Peritonitis

Peritonitis is characterized by severe general symptoms, including endogenous intoxication and multiple organ failure. Mortality in peritonitis has always remained one of the highest and reached 55-90% in postoperative surgical peritonitis. Despite the fact that such a formidable complication as peritonitis after cesarean section is currently relatively rare (0.2-0.8%), mortality in this form of purulent-septic diseases remains high and reaches 26-35%.

Peritonitis is an inflammation of the peritoneum, accompanied by the development of severe intoxication of the body. Peritonitis is understood as a diffuse spread of inflammation.

Local inflammations are defined as abdominal abscesses (limited peritonitis). Peritonitis is a secondary process that complicates the course of the underlying disease. Idiopathic (primary) peritonitis, when the source has not been identified in the last 20 years, does not occur at all and is excluded from the classification.

In diffuse peritonitis, according to the prevalence in the peritoneum, a distinction is made between: local peritonitis, when a part or one anatomical region of the cavity is affected; widespread peritonitis, when the process affects several areas, diffuse (general), with damage to the entire peritoneum. The severity of intoxication is explained by the enormous extent of the peritoneum - almost 10 sq. m with high exudation by the visceral layer and resorption by the parietal. Therefore, toxins quickly and in large quantities enter the blood.

According to etiology, peritonitis is divided into bacterial (infectious), developing with inflammatory diseases of internal organs or perforations of hollow organs, as well as with injuries; and aseptic peritonitis, when the inflammatory process of the peritoneum is caused by either irritating chemicals or biological fluids - bile, urine, blood. Exudate can be: serous, hemorrhagic, fibrinous, purulent, putrefactive. The clinical course is: acute, subacute and chronic. In acute peritonitis, reactive, toxic and terminal stages of the course are distinguished.

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Causes of peritonitis

Primary peritonitis is an inflammatory process that develops without disruption of the integrity of hollow organs, the result of spontaneous hematogenous dissemination of microorganisms into the peritoneal lining or translocation of a specific monoinfection from other organs.

Types of primary peritonitis:

• Spontaneous peritonitis in children.
• Spontaneous peritonitis in adults (ascites peritonitis, dialysis peritonitis, etc.).
• Tuberculous peritonitis

The causative agent is usually a certain type of microorganism. Secondary peritonitis is the most common type of the disease, it unites all forms of inflammation of the peritoneum that develops as a result of destruction or injury of the abdominal organs.

Types of secondary peritonitis:

• Peritonitis caused by perforation and destruction of abdominal organs.
• Postoperative peritonitis.
• Posttraumatic peritonitis:
  • in case of closed abdominal trauma,
  • for penetrating abdominal wounds

Tertiary peritonitis is an inflammation of the peritoneum of a “recurrent” nature (“persistent” or “recurrent” peritonitis).

It develops in the absence of infection sources and/or after surgery for secondary peritonitis, performed in full, but against the background of severe depletion of the body's defense mechanisms. The course of this form is characterized by an erased clinical picture, possible multiple organ dysfunction and manifestation of endotoxicosis, refractory to the treatment. The source of the pathological process is rarely established.

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Microbiological structure

Despite the diversity of microorganisms living in the intestine, only some of them can cause peritonitis. This is explained by the fact that a significant part of intestinal bacteria are strict anaerobes (they die in the presence of oxygen), while others are sensitive to the bactericidal factors of the peritoneum. Due to differences in the source of bacterial contamination of the abdominal cavity and the conditions of development of the pathological process, several forms of peritonitis (community-acquired or hospital-acquired) are distinguished.

Primary peritonitis

Primary peritonitis is an infection caused by one type of bacterial agent, developing in patients with liver cirrhosis (E. coli, Enterobacter spp., Citrobacter freundn, Klebsiella spp., S. vindans, S. pneumoniae, group B streptococci, in rare, severe cases - S. aureus) or in patients undergoing peritoneal dialysis (coagulase-negative staphylococci, in the most severe forms - S. aureus (MRSA), in case of nosocomial infection - Enterococcus spp., P. aeruginosa, rarely - Candida spp.).

Secondary peritonitis

The main pathogen in secondary peritonitis is E. coli (56-68%), less often Klebsiella spp (15-17%), P. aeruginosa (15-19%), Enterobacter spp. (6-14%), Citrobacter spp., Serratia marcescens and Morganella morganii. Often the main pathogen is associated with streptococci (26-35%) and enterococci (10-50%). Mixed (aerobic-anaerobic) flora is almost always found in patients with secondary peritonitis, with anaerobes represented mainly by the group Bacteroides spp., to a lesser extent Clostridium spp., Fusobacterium spp., Peptostreptococcus spp.

The causes of intra-abdominal infections in the postoperative period are somewhat different, with Enterococcus spp., coagulase-negative staphylococci, Enterobacter spp., Acinetobacter spp., and P. aeruginosa being the most common. With the development of complications against the background of immunosuppression, the likelihood of fungal infections increases, with the main pathogen being C. albicans.

Causes of peritonitis associated with pelvic infections in women include group B streptococci, N. gonorrhoeae, Prevotella spp., Peptococcus spp., Mobiluncus spp.

Pathogens when the source of infection is localized in the biliary tract are Enterobactenaceae and Enterococcus spp.

