Peritonitis

^r^^l^D; Peritonitis is inflammation of the peritoneal lining of the abdominal cavity, can be localised to one part or generalised, the latter primary or 2 secondary.

OA: Localised: Common causes are appendicitis, cholecystitis, diverticulitis, salpingitis.

Primary generalised peritonitis: bacterial infection of the peritoneal cavity without obvious focus responsible, possibly via haematogenous or lymphatic ^^ spread, or ascending infection from the female genital tract. More common in those with ascites, e.g. liver cirrhosis (SBP) or children with nephrotic syndrome. Seconday generalised peritonitis: Peritonitis due to bacterial translocation and spread, evolving from a localised focus (see above) or nonbacterial due to ^^ spillage of bile, blood, gastric contents, e.g. perforated peptic ulcer, pancreatic secretions (a chemical peritonitis that often becomes secondarily infected).

E: Primary peritonitis is rare, usually presents in adolescent females; localised and secondary generalised peritonitis are common in surgical patients.

_H: A careful history should be taken with exploration of the onset, nature, course and radiation of the abdominal pain as well as exacerbating, relieving and associated factors. Parietal pain from peritonitis is usually continuous, sharp, localised, exacerbated by movement and coughing (parietal peritoneum is supplied by somatic A-8 fibres arising from spinal nerves of T7-L2). In those with liver disease and ascites, symptoms can be vague (e.g. " confusion due to encephalopathy).

E: General state should be assessed, vital signs, signs of dehydration or compromised perfusion (e.g. due to hypovolaemia, sepsis or circulatory failure). Localised: Tenderness on examination with involuntary guarding: reflex contraction of overlying abdominal wall muscles; rebound tenderness: sudden removal of a palpating hand causes pain due to movement of the inflamed peritoneum, similarly demonstrated as percussion tenderness or pain evoked by coughing.

Generalised: Patient is usually very unwell with systemic signs of toxaemia or sepsis (e.g. fever, tachycardia). The patient lies still with shallow respiratory effort as movement exacerbates pain. The abdomen is rigid with generalised tenderness, bowel sounds are reduced or more typically absent due to paralytic ileus. Rectal examination allows direct palpation of the pelvic peritoneum usually demonstrating anterior tenderness.

P: The peritoneum consists of a single layer of flattened mesothelial cells over loose areolar tissue containing a rich network of capillaries, lymphatics, nerve endings, and immune-competent cells, particularly lymphocytes and macrophages. Secondary bacterial peritonitis is usually polymicrobial with synergistic growth of aerobic and anaerobic organisms, often arising from bowel flora. Primary peritonitis is often 'monomicrobial' (e.g. streptococcus, pneumococ-cus). When inflamed, the peritoneum loses its glistening appearance and becomes erythematous with production of copious serous inflammatory exudate, rich in white blood cells, protein and inflammatory mediators. The greater omentum often becomes adherent to inflamed organ, providing a barrier to spread of infection.

I: As indicated by history and clinical assessment.

Blood: FBC, U&Es, LFT, amylase, CRP, clotting, G&S or crossmatch, blood cultures, pregnancy test, ABG (looking for acidosis or respiratory failure). Imaging: Erect CXR (for pneumoperitoneum), AXR (e.g. in bowel obstruction), USS or CT abdomen. Laparoscopy.

Peritonitis continued 159

If ascites: Ascitic tap and cell count (diagnostic of SBP if > 250 neutrophils/ mm3), Gram stain and culture.

Localised: Treatment will depend on underlying cause (e.g. appendicectomy in appendicitis), whereas other conditions may be treated with IV antibiotics (e.g. cholecystitis, salpingitis and most cases of acute diverticulitis). Generalised: Patient is at risk of death from sepsis and shock. Needs IV fluid resuscitation and correction of volume and electrolyte imbalance (there is often severe hypovolaemia seconday to third space losses; hence fluid replacement is vital), IV antibiotics. Urinary catheter, NG tube and CVP line to monitor fluid balance. Urgent laparotomy should be performed to remove the infected or necrotic tissue, treat the cause and perform peritoneal washing with copious irrigation to remove all seropurulent exudate. An exception would be acute non-necrotising pancreatitis. Primary peritonitis is treated with antibiotics, but this diagnosis is often not apparent until after attempted operative intervention.

Spontaneous bacterial peritonitis: Medical treatment with quinolone antibiotic or cefuroxime and metronidazole combination.

Early: Septic shock, respiratory or multiorgan failure, paralytic ileus, wound infection, tertiary peritonitis (persistence of intra-abdominal infection), abscesses, portal pyaemia/hepatic abscesses. Late: Incisional hernia, adhesions.

With appropriate treatment of the underlying cause, localised peritonitis usually resolves. Generalised peritonitis has a much higher mortality, approaching 30-50%. The concurrent development of septic shock or multiorgan dysfunction can " the mortality rate to > 70%. Primary peritonitis has a good prognosis with appropriate antibiotic therapy. The overall mortality rate of patients with SBP may exceed 30% if diagnosis and treatment are delayed.

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