Peritonitis
Peritonitis is inflammation of the peritoneum, the thin membrane lining the abdominal cavity and covering the organs within it. It most often results from infection, and most commonly from bacteria entering the normally sterile abdominal cavity when a hollow organ perforates—a burst appendix, a perforated ulcer or diverticulum, or a leak after bowel surgery. It can also arise without any perforation, as when ascitic fluid becomes infected in patients with liver disease, or through chemical irritation from bile, stomach acid, or blood. Peritonitis is a medical emergency: the peritoneum’s enormous surface area allows infection and inflammatory fluid loss to overwhelm the body rapidly, and outcomes depend substantially on how quickly the underlying cause is identified and treated.
What is it?
The peritoneum is a thin, continuous membrane with two layers: one lining the inner surface of the abdominal wall, the other covering the abdominal organs. Between them lies a small volume of lubricating fluid. Under normal conditions this space is sterile and its total surface area is comparable to that of the skin.
That surface area is the key to understanding why peritonitis is so dangerous. When the peritoneum becomes inflamed, it behaves like a vast absorbing and weeping membrane. Bacteria and their toxins are absorbed rapidly into the bloodstream, and large volumes of fluid shift out of the circulation into the abdominal cavity and the inflamed tissues. A patient can lose several litres into this third space within hours, producing dehydration, falling blood pressure, and reduced blood flow to the kidneys and other organs, all while infection spreads systemically. The result is a condition that can progress from onset to septic shock in a matter of hours.
The peritoneum does have defences. It absorbs bacteria through lymphatic channels beneath the diaphragm, mounts a local immune response, and produces fibrin that walls off contamination—which is how a localised abscess forms rather than diffuse infection. The omentum migrates toward the site of injury and adheres to it, helping to contain the problem. When these mechanisms succeed, contamination stays localised; when they are overwhelmed, diffuse peritonitis develops.
Peritonitis is classified into three main categories, and the distinction determines treatment entirely.
Primary peritonitis, also called spontaneous bacterial peritonitis, occurs when the peritoneal fluid becomes infected without any perforation or surgically treatable source. It occurs almost exclusively in patients with pre-existing ascites, overwhelmingly from cirrhosis, and results from bacteria translocating across the bowel wall and seeding fluid that has reduced antibacterial capacity. It is treated with antibiotics alone. Recognising it is essential, because operating on a patient with spontaneous bacterial peritonitis is harmful rather than helpful.
Secondary peritonitis is the most common form and results from a breach of the gastrointestinal or genitourinary tract, allowing its contents into the peritoneal cavity. The causes span most of abdominal surgical practice: perforated appendicitis, perforated peptic ulcer, perforated diverticulitis, perforated colorectal cancer, bowel ischaemia with necrosis, strangulated hernia, traumatic injury, anastomotic leak after bowel surgery, gallbladder perforation, and pelvic inflammatory disease with tubo-ovarian abscess rupture. Secondary peritonitis requires source control—the underlying breach must be addressed.
Tertiary peritonitis describes persistent or recurrent peritoneal infection continuing beyond 48 hours after apparently adequate treatment of secondary peritonitis. It typically occurs in critically ill patients with impaired immune responses, frequently involves resistant or opportunistic organisms including fungi, and carries a poor prognosis.
Two further categories occur outside this framework and are worth understanding separately.
Peritoneal dialysis-associated peritonitis arises when bacteria enter through the dialysis catheter, usually from skin contamination during exchanges. It presents with cloudy dialysate effluent, abdominal pain, and sometimes fever, and is the leading complication of peritoneal dialysis. It is treated with antibiotics delivered directly into the dialysate.
Chemical or sterile peritonitis results from irritating material entering the peritoneal cavity without initial infection—bile from a leaking biliary system, gastric acid from a perforated ulcer in its earliest hours, pancreatic enzymes in severe pancreatitis, blood after trauma or a ruptured ectopic pregnancy, or urine from a bladder rupture. The inflammatory response can be severe, and bacterial infection frequently supervenes.
Tuberculous peritonitis develops more insidiously over weeks, with ascites, abdominal swelling, fever, night sweats, and weight loss rather than acute severe pain, and closely mimics peritoneal malignancy on imaging.
The clinical picture of acute secondary peritonitis is distinctive and, once recognised, difficult to mistake.
Pain is severe, constant rather than colicky, and markedly worsened by movement. Patients characteristically lie completely still, often with knees drawn up, and are reluctant to move, cough, or be jolted—a striking contrast to the restless movement of someone with colicky pain from a kidney stone or bowel obstruction. Pain may begin localised to the source, such as the right lower abdomen in appendicitis, then become generalised as contamination spreads.