Tertiary peritonitis

The pathogen in tertiary peritonitis often cannot be identified, but careful microbiological examination usually reveals multidrug-resistant enterococci, coagulase-negative staphylococci and C. albicans, less commonly Pseudomonas aeruginosa and enterobacteria. The role of anaerobes in tertiary peritonitis is not completely clear.

How does peritonitis develop?

The pathogenesis of peritonitis is very complex, it depends on the cause, virulence, microflora, state of reparative processes, presence of aggravating factors. The main factors determining the severity of the course are:

1. large loss of water, salts and proteins into the abdominal cavity and intestines, which are in paresis; per day, fluid loss is up to 4-8 liters, which leads to dehydration, hypovolemia, the development of cardiac and respiratory failure, acidosis;
2. the rate and volume of absorption of toxins from the surface of the peritoneum, which is determined by the prevalence of peritonitis and the state of delimitation;
3. autointoxication caused by anaphylaxin (it is formed when microbial lipopolysaccharides bind to antibodies and blood complements), which forms polyallergy and is the trigger for the development of intoxication syndrome.

With weakened reparative processes or massive invasion, delimitation does not develop and peritonitis takes the form of diffuse, with a slowdown with surgery, the process progresses. Delimitation is also hampered by hyperperistalsis, characteristic of the first hours of peritonitis, depleted omentum, the presence of blood and exudate in the abdominal cavity.

Symptoms of peritonitis

Clinical signs are largely determined by the cause of peritonitis, the localization of its source, and the duration of the disease. The results of treatment and outcome depend on the time of diagnosis and the timing of laparotomy, so it is important to know the early signs of this disease.

The earliest and most constant symptom of peritonitis is abdominal pain, which may arise suddenly, which is typical for perforation of hollow organs and disruption of mesenteric blood circulation, or develop gradually, which corresponds to an inflammatory-destructive process of any organ of the abdominal cavity. Localization of pain depends on the location and nature of the pathological process (the cause of peritonitis), but rather quickly becomes widespread. Abdominal pain is intense, intensifies with a change in body position, often accompanied by vomiting of gastric contents, which does not bring relief. The patient's position is forced "constrained", the abdomen does not participate in the act of breathing, its wall is tense.

On palpation, pain is felt in all parts of the abdomen, more pronounced in the projection of the pathological process. A positive Shchetkin-Blumberg symptom and symptoms characteristic of the disease are the causes of peritonitis. As the process progresses, the tongue becomes more dry, tachycardia, tension and pain in the abdominal wall increase, intestinal paresis occurs, stool retention and gas discharge are possible, signs of a systemic inflammatory reaction, dehydration and endotoxicosis appear.

Diffuse peritonitis

Symptoms of diffuse peritonitis are polymorphic. They depend on the primary focus and stage of the process; The volume and type of exudate (except for hemoperitoneum) do not have a significant impact on the clinical picture.

In the first 24 hours (reactive phase) the leading symptoms are as follows. The pain is sharp, constant, increasing with attempts to move, cough, deep breathing, palpation. To spare the abdomen, the patient takes a forced position: in case of local pain, presses the affected area with hands; in case of diffuse pain, lies on the back with legs drawn up, pressing the abdomen with hands during coughing. Dehydration: manifests itself as thirst, dry tongue, skin, tachycardia. Symptoms of tension and irritation of the peritoneum: the abdomen is drawn in, flat, does not participate in the act of breathing, tense to a "board-like" state; palpation is sharply painful over the affected organ or throughout the abdomen in case of diffuse peritonitis; positive symptoms of peritoneal irritation - Shchetkin-Blumberg symptom and others, specific for each affected organ. Hyperperistalsis is visible to the eye or determined by increased intestinal noise. Not obligatory, but may be: vomiting, diarrhea, tenesmus. In blood tests, leukocytosis, neutrophilia, ESR, LII, FSM increase rapidly, by the hour. These laboratory indicators are used for differential diagnostics, conducting dynamic hourly studies.

If surgical intervention is not performed, the toxic phase of peritonitis develops in the following 2-3 days, which is determined by the formation of intoxication syndrome, prevailing over local manifestations. Intoxication develops quickly and is very pronounced: facial features become sharper, the skin is pale, with an earthy tint, cyanosis of the lips, sunken eyes (Hippocratic face), the tongue is dry as a brush, may be varnished, hypotension, hypovolemia, tachycardia, hyperthermia increase.

Local manifestations decrease in severity, but the process itself increases and spreads throughout the abdominal cavity. Abdominal pains subside, become aching, they are constant, but spread throughout the abdomen. The protective tension of the abdominal wall is smoothed out, the Shchetkin-Blumberg symptom is less pronounced, but spreads throughout the abdomen. Peristalsis disappears, intestinal paresis develops, which is revealed by the symptom of "dead silence" during auscultation of the abdomen, the abdomen swells.

In the adynamic stage, contact with the patient is difficult due to the blockage or impossible due to the coma. Intoxication is pronounced, accompanied by the development of hypovolemic shock. The abdomen is swollen, the intestines are paresis, symptoms of abdominal wall tension and peritoneal irritation are not expressed, with a large effusion, fluid fluctuation is determined. Vomiting is uncontrollable, with a fecal odor.

