Peritonitis is the acute or chronic peritoneal inflammation with characteristic local and general changes in the organism and severe dysfunction of organs and vital systems of the organism. Peritonitis is an inflammation of the peritoneum, the thin tissue that lines the inner wall of the abdomen and covers most of the abdominal organs. Peritonitis may be localized or generalised, and may result from infection (often due to rupture of a hollow organ as may occur in abdominal trauma or appendicitis) or from a non-infectious process.




The peritoneum is the largest and most complex serous membrane in the body. It forms a closed sac (ie, coelom) by lining the interior surfaces of the abdominal wall (anterior and lateral), by forming the boundary to the retroperitoneum (posterior), by covering the extraperitoneal structures in the pelvis (inferior), and by covering the undersurface of the diaphragm (superior). This parietal layer of the peritoneum reflects onto the abdominal visceral organs to form the visceral peritoneum. It thereby creates a potential space between the 2 layers (ie, the peritoneal cavity).

The peritoneum consists of a single layer of flattened mesothelial cells over loose areolar tissue. The loose connective tissue layer contains a rich network of vascular and lymphatic capillaries, nerve endings, and immune-competent cells, particularly lymphocytes and macrophages. The peritoneal surface cells are joined by junctional complexes, thus forming a dialyzing membrane that allows passage of fluid and certain small solutes. Pinocytotic activity of the mesothelial cells and phagocytosis by macrophages allow for clearance of macromolecules.

Normally, the amount of peritoneal fluid present is less than 50 mL, and only small volumes are transferred across the considerable surface area in a steady state each day. The peritoneal fluid represents a plasma ultrafiltrate, with electrolyte and solute concentrations similar to that of neighboring interstitial spaces and a protein content of less than 30 g/L, mainly albumin. In addition, peritoneal fluid contains small numbers of desquamated mesothelial cells and various numbers and morphologies of migrating immune cells (reference range is < 300 cells/μ L, predominantly of mononuclear morphology).

The peritoneal cavity is divided incompletely into compartments by the mesenteric attachments and secondary retroperitonealization of certain visceral organs. A large peritoneal fold, the greater omentum, extends from the greater curvature of the stomach and the inferior aspect of the proximal duodenum downward over a variable distance to fold upon itself (with fusion of the adjacent layers) and ascends back to the taenia omentalis of the transverse colon. This peritoneal fold demonstrates a slightly different microscopic anatomy, with fenestrated surface epithelium and a large number of adipocytes, lymphocytes, and macrophages, and it functions as a fat storage location and a mobile immune organ.

The compartmentalization of the peritoneal cavity, in conjunction with the greater omentum, influences the localization and spread of peritoneal inflammation and infections.


Etiology and pathogenesis


The main causes of peritonitis are the acute inflammation of abdominal viscera, discontinuity and disturbed permeability of their walls, open and closed traumas of the abdomen with the damage of viscera with following microbial contamination of peritoneal space.

Despite the cause of peritonitis, the disease is characterized by a typical bacterial inflammation. The infectious agents are represented by Escherichia colli, Staphylococcus and Enterococcus, Proteus, Streptococcus and also nonclostridial anaerobes. At least in 30 % of cases association of two or more agents occur.

Primary peritonites occur very rarely and result from pneumococcal, streptococcal and staphylococcal infection.

Besides microbial peritonites, caused by peritoneal contamination, distinguished also aseptic peritoneal inflammation, which result from entering of different chemical noninfectious agents into peritoneal cavity (blood, urine, bile, pancreatic juice, etc.). Its so called toxico-chemical peritonitis. But with the development of aseptic inflammation bacteria penetrate into peritoneal space with transformation of peritonitis into bacterial.

Chronic peritonitis is mainly caused by tuberculosis, which agents are usually located extraperitoneally (lungs, mediastinal lymph nodes) or in mesenteric lymph nodes and by hematogenous way enter the peritoneum.


Risk Factors:


The following factors may increase the risk for primary peritonitis:


Infected peritonitis

Perforation of part of the gastrointestinal tract is the most common cause of peritonitis. Examples include perforation of the distal oesophagus (Boerhaave syndrome), of thestomach (peptic ulcer, gastric carcinoma), of the duodenum (peptic ulcer), of the remaining intestine (e.g., appendicitis, diverticulitis, Meckel diverticulum, inflammatory bowel disease (IBD), intestinal infarction, intestinal strangulation, colorectal carcinoma, meconium peritonitis), or of the gallbladder (cholecystitis). Other possible reasons for perforation include abdominal trauma, ingestion of a sharp foreign body (such as a fish bone, toothpick or glass shard), perforation by an endoscope or catheter, andanastomotic leakage. The latter occurrence is particularly difficult to diagnose early, as abdominal pain and ileus paralyticus are considered normal in patients who have just undergone abdominal surgery. In most cases of perforation of a hollow viscus, mixed bacteria are isolated; the most common agents include Gram-negative bacilli (e.g.,Escherichia coli) and anaerobic bacteria (e.g., Bacteroides fragilis). Fecal peritonitis results from the presence of faeces in the peritoneal cavity. It can result from abdominal trauma and occurs if the large bowel is perforated during surgery.


Table. Microbial Flora of Secondary Peritonitis







Gram negative

Escherichia coli











Gram positive




























Other rare, nonsurgical causes of intra-abdominal sepsis include the following:

Chlamydia peritonitis;

Tuberculosis peritonitis;

Acquired immunodeficiency syndrome (AIDS)-associated peritonitis.


Disruption of the peritoneum, even in the absence of perforation of a hollow viscus, may also cause infection simply by letting micro-organisms into the peritoneal cavity. Examples include trauma, surgical wound, continuous ambulatory peritoneal dialysis, and intra-peritoneal chemotherapy. Again, in most cases, mixed bacteria are isolated; the most common agents include cutaneous species such as Staphylococcus aureus, and coagulase-negative staphylococci, but many others are possible, including fungi such as Candida.

Spontaneous bacterial peritonitis (SBP) is a peculiar form of peritonitis occurring in the absence of an obvious source of contamination. It occurs in patients with ascites, in particular, in children. See the article on spontaneous bacterial peritonitis for more information.

Intra-peritoneal dialysis predisposes to peritoneal infection (sometimes named "primary peritonitis" in this context).

