Section 1: Epidemiology and aetiology
Acute cholecystitis (inflammation of the gallbladder) is one of the most common complications of gallstones, although it does rarely occur in the absence of gallstones (acalculous cholecystitis).
Gallstones consist of cholesterol (15 per cent), pigment (5 per cent), or a mixture of the two (80 per cent). The majority of mixed stones contain over 50 per cent cholesterol.
Factors linked to cholesterol stones include female sex and increasing age. Cholesterol stones form when the solubilising capacity of bile is exceeded. Supersaturated cholesterol leads to the formation of cholesterol microcrystals.
Acute acalculous cholecystitis
Acute acalculous cholecystitis may occur as a complication of severe burns or trauma.
The aetiology may be due to blood-borne infection, undetectable biliary sludge or an inflammatory response by the gall- bladder to concentrated bile salts.
If a gallstone remains in the gallbladder it does not cause symptoms - only 10-30 per cent of patients with gallstones will become symptomatic.
However, if the stone impacts in the gallbladder neck or cystic duct, it will result in pain as the gallbladder contracts behind the blockage. If the stone falls back, the gallbladder empties and the pain subsides (biliary colic).
If the stone remains impacted then trapped bile leads to elevated gallbladder pressure, resulting in reduced gallbladder mucosa blood flow.
This results in mucosal damage by bile with a consequential chemical irritation, inflammatory infiltration and oedema of the gallbladder wall.
Possible outcomes are summarised in the box.
|OUTCOMES FOLLOWING ACUTE CHOLECYSTITIS|
|Resolution||Stone spontaneously drops back into gallbladder, bile|
drains through cystic duct and sepsis settles
|RUQ pain, tenderness and signs of sepsis resolve.||Resolution Conservative management augments this process|
|Impacted stone isolates the gallbladder from the|
biliary tree without secondary infection. Gallbladder
mucosa continues to absorb water and bile pigment
while secreting mucus. A distended gallbladder forms
containing clear or bile-stained mucus
Previous episode of severe biliary pain consistent with cholecystitis. Symptoms may have resolved but ongoing RUQ ache/tenderness. RUQ mass may be present. No signs of sepsis.
|Empyema||As with a mucocele + superimposed infection.|
Bacterial proliferation leads to purulent contents
resulting in an abscess. The gallbladder may be
encased in inflammatory mass
|Rarely responds to conservative measures.|
|Emphysematous cholecystitis||Serious and rare progression of empyema. Gas in the gallbladder wall formed by Clostridium perfringens, Escherichia coli and anaerobic streptococci. Gallstones not always present||Resuscitation + broad-spectrum antibiotics|
|Serious sequelae of gallbladder wall inflammation. An|
inflammatory mass may adhere to the gallbladder, containing the perforation as a pericholecystic abscess
Section 2: Diagnosis
When a patient first presents with the principal symptom of acute cholecystitis it may be difficult to differentiate biliary colic from acute cholecystitis. However, the differentiation is important as treatment of the two conditions differs greatly.
Biliary colic occurs when a gallstone impacts in the neck of the gallbladder obstructing the cystic duct.
The pain resolves spontaneously as the stone falls back into the gallbladder or passes into the common bile duct (CBD). The elevated pressure within the gallbladder due to the temporary blockage leads to sustained gallbladder contraction.
The typical presentation is of sharp, sudden onset right upper quadrant (RUQ) or epigastric pain, radiating under ribs, to the right lower chest, directly through to back or to the lower tip of scapula. Despite its name it is not typically colicky in nature.
It usually lasts 30 minutes to two hours, and not more than about six hours. It can be precipitated by ingestion of a large or fatty meal. Nausea and vomiting may be present.
If a stone remains impacted in the neck of the gallbladder or cystic duct this results in acute cholecystitis. This may be preceded by attacks of biliary colic.
However, in cholecystitis the pain lasts for more than 12 hours and is worse on movement and inspiration.
In addition, inflammation leads to gallbladder tenderness and spreading inflammation to the diaphragm leads to referred pain over the acromion.
On examination the patient may look septic with systemic signs of infection (pyrexia and tachycardia) and local RUQ peritonism. Murphy's sign is usually positive. An oedematous gallbladder surrounded by omentum may be palpable as a tender mass in the RUQ.
Occasionally an inflamed and oedematous gallbladder will compress the common bile duct leading to obstructive jaundice (Mirizzi's syndrome).
Depending on the chronicity of the presentation the patient may have signs consistent with complications of acute cholecystitis.
An FBC and CRP determine the inflammatory component. LFTs are mandatory to identify any obstructive jaundice, with changes in enzyme levels being more reliable than plasma bilirubin alone.
Biliary scintigraphy and oral cholecystography are now almost obsolete in the era of ultrasonography, which is the gold standard test for detecting gallstones. If there is a strong clinical suspicion but an ultrasound is negative, a repeat scan will increase the sensitivity from >90 to >95 per cent.
In addition to the presence, number and size of gallstones, ultrasound can provide important supplementary information indicating cholecystitis, such as a thickened gallbladder wall (see figure, section 3) and presence of pericholecystic fluid.
Ultrasound can report the diameter of the CBD and the presence/absence of intrahepatic duct dilation. Stones within the CBD may be hidden behind a gas-filled duodenum reducing the sensitivity of ultrasound in this region.
Magnetic resonance cholangiopancreatography
MRCP provides exquisite images of the whole of the biliary tree and adjacent anatomy. Small stones can be detected, and 3D imaging of the biliary tree provides evaluation of an obstructed system (see figure, section 4).
CT may be used in the emergency setting, especially in elderly patients presenting with abdominal pain and peritonism. Although not as sensitive as ultrasound for visualising gallstones, it can be helpful in differentiating acute chole- cystitis.
