Obstetric peritonitis in the postpartum period

What is obstetric peritonitis in the postpartum period?

Peritonitis is an inflammation of the peritoneum, which is accompanied by a complex of severe pathophysiological reactions leading to dysfunction of all body systems. The nature and sequence of these changes are the same patterns that are observed in any inflammatory process.

Obstetric peritonitis, which is one of the most severe forms of postpartum infection, can develop as a result of the destruction of purulent formations of the uterus, appendicitis, cholecystitis, pancreatitis. However, peritonitis is most often caused by complications after cesarean section, which is currently one of the most frequently performed obstetric operations. The consequence of this is a more frequent and severe course of inflammatory complications, which make up 3/4 of all postoperative complications.

In the structure of purulent-inflammatory complications after cesarean section, the leading place in terms of frequency is occupied by complications from the wound of the anterior abdominal wall.

The higher frequency of inflammatory complications after abdominal delivery is due to several reasons:

• an incision in the uterus during cesarean section is accompanied by a violation of the integrity of the blood and lymphatic vessels, which contributes to direct bacterial invasion into the blood and lymphatic system of the uterus;
• an operation performed on the background of chorionamnionitis causes the direct spread of the infection to the peritoneum with the appearance of “early peritonitis”;
• infectious agents located in the uterine scar zone acquire the ability for rapid reproduction, their virulence increases, which leads to the spread of the process beyond the wound (myometrium, parametriums);
• the presence of a suture on the uterus contributes to the subinvolution of the uterus in the postpartum period, disrupts the normal outflow of lochia, creating favorable conditions for the reproduction of microorganisms and the occurrence of endometritis.

The clinical course and features of the pathogenesis of peritonitis after cesarean section are largely due to ways of infection of the peritoneum.

• In 30% of cases, peritonitis occurs due to infection of the peritoneum during the operation, which is performed against the background of the latent chorioamnionitis. Consequently, the source of infection in this case is the contents of the uterus, trapped in the abdominal cavity during the opening of the uterus.
• In 15% of cases, peritonitis is caused by impaired intestinal barrier function with infection penetrating the altered wall into the abdominal cavity as a result of prolonged paresis in postoperative endomyometritis.
• In 55% of cases, peritonitis develops due to the inferiority of the sutures in the uterus and their subsequent divergence (secondary peritonitis).

In some cases, peritonitis can develop when an intestinal injury occurs during surgery or when the purulent formations of the uterus rupture.

Causes of Obstetric Peritonitis in the Postpartum Period

Pathophysiological changes in peritonitis after cesarean section are determined not only by the type, virulence and number of microorganisms trapped in the abdominal cavity, but also by the state of reactivity of the microorganism, environmental factors including the prevalence and duration of the pathological process.

A single infection of the abdominal cavity during surgery is not always a decisive factor in the development of peritonitis. Of great importance in this sense is the state of the mother of the puerperal itself, its resistance to infection. It is important that every puerperal woman after cesarean section weakens the immune system due to operational stress, increased blood loss, microcirculation disorders, partial deposition of blood and other adverse factors. In addition, the response to infection in the body also depends on the state of general and organ hemodynamics, as well as the microcirculation system.

In this regard, the development of peritonitis after cesarean section as a serious risk factor is a chronic focus of infection in the form of chorioamnionitis in labor and endomyometritis in the postpartum period. The occurrence of chorioamnionitis, in turn, is directly dependent on the duration of the anhydrous period. In the presence of chorioamnionitis, cesarean section with the opening of the abdominal cavity is contraindicated.

It should be emphasized that the highest risk of peritonitis after cesarean section occurs in women with:

• exacerbation of chronic infectious diseases;
• duration of labor more than 12 hours;
• an anhydrous interval of more than 6 hours.

After cesarean section, the species composition of the microflora of the genital tract changes significantly. If before the operation, monocultures of conditionally pathogenic microflora are more often isolated, then in the postoperative period their associations are distinguished with the prevalence of enterobacteria (Escherichia, Klebsiella, Protei) and their number increases in the first days of the postoperative period. In an uncomplicated postoperative period, under the action of the immune system, the usual microflora of the genital tract gradually replaces microorganisms unusual for the birth canal. In conditions of sharply reduced reactivity of the organism in the first 3 days after the operation, the conditionally pathogenic microflora is significantly activated. The almost complete coincidence of the nature of the pathogen secreted from the vagina and uterus is determined, which may be due to both the upward penetration of the infection and the ingress of the uterus contents into the vagina.