Systemic infections (such as tuberculosis) may rarely have a peritoneal localisation.


Non-infected peritonitis

Leakage of sterile body fluids into the peritoneum, such as blood (e.g., endometriosis, blunt abdominal trauma), gastric juice (e.g., peptic ulcer, gastriccarcinoma), bile(e.g., liverbiopsy), urine (pelvic trauma), menstruum (e.g., salpingitis), pancreatic juice (pancreatitis), or even the contents of a ruptured dermoid cyst. It is important to note that, while these body fluids are sterile at first, they frequently become infected once they leak out of their organ, leading to infectious peritonitis within 24 to 48 hours.

Sterile abdominal surgery, under normal circumstances, causes localised or minimal generalised peritonitis, which may leave behind a foreign body reaction and/or fibroticadhesions. However, peritonitis may also be caused by the rare case of a sterile foreign body inadvertently left in the abdomen after surgery (e.g., gauze, sponge).

Much rarer non-infectious causes may include familial Mediterranean fever, TNF receptor associated periodic syndrome, porphyria, and systemic lupus erythematosus.



Peritonites are classified:

According to the character of microbial contamination:

A: primary

B: secondary.

According to clinical course:

A: acute

B: chronic.

According to the etiological agents:

A: peritonites, which caused by bacteria of digestive tract (E. colli, staphylococci, streptococci, proteus, anaerobes, etc.)

B: which caused by bacteria, which exist out of gastrointestinal tube (gonococci, pneumococci, streptococcus haemolyticus, etc.).

C: distinguished aseptic (nonbacterial peritonites), resulting from irritation by blood, bile, pancreatic juice or urine.

According to the character of exudate:

A: serous;

B: fibrinous;

C: fibrinopurulent;

D: purulent;

E: hemorrhagic;

F: "peritonitus sicca".

According to the extension of inflammatory process:

A: local;

B: diffuse;

C: generalized.


Dependent on duration of the disease and degree of pathological alterations in the clinical course of peritonitis distinguished three stages:

reactive (first 24 hours) maximal manifestation of local signs of the disease;

toxic (24-72 hours) gradual reducing of local signs and increasing of general intoxication.

terminal (after 72 hours) severe, often unreversable intoxication on the background of sharply expressed local manifestations of peritoneal inflammation.


Primary peritonitis.


Spontaneous bacterial peritonitis (SBP) is an acute bacterial infection of ascitic fluid. Contamination of the peritoneal cavity is thought to result from translocation of bacteria across the gut wall or mesenteric lymphatics and, less frequently, via hematogenous seeding in the presence of bacteremia.

SBP can occur as a complication of any disease state that produces the clinical syndrome of ascites, such as heart failure and Budd-Chiari syndrome. Children with nephrosis or systemic lupus erythematosus who have ascites have a high risk of developing SBP. The highest risk of SBP, however is in patients with cirrhosis who are in a decompensated state.  In particular, decreased hepatic synthetic function with associated low total protein level, low complement levels, or prolonged prothrombin time (PT) is associated with maximum risk. Patients with low protein levels in ascitic fluid (< 1 g/dL) have a 10-fold higher risk of developing SBP than those with a protein level greater than 1 g/dL. Approximately 10-30% of patients with cirrhosis and ascites develop SBP. The incidence rises to more than 40% with ascitic fluid protein contents of less than 1 g/dL (which occurs 15% of patients), presumably because of decreased ascitic fluid opsonic activity.

More than 90% of cases of SBP are caused by a monomicrobial infection.


Secondary peritonitis


Common etiologic entities of secondary peritonitis (SP) include perforated appendicitis; perforated gastric or duodenal ulcer; perforated (sigmoid) colon caused by diverticulitis, volvulus, or cancer; and strangulation of the small bowel. Necrotizing pancreatitis can also be associated with peritonitis in the case of infection of the necrotic tissue.

The pathogens involved in SP differ in the proximal and distal GI tract. Gram-positive organisms predominate in the upper GI tract, with a shift toward gram-negative organisms in the upper GI tract in patients on long-term gastric acid suppressive therapy. Contamination from a distal small bowel or colon source initially may result in the release of several hundred bacterial species (and fungi); host defenses quickly eliminate most of these organisms. The resulting peritonitis is almost always polymicrobial, containing a mixture of aerobic and anaerobic bacteria with a predominance of gram-negative organisms.

As many as 15% of patients who have cirrhosis with ascites who were initially presumed to have SBP have SP. In many of these patients, clinical signs and symptoms alone are not sensitive or specific enough to reliably differentiate between the 2 entities. A thorough history, evaluation of the peritoneal fluid, and additional diagnostic tests are needed to do so; a high index of suspicion is required.

Source Regions



Boerhaave syndrome
Trauma (mostly penetrating)


Peptic ulcer perforation
Malignancy (eg, adenocarcinoma, lymphoma, gastrointestinal stromal tumor)
Trauma (mostly penetrating)


Peptic ulcer perforation
Trauma (blunt and penetrating)

Biliary tract

Stone perforation from gallbladder (ie, gallstone ileus) or common duct
Choledochal cyst (rare)
Trauma (mostly penetrating)


Pancreatitis (eg, alcohol, drugs, gallstones)
Trauma (blunt and penetrating)

Small bowel

Ischemic bowel
Incarcerated hernia (internal and external)
Closed loop obstruction
Crohn disease
Malignancy (rare)
Meckel diverticulum
Trauma (mostly penetrating)

Large bowel and appendix

Ischemic bowel
Ulcerative colitis and Crohn disease
Colonic volvulus
Trauma (mostly penetrating)

Uterus, salpinx, and ovaries

Pelvic inflammatory disease (eg, salpingo-oophoritis, tubo-ovarian abscess, ovarian cyst)
Malignancy (rare)
Trauma (uncommon)

* Iatrogenic trauma to the upper GI tract, including the pancreas and biliary tract and colon, often results from endoscopic procedures; anastomotic dehiscence and inadvertent bowel injury (eg, mechanical, thermal) are common causes of leak in the postoperative period.