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Limited peritonitis

The state of reparative processes is important in pathogenesis, on which the delimitation of the process depends. Inflammation of the peritoneum causes a vascular reaction with exudation of plasma and blood cells. Fibrin precipitates from the plasma, which acts as glue, holding the intestinal loops and omentum together around the affected organ. Adhesions, initially loose, become denser, and an inflammatory infiltrate forms in the abdominal cavity, with the inflamed organ in the center. If this organ is destroyed, an abscess forms in the abdominal cavity, called delimited peritonitis. The most common localization of abscesses is Douglas abscess, subhepatic and subdiaphragmatic spaces, interintestinal abscesses. If the inflammation is stopped, the infiltrate slowly resolves.

Appendicular infiltrate and abscess - develops with non-operated acute appendicitis, more often with late presentation of patients, use of heating pads, etc.

In this case, the inflammation zone is first delimited by the omentum, then the intestinal loops are soldered, forming an elastic, dense, painful infiltrate. The condition of patients improves, the pain becomes less, the symptoms of peritoneal irritation disappear. Such patients are treated conservatively: massive anti-inflammatory therapy, cold on the abdomen; with constant monitoring of the process - the boundaries of the infiltrate are outlined with a marker. If the appendix is not destroyed and the inflammation is stopped, the infiltrate resolves in 2-3 weeks.

When the appendix is destroyed, an abscess is formed in the center of the infiltrate: abdominal pain does not subside, and even begins to progress, signs of intoxication appear, the abdomen becomes tense, painful when palpating over the infiltrate, there may be a Shchetkin-Blumberg symptom, the size of the infiltrate increases. In this case, surgical intervention is indicated, the volume of which depends on the findings

Douglas abscess is a limited accumulation of pus in the rectovesical (in men) and rectovaginal (in women) recesses of the small pelvis.

An abscess can develop with any pathology of the peritoneal cavity, when the exudate shifts to the small pelvis, is delimited and suppurates, the delimitation, as a rule, is quite powerful, but a breakthrough of pus into the abdominal cavity with the development of peritonitis can be. The clinical picture has characteristic features: high body temperature; the difference between the temperature in the armpit and rectum is more than 1 degree (Lennander's symptom); pain in the suprapubic area with deep palpation, overhanging rectal wall or bulging posterior vaginal fornix, a dense, painful, immobile infiltrate with softening in the center is determined by palpation. Tenesmus, frequent urination are characteristic. On radiographs standing in the small pelvis, gas with a fluid level, ultrasound reveals fluid in the small pelvis. In doubtful cases, puncture through the vagina or rectum.

Interintestinal abscess is quite difficult to detect, the starting points are the presence of intoxication, which does not decrease despite active therapy, prolonged intestinal paresis, pain during abdominal palpation, the presence of symptoms of peritoneal irritation to varying degrees. Given the poor delimitation of these abscesses, diffuse peritonitis often develops, so early relaparotomy is preferable to wait-and-see tactics.

Subdiaphragmatic abscess is an intraperitoneal abscess located in the subdiaphragmatic space.

The subdiaphragmatic space is divided into 2 parts - intraperitoneal and retroperitoneal.

An abscess most often forms in the intraperitoneal part - left-sided and right-sided, which communicates with the subhepatic space, where an abscess can also form. The causes are varied, they can be divided into 4 groups:

1. caused by pathology of the abdominal organs;
2. pathology of the pleural cavity;
3. purulent pathology of the kidneys;
4. mixed form, mainly with thoracoabdominal wounds.

The clinical picture is polymorphic, has an erased, atypical form, especially with massive antibacterial therapy. But some manifestations are characteristic: previous abdominal trauma, surgery or acute pathology of the internal organs of the abdominal cavity; persistent intoxication, despite active anti-inflammatory treatment; pain in the right hypochondrium, lower chest, back, right half of the abdomen, increasing with coughing, body movements, deep inspiration, which is accompanied by a dry cough (Troyanov's symptom). Patients acquire a forced semi-sitting position, the skin is pale, the sclera is subicteric, the intercostal spaces in the lower part of the dural cell are smoothed, the skin is pasty, the skin fold is thickened, there may be hyperemia of the skin. The same is noted with a retroperitoneal location of the abscess, "psoas syndrome" is often detected.

The anterior abdominal wall lags in the act of breathing, is painful on palpation, the diaphragm is high, its mobility is limited. Palpation of the XI-XII ribs on the right, especially at the place of their fusion at the costal arch, is painful (Kryukov's symptom). On radiographs, against the background of the high position of the diaphragm dome, gas with a horizontal border of liquid is sometimes visible. Early diagnosis can be made by ultrasound. Treatment is surgical, the method depends on the type of abscess.

Diagnosis of peritoneal pathology at home is based on the presence of: constant abdominal pain, maximally in the area of the affected organ or evenly throughout the abdomen, dry tongue, tachycardia. In all cases, the patient must be taken to a surgical hospital as an emergency aid.

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Classification of peritonitis

A distinction is made between primary and secondary peritonitis.

Primary (idiopathic) peritonitis is an infection of the peritoneum by hematogenous or lymphogenous routes (without the presence of a purulent focus in the abdominal cavity).

Secondary peritonitis is the spread of infection to the peritoneum from purulent-destructive foci of the abdominal cavity.

Depending on the extent of damage to the peritoneum during peritonitis and the degree of involvement of anatomical areas, the following types of peritonitis are distinguished:

• local (damage to one anatomical area);
• widespread (damage to several anatomical areas);
• general (diffuse) - damage to all parts of the abdominal cavity.

