Chronic 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], Aditya Govindavarjhulla, M.B.B.S. [3]

Chronic cholecystitis is the chronic inflammation of the gallbladder. Chronic calculous cholecystitis is usually caused by the mechanical obstruction due to gallstones. This obstruction leads to gallbladder stasis which is the primary mechanism leading to stone formation. Lith gene is also involved in the pathogenesis of cholecystitis. Cholecystitis is more common in siblings and first degree relatives of affected persons. On gross pathology, chronic cholecystitis usually shows enlarged or distended gallbladder and serosal or mucosal exudates. Fibrosis of gallbladder may also be seen. Microscopic pathology shows lymphocytic inflammatory infiltrates, metaplasia and lipid or mucolipid accumulations in the gallbladder wall. Chronic cholecystitis may be classified according to causes into two major subtypes, acute calculous cholecystitis and acute acalculous cholecystitis. Gallstones have been 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 chronic cholecystitis. Laparoscopic cholecystectomy was developed to treat chronic cholecystitis and the change in preference from open to laparoscopic cholecystectomy occurred in the late 1980s. Common causes of cholecystitis include cholelithiasis and infections. Common risk factors in the development of calculous cholecystitis (cholelithiasis) include female gender, increasing age, obesity, pregnancy, family history, genetic factors, and oral contraceptive use. Common risk factors in the development of acalculous cholecystitis include AIDS, diabetes mellitus, major surgery, burns, sepsis, and long term total parenteral nutrition use. It is estimated that 20 to 25 million Americans (10%–15% of the population) have gallstones. However, only 1-4% experience symptomatic gallstone diseases. Gallstone disease 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. Females are more commonly affected by gallstone diseases than males for calculous cholecystitis. Males are at increased risk compared to females for acalculous cholecystitis following trauma and burns. Chronic cholecystitis must be differentiated from other conditions that affect the gallbladder and biliary tract such as biliary colic, choledocholithiasis, and cholangitis. Chronic cholecystitis must also be differentiated from colitis, functional bowel syndrome, hiatal hernia, and peptic ulcer. Cholecystitis presents with abdominal pain, which is not relieved by antacids and postural changes and lasts longer than 6 hours. It is sometimes preceded by attacks of biliary pain (due to gallstones). Untreated cholecystitis resolves spontaneously in half of the uncomplicated cases without surgery in a span of 7 to 10 days. The complications of chronic cholecystitis include gangrenous cholecystitis, perforation of the gallbladder, Mirizzi syndrome, gallstone ileus, and gallbladder malignancies. The patients with chronic cholecystitis may have the history of recurrent episodes of biliary colic or acute cholecystitis. A positive history of biliary colic, nausea and vomiting are suggestive of chronic cholecystitis. The most common symptoms of chronic cholecystitis are right upper quadrant abdominal or epigastric pain, pain is usually prolonged and there is a positive history of pain after ingestion of heavy fatty meals. The pain is severe and steady and may radiate to the back or right shoulder. Patients with chronic cholecystitis may have malaise during the episode. The physical examination in chronic cholecystitis is remarkable for tender right upper quadrant, fever (usually low grade in uncomplicated cases), and a positive Murphy’s sign. Transabdominal ultrasonography is the initial study of choice for the diagnosis of chronic cholecystitis and gallstones. Cholescintigraphy is the gold standard for the diagnosis of chronic cholecystitis. HIDA cholescintigraphy findings for chronic cholecystitis include delayed gallbladder isotope accumulation, irregular gallbladder filling, or photopenic areas and septations. Patients with acute cholecystitis are much more likely to manifest abnormal laboratory values, while in chronic cholecystitis the laboratory values are frequently normal. Laboratory findings consistent with the diagnosis of chronic cholecystitis include elevated alkaline phosphatase, leukocytosis and elevated bilirubin. Amylase may also be elevated. CT scan findings associated with chronic cholecystitis include gallbladder wall thickening, gallbladder distension or contraction and subserosal edema. The mainstay of treatment for chronic cholecystitis is surgery. Supportive measures are instituted to prepare the patient for surgery. These include antimicrobial therapy and fluid resuscitation. If the chronic cholecystitis is superimposed by acute cholecystitis, antibiotics can be used. Commonly used antibiotics are Cefazolin, Cefuroxime, and Ceftriaxone. Gallbladder removal by cholecystectomy, can be accomplished by the open surgery or a laparoscopic procedure. Laparoscopic cholecystectomy is the operation of choice in uncomplicated calculous cholecystitis. Open cholecystectomy may be performed in complicated cases or when skilled personal for laparoscopic procedure is not available. Supportive measures are instituted in the meantime to prepare the patient for surgery. These measures include fluid resuscitation and antibiotics. Antibiotic regimens usually consist of a broad spectrum cephalosporin such as ceftriaxone and an antibacterial with good cover against anaerobic bacteria, such as metronidazole.