In case of peritonitis after cesarean section, both gram-negative and gram-positive microorganisms are distinguished, and in most cases there is a mixed nature of infection. E. coli and staphylococcus are most often sown from the abdominal cavity in association with Proteus, Enterococci, Streptococcus.

Pathogenesis during obstetric peritonitis in the postpartum period

The leading value in the pathogenesis of peritonitis belongs to intoxication.

Protein toxins (polypeptides, tissue proteases), microorganisms and their metabolic products, biogenic amines (histamine, serotonin) are absorbed into the bloodstream, causing disruption of metabolic processes in tissues, causing a shift towards catabolism.

Toxic products have a pathological effect on the nerve apparatus of the intestine and central nervous system.

The oppression of metabolic processes in all tissues of the body. There is a mobilization of vascular-active substances (kinin, catecholamines, glucocorticosteroids). As a result, the function of the cardiovascular system, liver, kidney, respiratory function and hemostasis are particularly affected.

In the process of toxic damage to the cells of the body, metabolic products of arachidonic acid (throm-boxane, prostacyclin and prostaglandins) are actively involved. Prostaglandin endoperoxides are vasoconstrictors, and thromboxane accelerates platelet aggregation and is a chemotactic factor for leukocytes. Prostacyclin, having the opposite effect, inhibits platelet aggregation, being a stabilizer of membranes and thromboxane. The ratio of prostacyclin and thromboxane determines the basal tone level of most blood vessels.

The toxic effect of oxygen radicals resulting from the inactivation of complement, the accumulation of enzymes (catalase, superoxide dismutase), an increase in the concentration of glucocorticosteroids results in circulatory hypoxia, which is accompanied by a disturbance of redox processes.

The progression of intoxication with peritonitis contributes to the depletion of the neutralizing function of the liver, resulting from the action of toxins, circulatory disorders, hypoxia, depression of sympathetic and parasympathetic impulses.

Catabolic processes in peritonitis and anabolic reactions (antibody formation, tissue regeneration) require large amounts of protein. However, due to the exudation and loss of protein in the intestinal lumen, hypoproteinemia develops, which is a poor prognostic sign and leads to a significant decrease in colloid-oncotic pressure. In turn, the reduction of colloid-oncotic pressure contributes to the passage of fluid into the interstitial space, contributing to the development of pulmonary edema, myocardium, brain, uterus.

As a result of increased vascular permeability and impaired absorption processes, large amounts of fluid accumulate in the intestines.

Ecto-and endogenous fluid loss leads to disruption of the ratio between the extracellular and intracellular space. The loss of fluid by the extracellular sector is accompanied by an increase in the osmolality of the blood and the movement of water from the cells, which causes cellular hypohydration.

The syndrome of cellular hypohydration is clinically manifested by arterial hypotension. There is a decrease in diuresis, blood viscosity increases, hyperosmolar syndrome (hypernatremia and hyperchloremia) is observed.

With preserved hormonal regulation, an increase in the secretion of ADH leads to an increase in water reabsorption in the renal tubules and additional hydration of the interstitial space and blood plasma, which causes a decrease in blood osmolality. If at the same time there is a significant loss of sodium, then hypo-osmolar syndrome (hyponatremia, hypochloremia, reduction of natriuresis) is formed.

With peritonitis, there is a deficiency of potassium, which moves to the area of ​​the pathological process directly from the cells. This is accompanied by adynamia, paresis of the gastrointestinal tract, bradyarrhythmia, a violation of intracardiac conduction and contractility of the myocardium. In the terminal stage of peritonitis during the development of oliguria and renal insufficiency, the excretion of potassium by the kidneys is disturbed, leading to progressive hyperkalemia.

Violations of the CRP with peritonitis occur again and are multidirectional in nature depending on the stage of the pathological process.

