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Peritonitis

Peritonitis is an inflammation of the , the thin that lines the and covers most of the abdominal organs, typically resulting from bacterial or and often leading to severe and potential life-threatening complications if untreated. The condition is classified into primary (or spontaneous) peritonitis, which occurs without an identifiable source of infection in the , often in patients with due to or other chronic conditions, and secondary peritonitis, which arises from a breach in the or other abdominal structures. Primary peritonitis, such as , is commonly associated with fluid accumulation in the from , , or certain cancers, allowing bacterial translocation from the gut. In contrast, secondary peritonitis frequently stems from of organs like the , rupture, , or , leading to contamination of the with gastrointestinal contents. Additional risk factors include , recent , or immunocompromised states, with an annual incidence of ranging from 7% to 30% in patients with . Symptoms of peritonitis typically develop rapidly and include severe abdominal tenderness and that worsens with movement, fever, chills, , , , and reduced bowel sounds or urine output. In patients undergoing , signs may manifest as cloudy dialysate fluid or the presence of strands. involves a revealing a rigid, tender , supported by blood tests showing , imaging such as X-rays or CT scans to identify free air or fluid, and to analyze for infection markers like elevated counts greater than 250 cells per microliter. Treatment requires urgent intervention, beginning with broad-spectrum intravenous antibiotics to target common pathogens such as , , or anaerobes. For primary peritonitis, management is primarily medical; for secondary peritonitis, it often includes surgical exploration to repair the underlying cause, drain abscesses, or lavage the . Supportive care includes fluid resuscitation, , and monitoring for in a setting, with peritoneal dialysis-related cases potentially managed by adjusting dialysis techniques or switching to . Complications can escalate to , multi-organ failure, formation, or death, particularly if is delayed, underscoring the need for prompt recognition and management to improve outcomes.

Overview

Definition and Classification

Peritonitis is defined as an inflammation of the , the thin serosal membrane that lines the and covers the abdominal organs. The peritoneum consists of two layers: the parietal peritoneum, which lines the (anteriorly and laterally), the retroperitoneum (posteriorly), the (inferiorly), and the (superiorly); and the visceral peritoneum, which directly covers the abdominal viscera, forming a known as the that normally contains less than 50 mL of fluid to facilitate organ movement. This membrane, composed of mesothelial cells overlying with vascular, lymphatic, and immune-competent elements, plays a key role in containing and lubricating abdominal fluids while providing a barrier against . Peritonitis is primarily classified based on into primary and secondary forms. Primary peritonitis, also known as spontaneous peritonitis, occurs without an identifiable intra-abdominal source of contamination, often arising from hematogenous or lymphatic spread of microorganisms, and is commonly seen in patients with or those undergoing . In contrast, secondary peritonitis results from direct contamination of the due to perforation of a hollow viscus, , or postoperative complications, making it the most frequent type. Additional classifications distinguish infectious peritonitis, caused by , fungi, or other pathogens, from noninfectious forms such as chemical peritonitis (e.g., due to , , or pancreatic enzymes) or sterile peritonitis (e.g., from foreign bodies or blood). Peritonitis can also be categorized by extent as generalized, involving the entire , or localized, confined to a specific region such as in or . A notable subtype of primary peritonitis is (SBP), particularly in patients with cirrhotic , where diagnostic criteria include an ascitic fluid polymorphonuclear leukocyte () count exceeding 250 cells/mm³ in the absence of an intra-abdominal surgically treatable source of infection. This threshold, supported by fluid analysis via , guides presumptive diagnosis and empiric antibiotic therapy, with common pathogens including and streptococcal species.

Epidemiology

Peritonitis represents a substantial burden globally, with acute generalized peritonitis serving as a frequent and a leading cause of non-trauma-related mortality in settings. Reported incidence rates for acute peritonitis vary by region, with one study in a West African district documenting 12.4 cases per 100,000 population annually. These figures underscore the condition's role as a major contributor to morbidity, particularly in resource-limited environments where access to timely intervention is constrained. In specific high-risk populations, peritonitis prevalence is markedly elevated. Among patients undergoing (PD), the incidence ranges from 0.2 to 0.6 episodes per patient-year, corresponding to an approximate risk of 18-45% for at least one episode annually, assuming a , which remains a primary cause of technique failure and mortality in 15-16% of affected individuals. Similarly, in patients with and , (SBP) affects 10-30% of hospitalized cases and 1.5-3.5% of outpatients, with a global pooled of approximately 17%. Demographic patterns reveal disparities in occurrence. Peritonitis is more common in males, who comprise 54-69% of cases across various cohorts, and incidence rises with age, particularly among those over 65 years, where older age independently predicts higher risk. These trends are exacerbated in elderly populations due to comorbidities and delayed diagnosis. Geographically, peritonitis rates are higher in low- and middle-income countries, where delayed care for underlying conditions like or peptic ulcers contributes to increased and secondary peritonitis. In contrast, high-income settings report lower SBP (around 11%) compared to middle-income regions (20%). From 2020 to 2025, epidemiological trends show declining peritonitis rates in high-income countries, attributed to advances in surgical techniques, antibiotic stewardship, and prevention; for instance, PD-associated rates fell from 0.6 episodes per patient-year in 1992 to 0.3 by 2019, with further reductions observed during the period due to enhanced hygiene measures. However, in PD populations, rates have shown variability, with some low-resource settings reporting increases to 0.96 episodes per patient-year amid socioeconomic challenges.

