Peritonitis: Primary, Secondary and Tertiary

Introduction

The peritoneum is a single continuous serous membrane with a surface area roughly equal to that of the skin, folded into a parietal layer lining the abdominal wall and a visceral layer covering the organs. It normally contains only a few millilitres of lubricating fluid. It is highly vascular, highly absorptive, and richly supplied with immune cells, and all three properties determine what happens when it becomes infected.

Peritonitis is inflammation of that membrane. It is worth learning as three separate diseases sharing a name, because the treatment of each is entirely different: one is treated with antibiotics and albumin, one with an operation, and one with critical care and microbiological persistence.

Anatomy and why abscesses form where they do

Peritoneal fluid does not stay where it is spilled. It moves under the influence of gravity and, in the supine patient, of the negative pressure generated beneath the diaphragm during respiration. Knowing the routes explains both the pattern of pain and the sites at which collections later appear.

• The subphrenic spaces, right and left, above the liver and spleen. Fluid is drawn upwards here by diaphragmatic movement, which is why a right subphrenic abscess can follow a pelvic appendicitis. Irritation of the diaphragm produces shoulder tip pain through the phrenic nerve.
• The subhepatic space (Morison pouch), the most dependent part of the upper abdomen in a supine patient and a common site for collections
• The paracolic gutters, lateral to the ascending and descending colon, which act as channels between the upper abdomen and the pelvis
• The pouch of Douglas (rectouterine) in women and the rectovesical pouch in men - the most dependent part of the peritoneal cavity when upright, and the classic site of a pelvic abscess presenting with diarrhoea, tenesmus and a swinging fever
• The lesser sac, behind the stomach, which communicates with the greater sac only through the epiploic foramen and so tends to trap pancreatic collections

The greater omentum is the peritoneum's principal defence mechanism and is sometimes called the abdominal policeman. It migrates towards an area of inflammation and adheres to it, walling off contamination and converting a potential generalised peritonitis into a localised phlegmon or abscess. This is why a perforated appendix in a young adult with a mobile omentum may be contained, while the same event in a very young child with a short omentum spreads freely.

Causes

Secondary peritonitis - the surgical causes

• Perforation - peptic ulcer, appendix, diverticulum, colorectal or gastric tumour, or a colonoscopic injury
• Ischaemia and infarction - mesenteric ischaemia, strangulated hernia, volvulus, closed loop obstruction
• Anastomotic leak after gastrointestinal surgery, classically presenting on day five to seven
• Inflammation without perforation - severe pancreatitis, cholecystitis, salpingitis and pelvic inflammatory disease
• Trauma - blunt or penetrating injury to a hollow viscus
• Foreign material - retained swab, a leaked biliary or urinary collection, or intraperitoneal chemotherapy
• Bile peritonitis, which is intensely irritant and may follow cholecystectomy or a liver biopsy

Primary peritonitis

• Spontaneous bacterial peritonitis in cirrhosis - by far the commonest cause, affecting around 10 to 30% of hospitalised patients with ascites
• Peritoneal dialysis-associated peritonitis - infection introduced along the catheter, usually with skin organisms
• Nephrotic syndrome in children, classically with pneumococcus
• Tuberculous peritonitis, which is subacute with weight loss, low-grade fever, ascites and a doughy abdomen

Pathophysiology

Contamination of the peritoneum triggers a stereotyped sequence whose consequences are both local and systemic.

1. Vasodilatation and increased permeability of the peritoneal capillaries, with an outpouring of protein-rich exudate. Several litres can be sequestered, producing hypovolaemia even before sepsis develops.
2. Fibrin deposition, which seals off contaminated areas but also impairs bacterial clearance by macrophages and forms the scaffold for later adhesions
3. Omental migration and adherence, walling off the source where possible
4. Paralytic ileus, as inflamed bowel stops propelling, adding further fluid loss and vomiting
5. Absorption of bacteria and endotoxin across the enormous absorptive surface directly into the portal and systemic circulations, producing bacteraemia and the systemic inflammatory response
6. Septic shock and multi-organ dysfunction - vasodilatation, capillary leak, acute kidney injury, respiratory failure and coagulopathy
7. Adhesion formation as the fibrin matures into fibrous bands, generating a lifelong risk of intestinal obstruction

Clinical features

Generalised secondary peritonitis

• Severe constant abdominal pain, worse with any movement, so the patient lies still with knees drawn up and breathes shallowly
• Generalised guarding and rigidity, with percussion tenderness across the abdomen and pain on coughing
• Absent bowel sounds from the accompanying ileus
• Fever, tachycardia and hypotension, with cool peripheries and reduced urine output
• Nausea, vomiting and absolute constipation
• A drawn, anxious facial appearance with sunken eyes in advanced disease, described historically as the Hippocratic facies

Spontaneous bacterial peritonitis

This is the important contrast. SBP is frequently silent. Up to a third of patients have no abdominal pain at all, and the classic peritonitic abdomen is rare because ascitic fluid separates the visceral and parietal peritoneum. Presentation may be nothing more than a deterioration in someone already known to have cirrhosis.