Metabolic acidosis develops with the loss of bases (bicarbonates) with the contents of the gastrointestinal tract or in violation of their reabsorption (dysfunction of the tubules in renal failure). In addition, the acidotic shift causes a violation of redox processes and blood circulation.

Metabolic alkalosis occurs due to a deficit of chlorine (loss of gastric contents due to vomiting), potassium, with excessive administration of bicarbonates.

A progressive decrease in the BCC is one of the main hemodynamic disorders in peritonitis after cesarean section.

Contribute to the increase of hypovolemia: exudation and transudation into the lumen of the gastrointestinal tract, into the abdominal cavity, into the tissue of the whole body, as well as large fluid loss (vomiting, respiration, evaporation from the skin).

Hemodynamic disorders in patients with peritonitis occur in phases, characterized by a consistent change of hyper-and hypodynamic syndromes.

Cardiovascular syndrome, complicating the course of peritonitis, is formed from three simultaneously occurring processes:

• reduce the contractile function of the myocardium;
• impaired vascular tone with the development of phleboparetichesky state and a progressive decrease in the level of CVP;
• changes in BCC with a persistent decrease in plasma and globular volumes.

Increasing hypovolemia leads to a mismatch between the BCC and the capacity of the vascular bed, to the appearance of insufficiency of the peripheral circulation and impaired microcirculation.

In the early stages of the development of the disease, there is vasoconstriction, an increase in the permeability of the vascular wall for protein and water, a decrease in the oncotic pressure of the blood, and the development of precapillary edema. With the progression of the process comes the expansion of pre- and postcapillaries and venules, slowing blood flow in them and the discharge of arterial blood into the venous system through arterio-venous shunts. The speed of blood flow in the tissues slows down, in the lumen of small vessels aggregates of formed elements (sludge-syndrome) are formed, stasis and hemolysis of erythrocytes are noted.

Disruption of metabolic processes leads to the development of tissue hypoxia, acidosis, increased blood clotting, the occurrence of DIC with consumption coagulopathy.

A sharp decrease in bcc, vasospasm, centralization and decentralization of blood circulation, impaired microcirculation lead to changes in regional blood flow and aggravate circulatory disorders in the liver, kidneys and other organs, reduce venous return and cardiac output. The result of the above changes is the formation of the syndrome of multiple organ failure (cardiac, pulmonary, renal, hepatic, DIC).

A special place in the pathogenesis of peritonitis after cesarean section is occupied by intestinal paresis. Overstretching the intestinal loops with fluid and gases leads to a violation of its functions (motor, secretory and suction) and dehydration of the body.

In connection with the growth of paralytic secretion in the lumen of the small intestine accumulates a large amount of fluid containing protein and electrolytes, especially potassium. The pressure in the intestinal lumen gradually increases, its overdistension occurs, the blood flow in the intestinal wall is disturbed, tissue ischemia is formed, paresis is aggravated, and the permeability of the intestinal wall to microorganisms and their toxins increases.

The high standing of the diaphragm that occurs during intestinal paresis, a decrease in its mobility worsens the ventilation of the lungs, leads to the formation of basal atelectases, and cardiac activity suffers.

Respiratory disorders, hypoxia are aggravated by increasing pain, hypoventilation, and severe veno-arterial blood shunting.

Massive fluid loss during intestinal paresis on the background of peritonitis after cesarean section, high fever, abundant perspiration, vomiting lead to a further decrease in the BCC, cardiac output, contributing to the development of septic shock.

Symptoms of obstetric peritonitis in the postpartum period

Peritonitis after cesarean section is often diffuse, since it has no tendency to delimit.

The reaction of the peritoneum to microbial aggression is characterized by hyperemia, minor hemorrhages, permeation of the peritoneum with inflammatory exudate, rich in white blood cells and fibrin.

Exudate with obstetric peritonitis can be serous, fibrinous, purulent and combined. The nature and amount of exudate in peritonitis depends on the stage of peritonitis, the type of infectious agent, the state of the body’s immune system, the duration of the disease.

The presence of purulent exudate in the abdominal cavity in most cases coincides with the clinical signs of divergence of the postoperative suture on the uterus.

The course of obstetric peritonitis is characterized by three phases.

