Acute cholecystitis is acute gallbladder inflammation and one of the major complications of cholelithiasis or gallstones.

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Essay describing cholecystitis
Definition
Acute cholecystitis is acute gallbladder inflammation and one of the major
complications of cholelithiasis or gallstones. It develops in up to 10% of
patients with symptomatic gallstones. In most cases (90%), it is caused by
complete cystic duct obstruction usually due to an impacted gallstone in the
gallbladder neck or cystic duct, which leads to inflammation within the
gallbladder wall. n 5% of cases, bile inspissation (due to dehydration) or bile
stasis (due to trauma or severe systemic illness) can block the cystic duct,
causing an acalculous cholecystitis.
Classification
Typesof acute cholecystitis
1. Calculous - 90% to 95%.
2. Acalculous - 3.7% to 14%.
Pathologic classification
1. Edematous
 2 to 4 days
 Gallbladder tissueis intact histological, with edema in the subserosallayer.
2. Necrotizing
 3 to 5 days
 Edema with areas of hemorrhageand necrosis
 Necrosis does not involve the full thickness of the wall.
3. Suppurative
 7 to 10 days
 WBCs present within the gallbladder wall, with areas of necrosis and
suppuration
 Intrawallabscesses involving theentire thickness of the wall
 Pericholecystic abscesses present.
4. Chronic

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 Occurs after repeated episodes of mild attacks
 Mucosalatrophy and fibrosis of the gallbladder wall.
5. Emphysematous
 Air appears in the gallbladder wall due to infection with gas-forming anaerobes
 Often found in diabetic patients.
Epidemiology
More than 20 million Americans are estimated to have gallstones, with
500,000 cholecystectomies performed annually. Most patients with gallstones
do not develop symptoms. About 1% to 2% of asymptomatic gallstones
become symptomatic each year. Acute cholecystitis is the most frequent
complication of gallstones and occurs in 10% of symptomatic patients.
Acute acalculous cholecystitis accounts for 5% to 14% of cases of acute
cholecystitis. The incidence is higher in the intensive care population,
particularly patients in burn and trauma units. The incidence of acute
cholecystitis is approximately the same in western Europe as in the US, but
worldwide the exact incidence is not known. The distribution and incidence
follow that of cholelithiasis because of the close relationship between
gallstones and acute cholecystitis.
Etiology
At least 90% of patients with the condition have gallstones. Helminthic
infection is one of the major causes of biliary disease in Asia, southern Africa,
and Latin America, but not the US. Infection with Salmonella organisms has
been described as a primary event in cholecystitis secondary to typhoid fever.
AIDS-related cholecystitis and cholangiopathy may be secondary to CMV
and Cryptosporidium organisms. Various microorganisms can be identified
early in the onset of disease.
These include Escherichia coli, Klebsiella, enterococci, Pseudomonas,
and Bacteroides fragilis. It has been suggested that this bacterial invasion is
not a primary perpetrator of injury, because in >40% of patients no bacterial
growth is obtained from surgical specimens. Generally, bacterial infection is a
secondary feature and not an initiating event. Occasionally, acute cholecystitis
occurs in the absence of gallstones. Starvation, total parenteral nutrition,