On examination, guarding is present: the abdominal muscles tense involuntarily when the abdomen is palpated. As inflammation progresses this becomes board-like rigidity, an abdomen that is hard and immobile. Rebound tenderness—pain that is worse when pressure is released than when applied—reflects peritoneal irritation. Bowel sounds diminish and eventually disappear as the intestine stops moving in response to inflammation.
Systemic features follow: fever, rapid heart rate, rapid breathing, and as the condition progresses, falling blood pressure, reduced urine output, confusion, and cold clammy skin indicating septic shock.
A critical point is that this classic presentation is frequently blunted or absent in certain groups. Older adults may have minimal pain and no fever. Patients on corticosteroids or immunosuppressants, those with diabetes, and those receiving chemotherapy may show remarkably few signs despite established infection. Patients with obesity can have significant peritonitis with an abdomen that feels deceptively soft. Postoperative patients may have their symptoms attributed to expected surgical pain. In all of these situations, unexplained deterioration, tachycardia, or a failure to recover as expected should raise the question of peritonitis even when the abdomen does not feel dramatic.
Spontaneous bacterial peritonitis deserves particular emphasis for the same reason. Its presentation is often subtle, and a substantial proportion of patients have no abdominal pain at all. It may declare itself only as fever, worsening confusion or hepatic encephalopathy, deteriorating kidney function, or unexplained clinical decline in someone with cirrhosis and ascites. This is why guidelines recommend diagnostic paracentesis in essentially all patients admitted to hospital with cirrhosis and ascites, regardless of whether they have abdominal symptoms.
Diagnosis combines examination, imaging, and fluid analysis.
Clinical examination frequently establishes that peritonitis is present. Rigidity, guarding, and rebound tenderness in a systemically unwell patient are strongly indicative, and in an unstable patient with clear signs, the priority is resuscitation and definitive treatment rather than further investigation.
CT of the abdomen and pelvis with intravenous contrast is the primary imaging test for identifying the cause and planning treatment. It demonstrates free gas outside the bowel lumen—the hallmark of perforation—along with free or loculated fluid, abscess collections, inflammatory changes, bowel wall thickening or lack of enhancement suggesting ischaemia, and the source organ itself. Oral or rectal contrast is used in some circumstances to identify the site of a leak. CT also determines whether a collection is amenable to percutaneous drainage rather than surgery.
Upright chest or abdominal X-rays can show free gas beneath the diaphragm and remain useful where CT is not immediately available, though they are far less sensitive and a normal film does not exclude perforation.
Ultrasound detects free fluid, can identify some causes such as gallbladder disease, and is used to guide paracentesis. It is particularly valuable in pregnancy and in unstable patients who cannot travel to a CT scanner.
Diagnostic paracentesis is the central test in suspected spontaneous bacterial peritonitis. A neutrophil count of 250 cells per cubic millimetre or greater in ascitic fluid establishes the diagnosis and prompts immediate antibiotic treatment, without waiting for culture results. Culture yield improves substantially when fluid is inoculated into blood culture bottles at the bedside. Additional fluid analysis including protein, glucose, and LDH helps distinguish spontaneous bacterial peritonitis from secondary peritonitis due to perforation, which is important because the latter requires surgery rather than antibiotics alone.
Blood tests assess severity and support management: complete blood count, inflammatory markers, lactate as a marker of tissue perfusion, kidney and liver function, coagulation, and blood cultures taken before antibiotics.
Important to Know
Peritonitis is a time-critical condition in which delays translate directly into worse outcomes. The two pillars of treatment are prompt resuscitation with antibiotics, and source control—eliminating whatever is contaminating the abdomen. Care is coordinated by emergency physicians, general and colorectal surgeons, intensivists, interventional radiologists, and, in the case of spontaneous bacterial peritonitis, hepatologists.
Initial management runs in parallel rather than in sequence. Intravenous fluid resuscitation addresses the substantial volume losses into the abdomen and tissues. Broad-spectrum intravenous antibiotics covering gram-negative and anaerobic organisms are started promptly after blood cultures are drawn, with early administration being one of the strongest determinants of survival in sepsis. Analgesia is provided—the old teaching that pain relief obscures the diagnosis has been abandoned, as adequate analgesia does not impair diagnostic accuracy. Patients are kept nil by mouth, with nasogastric decompression where there is vomiting or distension, and urine output, lactate, and haemodynamics are monitored closely, frequently in a critical care setting.
