Peritonitis is a serious condition where the peritoneum, the thin, protective layer that lines the inside of the abdomen and covers most abdominal organs becomes inflamed. This usually happens when bacteria or fungi enter the abdominal cavity, which is normally sterile. It can occur if an organ ruptures, such as with appendicitis or a stomach ulcer, if bile or stomach contents leak into the abdomen after an injury or surgery, or if germs are introduced during medical procedures like peritoneal dialysis.
The peritoneum helps support the organs and allows fluids and immune cells to move around the abdomen. When it becomes inflamed, infection spreads quickly and can trigger dangerous body-wide reactions. Peritonitis is a medical emergency that requires immediate treatment, since delays can lead to life-threatening complications such as sepsis (a severe bloodstream infection), organ failure, or death.
Symptoms often appear suddenly and may include intense, widespread abdominal pain, tenderness when the abdomen is touched, fever, chills, nausea, vomiting, bloating, constipation, or the inability to pass gas.
Treatment usually involves admission to the hospital for intravenous (IV) antibiotics to fight infection and, in many cases, surgery to fix the underlying cause (for example, repairing a ruptured appendix or ulcer). Commonly used antibiotics include cephalosporins, carbapenems, penicillins, and quinolones. Vancomycin may be given if the infection is caused by staphylococcal bacteria.
Prevention focuses on reducing the risk of germs entering the abdominal cavity. This includes careful hand washing, cleaning the skin around a peritoneal dialysis catheter, wearing a surgical mask during exchanges, storing supplies in a clean place, and applying antiseptic to the catheter exit site. In people with ascites (a buildup of fluid in the abdomen, often linked to liver disease), preventive antibiotics may also be prescribed.
Epidemiology
Peritonitis incidence varies globally, with increased rates in areas lacking prompt medical care. It is more common in patients with cirrhosis, undergoing peritoneal dialysis, or after abdominal surgery.
In developed countries, peritonitis typically affects less than 10 per 100,000 people annually. Mortality rates can reach 20-40% depending on the severity and speed of treatment.
Causes of Peritonitis
Peritonitis arises due to inflammation of the peritoneum, often triggered by infection or chemical irritation. The causes vary based on the source and the underlying medical conditions involved.
Primary Peritonitis
Primary peritonitis, also called spontaneous bacterial peritonitis (SBP), occurs in the absence of an obvious rupture or injury to the abdominal organs. Instead, microorganisms invade the peritoneal cavity through the bloodstream, lymphatic system, or direct movement across the intestinal wall. Because the peritoneal cavity is normally sterile, even a small introduction of bacteria can cause significant infection.
This type most commonly affects individuals with chronic liver disease and ascites. Ascitic fluid provides a favorable environment for bacterial growth, especially in patients with cirrhosis whose immune defenses are impaired. The most frequently identified bacteria are Escherichia coli and Streptococcus species, though Klebsiella pneumoniae and other enteric organisms may also be responsible. In patients undergoing peritoneal dialysis, Staphylococcus aureus and Staphylococcus epidermidis are additional important causes.
Primary peritonitis is strongly associated with immune compromise. Patients with conditions such as nephrotic syndrome, HIV infection, or those receiving immunosuppressive therapy for cancer or organ transplantation are also at higher risk. Diagnosis is usually confirmed by paracentesis, in which fluid from the abdominal cavity is tested for the presence of white blood cells and bacterial cultures. Unlike secondary peritonitis, there is no evidence of gastrointestinal perforation or injury.
If untreated, SBP can rapidly progress to sepsis and death, but with early recognition and intravenous antibiotics (commonly third-generation cephalosporins), outcomes improve significantly.
Secondary Peritonitis
Secondary peritonitis is the most common and clinically significant form. It results from direct contamination of the peritoneal cavity following a rupture or perforation of an abdominal organ. When an organ wall breaks, intestinal bacteria, bile, or digestive enzymes leak into the sterile peritoneal space, causing widespread infection and inflammation.
Typical causes include:
- Ruptured appendix in acute appendicitis.
- Perforated peptic ulcers of the stomach or duodenum.
- Diverticulitis with perforation, leading to fecal contamination.
- Ischemic bowel disease, where loss of blood supply causes tissue death and subsequent perforation.