According to another classification, depending on the characteristics of the spread of the inflammatory process (virulence of the pathogen, the body's ability to delimit the purulent focus due to the immune system, neighboring organs, peritoneum, omentum, fibrin deposits), a distinction is made between diffuse peritonitis (also known as general or diffuse) that does not have a tendency to delimit and delimited peritonitis (essentially encapsulated abscesses of the abdominal cavity). Examples of delimited surgical peritonitis are appendicular, subdiaphragmatic, subhepatic, and interintestinal abscesses.

In gynecology, examples of limited peritonitis may include the following diseases: pyosalpinx, pyovar, purulent tubo-ovarian formation (tubo-ovarian abscess), abscess of the Douglas space, and the uterus in the development of abscessing panmetritis. Symptoms, diagnosis and treatment of these diseases, as well as extragenital purulent foci.

In clinical practice, the term peritonitis usually refers to diffuse damage to the peritoneum, and henceforth, when using this term, we will mean diffuse peritonitis.

According to the type of clinical course, acute, subacute (sluggish) and chronic peritonitis are distinguished; some authors distinguish a fulminant form of the disease.

Acute peritonitis is a rapidly progressing severe disease, usually with a typical clinical picture, alternating phases of the disease and, in the absence of surgical treatment, quickly leading to death.

Subacute (sluggish) peritonitis is characterized by a longer course, more frequent delimitation of the purulent process and the formation of encapsulated abscesses, often with their subsequent perforation into adjacent hollow organs.

Chronic peritonitis is extremely rare, mainly with specific damage to the peritoneum (for example, carcinomatosis or tuberculosis).

Fulminant peritonitis is essentially peritonitis complicated by septic shock.

During the course of peritonitis, three stages (phases) are distinguished: reactive, toxic and terminal. The reactive stage in acute peritonitis lasts on average about a day, the duration of the toxic and terminal stages is variable and depends on many reasons (massiveness and nature of bacterial invasion, "volume" of the primary purulent focus, immunocompetence of the patient, nature of the treatment). According to the nature of the exudate, peritonitis is divided into:

• serous;
• fibrinous;
• purulent;
• hemorrhagic;
• uric;
• fecal.

It is impossible not to single out postoperative peritonitis separately.

N.A. Efimenko (1999) believes that primary postoperative peritonitis occurs after planned surgical interventions due to three main reasons:

• insufficiency of anastomotic sutures,
• intraoperative infection of the abdominal cavity,
• technical errors or mistakes in performing the operation.

Secondary postoperative peritonitis is the progression of peritonitis that was present during the first emergency surgical intervention.

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Diagnosis of peritonitis

The anamnesis of patients with peritonitis often includes inflammatory diseases of the abdominal cavity and pelvic organs, abdominal trauma, gastrointestinal ulcers of various localizations, cholelithiasis, previous laparotomies, and neoplastic processes.

When interviewing a patient, it is necessary to find out the duration of the disease, changes in the nature and localization of pain, the dynamics of manifestations, and signs of complications.

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Physical examination

It is necessary to pay attention to the severity of signs of systemic inflammatory reaction and organ dysfunction temperature, heart rate, blood pressure, frequency and depth of breathing, level of consciousness, condition of mucous membranes. In patients with peritonitis, tachycardia is more than 100-120 per minute, blood pressure can be increased or decreased, respiratory rate is more than 20 per minute. Manifestation of toxic encephalopathy - inhibition, agitation of the patient or delirium.

The abdomen is symmetrical, does not participate in the act of breathing, and is sharply painful upon palpation.

Rectal and vaginal examination reveals overhanging vaults and pain due to accumulation of inflammatory exudate.

Laboratory research

In laboratory studies, peritonitis is characterized by signs of increasing liver and kidney failure, uncontrolled decrease in protein levels, signs of azotemia, inflammatory changes in white blood cells, and anemia.

The simplest and most reliable method of laboratory diagnostics of purulent-inflammatory diseases of the abdominal organs is the determination of the leukocyte intoxication index (LII) (the formula was initially proposed for the diagnosis of acute appendicitis), in the calculation of which the modified formula of Ya. Ya. Kalf-Kalif is used.

LII = 32 Pl + 8 Mi + 4 Yu + 2 P + S/16 E +

2 B + Mo + L (norm 1.08±0.45),

Where Pl are plasma cells, Mi are myelocytes, Yu are juvenile neutrophils, P are band neutrophils, S are segmented neutrophils, E are eosinophils, B are basophils, Mo are monocytes, L are lymphocytes.

A promising additional laboratory indicator for the diagnosis of abdominal sepsis and peritonitis is the concentration of procalcitonin in blood plasma. This indicator is a marker in the differential diagnosis of SIRS of septic and abacterial origin, in particular, sterile and infected forms of pancreatic necrosis, acute respiratory distress syndrome, infected and uninfected intra-abdominal fluid collections. An excess of procalcitonin concentration in plasma above 2 ng/ml is a criterion for the development of a septic process. The indicator serves as a valuable aid in deciding on the tactics of surgical or intensive conservative treatment of purulent-septic complications in abdominal surgery.

Instrumental research

Instrumental methods of examination allow to identify the causes of peritonitis. Thus, in case of perforation of hollow organs, a strip of free gas under the diaphragm is visible on a survey radiograph, in case of acute cholecystitis, an ultrasound examination shows an enlarged gallbladder with heterogeneous contents, stones and a doubling of the contour of its wall. The same examination allows to identify free fluid in the abdominal cavity or an infiltrate in the ileocecal region in case of acute appendicitis.

