Tuesday, March 25, 2008

Acute cholecystitis

Acute cholecystitis
The inflammation of the gall bladder is most often caused by gall stones. Gall stones are one of the most common disorders of the gastrointestinal tract, affecting about 10% of people in Western society.
  • Occurs in 10 – 20% of symptomatic gallstones cases.
  • 7 to 15% have concomitant CBD stones.
  • Less than 1% have malignant tumor.
  • 60% are infected.
  • Diabetics are more labile for septic complications.
  • Anaerobic (clostridial) infection is more common in diabetics.
  • Repeated attacks results in chronic cholescystitis.


  • Fat, fertile,forty years female is the commonest in presentation.
  • Pain in URQ is like biliary colic but last longer(> than 6 hours) even for days which is associated with URQ tenderness.
  • Nausea, vomiting, anorexia,
  • Mild fever, seldom higher than 38°C.
  • Chills are unusual, and their presence suggests a complicated cholecystitis (abscess or associated cholangitis).
  • Mild jaundice is present in approximately 20% patients with AC, which may be related to common hepatic and/or bile duct edema and higher concentrations of bilirubin >60 µmol/l suggest a diagnosis of choledocholithiasis (a gall stone in the common bile duct) or Mirrizzi's syndrome (obstruction by a stone impacted in Hartmann's pouch that compresses the common hepatic duct).
  • Positive Murphy’s sign - inspiratory arrest on deep palpation in RUQ. The Murphy sign can be elicited with an ultrasound probe.
  • A palpable right upper quadrant mass – 1/3 of cases-
  • Usually represents omentum adhered in response to the inflammation.
  • Leucocytosis is pronounced with empyema and is usually in the range of 10,000-15,000/μL.
  • Mild rise (up to 5 fold)of AST , ALT & serum amylase.

Inflammation of gallbladder
Over 90% of cases of acute cholecystitis result from obstruction of the cystic duct by gall stones or by biliary sludge that has become impacted at the neck of the gall bladder.

  • Mechanical inflammation-
  • The sequence is - Obstruction-distension-increase in pressure- ischemia-injury-inflammation
  • Biochemical inflammation
  • Lysolecithin, Prostaglandin I2 and E2,
  • The trauma caused by the gall stones stimulates the synthesis of prostaglandins I2 and E2, which mediate the inflammatory response.
  • Infection –
    • Escherichia coli (41 percent), Enterococcus (12 percent), Klebsiella (11 percent), and Enterobacter (9 percent).
    • Positive bile culture is present in 50 to 80% of the patients with acute cholecystitis.

Acute Acalculous Cholecystitis

  • Acute acalculous cholecystitis accounts for 5% to 10% of all patients with acute cholecystitis.
  • The disease often has a more fulminant course than acute calculous cholecystitis and frequently progresses to gangrene, empyema, or perforation.
  • Acute acalculous cholecystitis usually occurs in the critically ill patient following trauma, burns, long-term parenteral nutrition, and major nonbiliary operations such as abdominal aneurysm repair and cardiopulmonary bypass.
  • The etiology of acute acalculous cholecystitis remains unclear although gallbladder stasis and ischemia have been most often implicated as causative factors.
  • Stasis is common in critically ill patients not being fed enterally and may lead to colonization of the gallbladder with bacteria.
  • Visceral ischemia is also a common denominator in patients with acute acalculous cholecystitis and may explain the high incidence of gallbladder gangrene.
  • Decreased arteriolar and capillary filling is present in acute acalculous cholecystitis in contrast to the dilation of these vessels observed in acute calculous cholecystitis.

Differential diagnosis

  • Pyogenic or amebic liver abscesses
  • Perforation or penetration of peptic ulcer
  • Pancreatitis
  • Appendicitis
  • Hepatitis
  • Myocardial ischemia or infarction
  • Pneumonia
  • Pleurisy
  • Herpes zoster involving an intercostal nerve
  • Gonococcal perihepatitis (Fitz-Hugh-Curtis syndrome) in women
  • Sickle cell crises, and
  • Leptospirosis


Abdominal Ultrasound

  • Gall stones along with wall (edema)thickness > 4mm
  • Pericholecystic fluid

Radionuclide scanning – HIDA – less frequently used

CT abdomen – if acutely ill and associated with complications – e.g. CBD stones and pancreatic pathology.