- Gallbladder rupture (often due to untreated gallstones or cholecystitis).
- Abdominal trauma, including stab wounds, gunshot injuries, or blunt trauma.
- Post-surgical complications, such as leakage from intestinal sutures or surgical sites.
Secondary peritonitis is typically polymicrobial, meaning it involves multiple types of bacteria at once. Aerobic bacteria such as E. coli and anaerobic bacteria such as Bacteroides fragilis are frequently identified, often in combination with enterococci and streptococci. Because digestive enzymes and bile can directly damage tissues, the infection spreads quickly and causes extensive inflammation.
This form generally has a more severe clinical course than primary peritonitis and almost always requires surgical intervention in addition to broad-spectrum intravenous antibiotics. Surgery may involve removing the ruptured organ (such as an appendectomy), repairing a perforation, or draining infected fluid. Without prompt treatment, secondary peritonitis often leads to sepsis, multiple organ failure, and death.
Tertiary Peritonitis
Tertiary peritonitis refers to persistent or recurrent infection that continues despite initial surgical and medical treatment of secondary peritonitis. It is most often seen in critically ill patients who are hospitalized for long periods and have weakened immune systems.
Unlike secondary peritonitis, which is typically caused by intestinal bacteria, tertiary peritonitis often involves low-virulence or opportunistic organisms that take advantage of a compromised immune state. These include Pseudomonas aeruginosa, Enterococcus species, Candida (fungal infections), and multidrug-resistant bacteria common in intensive care units.
Tertiary peritonitis is especially dangerous because it reflects a failure to clear infection even after surgery and antibiotics. Patients usually require prolonged antibiotic therapy, repeated surgical interventions, and intensive care support. The condition is frequently associated with immune system dysfunction, septic shock, and multiple organ failure, and it carries a poor prognosis.
Risk Factors
Several specific elements increase the likelihood of developing peritonitis. These factors relate to underlying health issues, recent medical interventions, and environmental influences.
Medical Conditions
Certain chronic diseases greatly increase susceptibility to peritonitis because they either weaken the immune system or create conditions that allow bacteria to multiply in the abdomen.
- Liver Cirrhosis and Ascites: Cirrhosis alters immune defenses and reduces the ability of the peritoneal fluid to clear infections. Ascites, a common complication of cirrhosis, provides an environment in which bacteria such as Escherichia coli or Streptococcus can grow, leading to spontaneous bacterial peritonitis (SBP). Patients with cirrhosis are often prescribed preventive antibiotics because of their high risk.
- Kidney Failure: Individuals with advanced kidney disease, particularly those on peritoneal dialysis (PD), are highly vulnerable. The dialysis catheter creates a direct pathway for microorganisms to enter the peritoneal cavity. Even minor lapses in technique or hygiene can result in infection.
- Diabetes Mellitus: Diabetes compromises immune function and slows wound healing, making infections both more likely and harder to control. Diabetic patients also face more severe outcomes from peritonitis due to their reduced ability to mount an effective immune response.
- Gastrointestinal Disorders: Conditions such as appendicitis, diverticulitis, Crohn’s disease, peptic ulcer perforation, and bowel obstruction can damage or perforate the intestinal wall. Once perforated, intestinal contents including bacteria, bile, and digestive enzymes spill into the abdominal cavity, triggering secondary peritonitis.
- Immune Suppression: Patients with HIV/AIDS, cancer, organ transplants, or those receiving long-term corticosteroids or chemotherapy are at higher risk. Their immune systems may not effectively control even small amounts of bacterial invasion, leading to rapid progression of infection.
Surgical Procedures
Surgical interventions in the abdomen carry inherent risks for peritonitis, especially when complications occur.
- Postoperative Peritonitis may arise after surgeries such as appendectomy, bowel resection, gastric surgery, or laparoscopic procedures. The most common causes include anastomotic leaks (leakage where two sections of the bowel are joined), surgical site infections, or unrecognized perforations made during surgery.
- Patients undergoing peritoneal dialysis are among the most frequently affected. The peritoneal catheter, if not handled under sterile conditions, can allow bacteria or fungi to enter. Repeated exchanges of dialysis fluid increase exposure risk, making careful training and strict adherence to hygiene protocols essential.