The most common cause of postoperative peritonitis is anastomotic leak, with symptoms generally appearing around postoperative days 5-7. After elective abdominal operations for noninfectious etiologies, the incidence of SP (caused by anastomotic disruption, breakdown of enterotomy closures, or inadvertent bowel injury) should be less than 2%. Operations for inflammatory disease (ie, appendicitis, diverticulitis, cholecystitis) without perforation carry a risk of less than 10% for the development of SP and peritoneal abscess. This risk may rise to greater than 50% in gangrenous bowel disease and visceral perforation.

After operations for penetrating abdominal trauma, SP and abscess formation are observed in a small number of patients. Duodenal and pancreatic involvement, as well as colon perforation, gross peritoneal contamination, perioperative shock, and massive transfusion, are factors that increase the risk of infection in these cases.

Peritonitis is also a frequent complication and significant limitation of peritoneal dialysis.  Peritonitis leads to increased hospitalization and mortality rates.


Tertiary peritonitis.


Tertiary peritonitis (see Table 3, below) develops more frequently in immunocompromised patients and in persons with significant preexisting comorbid conditions. Although rarely observed in uncomplicated peritoneal infections, the incidence of tertiary peritonitis in patients requiring ICU admission for severe abdominal infections may be as high as 50-74%.

Tuberculous peritonitis (TP) is rare in the United States (< 2% of all causes of peritonitis), but it continues to be a significant problem in developing countries and among patients with human immunodeficiency virus (HIV) infection. The presenting symptoms are often nonspecific and insidious in onset (eg, low-grade fever, anorexia, weight loss). Many patients with TP have underlying cirrhosis. More than 95% of patients with TP have evidence of ascites on imaging studies, and more than half of these patients have clinically apparent ascites.

In most cases, chest radiographic findings in patients with TP peritonitis are abnormal; active pulmonary disease is uncommon (< 30%). Results on Gram stain of ascitic fluid are rarely positive, and culture results may be falsely negative in up to 80% of patients. A peritoneal fluid protein level greater than 2.5 g/dL, a lactate dehydrogenase (LDH) level greater than 90 U/mL, or a predominantly mononuclear cell count of greater than 500 cells/μ L should raise suspicion of TP but have limited specificity for the diagnosis. Laparoscopy and visualization of granulomas on peritoneal biopsy specimens, as well as cultures (requires 4-6 wk), may be needed for the definitive diagnosis; however, empiric therapy should begin immediately.

Chemical peritonitis. Chemical (sterile) peritonitis may be caused by irritants such as bile, blood, barium, or other substances or by transmural inflammation of visceral organs (eg, Crohn disease) without bacterial inoculation of the peritoneal cavity. Clinical signs and symptoms are indistinguishable from those of SP or peritoneal abscess, and the diagnostic and therapeutic approach should be the same.

Peritoneal abscess. Peritoneal abscess describes the formation of an infected fluid collection encapsulated by fibrinous exudate, omentum, and/or adjacent visceral organs. The overwhelming majority of abscesses occurs subsequent to SP. Abscess formation may be a complication of surgery. The incidence of abscess formation after abdominal surgery is less than 1-2%, even when the operation is performed for an acute inflammatory process. The risk of abscess increases to 10-30% in cases of preoperative perforation of the hollow viscus, significant fecal contamination of the peritoneal cavity, bowel ischemia, delayed diagnosis and therapy of the initial peritonitis, and the need for reoperation, as well as in the setting of immunosuppression. Abscess formation is the leading cause of persistent infection and development of tertiary peritonitis.


Symptomatology and clinical course


The clinical picture of acute peritonitis is determined by the character of primary causative lesion, duration of inflammatory process, its extension and also the stage of the disease. Predominant clinical sign is the abdominal pain, which gradually increases. Firstly it is localized in the region of the source of peritonitis and then extends all over the abdomen. Elderly patients may experience lacking pain and even pay no attention on it, but general malaise, loss of appetite, and weakness are evident. This course is also characteristic for postoperative peritonitis, which results from parting of sutures (of anastomosis or site of perforation) or leaking colon carcinoma. Simultaneously with the increase of pain also change the general appearance. The patient looks anxious, with drawn features, hollowed-eyed. Further this is accompanied by nausea and vomiting: on initial stages vomit is of gastric contents, later duodenal and thereafter is of intestinal contents. With progression of the disease vomiting becomes constant, effortless and overcomes into frequent regurgitation by brown fluid with foul-smelling. Patient's lips and tongue are dry, with brown fur. Respiration is of thoracic type and is shallow and rapid. In order to prevent pain the patient speaks very quite. Every change of position results in increase of pain, thus the patient lies with the knee drawn up to relax the abdominal wall.

Often the vomiting is accompanied by hiccup, which results from irritation of diaphragmatic peritoneum. This is considered to be an unfavorable prognostic sign. The patient tries to retain distended abdomen by his hands during hiccup and thus provokes increase of pain.

During examination observed restricted movements of abdominal wall, which is mainly expressed over the inflammatory focus. Abdominal percussion reveals the region of maximal painfulness, which response the site of lesion, high tympanic sound as a result of intestinal gaseous dilatation, but sometimes dullness, caused by cumulation of great amount of exudate. On palpation revealed muscular tension of abdominal wall. Especially expressed the muscular rigidity in case of perforation of hollow organs ("board-like abdomen"). Pelvic location of peritonitis usually causes less clinical manifestations. In such cases a diagnostic value has digital examination of the rectum and bimanual palpation of the pelvis and lower abdomen, which reveals overhanging and painfulness of anterior rectal wall or posterior vaginal vault owing to accumulation of the exudate.

The clinical manifestation of peritonitis is various and individual. It depends on the character of primary lesion, extension of inflammatory process, and defensive properties of the organism. The main manifestations of peritonitis are acute abdominal pain, abdominal tenderness, and abdominal guarding, which are exacerbated by moving the peritoneum, e.g., coughing (forced cough may be used as a test), flexing one's hips, or eliciting the Blumberg sign (a.k.a. rebound tenderness, meaning that pressing a hand on the abdomen elicits less pain than releasing the hand abruptly, which will aggravate the pain, as the peritoneum snaps back into place). The presence of these signs in a patient is sometimes referred to as peritonism. The localization of these manifestations depends on whether peritonitis is localized (e.g., appendicitis or diverticulitis before perforation), or generalized to the whole abdomen. In either case, pain typically starts as a generalized abdominal pain (with involvement of poorly localizing innervation of the visceral peritoneal layer), and may become localized later (with the involvement of the somatically innervated parietal peritoneal layer). Peritonitis is an example of an acute abdomen.

