Peritonitis

Function of the peritoneum Pain perception (parietal peritoneum) Visceral lubrication Fluid and particulate absorption Inflammatory and immune response Fibrinolytic activity

Peritonitis is defined as inflammation of the peritoneal cavity. The peritoneal cavity includes an extensive serous membrane that covers the entire abdominal wall and is reflected over the contained viscera, the greater and lesser omentum, and the transverse mesocolon.

In early peritoneal inflammation, the condition is often localised because of containment of the affected area by surrounding structures e.g. omentum, adjacent bowel and fibrinous adhesions. However, this may not be sufficient to contain the inflammation and a condition that initially presented with localised peritonitis may eventually develop into generalised peritonitis. Precipitating factors include abrupt contamination, as occurs with penetrating wounds, continuing contamination from a large bowel defect, the bursting of a localised abscess, or the secondary infection of ascitic fluid.

Peritoneal infections are classified as: Primary (ie, spontaneous), Secondary (ie, related to a pathologic process in a visceral organ), or Tertiary (ie, persistent or recurrent infection after adequate initial therapy). The intra-abdominal infections are usually divided into Generalized (peritonitis) and Localized (intra-abdominal abscess). Primary (Spontaneous) peritonitis The symptoms of spontaneous peritonitis are often less dramatic than secondary peritonitis. Spontaneous peritonitis can occur in patients with severe liver disease, heart disease or kidney disease. Often these diseases cause the accumulation of fluid within the abdominal cavity. This is called ascites. The presence of ascites, together with the persons weakened defences against infection, often leads to bacterial infection. The most common etiology of primary peritonitis is spontaneous bacterial peritonitis (SBP) due to chronic liver disease. Approximately 10-30% of all patients with liver cirrhosis who have ascites develop bacterial peritonitis over time. SBP occurs in the absence of an apparent intra-abdominal source of infection and is observed almost exclusively in patients with ascites formation from chronic liver disease. Contamination of the peritoneal cavity is thought to result from translocation of bacteria across the gut wall or mesenteric lymphatics and, less frequently, via hematogenous seeding in the presence of bacteremia. More than 90% of cases of SBP are caused by a monomicrobial infection. The most common pathogens include gram-negative organisms (e.g., Escherichia coli [40%], Klebsiella pneumoniae [7%], Pseudomonas species, Proteus species, other gram-negative species [20%]) and gram-positive organisms (e.g., Streptococcus pneumoniae [15%], other Streptococcus species [15%], Staphylococcus species [3%]). Anaerobic microorganisms are found in less than 5% of cases, and multiple isolates are found in less than 10%. Secondary peritonitis The main cause of secondary peritonitis is the escape of pus from an infected abdominal organ, including:

Causative organisms: Pyogenic bacteria, E.coli, aerobic and anaerobic streptococci, Bacteroides, Pneumococci, Staphylococci Sources of infection: Local spread: 1- infected organs: appendicitis, cholecystitis, diverticulitis. 2- Leaking organs: perforated peptic ulcer, perforated typhoid ulcer, leaking anastomosis, ruptured gut, extravasated urine Direct entry (operative or traumatic) Blood spread (bacteremia, septicemia) Tertiary peritonitis Tertiary peritonitis represents the persistence or recurrence of peritoneal infection following apparently adequate therapy of SBP or SP, often without the original visceral organ pathology. Patients with tertiary peritonitis usually present with an abscess, or phlegmon, with or without fistulization. Tertiary peritonitis develops more frequently in patients with significant preexisting comorbid conditions and in patients who are immunocompromised. Although rarely observed in uncomplicated peritoneal infections, the incidence of tertiary peritonitis in patients requiring ICU admission for severe abdominal infections may be as high as 50-74%. Patients who develop tertiary peritonitis demonstrate significantly longer lengths of stay in the ICU and hospital, higher organ dysfunction scores, and higher mortality rates (50-70%). Resistant and unusual organisms (eg, Enterococcus, Candida, Staphylococcus, Enterobacter, and Pseudomonas species) are found in a significant proportion of cases of tertiary peritonitis. Most patients with tertiary peritonitis develop complex abscesses or poorly localized peritoneal infections that are not amenable to percutaneous drainage. Antibiotic therapy appears less effective compared to all other forms of peritonitis.