The first phase is initial or reactive (first 24 hours). This phase is characterized by the formation of exudate and an increase in the maximum severity of “local” clinical symptoms: abdominal pain, protective tension of the abdominal muscles, dyspeptic disorders (vomiting, diarrhea), motor agitation, an increase in the pulse rate and respiration, increased blood pressure.

The second phase is toxic (24-72 hours). In this period, “general” reactions begin to predominate: hemodynamic disorders, microcirculation develop, liver and kidney functions change, hypoxia gradually increases and tissue respiration deteriorates. Pain syndrome and protective tension of the abdominal muscles are reduced against the background of a sharp inhibition of intestinal peristalsis (paresis or paralysis), meteorism increases. A characteristic sign of the toxic phase of peritonitis is the formation of polyorgan failure syndrome.

The third phase is terminal (over 72 hours), characterized by decompensation of syndromic disorders that occur in the toxic phase of peritonitis. There is a complete absence of intestinal motility, pronounced flatulence, diffuse soreness throughout the abdomen. Hypovolemic and septic shock with polyorgan insufficiency is formed.

Treatment in the first phase of peritonitis, as a rule, is effective, and in the second and third phases, the prognosis becomes doubtful or unfavorable.

When evaluating the clinical picture of peritonitis after cesarean section, a number of factors should be taken into account.

• The clinical picture of peritonitis after cesarean section depends on the type of infection.
• The clinical picture is due to previous circumstances, the amount of blood loss and corrective therapy during surgery.
• Pronounced clinical signs of peritonitis may appear in an erased form or be absent.
• Due to the fact that during peritonitis after cesarean section no intestinal destruction occurs, functional disorders of the stomach and intestines are observed only in the toxic and terminal phases. This makes it difficult to diagnose in the reactive phase.
• Clinical manifestations depend on the nature, intensity and quality of the complex pathogenetic therapy being carried out.

Thus, in accordance with the etiology and pathogenesis, the previous course of pregnancy, the features of surgery, the microflora virulence, the stage of the disease and the body’s reactivity, the symptoms of peritonitis can be different.

The clinical course of peritonitis arising on the background of chorionamnionitis. Performing a caesarean section on the background of chorionamnionitis is a gross clinical error due to a violation of the correct prediction of the course and outcome of labor. The clinical picture of peritonitis in this situation is characterized by an early onset on days 1-2 after the operation, high body temperature, severe tachycardia, intestinal paresis. Protective tension of the abdominal muscles is missing. Symptom Shchetkina-Blumberg and abdominal pain is not expressed. Vomiting does not happen. Peristalsis of the intestine in the first 2 days of the disease is determined. After stimulation of the intestine there is a stool.

This picture is characteristic of the toxic phase. Early start eliminates the divergence of stitches in the uterus. High leukocytosis (15.0-16.0-109 / l), an increase in the number of stab leukocytes may be noted. When observed within 12-24 h, deterioration of the general condition is noted. Increasing intestinal paresis is persistent, peristalsis is not determined, measures of stimulation of the intestine are not effective. Thirst increases, tongue becomes dry, tachycardia increases. Every fifth patient develops hypotension and respiratory failure. Vomiting appears stagnant masses, there may be atony of the stomach with its significant expansion. In the absence of adequate therapy, fatal outcome occurs on the 5th – 16th day from bacterial shock or increasing cardiovascular insufficiency on the background of hypovolemia.

The clinical picture of this form of peritonitis resembles endometritis with intestinal paresis.

The clinical course of peritonitis, which develops as a result of paralytic ileus of the intestine when an infection enters the abdominal cavity through the intestinal wall. This form of peritonitis most often develops by the 3-4th day after the operation. As a rule, the development of peritonitis is preceded by the presence of endomyometritis, which is characterized by a severe course.

During the first 2 days the patient’s condition is satisfactory, the body temperature is low-grade, there is a moderate tachycardia, a transient feeling of thirst. No abdominal pain, “muscular protection” is absent, Shchetkin-Blumberg symptom is negative, intestinal paresis is noted. If within 24-40 hours it is not possible to eliminate intestinal paresis, restore hemodynamics and microcirculation in the intestinal wall, then its barrier function is disrupted and microorganisms begin to enter the abdominal cavity. In this case, the source of infection is not the uterus, but the intestine. Secondary stitches on the uterus are infected and suppuration is determined in the postoperative wound area.

