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Peritonitis

 
, medical expert
Last reviewed: 23.04.2024
 
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Peritonitis is characterized by severe general symptoms, including endogenous intoxication and multiple organ failure. Mortality in peritonitis was always one of the highest and reached 55-90% in postoperative surgical peritonitis. Despite the fact that such a formidable complication, like peritonitis after cesarean section, is now relatively rare (0.2-0.8%), the lethality with 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. By peritonitis is understood the diffuse spread of inflammation.

Local inflammations are defined as abscesses of the abdominal cavity (borderline peritonitis). Peritonitis is a secondary process that complicates the course of the underlying disease. Idiopathic (primary) peritonitis, when, no source is detected in the last 20 years, does not occur at all and is excluded from the classification.

In diffuse peritonitis, by prevalence along the peritoneum, there are: local peritonitis, when a part or one anatomical region of the cavity is affected; common peritonitis, when the process captures several areas, diffuse (general), with the defeat of the entire peritoneum. The severity of intoxication is explained by the enormous length of the peritoneum, almost 10 square kilometers. M with high exudation visceral leaf and parietal resorption. Therefore, toxins quickly and in large quantities enter the bloodstream.

On etiology, peritonitis is divided into bacterial (infectious), developing in inflammatory diseases of internal organs or perforations of hollow organs, as well as in traumas; and aseptic peritonitis, when the inflammatory process of the peritoneum causes 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, the reactive, toxic and terminal stages of the flow are isolated.

trusted-source[1], [2], [3], [4], [5]

Causes of peritonitis

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

Varieties of primary peritonitis:

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

The causative agent, as a rule, is a certain type of microorganism. Secondary peritonitis is the most common type of disease, it combines all forms of inflammation of the peritoneum, which developed as a result of destruction or trauma of the abdominal cavity organs.

Types of secondary peritonitis:

  • Peritonitis caused by perforation and destruction of abdominal organs.
  • Postoperative peritonitis.
  • Post-traumatic peritonitis:
    • with closed stomach injury,
    • with penetrating wounds of the abdomen

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

It develops in the absence of sources of infection and / or after surgery for a secondary peritonitis performed in full, but against the background of a pronounced depletion of the mechanisms of body protection. The course of this form is distinguished by an erased clinical picture, possible multi-organ dysfunction and the manifestation of endotoxicosis refractory to the treatment being administered. The source of the pathological process is rarely established.

trusted-source[6], [7], [8], [9], [10], [11]

Microbiological structure

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

Primary peritonitis

Primary peritonitis - infections caused by a single bacterial agent that develop in patients with cirrhosis of the liver (E. Coli, Enterobacter spp., Citrobacterfreundn, Klebsiella spp., S. Vindans, S. Pneumoniae, group B streptococcus, in rare, severe cases - S. Aureus) or in patients on 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 causative agent 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%). Almost always in patients with secondary peritonitis, a mixed (aerobic-anaerobic) flora is found, with anaerobes represented mainly by the group of Bacteroides spp., To a lesser extent Clostridium spp., Fusobacterium spp., Peptostreptococcus spp.

The causes of intra-abdominal infections of the postoperative period are somewhat different, in the first place - Enterococcus spp., Coagulase-negative staphylococci, Enterobacter spp., Acinetobacter spp., P. Aeruginosa. With the development of complications against the background of immunosuppression, the probability of fungal infections increases, the main pathogen is C. Albicans.

The causes of peritonitis associated with pelvic infections in women are group B Streptococcus, N. Gonorrhoeae, Prevotella spp., Peptococcus spp., Mobiluncus spp.

Pathogens with localization of the infection in the biliary tract - Enterobactenaceae and Enterococcus spp.

Tertiary peritonitis

The causative agent for tertiary peritonitis can often not be determined, however, with a careful microbiological examination, as a rule, multidrug-resistant enterococci, coagulase-negative staphylococci and C. Albicans, less often Pseudomonas aeruginosa and enterobacteria. The role of anaerobes in tertiary peritonitis is not fully understood.

How does peritonitis develop?

The pathogenesis of peritonitis is very complicated, depends on the cause, virulence, microflora, the state of reparative processes, the presence of aggravating factors. The main points that determine the severity of the current are:

  1. large loss of water, salts and proteins in the abdominal cavity and intestines, which is in the paresis; a day, the loss of fluid is up to 4-8 liters, which leads to dehydration, hypovolemia, the development of cardiac and respiratory failure, acidosis;
  2. speed 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 by binding of microbial lipopolysaccharides with antibodies and blood complement), which forms polyallergy and is a starting point for the development of intoxication syndrome.