Clinical Presentation

Signs and Symptoms

The hallmark symptom of peritonitis is diffuse, severe resulting from peritoneal irritation, which often intensifies with movement, coughing, or . Associated symptoms frequently include fever and chills, reflecting the systemic inflammatory response; gastrointestinal disturbances such as , , anorexia, , or ; and in advanced cases, or signaling or early . On , patients typically exhibit abdominal tenderness, involuntary guarding or rigidity of the , rebound tenderness upon release of pressure, and diminished or absent bowel sounds indicative of ; signs of , such as dry mucous membranes, or overt may also be evident in severe presentations. Symptom severity varies by type: primary peritonitis, often spontaneous bacterial in origin, may present with milder or even absent in up to 30% of cases, particularly in patients with , whereas secondary peritonitis typically features a more rapid onset of intense due to underlying visceral . In pediatric patients, presentations can be atypical, with , , or nonspecific distress substituting for clear verbalization of , alongside common features like fever and . Elderly individuals may exhibit subdued or atypical manifestations, such as , minimal fever, or reduced perception due to age-related physiological changes, potentially delaying recognition.

Complications

Peritonitis, if untreated or severe, can lead to a range of acute complications stemming from the systemic response and bacterial dissemination. occurs when the infection triggers a dysregulated host response, potentially progressing to characterized by profound and tissue hypoperfusion. is a frequent outcome in generalized peritonitis, with mortality rates reaching 35% in affected patients. This can escalate to multi-organ dysfunction (MODS), where multiple organs fail due to widespread and microvascular injury, often involving the kidneys, liver, and lungs. (ARDS) is another critical acute complication, arising in up to 40% of septic shock cases and contributing to high mortality through severe and lung . Local complications arise from persistent infection and inflammatory scarring within the . Intra-abdominal abscesses form as localized collections of , commonly following or inadequate source control, and can prolong recovery if not drained. Adhesions, fibrous bands resulting from peritoneal injury, may develop and lead to by kinking or compressing intestinal loops. formation, an abnormal connection between organs or to the skin, is another risk, often complicating severe cases with ongoing leakage of intestinal contents. Chronic sequelae can persist long after the acute episode, particularly from adhesion-related changes. These adhesions are implicated in chronic abdominal or due to ongoing and of or viscera. In women, pelvic adhesions may cause by distorting fallopian tubes or ovaries, representing a significant long-term impact. Extensive bowel resection, sometimes required in necrotizing peritonitis, can result in , characterized by , , and nutritional deficiencies due to insufficient intestinal length. Overall mortality in secondary peritonitis varies but can reach 20-40% in cases with delayed or severe , driven by the rapid progression to and . Complications differ by peritonitis type; for instance, perforated carries a higher risk of intra-abdominal formation, occurring in up to 39% of perforated cases compared to non-perforated ones. In (SBP), particularly in cirrhotic patients, may worsen as a complication, exacerbating neurological dysfunction through buildup and .

Etiology

Infectious Causes

Infectious causes of peritonitis are predominantly bacterial, arising either from direct contamination of the or spontaneous bacterial translocation in susceptible individuals. Secondary peritonitis, the most common form, results from or rupture of a hollow viscus in the , allowing luminal contents to spill into the . Common precipitating conditions include , , peptic ulcer , and . This leads to polymicrobial infection, typically involving a mix of enteric Gram-negative aerobes such as and species, anaerobes like , and occasionally Gram-positive organisms. Anaerobes are particularly prominent in cases of bowel due to their prevalence in the colonic flora. Primary peritonitis, also known as (SBP), occurs without an identifiable intra-abdominal source of contamination and is often monomicrobial. It is most frequently associated with cirrhotic patients who have , where translocate from the gut into the bloodstream and subsequently seed the ascitic fluid. Predominant pathogens include Gram-negative enteric such as E. coli (accounting for up to 40% of cases) and , alongside Gram-positive species like . In patients undergoing , primary peritonitis can present as polymicrobial, reflecting contamination via the dialysis catheter, with organisms including and enteric . The mechanism involves hematogenous spread or direct ascension through disrupted barriers in immunocompromised states. Fungal causes are less common but significant in immunocompromised hosts, those on prolonged broad-spectrum antibiotics, or peritoneal dialysis patients. species, particularly and , predominate and often arise as a complication of bacterial overgrowth suppression or catheter-related formation. In peritoneal dialysis, fungal peritonitis accounts for about 4-10% of episodes and carries higher morbidity due to poor response to therapy. Tuberculous peritonitis, caused by , is a rare but important infectious in endemic regions or among immigrants from high-prevalence areas. It typically manifests through hematogenous dissemination from a primary pulmonary focus, leading to chronic granulomatous inflammation of the . This form is more prevalent in patients with underlying or , where it presents insidiously with and constitutional symptoms.

