Acute cholecystitis

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Furqan M M. M.B.B.S[2]

Cholecystitis is the inflammation of the gallbladder. Acute cholecystitis may be classified according to causes into two major subtypes: Acute calculous cholecystitis and acute acalculous cholecystitis. Gallstones are found in 3500 years old Egyptian mummies during the autopsies. Common risk factors in the development of acute calculous cholecystitis include advanced age, female gender, obesity, and positive family history. Long periods of fasting, total parental nutrition (TPN), and weight loss are the common risk factors for the development of acute acalculous cholecystitis. Acute calculous cholecystitis is usually caused by the mechanical obstruction of the gallbladder due to gallstones. Acute acalculous cholecystitis is caused predominantly by the gallbladder stasis. Gallstones are the most common cause of physical obstruction of the gallbladder usually at the neck or in the cystic duct. Cholesterol gallstones are the most common type of gallstones. The obstruction causes an increased pressure as the gallbladder mucosa continues to produce mucus. This raised pressure may cause the venous congestion which is followed by the arterial congestion. Eventually, the raised pressure and stasis leads to the gallbladder ischemia and necrosis. Mechanical obstruction of the gallbladder as a result of polyps, malignancy, an infestation of the gallbladder with parasites, foreign bodies, and trauma may also lead to the acute cholecystitis. Acute cholecystitis is more common in siblings and first degree relatives of affected persons. Lith gene is involved in the pathogenesis of cholecystitis. Acute cholecystitis is associated with diabetes, insulin resistance, cardiovascular diseases, non-alcoholic fatty liver disease (NAFLD) and gastrointestinal malignancies. Microscopic histopathology shows edematous and hemorrhagic gallbladder wall, mucosal necrosis with neutrophil infiltration. Bile infiltration of the gallbladder wall and bile and leukocyte margination of blood vessels are specific findings for acalculous cholecystitis. Acute cholecystitis must be differentiated from other diseases that cause right upper quadrant abdominal pain and nausea/vomiting such as biliary colic, acute cholangitis, viral hepatitis, alcoholic hepatitis, acute pancreatitis, acute appendicitis, and irritable bowel syndrome. The incidence of acute cholecystitis is approximately 6,300 per 100,000 in individuals under 50 years age and 20,900 per 100,000 in individuals over 50 years age worldwide. The prevalence of acute cholecystitis is approximately 369 per 100,000 individuals in the United states. It is estimated from the population-based statistics, based on a comprehensive survey in the U.S. Acute cholecystitis is comparatively less prevalent in the developing countries. The mortality rate of acute cholecystitis is approximately 0.6%. Acute Cholecystitis most commonly occurs as a result of the prolonged obstruction of the cystic duct leading to inflammation of the gallbladder. The obstruction further contributes to the development of the complications associated with acute cholecystitis such as gangrene, empyema, perforation, cholecysto-enteric fistula, emphysematous cholecystitis, and gallstone ileus. Prognosis is generally good if the patient receives treatment. Acute cholecystitis occurs as a result of prolonged gallstone obstruction in the bile duct, one to four patients develop biliary colic and about 20% of these patients develop acute cholecystitis annually. The hallmark of acute cholecystitis is biliary colic. A positive history of biliary colic, nausea and vomiting is suggestive of acute cholecystitis. Patients with acute cholecystitis usually appear ill. Physical examination of patients with acute cholecystitis is remarkable for right upper quadrant abdominal tenderness, positive murphy’s sign, and fever. The presence of murphy’s sign on physical examination is highly suggestive of acute cholecystitis. Laboratory findings consistent with the diagnosis of acute cholecystitis include leukocytosis and elevated CRP. Transabdominal ultrasound is the initial test of choice for the diagnosis of acute cholecystitis. Findings on an ultrasound diagnostic of acute cholecystitis include thickened gallbladder, gallstones or sludge, and pericholecystic fluid. CT scan is usually used for the diagnosis of the complications of acute cholecystitis. These complications include emphysematous cholecystitis and gangrenous cholecystitis. Cholescintigraphy is the gold standard for the diagnosis of acute cholecystitis. Cholescintigraphy is an alternative method of imaging and uses technetium-labeled hepatic 2,6-dimethyl-iminodiacetic acid (HIDA) in difficult cases or uncertain diagnosis. Findings on a cholescintigraphy diagnostic of acute cholecystitis include lack of visualization of the gallbladder. The mainstay of treatment for acute cholecystitis (calculous and acalculous) is surgery. Laparoscopic cholecystectomy is the gold standard for the treatment of acute cholecystitis and is usually preferred over the open cholecystectomy. Percutaneous cholecystostomy (PC) is an alternative to emergency cholecystectomy in complicated cases of high-risk patients. Pharmacologic medical therapy is recommended for cases of acute cholecystitis in which surgery is delayed. Empiric pharmacologic medical therapies for acute cholecystitis include either amoxicillin-clavulanic acid, cefoxitin, cefotaxime, or ceftriaxone with metronidazole, and ciprofloxacin or levofloxacin with metronidazole. The duration of medical therapy after the cholecystectomy depends on the severity of the disease.