With weakened reparative processes or massive invasion, the delineation does not develop and the peritonitis takes the form of a diffuse one, with slowing down with the operation, the process progresses. The hyperperistalsis, characteristic of the first hours of peritonitis, the exhausted omentum, the presence of blood and exudate in the abdominal cavity, also hinders the delimitation.

Symptoms of peritonitis

Clinical signs are largely determined by the cause of peritonitis, the localization of its source, as well as the timing of the disease. From the time of diagnosis and the timing of laparotomy, the outcome of treatment and outcome depends, so it is important to know the early signs of this disease.

The earliest and permanent sign of peritonitis is abdominal pain, it can occur suddenly, which is typical for perforation of the hollow organs and disturbance of the mesenteric circulation, or develop gradually, which corresponds to the inflammatory-destructive process of any organ of the abdominal cavity. The localization of pain depends on the place and nature of the pathological process (causes of peritonitis), but rather quickly becomes widespread. Pain in the abdomen is intense, increases with a change in the position of the body, often accompanied by vomiting of gastric contents, not bringing relief. The position of the patient is forced "constrained", the stomach does not participate in the act of breathing, its wall is tense.

With palpation, soreness in all parts of the abdomen, more pronounced in the projection of the pathological process. The positive symptom of Shchetkin-Blumberg and the symptoms characteristic of the disease are the causes of peritonitis. As the process progresses, the dryness of the tongue becomes worse, tachycardia, tension and tenderness of the abdominal wall increase, intestinal paresis occurs, stool and gas retention may occur, signs of a systemic inflammatory reaction, dehydration and endotoxicosis appear.

Diffuse peritonitis

Symptoms of diffuse peritonitis are polymorphic. Depends on the primary focus and the stage of the process; The volume and type of exudate (with the exception of hemoperitoneum) have no significant effect on the clinic.

In the first 24 hours (reactive phase), the leading symptoms are as follows. The pain is sharp, constant, increasing when trying to move, cough, deep breathing, palpation. To shake the belly the patient takes a forced position: with local pains, he presses the affected department with his hands; with diffuse pain lies on his back with tightened legs, pressing his stomach with his hands during a cough. Dehydration: manifested by thirst, dryness of the 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, is strained to a "flattish" state; palpation is sharply painful over the affected organ or throughout the abdomen with diffuse peritonitis; positive symptoms of irritation of the peritoneum - a symptom of Shchetkin-Blumberg and others, specific for each affected organ. Hyperperistality is visible by eye or is determined by increased intestinal noise. Not mandatory, but can be: vomiting, diarrhea, tenesmus. In blood tests, rapidly, by the hour, increase: leukocytosis, neutrophilia, ESR, LII, FSM. These laboratory indicators are used for differential diagnosis, conducting in-hour studies.

If surgical intervention is not performed, the toxic phase of peritonitis develops in the next 2-3 days, which is determined by the formation of the intoxication syndrome, which predominates over local manifestations. Intoxication develops rapidly and is very pronounced: facial features are sharpened, the skin is pale, with an earthy tinge, cyanosis of the lips, eyes sunken (Hippocrates face), tongue dry like a brush, can be lacquer, hypotension, hypovolemia, tachycardia, hyperthermia.

Local manifestations decrease in severity, but the process itself grows and spreads throughout the abdominal cavity. The pains in the abdomen subside, become aching, they are permanent, but spread all over the stomach. The protective tension of the abdominal wall is smoothed, the Shchetkin-Blumberg symptom is less pronounced, but is common throughout the abdomen. Peristalsis disappears, paresis of the intestine develops, which in the belly auscultation is revealed by the symptom of "deathly silence", the stomach swells.

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

trusted-source[12], [13], [14], [15], [16], [17], [18], [19], [20], [21], [22],

Delimited peritonitis

Important in the pathogenesis is the state of the reparative processes, on which depends the process delimitation. Inflammation of the peritoneum develops a vascular reaction with the sweat of plasma and blood cells. From the plasma, fibrin falls out, which serves as a glue, securing the gland around the affected organ of the intestinal loop. Spikes, initially loose, are densified, and an inflammatory infiltrate is formed in the abdominal cavity, in the center of which is a sore organ. If there is a destruction of this organ - in the abdominal cavity an abscess is formed, called delimited peritonitis. The most frequent localization of abscesses: Douglas abscess, subhepatic and subdiaphragmatic spaces, interintestinal abscesses. If the inflammation stops, the infiltrate slowly resolves.