- In rare cases, procedures such as colonoscopy, paracentesis, or abdominal drain placements may inadvertently injure the bowel or introduce pathogens, leading to peritonitis.
Lifestyle and Environmental Risks
Lifestyle choices and environmental exposures can also increase the chances of peritonitis, either by weakening the body’s defenses or by raising exposure to infectious agents.
- Living in unsanitary conditions increases the risk of exposure to harmful bacteria and fungi. Inadequate handwashing, improper cleaning of medical devices, or unsafe food and water sources all contribute to higher infection rates.
- Chronic alcohol consumption damages the liver, predisposing individuals to cirrhosis and ascites, which are strong risk factors for primary peritonitis. Substance abuse in general weakens immunity, making the body less able to control infections.
- Physical injuries, such as those from car accidents, stab wounds, or blunt force trauma, can directly damage abdominal organs. This either introduces bacteria from outside or causes perforation of internal organs, both of which can lead to rapid-onset secondary peritonitis.
- Populations in crowded environments with limited access to clean water, medical care, and sterile equipment face higher risks. These conditions not only promote bacterial spread but also delay diagnosis and treatment, increasing the likelihood of severe outcomes.
Pathophysiology
Peritonitis results from the inflammation of the peritoneum, typically triggered by infection or chemical irritation. The biological response involves immune activation and structural changes in the abdominal cavity affecting multiple organs.
Inflammatory Process
The pathophysiological cascade begins with recognition of invading pathogens or irritants by resident immune cells in the peritoneum, including macrophages and mesothelial cells. These cells release pro-inflammatory cytokines—most notably interleukin-1 (IL-1), tumor necrosis factor-alpha (TNF-α), and interleukin-6 (IL-6)—that recruit neutrophils into the peritoneal cavity. Activated neutrophils release proteolytic enzymes and reactive oxygen species that directly kill pathogens but also damage host tissues. Complement system activation further enhances opsonization and pathogen clearance, but at the cost of escalating tissue injury.
Cytokine activity also increases vascular permeability, permitting plasma proteins, fibrinogen, and leukocytes to leak into the peritoneal cavity. Fibrinogen polymerizes into fibrin, coating inflamed surfaces and forming adhesions between bowel loops and other abdominal organs. While fibrin serves as a temporary defense to wall off infection, persistent fibrin deposition can entrap bacteria and hinder antibiotic penetration, leading to abscess formation. Exudate and pus accumulation interfere with peritoneal fluid resorption, worsening abdominal distension and pain. If uncontrolled, the localized immune response triggers a systemic inflammatory response syndrome (SIRS), predisposing to sepsis, septic shock, and multi-organ failure.
Impacts on Abdominal Organs
Peritonitis significantly alters the function of abdominal organs. The intestines are particularly vulnerable; inflammation and cytokine release suppress normal peristalsis, resulting in paralytic ileus. This leads to bowel distension, accumulation of gas and fluids, and impaired nutrient absorption. Dilated bowel loops also increase the risk of ischemia and perforation, exacerbating the cycle of infection.
The peritoneal membrane itself undergoes structural changes, including thickening, fibrosis, and impaired transport capacity. In patients on peritoneal dialysis, this damage compromises ultrafiltration and solute clearance, ultimately leading to encapsulating peritoneal sclerosis (EPS) in chronic cases. Hepatic function may deteriorate due to increased bacterial translocation and toxin absorption, which impose added strain on an already compromised liver in patients with cirrhosis or ascites. Similarly, renal perfusion is threatened by systemic hypotension and endotoxemia, which can result in acute kidney injury.
Persistent inflammation and fibrin deposition can lead to abscess formation within the peritoneal cavity, liver, or pelvis. These encapsulated pockets of infection are often resistant to systemic antibiotics and require drainage. Adhesions formed during healing may later cause chronic abdominal pain or bowel obstruction, representing long-term complications of peritonitis.
Systemic Consequences
Because of its vascularity and absorptive properties, the peritoneum serves as a conduit for systemic toxin and pathogen spread. Bacterial endotoxins absorbed from the peritoneal cavity activate coagulation pathways and contribute to disseminated intravascular coagulation (DIC). Prolonged inflammation leads to capillary leak syndrome, fluid shifts into the peritoneal cavity (“third spacing”), and hypovolemic shock. The cardiovascular system responds with tachycardia and hypotension, while respiratory compromise may result from diaphragmatic irritation, decreased lung expansion, and pleural effusions.