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 chronic cholecystitis. Laparoscopic cholecystectomy was developed to treat chronic cholecystitis and the shift from open to laparoscopic cholecystectomy occurred in the late 1980s.

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

Inflammation of the gallbladder is termed as cholecystitis. Chronic calculous cholecystitis is usually caused by the mechanical obstruction due to gallstones. Chronic acalculous cholecystitis is caused predominantly by the gallbladder stasis. Lith gene is also involved in the pathogenesis of cholecystitis. Cholecystitis is more common in siblings and first degree relatives of affected persons. On gross pathology, chronic cholecystitis usually shows enlarged/distended gallbladder and serosal or mucosal exudates. Fibrosis of gallbladder may also be seen. Microscopic pathology shows lymphocytic inflammatory infiltrates, metaplasia and lipid/mucolipid accumulations in the gallbladder wall.

Common causes of cholecystitis include cholelithiasis and infections.

Chronic cholecystitis must be differentiated from other conditions that affect the gallbladder and biliary tract such as biliary colic, choledocholithiasis, and cholangitis. Chronic cholecystitis must also be differentiated from colitis, functional bowel syndrome, hiatal hernia, and peptic ulcer.

It is estimated that 20 to 25 million Americans (10%–15% of the population) have gallstones. However, only 1-4% experience symptomatic gallstone diseases. Gallstone disease 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. Females are more commonly affected by gallstone diseases than males for calculous cholecystitis. Males are at increased risk compared to females for acalculous cholecystitis following trauma and burns.

Common risk factors in the development of calculous cholecystitis (cholelithiasis) include female gender, increasing age, obesity, pregnancy, family history, genetic factors, and oral contraceptive use. Common risk factors in the development of acalculous cholecystitis include AIDS, diabetes mellitus, major surgery, burns, sepsis, and long term total parenteral nutrition use.

There is insufficient evidence to recommend routine screening for chronic cholecystitis. However, screening ultrasound can be used in children presenting with abdominal pain. Bile amylase concentration may also be a useful screening tool for chronic cholecystitis.

Cholecystitis presents with abdominal pain, which is not relieved by antacids and postural changes and lasts longer than 6 hours. It is sometimes preceded by attacks of biliary pain (due to gallstones). Untreated cholecystitis resolves spontaneously in half of the uncomplicated cases without surgery in a span of 7 – 10 days. The complications of chronic cholecystitis include gangrenous cholecystitis, perforation of the gallbladder, Mirizzi syndrome, gallstone ileus, and gallbladder malignancies.

Cholescintigraphy is the gold standard for the diagnosis of chronic cholecystitis. Transabdominal ultrasonography is the initial study of choice for the diagnosis of chronic cholecystitis and gallstones.