Collateral manifestations: diffuse abdominal rigidity ("washboard abdomen") is often present, especially in generalized peritonitis, Fever, Sinus tachycardia, Development of ileus paralyticus (i.e., intestinal paralysis), which also causes nausea, vomiting and bloating.


In reactive stage of the disease the most common are the pain, muscular rigidity and positive Shchotkin-Blumberg's symptom. The general state changed a little the patient is active, sometimes excite. A moderate tachycardia and hypertension commonly observed.(Fig.1)




Fig.1. Shchotkin-Blumberg's symptom.


In toxic stage of the disease the pain and muscular defense tend to diminish, but on palpation the muscular tenderness and Shchotkin-Blumberg's symptom retain on the same level. More evident the signs of intestinal paresis (abdominal distension, absence of peristalsis). The general state is worsened. The patient is apathetic, the skin is blanched or cyanotic. Observed progressing of tachycardia, decreasing of blood pressure and rising of temperature. In blood analysis revealed leukocytosis and deviation of the differential count to the left.

In terminal stage of the disease the feeling of pain disappears, but the patient suffer from the uncontrollable vomiting by congested fecal contents. The patient is adynamic, with drawn features and blanched or cyanotic skin. The pulse becomes increasingly rapid small and thready. The arterial pressure tends to diminish. No peristalsis is evident and no bowel sounds are heard on auscultation. Shchotkin-Blumberg's symptom is slightly expressed. The respiration is rapid, with congested rales, and oliguria develops. This clinical pattern resembles a septic shock. The prognosis in this stage is serious and the patient will die if the urgent treatment is not be applied.

Plain films of the chest and abdomen with the patient in both supine and the erect position are essential. The chest x-ray examination assists in identifying thoracic causes of the acute abdomen and sometimes reveals specific x-ray findings of intraabdominal catastrophes (e.g. free air under the diaphragm associated with perforation of the gastrointestinal tract).

Laparoscopy is a rapid, direct, and often definitive method of identifying the cause of peritonitis in difficult cases. Finally, for patients who have acute intraabdominal problem of unknown nature and whose symptoms, signs, and laboratory findings are suggestive of a threat of life, exploratory laparotomy remains the most prudent diagnostic procedure.


Sequestration of fluid and electrolytes, as revealed by decreased central venous pressure, may cause electrolyte disturbances, as well as significant hypovolemia, possibly leading to shock and acute renal failure.

A peritoneal abscess may form (e.g., above or below the liver, or in the lesser omentum

Sepsis may develop, so blood cultures should be obtained.


Variants of clinical course and complications

Postoperative peritonitis is characterized by atypical and even asymptomatic course. This results from administering of analgesics, antibiotics and anesthetics. The general state of the patient after the operation is gradually worsens.

The most earliest and frequent sign of postoperative peritonitis is the increase of abdominal pain on the background of the previous satisfactory condition, tachycardia, high temperature, leukocytosis, deviation of the differential count to the left, elevation of erythrocyte sedimentation rate. The pain and muscular rigidity usually expressed slightly or absent at all. Later (on the 5-6th day) the general state continues to be worsened, which manifest by dry tongue, lack of peristalsis, expressed nausea, vomiting, tachycardia and shallow breathing. General weakness, adynamia, general intoxication and rebound tenderness symptoms progress. The outcomes of postoperative peritonitis are usually unfavorable, and they prevented by early repeated operation.

The specific complications of acute peritonitis include inflammatory infiltrates and abscesses of abdominal cavity (Fig.2) (subphrenic, subhepatic, interintestinal and pelvic), dynamic ileus, intestinal fistula, suppuration of postoperative wound, eventration, peritoneal adhesions, etc.

Fig.2.Localizations of abscesses of abdominal cavity

1, 2 Right and left subdiafragmatic abscesses

3 - Subhepatic abscess

4 Interintestinal abcesses

5, 6, 7 Right iliac abscesses

8 Left iliac abscess

9 Abscess of the small pelvis (Douglas space abscess)

The patients with subphrenic abscess (Fig.3) as a rule complain of the pain in epigastrium and lower chest, which irradiates into the shoulder and increases during cough and deep breathing. Sometimes revealed painfulness during digital pressing and swelling of soft tissues in the region of 7-10th Intercostals space. The patients are suffering from nausea, hiccup, and high temperature. Sometimes they must stay in forced position: supine or semisedentary. The tongue is dry, the abdomen is slightly bloated, and rebound tenderness symptoms are usually absent. In blood revealed leukocytosis, deviation of the differential count to the left. The abscess requires a surgical treatment. If the abscess is located near anterior abdominal wall, it is drained by means of oblique access under the costal arch. The abscesses, which located in posterior subphrenic space, are drained after the previous puncture through the access after resection of X rib. (Fig.4)

Fig.3. Subphrenic abscess


Fig.4. Dranaige of subdiafragmatic abscess


Subhepatic abscess is characterized by the pain and presence of infiltrate below right costal arch, positive Shchotkin-Blumberg symptom. The abscess is drained through the incision along right costal arch.

The clinical pattern of interintestinal abscess is vague. It is formed mostly on the 12-14th day after appearance of peritonitis. The patients complain of the high temperature and dull pain in the site of its location. The abdomen is soft, but during palpation revealed dense, painful infiltrate. In case of localization near to abdominal wall one can observe muscular tension and positive Shchotkin-Blumberg symptom. The roentgenological or ultrasound investigation often reveals focal shadow with air-fluid level. The abscess is drained over the site of its localization, dividing the bowel loops.

Abscesses of small pelvis mostly occur as a result of appendicitis(Fig.5) or accumulation of the exudates in Douglas space in diffuse peritonitis.


