Clinical Guides
Peritonitis
A clinically focused emergency guide to peritonitis in Indian practice, separating secondary intra-abdominal contamination from spontaneous bacterial peritonitis, with urgent resuscitation, CT and paracentesis pathways, source control, antimicrobial stewardship, albumin use and referral limits.
MedNext Academy | 14 min read
Peritonitis
A clinically focused emergency guide to peritonitis in Indian practice, separating secondary intra-abdominal contamination from spontaneous bacterial peritonitis, with urgent resuscitation, CT and paracentesis pathways, source control, antimicrobial stewardship, albumin use and referral limits.
Summary
Peritonitis is inflammation of the peritoneum caused most often by infection or leakage of gastrointestinal contents, but it is a syndrome rather than a single diagnosis. Primary peritonitis, especially spontaneous bacterial peritonitis (SBP), occurs without a surgically treatable perforation and is most commonly recognised in cirrhotic ascites. Secondary peritonitis results from a definable intra-abdominal source such as perforated viscus, anastomotic leak, ischaemic bowel, appendicitis, diverticulitis, biliary infection or trauma. Tertiary peritonitis describes persistent or recurrent infection after apparently adequate treatment in a severely ill host. These categories overlap clinically but differ decisively in source-control needs.
Generalised tenderness, involuntary guarding or rigidity with sepsis is a surgical emergency. Resuscitation, analgesia, blood tests, cultures and broad empirical antimicrobials should proceed alongside urgent imaging and surgical review; they are not reasons to postpone source control. Contrast-enhanced CT usually defines the source in a stable non-pregnant adult, while an unstable patient with convincing perforation may require theatre before complete imaging. Source control means stopping contamination and removing infected material using the least invasive definitive approach likely to work—surgery, percutaneous drainage or endoscopic intervention.
SBP demands a different reflex: perform prompt diagnostic paracentesis in hospitalised or deteriorating patients with cirrhotic ascites, culture fluid at the bedside and treat when the ascitic polymorphonuclear neutrophil count is at least 250 cells/mm³. Give intravenous albumin with antibiotics according to the validated SBP regimen and patient context. Failure of the neutrophil count to fall, polymicrobial culture or focal imaging should trigger investigation for secondary peritonitis. Local resistance and actual Indian source-control capacity must shape every antimicrobial and transfer decision.
How Common Is It?
There is no single meaningful incidence for “peritonitis” because it represents diverse diseases, settings and definitions. Secondary peritonitis is a major component of complicated intra-abdominal infection and emergency surgical workload, arising from appendiceal, gastroduodenal, small-bowel, colorectal, biliary, postoperative and traumatic sources. The distribution depends on age, local disease prevalence, referral pattern, antimicrobial exposure and access to timely imaging or surgery. Hospital series cannot be converted into a national community rate without careful denominators.
SBP occurs in people with cirrhosis and ascites, particularly during hospital admission or decompensation. Risk increases with advanced liver dysfunction, low ascitic protein, gastrointestinal bleeding, renal impairment and a previous episode. Published prevalence and recurrence estimates vary by inpatient status, diagnostic practices, prophylactic antibiotic exposure and geography. AASLD highlights that infection in cirrhosis can precipitate acute kidney injury and multiorgan failure; this clinical consequence is more useful than quoting an unverified Indian percentage. Tuberculous peritonitis remains an important Indian differential but is usually subacute and requires a separate diagnostic pathway rather than empirical labelling of every exudative ascites.
Indian data are fragmented across individual hospitals and procedure-based reports. Delayed presentation, prior community antibiotics, inter-facility transfer and limited microbiology can change both culture yield and organism distribution. Antimicrobial resistance also varies substantially between institutions. Therefore, avoid claims that one pathogen, perforation site or resistance rate represents all India. The robust teaching point is that peritonitis is common enough in acute care to require a rehearsed sepsis-and-source-control pathway, while SBP must be actively sought because abdominal signs may be mild or absent.
Risk Factors
Secondary peritonitis risk follows the diseases that disrupt an abdominal viscus. Important contexts include peptic ulcer perforation; appendicitis; diverticulitis; bowel obstruction, volvulus or strangulation; mesenteric ischaemia; inflammatory bowel disease; colorectal or gastric malignancy; gallbladder or biliary perforation; pancreatitis with infected necrosis; abdominal trauma; and recent endoscopy or surgery. Anastomotic leak, intra-abdominal drains, open abdomen, prolonged hospitalisation, immunosuppression, malnutrition and prior broad-spectrum antibiotics increase treatment-failure or resistant-organism risk. Extremes of age and limited physiological reserve amplify harm even when contamination appears anatomically modest.
