water deficiency and sodium loss, the normalization of the water-electrolyte balance is achieved by the simultaneous introduction of sodium and water.

A source: Ovsyannikov V.G. Pathological physiology, typical pathological processes. Tutorial... Ed. Rostov University, 1987 .-- 192 p.

Disorders of water and electrolyte metabolism in TBI are multidirectional changes. They arise due to reasons that can be divided into three groups:

1.Disorders typical for any resuscitation situation (the same for TBI, peritonitis, pancreatitis, sepsis, gastrointestinal bleeding).
2.Disorders specific to brain lesions.
3. Iatrogenic disorders caused by forced or erroneous use of pharmacological and non-pharmacological means of treatment.

It is difficult to find another pathological condition in which such a variety of water-electrolyte disturbances would be observed, as in TBI, and the threat to life was so great if they were untimely diagnosed and corrected. To understand the pathogenesis of these disorders, let us dwell in more detail on the mechanisms that regulate water-electrolyte metabolism.

A bit of physiology
The three "whales" on which the regulation of water-electrolyte metabolism rests are the antidiuretic hormone (ADH), the renin-angiotensin-aldosterone system (RAAS) and atrial natriuretic factor (PNF) (Fig. 3.1).

ADH affects the reabsorption (i.e. reabsorption) of water in the renal tubules. When triggers are turned on (hypovolemia, arterial hypotension and hypoosmolality), ADH is released into the blood from the posterior lobe of the pituitary gland, which leads to water retention and vasoconstriction. The secretion of ADH is stimulated by nausea and angiotensin II, while PNP inhibits the secretion. With an excessive production of ADH, the syndrome of excessive production of antidiuretic hormone (SIVADH) develops. For the realization of the effects of ADH, in addition to the adequate functioning of the posterior lobe of the pituitary gland, normal sensitivity of specific ADH receptors located in the kidneys is required. With a decrease in the production of ADH in the pituitary gland, the so-called central diabetes insipidus develops, with impaired receptor sensitivity - nephrogenic diabetes insipidus.

The RAAS affects the excretion of sodium by the kidneys. When the trigger (hypovolemia) is turned on, a decrease in blood flow in the juxtamedullary glomeruli is observed, which leads to the release of renin into the blood. An increase in renin levels causes the conversion of inactive angiotensin I to active angiotensin II. Angiotensin II induces vasoconstriction and stimulates the adrenal glands to release the mineralocorticoid aldosterone. Aldosterone causes retention of water and sodium, in exchange for sodium provides the excretion of potassium and calcium due to the reversible blockade of their tubular reabsorption.
PNP can, to a certain extent, be regarded as a hormone-antagonist for ADH and RAAS. With an increase in the volume of circulating blood (hypervolemia), pressure in the atria rises, which leads to the release of PNP into the blood and promotes the excretion of sodium by the kidneys. According to modern data, ouabain, a low molecular weight compound formed in the hypothalamus, acts similarly to PNP. Ouabain excess is most likely responsible for the development of cerebral salt-wasting syndrome.

3.1.1. Mechanisms of dysregulation of water-electrolyte metabolism in TBI
Volemic disorders are observed in any resuscitation situation. TBI is no exception to this rule. The activation of all links in the regulation of water-electrolyte metabolism in case of brain damage occurs due to the development of hypovolemia. In TBI, mechanisms of dysregulation specific to brain lesions are also activated. They are triggered when the diencephalic regions of the brain are damaged and the connections of the hypothalamus with the pituitary gland are disrupted due to direct trauma, increased dislocation of the brain, or vascular disorders. The activity of these specific mechanisms results in changes in the production of ADH, ouabain, and tropic hormones of the anterior pituitary gland (for example, adrenocorticotropic hormone, which indirectly affects the level of aldosterone), characteristic of cerebral pathology.

Hypertonic solutions, optimized hyperventilation, hypothermia used to relieve intracranial hypertension are forced iatrogenic measures that deepen water-electrolyte disorders. The use of saluretics in TBI most often (but not always!) Is an example of the use of drugs for erroneous indications, which causes gross violations of the water-electrolyte balance.