The patients with chronic cholecystitis may have the history of recurrent episodes of biliary colic or acute cholecystitis. A positive history of biliary colic, nausea and vomiting are suggestive of chronic cholecystitis. The most common symptoms of chronic cholecystitis are right upper quadrant abdominal or epigastric pain, pain is usually prolonged and there is a positive history of pain after ingestion of heavy fatty meals. The pain is severe and steady and may radiate to the back or right shoulder.

Patients with chronic cholecystitis may have malaise during the episode. The physical examination in chronic cholecystitis is remarkable for tender right upper quadrant, fever (usually low grade in uncomplicated cases) and a positive Murphy’s sign.

Patients with acute cholecystitis are much more likely to manifest abnormal laboratory values, while in chronic cholecystitis the laboratory values are frequently normal. Laboratory findings consistent with the diagnosis of chronic cholecystitis include elevated alkaline phosphatase, leukocytosis and elevated bilirubin. Amylase may also be elevated.

There are no associated EKG findings associated with chronic cholecystitis. However, chronic 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 does not aid diagnosis of chronic cholecystitis. It is performed as an initial evaluation to diagnose the complicated gallbladder disease.

Sonography is the most effective initial modality for the diagnosis of chronic cholecystitis. The 2 major diagnostic criteria are cholelithiasis and sonographic Murphy’s sign. Other findings may include gallbladder wall thickening, and gallbladder dilatation or contraction.

CT scan findings associated with chronic cholecystitis include gallbladder wall thickening, gallbladder distension or contraction and subserosal edema.

Abdominal MRI may be helpful in the diagnosis of chronic cholecystitis. Findings on MRI suggestive of chronic cholecystitis include thickening of the gallbladder and gallstones.

HIDA cholescintigraphy is the most sensitive and accurate modality for the diagnosis of chronic cholecystitis. HIDA cholescintigraphy findings for chronic cholecystitis include delayed gallbladder isotope accumulation, irregular gallbladder filling, or photopenic areas and septations.

The histopathological analysis may be helpful in the diagnosis of chronic cholecystitis. Findings suggestive of chronic cholecystitis include lymphocytic inflammatory infiltrates, metaplasia, fibrosis, lipid and mucolipid accumulation in gallbladder wall.

The mainstay of treatment for chronic cholecystitis is surgery. Supportive measures are instituted to prepare the patient for surgery. These include antimicrobial therapy and fluid resuscitation. If the chronic cholecystitis is superimposed by acute cholecystitis antibiotics can be used. Commonly used antibiotics are Cefazolin, Cefuroxime, and Ceftriaxone.

Gallbladder removal, cholecystectomy, can be accomplished by the open surgery or a laparoscopic procedure. Laparoscopic cholecystectomy is the operation of choice in uncomplicated calculous cholecystitis. Open cholecystectomy may be performed in complicated cases or when trained/skilled personal for laparoscopic procedure is not available. Supportive measures are instituted in the meantime to prepare the patient for surgery. These measures include fluid resuscitation and antibiotics. Antibiotic regimens usually consist of a broad spectrum cephalosporin such as ceftriaxone and an antibacterial with good cover against anaerobic bacteria, such as metronidazole.

There are no established measures for the primary prevention of 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], Aditya Govindavarjhulla, M.B.B.S. [3]

Gallstones have been 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 chronic cholecystitis. Laparoscopic cholecystectomy was developed to treat chronic 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][7]

• 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%.
• In 1949, eosinophilic cholecystitis was first described.^[8]
• In 1976, xanthogranulomatous cholecystitis (XGC) was discovered by J.J. McCoy, Jr., and colleagues. Xanthogranulomatous cholecystitis is a rare form of gallbladder disease which mimics gallbladder cancer although it is not cancerous.
• Historically, open cholecystectomy was the treatment employed for the treatment of chronic cholecystitis.
• Laparoscopic cholecystectomy was developed to treat chronic cholecystitis and the shift from open to laparoscopic cholecystectomy occurred in the late 1980s.

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

Common causes of cholecystitis include cholelithiasis and infections.