SBP occurs mainly in cirrhotic ascites and becomes more likely with previous SBP, advanced decompensation, gastrointestinal haemorrhage, renal dysfunction, severe jaundice and low-protein ascitic fluid. Long hospital exposure and repeated antibiotics shift flora toward multidrug-resistant organisms, so a regimen that was reasonable during a first community presentation may be inadequate for nosocomial infection. Ascites from heart failure, malignancy, pancreatitis or tuberculosis has a different baseline risk and requires aetiological assessment rather than automatic SBP prophylaxis.
Peritoneal dialysis introduces a separate catheter-associated peritonitis pathway that this guide does not cover in prescribing detail. Female genital tract infection, postpartum infection and pelvic inflammatory disease may produce pelvic peritonitis and need gynaecological assessment. Steroids, chemotherapy, transplantation, diabetes and neutropenia may blunt fever or guarding. NSAIDs and analgesics can alter symptoms but do not reliably erase peritoneal inflammation. Risk factors guide empirical cover and urgency; none replaces examination, imaging, paracentesis or operative findings, and absence of a recognised risk cannot exclude perforation.
Diagnosis
History
Clarify onset, site, migration and spread of pain; vomiting; distension; obstipation; diarrhoea; gastrointestinal bleeding; fever; rigors; anorexia; syncope; urinary or gynaecological symptoms; trauma; and recent procedures. Ask about ulcer disease, gallstones, diverticular disease, cancer, inflammatory bowel disease, cirrhosis, ascites, prior SBP, dialysis and operations. Reconcile antibiotics, anticoagulants, NSAIDs, steroids, immunosuppression and allergies. In cirrhosis, new encephalopathy, kidney injury, hypotension or hospital admission warrants SBP assessment even without marked pain. Establish pregnancy possibility without delaying lifesaving care.
Examination
Begin with airway, breathing, circulation, mental state, perfusion, temperature and urine output. Inspect for distension, scars, hernias, drains and stigmata of chronic liver disease. Gently assess focal and generalised tenderness, percussion tenderness, involuntary guarding, rigidity, masses and bowel sounds. Rebound is painful and unnecessary when clear peritonism exists. Examine hernial orifices and selectively perform rectal or pelvic examination when findings will alter the pathway. Frail, immunosuppressed or encephalopathic patients may lack classic rigidity.
Investigations
Obtain blood count, electrolytes, renal and liver profile, glucose, coagulation, blood gas with lactate, CRP, group and crossmatch, pregnancy test where relevant and blood cultures before antibiotics when this creates no delay. Contrast CT of abdomen and pelvis usually identifies free air, leak, inflamed organ, collection, ischaemia or obstruction and guides drainage or surgery; ultrasound is valuable for biliary, pelvic or ascitic assessment. In cirrhotic ascites, perform prompt paracentesis for cell count with differential, albumin/protein and bedside inoculation into aerobic and anaerobic blood-culture bottles. An ascitic neutrophil count at least 250 cells/mm³ establishes the treatment threshold for SBP, but imaging and fluid chemistry must assess secondary causes when the pattern is atypical.
Differential Diagnosis
Peritonitis must first be separated from abdominal pain without peritoneal inflammation. Pancreatitis, biliary colic, renal colic, gastroenteritis, pyelonephritis, diabetic ketoacidosis, adrenal crisis, myocardial infarction, pneumonia, pulmonary embolism and abdominal-wall pain can mimic an acute abdomen. Early mesenteric ischaemia may cause intense pain before guarding develops and should not be excluded by a soft abdomen. Ileus may be a consequence of peritoneal inflammation or a manifestation of severe metabolic illness. In pregnancy-capable patients, ectopic pregnancy, ovarian torsion and pelvic infection require urgent consideration.
Within peritonitis, identifying the source changes treatment. Free intraperitoneal air, a focal inflammatory lesion, an abscess, anastomotic leak, bowel-wall non-enhancement or polymicrobial ascitic culture supports secondary peritonitis. In cirrhotic ascites, a monomicrobial culture and neutrophil count at least 250 cells/mm³ without a surgically remediable lesion support SBP. Very high ascitic protein, low glucose, high lactate dehydrogenase, multiple organisms, poor clinical response or a neutrophil decline of less than 25% after about 48 hours should increase concern for a secondary source; no single fluid rule is infallible.