Increased endotoxicosis, tension and pain in the anterior abdominal wall upon palpation, pronounced Shchetkin-Blumberg symptom do not require additional research methods. In case of an erased clinical picture, especially in elderly people, diagnostic laparoscopy should be performed to clarify the diagnosis and extent of the pathological process. Cloudy exudate in the abdominal cavity, fibrin threads on the visceral peritoneum, bile leakage, perforation or contents of the stomach or intestine in the free abdominal cavity and other pathological changes are visible.

Early signs of secondary peritonitis (signs of underlying diseases) are diagnosed using ultrasound of the abdominal cavity and retroperitoneal space, X-ray examination of the abdominal cavity and chest, CT, and, as the final stage of diagnosis, diagnostic laparoscopy is performed.

Objective assessment of the severity of the condition and prognosis in patients with peritonitis

An objective assessment of the severity of a patient's condition takes into account a large number of factors.

Integral scales for assessing the severity of the condition (APACHE, APACHE II, APACHE III, SAPS, SAPS II, SOFA, MODS) and scales that take into account the characteristics of peritonitis (Mannheim Peritonitis Index - MPI, Prognostic Index of Relaparotomies - PIR) are widely used.

Individual homeostasis parameters are used as independent predictors of adverse outcome.

Systemic inflammatory response syndrome and objective assessment of the severity of the condition in peritonitis

The basis of the modern understanding of the body's response to infection is the concept of abdominal sepsis (a pathological process based on the body's reaction in the form of generalized inflammation in response to a surgical infection in the abdominal cavity). The clinical interpretation of this view on the pathogenesis of sepsis (including abdominal) is the criteria for the diagnosis of SIRS and the classification of sepsis proposed by the consensus conference of the American College of Chest Physicians and the Society of Critical Care Medicine Specialists - ACCP/SCCM.

In abdominal sepsis caused by widespread peritonitis, there is a correlation between the severity of SIRS (three signs of SIRS - SIRS-3, four signs of SIRS - SIRS-4, severe sepsis, septic shock) and the severity of the patient's condition according to the severity assessment scales - APACHE II, SAPS, MODS, SOFA.

Mannheim Peritonitis Index (MPI)

M. Linder and a group of German surgeons from Mannheim developed an index for the prognosis and outcome of purulent peritonitis, which included 8 risk factors:

1. patient's age,
2. floor,
3. organ failure,
4. the presence of a malignant neoplasm,
5. duration of peritonitis before surgery more than 24 hours,
6. generalized peritonitis,
7. site of the primary lesion,
8. type of peritoneal exudate.

MPI values can range from 0 to 47 points. MPI provides for three degrees of peritonitis severity. With an index of less than 21 points (severity degree I), the mortality rate is 2.3%, from 21 to 29 points (severity degree II) - 22.3%, more than 29 points (severity degree III) - 59.1%. A formula for calculating the predicted mortality rate based on MPI is also proposed.

Mortality (%) = 0.065 x (MPI - 2) - (0.38 x MPI) - 2.97. However, even with the help of this specially developed scale, it was impossible to predict the outcome in a specific patient and determine treatment tactics.

Mannheim Peritonitis Index

Age over 50 years	1
Female gender	5
Presence of organ failure	7
Presence of a malignant tumor	4
Duration of peritonitis more than 24 hours	4
The colon as a source of peritonitis	4
Diffuse peritonitis	6
Exudate (only one answer)
Transparent	0
Turbid and putrid	6
Fecal-putrefactive	12

To objectify the assessment of the condition of the abdominal organs, the Altona peritoneal index (PIA) and PIA II are used, but they have less prognostic significance in comparison with MPI. At the Department of Faculty Surgery of the Russian State Medical University, under the leadership of Academician of the Russian Academy of Medical Sciences V. S. Savelyev, similar systems have been developed that allow optimizing the choice of treatment tactics for widespread peritonitis and pancreatic necrosis (abdominal cavity index - ACI).

Abdominal cavity index in peritonitis

Prevalence of peritonitis	Local (or abscess)	1
	Spilled	3
Nature of exudate	Serous	1
	Purulent	3
	Hemorrhagic	4
	Fecal	4
Fibrin overlays	In the form of a shell	1
	In the form of loose masses	4
Bowel condition	Wall infiltration	3
	Absence of spontaneous and stimulated peristalsis	3
	Intestinal fistula or anastomotic leak	4
Condition of the abdominal wall	Suppuration or necrosis of the wound	4
	Eventration	3
	Unremoved devitalized tissue	3
Total score - abdominal cavity index (ACI)

Treatment of peritonitis

Treatment of patients with peritonitis is carried out only in a surgical hospital. Treatment objectives:

• Sanitation/elimination of purulent-inflammatory focus.
• Adequate antibacterial therapy.
• Optimization of tissue perfusion and oxygen transport.
• Nutritional support.
• Immunocorrection.
• Prevention of complications.
• Effective intensive therapy of sepsis is possible only if the source of infection is sanitized and adequate antimicrobial therapy is provided.

Surgical treatment

Stages of surgical treatment:

• Rational access.
• Removal of pathological contents.
• Revision of abdominal organs, elimination or localization of the source of peritonitis (includes the choice of further patient management tactics - establishing indications for staged treatment of peritonitis).
• Abdominal cavity sanitation.
• Drainage of the small intestine.
• Drainage of the abdominal cavity

The options for the final stage of surgery for widespread peritonitis depend on the further tactics of surgical treatment in the “on demand” or “according to the program” mode.