Gallstones are found in 3500 years old Egyptian mummies during the autopsies. In 1420, Antonio Benivieni was the first to describe gallstones. Carl Langenbuch performed the first cholecystectomy of a 43-year-old man who had suffered from biliary colic for sixteen years. Historically, open cholecystectomy was the treatment employed for the treatment of acute cholecystitis. Laparoscopic cholecystectomy was developed to treat acute cholecystitis and the shift from open to laparoscopic cholecystectomy occurred in the late 1980s.

Acute cholecystitis may be classified according to causes into two major subtypes: Acute calculous cholecystitis and acute acalculous cholecystitis.

Acute calculous cholecystitis is usually caused by the mechanical obstruction of the gallbladder due to gallstones. Acute acalculous cholecystitis is caused predominantly by the gallbladder stasis. Gallstones are the most common cause of physical obstruction of the gallbladder usually at the neck or in the cystic duct. Cholesterol gallstones are the most common type of gallstones. The obstruction causes an increased pressure as the gallbladder mucosa continues to produce mucus. This raised pressure may cause the venous congestion which is followed by the arterial congestion. Eventually, the raised pressure and stasis leads to the gallbladder ischemia and necrosis. Mechanical obstruction of the gallbladder as a result of polyps, malignancy, an infestation of the gallbladder with parasites, foreign bodies, and trauma may also lead to the acute cholecystitis. Acute cholecystitis is more common in siblings and first degree relatives of affected persons. Lith gene is involved in the pathogenesis of cholecystitis. Mutations in the hepatic cholesterol transporter ABCG8 also predispose an individual to the develop gallstones. Acute cholecystitis is associated with diabetes, insulin resistance, cardiovascular diseases, non-alcoholic fatty liver disease (NAFLD) and gastrointestinal malignancies. Microscopic histopathology shows edematous and hemorrhagic gallbladder wall, mucosal necrosis with neutrophil infiltration. Bile infiltration of the gallbladder wall and bile and leucocyte margination of blood vessels are specific findings for acalculous cholecystitis.

The most common cause of acute cholecystitis is gallstones. Less common causes of acute cholecystitis include gallbladder stasis, gallbladder polyp, gallbladder malignancy, parasites, and foreign

Acute cholecystitis must be differentiated from other diseases that cause right upper quadrant abdominal pain and nausea/vomiting such as biliary colic, acute cholangitis, viral hepatitis, alcoholic hepatitis, acute pancreatitis, acute appendicitis, and irritable bowel syndrome.

The incidence of acute cholecystitis is approximately 6,300 per 100,000 in individuals under 50 years age and 20,900 per 100,000 in individuals over 50 years age worldwide. The prevalence of acute cholecystitis is approximately 369 per 100,000 individuals in the United states. It is estimated from the population-based statistics, based on a comprehensive survey in the U.S. Acute cholecystitis is comparatively less prevalent in the developing countries. The mortality rate of acute cholecystitis is approximately 0.6%. Acute cholecystitis usually affects individuals of the North American Indian race. Females are more commonly affected by acute cholecystitis than males. Acute cholecystitis cases are reported worldwide. Acute cholecystitis accounts for 700,000 cholecystectomies and costs of ∼$6.5 billion annually only in the United States.

Common risk factors in the development of acute calculous cholecystitis include advancing age, female gender, obesity, and family history. Long periods of fasting, total parental nutrition (TPN), weight loss are the common risk factors for the development of acute acalculous cholecystitis.

There is insufficient evidence to recommend routine screening for acute cholecystitis.

Acute Cholecystitis most commonly occurs as a result of the prolonged obstruction of the cystic duct leading to inflammation of the gallbladder. The obstruction further contributes to the development of the complications associated with acute cholecystitis such as gangrene, empyema, perforation, cholecysto-enteric fistula, emphysematous cholecystitis, and gallstone ileus. Prognosis is generally good if the patient receives treatment. The majority of the patients undergo cholecystectomy.