Appendicular infiltration and abscess - develops with unoperated acute appendicitis, more often with late treatment of patients, use of warmers, etc.

In this case, the inflammation zone is first delimited by the omentum, in the subsequent loops of the intestine are soldered, forming an elastic, dense, painful infiltrate. The condition of the patients improves, the pain becomes less, the symptoms of irritation of the peritoneum disappear. Such patients are conservative: massive anti-inflammatory therapy, cold on the stomach; with constant monitoring of the course of the process - the boundaries of the infiltrate are drawn around the marker. If the process does not degenerate and the inflammation stops, the infiltrate dissolves in 2-3 weeks.

When the appendix is destroyed in the center of the infiltrate, an abscess forms: the abdominal pain does not subside, and even begins to progress, signs of intoxication appear, the stomach becomes tense, painful when palpation over the infiltrate, may be a symptom of Schetkina-Blumberg, the size of the infiltrate increases. In this case the operative intervention is shown, the volume of which depends on the findings

Douglas abscess - a limited accumulation of pus in the rectum-vesicle (in men) and rectal-vaginal (in women) deepening of the pelvis.

An abscess can develop with any pathology of the peritoneal cavity, when the exudate is shifted to a small pelvis, it is delimited and suppressed, the delimitation is usually quite powerful, but the breakdown of pus into the abdominal cavity with the development of peritonitis can be. The clinical picture has the following characteristics: 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 zone with deep palpation, overhanging the rectum wall or swelling of the posterior vaginal fornix, palpation is determined by a dense, painful »immobile infiltration with a softening in the center. Characteristic are tenesmus, frequent urination. On radiographs standing in a small pelvis gas with liquid level, on ultrasound reveal fluid in the small pelvis, In doubtful cases, puncture through the vagina or rectum.

Meskheshechny abscess is difficult to identify, the starting points are the presence of intoxication, which does not decrease, despite active therapy, prolonged intestinal paresis, pain in palpation of the abdomen, the presence of varying degrees of symptoms of irritation of the peritoneum. Given the weak delimitation of these abscesses, diffuse peritonitis often develops, so early relaparotomy, rather than wait-and-see tactics, is preferable.

Subdiaphragmatic abscess is an intraperitoneal abscess located in the sub-diaphragmatic space.

Subdiaphragmatic space is divided into 2 parts - intraperitoneal and retroperitoneal.

The abscess is most often formed in the intraperitoneal part - the left-sided and right-sided, which communicates with the sub-hepatic space, where an abscess can also form. The reasons are diverse, they can be divided into 4 groups:

  1. the pathology of the abdominal cavity;
  2. pathology of the pleural cavity;
  3. purulent kidney pathology;
  4. mixed form, mainly with thoracoabdominal injuries.

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

The anterior abdominal wall lags behind in the act of breathing, is painful on palpation, the standing of the diaphragm is high, its mobility is limited. Palpation of the XI-XII ribs on the right, especially at the point of their fusion at the costal arch, is painful (Kryukov's symptom). On radiographs, against the background of a high standing dome of the diaphragm, sometimes a gas with a horizontal boundary of the liquid is visible. Early diagnosis allows you to perform ultrasound. Treatment is prompt, the method depends on the type of abscess.

Diagnosis of peritoneal pathology at home is based on the presence of: permanent pain in the abdomen, maximum in the area of the affected organ or evenly throughout the abdomen, dryness of the tongue, tachycardia. In all cases, the patient must be taken to a surgical hospital in order of emergency care.

trusted-source[23], [24]

Where does it hurt?

Classification of peritonitis

There are primary and secondary peritonitis.

Primary (idiopathic) peritonitis - infection of the peritoneum with hematogenous or lymphogenous pathways (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 vastness of the peritoneal lesion in peritonitis and the degree of involvement of the anatomical areas, the following types of peritonitis are distinguished:

  • local (lesion of one anatomical area);
  • widespread (lesion of several anatomical regions);
  • general (diffuse) - the defeat of all parts of the abdominal cavity.