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narcotic analgesics, and immobility are predisposing factors for acalculous
acute cholecystitis. Secondary infection with gram-negative flora occurs in
most cases.
Pathophysiology
Fixed obstruction or passage of gallstones into the gallbladder neck or cystic
duct causes acute inflammation of the gallbladder wall. The impacted gallstone
causes bile to become trapped in the gallbladder, which causes irritation and
increases pressure in the gallbladder. Trauma caused by the gallstone
stimulates prostaglandin synthesis (PGI2, PGE2), which mediates the
inflammatory response. This can result in secondary bacterial infection leading
to necrosis and gallbladder perforation.
The pathophysiology of acalculous cholecystitis is poorly understood, but it is
most likely multifactorial. Functional cystic duct obstruction is often present
and related to biliary sludge or bile inspissation caused by dehydration or bile
stasis (due to trauma or systemic illness). Occasionally, extrinsic compression
may play a role in the development of bile stasis. Some patients with sepsis
may have direct gallbladder wall inflammation and localized or generalized
tissue ischemia without obstruction.
Jaundice occurs in up to 10% of patients and is caused by inflammation of
contiguous biliary ducts (Mirizzi syndrome).
Acute cholecystitis may resolve spontaneously 5 to 7 days after symptom
onset. The impacted stone becomes dislodged, with re-establishment of cystic
duct patency. If cystic duct patency is not re-established, inflammation and
pressure necrosis may develop, leading to mural and mucosal hemorrhagic
necrosis. Untreated acute cholecystitis can lead to suppurative, gangrenous,
and emphysematous cholecystitis.
Diagnostic Approach
Early diagnosis is essential for prompt therapeutic decisions and prevention of
complications. Diagnosis is based on the signs and symptoms of inflammation
in the presence of peritonitis localized to the RUQ of the abdomen. However,
no clinical or laboratory finding has a high or low enough likelihood ratio to
predict the presence or absence of the condition.

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History
Patients typically complain of nausea and pain that lasts >3 to 6 hours, which is
unremitting and may be associated with fever. The pain is severe and steady.
The duration of pain can be shorter if the gallstone returns into the gallbladder
lumen or passes into the duodenum.
Physical exam
Physical exam may reveal RUQ tenderness or a palpable mass. A positive
Murphy sign (the examiner's hand rests along the costal margin and deep
inspiration causes pain) has a specificity of 79% to 96% for acute cholecystitis.
Persistent pain, fever, chills, and more severe localized or generalized
tenderness may indicate complicated disease (e.g., abscess formation or
gallbladder perforation).
Acalculous cholecystitis is more difficult to diagnoseclinically, as it often occurs
in critically ill patients who may not be able to express pain. Patients receiving
total parental nutrition are at increased risk. Fever, jaundice, vomiting,
abdominal tenderness, leukocytosis, and hyperbilirubinemia should lead to a
high index of clinical suspicion. Typically acalculous cholecystitis is a diagnosis
of exclusion.
Blood tests
CBC and C-reactive protein (CRP) should be assessed to look for evidence of an
inflammatory process. LFTs may show elevated bilirubin, alkaline phosphatase,
and gamma-GT.
Imaging
RUQ ultrasound should be the first test ordered and can be performed at the
patient's bedside. Detection of gallstones alone does not definitively diagnose
the condition. To make an accurate diagnosis the findings of stones and an
ultrasonographic Murphy sign are required. About 92% of patients with a
positive Murphy sign in the presence of gallstones have the condition. [29]
Ultrasound allows for evaluation of all the abdominal structures. It provides
anatomic information about gallbladder size, stone size, gallbladder wall, and
bile duct size.
Scintigraphy with hepatobiliary iminodiacetic acid (HIDA) scan should be
obtained if ultrasound results are equivocal.

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Abdominal CT scan is inferior to ultrasound in assessing acute biliary disease,
but it is useful when obesity or gaseous distension limits ultrasound
interpretation. It is also indicated for evaluation of suspected complications
(such as abscess) and concurrentintra-abdominalconditions. Abdominal MRI is
appropriate for pregnant patients with abdominal pain.
Plain radiographs may detect a radiopaque gallstone in 15% of cases and
provide information about bowel gas pattern or free air, but offer no
incremental information if ultrasound or CT is performed.
Treatment Approach
When a diagnosis of acute cholecystitis is suspected, medical treatment,
including NPO, intravenous fluids, antibiotics, and analgesia, together with
close monitoring of blood pressure, pulse, and urinary output, should be
initiated. Simultaneously, the grade of severity needs to be established.
Appropriate treatment should be performed in accordance with the severity
grade. Operative risk should also be evaluated based on the severity grade.
Cholecystectomy
Cholecystectomy is the definitive treatment, as gallbladder inflammation often
persists despite medical therapy. This can be performed by laparoscopy or
laparotomy (i.e., open approach). It is carried out as soon as possible after the
onset of cholecystitis unless the patient is critically ill with severe cholecystitis
and is thoughtto havea high operativerisk, or inflammation is thought to have
been present for more than 7 days. This is because of the high risk of liver
failure and heavy hemorrhage.
Laparoscopic
 Now the preferred treatment. Early laparoscopic cholecystectomy (ELC)
showed a significant reduction in hospital stay evidence but did not
significantly affect conversion rate to open cholecystectomy. Evidence Optimal
timing (≤7 days after symptomonset) is critical for the best results. Conversion
to the open procedure may be required if there is significant inflammation,
difficulty delineating the anatomy, or significant bleeding.
 Conversion rates vary depending on the patient population but not the
surgeon's experience. Patients with Child-Turcotte-Pugh grade A or B liver