Cholescintigraphy is the gold standard for the diagnosis of acute cholecystitis. Transabdominal ultrasonography is the initial study of choice for the diagnosis of acute cholecystitis and gallstones. Thickened gallbladder, gallstones or sludge, and pericholecystic fluid are the findings associated with transabdominal ultrasound in patients with acute cholecystitis.

The majority of patients with cholelithiasis are asymptomatic. Acute cholecystitis occurs as a result of prolonged gallstone obstruction in the bile duct, one to four patients develop biliary colic and about 20% of these patients develop acute cholecystitis annually. The hallmark of acute cholecystitis is biliary colic. A positive history of biliary colic, nausea and vomiting is suggestive of acute cholecystitis.

Patients with acute cholecystitis usually appear ill. Physical examination of patients with acute cholecystitis is remarkable for right upper quadrant abdominal tenderness, positive murphy’s sign, and fever. The presence of murphy’s sign on physical examination is highly suggestive of acute cholecystitis.

Laboratory findings consistent with the diagnosis of acute cholecystitis include leukocytosis and elevated CRP.

There are no ECG findings associated with acute cholecystitis. However, acute cholecystitis presents with pain in the epigastrium, which can be confused with an acute myocardial infarction. ECG can be useful in excluding an MI.

Abdominal X-Ray (AXR) does not aid diagnosis of acute cholecystitis. AXR is performed as an initial evaluation to diagnose the complicated gallbladder disease.

Transabdominal ultrasound is the initial test of choice for the diagnosis of acute cholecystitis. Findings on an ultrasound diagnostic of acute cholecystitis include thickened gallbladder, gallstones or sludge, and pericholecystic fluid.

CT scan is usually used for the diagnosis of the complications of acute cholecystitis. These complications include emphysematous cholecystitis and gangrenous cholecystitis.

Abdominal MRI may be helpful in the diagnosis of acute cholecystitis. Findings on MRI suggestive of acute cholecystitis include thickening of the gallbladder and pericholecystic fluid.

Cholescintigraphy is the gold standard for the diagnosis of acute cholecystitis. Cholescintigraphy is an alternative method of imaging and uses technetium-labeled hepatic 2,6-dimethyl-iminodiacetic acid (HIDA) in difficult cases or uncertain diagnosis. Findings on a cholescintigraphy diagnostic of acute cholecystitis include lack of visualization of the gallbladder.

The histopathological analysis may be helpful in the diagnosis of acute cholecystitis. Findings suggestive of acute cholecystitis include edematous and hemorrhagic gallbladder wall, mucosal necrosis with neutrophil infiltration, eosinophilic infiltration of the gallbladder mucosa, and bile infiltration and leucocyte margination of blood vessels.

The mainstay of treatment for acute cholecystitis (calculous and acalculous) is surgery. Pharmacologic medical therapy is recommended for cases of acute cholecystitis in which surgery is delayed. Empiric pharmacologic medical therapies for acute cholecystitis include either amoxicillin-clavulanic acid, cefoxitin, cefotaxime, or ceftriaxone with metronidazole, and ciprofloxacin or levofloxacin with metronidazole. The duration of medical therapy after the cholecystectomy depends on the severity of the disease.

Surgery is the mainstay of treatment for acute cholecystitis (calculous and acalculous).Laparoscopic cholecystectomy is the gold standard for the treatment of acute cholecystitis and is usually preferred over the open cholecystectomy. Percutaneous cholecystostomy (PC) is an alternative to emergency cholecystectomy in complicated cases of high-risk patients.

Administration of NSAIDs in the patients with biliary colic prevents the progression to acute cholecystitis.

There are no established measures for the secondary prevention of acute cholecystitis.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Furqan M M. M.B.B.S[2]

Gallstones are found in 3500 years old Egyptian mummies during the autopsies. In 1420, Antonio Benivieni was the first to describe gallstones. Carl Langenbuch performed the first cholecystectomy of a 43-year-old man who had suffered from biliary colic for sixteen years. Historically, open cholecystectomy was the treatment employed for the treatment acute cholecystitis. Laparoscopic cholecystectomy was developed to treat acute cholecystitis and the shift from open to laparoscopic cholecystectomy occurred in the late 1980s.