Noninfectious Causes

Noninfectious peritonitis, also known as sterile or chemical peritonitis, arises from non-microbial irritants that trigger an inflammatory response in the without bacterial involvement. This condition often presents with symptoms mimicking infectious peritonitis, such as and tenderness, but peritoneal fluid cultures remain negative for organisms. Differentiation typically relies on clinical history, imaging, and laboratory analysis confirming the absence of . Chemical peritonitis commonly results from the leakage of irritating substances due to organ or rupture. spillage from , as seen in acute or , induces a potent inflammatory reaction owing to its caustic properties on the . Similarly, from a perforated peptic can cause severe peritoneal irritation, leading to rapid onset of shortly after . Pancreatic enzymes leaking into the peritoneal space during provoke autodigestion and sterile , often complicating severe cases with elevated amylase levels in ascitic fluid. Sterile peritonitis can also stem from , where blood accumulation from trauma, ruptured , or vascular injury acts as an irritant, potentially leading to secondary complications like adhesions if untreated. In neonates, meconium peritonitis occurs due to in utero bowel , allowing sterile to spill into the and cause chemical , often detected prenatally via calcifications on . Iatrogenic causes are prominent in patients undergoing , where noninfectious peritonitis may arise from reactions to dialysate components, such as icodextrin-induced chemical irritation or eosinophilic responses to allergens in the solution. Post-procedural events, including or , can introduce sterile irritants like from contrast studies, exacerbating peritoneal . Rarely, autoinflammatory disorders contribute to recurrent sterile peritonitis. (FMF), an autosomal recessive condition, manifests with episodic , including acute peritoneal attacks simulating peritonitis, driven by gene mutations and responsive to therapy. Other entities, such as systemic lupus erythematosus, can similarly produce aseptic peritoneal inflammation through immune-mediated mechanisms.

Risk Factors

Peritonitis development is influenced by various individual and procedural factors that compromise the peritoneal barrier or immune defenses. Patients with liver cirrhosis and ascites are at heightened risk for spontaneous bacterial peritonitis (SBP), a subtype of primary peritonitis, due to impaired immune function and translocation of gut bacteria across the intestinal wall. Immunosuppression, such as that seen in HIV infection or from chemotherapy, further exacerbates this vulnerability by reducing the body's ability to combat bacterial invasion in the peritoneal cavity. Diabetes mellitus independently increases the risk of SBP in cirrhotic patients with ascites, likely through hyperglycemia-induced immune dysfunction and endothelial damage. Similarly, obesity, often measured by higher body mass index, correlates with elevated peritonitis rates, possibly due to associated metabolic inflammation and reduced peritoneal clearance. Procedural interventions also predispose individuals to peritonitis. , commonly used in , carries a significant risk from catheter-related infections, with patients experiencing approximately 0.2 to 0.5 episodes per patient-year at risk, though rates can vary by facility and adherence to protocols.31105-9/fulltext) Recent introduces contamination risks during the procedure or postoperative period, allowing bacterial entry into the . Endoscopic procedures, such as in dialysis patients, have been linked to peritonitis episodes, potentially from transient bacteremia or mucosal disruption. Lifestyle factors contribute to peritonitis susceptibility, particularly in vulnerable populations. Chronic promotes liver and formation, thereby elevating SBP risk through and gut barrier impairment. Intravenous drug use indirectly heightens risk by increasing the likelihood of hepatitis C acquisition, leading to and subsequent SBP predisposition. In peritoneal dialysis patients, poor hygiene practices, including inadequate handwashing or improper equipment handling, significantly contribute to infection rates. Certain comorbidities amplify peritonitis risk beyond isolated conditions. necessitates , inherently exposing patients to recurrent infection threats. , exemplified by , predisposes to secondary peritonitis through chronic intestinal inflammation and potential fistulas.

Pathophysiology

Inflammatory Mechanisms

Peritonitis involves the of peritoneal mesothelial cells as the initial response to inflammatory stimuli, where these cells rapidly release proinflammatory such as interleukin-1 (IL-1) and tumor necrosis factor-alpha (TNF-α), along with like IL-8, to orchestrate the local immune defense. This release induces endothelial and increases , marking the onset of acute in the . The immune cascade follows, characterized by the recruitment of neutrophils via gradients, which migrate into the peritoneal space to perform of invading . Complement activation occurs concurrently, enhancing opsonization and amplifying the phagocytic activity of neutrophils and macrophages, thereby facilitating clearance but also contributing to tissue damage through the release of . Macrophages further propagate the response by secreting additional cytokines and promoting the resolution phase once the threat is neutralized. Fluid dynamics are profoundly altered during peritonitis, with cytokine-mediated and increased capillary permeability leading to exudative fluid accumulation in the , resulting in formation. This third-spacing of fluid can cause and hemodynamic instability, as volume shifts into the peritoneal compartment, exacerbating systemic physiological . In severe cases, the inflammatory process escalates systemically through a , where elevated levels of IL-1, TNF-α, and IL-6 spill over into the bloodstream, triggering (SIRS) with widespread and potential multi-organ involvement. Resolution of the inflammatory response depends on the balance between pro- and anti-inflammatory signals; anti-inflammatory cytokines like IL-10 promote apoptosis and by macrophages, aiding clearance. However, if unresolved, excessive deposition occurs due to impaired , leading to adhesion formation and progressive peritoneal characterized by accumulation driven by transforming growth factor-beta (TGF-β).

