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PeritonitisEdit

Peritonitis is an acute inflammation of the peritoneum, the serous membrane that lines the abdominal cavity and covers most intra-abdominal organs. It is a medical emergency characterized by rapid onset of abdominal pain and systemic illness, and it requires prompt assessment and often urgent intervention to prevent organ failure and death. The condition can arise from a variety of causes and is commonly categorized into primary, secondary, and tertiary forms, each with distinct pathophysiology, clinical features, and management strategies peritoneum abdomen.

The peritoneal cavity normally contains a small amount of lubricating fluid that minimizes friction between abdominal organs. When infection or chemical irritation disrupts this calm environment, inflammatory mediators are released, vascular permeability increases, and the resulting edema and purulent exudate can impair organ function. The severity of peritonitis is influenced by the source of contamination, the patient’s underlying health, and the timeliness of treatment, with delays associated with higher mortality rates infection inflammation.

Causes and classification

  • Primary peritonitis (spontaneous bacterial peritonitis) occurs without an evident intra-abdominal source and is most commonly seen in people with cirrhosis and ascites. Bacteria access the peritoneal cavity through the bloodstream or lymphatics, or originate from translocation of gut flora. Management emphasizes targeted antibiotic therapy and control of the underlying liver disease cirrhosis ascites.

  • Secondary peritonitis results from a tangible intra-abdominal source of contamination, such as perforation of a hollow viscus (e.g., stomach, intestine, appendix) or traumatic injury. Contamination with fecal material or purulent fluid typically necessitates operative source control to repair the defect and remove infected material. This form is the most common and carries substantial risk if not treated promptly appendix perforation trauma.

  • Tertiary peritonitis refers to persistent or recurrent intra-abdominal infection after initial control, often in hospitalized or immunocompromised patients. It may involve a more indolent course but can still lead to sepsis and organ dysfunction if inadequately managed. Long-term antibiotic strategies and surveillance for resistant organisms are central here sepsis antibiotics.

See also: secondary peritonitis primary peritonitis tertiary peritonitis peritonitis in surgical literature

Pathophysiology

In secondary peritonitis, a breach in the gastrointestinal tract introduces bacteria, enzymes, and inflammatory mediators into the peritoneal cavity. The ensuing inflammatory cascade recruits neutrophils and macrophages, increases vascular permeability, and can cause systemic inflammatory response syndrome (SIRS). If the infection is not controlled, sepsis, septic shock, organ failure, and death can follow. In primary peritonitis, bacteria reach the peritoneum via translocation or hematogenous spread rather than a local perforation. The host response in tertiary peritonitis is complex and often involves antibiotic-resistant organisms and a fragile immune status sepsis inflammation.

Signs and symptoms

  • Sudden onset or rapidly escalating abdominal pain, often generalized or localized to the area of inflammation
  • Abdominal tenderness, guarding, and sometimes rebound tenderness
  • Fever, tachycardia, tachypnea, and leukocytosis; in severe cases, hypotension and confusion may occur
  • Nausea, vomiting, ileus, abdominal distension, and reduced or absent bowel sounds
  • In individuals with cirrhosis and ascites, fever and abdominal pain plus changes in ascitic fluid can signal primary peritonitis

Clinical presentation can vary, particularly in elderly, immunocompromised, or critically ill patients, where symptoms may be blunted. Rapid recognition and differentiation from other causes of acute abdomen are essential to guide timely management diagnosis.

Diagnosis

  • Laboratory tests: complete blood count, metabolic panel, coagulation profile, inflammatory markers (e.g., CRP, procalcitonin). Blood cultures are often obtained given the risk of bacteremia; cultures from ascitic fluid may be informative in primary peritonitis with ascites ascites.
  • Diagnostic paracentesis: in patients with ascites, sampling and analysis of ascitic fluid helps distinguish primary from secondary infection and guides antimicrobial therapy. Key fluid findings include high neutrophil counts and positive cultures in infectious peritonitis paracentesis.
  • Imaging: ultrasound or computed tomography (CT) can identify free intraperitoneal fluid, hidden perforations, abscesses, or the source of contamination. Imaging assists in planning source control in secondary peritonitis and can help rule out alternative diagnoses CT ultrasound.
  • Microbiologic testing: cultures from blood, ascitic or peritoneal fluid, and any drained collections inform antibiotic selection and help monitor resistance patterns antibiotics.