Dysfunction of hormones that regulate water and electrolyte balance leads to violations of the volemic status (hypo- and hypervolemia), sodium content (hypo- and hypernatremia), osmolality (hypo- and hyperosmolality). There are violations of the content of potassium, magnesium, calcium, acid-base state. All of these disorders are interrelated. However, we begin with a description of abnormalities in sodium concentration, which is the central ion that regulates the osmotic pressure of the blood and determines the water balance between the intravascular bed and the interstitial space of the brain.

Sodium disorders

Hypernatremia
Hypernatremia, depending on the presence of volemic disorders, is divided into hypovolemic, euvolemic and hypervolemic. Hypernatremia is always accompanied by an increase in effective blood osmolality, that is, it is hypertensive.

Hypovolemic hypernatremia
Hypovolemic hypernatremia is most often observed in the initial stages of TBI. The causes of hypovolemic hypernatremia at this stage are renal and extrarenal fluid losses, which are not compensated by a sufficient intake of it into the body. Often there is blood loss, as well as associated injuries. Since the victim is in an altered consciousness, he loses the ability to adequately respond to water losses through the kidneys and skin. Frequent symptom intracranial hypertension is vomiting. Therefore, fluid loss through the gastrointestinal tract can also play a significant role in the development of hypovolemia. It is also possible to move fluid into the so-called third space due to sequestration in the paretic intestine.

The result of activation of the described mechanisms is hypovolemia. The body tries to compensate for the loss of intravascular volume by attracting fluid from the interstitial space. This space is dehydrated, but the attracted fluid is not enough to "fill" the intravascular space. As a result, extracellular dehydration occurs. Since water is mainly lost, the sodium level in the extracellular sector (interstitial and intravascular space) increases.

Hypovolemia triggers another mechanism of hypernatremia: hyperaldosteronism develops, which leads to sodium retention in the body (J.J. Marini, A.P. Wheeler, 1997). This reaction is also adaptive, since the osmotically active properties of sodium make it possible to retain water in the body and compensate for hypovolemia. At the same time, sodium retention leads to compensatory excretion of potassium, which is accompanied by a number of negative consequences.

The inclusion of the described pathological mechanism is possible in later periods of TBI, however, such a pronounced hypovolemia, as in the early stages, is not noted, since the patient is already receiving treatment by this time.

Euvolemic hypernatremia
This type of hypernatremia occurs when water loss prevails over sodium loss. It is observed with a deficiency or ineffectiveness of ADH, the use of diuretics, osmostat reinstallation syndrome.
ADH deficiency is called tasteless, salt-free diabetes, diabetes insipidus (since urine is low in salt) and otherwise central diabetes insipidus. Central diabetes insipidus occurs due to direct damage to the pituitary gland or a violation of its blood supply. The syndrome is characterized by impaired production of ADH and is accompanied by hypernatremia due to excessive secretion of hypotonic urine with a low sodium content. Treatment of the syndrome is reduced to the use of synthetic antidiuretic hormone substitutes and correction of water losses.

Ineffectiveness of ADH, otherwise called nephrogenic diabetes insipidus, can develop with concomitant kidney disease, hypercalcemia, hypokalemia. Chronic intake of certain drugs (for example, lithium for depressive disorders) can reduce the sensitivity of the renal receptors to the action of ADH.

Loop diuretics such as furosemide have unpredictable effects on sodium and water excretion. In some situations, more water is lost than sodium, resulting in hypernatremia. It is assumed that the mechanism of this phenomenon is associated with the effect of a loop diuretic on the sensitivity of renal ADH receptors, that is, in fact, it is a variant of nephrogenic diabetes insipidus. In other cases, more sodium is lost than water and hyponatremia develops.

Osmostat reinstallation syndrome is a peculiar condition characterized by the establishment of a new normal blood sodium level and a corresponding change in its osmolality. According to our data, in TBI, osmostat reinstallation syndrome often leads to a lower, rather than a higher, sodium norm, so we will consider it in more detail in the section on hyponatremia.