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cirrhosis have fewer overall postoperative complications than those who
undergo the open procedure.
Open
 May be appropriate for patients with gallbladder mass, extensive upper
abdominal surgery, suspicion of malignancy, or late third trimester of
pregnancy. It is also indicated if there is significant gallbladder inflammation,
difficulty delineating the anatomy, significant bleeding, presence of adhesions,
or laparoscopic cholecystectomy complications.
Percutaneous cholecystostomy tube
If medical management fails, and patients are poor surgical candidates (e.g.,
medically not suitable for surgery), a percutaneous cholecystostomy tube
should be considered. This has been shown to give clinical improvement in
80% of patients within 5 days after placement.
Age over 70 years, diabetes, a distended gallbladder, and persistently elevated
WBC (>15,000 cells/microliter) are prognostic factors for the development of
complications such as gangrenous cholecystitis and predictors for failure of
conservative treatment. These patients should be considered for early
percutaneous cholecystostomy tube.
It is a minimally invasive procedure most often performed in patients who
have a high surgical risk and occasionally in critically ill patients. Initially it was
used as a bridging procedure to help patients recover from a serious
underlying illness and before definitive surgery.
Based on available evidence from RCTs, the management of people at high risk
of perioperative death due to their general condition (i.e., high-risk surgical
patients) with percutaneous cholecystostomy is unclear. Further data are
needed.
The inflamed gallbladder is localized with sonography or fluoroscopy after the
oral administration of contrast medium. CT-guided access may help if no
sonographic window is found. A tube is then placed through the skin to drain
or decompress the gallbladder.
An incomplete or poor response within the first 48 hours may indicate
complications (e.g., tube dislodgment, gallbladder wall necrosis) or the wrong
diagnosis. Extrahepatic and transhepatic approaches have been advocated. A

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transhepatic route minimizes the risk of intraperitoneal bile leakage and
inadvertent injury to the hepatic flexure of the colon. A subhepatic or
transperitoneal approach is more favorable if stone extraction is planned due
to the need for tract dilation.
Contraindications include coagulopathy that cannot be corrected, massive
ascites that cannot be drained, and suspicion for gangrenous or perforated
cholecystitis. Technical success of percutaneous cholecystostomy is high in
experienced hands (95% to 100%), and complication rates are low.
Complications include catheter dislodgment, vagal reaction, bile leakage and
peritonitis, and hemorrhage.
Patients treated with cholecystostomy tube can be discharged with their tube
in place after the inflammatory process has resolved clinically. These patients
should subsequently undergo a cholangiogram through the cholecystostomy
tube (6-8 weeks) to see whether the cystic duct is open. If the duct is open and
the patient is a good surgical candidate, he or she should be referred for
cholecystectomy.
Management based on severity grade
Mild (grade I)
 Defined as acute cholecystitis in a healthy patient with no organ dysfunction
and mild inflammatory changes in the gallbladder; responds to initial medical
treatment.
 Patients are observed and treated with oral antibiotic drugs or even observed
without antibiotics. The pathophysiology of acute cholecystitis is cystic duct
obstruction, which causes an acute sterile inflammation. Secondary infection
of the gallbladder space by bacteria may follow. Antibiotics are required if
infection is suspected on the basis of laboratory and clinical findings.
 Antibiotic therapy should include coverage against microorganisms in the
Enterobacteriaceae family (e.g., a second-generation cephalosporin or a
combination of a quinolone and metronidazole); activity against enterococci is
not required.
 Nonsteroidal anti-inflammatory drugs (NSAIDs) such as diclofenac or
indomethacin are recommended as part of the medical treatment for their