Fig.5. The localization of appendiceal abscess

depending the appendix location


Such patients complain of constant pain in the lower abdomen, high temperature, painful urinary excretion and tenesmus. The palpation of the abdomen usually reveals no pathology. But the digital rectal examination finds out a painful infiltrate that drawn into the rectum. (Fig.6) The mucosa over the infiltrate is edematous and immovable. The vaginal examination of the female patients reveals overhanging of posterior vaginal vault and painfulness of cervical shift. Often on the background of solid consistency of the infiltrate the softened regions are palpated, which respond to accumulation of pus. The purulent sites of small pelvis in males are drained through the anterior wall of the rectum and in females through the posterior vaginal vault. For this purpose the infiltrate is punctured by thick needle and under its check the abscess is drained by means of scalpel incision. Then the incision is expanded by clamp, the pus is aspirated and the abscess cavity is drained by rubber strap, which is fixed to perineum.







Fig. 6. Diagnotic and management of Douglas space abscess

A - Digital rectal examination

B Diagnostic puncture through anterior rectal wall

C The drainage is placed through anterior rectal wall


The diagnostic program


Complaints and history of the disease.

Physical findings.

General blood and urine analyses.

Biochemical blood analysis (protein and its fractions).

Examination of the exudate (bacteriological, cytological).

Laparoscopy. (Fig.7)

Plain film of the abdomen.



Fig.7. Purulent peritonitis(Laparoscopic picture)


Tests and diagnosis


To diagnose peritonitis, your doctor will talk with you about your medical history and perform a physical exam. When peritonitis is associated with peritoneal dialysis, your signs and symptoms, particularly cloudy dialysis fluid, may be enough for your doctor to diagnose the condition.

In cases of peritonitis in which the infection may be a result of other medical conditions (secondary peritonitis) or in which the infection arises from fluid buildup in your abdominal cavity (spontaneous peritonitis), your doctor may recommend the following tests to confirm a diagnosis:

Peritoneal fluid analysis. Using a thin needle, your doctor may take a sample of the fluid in your peritoneum (paracentesis). If you have peritonitis, examination of this fluid may show an increased white blood cell count, which typically indicates an infection or inflammation. A culture of the fluid may also reveal the presence of bacteria.

Diagnostic paracentesis should be performed in all patients who do not have an indwelling peritoneal catheter and are suspected of having SBP. In peritoneal dialysis patients with a peritoneal catheter, fluid should be withdrawn using sterile technique. Ultrasonography may aid paracentesis if ascites is minimally detectable or questionable.

The results of aerobic and anaerobic bacterial cultures, used in conjunction with the cell count, prove the most useful in guiding therapy for those with SBP. With regard to ascitic fluid culture, direct inoculation of routine blood culture bottles at the bedside with 10 mL of ascitic fluid has been reported to significantly increase the sensitivity of microbiologic studies.

The single best predictor of SBP is an ascitic fluid neutrophil count of greater than 500 cells/L, which carries a sensitivity of 86% and a specificity of 98%. By lowering the ascitic fluid neutrophil count threshold to 250 cells/μ L, the sensitivity increases to 93% with only a minimal decrease in specificity to 94%.

The fluid should be evaluated for glucose, protein, lactate dehydrogenase (LDH), cell count, Gram stain, and aerobic and anaerobic cultures. If pancreatitis or a pancreatic leak is suspected, amylase analysis should be added to the panel. Bilirubin and creatinine levels can be analyzed as well, if a biliary or urinary leak is suspected as a possible etiology. The peritoneal/ascitic fluid characteristics or levels are then compared with their respective serum values.

The fluid in bacterial peritonitis generally demonstrates a low pH and low glucose levels with elevated protein and LDH levels. Traditionally, ascitic fluid pH of less that 7.34 was consistent with a diagnosis of SBP; however, ascitic pH is less commonly measured because it is unreliable and lacks specificity for the condition.

SBP is established when the polymorphonuclear neutrophil (PMN) count is 250 cells/L or greater in conjunction with a positive bacterial culture result. In most of these cases, as mentioned previously, cultures are positive for a single organism. Obviously, these patients should receive antibiotic therapy. Although up to 30% of cultures remain negative, most of these patients are presumed to have bacterial peritonitis; they should be treated. A significantly decreased peritoneal fluid glucose level (< 50 mg/dL), a peritoneal fluid LDH level much greater than the serum LDH, a peritoneal fluid WBC count greater than 10,000 cells/L, a pH lower than 7.0, high amylase levels, multiple organisms on Gram stain, or recovery of anaerobes from the culture raises the suspicion of SP in these patients. Some authors recommend repeating the paracentesis in 48-72 hours to monitor treatment success (decrease in neutrophil count to < 50% of the original value).

Culture-negative neutrocytic ascites (probable SBP) is established when the ascitic fluid culture results are negative but the PMN count is 250 cells/L or greater. This may happen in as many as 50% of patients with SBP and may not actually represent a distinctly different disease entity. Rather, it may be the result of poor culturing techniques or late-stage resolving infection. Nonetheless, these patients should be treated just as aggressively as those with positive culture results.

Monomicrobial nonneutrocytic bacterascites exists when a positive culture result coexists with a PMN count 250 cells/L or greater. Although this may often be the result of contamination of bacterial cultures, 38% of these patients develop SBP. Therefore, monomicrobial nonneutrocytic bacterascites may represent an early form of SBP. All study patients described who eventually developed SBP were symptomatic. For this reason, any patient suspected clinically of having SBP in this setting must be treated.

Tuberculous peritonitis is identified by ascites with high protein content, a low glucose and low SAAG, elevated ascitic fluid WBC count, and lymphocyte predominance. In TP, the fluid Gram stain and acid-fast stain results are rarely positive, and routine culture results are falsely negative in as many as 80% of cases. A peritoneal fluid protein level greater than 2.5 g/dL, LDH level greater than 90 U/mL, and predominantly mononuclear cell count of more than 500 cells/L should raise the suspicion of TP, but specificity for the diagnosis is limited. Laparoscopy with visualization of granulomas on peritoneal biopsy and specific culture (which requires 4-6 wk) may be needed for definitive diagnosis.

Peritonitis in patients receiving continuous ambulatory peritoneal dialysis (CAPD) is indicated by contamination of the dialysis catheter; cloudy effluent, total fluid WBC count of greater than 100 neutrophils/L, or presence of organisms on Gram stain.