Hypervolemic hypernatremia
This form of hypernatremia in TBI is rare. It always arises iatrogenically. The main reason is the introduction of an excess of sodium-containing solutions - hypertonic (3-10%) sodium chloride solutions, as well as 4% sodium bicarbonate solution. The second reason is the exogenous administration of corticosteroids, which have more or less mineralocorticoid properties. Due to the excess of aldosterone, sodium and water are retained by the kidneys, and potassium is lost in exchange for sodium. As a result, hypervolemic hypernatremia and hypokalemia develop.

Diagnosis of hypernatremia
To clarify the mechanisms of hypernatremia, it is very important to study the osmolality of urine and the sodium content in it.

A bit of physiology
Osmolality of urine, like total osmolality of blood, depends on the concentration of sodium, glucose and urea. In contrast to the value of blood osmolality, it varies widely: it can increase (more than 400 mOsm / kg water), be normal (300 - 400 mOsm / kg water) and low (less than 300 mOsm / kg water). If it is not possible to measure urine osmolality, the specific gravity of urine can be used for a rough estimate.

The combination of high urine osmolality and hypernatremia suggests three possible conditions:

Dehydration and reduced water intake (hypodipsia),
excess mineralocorticoids,
significant exogenous sodium administration.

For differential diagnosis of these conditions, it is useful to study the sodium content in urine. The concentration of sodium in the urine is low with dehydration and other extrarenal causes of hypernatremia, high - with an excess of mineralocorticoids and exogenous administration of sodium.

Normal urine osmolality and hypernatremia are observed with the use of diuretics, with a mild course of diabetes insipidus. Low urine osmolality and hypernatremia are indicative of severe central or nephrogenic diabetes insipidus. The sodium content in urine is variable in all these cases.

Hyponatremia
Hyponatremia is not an early symptom of TBI. Its development, as a rule, is noted already in the conditions of treatment, therefore, with hyponatremia, the volume of circulating blood is almost normal or slightly increased. Unlike hypernatremia, which is always accompanied by a hyperosmolality of the blood, hyponatremia can be combined with both hyperosmolality and normo- and hypoosmolality.

Hypertensive hyponatremia
Hypertensive hyponatremia is the rarest and least logical form of blood sodium reduction. Reduced level of sodium - the main agent providing osmotic properties of blood, and increased osmolality! This type of hyponatremia can develop only when a significant amount of other osmotically accumulates in the blood. active substances - glucose, urea, starch, dextrans, alcohol, mannitol. These agents can be introduced externally or produced endogenously. An example of an endogenous mechanism for the development of hypertensive hyponatremia is hyperglycemia due to decompensation of diabetes mellitus. This situation is often encountered in elderly patients with TBI. With an increase in blood osmolality, the sodium level in it decreases compensatory. If the osmolality exceeds 295 mOsm / kg water, the mechanisms that remove sodium from the body are activated. As a result, not only the concentration of sodium in the blood decreases, but also its absolute amount.

Hypo- and normotonic hyponatremia
Hypo- and normotonic hyponatremia reflect different degrees of activity of the same pathological processes. In milder cases, normosmolality is observed. Most often, a decrease in the level of sodium in the blood is accompanied by its hypoosmolality. Five mechanisms can lead to hypotonic hyponatremia in TBI:

1. Water intoxication.
2. Syndrome of excess production of ADH.
3. Renal and cerebral salt wasting syndromes.
4. Mineralocorticoid insufficiency.
5.Syndrome reset osmostat (osmostat's reset).

The first two mechanisms cause excess water, the second two cause sodium deficiency. The latter mechanism most likely reflects the so-called “stress norm”.

Water intoxication
Water intoxication develops more often iatrogenically, as a result of inadequate correction of hypovolemia, accompanied by water and sodium losses. Adequate replacement of water losses and insufficient correction of sodium losses lead to water intoxication. One of the arguments of the supporters of limiting the use of glucose solutions in TBI is the development of water intoxication when using these funds. The explanation is as follows: glucose is metabolized to carbon dioxide and water. As a result, when pouring glucose solutions, in fact, only water is introduced. How important this mechanism is for the development of cerebral edema and increased ICP remains unclear.

Overproduction of ADH syndrome
The syndrome of excessive production of ADH, also called the syndrome of inadequate secretion of ADH, leads to water retention in the body due to its increased reabsorption in the renal tubules. As a result, urine volume and blood sodium levels decrease. Despite hyponatremia, urinary sodium concentration exceeds 30 mEq / L due to compensatory stimulation of atrial natriuretic factor and suppression of aldosterone secretion.