• Gallstone related diseases have an ancient history. Gallstones are found in 3500 years old Egyptian mummies during the autopsies.^[1]
• In 1420, Antonio Benivieni was the first to describe gallstones.^[2]
• In 1658, Francis Glisson described his own biliary colic attacks, “from which there is no release except by death”. He also described the liver capsule that bears his name.^[3]
• In 1687, Stalpert von der Wiel found gallstones accidentally during the surgery of a purulent upper abdominal abscess in a patient with a long history of abdominal pain.^[4]

The landmarks in the development of treatment strategies for acute cholecystitis are:^[5][6]

• In 1733, Jean-Louis Petit, a Parisian surgeon suggested that if biliary colic occurred in association with reddening of the abdominal skin, the surgeon should lance the area, remove the gallstones, and leave a gall fistula. In 1743, he performed this procedure.
• In 1859, when J. L. W. Thudichum proposed a two-stage elective cholecystostomy.
• In 1882, Langenbuch performed the first cholecystectomy of a 43-year-old man who had suffered from biliary colic for sixteen years.
• By 1890, 47 cholecystectomies were performed by twenty-seven surgeons, and in 1897 the number had risen to nearly a hundred operations with a mortality of less than 20%.
• Historically, open cholecystectomy was the treatment employed for the treatment of acute cholecystitis.
• Laparoscopic cholecystectomy was developed to treat acute cholecystitis and the shift from open to laparoscopic cholecystectomy occurred in the late 1980s.

Template:WH Template:WS

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Furqan M M. M.B.B.S[2]

Acute cholecystitis may be classified according to causes into two major subtypes: Acute calculous cholecystitis and acute acalculous cholecystitis.

• Acute cholecystitis may be classified according to causes into two major subtypes:^[1][2][3]
  • Acute calculous cholecystitis
    • Acute calculous cholecystitis is caused by gallstones or biliary sludge.
  • Acute acalculous cholecystitis
    • Acute acalculous cholecystitis is caused by the gallbladder stasis.

Template:WH Template:WS

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Furqan M M. M.B.B.S[2]

Acute calculous cholecystitis is usually caused by the mechanical obstruction of the gallbladder due to gallstones. Acute acalculous cholecystitis is caused predominantly by the gallbladder stasis. Gallstones are the most common cause of physical obstruction of the gallbladder usually at the neck or in the cystic duct. Cholesterol gallstones are the most common type of gallstones. The obstruction causes an increased pressure as the gallbladder mucosa continues to produce mucus. This raised pressure may cause the venous congestion which is followed by the arterial congestion. Eventually, the raised pressure and stasis leads to the gallbladder ischemia and necrosis. Mechanical obstruction of the gallbladder as a result of polyps, malignancy, an infestation of the gallbladder with parasites, foreign bodies, and trauma may also lead to the acute cholecystitis. Acute cholecystitis is more common in siblings and first degree relatives of affected persons. Lith gene is involved in the pathogenesis of cholecystitis. Mutations in the hepatic cholesterol transporter ABCG8 also predispose an individual to the develop gallstones. Acute cholecystitis is associated with diabetes, insulin resistance, cardiovascular diseases, non-alcoholic fatty liver disease (NAFLD) and gastrointestinal malignancies. Microscopic histopathology shows edematous and hemorrhagic gallbladder wall, mucosal necrosis with neutrophil infiltration. Bile infiltration of the gallbladder wall and bile and leucocyte margination of blood vessels are specific findings for acalculous cholecystitis.

Inflammation of the gallbladder is termed as cholecystitis. Acute calculous cholecystitis is usually caused by the mechanical obstruction due to gallstones. Acute acalculous cholecystitis is caused predominantly by the gallbladder stasis. The pathogenesis of acute cholecystitis involves the following:^{[1][2][3][4][5][6][7][8][9][10][11]}

• Obstruction of the gallbladder:
  • Gallstones are the most common cause of physical obstruction of the gallbladder usually at the neck or in the cystic duct. The obstruction causes an increased pressure as the gallbladder mucosa continues to produce mucus. This raised pressure may cause the venous congestion which is followed by the arterial congestion. Eventually, the raised pressure and stasis leads to the gallbladder ischemia and necrosis.
    • There are two major types of gallstones:
      • Cholesterol gallstones:
        • Cholesterol gallstones are the most predominant form of the gallstones. They account for approximately 80% of the total gallstones.
        • The formation of gallstones is dependant on the following factors:
          • Cholesterol supersaturation in the bile
          • Crystal nucleation
          • Gallbladder dysmotility
          • Gallbladder absorption
      • Pigmented gallstones:
        • There are two types of pigmented gallstones.
          • Black stones
            • Black stones consist of calcium bilirubinate and mucin glycoproteins.
            • Black stones are predominantly associated with hemolytic conditions or cirrhosis (as a result of increased levels of unconjugated bilirubin).
            • These stones are usually located in the gallbladder.
          • Brown stones
            • Brown stones are usually associated with bacterial infection.
            • Brown stones are usually located elsewhere in the biliary tree as opposed to the gallbladder.
  • Mechanical obstruction of the gallbladder as a result of polyps, malignancy, an infestation of the gallbladder with parasites, foreign bodies, and trauma may also lead to the acute cholecystitis.
• Gallbladder stasis:
  • Gallbladder stasis is usually due to the lack of gallbladder stimulation and contractility.
  • This leads to concentration of the bile salts with a build-up of pressure within the organ. An increased intraluminal pressure results in ischemia and necrosis of the gallbladder.
  • The gallbladder stasis also facilitates the proliferation of the bacteria such as Escherichia coli, Klebsiella, Bacteroides, Proteus, Pseudomonas, and Enterococcus faecalis. This can also cause an inflammatory reaction in the gallbladder.