Routine intraoperative peritoneal fluid cultures in defined acute disease entities (ie, gastric or duodenal ulcer perforation, appendicitis, diverticulitis or perforation of the colon caused by obstruction or ischemia) are controversial. Several studies found no significant difference in patients with appendicitis, diverticulitis, and other common etiologies for bacterial peritonitis with regard to postoperative complication rates or overall outcomes. The antibiotic regimen was altered only 8-10% of the time based on operative culture data. In patients who had previous abdominal operations or instrumentation (eg, peritoneal dialysis catheter, percutaneous stents) and patients with prolonged antibiotic therapy, critical illness, and/or hospitalization, these cultures may reveal resistant or unusual organisms that should prompt alteration of the antibiotic strategy.

For a summary of ascitic fluid analysis, see table, below.

Table. Ascitic Fluid Analysis Summary




Less Helpful

Cell count

Obtain culture in blood culture (BC) bottles.

Tuberculosis (TB) smear and culture






Total protein

Lactate dehydrogenase (LDH)








Gram stain


Alpha 1-antitrypsin






Blood tests. A sample of your blood may be drawn and sent to a lab to check for a high white blood cell count. A blood culture also may be performed to determine if there are bacteria in your blood.

Most patients will have leukocytosis (>11,000 cells/μ L), with a shift to the immature forms on the differential cell count. Patients who have severe sepsis, are immunocompromised, or have certain types of infections (eg, fungal, cytomegaloviral) may not have leukocytosis or leukopenia. In cases of suspected SBP, hypersplenism may reduce the polymorphonuclear leukocyte count.

Blood chemistry findings may reveal dehydration and acidosis. PT, PTT, and INR are indicated. Liver function tests may be indicated. Amylase and lipase levels should be obtained if pancreatitis is suspected. Blood culture results are positive for the offending agent in as many as 33% of patients with SBP and may help guide antibiotic therapy. Measurement of serum albumin allows calculation of the serum-to-ascites albumin gradient (SAAG). A SAAG of more than 1.1 is noted in SBP.

Imaging tests. Your doctor may want to use an X-ray to check for holes or other perforations in your gastrointestinal tract. Ultrasound may also be used. In some cases, your doctor may use a computerized tomography (CT) scan instead of an X-ray.

Radiography.Plain films of the abdomen (eg, supine, upright, and lateral decubitus positions) are often the first imaging studies obtained in patients presenting with peritonitis. Their value in reaching a specific diagnosis is limited.

Ultrasonography. Abdominal ultrasonography may be helpful in the evaluation of pathology in the right upper quadrant (eg, perihepatic abscess, cholecystitis, biloma, pancreatitis, pancreatic pseudocyst), right lower quadrant, and pelvis (eg, appendicitis, tubo-ovarian abscess, Douglas pouch abscess). However, the examination is sometimes limited because of patient discomfort, abdominal distention, and bowel gas interference. Ultrasonography may detect increased amounts of peritoneal fluid (ascites), but its ability to detect quantities of less than 100 mL is limited. The central (perimesenteric) peritoneal cavity is not visualized well with transabdominal ultrasonography. Examination from the flank or back may improve the diagnostic yield, and providing the ultrasonographer with specific information about the patient's condition and the suspected diagnosis before the examination is important. With an experienced ultrasonographer, a diagnostic accuracy of greater than 85% has been reported in several series. Ultrasonographically guided aspiration and placement of drains has evolved into a valuable tool in the diagnosis and treatment of abdominal fluid collections. Advantages of ultrasound include low cost, portability, and availability. Disadvantages are that the test is operator dependent, and there is reduced visualization in the presence of overlying bowel gas and abdominal dressings.

CT scanning. If the diagnosis of peritonitis is made clinically, a CT scan is not necessary and generally delays surgical intervention without offering clinical advantage. However, CT scanning is indicated in all cases in which the diagnosis cannot be established on clinical grounds and findings on abdominal plain films. CT scans of the abdomen and pelvis remain the diagnostic study of choice for peritoneal abscess and related visceral pathology.

Whenever possible, the CT scan should be performed with enteral and intravenous contrast. CT scans can detect small quantities of fluid, areas of inflammation, and other GI tract pathology, with sensitivities that approach 100%. (See the image below.) CT scanning can be used to evaluate for ischemia, as well as to determine bowel obstruction. An abscess is suggested by the presence of fluid density that is not bound by the bowel or other known structures. Gas within an abdominal mass or the presence of an enhancing wall and adjacent inflammatory changes are also highly suggestive of an abscess. Ischemia can be demonstrated by a clot in a large vessel or by the absence of blood flow. Gas within the intestinal wall or in the portal vein may also suggest ischemia.

Free air is present in most cases of anterior gastric and duodenal perforation but is much less frequent with perforations of the small bowel and colon and is unusual with appendiceal perforation. Upright films are useful for identifying free air under the diaphragm (most often on the right) as an indication of a perforated viscus. Remember that the presence of free air is not mandatory with visceral perforation and that small amounts of free air are missed easily on plain films.

In abscess formation subsequent to secondary peritonitis (SP), approximately half of patients have a simple abscess without loculation, and the other half have complex abscesses secondary to fibrinous septation and organization of the abscess material. Abscess formation occurs most frequently in the subhepatic area, the pelvis, and the paracolic gutters, but it may also occur in the perisplenic area, the lesser sac, and between small bowel loops and their mesentery.

Peritoneal abscesses and other fluid collections may be aspirated for diagnosis and drained under CT guidance; this technique has become a mainstay of therapy.

MRI. MRI is an emerging imaging modality for the diagnosis of suspected intra-abdominal abscesses. Abdominal abscesses demonstrate decreased signal intensity on T1-weighted images and homogeneous or heterogeneous increased signal intensity on T2-weighted images; abscesses are observed best on gadolinium-enhanced, T1-weighted, fat-suppressed images as well-defined fluid collections with rim enhancement.

Limited availability and high cost, as well as the need for MRI-compatible patient support equipment and the length of the examination, currently limit its usefulness as a diagnostic tool in acute peritoneal infections, particularly for patients who are critically ill.


The above tests may also be necessary if you're receiving peritoneal dialysis and a diagnosis of peritonitis is uncertain after a physical exam and an examination of the dialysis fluid.\


Differential diagnostics


Thoracic processes with diaphragmatic irritation (eg, empyema), extraperitoneal processes (eg, pyelonephritis, cystitis, acute urinary retention), and abdominal wall processes (eg, infection, rectus hematoma) may mimic certain signs and symptoms of peritonitis. Always examine the patient for the presence of external hernias to rule out intestinal incarceration.

