Secondary peritonitis

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Shivani Chaparala M.B.B.S [2]
Synonyms and keywords:: Surgical peritonitis, Perforation peritonitis, Acute peritonitis, Acute bacterial peritonitis, Acute generalized peritonitis, Abscess of suppurative peritonitis, Purulent peritonitis, Chemical peritonitis, Peritoneal abscess.

Secondary peritonitis is the most common cause of peritonitis, seen in 80-90% of patients, as a result of inflammation, perforation, or gangrene of an intra-abdominal or retroperitoneal organ. Surgical intervention is typically required to treat these processes. Antibiotics play an adjunctive role in severe intra-abdominal infection. If left untreated, patients with secondary peritonitis usually die due to life-threatening sepsis and shock.

Secondary peritonitis is defined as the infection of the peritoneum due to spillage of organisms into the peritoneal cavity resulting from hollow viscus perforation, anastomotic leak, ischemic necrosis, or other injuries of the gastrointestinal tract.^[1]

• Mikulicz 1889; Krönlein 1885; Körte 1892 reported the surgical treatment of peritonitis.
• Kirschner in 1926 was the first to demonstrate a reduction in mortality rate by surgical treatment from 80–100% to about 60% in 1926.

Secondary peritonitis is classified based on the etiology and extension of inflammation.

Disturbances in the intestinal mucosal barrier as a result of spontaneous disease, trauma, or surgical operations permit the escape of indigenous bacteria causing infection of the peritoneum.

Risk factors of Secondary peritonitis are numerous intraabdominal disorders involving the gastrointestinal or genitourinary tract with spillage of material into the peritoneal space.

The prognosis and outcome of patients with postoperative peritonitis is directly related to early diagnosis and stringent treatment interventions along with the complex interaction of factors related to: patient, disease and intervention and the chronic health status. Septicemia, shock and renal failure account for life threatening complications of peritonitis.^[7]The mortality of generalized postoperative peritonitis is high at 22-55%. Inability to clear the abdominal infection or to control the septic source, older age, and unconsciousness were significant factors related to mortality. Failure to control the peritoneal infection (15%) increases fatality and correlates with failed septic source control, high Acute Physiology and Chronic Health Evaluation (APACHE) II score, and male gender. Failure to control the septic source (8%) also was always fatal and correlated with high APACHE II score and therapeutic delay. In patients with immediate source control, residual peritonitis occurred in 9% after purulent or biliary peritonitis and in 41% after fecal peritonitis. In patients without immediate control of the septic source, delayed control was still achieved in 100% after a planned relaparotomy (PR) strategy versus 43% after an on-demand relaparotomy (ODR). ^[8]

Diagnostic criteria for peritonitis associated with perforation on the basis of the initial ascitic fluid analysis include fulfilling at least two of the following criteria:[8]

• Total protein > 1 g/dl
• Glucose < 50 mg/dl
• Lactate dehydrogenase (LDH) greater than the upper limit of normal for serum.

Non perforated secondary peritonitis such as perinephric abscess, cannot be readily apparent on the basis of the initial ascitic fluid analysis, but the response of the ascitic fluid cell count and cultures to treatment can raise suspicion of this form of secondary peritonitis.

The clinical picture of peritonitis is determined by the nature of the causative lesion, duration and extension of the inflammatory process, and stage of the disease.

The main manifestations of peritonitis are acute abdominal pain, tenderness, and guarding, which are exacerbated by moving the peritoneum, e.g. coughing, flexing the hips, or eliciting the Blumberg sign (a.k.a. rebound tenderness, meaning that pressing a hand on the abdomen elicits pain, but releasing the hand abruptly will aggravate the pain, as the peritoneum snaps back into place). Abdominal rigidity, generalized peritonitis (versus localized), hypotension, tachycardia and anemia were significantly associated with mortality.

As the clinical signs and symptoms are not a good representation for the diagnosis of secondary peritonitis, initial ascitic fluid analysis and the response of ascitic fluid parameters to treatment have been found to be of great value in differentiating secondary peritonitis from spontaneous bacterial peritonitis.

An upright and supine plain films of the chest and abdomen should be performed in patients with abdominal pain to exclude free air under the diaphragm (most often on the right), which signals a bowel perforation and associated peritonitis.