Salt-wasting syndromes and mineralocorticoid insufficiency
In renal and cerebral salt-wasting syndromes, as well as in mineralocorticoid insufficiency, excessive sodium losses in the urine are noted. Their direct culprit in cerebral salt wasting syndrome is ouabain, which enhances sodium excretion by the kidneys.

The reasons for the development of renal salt wasting syndrome most often remain unclear. Perhaps previous kidney disease or genetic defects with impaired sensitivity to PNP and ouabain are important. Excessive sodium loss compared to water loss can be observed with saluretics. In mineralocorticoid insufficiency, a low aldosterone content causes impaired sodium reabsorption in the renal tubules with the development of natriuresis and hyponatremia.

The syndrome of reinstallation of the osmostat ("osmostat's reset")
In this syndrome, for unclear reasons, a new normal sodium level is established, so the kidneys do not respond to this level with compensatory changes in sodium and water excretion.

Diagnosis of hypotonic hyponatremia
For differential diagnosis the causes of hypotonic hyponatremia in our clinic uses the following algorithm (Fig. 3.2). According to this algorithm, in addition to studying the osmolality of blood and the level of sodium in it, it is mandatory to determine the osmolality of urine and the concentration of sodium in it. Sometimes pharmacological tests are needed to detail the diagnosis. In all cases, treatment begins with the introduction of hypertonic (3%) sodium chloride solutions.

High urine osmolality (more than 400 mOsm / kg water) in combination with hyponatremia indicates syndrome of excess production of ADH... At the same time, there is an increase in the concentration of sodium in the urine - more than 30 meq / l. Osmolality of urine remains almost constant when the amount of fluid and the rate of its administration change. This is a very important symptom, since in other cases of hyponatremia, infusion loading and fluid restriction cause corresponding changes in urine osmolality. Administration of a 3% sodium chloride solution temporarily increases the level of sodium in the blood without significantly affecting the sodium content in urine.

Hyponatremia and low urine osmolality can be combined with low or low high level sodium in the urine. Low sodium levels (less than 15 mEq / L) indicate water intoxication or osmostat reinstallation syndrome... To diagnose water intoxication, it is necessary to conduct a thorough analysis of the clinical picture, the composition of the administered drugs, a study of renal function and biochemical blood tests. The diagnosis of water intoxication is made by excluding all possible reasons sodium loss, except for sodium restriction in diet and as part of fluid therapy. For the differential diagnosis between these syndromes, it is necessary to administer a hypertonic sodium chloride solution. With water intoxication, this pharmacological test leads to the restoration of the sodium concentration in the blood with a gradual increase in the level of sodium in the urine.

Urine osmolality is gradually normalized. The introduction of a hypertonic sodium chloride solution with osmostat reinstallation syndrome has a temporary effect on the level of sodium in the blood. In the urine after this test, transient hypernatremia and hyperosmolality are noted.

Low or normal urine osmolality with a high sodium content in the urine (more than 30 meq / l) indicates either salt wasting syndromes (including those due to the use of saluretics) or mineralocorticoid insufficiency. The administration of a 3% sodium chloride solution causes a temporary increase in the level of sodium in the blood. At the same time, sodium losses in the urine increase. For the differential diagnosis of mineralocorticoid insufficiency and salt-wasting syndromes, the administration of drugs with mineralocorticoid effects (for example, fludrocortisone) is used.

After the use of exogenous mineralocorticoids in mineralocorticoid insufficiency, the concentration of sodium in the urine decreases and its content in the blood rises; in case of salt-wasting syndromes, these indicators remain unchanged.

Hypokalemia
A bit of physiology
For a correct assessment of the causes of hypokalemia, it is necessary to use the Gamble rule and the concept of anion gap.

According to the Gamble rule, the body always maintains the electroneutrality of the blood plasma (Fig. 3.3). In other words, the blood plasma must contain the same amount of oppositely charged particles - anions and cations.