Primary Versus Secondary Peritonitis

Peritonitis is classified into primary and secondary forms based on the underlying and presence of an identifiable intra-abdominal source of infection. Primary peritonitis, also known as (SBP), arises without a detectable in the gastrointestinal or genitourinary tract, typically resulting from bacterial translocation across the gut mucosa or hematogenous spread in susceptible individuals. It is commonly observed in patients with due to liver , where fluid accumulation facilitates bacterial seeding, or in those undergoing , where the procedure introduces risk without an intra-abdominal perforation. Microbiologically, primary peritonitis is usually monomicrobial; in SBP associated with , it typically involves aerobic gram-negative enteric bacteria such as or gram-positive organisms like streptococci, whereas in peritoneal dialysis-associated cases, gram-positive cocci such as coagulase-negative staphylococci or predominate due to catheter . In contrast, secondary peritonitis develops from direct contamination of the due to visceral , such as from , , or , or from intra-abdominal inflammatory processes like . This form is the most prevalent type of peritonitis in non-cirrhotic patients and is characterized by polymicrobial , encompassing a mix of aerobic and from the gastrointestinal flora, depending on the site of . Unlike primary peritonitis, secondary cases often involve a surgically treatable source, such as a ruptured viscus, necessitating beyond antimicrobial therapy.

Diagnosis

Clinical Assessment

The clinical assessment of suspected peritonitis begins with a detailed history taking to evaluate the onset, location, and character of abdominal pain, which is typically sudden and severe, often becoming diffuse as the condition progresses. Associated symptoms such as fever, nausea, vomiting, and anorexia are commonly reported, helping to distinguish peritonitis from other acute abdominal conditions. Relevant risk factors, including recent abdominal surgery, peritoneal dialysis, liver cirrhosis, or immunocompromise, are elicited to guide suspicion toward primary or secondary etiologies. Physical examination starts with vital signs assessment, revealing , fever, and potentially in advanced cases indicative of systemic inflammatory response. Abdominal inspection may show distension and diminished bowel sounds, while elicits marked tenderness, often with guarding, rigidity, and rebound tenderness upon release of pressure, reflecting peritoneal irritation. Systemic signs such as altered mental status or further support the . Severity assessment may include tools like the Acute Physiology and Chronic Health Evaluation II () score for risk stratification in complicated intra-abdominal infections. Differential diagnosis encompasses mimics of acute abdomen, including (presenting with epigastric pain radiating to the back), (with sudden severe pain and hemodynamic instability), and lower lobe (causing referred abdominal pain via diaphragmatic irritation). In cases where is suspected as the underlying cause of secondary peritonitis, the —a clinical tool incorporating symptoms like right lower quadrant pain, anorexia, and rebound tenderness, along with signs such as fever and —can help stratify risk and inform urgency of intervention. Due to the high mortality risk, ranging from 6% overall to 35% in patients developing , clinical assessment must be expedited, with immediate hospitalization and further prioritized to mitigate deterioration.

Laboratory Tests

Laboratory tests play a crucial role in confirming the of peritonitis, assessing its severity, and guiding therapeutic decisions by providing objective evidence of , , and . Blood tests are typically the initial step, revealing systemic responses to the inflammatory process. A often shows , characterized by an elevated count greater than 11,000 cells/μL, frequently with a left shift indicating , which supports the presence of an acute bacterial . Inflammatory markers such as (CRP) and are commonly elevated; CRP levels above 10 mg/L indicate , while greater than 0.5 ng/mL suggests a bacterial and helps differentiate from non-infectious causes. In cases of suspected , serum lactate levels are measured, with values exceeding 2 mmol/L signaling tissue hypoperfusion and poor . Additionally, electrolyte panels and (BUN)/ ratios evaluate and renal impairment, as peritonitis can lead to third-spacing of fluids and , often showing elevated BUN (>20 mg/dL) and (>1.2 mg/dL). Paracentesis, the aspiration of peritoneal or ascitic fluid, is the gold standard for direct evaluation in patients with or suspected intra-abdominal fluid collections, prompted by clinical signs such as abdominal tenderness. Analysis of the fluid includes a cell count, where a polymorphonuclear leukocyte () count greater than 250 cells/μL is diagnostic for (SBP), a common subtype, even in the absence of positive cultures. The total nucleated cell count exceeding 500 cells/μL with a predominance of degenerative neutrophils further confirms an exudative inflammatory process. Biochemical assessment measures protein levels (typically >2.5 g/dL in exudates), (LDH > upper limit of normal serum value), and glucose, where low glucose (<60 mg/dL) or a fluid-to-blood glucose ratio less than 0.4 strongly suggests bacterial infection due to bacterial consumption. Microbiological evaluation of the peritoneal fluid is essential for identifying pathogens and determining antibiotic sensitivity. Gram staining provides rapid preliminary identification of bacterial morphology, though it has low sensitivity (10-30%) and is positive in only a minority of cases. Cultures of the fluid, ideally inoculated at the bedside into blood culture bottles to enhance yield, detect organisms such as or in up to 40-60% of SBP cases; fungal cultures are pursued if bacterial cultures are negative and risk factors like immunosuppression are present. For culture-negative cases, molecular techniques such as 16S rRNA PCR can detect bacterial DNA directly from ascitic fluid, improving identification in up to 20-30% of cases and associating with poorer prognosis. Emerging point-of-care tests, including IL-6-based lateral flow assays on peritoneal effluent, provide rapid diagnosis (within 5 minutes) with high sensitivity (97.6%) and negative predictive value (98.3%), particularly useful in peritoneal dialysis-associated peritonitis. Additionally, artificial intelligence and machine learning models using clinical and laboratory variables offer predictive scoring for SBP with sensitivities up to 94.7% as of 2025. Sensitivity testing on positive isolates guides targeted antimicrobial therapy. Blood cultures should be obtained concurrently in all patients to assess for bacteremia, which occurs in approximately 20-40% of peritonitis cases with systemic involvement, particularly in those with elevated temperature or suspected resistant organisms. Other laboratory tests help exclude alternative diagnoses. Serum amylase and levels are checked to rule out pancreatitis, with elevations above three times the upper limit of normal (amylase >300 U/L, lipase >180 U/L) indicating possible pancreatic involvement rather than primary peritonitis. Interpretation of results must consider the clinical context, as isolated elevations in blood markers may occur in non-peritoneal infections, while fluid analysis provides the most specific evidence; for instance, a count between 100-250 cells/μL warrants close monitoring and repeat testing.