In some cases, the operation is completed with layer-by-layer suturing of the anterior abdominal wall wound. Indications for repeated laparotomy arise with the progression of the intra-abdominal inflammatory process or its complications. With severe intestinal paresis or signs of inflammation of the visceral and parietal peritoneum, suturing of only the subcutaneous tissue and skin is possible. With this surgical technique, a ventral hernia is formed, but the patient's death from progressive peritonitis or intra-abdominal hypertension syndrome is prevented.

Indications for choosing a staged treatment method:

• diffuse fibrinous-purulent or fecal peritonitis,
• signs of anaerobic infection of the abdominal cavity,
• the impossibility of immediate elimination or reliable localization of the source of peritonitis,
• the condition of the laparotomy wound that does not allow the defect of the anterior abdominal wall to be closed,
• intra-abdominal hypertension syndrome,
• stage of peritonitis corresponding to severe sepsis or septic shock.

Postoperative intra-abdominal complications of peritonitis and conditions requiring repeated surgical treatment.

These conditions include:

• abdominal abscesses,
• SKN,
• eventration,
• failure of the sutures of hollow organs, anastomoses and stomas, formation of intestinal fistulas,
• postoperative bleeding,
• intra-abdominal hypertension syndrome.

Preliminary preparation

High-risk patients:

• age over 60 years,
• AAA score - 3-4,

Acute myocardial ischemia suffered within the last year. Standard preoperative preparation in patients with peritonitis should not exceed 2-3 hours. In special cases (severe hypovolemia, severe cardiovascular failure), preoperative preparation can be extended to 4-5 hours.

Failure to achieve the required level of correction within the specified time frame is not a reason for further delay of surgical intervention.

The main objectives of preoperative preparation are to predict and prevent possible deterioration of the patient’s condition during anesthesia.

Anesthesia can cause a breakdown of hemodynamic compensation mechanisms due to the vasodilating and negative inotropic effects of the drugs used. In this regard, a very important factor for the prognosis of surgical treatment as a whole is careful preoperative correction of the patient's volemic status.

Clinical assessment of extracellular fluid deficiency presents certain difficulties. In intestinal paresis, there is 1500-3000 ml or more of fluid in its lumen. In patients with good compensatory capabilities of the cardiovascular system, blood pressure and heart rate are inadequate criteria for the state of pulmonary blood flow. In elderly and senile patients with limited compensatory capabilities of the myocardium and increased total peripheral vascular resistance, clinical signs of hypovolemia may appear with a circulating fluid volume deficit of at least 15-20%. Due to age-related decrease in baroreceptor sensitivity, compensatory tachycardia may not correspond to the severity of hypovolemia. At the same time, orthostatic hypotension is an accurate sign of significant fluid deficiency, which can (with inadequate correction) lead to a significant decrease in blood pressure at the stage of anesthesia induction.

Estimation of extracellular fluid loss volume

Degree	Volume of fluid loss in ml in a patient weighing 70 kg	Clinical signs
Minimum	More than 2500	Thirst, decreased elasticity of the skin, decreased intraocular pressure, dry tongue, decreased sweating
Moderate	More than 4500	All of the above plus orthostatic hypotension, decreased peripheral venous filling, oliguria, nausea, decreased CVP, apathy, hemoconcentration
Average	More than 5500	All of the above plus hypotension, thready pulse, cold skin
Heavy	7000-10 500	Shock, coma, death

Preoperative preparation and monitoring

• Central venous catheterization
• Catheterization of the urinary bladder
• Nasogastric tube placement
• Oxygen therapy via face mask
• Infusion of crystalloid and colloidal solutions in a volume of at least 1500 ml

Administration of drugs that increase the pH of gastric contents: proton pump inhibitors (omeprazole 40 mg intravenously) or H2-receptor blockers ₍ ranitidine 50 mg intravenously).

The problem of regurgitation of gastric contents with their subsequent aspiration into the tracheobronchial tree is one of the most serious problems of anesthesia during operations for peritonitis. The threat of regurgitation and aspiration exists in cases where the residual volume of gastric contents exceeds 25 ml. Aspiration of fluid with a pH <2.5 causes a burn of the mucous membrane of the bronchi, bronchioles and alveoli, resulting in atelectasis, OL and decreased pulmonary compliance. In addition, bronchospasm may develop. In some cases, regurgitation is latent and manifests itself only later as pneumonia or aspiration pneumonitis. The likelihood of gastric reflux is determined by the difference in pressure in the stomach and the lower third of the esophagus.

Drugs that reduce the tone of the esophageal sphincter, in particular anticholinergics and ganglionic blockers, should not be used; this explains the refusal to use atropine in premedication in patients with peritonitis.

Preoperative antibacterial therapy Before the operation, it is necessary to start empirical antibacterial therapy, the regimen of which is determined by the etiology of peritonitis.

Approximate regimens of antibacterial therapy:

• Community-acquired peritonitis - cefotaxime (2 g) + metronidazole (500 mg) intravenously.
• Nosocomial peritonitis - cefepime (2 g) + metronidazole (500 mg) intravenously.
• In-hospital against the background of previous antibacterial therapy - meropenem (1 g) intravenously.

