Chapter 2 Acute cholecystitis

Acute cholecystitis is nonspecific inflammation of gallbladder. By frequency this disease takes second place after acute appendicitis and makes about 10% in relation to all acute surgical diseases of abdominal cavity organs.

Acute cholecystitis occurs most commonly because of an obstruction of the cystic duct from cholelithiasis. Ninety percent of cases involve stones in the cystic duct (i.e., calculous cholecystitis), with the other 10% representing acalculous cholecystitis.

Acalculous acute cholecystitis is associated with biliary stasis, including debilitation, major surgery, severe trauma, sepsis, long-term total parenteral nutrition and prolonged fasting. Other causes of acalculous cholecystitis include cardiovascular attacks; sickle cell disease; Salmonella infections; diabetes mellitus; and cytomegalovirus, cryptosporidiosis or microsporidiosis infections in patients with AIDS.

Although bile cultures are positive for bacteria in 50–75% of cases, bacterial proliferation may be a result of cholecystitis and not the precipitating factor.

Risk factors for cholecystitis include increasing  age, female sex, certain ethnic groups, obesity or rapid weight loss, drugs and pregnancy.

As a result inflammatory process develops from simple  (catarrhal or superficial) cholecystitis till destructive cholecystitis (phlegmonous, gangrenous) and complicated cholecystitis.

Classification. Acute cholecystitis is divided into:

I. Acute calculous cholecystitis.

II. Acute non-calculous cholecystitis:

1. Catarrhal.

2. Phlegmonous.

3. Gangrenous.

4. Complicated:

a) hydropsy;

b) empyema;

c) biliary pancreatitis;

d) choledocholithiasis;

e) hepatitis;

f) cholangitis;

g) mass;

h) abscess;

i) hepatorenal insufficiency;

j) peritonitis (local, general).

Clinical diagnostic of acute cholecystitis

Most patients with acute cholecystitis describe a history of biliary pain. Some patients may have documented gallstones.

The disease, as a rule, begins after violation of diet: intake of much of fatty foods.

Pain syndrome. Frequently, the pain begins in the epigastric region and then localizes to the right upper quadrant.

Although the pain may initially be described as colicky, it becomes constant in virtually all cases. The pain may radiate to the right shoulder or scapula.

Dyspepsia syndrome. Frequent symptoms which disturb a patient are nausea, vomiting, at first by gastric content, and later – with a part of bile. Afterwards feelings of swelling of stomach, delay of emptying and gases often join to them.

Examination. During examination almost in all patients subicterus of sclera even at the normal passage of bile can be observed. Patients complain of dryness in mouth. In difficult cases the tongue is usually dry, assessed by white stratification with a yellow spot in the center.

The temperature of body of most patients rises (37.2 С in patients with catarrhal cholecystitis, 38.0–39.0  С at its destructive forms and cholangitis).

At first hours of disease the pulse rate usually is relevant to the temperature, and at progress of process, especially with development of peritonitis, it becomes frequent and weak.

During palpation painfulness in the place of crossing of right costal arc with the external edge of direct muscle of abdomen can be observed (the Kehrs point). By superficial and deep palpation of right hypochondrium, as a rule, painfulness and increased gallbladder are exposed.

Murphy’s sign – a delay of breathing during palpation of gallbladder on inhalation because of pain increasing.

Kehr’s sign – strengthening of pain at pressure on the region of gallbladder.

Ortner’s sign – painfulness at the easy pattering on right costal arc by the edge of palm.

Mussy’s sign – increasing  of pain after palpation between the legs of right nodding muscle.

Blumberg’s sign may be positive in patients with peritonitis. In elderly patients, pain and fever may be absent, and localized tenderness may be the only present sign.

Patients with acalculous cholecystitis may present similarly to patients with calculous cholecystitis, but acalculous cholecystitis frequently occurs suddenly in severely ill patients without a prior history of biliary colic.

Special examinations

Laboratory studies

Patients with uncomplicated cholelithiasis or simple biliary colic typically have normal laboratory test results.

Acute cholecystitis is associated with polymorphonuclear leukocytosis.