According to another classification, depending on the specific features of the spread of the inflammatory process (the virulence of the pathogen, the ability of the organism to delimit the purulent focus due to the immune system, neighboring organs, peritoneum, epiploon, fibrin deposits) distinguish diffuse peritonitis (which is common or diffuse) and delimited peritonitis (essentially - encysted abscesses of the abdominal cavity). Examples of delimited surgical peritonitis are appendicular, sub-diaphragmatic, sub-hepatic, interintestinal abscesses.

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

In clinical practice, the term peritonitis usually means a diffuse lesion of the peritoneum, and in the future, using this term, we will keep in mind exactly the diffuse peritonitis.

By the type of clinical course distinguish acute, subacute (chronic) and chronic peritonitis, some authors distinguish the fulminant form of the disease.

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

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

Chronic peritonitis is extremely rare, mainly with a specific lesion of the peritoneum (eg, carcinomatosis or tuberculosis).

Lightning peritonitis is, in fact, peritonitis complicated by septic shock.

In the course of peritonitis, three stages (phases) are identified: reactive, toxic and terminal. The reactive stage in acute peritonitis lasts about a day on average, the duration of the toxic and terminal stages is variable and depends on a variety of causes (massiveness and nature of bacterial invasion, the volume of the primary purulent focus, the patient's immunocompetence, the nature of the treatment). By the nature of exudate peritonitis is divided into:

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

It is impossible not to distinguish separately postoperative peritonitis.

NA Efimenko (1999) considers that the primary postoperative peritonitis occurs after planned surgical interventions for three main reasons:

  • insufficiency of the seams of anastomoses,
  • intraoperative infection of the abdominal cavity,
  • technical errors or errors in the operation.

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

trusted-source[25], [26], [27], [28], [29], [30], [31], [32]

Diagnosis of peritonitis

In the history of patients with peritonitis, inflammatory diseases of the abdominal and pelvic organs, abdominal trauma, gastrointestinal ulcers of various localizations, cholelithiasis, advanced laparotomy, and neoplastic processes are often noted.

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

trusted-source[33], [34], [35], [36], [37], [38], [39]

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, on the level of consciousness, the condition of mucous membranes. In patients with peritonitis tachycardia is more than 100-120 per minute, BP can be increased or decreased, respiratory rate more than 20 per minute. The manifestation of toxic encephalopathy is inhibition, excitation of the patient or delirium.

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

When rectal and vaginal examination - overhanging arches and soreness due to the accumulation of inflammatory exudates

Laboratory research

In a laboratory study, peritonitis is characterized by signs of increasing liver-kidney failure, uncontrolled reduction in protein levels, signs of azotemia, inflammatory changes in white blood, anemia.

The simplest and most reliable method for laboratory diagnosis of purulent inflammatory diseases of the abdominal cavity organs is the determination of the leukocyte index of intoxication (LII) (originally the formula was proposed for the diagnosis of acute appendicitis), the calculation of which uses the modified formula of J. Ya. Kalf-Kalifa.

LII = 32 Pl + 8 Mi + 4 10 + 2 P + C / 16 E +

2 B + Mo + L (norm 1.08 ± 0.45),

Where Pl are plasma cells, Myelocytes, Yu - neutrophils, P - stab neutrophils, C - segmented neutrophils, E - eosinophils, B - basophils, Mo - monocytes, L - lymphocytes.

A promising additional laboratory indicator of the diagnosis of abdominal sepsis and peritonitis is the concentration of procalcitonin in the blood plasma. This indicator is a marker in the differential diagnosis of SSEP of septic and abacterial origin, in particular sterile and infected forms of pancreatonecrosis, acute respiratory distress syndrome, infected and uninfected intra-abdominal fluid clusters. Exceeding the concentration of procalcitonin in the plasma above 2 ng / ml is the criterion for the development of the septic process. The index is a valuable help in deciding the question of the tactics of surgical or intensive conservative treatment of purulent-septic complications in abdominal surgery.

Instrumental research

Instrumental methods of research can identify the causes that caused peritonitis. Thus, in the perforation of hollow organs, a strip of free gas under the diaphragm is seen on the overview radiograph, in acute cholecystitis with ultrasound, an increase in the gallbladder with heterogeneous contents, concrements and a doubling of the contour of its wall. This same study allows you to identify free fluid in the abdominal cavity or infiltrate in the ileocecal region with acute appendicitis.