Premedication

It is performed on the operating table. Intravenous administration of midazolam (5 mg) and metoclopramide (10-20 mg) is recommended. The use of atropine or metocinium iodide is limited to strict indications (pronounced bradycardia) for the above reasons.

The main problems of the early postoperative period and ways to solve them

Recommendations:

• Hypothermia. It is necessary to warm patients with warm infusion media and modern warming devices.
• Hypoxia. Oxygen therapy (or prolonged mechanical ventilation) is required for 72 hours.
• Hypovolemia. Corrected by adequate infusion therapy, volume status is monitored by constant assessment of heart rate, blood pressure, diuresis, central venous pressure, fluid loss through drains, stomas, etc.
• Gastrointestinal paresis. Optimally, early restoration of gastrointestinal motility using prolonged epidural blockade with local anesthetics (at least 72 hours).
• Pain syndrome. The optimal method for relieving postoperative pain syndrome is a combination of prolonged epidural analgesia with 0.2% ropivacaine solution (rate 5-7 ml/h + fentanyl 0.1-0.2 mg/day) with intravenous administration of NSAIDs - lornoxicam (up to 24 mg/day) or ketorolac (up to 90 mg/day). The combination of prolonged epidural anesthesia and NSAIDs helps reduce the loss of patient muscle mass by reducing protein degradation caused by hyperproduction of cortisol and prostaglandin E2.

Antimicrobial therapy for peritonitis

The diagnosis of peritonitis is an absolute indication for the prescription of antibacterial therapy. Treatment must be started in advance, since massive contamination of the surgical wound is inevitable during the operation, and early prescription of antibiotics will reduce the frequency of infections after surgery.

The choice of drugs is based on the most probable cause of the infectious process. It is inappropriate to prescribe antibacterial drugs or their combinations, the spectrum of action of which is wider than the list of probable pathogens. It is also inappropriate to prescribe drugs active against multiresistant bacteria for infections caused by sensitive strains.

When choosing antibacterial drugs, it is necessary to consider:

• localization of the lesion,
• probable microbiological structure,
• pharmacodynamics and pharmacokinetics of antibiotics,
• severity of the condition (APACHE II),
• economic realities.

[ 40 ], [ 41 ], [ 42 ], [ 43 ]

Antimicrobial therapy for secondary peritonitis

Drugs and their combinations for mild and moderate severity of community-acquired peritonitis:

• protected aminopenicillins (amoxicillin and ampicillin/sulbactam),
• combinations of second- and third-generation cephalosporins (cefuroxime, cefotaxime, ceftriaxone) with antianaerobic drugs,
• combinations of fluoroquinolones (levofloxacin, moxifloxacin, ofloxacin, pefloxacin, ciprofloxacin) with antianaerobic drugs.

Of the anaerobic drugs, metronidazole is currently the most appropriate to use, since resistance to it is virtually absent. Growing resistance is observed to clindamycin (lincomycin) and antianaerobic cephalosporins (cefoxitin).

The use of cheaper combinations of antibacterial drugs (ampicillin/gentamicin, cefazolin/gentamicin, gentamicin/metronidazole or gentamicin/clindamycin) for the treatment of community-acquired peritonitis is ineffective due to the high frequency of development of resistance to them by microorganisms, primarily E. coli.

If the source of infection is the biliary tract or upper gastrointestinal tract, then in the absence of obstruction or oncological diseases, it is possible to use drugs without antianaerobic activity.

In case of severe community-acquired peritonitis with manifestations of severe sepsis and/or septic shock, at the first stage of therapy it is justified to prescribe antibacterial therapy regimens that maximally cover the spectrum of possible pathogens with minimal resistance to them of community-acquired strains of pathogens: cefepime + metronidazole, ertapenem, levofloxacin + metronidazole, moxifloxacin.

A separate group should include peritonitis that develops in patients with concomitant diseases or risk factors that seriously aggravate the course of the infectious process and increase the etiological role of multiresistant hospital microflora:

• long hospital stay before surgery (it is not possible to establish a critical duration),
• previous antibacterial therapy (more than 2 days),
• immunodeficiency states (oncological diseases, transplantation, treatment with glucocorticoids or cytostatics, HIV infection),
• pancreatic necrosis,
• previous surgeries on abdominal organs,
• impossibility of adequate sanitation of the source of infection,
• diabetes mellitus.

The following drugs or their combinations cover the maximum spectrum of potential pathogens for postoperative peritonitis and peritonitis in patients with the indicated risk factors:

• carbapenems (meropenem),
• protected cephalosporins (cefoperazone/sulbactam),
• fourth generation cephalosporins (cefepime) in combination with metronidazole.

Controlled clinical trials have confirmed the high clinical efficacy of other treatment regimens for severe peritonitis. However, their use in this category of patients may be associated with an increased risk of ineffective treatment due to the high frequency of resistance of pathogens of nosocomial infections:

• combinations of fluoroquinolones with metronidazole,
• combinations of second-generation cephalosporins (cefotaxime, ceftriaxone, ceftazidime, cefoperazone) with metronidazole.

The possibility of using a fluoroquinolone with antianaerobic activity, moxifloxacin, for the treatment of nosocomial peritonitis has not been definitively confirmed.

The advisability of combining cephalosporins or carbapenems with aminoglycosides (amikacin, netilmicin) has not been confirmed in controlled studies.

Although staphylococci are rare pathogens for peritonitis, except in cases of peritonitis associated with PD, caution is required in hospitals with a high incidence of methicillin-resistant strains. In some cases, vancomycin may be included in empirical therapy regimens.