The main cations in plasma are sodium and potassium. The main anions are chlorine, bicarbonate and proteins (mainly albumin). Besides them, there are many other cations and anions, the concentration of which is difficult to control in clinical practice. The normal plasma concentration of sodium is 140 meq / l, potassium - 4.5 meq / l, calcium - 5 meq / l, magnesium - 1.5 meq / l, chloride - 100 meq / l, and bicarbonate - 24 meq / l. About 15 meq / l is provided by the negative charge of albumin (at its normal level). The difference between the content of cations and anions is:
(140 + 4.5 + 5 + 1.5) - (100 + 24 + 15) \u003d 12 (meq / l).

The remaining 12 meq / L is provided by undetectable anions and is called the “anion dip”. Undetectable anions are ions of mineral acids secreted by the kidneys (sulfate ion, phosphate ion, etc.). When calculating the size of the anion gap, the albumin level must be taken into account. With a decrease in the level of this protein for every 10 g / l, the charge created by it decreases by 2-2.5 meq / l. The anion gap increases accordingly.

The most common cause of hypokalemia is hypovolemia. A decrease in the volume of circulating blood causes the activation of the secretion of aldosterone, which provides compensatory sodium retention. In order to maintain the electroneutrality of blood plasma during sodium retention in the body, the kidneys excrete another cation - potassium (Fig. 3.4).

Another cause of hypokalemia is an iatrogenic excess of the mineralocorticoid hormone aldosterone. In TBI, this cause can lead to hypokalemia with exogenous administration of hydrocortisone, prednisolone, dexamethasone and other corticosteroid drugs with mineralocorticoid properties (Fig. 3.5).

Similar mechanisms lead to hypokalemia with saluretic use. Furosemide and other saluretics cause sodium and water loss by blocking the reabsorption of these substances in the renal tubules. Water loss leads to secondary hyperaldosteronism, sodium retention and potassium excretion (Fig. 3.6).

Another cause of hypokalemia in TBI can be vomiting and constant active aspiration of gastric contents through a tube (Fig. 3.7). In these cases, hydrochloric acid is lost, that is, hydrogen and chlorine ions, as well as water. A decrease in the content in blood plasma of each of them can cause hypokalemia by activating various mechanisms.

Water loss induces secondary aldosteronism, and the kidneys compensatory retain sodium and excrete potassium.
A decrease in the concentration of hydrogen and chlorine ions in the blood plasma causes hypochloremic alkalosis.

Alkalosis is an excess of bicarbonate ions. To compensate for this excess and maintain a normal pH of the plasma, hydrogen ions are involved, which come from the intracellular space. In return for the lost hydrogen ions, the cells capture potassium from the plasma, and it passes into the cells. As a result, hypokalemia develops. Metabolic alkalosis and hypokalemia are a very common combination, regardless of which of them is the cause and which is the effect.

Frequent use of β-adrenergic agonists in TBI also leads to hypokalemia as a result of activation of the mechanisms of potassium redistribution from plasma into the cell (Fig. 3.8).

To clarify the etiology of hypokalemia, the study of chlorides in the urine is informative. Their high content (more than 10 meq / l) is characteristic of an excess of mineralocorticoids (hyperaldosteronism, hypovolemia). Low chloride content (less than 10 meq / l) is characteristic of other mechanisms of hypokalemia.

A bit of physiology
The main extracellular cation is sodium. The main intracellular cation is potassium. Normal concentration of ions in blood plasma: sodium - 135-145 meq / l, potassium - 3.5-5.5 meq / l. Normal concentration of ions inside cells: sodium - 13-22 meq / l, potassium - 78-112 meq / l. Maintaining a sodium and potassium gradient on both sides of the cell membrane ensures the vital activity of the cell.

