Write a short note on spontaneous bacterial peritonitis and secondary peritonitis.

Spontaneous Bacterial Peritonitis (SBP)

Definition: infection of pre-existing ascitic fluid without any identifiable intra-abdominal, surgically treatable source. It is a common and serious complication of cirrhosis, occurring in 10–30% of hospitalised cirrhotic patients with ascites, with substantial mortality and a high rate of recurrence.

Pathogenesis: bacterial translocation from the gut lumen to mesenteric lymph nodes and then to ascitic fluid, facilitated by increased intestinal permeability, small bowel bacterial overgrowth, and impaired local and systemic immune defences in cirrhosis. Ascitic fluid with low protein (< 1.5 g/dL) has poor opsonic activity, which is why such patients are at highest risk.

Organisms: predominantly Gram-negative enteric organisms — *Escherichia coli* (commonest), *Klebsiella* — and streptococci; usually a monomicrobial infection, which is an important contrast with secondary peritonitis.

Clinical features: the crucial point is that presentation is frequently subtle or silent.

• Fever and abdominal pain with generalised tenderness — but these may be absent.
• Worsening or new-onset hepatic encephalopathy — often the only clue.
• Deterioration in renal function; refractory or newly worsening ascites.
• Hypotension, shock, ileus, diarrhoea.
• Any unexplained clinical deterioration in a cirrhotic with ascites should prompt a diagnostic tap.

Diagnosis — by ascitic fluid analysis:

• Ascitic fluid polymorphonuclear (neutrophil) count ≥ 250 cells/µL is diagnostic, regardless of culture result. Treatment is started on this count alone.
• Culture — inoculate at the bedside directly into blood culture bottles, which raises the yield from around 50% to 80%; nevertheless, culture-negative neutrocytic ascites is common and is treated as SBP.
• Bacterascites — positive culture with a neutrophil count below 250: repeat the tap; treat if the patient is symptomatic.
• Also send total protein, albumin (for SAAG), glucose and LDH.

Distinguishing SBP from SECONDARY bacterial peritonitis — essential, because secondary peritonitis needs surgery, and antibiotics alone will fail:

Management of SBP:

• Start empirical intravenous antibiotics immediately once the neutrophil count is ≥ 250 — do not wait for culture. Third-generation cephalosporins (cefotaxime, ceftriaxone) are standard; adjust for local resistance patterns, and consider broader cover for hospital-acquired or recent-antibiotic-exposed patients, where resistant organisms are an increasing problem in India.
• INTRAVENOUS ALBUMIN — given on day 1 and day 3, this reduces the incidence of hepatorenal syndrome and improves survival, particularly in those with renal impairment or a high bilirubin. It is one of the strongest evidence-based interventions in hepatology and is frequently omitted.
• Stop non-selective beta-blockers during an episode with hypotension or renal impairment.
• Avoid nephrotoxins; monitor renal function.
• Repeat the ascitic tap at 48 hours if there is doubt — a fall in the neutrophil count of more than 25% confirms response; failure to fall suggests resistance or secondary peritonitis.
• Secondary prophylaxis — long-term norfloxacin or ciprofloxacin after an episode, since recurrence approaches 70% at one year.
• Primary prophylaxis — for low ascitic protein (< 1.5 g/dL) with advanced disease, and short-course prophylaxis during gastrointestinal bleeding in all cirrhotics.
• Refer for liver transplant assessment — an episode of SBP marks a poor prognosis.

Secondary Peritonitis

Definition: peritoneal inflammation resulting from a defined intra-abdominal source — perforation, ischaemia or transmural inflammation of a viscus.

Causes:

• perforated peptic ulcer, perforated appendix, typhoid ileal perforation and tuberculous intestinal perforation (both important in India), diverticular perforation, perforated malignancy, gangrenous bowel from strangulation or mesenteric ischaemia, acute cholecystitis with perforation, pancreatitis with infected necrosis, and post-operative anastomotic leak.
• Tertiary peritonitis is persistent or recurrent infection after apparently adequate treatment, typically in critically ill patients.

Clinical features:

• severe, constant abdominal pain, worse on movement and coughing
• the patient lies still (in contrast to the restlessness of colic)
• generalised tenderness with guarding, rigidity ("board-like abdomen") and rebound tenderness
• absent bowel sounds (ileus)
• loss of liver dullness with free gas
• fever, tachycardia, dehydration and septic shock.

Investigations:

• erect chest or abdominal X-ray showing free gas under the diaphragm (absent in up to 30%)
• CECT abdomen — the investigation of choice for identifying the source
• CBC with leucocytosis, raised CRP and lactate, renal function, amylase, and blood cultures.

Management:

1. Resuscitation — fluids, correction of electrolytes, analgesia, nasogastric decompression, urinary catheter and monitoring.

2. Broad-spectrum intravenous antibiotics covering Gram-negatives and anaerobes.

3. SOURCE CONTROL — the definitive treatment: urgent surgery (or percutaneous drainage for a localised collection) to close the perforation, resect necrotic bowel, drain pus and lavage the peritoneum. Antibiotics alone will not cure secondary peritonitis.

4. Intensive care support for organ failure; nutritional support; management of complications (abscess, fistula, adhesions).