Choledocholithiasis with acute common bile duct obstruction initially produces an acute increase in the level of liver transaminases (alanine and aspartate aminotransferases), followed within hours by a rising serum bilirubin level. If obstruction persists, a progressive decline in the level of transaminases with rising alkaline phosphatase and bilirubin levels may be noted over several days. Concurrent obstruction of the pancreatic duct by a stone in the Vater’s ampulla may be accompanied by increases in circulating lipase and amylase levels.

Repeated testing over hours to days may be useful in evaluating patients with gallstone complications. Improvement of the levels of bilirubin and liver enzymes may indicate spontaneous passage of an obstructing stone. Conversely, rising levels of bilirubin and transaminases with progression of leukocytosis in the face of antibiotic therapy may indicate ascending cholangitis.

Investigations in acute cholecystitis

Ultrasonography. Ultrasonographic findings that are suggestive of acute cholecystitis include the following: pericholecystic fluid, gallbladder wall thickening greater than 4 mm and sonographic Murphy’s sign. The presence of gallstones also helps to confirm the diagnosis (fig. 7, 8).

The sensitivity and specificity of CT/MRT scans for predicting acute cholecystitis have been reported to be greater than 95%. Spiral CT scans and MRI have the advantage of being noninvasive, but they have no therapeutic potential and are most appropriate in cases where stones are unlikely.


Findings suggestive of cholecystitis include wall thickening (>4 mm), pericholecystic fluid, subserosal oedema, intramural gas, and sloughed mucosa (fig. 9).

Endoscopic retrograde cholangiopancreatography may be useful in patients at high risk for common duct gallstones, if signs of common bile duct obstruction are present (fig. 10).

Endoscopic retrograde cholangiopancreatography allows visualization of the anatomy and may be therapeutic by removing stones from the common bile duct. Disadvantages include the need for a skilled operator, high cost, and complications such as pancreatitis, which occurs in 3–5% of cases.

Differential diagnosis of acute cholecystitis

Perforated peptic ulcer. For this disease the Mondor’s triad (“knife-like” pain, tension of muscles of front abdominal wall and ulcerous anamnesis) and positive Spizharny’s sign are characteristic (disappearance of hepatic dullness). On the abdominal X-ray gram under the right copula of diaphragm free gaze can be found.

Right-side kidney colic. Pain at right-side kidney colic also can be localized in right hypochondrium. However, it is always accompanied by disorders of urination. Kidney pain often irradiates downward along passing of ureter. For this pathology micro- or macrohaematuria, presence of renal concrements exposed at sonography and on the urograms. Absence of renal function during chromocystoscopy can be characteristic.

Acute appendicitis. It is needed always to remember, that the subhepatic location of the pathologically changed appendix is also able to show up pain in right hypochondrium. However, for patients with acute appendicitis beginning of pain in epigastric region, absence of hepatic anamnesis, expressed dyspeptic phenomena, inflammatory changes from the side of gallbladder at sonography are inherent.

Heart attack, myocardial infarction. The so called cholecystocardial syndrome which often imitates stenocardia pain, suspicion of heart attack or myocardial infarction can develop. Electrocardiography examination is decisive in establishment of diagnosis. However, laparoscopy is applied in doubtful cases.

Acute pancreatitis. Acute pancreatitis is accompanied by the expressed upper abdominal pain. During palpation in left costovertebral corner patients feel painfulness (Mayo-Robson’s sign).

Treatment of acute cholecystitis

For acute cholecystitis, initial treatment is conservative:

local abdominal hypothermia;

bowel rest;

intravenous hydration;

analgesia with NSAID;

spasmolytical therapy;

intravenous antibiotics.

Although not initially an infective process, broad-spectrum antibiotics are used and should be guided by local microbiological policy to target the most common organisms found in the biliary tract. These include Escherichia coli, klebsiella, enterobacter and enterococcus species. Anaerobes are less significant but include clostridium and bacteroides species.

Following successful conservative treatment most patients are discharged from hospital for future elective laparoscopic cholecystectomy. If acute cholecystitis resolves, laparoscopic cholecystectomy may be carried out 4–6 weeks later. Delayed surgery carries the risk of recurrent biliary complications.

For frail and elderly patients who have only a signle attack, or mild recurrent episodes, conservative management may be the mainstay of treatment.

Indications for urgent operation are:


inefficacy of conservative treatment during 24–48 hours (retention of abdominal pain and muscles resistance, increasing of body temperature and polymorphonuclear leukocytosis, signs of peritonitis, jaundice).