• Acute cholecystitis is more common in siblings and first degree relatives of affected persons.^[12][13]
• Lith gene is involved in the pathogenesis of cholecystitis.^[6]
• Mutations in the hepatic cholesterol transporter ABCG8 also predispose an individual to the develop gallstones.^[9]

The following conditions are associated with acute cholecystitis:^[14]

• Diabetes
• Insulin resistance
• Cardiovascular diseases
• Non-alcoholic fatty liver disease (NAFLD)
• Gastrointestinal malignancies:
  • Gastric cancer
  • Hepatocellular carcinoma
  • Cholangiocarcinoma
  • Pancreatic cancer
  • Cancer of the ampulla of Vater

• On gross pathology, acute cholecystitis has the following features:^{[15][16][17][18][2]}
  • Enlarged/distended gallbladder
  • Serosal or mucosal exudates
  • Thickened wall with hemorrhage and edema
  • Ulcers, pus, bile, and gallstones

• On microscopic histopathological analysis, acute cholecystitis has the following features:^{[16][17][19][20]}
  • Edematous and hemorrhagic gallbladder wall
  • Mucosal necrosis with neutrophil infiltration
  • Eosinophilic infiltration of the gallbladder mucosa
• Specific microscopic features of acalculous cholecystitis:^[15]
  • Bile infiltration of gallbladder wall
  • Bile infiltration and leucocyte margination of blood vessels
  • Lymphatic dilation

Template:WH Template:WS

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Furqan M M. M.B.B.S[2]

The most common cause of acute cholecystitis is gallstones. Less common causes of acute cholecystitis include gallbladder stasis, gallbladder polyp, gallbladder malignancy, parasites, and foreign bodies.

The most common cause of acute cholecystitis is gallstones. Less common causes of acute cholecystitis include gallbladder stasis, gallbladder polyp, gallbladder malignancy, parasites, and foreign bodies..^[1][2][3]

Acute cholecystitis may be caused by:

• Gallstones

Less common causes of acute cholecystitis include:

• Gallbladder stasis
• Gallbladder polyp
• Gallbladder malignancy
• Genetic causes
• Parasites
• Foreign bodies

For the risk factors involved in the development of Acute cholecystitis, please click here.

Cardiovascular	No underlying causes
Chemical/Poisoning	No underlying causes
Dental	No underlying causes
Dermatologic	No underlying causes
Drug Side Effect	No underlying causes
Ear Nose Throat	No underlying causes
Endocrine	No underlying causes
Environmental	No underlying causes
Gastroenterologic	Gallstones, gallbladder stasis
Genetic	Lith gene, mutations in the hepatic cholesterol transporter ABCG8
Hematologic	No underlying causes
Iatrogenic	No underlying causes
Infectious Disease	Parasitic infiltration of gallbladder
Musculoskeletal/Orthopedic	No underlying causes
Neurologic	No underlying causes
Nutritional/Metabolic	No underlying causes
Obstetric/Gynecologic	No underlying causes
Oncologic	Gallbladder polyp, gallbladder malignancy
Ophthalmologic	No underlying causes
Overdose/Toxicity	No underlying causes
Psychiatric	No underlying causes
Pulmonary	No underlying causes
Renal/Electrolyte	No underlying causes
Rheumatology/Immunology/Allergy	No underlying causes
Sexual	No underlying causes
Trauma	Foreign body
Urologic	No underlying causes
Miscellaneous	No underlying causes

List the causes of the disease in alphabetical order.