Medical management

  • Most patients with acute cholecystitis respond to conservative, first line management: the gall stone disimpacts and falls back into the gall bladder, which allows the cystic duct to empty.
  • If the gall stone does not disimpact, complications such as advanced cholecystitis (gangrenous cholecysytitis or empyema of the gall bladder) or perforation may result.
  • Immediate measures should be taken to rest the gall bladder; this will subdue the inflammatory process in most patients.
  • Patients should be fasted, rehydrated with intravenous fluids, and given oxygen therapy and adequate analgesia.
  • A single intramuscular dose of diclofenac (75 mg) may substantially decrease the rate of progression to acute cholecystitis in patients with symptomatic gall stones.
  • Because of the risk of superimposed infection, intravenous antibiotics should be started empirically if the patient has systemic signs or if no improvement is seen after 12-24 hours.
  • A second generation or newer cephalosporin should be used (for example, cefuroxime 1.5 g every 6-8 hours) with metronidazole (500 mg every 8 hours).
  • Acute inflammation subsides in 5 – 7 days with conservative treatment

    Non-operative management solvent dissolution therapy or extracorporeal shockwave lithotripsy has been used with variable results to treat chronic cholecystitis in patients unfit for surgery, but it has no place in the management of acute cholecystitis.

Surgical treatment

  • The treatment of choice for acute cholecystitis is cholecystectomy.
  • Open cholecystectomy had been the standard treatment for acute cholecystitis for many years.
  • Initially, acute cholecystitis was felt to be a contraindication to laparoscopic cholecystectomy.
  • As experience has increased, however, it has become clear that laparoscopic cholecystectomy can be performed safely in the setting of acute cholecystitis.
  • In prospective, randomized trials, the morbidity rate, length of hospital stay, and time to return to work have all been lower in patients undergoing laparoscopic cholecystectomy than open cholecystectomy.
  • However, the conversion rate in the setting of acute cholecystitis (10% to 35%) is higher than with chronic cholecystitis.

The timing of cholecystectomy for acute cholecystitis has been studied for several decades.

  • In the distant past, delayed cholecystectomy was preferred in the setting of acute cholecystitis.
  • Patients were initially managed nonoperatively and discharged home after their symptoms resolved.
  • Elective cholecystectomy was then performed 6 weeks later after the acute inflammation had resolved.
  • Recent prospective randomized trials have shown that early laparoscopic cholecystectomy (within 3 days of symptom onset) can be accomplished with a similar morbidity and mortality rate as delayed cholecystectomy.
  • No significant differences were observed in the conversion rate to open cholecystectomy among patients undergoing early cholecystectomy versus those managed with delayed surgery.
  • Hospital stay, and therefore cost, however, were significantly reduced in both trials in the early laparoscopic cholecystectomy group.
  • In addition, approximately 20% of patients in the delayed surgery arm failed initial medical therapy and required operation during the initial admission or before the end of the planned cooling-off period.
  • Laparoscopic cholecystectomy should be performed within 24 to 72 hours of diagnosis.
  • Early conversion to an open procedure should be considered if dissection is difficult or clear progress cannot be made by the laparoscopic technique.
  • In certain high-risk patients whose medical conditions precludes cholecystectomy, a cholecystostomy can be performed for acute cholecystitis.
  • Although previously performed operatively and under local anesthesia, percutaneous drainage techniques can usually be accomplished (Fig. 62.12).
  • In most cases, prompt improvement is seen after gallbladder drainage and appropriate antibiotics.
  • These patients must be observed closely, however, and if improvement does not occur within 24 hours, laparotomy is indicated.
  • Failure to improve after percutaneous cholecystostomy is usually caused by gangrene of the gallbladder or perforation.
  • After the acute episode resolves, the patient can undergo either cholecystectomy or percutaneous stone extraction and removal of the cholecystostomy tube.
  • The latter is an option in elderly or debilitated patients for whom a general anesthetic is contraindicated.

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