The increase in endotoxicosis, tension and tenderness of the anterior abdominal wall during palpation, expressed by the Shtetkin-Blumberg symptom, does not require additional methods of investigation. With an erased clinical picture, especially in the elderly, a diagnostic laparoscopy should be performed to clarify the diagnosis and the extent of the pathological process. Visible exudate in the abdominal cavity, the imposition of filaments of fibrin on the visceral peritoneum, the flow of bile, perforation or contents of the stomach or intestine in the free abdominal cavity and other pathological changes.

Early signs of secondary peritonitis (signs of initial diseases) are diagnosed with ultrasound of the abdominal cavity and retroperitoneal space, radiographic examination of the abdominal cavity and chest, CT, and, as the last stage of diagnosis, perform diagnostic laparoscopy.

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

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

Common scales for assessing the severity of the condition (APACHE, APACHE II, APACHE III, SAPS, SAPS II, SOFA, MODS), scales taking into account the peculiarities of peritonitis (Mannheim peritonitis index - MPI, prognostic index of relaparotomy - PID) are widely used.

Individual indices of homeostasis are used as independent predictors of an unfavorable outcome.

Syndrome of a systemic inflammatory reaction and an objective assessment of the severity of a condition with peritonitis

The basis of modern understanding of the body's response to infection is the concept of abdominal sepsis (a pathological process based on the body's response in the form of generalized inflammation in response to a surgical infection in the abdominal cavity). Clinical interpretation of this view on the pathogenesis of sepsis (including abdominal) - the criteria for diagnosing CVD and the classification of sepsis, proposed by the conciliation conference of the American College of Pulmonology and the Society of Specialists in Critical Medicine - ACCP / SCCM.

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

Mannheim's peritonitis index (IIP / MP1)

M Linder and a group of German surgeons in Mannheim developed an index for the prediction and outcome of purulent peritonitis, including 8 risk factors:

  1. age of the patient,
  2. floor,
  3. organ failure,
  4. the presence of malignant neoplasm,
  5. duration of peritonitis before surgery more than 24 hours,
  6. common peritonitis,
  7. place of primary focus,
  8. type of peritoneal exudate.

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

Lethality (%) = 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 of a particular patient and determine the tactics of treatment.

Mannheim's peritonitis index

Age over 50 years

1

Female

5

The presence of organ failure

7th

The presence of a malignant tumor

4

Duration of peritonitis more than 24 hours

4

Large intestine as a source of peritonitis

4

Peritonitis diffuse

6th

Exudate (only one answer)

Transparent

0

Dull-rotting

6th

Calico-putrefactive

12

To objectify the assessment of the state of the abdominal cavity organs, the peritoneal index of Altona (PIA) and PIA II is used, but they have less prognostic significance than MPI. At the Department of Faculty Surgery of the Russian State Medical University under the guidance of Academician VS Savelyev, the academician of the Russian Academy of Medical Sciences, similar systems have been developed to optimize the choice of therapeutic tactics with widespread peritonitis and pancreatic necrosis (abdominal index - UPS).

Abdominal cavity index for peritonitis

Prevalence of peritonitis

Local (or abscess)

1

Spilled

3

The nature of the exudate

Serous

1

Purulent

3

Hemorrhagic

4

Feces

4

Fibrin overlays

In the form of shell

1

In the form of loose masses

4

Condition of the intestine

Infiltration of the wall

3

Absence of spontaneous and stimulated peristalsis

3

Intestinal fistula or inconsistency of anastomosis

4

Condition of abdominal wall

Suppuration or necrosis of the wound

4

Eventing

3

Undefined devitalized tissues

3

The total number of points is the abdominal cavity index (UPS)

What do need to examine?

Who to contact?

Treatment of peritonitis

Treatment of patients with peritonitis is carried out only in the conditions of a surgical hospital. Tasks of treatment:

  • Sanitation / elimination of a 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 focus of infection is sanitized and adequate antimicrobial therapy is provided.

Surgery

Stages of surgical treatment:

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

Variants of the final stage of the operation with advanced 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 by layer-by-layer suturing of the wound of the anterior abdominal wall. Indications for re-laparotomy occur with the progression of the intra-abdominal inflammatory process or its complications. With expressed intestinal paresis or signs of inflammation of the visceral and parietal peritoneum, it is possible to suture only the subcutaneous tissue and skin. With this technique of surgery, a ventral hernia is formed, but the patient's death from progressive peritonitis or the syndrome of intra-abdominal hypertension is prevented.