In immunocompromised patients, the probability of fungal etiology of peritonitis increases, primarily Candida spp. When Candida albicans is isolated, the drug of choice is fluconazole. Other types of Candida (C. crusei, C. glabrata) are less sensitive or resistant to azoles (fluconazole), in which case it is advisable to use voriconazole or caspofungin.

After laboratory determination of the antibiotic sensitivity of the pathogen, the necessary adjustments are made to the therapy.

[ 44 ], [ 45 ], [ 46 ], [ 47 ], [ 48 ], [ 49 ]

Route of administration of antimicrobial agents

In peritonitis, antibacterial agents are administered intravenously; there is no convincing evidence in favor of intra-arterial or endolymphatic administration.

Intracavitary administration of antibacterial drugs

The main drug for intracavitary administration is dioxidine. With intracavitary administration, it is impossible to predict what concentration of the drug will be in the blood serum and whether toxic reactions are possible - dystrophy and destruction of the adrenal cortex (dose-dependent reaction), embryotoxic, teratogenic and mutagenic action. In this regard, the main reasons for refusing intracavitary administration of dioxidine and other antibacterial drugs are the unpredictability of their pharmacokinetics and the ability of modern antibacterial drugs to penetrate well into organs, tissues and cavities when administered intravenously, creating therapeutic concentrations in them.

The duration of antibiotic therapy is determined by its effectiveness, which is assessed 48-72 hours after its start. Therapy is adjusted by prescribing more effective drugs when resistant flora is isolated and using drugs with a narrower spectrum of action when highly sensitive pathogens are isolated (de-escalation therapy).

Criteria for the effectiveness (48-72 hours after the start) of antibacterial therapy for peritonitis:

• positive dynamics of abdominal infection symptoms,
• reduction of fever (maximum temperature no higher than 38.9 °C),
• reduction of intoxication,
• reduction in the severity of the systemic inflammatory response.

If there is no persistent clinical and laboratory response to the antibacterial therapy within 5-7 days, additional examination (ultrasound, CT, etc.) is necessary to identify complications or another source of infection.

Criteria for adequacy (discontinuation) of antibacterial therapy:

• Absence of symptoms of systemic inflammatory response.
• Temperature <38 °C and >36 °C.
• Heart rate <90 beats per minute.
• Respiratory rate <20 per minute.
• Leukocytes <12x10 ⁹ /l or >4x10 ⁹ /l with the number of band neutrophils <10%.
• Absence of PON if the cause was related to infection.
• Restoration of gastrointestinal function.
• No impairment of consciousness.

The persistence of only one sign of bacterial infection (fever or leukocytosis) is not an absolute indication for continuing antibacterial therapy. An isolated increase in temperature to subfebrile numbers (maximum daytime temperature within 37.9 °C) without chills and changes in the peripheral blood may be a manifestation of postinfectious asthenia or nonbacterial inflammation after surgery and does not require continued antibacterial therapy. The persistence of moderate leukocytosis (9-12x10 ⁹ /l) in the absence of a left shift and other signs of bacterial infection also does not require continued antibiotic treatment.

The duration of effective antibacterial therapy in the vast majority of cases is 7-10 days; longer is undesirable due to the risk of developing possible complications of treatment, selection of resistant strains of microorganisms and the development of superinfection.

Evidence-based effectiveness of intensive care methods for abdominal sepsis

Methods that have been tested for their effectiveness in multicenter, high-level evidence studies:

• Use of antibiotics.
• Providing nutritional support.
• Use of Activated Protein C* in the treatment of severe sepsis.
• Use of polyvalent immunoglobulins for replacement immunotherapy.
• Use of low volume respiratory ventilation.

Methods that have been tested in a number of studies but not in multicenter trials:

• Use of anticoagulants in the treatment of sepsis.
• Use of low doses of hydrocortisone (300 mg/day) in refractory septic shock.
• Control and correction of glycemic levels.
• Methods that cannot be recommended for use in widespread clinical practice as they do not have sufficient evidence base.
• Ultraviolet and laser irradiation of blood.
• Hemosorption.
• Lymphosorption.
• Discrete plasmapheresis.
• Electrochemical oxidation of blood, plasma, lymph.
• Xenoperfusate infusion.
• Infusion of ozonated crystalloid solutions.
• Endolymphatic antibiotic therapy.
• Immunoglobulins for intramuscular administration.

The main directions and objectives of treatment of patients with abdominal sepsis, confirmed by evidence of levels I and II:

• Hemodynamic support: CVP 8-12 mm Hg, _{mean BP} more than 65 mm Hg, diuresis 0.5 ml/kg per hour, hematocrit more than 30%, mixed venous blood saturation not less than 70%.
• Respiratory support peak airway pressure below 35 cm H2O, inspiratory fraction of oxygen below 60%, tidal volume less than 6 ml/kg, non-inverted inspiratory to expiratory ratio.
• Glucocorticoids "low doses" - 240-300 mg per day.
• Activated protein C 24 mcg/kg per hour for 4 days in severe sepsis (APACHE II more than 25).
• Immunocorrection replacement therapy with the drug "Pentaglobin".
• Prevention of deep vein thrombosis.
• Prevention of the formation of stress ulcers of the gastrointestinal tract: use of H2-receptor blockers and proton pump inhibitors.
• Renal replacement therapy for acute renal failure due to severe sepsis.