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analgesic effects and their inhibition of prostaglandin release from the
gallbladder wall.
Medical treatment may be sufficient for patients with mild (grade I) disease,
and urgent surgery may not be required. However, for most patients ELC
should be considered the primary approach (within 1 week of onset of
symptoms). For patients who received preoperative and intraoperative
antibiotics, postoperative antibiotic therapy may not be required.
The Tokyo guidelines state that ELC is the preferred treatment. ELC (within 72
hours of onset of symptoms) has a clear benefit compared with delayed
cholecystectomy (>6 weeks after index admission) in terms of complication
rate, cost, quality of life, and hospital stay.
There is no advantage to delaying cholecystectomy for acute cholecystitis on
the basis of outcomes. Also favoring early cholecystectomy is that
approximately 15% to 20% of patients who underwent delayed procedures in
the randomized trials had persistent or recurrent symptoms requiring
intervention before their planned operation.
If medical management fails, and patients are poor surgical candidates, a
percutaneous cholecystostomy tube should be considered, with consideration
of referral for cholecystectomy if clinical situation improves.
Moderate (grade II)
 Defined as acute cholecystitis associated with any one of the following:
elevated white blood cell count (>18,000/microliter), palpable tender mass in
the right upper abdominal quadrant, duration of complaints >72 hours, and
marked local inflammation (gangrenous cholecystitis, pericholecystic abscess,
hepatic abscess, biliary peritonitis, emphysematous cholecystitis).
Moderate-grade cholecystitis usually does not respond to the initial medical
treatment. Patients who do not improve under conservative treatment are
referred for either surgery or percutaneous cholecystostomy, usually within 1
week of onset of symptoms.
ELC could be indicated if advanced laparoscopic techniques and skills are
available. Controversy lies within the group with moderately severe
cholecystitis, where there is no organ dysfunction but there is extensive

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disease in the gallbladder, which can confer difficulty in safely carrying out a
cholecystectomy. In this group, ELC or open cholecystectomy is preferred but
should be carried out only by a highly experienced surgeon. If operative
conditions make anatomic identification difficult, ELC should be promptly
terminated by conversion to open cholecystostomy.
Interval cholecystectomy can then be performed in 6 to 8 weeks. Limiting
factors to emergency surgery include availability of surgical staff, theatre
space, and radiologic investigations. Percutaneous cholecystostomy tube
should be considered for poor surgical candidates, with consideration of
referral for cholecystectomy if clinical situation improves.
Severe (grade III)
 Defined as organ dysfunction in at least any one of the following
organs/systems of cardiovascular (hypotension requiring treatment with
dopamine ≥5 micrograms/kg per minute, or any dose of norepinephrine), CNS
(decreased level of consciousness), respiratory (PaO2/FiO2 ratio <300), renal
(oliguria, creatinine >2.0 mg/dL), hepatic (INR >1.5), or hematologic (platelet
count <100,000 cells/microliter), and/or severe local inflammation.
Intensive supportive care is required to monitor and treat organ dysfunction.
Requires urgent management of severe local inflammation by percutaneous
gallbladder drainage (i.e., percutaneous cholecystostomy tube) followed where
indicated by delayed elective cholecystectomy 2 to 3 months later, when the
patient's general condition has improved.
Patients treated with cholecystostomy tube can be discharged with their tube
in place after the inflammatory process has resolved clinically. These patients
should subsequently undergo a cholangiogram through the cholecystostomy
tube (6-8 weeks) to see whether the cystic duct is open. If the duct is open and
the patient is a good surgical candidate, he or she should be referred for
cholecystectomy.

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References
 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2784509/
 https://en.wikipedia.org/wiki/Cholecystitis
 http://www.uptodate.com/contents/acute-cholecystitis-
pathogenesis-clinical-features-and-diagnosis
 https://online.epocrates.com/diseases/7811/Cholecystitis/Key-
Highlights
 http://www.mayoclinic.org/diseases-
conditions/cholecystitis/basics/definition/con-20034277