Indications for the selection of the terminal method of treatment:

  • diffuse fibrinous-purulent or fecal peritonitis,
  • signs of anaerobic infection of the abdominal cavity,
  • the impossibility of instantaneous elimination or reliable localization of the source of peritonitis,
  • the state of the laparotomic wound, which does not allow to close the defect of the anterior abdominal wall,
  • a syndrome of intra-abdominal hypertension,
  • stage of peritonitis, corresponding to severe sepsis or septic shock.

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

These states include:

  • abscesses of the abdominal cavity,
  • SKN,
  • event,
  • inconsistency of the seams of hollow organs, anastomoses and stoma, the formation of intestinal fistula,
  • postoperative bleeding,
  • syndrome of intra-abdominal hypertension.

Pre-training

Patients at high risk:

  • age over 60 years,
  • the estimate for ABA is 3-4,

Acute myocardial ischemia, suffered during 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 up to 4-5 hours.

The inability to achieve the required level of correction for the specified timeframe is not a basis for further postponement of the surgical intervention.

The main tasks of preoperative preparation are to predict and prevent possible deterioration of patients during anesthesia.

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

Clinical evaluation of the deficiency of extracellular fluid presents certain difficulties. When paresis of the intestine in its lumen is 1500-3000 ml of fluid and more. In patients with good compensatory capabilities of the cardiovascular system, indicators of 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 elevated OPSS, the clinical signs of hypovolemia can manifest themselves when the volume of circulating fluid is not less than 15-20%. Because of the age-related decrease in the sensitivity of baroreceptors, compensatory tachycardia may not correspond to the severity of hypovolemia. At the same time, orthostatic hypotension is an accurate sign of a significant fluid deficit that, if inadequately corrected, leads to a significant reduction in blood pressure during the induction of anesthesia.

Estimation of extracellular fluid loss volume

 Power

 The volume of fluid loss in ml in a patient weighing 70 kg

Clinical signs

The minimum

More than 2500

Thirst, decreased elasticity of the skin, decreased intraocular pressure, dryness of the tongue, decreased sweating

Moderate

More than 4500

All of the above plus orthostatic hypotension, decreased filling of peripheral veins, oliguria, nausea, decreased CVP, apathy, hemoconcentration

Average

More than 5500

All of the above plus hypotension, thread-like pulse, cold skin

Heavy

7000-10 500

Shock, coma, death

Pre-preoperative preparation and monitoring

  • Central vein catheterization
  • Catheterization of the bladder
  • Installation of a nasogastric tube
  • Oxygenotherapy through the face mask
  • Infusion of crystalloid and colloidal solutions in a volume of not less than 1500 ml

Administration of drugs that increase the pH of gastric contents of proton pump inhibitors (omeprazole 40 mg intravenously) or H 2 -receptor blockers (ranitidine 50 mg intravenously).

The problem of regurgitation of gastric contents with its subsequent aspiration into the tracheo-bronchial tree is one of the most serious problems of anesthetic management in cases of peritonitis. The threat of regurgitation and aspiration exists when the residual volume of stomach contents exceeds 25 ml. Aspiration of a liquid with a pH <2.5 causes a burn of bronchial mucosa, bronchioles and alveoli, resulting in the development of atelectasis, OL and a decrease in pulmonary compliance. In addition, bronchospasm may develop. In a number of cases, regurgitation is hidden and manifests itself only after pneumonia or aspiration pneumonitis. The likelihood of gastric reflux is determined by the difference in pressure in the stomach and lower third of the esophagus.

Do not use drugs that reduce the tone of the esophageal sphincter, in particular cholinolytics, ganglion blockers, which explains the refusal to use atropine in premedication in patients with peritonitis.

Preoperative antibacterial therapy before the operation begins, it is necessary to begin empirical antibiotic therapy, the regimen of which is determined by the etiology of peritonitis.

Approximate schemes of antibacterial therapy:

  • The out-of-hospital peritonitis is cefotaxime (2 g) + metronidazole (500 mg) IV.
  • Intra-hospital peritonitis - cefepime (2 g) + metronidazole (500 mg) IV.
  • Intrahospital on the background of the previous antibiotic therapy - meropenem (1 g) IV.