Peritonitis may be also classified as local and generalised causes. Note that some of the causes of local peritonitis may eventually cause generalised peritonitis. Localised peritonitis can be caused by:

transmural bowel inflammation, e.g. appendicitis, diverticulitis, Crohn's disease transmural inflammation of other viscera, e.g. salpingitis, cholecystitis transmural ischaemia, e.g. ischaemic bowel obstruction - strangulating hernia

Generalised peritonitis can be caused by the following:

any cause of localised peritonitis if left for long enough perforation of a viscus causing generalised peritoneal irritation, e.g. stomach, colon, gall bladder, enzymatic discharge in acute pancreatitis chemical peritonitis may be caused by any foreign substance introduced into the peritoneum, for example talcum powder from operating gloves spreading intraperitoneal infection, e.g. faecal contamination following bowel perforation, rupture of an intra-abdominal abscess, anastomotic leak, trauma, surgery

The clinical features of localised peritonitis are:

a primary intra-abdominal process, e.g. appendicitis localised abdominal pain - made worse by movement of the abdomen e.g. coughing. on examination there are signs of localised peritonism: o localised tenderness

contraction of the abdominal muscles over the area of tenderness when palpation is attempted - guarding o rebound tenderness - when the examining hand is quickly examined the movement of the peritoneum causes intense pain. This sign may be better elicited by percussion or asking the patient to cough. rectal tenderness - anterior tenderness may be elicited features of mild systemic toxicity, e.g. malaise, low-grade fever, tachycardia, leucocytosis on FBC.

The clinical features of generalised peritonitis include:

patient is systemically very ill - fever, tachycardia, prostration postural hypotension - there may be a massive exudation of inflammatory fluid into the peritoneal cavity causing hypovolaemia severity of symptoms depends on cause of the peritonitis: o if there is infection, i.e. faeces, pus, infected bile, then the initial presentation may not be severe initially; eventually, with spread the peritonitis becomes very severe o with chemical peritonitis, e.g. perforated peptic ulcer, then the initial presentation may be very severe but becomes less so with inflammatory dilution on examination: o rigidity of the abdominal wall o diffuse abdominal tenderness o bowel sounds may be absent because of peristaltic paralysis o if there is severe peritonitis, e.g. faecal, there may be signs of gram-negative bacteraemic shock, i.e. hypotensive, cold patient o rectal tenderness radiographically: o may be air under the diaphragm if perforated viscus o the majority of patients will show signs of intestinal ileus

Investigation in peritonitis raised white cell count is usual serum amylase > 4x normal indicates acute pancreatitis abdominal radiographs occasionally helpful erect chest radiographs may show free peritoneal gas (perforated viscus) ulstrasound / CT scanning increasingly used peritoneal fluid aspiration (with or without ultrasound guidance) may be helpful

Treatment for peritonitis Treatment options for peritonitis depend on the cause, but may include: Hospitalisation often in an intensive care unit Antibiotics tailored to the specific bacteria to kill the infection

 Intravenous fluids to rehydrate the body and replace lost electrolytes Surgery to repair the ruptured organ and wash out the abdominal cavity of blood and pus Treatment for the underlying cause such as a perforated ulcer. The management of peritonitis is dependent on location and aetiology:

localised peritonitis: management dependent on cause, e.g. acute appendicitis necessitates urgent appendicetomy, acute diverticulitis or acute salpingitis are usually managed with antibiotics generalised peritonitis: management consists of preoperative, operative and postoperative steps