• Foreign body
• Gallbladder malignancy
• Gallbladder polyp
• Gallbladder stasis
• Gallstones
• Genetic causes
• Parasites

Template:WH Template:WS

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Furqan M M. M.B.B.S[2]

Acute cholecystitis must be differentiated from other diseases that cause right upper quadrant abdominal pain and nausea/vomiting such as biliary colic, acute cholangitis, viral hepatitis, alcoholic hepatitis, acute pancreatitis, acute appendicitis, and irritable bowel syndrome.

Acute cholecystitis must be differentiated from other diseases that cause right upper quadrant pain and nausea/vomiting such as:^[1][2][3]

• Biliary colic
• Acute cholangitis
• Viral hepatitis
• Alcoholic hepatitis
• Acute pancreatitis
• Acute appendicitis
• Irritable bowel syndrome

Abbreviations: RUQ= Right upper quadrant of the abdomen, LUQ= Left upper quadrant, LLQ= Left lower quadrant, RLQ= Right lower quadrant, LFT= Liver function test, SIRS= Systemic inflammatory response syndrome, ERCP= Endoscopic retrograde cholangiopancreatography, IV= Intravenous, N= Normal, AMA= Anti mitochondrial antibodies, LDH= Lactate dehydrogenase, GI= Gastrointestinal, CXR= Chest X ray, IgA= Immunoglobulin A, IgG= Immunoglobulin G, IgM= Immunoglobulin M, CT= Computed tomography, PMN= Polymorphonuclear cells, ESR= Erythrocyte sedimentation rate, CRP= C-reactive protein, TS= Transferrin saturation, SF= Serum Ferritin, SMA= Superior mesenteric artery, SMV= Superior mesenteric vein, ECG= Electrocardiogram, US = Ultrasound