Premedication

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

The main problems of the early peslooperational 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 ventilation) is required for 72 hours.
  • Hypovolemia. It is corrected by adequate infusion therapy, the vollemic status is monitored continuously assessment of heart rate, blood pressure, diuresis, CVP, fluid drainage through drainage, through stoma, etc.
  • Gastrointestinal paresis. Optimal - early recovery of GI motility with the help of prolonged epidural blockade with local anesthetics (at least 72 hours).
  • Pain syndrome. The optimal technique for arresting postoperative pain syndrome is the combination of prolonged epidural analgesia with a 0.2% solution of ropivacaine (a rate of 5-7 ml / h + fentanyl 0.1-0.2 mg / day) with intravenous NSAIDs - lornoxicam (up to 24 mg / day ) or ketorolac (up to 90 mg / day). The combination of extended epidural anesthesia and NSAIDs can reduce the loss of muscle mass of the patient by reducing the degradation of the protein caused by hyperproduction of cortisol and prostaglandin E2.

Antimicrobial therapy of peritonitis

The diagnosis of "peritonitis" is an indisputable indication for the appointment of antibiotic therapy. Treatment should be started in advance, because during the operation, a massive contamination of the operating wound is inevitable, and the early administration of antibiotics will reduce the incidence of infections after surgery.

The choice of drugs is based on the most likely cause of the infection process. It is not advisable to prescribe antibacterial drugs or their combinations, whose spectrum of action is broader than the list of probable pathogens. It is also not advisable to prescribe drugs that are active against multi-resistant bacteria in infections caused by sensitive strains.

When choosing antibacterial drugs, it is necessary to take into account:

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

trusted-source[40], [41], [42], [43]

Antimicrobial therapy of secondary peritonitis

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

  • protected aminopenicillins (amoxicillin and ampicillin / sulbactam),
  • combinations of cephalosporins II-III generations (cefuroxime, cefotaxime, ceftriaxone) with antineaerobic drugs,
  • a combination of fluoroquinolones (levofloxacin, moxifloxacin, ofloxacin, pefloxacin, ciprofloxacin) with anti-anaerobic drugs.

Of the anaerobic drugs, metronidazole is currently the most useful, since resistance to it is practically absent. Clindamycin (lincomycin) and anti-anaerobic cephalosporins (cefoxytin) are observed to increase in resistance.

The use of cheaper combinations of antibacterial drugs (ampicillin / gentamicin, cefazolin / gentamicin, gentamicin / metronidazole or gentamicin / clindamycin) for inpatient peritonitis therapy is ineffective because of the high incidence of resistance to microorganisms, especially E. Coli.

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

In the case of community-acquired peritonitis of severe course with PON (severe sepsis) and / or septic shock phenomena, the first stage of therapy is justified by prescribing antibiotic regimens that maximally overlap the spectrum of possible pathogens with minimal resistance to community-acquired strains of cephepin + metronidazole, ertapenem, levofloxacin + metronidazole , moxifloxacin.

In a separate group should be allocated peritonitis, developed in patients with concomitant diseases or risk factors, seriously burdening the course of the infectious process and increasing the etiological role of the multi-resistant hospital microflora:

  • long stay in the hospital before surgery (it is not possible to establish a critical duration),
  • previous antibiotic therapy (more than 2 days),
  • immunodeficiency states (oncological diseases, transplantation, treatment with glucocorticoids or cytostatics, HIV infection),
  • pancreatic necrosis,
  • the transferred surgical interventions on the organs of the abdominal cavity,
  • impossibility of adequate sanation of the focus of infection,
  • diabetes.

The maximum spectrum of potential causative agents of postoperative peritonitis and peritonitis in patients with these risk factors is covered by the following drugs or their combinations:

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

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

  • a combination of fluoroquinolones with metronidazole,
  • a combination of cephalosporins of the second generation (cefotaxime, ceftriaxone, ceftazidime, cefoperazone) with metronidazole.

The possibility of using for the treatment of nosocomial peritonitis fluoroquinolone, which has antianaerobic activity - moxifloxacin - has not been fully confirmed.

The feasibility of a combination of cephalosporins or carbapenems with aminoglycosides (amikacin, netilmicin) is not confirmed in controlled studies.

Despite the fact that staphylococci are rare pathogens of peritonitis, with the exception of cases of its development against the background of PD, in hospitals with a high incidence of methicillin-resistant strains, caution is necessary. In some cases, it is possible to include vancomycin in empiric therapy regimens.