According to Adler and Gasbarra, the following should be considered in the differential diagnosis:

Aneurysm, Abdominal


Appendicitis, Acute

Mesenteric Ischemia

Urinary Tract Infection in Females

Whipple Disease

Chemical irritants (eg, bile, blood, gastric juice, barium, enema or douche contents)

Chronic peritoneal dialysis

Chylous peritonitis

Eosinophilic peritonitis

Familial Mediterranean fever

Fungal infections (eg, histoplasmosis, cryptococcosis, coccidioidomycosis)

Granulomatous peritonitis (eg, parasitic infestations, sarcoidosis, tumors, Crohn disease, starch granules)

Gynecologic disorders (Chlamydia peritonitis, salpingitis, endometriosis, teratoma, leiomyomatosis, dermoid cyst)

HIV-associated peritonitis (from opportunistic organisms)

Mesothelial hyperplasia and metaplasia

Neoplasms (eg, primary mesothelioma, secondary carcinomatosis, Pseudomyxoma peritonei)

Parasitic infections (eg, schistosomiasis, ascariasis, enterobiasis, amebiasis, strongyloidiasis)

Perforated viscus

Peritoneal encapsulation

Peritoneal loose bodies and peritoneal cysts

Peritoneal lymphangiectasis


Sclerosing peritonitis


Vascular conditions (eg, mesenteric embolus, mesenteric nonocclusive ischemia, ischemic colitis, portal vein thrombosis, mesenteric vein thrombosis)

Vasculitis (eg, systemic lupus erythematosus, allergic vasculitis [Henoch-Schönlein purpura], Kohlmeier-Degos disease, polyarteritis nodosa)


The differential diagnostics in toxic and terminal stage of peritonitis when the typical signs of the disease are present commonly makes no difficulties. But in initial (reactive) stage the sings are similar to manifestation of causative disease appendicitis, cholecystitis, pancreatitis, etc.). But there are variety of disorders, which according to their manifestation resemble peritonitis, renal colic for instance. A sharp pain, nausea, vomiting, intestinal paralysis, and false Shchotkin-Blumberg symptom (peritonism) frequently lead to misdiagnostics. A periodical pain attack with typical irradiation in thigh, perineum, dysuria, positive Pasternatsky's symptom, lack of inflammatory changes in blood analysis, presence of erythrocytes in urine help to make correct diagnosis. For its improvement applied x-ray film of the abdomen, urography and chromocystoscopy.

A diffuse abdominal pain, muscular tension of abdominal wall and peritonism often accompany hemorrhagic diatheses (Schonlein-Henoch's disease). This disorder mostly occurs in young people and manifests by multiple small hemorrhages on skin (forearm, chest, and thigh), mucous membranes of cheeks, tongue and peritoneum as well. The rectal examination reveals tarry stool or melena. In blood thrombocytopenia is observed.

Myocardial infarction especially in its location on posterior wall (abdominal form) usually accompanied by epigastric pain, nausea and vomiting. Also revealed abdominal wall tension with phenomena of peritonism. But ischemic heart disease in history and characteristic ECG changes can favor correct diagnostics.

Basal pleurisy and acute lower lobe pneumonia, causing the pain and muscular guard in epigastrium, also resemble peritonitis. Only thorough clinical examination leads to correct diagnostics.


Tactics and choice of treatment


Approach considerations. The current approach to peritonitis and peritoneal abscesses targets correction of the underlying process, administration of systemic antibiotics, and supportive therapy to prevent or limit secondary complications due to organ system failure. treatment success is defined as adequate source control with resolution of sepsis and clearance of all residual intra-abdominal infection.

Early control of the septic source is mandatory and can be achieved by operative and nonoperative means.


Nutrition and Dietary Supplements


Peritonitis is a medical emergency and should be treated by a medical doctor. Do not try to treat peritonitis with herbs or supplements. However, a comprehensive treatment plan for recovering from peritonitis may include a range of complementary and alternative therapies. Ask your team of health care providers about the best ways to incorporate these therapies into your overall treatment plan. Always tell your health care provider about the herbs and supplements you are using or considering using.

These good nutrition habits may help you recover from any serious illness:

                   Eat antioxidant foods, including fruits (such as blueberries, cherries, and tomatoes) and vegetables (such as squash and bell peppers).

                   Eat foods high in B-vitamins and calcium, such as almonds, beans, whole grains (if no allergy), dark leafy greens (such as spinach and kale), and sea vegetables.

                   Avoid refined foods, such as white breads, pastas, and especially sugar.

                   Eat fewer red meats and more lean meats, cold-water fish, tofu, or beans for protein.

                   Use healthy oils in foods, such as olive oil or vegetable oil.

                   Avoid caffeine, alcohol, and tobacco.

                   Drink 6 - 8 glasses of filtered water daily.

                   Ask your doctor about taking a multivitamin daily, containing the antioxidant vitamins A, C, E, the B-complex vitamins, and trace minerals such as magnesium, calcium, zinc, and selenium.

                   Probiotic supplement (containing Lactobacillus acidophilus among other species), 5 - 10 billion CFUs (colony forming units) a day, for gastrointestinal and immune health. Probiotics can be especially helpful when taking antibiotics, because probiotics can help restore the balance of "good" bacteria in the intestines.

Operative management addresses the need to control the infectious source and to purge bacteria and toxins.

The type and extent of surgery depends on the underlying disease process and the severity of intra-abdominal infection. Definitive interventions to restore functional anatomy involve removing the source of the antimicrobial contamination and repairing the anatomic or functional disorder causing the infection. This is accomplished by surgical intervention. Occasionally, this can be achieved during a single operation; however, in certain situations, a second or a third procedure may be required. In some patients, definitive intervention is delayed until the condition of the patient improves and tissue healing is adequate to allow for a (sometimes) lengthy procedure.

To see complete information on the Surgical Approach to Peritonitis and Abdominal Sepsis, please go to the main article by clicking here.