Imaging Modalities

Imaging plays a crucial role in the of peritonitis by visualizing structural abnormalities such as free fluid, abscesses, perforations, and the underlying source of or . While clinical assessment and laboratory tests provide initial clues, modalities help confirm the presence of peritonitis and guide decisions, particularly in distinguishing primary from secondary causes. Plain abdominal radiography, often performed as an upright chest-abdomen , is a rapid initial imaging tool used to detect free intraperitoneal air, which indicates as a common cause of secondary peritonitis. The classic finding is subdiaphragmatic free air, appearing as a crescent-shaped lucency under the on upright views, with a sensitivity of approximately 89% for in cases of gastric or duodenal but lower for other sites. However, its overall sensitivity is limited, missing small amounts of free air or non-perforative causes of peritonitis, and it rarely identifies abscesses or fluid collections directly. Ultrasound serves as a first-line imaging modality, particularly in hemodynamically unstable patients, pregnant individuals, or resource-limited settings, due to its portability, lack of , and ability to detect free or abscesses in . Key findings include echogenic free fluid exceeding 100 , loculated collections with internal debris suggesting abscesses (e.g., perihepatic or pelvic), and bowel wall thickening or abnormalities; it also guides diagnostic . Its accuracy reaches about 83% for peritonitis diagnosis, outperforming clinical impression alone, though it is operator-dependent and hindered by bowel gas or . Per 2024 IDSA guidelines, is recommended as initial for suspected or in children and pregnant patients. Computed tomography (CT) is considered the gold standard imaging modality for peritonitis, offering high sensitivity (up to 100%) for detecting small volumes of free fluid, pneumoperitoneum, abscesses, bowel wall thickening, and the precise source of perforation or inflammation. Contrast-enhanced CT protocols enhance visualization of peritoneal enhancement, vascular complications like ischemia, and loculated collections (e.g., subhepatic abscesses), aiding in preoperative planning and percutaneous drainage. It excels in evaluating complex cases, such as identifying smooth peritoneal thickening in infectious peritonitis versus nodular patterns in malignancy mimics. The 2024 IDSA guidelines suggest CT as initial imaging for appendicitis in adults. Magnetic resonance imaging (MRI) is rarely employed in acute peritonitis due to its limited availability, longer acquisition time, and unsuitability for critically ill patients, but it may be useful in complex or chronic cases, such as suspected , or when is contraindicated (e.g., renal impairment). Findings include decreased T1 signal and increased signal in fluid collections with rim enhancement on gadolinium-enhanced sequences, providing detailed soft-tissue characterization comparable to for peritoneal abnormalities. is recommended after inconclusive for in children and pregnant patients per 2024 guidelines. Despite their utility, imaging modalities have limitations including radiation exposure from X-ray and CT (a concern in younger patients or repeated scans), variable availability in emergency settings, and potential delays in definitive surgical intervention if over-relied upon when clinical diagnosis is evident. Ultrasound's effectiveness can be reduced in distended bowels, while MRI's high cost and contraindications (e.g., pacemakers) restrict its routine use.

Pathological Examination

In gross pathological examination of peritonitis, the often contains variable amounts of purulent or fibrinous fluid, with congestion and hyperemia of the peritoneal surfaces evident. In cases of secondary peritonitis due to organ , such as appendiceal rupture or bowel , a focal site of is typically identified, surrounded by adherent inflammatory and possibly localized formation. Fibrinous may form shaggy, yellow-white plaques over visceral and parietal , while purulent fluid appears thick and creamy, reflecting bacterial contamination in infectious etiologies. Microscopically, acute peritonitis demonstrates dense neutrophilic infiltration within the submesothelial and overlying the , often with deposition on the surface. Mesothelial cells show reactive changes including , , or sloughing due to inflammatory damage, contributing to impaired . In infectious cases, bacterial colonies may be visible within the or tissue, particularly in secondary peritonitis from . In resolving or chronic peritonitis, pathological features shift toward of the submesothelial layer, with deposition leading to peritoneal thickening and adhesions. may appear in areas of organization, featuring proliferating fibroblasts, new blood vessels, and mixed inflammatory cells as the acute response subsides. Special stains play a key role in identifying causative organisms; Gram staining highlights bacterial morphology and aids in classifying infectious peritonitis, while acid-fast bacilli (AFB) stains, such as Ziehl-Neelsen, detect in tuberculous peritonitis, often revealing caseating granulomas. Biopsy of peritoneal tissue, obtained intraoperatively during or , or post-mortem, confirms the by demonstrating the above features and distinguishing peritonitis from mimics like ; imaging-guided sampling may occasionally assist but is less common for direct pathological evaluation.