Section 3: Management
Biliary colic is treated with analgesia and does not require emergency referral to hospital.
Mild cases of acute cholecystitis in young fit patients may be treated in primary care with appropriate antibiotics, with the proviso that such patients are reviewed regularly and referred immediately if there is any deterioration in their condition.
The initial treatment of acute cholecystitis is conservative, comprising bed-rest, gut-rest, analgesia with NSAIDs and opiates, anti-emetics, IV fluids and 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, or undergo early cholecystectomy during their emergency admission.
For frail and elderly patients who have only a single attack, or mild recurrent episodes, conservative management may be the mainstay of treatment.
The incidence of cholecystostomy has reduced with the increased use of emergency laparoscopic cholecystectomy.
Elderly patients are prone to infective complications of acute cholecystitis, such as intra-abdominal abscess and basal pneumonia. It may therefore be preferential to control the acute phase by percutaneous drainage of the gallbladder.
After resolution the causative gallstones can be dealt with by laparoscopic cholecystectomy, percutaneous stone extraction along the drain tract or may be left in situ.
The classical open cholecystectomy and the minimally invasive laparoscopic cholecystectomy are two operations for removal of the gallbladder. There are no significant differences in mortality and complications between the two techniques, although the laparoscopic operation has advantages regarding duration of hospital stay and convalescence, and so is the treatment of choice.
Early laparoscopic cholecystectomy
Common practice is to treat acute cholecystitis conservatively and then bring the patient back for elective cholecystectomy several weeks later.
The principal rationale of this policy is the fear of higher morbidity and conversion from laparoscopic cholecystectomy to open cholecystectomy during acute cholecystitis.
However, a Cochrane systematic review has demonstrated that there is no significant difference in the complication or conversion rate in regard to the time when the laparoscopic cholecystectomy is performed during acute cholecystitis.1 There is an almost 30 per cent re-admission rate with gallstone-related complications prior to the scheduled operation date in patients discharged for future surgery.
Open cholecystectomy is less frequently performed with the advent of the laparoscopic approach, and most commonly performed when the laparoscopic technique fails. This is usually due to adhesions, inflammation, bleeding, inability to define anatomy and suspected bile duct injury.
Non-operative treatment of gallstones
The non-operative treatment of gallstones using extracorporeal shock wave lithotripsy and bile salt therapy has become obsolete with the introduction of laparoscopic cholecystectomy.
Such methods required prolonged treatment, were only suitable for 30-40 per cent of patients with gallstones, and had a recurrence rate of 10 per cent at five years.
Section 4: Prognosis and follow-up
Complications following acute cholecystitis
The complications of acute cholecystitis should be considered in any patient seeking medical advice following an attack of either cholecystitis or biliary colic.
If a patient is on a waiting list for elective cholecystectomy following a hospital admission for acute cholecystitis, it must be remembered that there is an almost 30 per cent re-admission rate with gallstone-related complications.
Postcholecystectomy syndrome (PCS) refers to the presence of symptoms after cholecystectomy and occurs in 10-15 per cent of patients.2
It encompasses a collection of symptoms that are due to either a failure to recognise the correct cause of symptoms leading to cholecystectomy or new symptoms normally attributed to the gallbladder.
Removal of the gallbladder can lead to alterations in bile flow due to the loss of the reservoir function of the gallbladder.
The best way of avoiding PCS is to avoid cholecystectomy in patients without convincing symptoms. Although it is easy to attribute vague mild and non-specific abdominal pain to gallstones it must be remembered that approximately 90 per cent of gallstones are asymptomatic.
In one study, only 18 per cent of men with asymptomatic gallstones developed symptoms over 24 years of follow-up.3
It has been shown that 40 per cent of normal individuals experience upper abdominal dyspepsia, and that of the 25 per cent of these that visit their GP for these symptoms, there was no difference in these patients compared with those with gallstones.4
Therefore attributing vague symptoms to the presence of gallstones is tenuous, with little evidence that 'biliary dyspepsia' is associated with the presence of stones. There is no evidence to link gallstones with epigastric pain, belching or indigestion. Heartburn and reflux symptoms are not directly related to the presence of gallstones.
Chronic cholecystitis results from incompletely resolved acute cholecystitis resulting in a contracted and fibrosed gallbladder that may be susceptible to further attacks. Elective cholecystectomy should be considered if the patient is considered fit for surgery.
1. Gurusamy K S, Samraj K. Early versus delayed laparoscopic cholecystectomy for acute cholecystitis. Cochrane Database Syst Rev 2006, Issue 4. Art. No.: CD005440. DOI: 10.1002/14651858.CD005440.pub2.
2. Jenson S W. Postcholecystectomy Syndrome. Jan 2008. http://emedicine.medscape.com/article/192761
3. Gracie W A, Ransohoff D F. The natural history of silent gallstones. N Engl J Med 1982; 307: 798.
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- Karanjia N, Ali T. Gallstones. Surgery 2006; 25(1): 16-21.
- Peel A L. Gallbladder stones. Surgery 1997; 15(4): 82-9.
- Howard E R, Peel A L G. The gallbladder and bile ducts. In: The New Aird's Companion in Surgical Studies (2nd Ed). Bernand KG, Young AE (ed). Churchill Livingston: 907-41.
- Motson R W, Menzies D. Gallstones. In: Hepatobiliary & Pancreatic Surgery - A Companion to Specialist Surgical Practice. O J Garden (ed). W B Saunders: 175-201
- Keus F, de Jong J A F, Gooszen H G, van Laarhoven C J. Laparoscopic versus open cholecystectomy for patients with symptomatic cholecystolithiasis. Cochrane Database Syst Rev 2006, Issue 4. Art. No.: CD006231. DOI: 10.1002/14651858.CD006231.
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