In cases of severe inflammation, shock, or if the patient has higher risk for general anaesthesia (required for cholecystectomy), the managing physician may elect to have an interventional radiologist insert a percutaneous drainage catheter into the gallbladder (“percutaneous cholecystostomy tube”) and treat the patient with antibiotics until the acute inflammation resolves. The patient may later warrant cholecystectomy if their condition improves.

Gallbladder removal, cholecystectomy, can be accomplished via open surgery or a laparoscopic procedure. Laparoscopic procedures can have less morbidity and a shorter recovery stay. Open procedures are usually carried out if complications have developed or the patient has had prior surgery to the region, making laparoscopic surgery technically difficult. A laparoscopic procedure may also be “converted” to an open procedure during the operation if the surgeon feels that further attempts at laparoscopic removal might harm the patient. Open procedure may also be carried out if the surgeon does not know how to perform a laparoscopic cholecystectomy. Preparation of patients undergoing cholecystectomy is similar for both urgent open and laparoscopic procedures.

Surgical incisions for open cholecystectomy are: line oblique incision in right subcostal region (is rarely performed because of the tendency for herniation); upper middle line laparotomy. Laparoscopic cholecystectomy is performed using 4 considerably smaller incisions (fig. 11).

The phases of operation are: visual inspection of abdominal cavity and operative confirmation of diagnosis; puncture of gallbladder if it is distending; dissection and visualization of Kalo’s trigonum structures; cutting of cystic duct and artery with ligation or clipping (fig. 12); removing of gallbladder (fig. 13); control of bleeding and bile leak; sanation and drainage of abdominal cavity.

Complications of cholecystectomy:

bile leak (“biloma”);

bile duct injury (about 5–7 out of 1000 operations. Open and laparoscopic surgeries have essentially equal rate of injuries, but the recent trend is towards fewer injuries with laparoscopy. It may be that the open cases often result because the gallbladder is too difficult or risky to remove with laparoscopy);


wound infection;

bleeding (liver surface and cystic artery are most common sites);


organ injury (intestine and liver are at highest risk, especially if the gallbladder has become adherent/scarred to other organs due to inflammation (e.g. transverse colon);

deep vein thrombosis, pulmonary embolism (risk can be decreased through use of sequential compression devices on legs during surgery);

fatty acid and fat-soluble vitamin malabsorption.

Postoperative treatment

Administer intravenous antibiotics postoperatively. The length of administration is based on the operative findings and the recovery of the patient.

Antiemetics and analgesics are administered to patients experiencing nausea and wound pain.

A liquid diet may be started when bowel function returns.

Follow-up care

After hospital discharge, patients must have a light diet and limit their physical activity for a period of 4 weeks – 3 months based on the surgical approach (i.e., laparoscopic or open cholecystectomy). The patient should be evaluated by the surgeon in the clinic to determine improvement and to detect any possible complications.

Following cholecystectomy, about 5–10% of patients develop chronic diarrhoea. This is usually attributed to bile salts. The frequency of enterohepatic circulation of bile salts increases after the gallbladder is removed, resulting in more bile salt reaching the colon. In the colon, bile salts stimulate mucosal secretion of salt and water.

Postcholecystectomy diarrhoea usually is mild and can be managed with occasional use of over-the-counter antidiarrhoeal agents. More frequent diarrhoea can be treated with daily administration of a bile acid binding resin.

Following cholecystectomy, a few individuals experience recurrent pain resembling biliary colic. The term “postcholecystectomy syndrome” is sometimes used for this condition.

Many patients with postcholecystectomy syndrome have long-term functional pain that was originally misdiagnosed as being of biliary origin. Diagnostic and therapeutic efforts should be directed at the true cause.

Some individuals with postcholecystectomy syndrome have an underlying motility disorder of Oddi’s sphincter, termed biliary dyskinesia, in which the sphincter fails to relax normally following ingestion of a meal. The diagnosis can be established in specialized centers by endoscopic retrograde cholangiopancreatography.


For uncomplicated cholecystitis, the prognosis is excellent, with a very low mortality rate. In patients who are critically ill with cholecystitis, the mortality rate approaches 50–60%, especially in the setting of peritonitis.