CT may be positive in unto 82%. Indicated in all patients with acute abdomen. However, CT can be omitted when a diagnosis is made according to the results of precedent examinations such as Ultrasound. Radiation exposure should be considered with the use of CT.

Ultrasound may be positive in unto 72%. It is recommended as a screening test for acute abdomen and strongly recommended particularly when abdominal aortic aneurysm rupture or acute cholecystitis is suspected. Ultrasound is recommended in pregnant women, young women or children in whom radioactive exposure is not desirable.

Medical management of secondary peritonitis includes hydration, prevention of septicemia, and correction of electrolytes. Empiric coverage for gram positive, gram negative, and anaerobic bacteria should be initiated promptly while awaiting culture results. Either open abdominal surgery or an exploratory laparotomy is recommended.

The surgical treatment of postoperative peritonitis is primarily aimed at defining source control, followed by debridement of fibrin bedding and abdominal lavage of contaminants and infectious fluids. In cases of suspected diffuse secondary peritonitis, indication for relaparotomy after positive findings in CT were based on the following citeria: Evidence of leakage, intraabdomnal air after more than five days postoperatively, and/or massive collection of intraabdominal fluid. Re-laparotomy has to be performed immediately following positive radiological examination and/or clinical/laboratory signs. In postoperative peritonitis, negative radiological findings and persistent symptoms of sepsis for longer than 24 hours were also indications for relaparotomy.^[9][10][11]

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Shivani Chaparala M.B.B.S [2]

Surgical treatment was described in 1885 while its effectiveness was proven in 1926.

• Mikulicz (1889), Krönlein (1885) ,and Körte (1892) reported the surgical treatment of peritonitis.
• Kirschner in 1926 was the first to demonstrate a reduction in mortality rate by surgical treatment from 80–100% to about 60% in 1926.^[1]

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Shivani Chaparala M.B.B.S [2]

Secondary peritonitis can be classified according to the origin and extent of inflammation into Acute perforation peritonitis, Postoperative peritonitis, and Post-traumatic peritonitis.

Secondary peritonitis can be classified according to the origin and extent of inflammation into:^[1]

• Gastrointestinal perforation
• Intestinal ischemia
• Pelvi-peritonitis and other forms

• Anastomotic leak
• Accidental perforation and devascularization

• After blunt abdominal trauma
• After penetrating abdominal trauma

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Shivani Chaparala M.B.B.S [2]

Secondary bacterial peritonitis is caused by inoculation of bacteria from the (GI lumen or during surgical procedures) in the peritoneal cavity.

• Bacteria can reach the peritoneal cavity by a variety of pathologic processes:
  • Transmural inflammation with luminal obstruction
  • Perforation of the GI tract
  • Intestinal ischemia
• The initial inoculum of bacteria is determined by the normal flora in the involved portion of the GI tract.

Microbial organisms causing secondary peritonitis depends on the site of the gut perforation.^[1]

• Small bowel perforation: Consist mainly of enterococci and Escherichia coli
• Distal small bowel lumen perforation: Mostly Enterobacteriaceae and anaerobic organisms, including the Bacteroides spp.
• Colon: Mostly anaerobes (e.g. Peptostreptococcus, Clostridium, and most commonly Bacteroides sis)

Bacteria and digestive enzymes act on the peritoneal serosal surface resulting in enzymatic digestion, necrosis and an outpouring of serum protein and electrolytes from the blood into the peritoneal cavity, together with the formation of an exudate rich in granulocytes. The inflammatory process may be diffuse or confined to an abscess. Systemically, there is paralysis of the bowel, hemoconcentration, and decrease in the cardiac output due to the shift of fluids and later acidosis. Intrapulmonary shunting, hypo/hypercapnia, hypoxemia, progressive azotemia, acute tubular necrosis, weight loss by protein consumption, fall of body temperature, loss of heat production, and exhaustion are other complications that may lead to the death of the patient if the process is not interrupted.

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Shivani Chaparala M.B.B.S [2]

Secondary peritonitis has numerous causes. It most often results from entry of enteric bacteria into the peritoneal cavity through a necrotic defect in th wall of the intestines or other viscus as a result of obstruction, infarction or after rupture of an intra-abdominal visceral abscess. It most often occurs after perforation of appendix. Nonbacterial causes of peritonitis include leakage of blood into the peritoneal cavity due to rupture of a tubal pregnancy, ovarian cyst, or aneurysmal vessel.