• New or worsening hepatic encephalopathy - often the only clue
• Fever or hypothermia, and unexplained tachycardia
• Deteriorating renal function or a rising bilirubin
• Diffuse abdominal tenderness without guarding
• Diuretic-resistant ascites, or hypotension in a patient previously stable
• Unexplained gastrointestinal bleeding, which both predisposes to SBP and may be precipitated by it

Investigations

Ascitic fluid analysis

The diagnostic ascitic tap is the single most important investigation in suspected primary peritonitis, and it should be performed and sent before antibiotics are given wherever this does not cause delay.

Other investigations

• FBC, U&Es, LFTs, CRP, clotting, lactate and blood cultures in all patients
• Contrast-enhanced CT of the abdomen and pelvis - essential where secondary peritonitis is suspected, to find and localise the source and to identify drainable collections
• Erect chest radiograph for free subdiaphragmatic gas, remembering its limited sensitivity
• Ultrasound to confirm ascites, guide the tap, and assess the liver and biliary tree
• Beta-hCG in women of childbearing age, since pelvic inflammatory disease and ruptured ectopic pregnancy both enter the differential

Management

Spontaneous bacterial peritonitis

1. Empirical intravenous antibiotics immediately - typically cefotaxime, or piperacillin-tazobactam where healthcare-associated infection or resistance is likely, following local microbiology policy. A five-day course is usually sufficient once the patient responds.¹
2. Intravenous human albumin solution, 1.5 g/kg on day 1 and 1 g/kg on day 3. This is not simply volume replacement - it reduces the incidence of hepatorenal syndrome and improves survival, and is one of the few interventions in hepatology with a clear mortality benefit.²
3. Stop non-selective beta-blockers, nephrotoxic drugs and diuretics during the acute episode
4. Repeat the ascitic tap at 48 hours if the response is uncertain; a fall in the neutrophil count of at least 25% indicates the antibiotics are working
5. Secondary prophylaxis with an oral quinolone such as ciprofloxacin after a first episode, since recurrence is otherwise around 70% within a year
6. Refer for liver transplant assessment, because an episode of SBP marks a significant deterioration in prognosis

Secondary peritonitis

The governing principle is source control: antibiotics cannot sterilise a peritoneum that is being continuously contaminated. Resuscitate and give antibiotics, but the definitive treatment is mechanical.

• A to E assessment, large-bore access, balanced crystalloid resuscitation guided by lactate and urine output, and early critical care involvement
• Broad-spectrum intravenous antibiotics within one hour after blood cultures, covering enteric Gram-negatives and anaerobes³
• Nil by mouth, nasogastric decompression, catheterisation, analgesia and thromboprophylaxis
• Definitive source control - laparotomy or laparoscopy to close, resect or divert the source, with thorough peritoneal lavage. Radiologically guided percutaneous drainage is preferred where the source is a discrete abscess and the patient is stable.
• Relook laparotomy or laparostomy in severe contamination or where viability was uncertain, with a planned return to theatre rather than a reactive one
• Nutritional support, since these patients are catabolic and often have a prolonged ileus

Peritoneal dialysis-associated peritonitis

Suspect it in any peritoneal dialysis patient with a cloudy dialysate bag, with or without abdominal pain. Send the effluent for cell count, Gram stain and culture: a white cell count above 100 cells/microlitre with more than 50% neutrophils is diagnostic. Treatment is with intraperitoneal antibiotics delivered in the dialysate, covering both Gram-positive and Gram-negative organisms, and the catheter is removed for refractory, relapsing or fungal infection.⁴

Tertiary peritonitis

This is a problem of critical care rather than of the operating theatre. It occurs in patients with an impaired immune response after severe secondary peritonitis, and the organisms recovered are typically resistant Gram-negatives, enterococci, coagulase-negative staphylococci and Candida. Management involves repeated imaging to identify any remaining focus, targeted antimicrobials including antifungals guided by cultures, organ support, and nutritional and metabolic care. Mortality is high.

Complications

• Septic shock and multi-organ failure - the principal cause of death
• Intra-abdominal abscess in the subphrenic, subhepatic, paracolic or pelvic spaces, typically presenting five to ten days after the initial event with a swinging fever, ileus and rising inflammatory markers
• Hepatorenal syndrome following SBP, which is the reason albumin is given
• Adhesions, and consequent small bowel obstruction and subfertility
• Enterocutaneous fistula and wound dehiscence after laparotomy for contamination
• Abdominal compartment syndrome, particularly after massive resuscitation or laparostomy
• Prolonged ileus with malnutrition and the need for parenteral nutrition
• Recurrence - around 70% within a year after a first episode of SBP without prophylaxis

Red flags

Prognosis

Outcome varies enormously by category. Secondary peritonitis treated with prompt source control in a physiologically robust patient carries a good prognosis, while faecal peritonitis in a frail patient with delayed treatment carries a mortality above 30%.

Spontaneous bacterial peritonitis has an in-hospital mortality of around 20% even with prompt treatment, and the one-year mortality after a first episode approaches 50 to 70%. That figure reflects the underlying liver disease more than the infection itself: SBP is best regarded as a marker that the cirrhosis has decompensated to a point where transplantation should be considered, rather than as an isolated infective episode.

Tertiary peritonitis carries the worst prognosis of the three, with mortality frequently above 50%, because it arises in patients whose immune response has already failed. The practical implication runs backwards through the whole topic: the best treatment for tertiary peritonitis is adequate source control of the secondary peritonitis that preceded it.