Tuberculous peritonitis commonly evolves subacutely with fever, weight loss, pain and ascites. Lymphocytic fluid, elevated adenosine deaminase and imaging may support suspicion, but microbiological or histological confirmation is often needed and sensitivity varies. Peritoneal carcinomatosis, pancreatic ascites and chylous ascites also require targeted testing. Chemical peritonitis from blood, bile, gastric contents or pancreatic enzymes can become secondarily infected. The diagnostic obligation is to explain why the peritoneum is inflamed, not merely attach the syndrome label.
Management
Treat generalised secondary peritonitis as sepsis with a source-control emergency. Obtain intravenous or intraosseous access, give oxygen when indicated, monitor continuously, provide opioid-sparing multimodal analgesia and use reassessed balanced crystalloid boluses rather than indiscriminate large volumes. Measure urine output, correct glucose and electrolytes, decompress the stomach when obstruction or major vomiting warrants it, and provide venous-thromboembolism and stress-ulcer prophylaxis according to bleeding and operative risk. Start empirical intravenous antibiotics promptly, within the sepsis timeframe, after cultures when sampling does not delay therapy. Resuscitation and operative preparation occur simultaneously.
Source control removes infected material, stops ongoing contamination and restores anatomy or drainage. Depending on the cause, it may require repair or resection of a perforation, appendicectomy, cholecystectomy, stoma creation, debridement, percutaneous drainage or an endoscopic procedure. Use the least invasive method that is likely to achieve definitive control; a technically small procedure is not safer if it leaves contamination. Diffuse peritonitis, uncontrolled leak, ischaemic bowel or physiological collapse usually needs urgent surgery. Critically ill patients may require damage-control laparotomy and planned reassessment. After adequate control, short antimicrobial courses are generally effective; continued fever should trigger a search for failed control rather than automatic antibiotic extension.
For SBP, perform paracentesis then begin protocol-led intravenous therapy active against the likely setting-specific flora. Give intravenous albumin alongside antibiotics using the established day-one/day-three regimen, while monitoring respiratory and renal status. Repeat paracentesis at about 48 hours when response is uncertain, nosocomial infection or resistant organisms are concerns, or secondary peritonitis remains possible. Manage gastrointestinal bleeding, renal dysfunction and encephalopathy concurrently and arrange hepatology/transplant evaluation where appropriate.
Prescribing Information
Empirical treatment for secondary peritonitis must cover enteric Gram-negative organisms and anaerobes. The regimen depends on community versus healthcare acquisition, shock, previous cultures, recent antibiotics, renal and hepatic function, allergy, pregnancy and the local antibiogram. Broader anti-pseudomonal or resistant Gram-negative cover is reserved for patients whose severity or exposure justifies it; enterococcal, MRSA or antifungal treatment is not automatically required for every perforation. Obtain operative or drainage cultures in complicated infection when results can guide narrowing. After adequate source control, the Surgical Infection Society recommends no more than four days of therapy for most adults; ongoing infection demands reassessment of control, not reflexively prolonged drugs.
In SBP, select empirical intravenous antibiotics by acquisition setting and resistance risk. A third-generation cephalosporin may suit susceptible community-acquired disease, while nosocomial infection often requires broader local-protocol cover. AASLD recommends intravenous albumin 1.5 g/kg on day 1 and 1 g/kg on day 3 with antibiotics; benefit is especially relevant with kidney dysfunction or jaundice. Albumin can cause circulatory overload and requires clinical monitoring. Secondary prophylaxis after SBP and prophylaxis during selected gastrointestinal bleeding or high-risk low-protein ascites require specialist assessment, renal-dose review and stewardship because long-term antibiotics select resistance.
NCDC guidance supplies an Indian national stewardship framework but older syndrome tables are not a substitute for current hospital susceptibility data. Verify dose, infusion, maximum dose, allergy, renal adjustment and surgical timing in the live formulary. Avoid NSAIDs in cirrhosis, kidney injury or shock. Hold or review diuretics, nephrotoxins and non-selective beta blockers when hypotension or acute kidney injury complicates SBP. This educational guide cannot safely prescribe for an individual patient.
When to Refer
Generalised peritonitis, septic shock, free perforation, ischaemic bowel, uncontrolled leak or rapidly worsening physiology requires immediate senior surgical involvement and a facility capable of emergency source control, anaesthesia, blood products and postoperative critical care. Refer early to interventional radiology when a drainable collection may be controlled percutaneously, but do not let a pending drainage opinion delay surgery for diffuse contamination. Gastroenterology or therapeutic endoscopy may contribute to selected biliary, pancreatic or luminal leaks. Complex postoperative infection should involve the operating team whenever possible.