Management

Initial Medical Therapy

Initial medical therapy for peritonitis primarily involves prompt initiation of broad-spectrum intravenous to cover the most likely pathogens, including Gram-negative aerobes, anaerobes, and enterococci, pending results. For community-acquired secondary peritonitis in adults, recommended empirical regimens include monotherapy with piperacillin-tazobactam (3.375 g IV every 6 hours) or a such as (1 g IV every 8 hours), which provide adequate coverage for enteric bacteria and anaerobes. In high-risk patients, such as those with healthcare-associated infections or recent exposure, broader coverage with addition of an agent active against resistant organisms, like for , may be necessary. Therapy should be de-escalated to narrower agents based on microbiological and sensitivities, typically within 48-72 hours, to minimize resistance and toxicity. For primary peritonitis, particularly (SBP) in patients with , empirical therapy consists of a third-generation such as (2 g IV every 8 hours) or (2 g IV every 24 hours), which effectively targets common Gram-negative pathogens like . The standard duration for SBP treatment is 5 days, provided clinical response is observed and complications are absent. Adjunctive is recommended in SBP to prevent renal impairment: 1.5 g/kg body weight on day 1 and 1 g/kg on day 3, reducing the risk of by improving effective circulating volume. For peritoneal dialysis-associated peritonitis, empirical intraperitoneal antibiotics are recommended per International Society for Peritoneal Dialysis guidelines, typically (15-30 mg/L per exchange) or (15 mg/L) plus ceftazidime (250 mg/L , then 125 mg/L maintenance) for Gram-positive and Gram-negative coverage, respectively, with intermittent dosing in automated . Therapy is adjusted based on effluent cultures; total duration is 14-21 days for most organisms, with removal indicated for peritonitis (no response after 5 days) or fungal/relapsing cases to prevent recurrence. Empirical antifungal therapy is reserved for cases with suspected fungal involvement, such as in peritoneal dialysis-associated peritonitis or immunocompromised patients with risk factors like recent broad-spectrum antibiotics; fluconazole (400 mg IV/PO daily) or an echinocandin like caspofungin (70 mg IV loading dose, then 50 mg daily) is used if Candida is suspected. For secondary peritonitis, antibiotic duration is generally 4-7 days after source control, as shorter courses (e.g., 4 days) are noninferior to longer ones (8-10 days) in resolving infection without increasing recurrence. These recommendations align with the 2024 World Society of Emergency Surgery (WSES) guidelines on intra-abdominal infections, emphasizing early empirical coverage and stewardship.

Surgical Interventions

Surgical interventions are the cornerstone of managing secondary peritonitis, particularly when source control is required to eliminate the infectious focus, such as in cases of gastrointestinal perforation, anastomotic dehiscence, or failure of initial medical therapy to resolve diffuse infection or sepsis. Indications typically arise in patients with generalized peritonitis exhibiting signs like abdominal rigidity, rebound tenderness, or systemic inflammatory response, where non-operative approaches are inadequate. These procedures aim to interrupt the cycle of ongoing contamination and bacterial proliferation, thereby supporting resuscitation and antimicrobial therapy. The primary procedures involve either open or laparoscopic exploration to identify and address the underlying . For instance, in perforated , an is performed, while colonic perforations from may necessitate resection with or without formation; abscesses are drained percutaneously or surgically as needed. remains the standard for most emergency cases due to its reliability in extensive exploration and control of , though is increasingly favored for stable patients with localized disease, such as uncomplicated or early , offering reduced morbidity when expertise is available. Intraoperative peritoneal lavage with copious saline irrigation is routinely incorporated to remove purulent material and debris. In critically ill patients with or hemodynamic instability, is employed as a staged technique, focusing on rapid source control through resection of necrotic bowel, thorough washout of the , and temporary closure of the abdomen to prevent . Open abdomen management may follow, utilizing or mesh-mediated traction to facilitate relaparotomy on demand—guided by clinical deterioration rather than scheduled reoperations—while minimizing formation and risks. These approaches are complemented by broad-spectrum antibiotics initiated preoperatively. Timing of is critical, with source control ideally achieved emergently upon , particularly within 12-24 hours for diffuse peritonitis, as delays beyond this threshold are associated with increased mortality rates exceeding 30% in severe cases. Early in the setting of recognition allows for better hemodynamic stabilization and reduces the progression to multi-organ failure. Complications from these interventions include wound infections, occurring in up to 20% of open procedures, and anastomotic leaks, which can necessitate reoperation and prolong recovery. Other risks encompass enteric fistulas (10-20% in open abdomen cases) and incisional hernias, underscoring the need for meticulous and postoperative .