Preoperative treatment in the patient with generalised peritonitis is as important as surgery:

correct fluid balance due to lost extracellular fluid: o give a rapid IV infusion of Hartmann's solution, 2.5-3.0 litres over 3 hours in a 70kg adult o monitor central venous pressure in elderly patients to ensure that infusion is not given too quickly o insert a urinary catheter to monitor urinary output o give additional colloid if there is evidence of hypovolaemia remove blood for culture, then give parenteral antibacterial treatment, e.g. metronidazole for anaerobes and cephalexin for aerobes give analgesic, preferably IV slowly, after consulting with the anaesthetist

give oxygen via a face mask as diaphragmatic movements are likely to be reduced before inducing anaesthesia, pass a 16F nasogastric tube to keep the stomach empty

There are several contentious issues in the operative management of generalised peritonitis:

incision: a long midline incision provides ample access to most perforation sites and allows ready toilet. source of contamination: o appendicectomy for acute appendicitis o cholecystectomy for perforation of acute cholecystitis o oversew peptic ulcers o in perforated diverticular disease and faecal ulceration, one approach is colonic resection, e.g. Hartmann's resection, +/- raising of a stoma, e.g. Paul-Mickulicz double-ended colostomy; when a single perforated diverticulum is found, trimming, suturing and drainage may be adequate steps o in perforation secondary to fulminant colitis, the whole colon is usually severely ulcerated and a total colectomy with ileostomy is indicated peritoneal lavage nasogastric intubation is continued until the return of intestinal function closure of the wound with non-absorbable sutures

There are several practices that are of value to the surgical patient in the postoperative period:

nasogastric suction evacuates swallowed air which potentiates postoperative ileus intravenous fluids antibiotic treatment; this is discontinued with resolution of peritonitis treat postoperative shock; this complication is unlikely if earlier measures have been successfully carried through, although it is prudent to monitor and correct the fluid balance and operative blood losses o in the elderly, monitor blood gases to guard against metabolic acidosis and hypoxia o carefully used, dopamine can increase cardiac output and renal blood flow sedation respiratory complications: o promote the cough reflex by injecting bupivacaine into the wound for 48-72 hours in those with existing respiratory disease o be wary of ARDS, liase with the anaesthetist if there was major sepsis and respiratory signs are worsening watch for paralytic ileus and consider metabolic abnormalities, residual intraperitoneal abscess or mechanical adhesive obstruction residual abscesses are common and may need drainage

Complication of peritonitis systemic abdominal

Systemic complications of peritonitis bacteraemic/ endotoxic shock bronchopneumonia/ respiratory failure renal failure bone marrow suppression multisystem failure

Abdominal complications of peritonitis adhesional small bowel obstruction paralytic ileus residual or recurrent abscess portal pyaemia/ liver abscess

Clinical features of an abodominal / pelvic abscess: malaise sweat with or without rigors abdominal/pelvic (with or without shoulder tip ) pain anorexia and weight loss symptoms from local irritation, e.g hiccoughs (subphrenic), diarrhea and mucus (pelvic) swinging pyrexia localized abdominal tenderness

Subphrenic abscess

Other types of peritonitis Chemical (sterile) peritonitis Chemical (sterile) peritonitis may be caused by irritant substances such as bile, blood, barium, and other substances or by transmural inflammatory processes of visceral organs (eg, Crohns disease) without bacterial inoculation of the peritoneal cavity. Clinical signs and symptoms are indistinguishable from those of SP or peritoneal abscess, and the diagnostic and therapeutic approach should be the same. Bile peritonitis perforated cholecystitis post cholecystectomy (cystic duct stump leakage, divison of accessory duct in gall bladder bed, bile duct injury) following other operation and procedures leaking duodenal stump post gastrectomy leaking biliary enteric anastamosis leaking around percutaneous placed biliary drains

Tuberculous peritonitis acute and chronic forms abdominal pain, sweats, malaise and weight loss are frequent caseating peritoneal nodules are common-distinguish from metastatic carcinoma and fat necrosis of pancreatitis ascites common intestinal obstruction may respond to anti-tuberculous treatment without surgery