Ultimately, untreated peritonitis causes a downward spiral from localized infection to generalized sepsis, shock, and multiple organ dysfunction syndrome (MODS). Mortality rates remain high without prompt and aggressive treatment, reflecting the profound systemic impact of the peritoneal inflammatory process.
Clinical Presentation
Peritonitis manifests through distinct symptoms and physical signs that help guide diagnosis. Key features involve acute abdominal pain and systemic responses to inflammation or infection.
Common Symptoms
The most striking and universal symptom of peritonitis is abdominal pain. This pain often begins suddenly and is described as sharp, severe, and diffuse, but it can initially localize to the region of the affected organ (e.g., right lower quadrant in appendicitis or left lower quadrant in diverticulitis). Patients typically report that the pain worsens with movement, coughing, or deep inspiration, a phenomenon sometimes referred to as “guarding against pain.” In generalized peritonitis, the pain quickly becomes widespread, making even small movements unbearable.
Gastrointestinal symptoms often accompany abdominal pain. These include nausea, persistent vomiting, abdominal bloating, and distension. Many patients lose their appetite and experience early satiety. Altered bowel function is common: some patients develop constipation or paralytic ileus (reflecting bowel immobility), while others may experience diarrhea in cases of infectious or localized peritonitis.
Systemic symptoms arise as the infection and inflammatory mediators spread. Fever, chills, malaise, and profound fatigue indicate systemic involvement. As sepsis progresses, patients may also present with confusion, dizziness, or altered mental status, particularly in elderly or immunocompromised individuals. In patients with liver disease and ascites, spontaneous bacterial peritonitis (SBP) may cause only vague symptoms such as low-grade fever, mild abdominal discomfort, or even no abdominal pain, making diagnosis more challenging.
Physical Examination Findings
Physical examination is central to the diagnosis of peritonitis. The hallmark sign is abdominal rigidity, where the abdominal wall becomes involuntarily stiff due to reflex contraction of muscles in response to peritoneal irritation. This is often accompanied by voluntary guarding, where patients tighten their abdominal muscles when touched, and rebound tenderness, where pain intensifies upon sudden release of pressure after palpation. These signs strongly suggest peritoneal inflammation.
Other key findings include abdominal distension from paralytic ileus or fluid accumulation (ascites). Bowel sounds are usually reduced or absent, reflecting intestinal paralysis secondary to inflammation. Percussion may reveal diffuse tenderness and tympany if bowel distension is significant. In advanced cases, shifting dullness or fluid wave tests may demonstrate free fluid in the abdomen.
Systemic signs often mirror the severity of infection. Patients typically exhibit fever and tachycardia, which correlate with systemic inflammatory response. In severe or advanced peritonitis, hypotension, tachypnea, and diaphoresis suggest progression to septic shock. Orthostatic hypotension, dry mucous membranes, and reduced skin turgor may be present due to dehydration from vomiting and third spacing of fluids into the peritoneal cavity.
In elderly patients, children, or the immunocompromised, physical signs may be subtle or atypical. For example, neonates with peritonitis may present only with abdominal distension and irritability, while elderly patients may show fewer localizing signs but develop rapid systemic deterioration.
Atypical and Special Presentations
Not all cases follow the classical pattern. Patients undergoing peritoneal dialysis may present with cloudy peritoneal fluid, abdominal pain, or catheter site tenderness rather than classic rigidity and rebound tenderness. Similarly, in spontaneous bacterial peritonitis (SBP), symptoms may be nonspecific, such as low-grade fever or confusion, particularly in cirrhotic patients with hepatic encephalopathy.
Another important consideration is that patients with immunosuppression (e.g., due to diabetes, HIV, chemotherapy, or corticosteroids) may have blunted inflammatory responses. They can develop severe peritonitis without pronounced fever or leukocytosis, making a high index of suspicion essential.
Diagnostic Evaluation
Diagnosing peritonitis requires a combination of clinical data, laboratory results, and imaging studies. Specific criteria help confirm the presence and severity of infection within the peritoneal cavity.