Treatment

  • Medical stabilization: aggressive fluid resuscitation, hemodynamic monitoring, analgesia, and correction of electrolyte and acid-base disturbances are foundational steps. Early involvement of surgeons or interventional radiologists is common when source control is indicated surgery.
  • Antibiotic therapy: empiric broad-spectrum antibiotics are started promptly in suspected peritonitis, then narrowed based on culture results and local resistance patterns. Choices vary by patient factors and setting but commonly target gram-negative and anaerobic organisms; adjustments are made for known risk factors such as cirrhosis or prior antibiotic exposure antibiotics.
  • Source control: most secondary peritonitis requires prompt surgical intervention to repair perforations, resect nonviable tissue, drain purulent collections, and wash out contaminated areas. Laparoscopic or open approaches may be used depending on patient status and intra-abdominal findings. In selected stable patients with localized contamination, percutaneous drainage of abscesses may be appropriate surgery laparotomy percutaneous drainage.
  • Adjuncts and postoperative care: intensive care support for organ dysfunction, nutritional support, and careful monitoring for nosocomial infection and antibiotic-associated complications. Recurrent or persistent infection may necessitate repeat imaging or surgical revisit ICU nutrition.

Prognosis

Mortality and morbidity depend on the etiology, timeliness of treatment, and the patient’s baseline health. Secondary peritonitis generally carries a higher risk than primary peritonitis due to the underlying perforation and the potential for extensive contamination. Early source control and appropriate antibiotic therapy substantially improve outcomes, but delays or inadequate treatment can lead to sepsis, multi-organ failure, and death. Prognostic indicators include the degree of systemic inflammation, organ dysfunction at presentation, and the speed of clinical improvement after initiation of treatment sepsis.

Prevention and public health considerations

  • For patients with cirrhosis and ascites, secondary prevention strategies include prophylactic antibiotics in specific high-risk situations (e.g., GI bleeding) and careful management of ascites to reduce infection risk cirrhosis ascites.
  • Standard infection control practices in surgical and hospital settings help prevent postoperative and nosocomial peritonitis, including sterile technique, timely removal of contaminated material, and appropriate antibiotic stewardship to reduce resistance development antibiotics.
  • Education on recognizing early signs of severe abdominal illness and seeking prompt care can reduce delays in treatment and improve outcomes emergency medicine.

Controversies and debates

  • Antibiotic stewardship vs broad empiric coverage: there is ongoing discussion about balancing immediate broad-spectrum antibiotic therapy to prevent sepsis progression with the need to minimize resistance and collateral damage from overuse. Clinicians weigh local antibiograms, patient risk factors, and prior antibiotic exposure when deciding initial therapy antibiotics.
  • Timing and route of source control: while many cases of secondary peritonitis require urgent surgical intervention, certain stable patients with localized contamination or abscesses may be managed with image-guided drainage and antibiotics alone. The decision hinges on the infection’s extent, patient stability, and the feasibility of definitive source control drainage.
  • Approach to suspected tertiary peritonitis: in immunocompromised or critically ill patients, recurrent or resistant infections may prevail, raising questions about prolonged or combination antibiotic strategies versus de-escalation and deintensification guided by cultures and clinical response tertiary peritonitis.
  • Role of minimally invasive techniques: laparoscopy can offer diagnostic clarity and less invasiveness in selected patients, but conversion to open surgery may be necessary for thorough source control. The choice of approach depends on patient condition, surgeon expertise, and intra-abdominal findings laparoscopic.

See also