In immunocompromised patients, the likelihood of fungal etiology of peritonitis, especially Candida spp., Increases. With the isolation of Candida albicans, the drug of choice is fluconazole. Other species 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 susceptibility of the pathogen, the necessary adjustments are made to the therapy.

trusted-source[44], [45], [46], [47], [48], [49],

The route of administration of antimicrobial agents

With peritonitis, antibacterial agents are administered intravenously, there is no conclusive evidence for intraarterial or endolymphatic administration

Intraluminal administration of antibacterial drugs

The main drug for intracavitary administration is dioxidine. With intracavitary injection, 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 effects. In this regard, the main reasons for refusing intracavitary injection of dioxin 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 with intravenous administration, creating therapeutic concentrations in them.

The duration of antibiotic therapy is determined by the efficacy, which is evaluated after 48-72 hours after its onset. Therapy is corrected by prescribing more effective drugs in isolating a stable flora and applying preparations of a narrower spectrum of action in the isolation of highly sensitive pathogens (de-escalation therapy).

The efficacy criteria (48-72 hours after the onset) of antibacterial therapy of peritonitis:

  • positive dynamics of symptoms of abdominal infection,
  • decrease in fever (maximum temperature not higher than 38.9 ° C),
  • reduction of intoxication,
  • decrease in the severity of the systemic inflammatory reaction.

In the absence of a persistent clinico-laboratory response to ongoing antibiotic therapy for 5-7 days, an additional examination (ultrasound, CT, etc.) is needed to detect complications or another focus of infection.

Criteria for sufficiency (cessation) of antibiotic therapy:

  • Absence of symptoms of systemic inflammatory reaction.
  • The temperature is <38 ° C and> 36 ° C.
  • Heart rate <90 per minute.
  • Respiratory rate <20 per minute.
  • Leukocytes <12x10 9 / l or> 4x10 9 / l with the number of rod- trophy trophils <10%.
  • Absence of PON, if the cause was associated with an infection.
  • Restoration of the function of the digestive tract.
  • Absence of impaired consciousness.

Preservation of only one sign of bacterial infection (fever or leukocytosis) is not an absolute indication for the continuation of antibiotic therapy. Isolated temperature rise to low-grade figures (maximum daily temperature within 37.9 ° C) without chills and changes in peripheral blood may be a manifestation of post-infection asthenia or non-bacterial inflammation after surgery and does not require the continuation of antibiotic therapy. Preservation of moderate leukocytosis (9-12x10 9 / L) in the absence of a left shift and other signs of bacterial infection also does not require continuation of antibiotic treatment.

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

Proof of the effectiveness of intensive care for abdominal sepsis

Methods that have been tested for their effectiveness in multicenter studies of a high level of evidence:

  • Use of antibiotics.
  • Carrying out nutritional support.
  • Use of "Activated Protein C" * in the treatment of severe sepsis.
  • Use of polyvalent immunoglobulins for replacement immunotherapy.
  • Use of small volumes of 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.
  • The use of small doses of hydrocortisone (300 mg / day) with refractory septic shock.
  • Control and correction of the level of glycemia.
  • Methods that can not be recommended for use in broad clinical practice as not having sufficient evidence.
  • Ultraviolet and laser irradiation of blood.
  • Hemosorption.
  • Lymphosorption.
  • Discrete plasmapheresis.
  • Electrochemical oxidation of blood, plasma, lymph.
  • Infusion of xeno perfusate.
  • Infusion of ozonized solutions of crystalloids.
  • Endolymphatic antibiotic therapy.
  • Immunoglobulins for intramuscular injection.

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

  • Hemodynamic support HPC 8-12 mm RTST, BP Wed 65 mm RTST, diuresis 0.5 ml / kg per hour for more than 30% hematocrit, oxygen saturation of mixed venous blood is not less than 70%.
  • Respiratory support peak pressure in the airways below 35 cm water, oxygen inspiratory fraction below 60%, respiratory volume less than 6 ml / kg, non-inverted inspiration-to-exhalation ratio.
  • Glucocorticoids "small doses" - 240-300 mg per day.
  • Activated protein C 24 μg / kg per hour for 4 days with severe sepsis (APACHE II more than 25).
  • Immunocorrection substitution therapy with Pentaglobin.
  • Prophylaxis of deep vein thrombosis.
  • Preventing the formation of stress ulcers of the gastrointestinal tract using H2-receptor blockers and proton pump inhibitors.
  • Replacement renal therapy in acute renal failure due to severe sepsis.

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