The leading persistently persistent symptom is intestinal paresis, turning into paralytic obstruction. Since then, the patient’s condition worsens dramatically: severe fever, tachycardia, general depression or euphoria appear. In the abdominal cavity is determined and increased exudate. A significant amount of stagnant content accumulates in the stomach.

When comparing the first two forms, the following features can be distinguished.

• The first type is characterized by early onset at 1-2 days, severe intoxication, recurrent paresis.
• In the presence of a complication in the second type, there is first marked unexpressed intoxication, increasing paresis. From the 3-4th day, signs of intoxication, exudation into the abdominal cavity, transudation into the intestine appear and quickly aggravate.
• Both clinical forms have common features: there is no muscle defense syndrome and Shchetkin-Blumberg symptom.

Peritonitis due to inferiority of stitches in the uterus. This form of peritonitis is characterized by a relatively late start on the 4-9th day.

Peritonitis develops gradually. Initially, there is a soreness of the uterus, defined symptom Shchetkina-Blumberg, unexpressed muscle tension. At the same time, intestinal paresis occurs. In the abdominal cavity is determined by the exudate. On the background of increasing intoxication, the patient is worried about pain. For a relatively short period of time (4-12 hours), the patient’s condition worsens, the reactive phase is replaced by a phase of intoxication.

Diagnosis of obstetric peritonitis in the postpartum period

Diagnosis of peritonitis after cesarean section in some cases may present certain difficulties due to insufficiently expressed symptoms. By itself, the diagnosis of peritonitis inevitably entails a traumatic surgical intervention.

Early diagnosis of peritonitis is necessary due to the fact that in the reactive phase of the disease treatment can be effective, while in the phase of intoxication the prognosis becomes doubtful.

In establishing the diagnosis of peritonitis after cesarean section, the assessment of the dynamics of the clinical picture against the background of therapy is of great importance. It is necessary to pay attention to the recurrence of symptoms and increasing signs of intoxication.

There is a discrepancy between the clinical symptoms of postoperative peritonitis and laboratory signs of a developing complication, which is manifested in the delay of laboratory data with a bright clinical picture of peritonitis.

Laboratory diagnosis

• According to the results of a clinical analysis of blood, there is an increase in the total number of leukocytes, a shift in leukocyte formula towards the young and stab cells, the appearance of toxic granularity of neutrophils, and anemia. Leukopenia with an increasing shift of the leukocyte formula to the left is a poor prognostic sign of peritonitis.
• According to the biochemical analysis of blood, there is hypo- and dysproteinemia, hypokalemia (with the development of renal failure – hyperkalemia); metabolic acidosis or alkalosis.
• When studying a coagulogram, coagulopathy and thrombocytopathy are detected.
• In the general analysis of urine, a decrease in the relative density of urine, the appearance of protein, hyaline and granular cylinders are noted.

Echographic criteria for peritonitis

According to the echographic study, when peritonitis is detected:

• free fluid in the uterine-rectus space, lateral channels of the abdominal cavity, between the intestinal loops, under the liver and the diaphragm;
• accumulation of gas and liquid in overstretched intestinal loops;
• weakening or absence of intestinal motility.

The X-ray picture of paralytic intestinal obstruction is characterized by overstretching of the intestinal walls with the presence of multiple horizontal fluid levels and Kloyber bowls.

Laparoscopy is performed in cases where the clinical symptoms do not allow a differential diagnosis between endometritis and peritonitis.

Treatment of obstetric peritonitis in the postpartum period

Treatment of peritonitis should be comprehensive. Surgical treatment in all patients is combined with intensive conservative therapy.

In the clinical form of peritonitis caused by infection of the peritoneum during surgery on the background of chorionamnionitis, conservative therapy may be the decisive method that will help localize and neutralize the infection. With intensive pathogenetically substantiated therapy, a favorable outcome is possible. However, it should be borne in mind that conservative therapy should be carried out no more than within a day.

Peritonitis, developing as a result of intestinal paresis, can be prevented provided proper therapy is provided in the first days after surgery. However, if peritonitis has already occurred, then with this form of delay with the operation is unacceptable.