Classification of pain in the abdomen based on etiology Disease Clinical manifestations Diagnosis Comments Symptoms Signs Abdominal Pain Fever Rigors and chills Nausea or vomiting Jaundice Constipation Diarrhea Weight loss GI bleeding Hypo- tension Guarding Rebound Tenderness Bowel sounds Lab Findings Imaging Abdominal causes Inflammatory causes Pancreato-biliary disorders Acute cholecystitis RUQ + − + + − − − − − − − Hypoactive Hyperbilirubinemia Leukocytosis Ultrasound shows: Gallstone Inflammation Murphy’s sign Acute suppurative cholangitis RUQ + + + + − − − − + + + N Abnormal LFT WBC >10,000 Ultrasound shows biliary dilatation/stents/tumor Septic shock occurs with features of SIRS Acute cholangitis RUQ + − − + − − − − − − − N Abnormal LFT Ultrasound shows biliary dilatation/stents/tumor Biliary drainage (ERCP) + IV antibiotics Cholelithiasis RUQ/Epigastric ± − ± ± − − − − − − − Normal to hyperactive for dislodged stone Leukocytosis Ultrasound shows gallstone Fatty food intolerance Acute pancreatitis Epigastric + − + ± − − + − ± − − N Increased amylase / lipase Ultrasound shows evidence of inflammation CT scan shows severity of pancreatitis Pain radiation to back Primary biliary cirrhosis RUQ/Epigastric − − − + − − − − − − − N Increased AMA level, abnormal LFTs ERCP Pruritis Primary sclerosing cholangitis RUQ + − − + − − − − − − − N Increased liver enzymes Increased IgM, IgG4 Anti-neutrophil cytoplasmic antibody (p-ANCA) Anti-nuclear antibody (ANA) Anti-smooth muscle antibody (Anti-Sm) Anti-endothelial antibody Anti-cardiolipin antibody ERCP and MRCP shows Multiple segmental strictures Mural irregularities Biliary dilatation and diverticula Distortion of biliary tree The risk of cholangiocarcinoma in patients with primary sclerosing cholangitis is 400 times higher than the risk in the general population. Hepatic causes Viral hepatitis RUQ + − + + − Positive in Hep A and E + − Positive in fulminant hepatitis Positive in acute + N Abnormal LFTs Viral serology US Hep A and E have fecal-oral route of transmission Hep B and C transmits via blood transfusion and sexual contact. Liver abscess RUQ + + + + − ± + − + + ± Normal or hypoactive CBC Blood cultures Abnormal liver function tests US CT Hepatocellular carcinoma/Metastasis RUQ + − − + − − + − − − − Normal Hyperactive if obstruction present High levels of AFP in serum Abnormal liver function tests US CT Liver biopsy Other symptoms: Splenomegaly Variceal bleeding Ascites Spider nevi Asterixis Disease Abdominal Pain Fever Rigors and chills Nausea or vomiting Jaundice Constipation Diarrhea Weight loss GI bleeding Hypo- tension Guarding Rebound Tenderness Bowel sounds Lab Findings Imaging Comments Budd-Chiari syndrome RUQ ± − − ± − − − Positive in liver failure leading to varices − − − N Elevated serum aspartate aminotransferase and alanine aminotransferase levels may be more than five times the upper limit of the normal range. Elevated serum alkaline phosphatase and bilirubin levels, decreased serum albumin level. Findings on CT scan suggestive of Budd-Chiari syndrome include: Early enhancement of the caudate lobe and central liver around the inferior vena cava Delayed enhancement of the peripheral liver with accompanying central low density (flip-flop appearance) Peripheral zones of the liver show reversed portal venous blood flow In the chronic phase, there is caudate lobe enlargement and atrophy of the peripheral liver in affected areas Ascitic fluid examination shows: Total protein more than 2.5 g per deciliter White blood cells are usually less than 500/μL. Hemochromatosis RUQ − − − − − − − Positive in cirrhotic patients − − − N >60% TS >240 μg/L SF Raised LFT Hyperglycemia Ultrasound shows evidence of cirrhosis Extra intestinal findings: Hyperpigmentation Diabetes mellitus Arthralgia Impotence in males Cardiomyopathy Atherosclerosis Hypopituitarism Hypothyroidism Extrahepatic cancer Prone to specific infections Cirrhosis RUQ − − − + − − + + + − − N Hypoalbuminemia Prolonged PT Abnormal LFTs Hyponatremia Thrombocytopenia US Nodular, shrunken liver Ascites Stigmata of liver disease Cruveilhier- Baumgarten murmur Disease Abdominal Pain Fever Rigors and chills Nausea or vomiting Jaundice Constipation Diarrhea Weight loss GI bleeding Hypo- tension Guarding Rebound Tenderness Bowel sounds Lab Findings Imaging Comments Intestinal causes Acute appendicitis Starts in epigastrium, migrates to RLQ + Positive in pyogenic appendicitis + − − ± − − Positive in perforated appendicitis + + Hypoactive Leukocytosis Ct scan Ultrasound Positive Rovsing sign Positive Obturator sign Positive Iliopsoas sign Irritable bowel syndrome Diffuse − − − − ± ± + − − − − N Normal Normal Symptomatic treatment High dietary fiber Osmotic laxatives Antispasmodic drugs Hollow Viscous Obstruction Biliary colic RUQ − − + + − − − − − − − N ↑ bilirubin and alkaline phosphatase Ultrasound Extra-abdominal causes Pulmonary causes Pulmonary embolism RUQ/LUQ ± − − − − − − − ± − − N ABGs D-dimer CXR V/Q scan Spiral CT pulmonary angiogram Dyspnea Tachycardia Pleuretic chest pain Pneumonia RUQ/LUQ + + + − − ± − − + − − Normal or hypoactive ABGs Leukocytosis Pancytopenia CXR CT chest Bronchoscopy Shortness of breath Cough

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Furqan M M. M.B.B.S[2]

The incidence of acute cholecystitis is approximately 6,300 per 100,000 in individuals under 50 years age and 20,900 per 100,000 in individuals over 50 years age worldwide. The prevalence of acute cholecystitis is approximately 369 per 100,000 individuals in the United States. It is estimated from the population-based statistics, based on a comprehensive survey in the U.S. Acute cholecystitis is comparatively less prevalent in the developing countries. The mortality rate of acute cholecystitis is approximately 0.6%. Acute cholecystitis usually affects individuals of the North American Indian race. Females are more commonly affected by acute cholecystitis than males. Acute cholecystitis cases are reported worldwide. Acute cholecystitis accounts for 700,000 cholecystectomies and costs of ∼$6.5 billion annually only in the United States.

• The incidence of acute cholecystitis is approximately 6,300 per 100,000 in individuals under 50 years age and 20,900 per 100,000 in individuals over 50 years age worldwide.^[1][2]

• The prevalence of acute cholecystitis is approximately 369 per 100,000 individuals in the United states. It is estimated from the population-based statistics, based on a comprehensive survey in the U.S.^[3]

• The mortality rate of Acute cholecystitis is approximately 0.6%.^[3]

• The incidence of acute cholecystitis increases with age.^[2][3][4]

• Gallstone diseases usually affects individuals of the North American Indian race. White Americans, Asians, African Americans, and Africans are less likely to develop acute cholecystitis.^[3][4]