• Solid organ rupture
• Perforated peptic ulcer
• Tubo-ovarian abscess
• Small bowel perforation

Common causes of secondary peritonitis include:^[1][2]

• Perforated PUD
• Appendicitis
• Diverticulitis
• Acute cholecystitis
• Pancreatitis
• Post-surgical complications

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Shivani Chaparala M.B.B.S [2]

Secondary peritonitis has to be differentiated from spontaneous bacterial peritonitis which is also seen in cirrhotics and also from other causes of peritonitis.

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Shivani Chaparala M.B.B.S [2]

Despite the recent advances in treatment modalities, morbidity and mortality rates caused by peritonitis remain high.

• The incidence of secondary peritonitis can not be measured accurately as it occurs in the context of a wide spectrum of diseases and conditions.
• At one study, the incidence of diffuse postoperative peritonitis was 25% in the surgical ICU especially in patients with multi-organ failure.^[1]

• Morbidity and mortality of patient with secondary peritonitis is ~30%.^[2][3].
• Despite the development of antibiotics and significant improvement in intensive care support, morbidity is high and mortality rates remain between 30-66%.

• The mean age of perforation peritonitis is more than 60 years.

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Shivani Chaparala M.B.B.S [2]

Risk factors of Secondary peritonitis are numerous intraabdominal disorders involving the gastrointestinal or genitourinary tract with spillage of material into the peritoneal space.

• Ruptured gastric ulcer, appendicular abscess or diverticular abscess^[1]
• Recent surgical procedures
• Recent trauma to the abdomen (e.g. Stab injury or gun shot injury)

Common risk factors for peritonitis include:^[2]

• Perforating peptic ulcer disease
• Cholecystitis
• Pancreatitis
• Appendicitis
• Diverticulitis
• Inflammatory bowel disease such as crohn’s disease or ulcerative colitis with toxic megacolon
• Pelvic inflammatory disease

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Shivani Chaparala M.B.B.S [2]

There are no specific screening studies for secondary peritonitis.

There are no specific screening studies for secondary peritonitis.

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Shivani Chaparala M.B.B.S [2]

With treatment, patients usually do well. Without treatment, the outcome is usually poor. However, in some cases, patients do poorly even with prompt and appropriate treatment.

With treatment, patients usually do well. Without treatment, the outcome is usually poor. However, in some cases, patients do poorly even with prompt and appropriate treatment.

• With the progression of infection, septicaemia ensues with its classic symptoms and signs. Septicaemia and shock are associated with very bad prognosis.

• With the progression of shock, blood supply to the brain might be compromised leading to altered mental status. Associated comorbidities and poor general status make the development of altered mental status more likely.

• Peritoneal inflammation can be complicated with paralytic ileus. Paralytic ileus is a very poor prognostic sign with increased mortality rate.

• Diarrhea occurs due to peritoneal inflammation and secondary irritation of the intestines.

• Shock and septicemia can develop into renal failure. Renal failure can be reversible if proper management is done at timeproper .

Peritonitis is a frequent cause of morbidity.The prognosis greatly depends on the degree of intra-abdominal contamination, the severity of underlying disease, the immune response of the host and associated organ dysfunction.^[1] Associated mortality rates vary from less than 1% to more than 60% Factors affecting prognosis are:

• Age
• Blood pressure
• Cause of infection
• Site of origin of peritonitis
• Number of organs involved in multi-organ-failure (MOF)
• Pre-operative organ failure
• Presence of metabolic acidosis
• Serum albumin
• New York Heart Association cardiac function status
• Malnutrition
• Malignoma
• Fecal peritonitis
• Immunosuppression

The prognosis risk of peritonitis may be stratified using the Mannheim’s Peritoneal index score (MPI) as shown below:^[2][3]

• For a score of 27, the sensitivity was 66.67%, specificity was 100%, and positive predictive value for mortality is 100% at an accuracy of 94%.^[2]

Factors that were found to be independently significant factors in predicting the mortality:

• Duration of pain for >24 h
• Organ failure on admission
• Female sex and
• Feculent exudate
• Early prognostic evaluation of abdominal sepsis is useful in the assessment of the severity of the disease and to select high-risk patients for early surgical reintervention.