Peritonitis, the source of which are defective sutures on the uterus, occurs somewhat later, proceeds quite typically and dictates active surgical tactics.

Of course, only one surgery for peritonitis does not eliminate the development of the pathological process. It is necessary to conduct complex therapy.

Surgical treatment. The purpose of the operation in obstetric peritonitis is to remove the source of the infection – the infected uterus and drain the abdominal cavity. The uterus must be removed along with the fallopian tubes. Removal of the ovaries (a) is justified only in the presence of pyovar or tubo-ovarian purulent formation.

The technical features of the operation include:

• aspiration of the pathological effusion from the abdominal cavity (removal of exudate during drainage is necessary because it contains a large number of biologically active substances that cause a violation of microcirculation, hemostasis);
• restoration of normal anatomical relationships between the organs of the abdominal cavity and the small pelvis (separation of adhesions by blunt and acute means);
• revision of the abdominal organs;
• transnasal intubation of the small intestine probe with extensive adhesions to prevent intestinal obstruction;
• thorough rehabilitation of the abdominal cavity with antiseptic solutions (dioxidine, chlorhexidine, ozonized isotonic sodium chloride solution, sodium hypochlorite);
• stitching the anterior abdominal wall with separate sutures through all layers into two floors (peritoneum – aponeurosis and subcutaneous fatty tissue – skin) to prevent the development of postoperative eventration and hernias;
• drainage of the abdominal cavity; the main drains (2) are always injected transvaginally, in addition to them, transabdominally through contraceptives in the mesogastral and epigastric areas to the places of greatest destruction spend 2-3 additional drainage.

Infusion and detoxification therapy.

As part of infusion-transfusion therapy, a variety of therapeutic measures are performed.

Detoxification therapy is carried out by the method of controlled hemodilution with forced diuresis. To perform this procedure, blood substitutes of directional action and solutions with a balanced ionic composition are used under monitor monitoring of indicators of the colloid-osmotic state.

Therapy begins with the introduction of solutions of colloids 400-1000 ml / day (reopolyglukine, reoglyuman, gelatinol, infukol HES 6% or 10%, albumin and FFP), which improve the rheological properties of blood, reduce the pathological permeability of the vascular wall for protein and water.

The introduction of hemodez causes the binding and elimination of toxins from the body, increases diuresis and lymph flow.

The use of fresh blood, red blood cell mass eliminates anemia and hypoxia, stimulates the protective functions of the body.

The use of solutions of plasma, protein and albumin contributes to detoxification, improve the rheological properties of blood, eliminate violations of protein metabolism and BCC, restore hemodynamics.

In case of severe disease, large amounts of fluid (up to 4-6 liters) are administered with simultaneous use of forced diuresis. To do this, use 1000 ml of crystalloids, 500 ml of 3% sodium bicarbonate solution and 400 ml of reopolyglukine, then 20 mg of lasix in combination with antispasmodics after each liter of injected liquid, then 1000-1500 ml of protein preparations (albumin, plasma, amino acids) with hourly diuresis.

Elimination of rheological disorders and correction of blood coagulation properties. Against the background of severe intoxication and deep metabolic disturbances, hypercoagulative processes develop and the risk of thrombosis and thromboembolism increases.

To improve the rheological properties of blood, microcirculation and prevention of DIC, anticoagulants, antiplatelet agents, vasoactive drugs are used under the control of the state of the hemostasis system.

The average daily dose of heparin is 10 000 IU per day. Heparin not only has an anticoagulant effect, but also has the ability to increase immunological reactivity and positively affect local inflammatory processes.

More effective is the appointment of LMWH: fraxiparin, 0.3 ml 1 time per day, clexane at a dose of 0.2 ml 1 time per day.

The composition of infusion therapy include reopolyglukine in combination with trental 100-200 mg / day.

Elimination of violations of water-electrolyte metabolism and restoration of the acid-base state. In case of metabolic acidosis, the introduction of 4% solution of sodium bicarbonate in the amount of 150-200 ml or buffer solutions is recommended.

In hypokalemic alkalosis, administration of solutions containing potassium is indicated (4% potassium chloride solution). The daily dose should not exceed 6-12 g. Potassium preparations are administered under the strict control of its content in blood serum.