• Females are more commonly affected by gallstone diseases than males. The female to male ratio ranges from 10:1 in Pima Indians to 2–3:1 in Europeans women.^[3][4]

• Acute cholecystitis cases are reported worldwide. America and Europe have high rates of gallbladder stones as compared to Asia and Africa.^[3]

• Gallstone disease accounts for 700,000 cholecystectomies and costs of ∼$6.5 billion annually only in the United States.^[3]
  • Gallstone disease is prevalent in North America with a racial predisposition to the American Indians.
  • South American countries have slightly more prevalence than North America.
  • In Europe, Scandinavian countries have the highest prevalence of acute cholecystitis.
  • Italy, Austria, England, Germany, and Poland have a higher prevalence among the rest of Europe.

• Gallstone diseases are comparatively less prevalent in the developing countries.^[3]
  • India and Taiwan have a higher prevalence of acute cholecystitis in the developing countries.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Furqan M M. M.B.B.S[2]

Common risk factors in the development of acute calculous cholecystitis include advancing age, female gender, obesity, and family history. Long periods of fasting, total parental nutrition (TPN), weight loss are the common risk factors for the development of acute acalculous cholecystitis.

• Common risk factors in the development of acute calculous cholecystitis include advancing age, female gender, obesity, and family history. Long periods of fasting, total parental nutrition (TPN), weight loss are the common risk factors for the development of acute acalculous cholecystitis.

• Common risk factors in the development of acute calculous cholecystitis are:^[1][2][3]
  • Advancing age
  • Female gender
  • Obesity
  • Multi parity
  • Family history
  • Genetic factors
  • Oral contraceptives
  • Diabetes
• Common risk factors in the development of acute acalculous cholecystitis are:^[4]
  • Long lasting fasting
  • Total parenteral nutrition (TPN)
  • Weight loss
  • Severe burns
  • Sepsis

• Less common risk factors in the development of acute cholecystitis include:^[5]
  • AIDS

For the causes of Acute cholecystitis, please click here.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Furqan M M. M.B.B.S[2]

There is insufficient evidence to recommend routine screening for acute cholecystitis.

There is insufficient evidence to recommend routine screening for acute cholecystitis.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Dildar Hussain, MBBS [2]

Acute Cholecystitis most commonly occurs as a result of the prolonged obstruction of the cystic duct leading to inflammation of the gallbladder. The obstruction further contributes to the development of the complications associated with acute cholecystitis such as gangrene, empyema, perforation, cholecystoenteric fistula, emphysematous cholecystitis, and gallstone ileus. Prognosis is generally good if the patient receives treatment. The majority of the patients undergo cholecystectomy.

• In calculus cholecystitis, symptoms of acute cholecystitis usually develop after the obstruction of a gallstone in the bile ducts for more than 7 to 10 days. Female sex, obesity, oral contraceptives, and an underlying disease, such as diabetes are associated with the development of acute cholecystitis. Acute cholecystitis presents with the symptoms, such as right upper quadrant abdominal pain (biliary colic), nausea, and vomiting.^[1][2]
  • If left untreated acute cholecystitis further leads to the development of gangrene, empyema, perforation, cholecystoenteric fistula, emphysematous cholecystitis, and gallstone ileus.

Common complications of acute cholecystitis include:^{[3][4][5][6][7][8]}

Complication	Explanation
Gangrene	Gangrene of gallbladder is the most common complication of acute cholecystitis, if left untreated and in elderly patients with an underlying disease of diabetes.
Empyema	Prolonged untreated acute cholecystitis worsens the inflammation of the gallbladder leading to the collection of pus around the gallbladder called the empyema of the gallbladder.
Perforation	Perforation of the gallbladder is a result of the gangrene of the gallbladder and lead to the pericholecystic abscess. Peritonitis may also occur as a result of gallbladder perforation, such patients develop septicemia and have a high mortality rate.
Cholecystoenteric fistula	The cholecystoenteric fistula usually occurs due to the perforation of the gallbladder associated with the long-standing pressure necrosis due to gallstones than acute cholecystitis.
Emphysematous cholecystitis	It is associated with secondary infection of the gall bladder wall with gas forming organisms i.e Clostridium welchii, other organisms which can be found are Escherichia coli, Staphylococci, Streptococci, Pseudomonas, and Klebsiella.
Gallstone Illeus	Gallstone ileus is associated with the passage of gall stone through the cholecystoenteric fistula leading to mechanical obstruction of bowel in the terminal ileum.

• Prognosis is generally good after the timely treatment (cholecystectomy).^[9][10]

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