Source control is the defining intervention in secondary peritonitis and should not be delayed for extended investigation in a deteriorating patient. Surgery is the usual route and may involve appendicectomy, repair or patching of a perforated ulcer, resection of perforated bowel with either primary anastomosis or a stoma, drainage and washout of the peritoneal cavity, or diversion. The specific operation depends on the cause, the degree of contamination, and the patient’s physiological state. In severely unstable patients, a damage-control approach is sometimes used: a limited initial operation to control contamination, followed by resuscitation in intensive care and a planned return to theatre once the patient has stabilised, occasionally with the abdomen left temporarily open.
Image-guided percutaneous drainage is an important alternative for well-defined, accessible collections such as a diverticular or appendiceal abscess. It frequently settles the acute episode without emergency surgery and allows any subsequent operation to be performed electively under far better conditions.
Spontaneous bacterial peritonitis is managed entirely differently and must not be operated on. Treatment is with intravenous antibiotics, typically a third-generation cephalosporin, guided by local resistance patterns and by whether the infection was acquired in hospital. Intravenous albumin given alongside antibiotics reduces the risk of kidney injury and improves survival, and is recommended particularly for patients with impaired kidney function or significant jaundice. Repeat paracentesis after 48 hours is used when the response is uncertain, and a failure to improve raises the possibility of secondary peritonitis from a perforation, which changes management fundamentally. After an episode, long-term preventive antibiotics substantially reduce recurrence, and an episode of spontaneous bacterial peritonitis is generally an indication to assess the patient for liver transplantation, since it marks a significant deterioration in prognosis.
Peritoneal dialysis-associated peritonitis is treated with antibiotics delivered into the dialysate, allowing high local concentrations. Most episodes resolve without removing the catheter, but refractory infection, relapsing infection, fungal peritonitis, and certain organisms require catheter removal. Meticulous exchange technique and exit-site care are the mainstays of prevention.
Complications of peritonitis include sepsis and septic shock, acute kidney injury, respiratory failure, residual or recurrent intra-abdominal abscess, prolonged ileus, wound infection and dehiscence, enterocutaneous fistula, and dense adhesions that can cause bowel obstruction years later. Tertiary peritonitis in critically ill patients is particularly difficult to treat.
Outcomes depend heavily on the cause, the patient’s baseline health, and the speed of treatment. A young patient with a perforated appendix treated promptly generally recovers fully. An older patient with multiple comorbidities, a faecally contaminated abdomen from a perforated colon, and established septic shock faces a substantially higher risk, and mortality in that setting remains significant despite modern care. This variation is why urgency matters so much and why delayed presentation is consequential.
Recovery after treatment for severe peritonitis often takes considerably longer than patients expect, involving a period of weakness, poor appetite, and fatigue lasting weeks to months, particularly after critical illness. Nutritional support and graduated rehabilitation form part of care.
Prevention is limited but relevant in specific situations: preventive antibiotics after an episode of spontaneous bacterial peritonitis and for patients with cirrhosis and gastrointestinal bleeding or low-protein ascites; careful technique and exit-site care in peritoneal dialysis; timely treatment of appendicitis, diverticulitis, and peptic ulcer disease before perforation occurs; and prompt repair of symptomatic hernias.
Care is coordinated by emergency, surgical, critical care, radiology, and hepatology teams as appropriate. Imaging, laboratory, and clinical findings are interpreted alongside the patient’s symptoms, examination, comorbidities, immune status, and recent surgical history rather than in isolation.
Patient education plays an important role. Understanding why urgent assessment matters, why some cases require surgery while others are treated with antibiotics alone, why patients with cirrhosis need a diagnostic tap even without abdominal pain, why preventive antibiotics are continued afterwards, and what a realistic recovery looks like all contribute to appropriate care.
Red flag symptoms include severe constant abdominal pain that worsens with any movement or coughing; an abdomen that is rigid, hard, or exquisitely tender; fever with abdominal pain; persistent vomiting with abdominal distension and inability to pass gas or stool; rapid heart rate, rapid breathing, or low blood pressure; confusion, drowsiness, or new disorientation; cold clammy skin or markedly reduced urine output; cloudy dialysate fluid or abdominal pain in a patient on peritoneal dialysis; and fever, confusion, or unexplained deterioration in a patient with cirrhosis and ascites, even without abdominal pain. These warrant immediate emergency evaluation, as they may indicate perforation, established peritonitis, or sepsis.