Supportive Measures

Supportive measures in peritonitis focus on stabilizing , preventing , and promoting recovery through ancillary care, often provided in an (ICU) setting. These interventions address the systemic inflammatory response and complications such as , which can exacerbate the condition. Early and aggressive supportive is essential to improve outcomes in critically ill patients. Fluid is a cornerstone of supportive care, particularly in cases of associated with peritonitis. At least 30 mL/kg body weight of intravenous crystalloids, such as normal saline or , should be administered within the first 3 hours to restore intravascular volume and maintain tissue perfusion. If persists despite adequate fluid loading, vasopressors like norepinephrine or inotropes such as are initiated to achieve a greater than 65 mmHg. Monitoring to guide therapy includes dynamic parameters such as passive or variation for further fluid administration, output (>0.5 mL/kg/hour), and clearance to detect ongoing hypoperfusion. Nutritional support is initiated early to counteract and support immune function, with enteral preferred when gastrointestinal function allows, typically via nasogastric or nasojejunal tubes. This approach helps maintain gut barrier integrity and reduces bacterial translocation. In patients with or bowel rest, total parenteral (TPN) is used to provide adequate calories (approximately 25-30 kcal/kg/day) and protein (1.2-1.5 g/kg/day), though it carries risks of and line . nutritional supplementation has been shown to shorten hospital stays and enhance recovery in abdominal cases. Pain management is crucial for comfort but must be balanced to avoid masking clinical signs of deterioration. Opioids, such as or , are commonly employed as first-line agents for severe , administered intravenously in the acute phase. These can be safely used without significantly impairing diagnostic accuracy in acute abdominal conditions. analgesia, including non-opioid adjuncts like acetaminophen, may be incorporated to minimize opioid requirements and mitigate side effects such as respiratory . Organ support is tailored to specific failures, with mechanical ventilation using low tidal volumes (6-8 mL/kg) recommended for (ARDS), which occurs in up to 30% of severe peritonitis cases. For , continuous or is employed to manage fluid overload, electrolyte imbalances, and . These measures, often in conjunction with vasopressor support, aim to sustain vital organ function during the inflammatory cascade. Close monitoring in the ICU involves serial abdominal examinations to assess for worsening peritonitis, tracking, and evaluations of inflammatory markers and organ function. Repeat imaging, such as computed tomography or , is performed as needed to evaluate response to therapy and detect complications. Severity scoring systems like help stratify risk and guide resource allocation.

and Prevention

Prognostic Factors

Prognostic factors in peritonitis significantly influence survival and recovery, encompassing clinical, microbiological, and patient-specific elements that determine outcomes following and intervention. Early and prompt source control, ideally achieved within 24 hours of symptom onset, are critical positive predictors, substantially improving survival rates by limiting the progression to severe and multi-organ dysfunction. Monomicrobial infections, particularly those caused by single gram-negative organisms, also correlate with better compared to more complex cases, as they respond more effectively to targeted antimicrobial therapy. Conversely, several negative factors adversely affect outcomes. Delayed treatment beyond the initial 24-hour window markedly increases mortality risk, often due to escalating and organ failure. Polymicrobial infections, common in secondary peritonitis, are associated with higher complication rates and poorer resolution, as they complicate management and promote persistent intra-abdominal contamination. Advanced age, typically over 65 years, serves as an independent , with elderly patients exhibiting reduced physiological reserve and higher susceptibility to . Comorbidities such as , , diabetes mellitus, and further worsen prognosis by impairing immune response and increasing vulnerability to . Elevated severity scores, including a high score (greater than 15), strongly predict adverse events, reflecting acute physiological derangements and chronic health burdens. Recent validations of such scores, along with emerging models for risk stratification as of 2025, have enhanced predictive accuracy in intensive care settings. Mortality rates vary by peritonitis type and severity. Primary peritonitis, often spontaneous and community-acquired, carries a lower mortality of approximately 10-20% at 30 days, primarily in non-cirrhotic patients without . Secondary peritonitis, resulting from or postoperative complications, has higher rates of 20-50%, driven by the need for surgical source control and frequent polymicrobial involvement. In cases complicated by , mortality can range from 30-50%, underscoring the role of rapid hemodynamic stabilization. Long-term outcomes include risks of recurrence and diminished . In peritoneal dialysis-associated peritonitis, recurrence or relapse occurs in 20-30% of cases within the first year, often necessitating removal and technique failure. Survivors frequently experience persistent abdominal symptoms, reduced physical function, and psychological impacts, contributing to overall morbidity beyond the acute phase. As of 2025, outcomes have improved in high-resource settings through standardized protocols like those from the International Society for Peritoneal Dialysis, which emphasize early empirical antibiotics and audit-driven care, reducing peritonitis rates to below 0.40 episodes per patient-year. However, in low-resource areas, mortality remains elevated at approximately 25-30% due to delayed access to and challenges.