Laboratory Tests
Laboratory tests evaluate inflammation and infection. A complete blood count (CBC) typically shows elevated white blood cells (leukocytosis). Elevated C-reactive protein (CRP) and erythrocyte sedimentation rate (ESR) indicate systemic inflammation.
Peritoneal fluid analysis is essential in cases like spontaneous bacterial peritonitis (SBP). This includes cell count with differential, Gram stain, and culture to identify causative organisms. A polymorphonuclear leukocyte (PMN) count greater than 250 cells/mm³ supports the diagnosis of SBP.
Blood cultures may be positive if bacteremia is present. Serum electrolytes and renal function tests help assess patient status and guide treatment.
Imaging Studies
Imaging confirms peritoneal inflammation, detects complications, and identifies underlying causes. Abdominal ultrasound is often the first-line imaging to detect free fluid, abscesses, or perforations.
Computed tomography (CT) offers detailed visualization of the peritoneal cavity and adjacent organs. It can identify bowel wall thickening, free air, abscesses, or fluid collections. Contrast-enhanced CT is preferred when perforation or intra-abdominal abscess is suspected.
X-rays may show free intraperitoneal air, indicating a perforated viscous. However, they have limited sensitivity and are less commonly used alone.
Diagnostic Criteria
Peritonitis diagnosis relies on clinical presentation combined with objective findings. A key diagnostic marker in peritoneal fluid is the PMN count above 250 cells/mm³ in patients with ascites.
Additional criteria include positive peritoneal fluid cultures or evidence of infection on imaging. Signs of systemic infection such as fever, abdominal tenderness, and guarding support the diagnosis.
In surgical peritonitis, observation of pus or inflamed peritoneum during operation confirms the diagnosis. Laboratory and imaging findings guide the decision between medical and surgical management.
Complications
Peritonitis can lead to serious health issues if untreated or poorly managed. Two primary complications include widespread infection in the bloodstream and localized pockets of infection within the abdominal cavity.
Sepsis
One of the most severe complications of peritonitis is sepsis, which occurs when bacteria, fungi, or their toxins gain access to the bloodstream. The systemic immune response that follows leads to widespread inflammation, vascular dilation, increased capillary permeability, and eventual tissue hypoperfusion. This progression can culminate in septic shock, characterized by severe hypotension unresponsive to fluids, requiring vasopressors to maintain adequate organ perfusion.
Patients who develop sepsis often present with fever, tachycardia, tachypnea, and low blood pressure, alongside signs of altered mental status such as agitation, drowsiness, or confusion. Laboratory findings may reveal elevated lactate levels, leukocytosis or leukopenia, and evidence of organ dysfunction (e.g., rising creatinine, abnormal liver enzymes, or coagulopathy).
Uncontrolled sepsis can lead to multiple organ dysfunction syndrome (MODS), where the lungs, kidneys, liver, and cardiovascular system progressively fail. Mortality in untreated septic shock is extremely high.
Abscess Formation
Intra-abdominal abscesses represent another major complication of peritonitis. These localized pus-filled collections develop when the body attempts to wall off infection to prevent its spread. While protective in theory, abscesses harbor persistent pathogens and inflammatory debris, which can prolong illness and undermine recovery.
Clinically, abscesses may cause persistent abdominal pain, fever, localized tenderness, anorexia, and prolonged malaise even after initial peritonitis treatment. They are often suspected when a patient fails to improve or deteriorates after seemingly appropriate therapy.
Diagnosis typically requires imaging studies such as ultrasound or computed tomography (CT), which help identify the location and size of the abscess. Treatment usually involves drainage, either through image-guided percutaneous catheter insertion or open/laparoscopic surgery, depending on the complexity and accessibility of the collection. Antibiotics alone are insufficient because drug penetration into pus is poor. If untreated, abscesses can rupture, leading to recurrent peritonitis or systemic sepsis.
Adhesion Formation and Bowel Obstruction
The inflammatory and fibrinous exudate associated with peritonitis often promotes the development of intra-abdominal adhesions. These fibrous bands can tether organs together, disrupting normal anatomy and mobility. Over time, adhesions may cause chronic abdominal pain, infertility (in women due to tubal involvement), or intestinal obstruction.