Normalization of hemodynamic parameters and circulating blood volume. Cardiac glycosides, corticosteroids, ATP, cocarboxylase and tren-tal are used to solve this problem. Prescribed prednisone in a daily dose of 90-120 mg with a gradual decrease and cancellation of the drug in 5-7 days.

Elimination of disorders in the immune system of the body. Stimulation of non-specific protective forces of the body consists in the use of solutions of immunoglobulins (pentaglobin, intraglobin, normal human immunoglobulin), interferon and its inducers (cycloferon).

Antibacterial therapy.

Conducting antibiotic therapy is advisable only against the background of infusion and restorative treatment by intravenous administration. Antibacterial therapy is carried out simultaneously with two or three drugs, preferably taking into account the sensitivity of microflora. The combination of antibiotics should include cephalosporins (kefzol, fortum, cefamezin, claforan), aminoglycosides (gentamicin), nitroimidazole group antibacterial drugs that are effective against anaerobic flora (trichopol, tinidazole, metrogil). The treatment is carried out with maximum single and daily doses of antibiotics. Duration of therapy is 7-10 days.

Given the possibility of intestinal dysbiosis, candidiasis of the mucous membranes in patients receiving massive doses of antibiotics, the use of eubiotics (bifidumbacterin and lactobacterin) and antifungal drugs (nystatin, levorin, diflucan, amphotericin B) should be included in the therapy complex.

Within 12-20 hours on clinical grounds, it is possible to establish the effectiveness of antibiotic therapy. The reduction of tachycardia, stabilization of blood pressure, elimination of discrepancies between heart rate and body temperature, improvement of sleep and appetite are especially indicative in this sense. If necessary, long-term use of antibiotics after 7-8 days they are changed.

Hormone therapy.

Given the severity of stressful situations in peritonitis and impaired adrenal function, an important component of the complex treatment of peritonitis is the use of glucocorticosteroids. With normal blood pressure, the patient should receive 60-80 mg of prednisone per day. If there is a tendency to hypotension, the doses of prednisolone may be increased.

Elimination of intestinal paresis. An important aspect of the treatment of peritonitis is the elimination of intestinal paresis and the prevention of paralytic obstruction by restoring the balance of electrolytes and, above all, the elimination of hypokalemia. It should be taken into account that in patients with peritonitis, hypokalemic alkalosis often occurs, the treatment of which is crucial for the restoration of bowel function. In this regard, shows the introduction of 6-12 g of potassium during the day. Potassium preparations are administered under the careful control of diuresis. Potassium deficiency is restored only with a stable diuresis.

When the paralytic state of the intestine fluid loss is large enough. Fluid deficiency reaches 4-6 liters.

In the postoperative period, it is also advisable to conduct “soft”, physiological stimulation of the intestine, which is achieved by applying:

• adequate pain relief;
• rational infusion therapy in the mode of normal or minor hypervolemia;
• preemptive use of drugs metoclopramide (Reglan, raglan).

Only in the absence of the effect of the above methods is shown to stimulate the motility of the gastrointestinal tract with the help of prozerin, kalimin, ubretida.

Syndromic therapy of hypovolemic shock, pulmonary, cardiac, renal-hepatic failure, elimination of CNS dysfunction.

With the development of pulmonary insufficiency, the patient is transferred to a ventilator in the mode of moderate hyperventilation with positive pressure at the end of expiration. Control of CVP allows detecting increasing pulmonary hypertension and preventing pulmonary edema.

Treatment of hepatorenal syndrome includes the use of all methods of detoxification (hemosorption, hemodialysis, plasmapheresis, peritoneal dialysis).

Normalization of parenchymal organ function and tissue metabolism. To normalize the function of parenchymal organs and tissue metabolism, glutamic and folic acids, cocarboxylase, cerebrolysin, nootropil, cardiac glycosides, Essentiale, protease inhibitors (trasilol, contrycal, gordox) are administered.

Daily doses of gordox are 300’000-500’000 U, contrikal – 800’000-1’500’000 U and trasilola 125’000-200’000 U.

In the process of treatment, it is necessary to constantly monitor diuresis, the nature of the pulse, the amount of blood pressure, the frequency of respiratory movements, KOS.