Nonoperative interventions include percutaneous abscess drainage, as well as percutaneous and endoscopic stent placements. If an abscess is accessible for percutaneous drainage and if the underlying visceral organ pathology does not clearly require operative intervention, percutaneous drainage is a safe and effective initial treatment approach. With percutaneous treatment, the definition of success includes the avoidance of further operative intervention and, in some cases, the delay of surgery until after resolution of the initial sepsis.

The general principles guiding the treatment of infections are 4-fold, as follows:

Control the infectious source

Eliminate bacteria and toxins

Maintain organ system function

Control the inflammatory process

The treatment of peritonitis is multidisciplinary, with complementary application of medical, operative, and nonoperative interventions. Medical support includes the following:

Systemic antibiotic therapy

Intensive care with hemodynamic, pulmonary, and renal support

Nutrition and metabolic support

Inflammatory response modulation therapy

Early control of the septic source is mandatory and can be achieved by operative and nonoperative means. Nonoperative interventional therapies include percutaneous drainage of abscesses and percutaneous and endoscopic stent placements.

Treatment of peritonitis and intra-abdominal sepsis always begins with volume resuscitation, correction of potential electrolyte and coagulation abnormalities, and empiric broad-spectrum parenteral antibiotic coverage.

The treatment of acute peritonitis should be always carried out with appreciation of clinical form and stage of the disease, causative factor, extension of inflammatory process, degree of metabolic disturbances and dysfunction of vital organs of the patient.

The complex of treatment of peritonitis should include:

early operative approach in order to liquidate the source of peritonitis;

sanation of peritoneal cavity by means of lavage, adequate drainage and antibiotic therapy;

intubation and decompression of gastrointestinal tract and liquidation of paralytic ileus; (Fig.8)

metabolic correction (acid-base balance, blood electrolytes, protein metabolism, energetic metabolism);

restore and support of visceral function (kidney, liver, heart, lung) and prevention of complications.


Fig.8. Principles of nasogastrointestinal intubation



Gastric probe-guide is placed


2. Beginning of intubation


3. Intubation till caecum

through the gastric probe-guide

distally to pylorus per os


4. Removing of gastric probe

5. Fixation of proximal part

of intestinal probe to the nasal cathether





6. Removing of proximal part of intestinal


7. Proximal part is removed through the nose

probe from the oral cavity through the nose



8. Final view of nasogastrointestinal intubation


Fig.8. Principles of nasogastrointestinal intubation

The preoperative preparation in patients with peritonitis should be individual and lasted at least 2-3 hours. In extremely advanced cases, which associated with toxic shock and low arterial pressure it can last to 4-6 hours and must include nasogastric decompression of the stomach with active aspiration, catheterization of two veins, one of which is central, catheterization of bladder for diuresis control, infusion therapy.

The infusion therapy includes 5 % solution of glucose, solution of albumins, plasma, rheopolyglucin, vitamins of B and C group, solution of sodium hydrocarbonatis. The volume of fluid infusion should be at least 1.5-2 l. If there are no improvement of patient's condition before the operation, the infusion therapy must go on during operative approach.

The most common access in diffuse peritonitis is a median laparotomy, which is the most suitable for abdominal revision. In case of localized peritonitis (acute appendicitis) oblique incision may be used. The main goal of surgery must be elimination of infectious focus (appendectomy, cholecystectomy) or closure of stomach opening (perforating ulcer) or disrupture of hollow viscera. The exudate must be maximum removed and peritoneal cavity washed up by antiseptic solutions and thereafter the intestinal decompression and draining of peritoneal space is performed.

Fig.9. Scheme of the draining abdominal cavity

at extensive purulent peritonitis


In diffuse peritonitis the peritoneal cavity is drained in right and left hypochondrium and both left and right inguinal regions. It is better to use double or multiple polyethylene tubes, which are the most suitable for peritoneal dialysis. ( Fig.9);( Fig.10);( Fig.11)


Fig.9. Localization of the drainages at peritoneal dialysis



Fig.10. Scheme of localization of the drainages

at peritoneal dialysis(Lateral view)




Fig.11. The position of the patient at peritoneal dialysis


Thus the infectious exudate and toxic substances are eliminated and antibiotics and antiseptic solutions are flown into the abdomen through these tubes. In 1.5-2 hours after the operation before the dialysis the patient takes a semisedentary position. Then the solutions flow in through the upper tubes and flow out through the lower. This procedure is performed as far as the solution from the lower tubes becomes clear, using for this purpose 10-25 l. of fluid.

In recent years instead of dialysis applied peritoneal lavage. Controllable peritoneostomy(Fig.12) in association with lavage, epidural anesthesia and intestinal intubation allow to rather promptly carry out sanation of peritoneal cavity and liquidation of inflammatory process. These procedures are repeated in 1-2 days up to complete elimination of pus, fibrin and necrotic tissues. After the last sanation the abdominal wall is closed.



Fig.12. Wide plane drainage of abdominal cavity(begining):

bottom of operative wound


tube for irrigation

gauze drainages

laparotomy wound margins





Fig.12. Wide plane drainage of abdominal cavity(finishing):

laparotomy wound margins

sutures on the skin

gauze(matrix), which covers drainages

tube for irrigation



Fig.13. Reconstruction of anterior abdominal wall

laparotomy wound margins

rubber-line dranaige

primary delayed suture


Antibacterial therapy is performed by means of intraabdominal and parenteral (intramuscular, intravenous, endolymphatic) administering of antibiotics. It is desirable to use broad-spectrum antibiotics and after results of antibioticogram possible to apply direct correction. The antibiotics are advisable to use in combination with sulfanilamides, metrogyl, immunostimulators.

A struggle against paralytic ileus is a very important in the complex of treatment of peritonitis. It should begin during operation by means of intestinal decompression, mesenteric blockade, gastric lavage, and detoxycation therapy. For restitution of peristalsis used proserin, 10 % solution of sodium chloride, hypertonic enema. One of the most important factors in the treatment of peritonitis is the complete restore of the volume of circulating blood, correction of acid-base balance, blood electrolytes, protein metabolism. The total amount of fluid is calculated with account of its loss during vomiting, urinary excretion, drainage discharges and also respiration. For energetic compensation infused concentrated solution of glucose, sorbitol and lipid emulsion. Also plasma, erythrocyte and blood transfusions are used. In order to prevent hypoxia oxygenotherapy or hyperbaric oxygenation are applied.



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