Small bowel obstruction caused by adhesions is a particularly troublesome long-term complication. Patients may present weeks to months after an episode of peritonitis with crampy abdominal pain, vomiting, distension, and constipation. Severe obstruction may require surgical intervention to release the adhesions, though surgery itself increases the risk of new adhesions, creating a vicious cycle.
Fluid and Electrolyte Imbalance
Because peritonitis increases vascular permeability and promotes the leakage of fluid into the abdominal cavity (“third spacing”), patients often develop significant fluid depletion. This can cause hypovolemia, hypotension, and electrolyte disturbances such as hyponatremia, hypokalemia, or metabolic acidosis. Vomiting and reduced oral intake further exacerbate the problem. If left uncorrected, these imbalances contribute to shock, arrhythmias, and kidney injury.
Multi-Organ Dysfunction
Severe or untreated peritonitis often results in multi-organ involvement beyond sepsis.
- The lungs may be affected by acute respiratory distress syndrome (ARDS), where inflammatory mediators increase capillary permeability in the alveoli.
- The kidneys are vulnerable to acute kidney injury due to hypoperfusion, nephrotoxic drugs, or septic shock.
- The liver can suffer from reduced perfusion and sepsis-related injury, especially in patients with pre-existing liver disease.
- The heart may develop septic cardiomyopathy, leading to impaired contractility and worsening shock.
Treatment Options
Treatment for peritonitis requires prompt medical action to control infection and address any underlying causes. Management typically involves antimicrobial drugs and, in some cases, surgical procedures to eliminate infection sources.
Antibiotic Therapy
Antibiotics remain the cornerstone of peritonitis treatment because the infection can spread rapidly throughout the peritoneal cavity, leading to sepsis and potentially life-threatening complications. In most cases, broad-spectrum antibiotics are administered immediately once peritonitis is suspected, even before laboratory confirmation is obtained. This empiric approach ensures early coverage of the most common organisms associated with peritonitis, including Escherichia coli, Klebsiella pneumoniae, Enterococcus species, and anaerobic bacteria such as Bacteroides fragilis. Prompt initiation of therapy is crucial, as delays in antibiotic administration are associated with significantly higher morbidity and mortality.
Empiric therapy often includes third-generation cephalosporins such as cefotaxime or ceftriaxone, which provide strong coverage against Gram-negative organisms. Beta-lactam/beta-lactamase inhibitor combinations, such as piperacillin-tazobactam, are also widely used because they offer broad coverage against both Gram-negative and anaerobic bacteria. In severe or resistant cases, carbapenems such as imipenem or meropenem are preferred due to their ability to target multidrug-resistant organisms. For enhanced anaerobic coverage, metronidazole is frequently added to cephalosporin regimens to ensure adequate control of Bacteroides and other obligate anaerobes.
Once culture and sensitivity results are available from blood, ascitic fluid, or peritoneal fluid samples, therapy should be tailored to target the specific pathogens identified. This process, known as de-escalation, helps minimize unnecessary exposure to broad-spectrum antibiotics, thereby reducing the risk of antibiotic resistance and adverse effects. In cases of spontaneous bacterial peritonitis (SBP), commonly seen in patients with liver cirrhosis, fluoroquinolones such as ciprofloxacin may be used for both prophylaxis and treatment. In contrast, hospital-acquired or tertiary peritonitis may involve multidrug-resistant organisms, requiring more advanced options such as vancomycin for methicillin-resistant Staphylococcus aureus (MRSA), linezolid for vancomycin-resistant enterococci (VRE), or antifungal therapy such as fluconazole or echinocandins if Candida species are implicated.
Antibiotics are generally administered intravenously to achieve rapid and effective drug levels in both the bloodstream and the peritoneal cavity. The typical course of treatment ranges from 7 to 14 days, although the duration may be extended in cases involving inadequate source control, persistent infection, or immunocompromised patients. The choice of agent, route of administration, and duration of therapy must therefore be individualized, guided by both the clinical response and the results of microbiological testing.