Transfer from a resource-limited Indian facility should begin as soon as the need exceeds local capability. Communicate vital trends, peritoneal findings, organ dysfunction, pregnancy status, anticoagulants, antibiotics and fluids given, laboratory results, CT images and the suspected control procedure. Keep the patient nil by mouth, continue resuscitation and antimicrobials, provide adequate analgesia and arrange an escort capable of recognising deterioration. Do not require CT before transfer if an unstable patient has an obvious surgical abdomen and imaging is unavailable; conversely, do not repeat imaging merely because the receiving hospital uses a different system.
Cirrhotic patients with SBP need hepatology input for decompensation, renal injury, prophylaxis and transplant eligibility, but surgical consultation remains urgent when secondary peritonitis is possible. Peritoneal-dialysis peritonitis requires the dialysis service because sampling and intraperitoneal antimicrobial protocols differ. Suspected tuberculous or malignant peritonitis needs gastroenterology, infectious-disease, respiratory or oncology pathways after acute instability is addressed. After discharge, unresolved fever, feeding failure, drain problems, recurrent ascites or wound complications require an explicit review destination rather than an open-ended return instruction.
Red Flags
Generalised involuntary guarding or board-like rigidity, shock, altered consciousness, oliguria, rising lactate, severe metabolic acidosis, hypoxaemia, rapidly progressive distension, gastrointestinal bleeding or free intraperitoneal gas is an emergency. Pain may temporarily diminish after a viscus perforates or as bowel becomes necrotic; apparent relief does not prove recovery. Older adults, steroid-treated patients, people with neutropenia and those with advanced cirrhosis may show little fever or guarding despite life-threatening infection. Persistent tachycardia or worsening organ function deserves more weight than a single benign abdominal examination.
After source control, continuing vasopressor need, recurrent pain, bilious or faeculent drain output, wound dehiscence, feeding intolerance, new organ failure or inflammatory markers that fail to improve suggests an uncontrolled source, missed ischaemia or anastomotic leak. Repeat CT or re-intervention should be considered according to stability; simply adding another antimicrobial is not source control. Abdominal-compartment physiology, enterocutaneous fistula and open-abdomen fluid losses require specialist critical-care and surgical management.
In cirrhotic ascites, fever, abdominal pain, encephalopathy, hypotension, ileus, gastrointestinal bleeding, kidney injury or unexplained decompensation should prompt immediate paracentesis and infection treatment. A polymicrobial culture, focal tenderness, free air, very abnormal fluid chemistry, inadequate neutrophil decline or clinical deterioration despite therapy is a red flag for secondary peritonitis. Albumin does not replace antimicrobial therapy or control of a perforation. New breathlessness during albumin infusion suggests overload and needs urgent assessment. Discharging a patient before a responsible team has reconciled the underlying source and follow-up is unsafe.
Indian Clinical Context
Indian practice spans high-volume tertiary emergency surgery units, district hospitals with variable CT availability and smaller facilities that must stabilise and transfer. The safest local protocol identifies the nearest 24-hour operating theatre, anaesthetist, blood bank, CT, interventional radiology and critical-care bed before a crisis. If source control cannot be delivered locally, referral starts during resuscitation. Family travel, payment mechanisms and bed searches must not turn into undocumented clinical delay; use named clinician-to-clinician handover and send images electronically where possible.
Resistance patterns vary across regions and hospitals, and many patients have already received antibiotics before culture. NCDC national guidance supports syndrome-based empirical treatment and stewardship, but institutional antibiograms and recent patient microbiology must determine whether community regimens remain credible. Samples from blood, ascitic fluid, drainage or operation should be collected correctly and treatment narrowed when results arrive. Reserve drugs should not be advertised as universally stronger. Short courses after adequate source control reduce exposure, whereas persistent sepsis requires evaluation for failed control and resistant or opportunistic infection.
Cirrhosis in India has diverse viral, alcohol-related and metabolic causes, and access to albumin, hepatology and transplantation is uneven. Diagnostic paracentesis is a high-value bedside test and should not be deferred solely for a modestly abnormal INR or platelet count without an individualized bleeding assessment. Tuberculosis remains a relevant subacute alternative, but empirical antituberculous therapy without adequate sampling can obscure malignancy and other diagnoses. International guidance informs care but is not an Indian national drug mandate; many source-control recommendations combine trial evidence with observational data and expert consensus from settings unlike a district Indian hospital. This guide therefore states principles, documents evidence limitations and requires local verification of every regimen and referral route.