This gradient is supported by the operation of the sodium-potassium pump. During depolarization of the cell membrane, sodium enters the cell, and potassium leaves it according to the concentration gradient. Inside the cell, the concentration of potassium decreases, the level of sodium increases. Then the ion level is restored. A potassium-sodium pump "pumps" potassium against the concentration gradient into the cell, and sodium "pumps out" it (Fig. 3.9). Due to the fact that the level of potassium in the blood plasma is low, insignificant changes in the concentration of this cation significantly affect its absolute value. An increase in plasma potassium from 3.5 to 5.5 meq / l, that is, by 2 meq / l, means an increase of more than 50%. An increase in the concentration of potassium inside the cell from 85 to 87 meq / l, that is, by the same 2 meq / l, is an increase of only 2.5%! It would not be worthwhile to engage in these arithmetic operations if it were not for the constant confusion with hypokalemia and hypokaligism in textbooks, journal publications and during professional discussions. You can often find "scientific" reasoning of this kind: "You never know what the level of potassium in the plasma, it is important - what it is in the cells!" Apart from the fact that in clinical practice it can be difficult to assess the level of potassium inside cells, it is fundamentally important to understand that most of the known physiological effects potassium are associated with its content in blood plasma and do not depend on the concentration of this cation in cells.

Hypokalemia leads to the following negative consequences.
Weakness of striated and smooth muscles develops. The muscles of the legs are the first to suffer, then the arms, up to the development of tetraplegia. At the same time, dysfunctions of the respiratory muscles are noted. Even with moderate hypokalemia, intestinal paresis appears due to dysfunction of smooth muscles.
The sensitivity of the vascular muscles to catecholamines and angiotensin worsens, as a result of which the instability of blood pressure is noted.
The sensitivity of the renal epithelium to ADH is impaired, resulting in the development of polyuria and polydipsia.
A very important negative consequence of hypokalemia is a decrease in the threshold for ventricular fibrillation and an acceleration of the mechanisms of circulation of the excitatory impulse through the cardiac conduction system - re-entry. This leads to an increase in the frequency of cardiac arrhythmias triggered by this mechanism. The ECG shows depression of the ST segment, the appearance of U waves, smoothing and inversion of the T waves (Fig. 3.10). Contrary to popular belief, changes in potassium levels do not significantly affect the frequency of normal (sinus) rhythm.

Long-term maintenance of hypovolemia leads to depletion of not only potassium reserves in the blood, but also in cells, that is, hypokalemia may be accompanied by hypokalygisti. Hypokaligistia has less obvious negative consequences than hypokalemia. These consequences do not develop for a long time due to the large stores of potassium in cells, but, in the end, they disrupt metabolic processes in the cell due to disruption of the potassium-sodium pump.

These pathophysiological mechanisms explain the feeling of a "black hole" known to many resuscitators, when daily administration of large doses of exogenous potassium allows maintaining the level of potassium in blood plasma only at the lower limit of the norm. Exogenously administered potassium is directed to arresting hypokalygism and it takes a long time to replenish the potassium deficiency in the body. An increase in the rate of introduction of exogenous potassium does not allow to resolve the indicated problem, since in this case there is a threat of hyperkalemia with persisting hypokalygism.

Hyperkalemia
Hyperkalemia with isolated TBI is rare. Two mechanisms can lead to its development. The first is iatrogenic. Ineffective attempts to control hypokalemia may prompt the physician to increase the rate of administration of potassium-containing solutions excessively. The intracellular sector can hold a lot of potassium. But for potassium to enter the intracellular space, a certain time is required, therefore, clinical effects develop not due to changes in the level of potassium in cells, but due to a temporary increase in the content of this ion in blood plasma.

The second cause of hyperkalemia in TBI is kidney damage due to trauma, circulatory disorders, or the use of nephrotoxic drugs. In this case, hyperkalemia is necessarily combined with oliguria and is one of the signs of the true form of acute renal failure.

The clinical manifestations of hyperkalemia are mainly associated with disturbances in heart rhythm and conduction. The ECG shows the expansion of the QRS complex, the narrowing and growth of the T wave. The PQ and QT intervals increase (Fig. 3.11). Muscle weakness is noted, as well as arterial hypotension due to peripheral vasodilation and a decrease in the pumping function of the heart.

Other electrolyte disturbances
Violations of the content of calcium, magnesium, phosphates should be assumed in the event of unexplained neuromuscular disorders. Hypomagnesemia is more common. In this regard, in case of malnutrition, alcoholism, inflammatory diseases intestines and diarrhea, diabetes, the use of a number of drugs (saluretics, digitalis, aminoglycosides), it is necessary to remember to compensate for a possible magnesium deficiency.