Surgical Interventions
While antibiotics are essential for treating peritonitis, surgery is often required in secondary or tertiary cases, where the infection originates from a perforated organ, necrotic tissue, or abscess formation that cannot be resolved with antibiotics alone. In these situations, failure to address the underlying source of infection can result in persistent contamination of the peritoneal cavity, leading to uncontrolled sepsis and organ failure. Surgical management aims to identify and eliminate the source of infection, repair structural damage, and restore the normal function of affected organs.
A laparotomy, or open abdominal surgery, is traditionally performed in severe or unstable cases because it provides surgeons with full access to the abdominal cavity. This approach allows for direct visualization and repair of perforations, control of intra-abdominal bleeding, removal of infected or necrotic tissue, and irrigation of contaminated peritoneal fluid. Alternatively, laparoscopy, a minimally invasive surgical technique, is increasingly being adopted for stable patients. With smaller incisions and the use of a camera-guided system, laparoscopy allows for targeted interventions, lavage, and repair, often resulting in shorter recovery times, reduced postoperative pain, and fewer complications compared to open surgery.
Specific surgical procedures depend on the source of infection. For instance, a perforated appendix requires appendectomy, while a gastric or duodenal ulcer may be repaired using an omental patch (Graham patch technique). In cases of intestinal necrosis or perforation, a segmental bowel resection may be necessary, sometimes requiring temporary or permanent stoma formation. If the gallbladder is identified as the infectious source, a cholecystectomy is performed. In addition, localized abscesses may be drained surgically or, when appropriate, through image-guided percutaneous catheter placement—a less invasive option that avoids major abdominal surgery.
Prognosis and Outcomes
The success of treatment and recovery for peritonitis depends on multiple factors, including the underlying cause and timeliness of intervention. Complications and lasting effects vary widely among patients.
Recovery Rates
Recovery rates for peritonitis improve significantly with early diagnosis and prompt treatment. Bacterial peritonitis treated with appropriate antibiotics has mortality rates as low as 10-15% in otherwise healthy individuals. Surgical intervention may be necessary in cases where infection results from organ perforation or abscess. Delays in treatment can increase mortality rates to over 50%.
Factors influencing recovery include patient age, immune status, and presence of chronic conditions such as liver disease or diabetes. Patients without severe comorbidities generally experience faster resolution of symptoms and shorter hospital stays. Supportive care, including fluid management and pain control, also plays an important role.
Long-Term Effects
Long-term effects of peritonitis can include chronic abdominal pain, adhesions, and bowel obstruction. Adhesions occur in up to 30% of patients following severe infection, potentially complicating future surgeries. In some cases, persistent inflammation may lead to impaired organ function.
Patients who suffer from secondary bacterial peritonitis due to diseases like appendicitis or diverticulitis may face recurrent infections if underlying issues are untreated. Continuous monitoring and follow-up imaging can help detect complications early. Psychological effects such as anxiety or depression may arise due to prolonged hospitalization or the severity of illness.
Prevention Strategies
The prevention of peritonitis centers on minimizing the risk of bacterial entry into the peritoneal cavity and ensuring that both healthcare providers and patients are equipped with the knowledge and skills needed to maintain strict hygiene. Since peritonitis can progress rapidly to sepsis and life-threatening complications, prevention is particularly critical in patients with risk factors such as those undergoing peritoneal dialysis, individuals with abdominal catheters, or patients recovering from abdominal surgery.
Infection Control
Strict adherence to sterile technique is one of the most important measures in preventing peritonitis. Any medical procedure that breaches the peritoneal cavity such as catheter insertion, paracentesis, peritoneal dialysis, or abdominal surgery creates a potential pathway for pathogens.
Healthcare providers must therefore comply with standardized infection control protocols, which include meticulous hand hygiene, proper use of sterile gloves, face masks, gowns, and strict disinfection of instruments and equipment. Even minor lapses in these practices can result in bacterial contamination, significantly increasing the risk of infection.
For patients with indwelling catheters, particularly those on long-term peritoneal dialysis, ongoing maintenance is crucial. Catheter exit sites must be cleaned regularly with antiseptic solutions such as chlorhexidine, and dressings should only be changed under sterile conditions.
Healthcare providers and patients should also be trained to recognize early warning signs of contamination, such as redness, discharge, or tenderness at the insertion site. Any potential contamination event, such as accidental disconnection or improper handling of dialysis tubing, should be promptly reported and managed to prevent bacterial invasion.