NMC Competency Mapping
This guide maps directly to NMC General Surgery competency SU28.3: describe the causes, clinical features, complications and principles of management of peritonitis. Related learning includes abdominal examination, shock and sepsis recognition, gastrointestinal perforation, intestinal obstruction, perioperative resuscitation, antimicrobial safety and timely referral. A learner should take a focused history, identify peritoneal signs without repeatedly causing pain, recognise organ dysfunction, generate a source-oriented differential and select appropriate first-line investigations under supervision. Institutions should confirm the mapping against their adopted 2024 CBME implementation rather than relying on superseded local schedules.
At an applied level, the student should distinguish primary, secondary and tertiary peritonitis; explain why secondary disease requires source control; interpret free air, focal collections and bowel-compromise findings; and describe why resuscitation, antibiotics and operative planning occur in parallel. In a patient with cirrhotic ascites, the student should know the diagnostic paracentesis threshold, correct bedside culture technique, the role of albumin, and features suggesting a secondary source. Antimicrobial exercises should use local susceptibility information and teach de-escalation rather than memorising one universal combination.
Procedural competence requires supervised clinical training. This guide does not certify independent paracentesis, drain placement, laparotomy, bowel resection or management of septic shock. Simulation can assess closed-loop escalation, consent in an emergency, safe transfer and recognition of deterioration after surgery. Learners should document uncertainty and call for help early. The educational outcome is not recall of a rigid recipe; it is the ability to identify peritonitis, begin safe supportive care and connect the patient rapidly to definitive source control or a verified SBP pathway.
Key Exam Pearls for NEET PG
Peritonitis produces tenderness with involuntary guarding or rigidity, percussion tenderness and reduced bowel activity, but signs may be muted in older, immunosuppressed or critically ill patients. Primary peritonitis occurs without a surgically correctable perforation; secondary peritonitis follows contamination from a defined intra-abdominal source; tertiary peritonitis is persistent or recurrent infection after treatment in a severely ill host. Pneumoperitoneum supports perforation, yet its absence does not exclude a leak. Contrast CT is the principal source-defining study in a stable adult.
The core treatment of secondary peritonitis is resuscitation plus prompt broad enteric antimicrobial treatment plus definitive source control. Surgery, percutaneous drainage or endoscopic control is selected by source and physiology. After adequate control, an unnecessarily prolonged antimicrobial course offers little benefit and increases harm; persistent sepsis suggests failed control until proved otherwise. Damage-control surgery may be used in profound physiological derangement. Cultures allow later narrowing, especially in healthcare-associated or resistant-risk infection.
For SBP, perform diagnostic paracentesis in hospitalised or deteriorating cirrhotic ascites. An ascitic polymorphonuclear neutrophil count of at least 250 cells/mm³ triggers treatment even if culture is negative. Inoculate culture bottles at the bedside. Treat with setting-appropriate intravenous antibiotics and albumin 1.5 g/kg on day 1 then 1 g/kg on day 3, with monitoring. Failure of the neutrophil count to fall by at least 25% at about 48 hours, polymicrobial growth or focal imaging should raise secondary peritonitis. The common exam error is treating a perforation as SBP or giving antibiotics while omitting source control.
Frequently Asked Questions
Does every patient with peritonitis require an open emergency operation?
No. Diffuse contamination, perforation, ischaemic bowel or uncontrolled leak commonly requires urgent surgery, but selected collections can be drained percutaneously and some leaks can be controlled endoscopically. SBP is treated medically. The correct question is which intervention will achieve timely definitive source control for the identified cause.
How is spontaneous bacterial peritonitis diagnosed in cirrhotic ascites?
Perform diagnostic paracentesis and count ascitic polymorphonuclear neutrophils. A count of at least 250 cells/mm³ is the treatment threshold, whether or not culture later grows an organism. Inoculate aerobic and anaerobic blood-culture bottles at the bedside, and investigate a secondary source when imaging, culture, chemistry or response is atypical.
Why is intravenous albumin given with antibiotics for spontaneous bacterial peritonitis?
In SBP, albumin reduces progression of kidney injury and improves outcomes when combined with antibiotics, with greatest benefit seen in patients with renal dysfunction or marked jaundice. AASLD uses 1.5 g/kg on day 1 and 1 g/kg on day 3. Clinicians must monitor for circulatory overload and individual contraindications.
Should antibiotics simply be continued when fever persists after source control?
Not automatically. Ongoing fever, organ dysfunction or inflammatory deterioration may indicate an undrained collection, leak, ischaemic bowel, resistant organism or another infection. After adequate source control, short courses are usually sufficient. The team should reassess anatomy, cultures and the patient rather than extending broad therapy without a defined reason.
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