Preventive Strategies

Preventive strategies for peritonitis focus on addressing underlying risk factors through early intervention, strict protocols, and targeted prophylaxis in vulnerable populations. recognition and of abdominal infections, such as or , can prevent perforation and subsequent secondary peritonitis by reducing bacterial translocation into the . In surgical settings, adherence to evidence-based measures significantly lowers the risk of postoperative peritonitis arising from surgical site infections. Key practices include preoperative patient bathing with antimicrobial soap, alcohol-based skin preparation, surgical hand antisepsis with alcohol-based rubs, and timely administration of prophylactic antibiotics within 120 minutes before incision. For elective colorectal procedures, combining mechanical bowel preparation with oral antibiotics further mitigates contamination risks. For patients undergoing (PD), comprehensive training by experienced nurses on aseptic techniques, including hand and proper connection-disconnection methods, is essential to minimize contamination-related peritonitis. Structured programs, often exceeding 15 hours of cumulative training, enhance knowledge and behaviors, with home visits and retraining for non-compliance further supporting adherence. Exit-site care protocols involve daily application of topical like or gentamicin cream, alongside antiseptic cleaning with , which reduces aureus-related exit-site infections and peritonitis by 40-70%. Use of Y-connection or double-bag systems with flush-before-fill designs decreases peritonitis rates by approximately 33% compared to traditional spike systems. prophylaxis at PD catheter insertion and before invasive procedures, such as , is recommended to prevent early infections. Antifungal prophylaxis, such as during systemic courses, prevents secondary fungal peritonitis. Overall, these protocols and quality improvement initiatives can achieve peritonitis rates below 0.40 episodes per patient-year at risk. In patients with and , antibiotic prophylaxis targets (SBP), particularly in high-risk groups with ascitic fluid protein below 1.5 g/dL or prior episodes. Primary prophylaxis with (400 mg daily) or trimethoprim-sulfamethoxazole (one double-strength tablet daily) is advised for those without prior SBP, while secondary prophylaxis uses the same regimens post-resolution of an episode. These interventions reduce SBP incidence by 50-70% and lower infection-related mortality. Pneumococcal vaccination is also recommended for cirrhotics to prevent bacterial infections that may contribute to SBP. Public health efforts emphasize education on early symptom recognition, such as and fever, to facilitate timely medical access and reduce peritonitis complications in at-risk communities. In resource-limited settings, improving infrastructure and multidisciplinary training programs can lower peritonitis rates through better and practices.

History and Terminology

Historical Development

Peritonitis, an of the peritoneum, was first recognized in ancient medicine by in the BCE, who described symptoms including severe , fever, and rigidity, often leading to fatal outcomes without effective intervention. Early observations in texts noted similar symptoms of but lacked etiological understanding, attributing it to imbalances in bodily humors. In the , surgical advancements were hampered by high rates of postoperative peritonitis due to infection, with mortality exceeding 80% in abdominal procedures. Joseph Lister's introduction of antiseptic techniques in 1867, using carbolic acid to sterilize wounds and instruments, dramatically reduced these infections by targeting microbial causes, as inspired by Pasteur's germ theory. Concurrently, developed the Gram staining method in 1884, enabling differentiation of bacterial pathogens—crucial for identifying causative agents in peritonitis samples and guiding early microbiological diagnosis. The marked a turning point with the advent of antibiotics in the , which improved management of bacterial infections including peritonitis; sulfonamides and penicillin contributed to better outcomes in secondary peritonitis following or , though diagnostic delays continued to pose challenges. (SBP), particularly in cirrhotic patients, was initially reported in 1907 with cases of infection in ascitic fluid, though its distinct was not clarified until the 1960s through studies confirming bacterial translocation without intra-abdominal sources. From the 1980s onward, the adoption of laparoscopic surgery allowed minimally invasive exploration and source control in peritonitis, reducing operative trauma and complications compared to open . By the , evidence-based guidelines from organizations like the World Society of Emergency Surgery standardized multimodal approaches, integrating early antibiotics, imaging, and surgery, leading to improved outcomes—such as targets for technique survival exceeding 80% in peritoneal dialysis-related cases (as of 2022) and reduced overall mortality through refined protocols, including 2024 updates emphasizing .

Etymology

The term peritonitis derives from the Greek peritonaion (περιτόναιον), referring to the peritoneum or abdominal membrane, combined with the suffix -itis, which denotes inflammation in medical terminology. This etymological construction reflects the condition's core pathology: inflammation of the serous membrane lining the abdominal cavity. The word peritoneum itself originates from the Greek roots peri- ("around") and teinein ("to stretch"), literally meaning "stretched around," alluding to the membrane's enveloping role over abdominal viscera; it entered Late Latin as peritonaeum before adoption into English in the early 15th century. The full term peritonitis was coined in medical Latin around 1750 by the French pathologist François Boissier de Sauvages, marking its formal introduction into nosological classifications. In early , peritonitis was often described using phrases like "peritoneal " to emphasize the localized inflammatory process within the . A related descriptor, "," emerged as a broader clinical term encompassing sudden-onset syndromes, including peritonitis, and gained traction in diagnostic contexts from the onward. The modern usage of peritonitis became standardized during the amid advances in and , as detailed in seminal texts that clarified its association with perforations and infections. As of 2025, no significant variants or alternative have supplanted this term in international medical practice, maintaining its precision in describing peritoneal inflammation across subtypes.