Life-threatening causes include conditions which may result in death or permanent disability within 24 hours if left untreated. Acute cholecystitis may become complicated as abscess, gangrene or perforation in patients who are older, with diabetes or who delay seeking treatment. This complicated acute cholecystitis can by itself be life-threatening.^{[1][2][3][4][5]}

Common causes of chronic cholecystitis include:

• Bacteroides
• Cholelithiasis
• Escherichia coli

Less common causes of chronic cholecystitis include:

• Sickle cell disease
• Drugs such as:
  • Octreotide
  • Oral contraceptives
  • Estrogen

Cardiovascular	Cholesterol emboli, gall bladder ischemia, hemobilia, vasculitis
Chemical/Poisoning	No underlying causes
Dental	No underlying causes
Dermatologic	No underlying causes
Drug Side Effect	Ceftriaxone, clofibrate, febuxostat, estrogen, octreotide, opiates, oral contraceptives, Pergolide, pramipexole, Rilpivirine, Sorafenib, sunitinib, Teduglutide, Tiagabine, zonisamide
Ear Nose Throat	No underlying causes
Endocrine	No underlying causes
Environmental	No underlying causes
Gastroenterologic	Acalculous cholecystitis, ampullary stenosis, calculous cholecystitis, cholelithiasis, cirrhosis, Crohn’s disease, gall bladder ischemia, gallbladder carcinoma, gallstones, hemobilia, hepatocellular carcinoma, liver abscess, pancreatic tumor
Genetic	Choledochal cyst, sickle cell disease
Hematologic	Hemolysis, sickle cell disease
Iatrogenic	Percutaneous transhepatic cholangiography
Infectious Disease	Ascaris lumbricoides, bacteroides, brucella, campylobacter jejuni, candida, choledochal cyst, coxiella burnetii, echinococcus granulosus, edwardsiella tarda, epstein-barr virus, escherichia coli, flavivirus, hepatitis A, hepatitis B, HIV, infections, isospora, klebsiella, leptospira, liver abscess, microsporidiosis, mycobacterium tuberculosis, opisthorchiasis, plasmodium, salmonella enterica, salmonella infections, salmonella typhi, typhoid fever, vibrio cholerae
Musculoskeletal/Orthopedic	No underlying causes
Neurologic	No underlying causes
Nutritional/Metabolic	No underlying causes
Obstetric/Gynecologic	No underlying causes
Oncologic	Acute myelogenous leukemia, gallbladder carcinoma, hepatocellular carcinoma, malignancy, pancreatic tumor
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	Crohn’s disease, Sjogren’s syndrome, SLE, vasculitis
Sexual	No underlying causes
Trauma	Cholesterol emboli
Urologic	No underlying causes
Miscellaneous	Idiopathic

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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]

Chronic cholecystitis must be differentiated from other conditions that affect the gallbladder and biliary tract such as biliary colic, choledocholithiasis, and cholangitis. Chronic cholecystitis must also be differentiated from colitis, functional bowel syndrome, hiatal hernia, and peptic ulcer disease.

Cholecystitis must be differentiated from other conditions that affect the gallbladder and biliary tract such as biliary colic, choledocholithiasis, and cholangitis. Chronic cholecystitis must be differentiated from colitis, functional bowel syndrome, hiatal hernia, and peptic ulcer diseasse.^[1][2][3]

• The symptoms of chronic cholecystitis are non-specific, thus chronic cholecystitis may be mistaken for other common disorders such as:
  • Colitis
  • Functional bowel syndrome
  • Hiatus hernia
  • Peptic ulcer

• Cholecystitis must be differentiated from other diseases that cause right upper quadrant pain and nausea/vomiting such as:
  • Biliary colic
  • Cholangitis
  • Viral hepatitis
  • Alcoholic hepatitis
  • Pancreatitis
  • Irritable bowel syndrome

• Biliary colic
  • Caused by obstruction of the cystic duct
  • Sharp and constant epigastric pain without fever
  • Murphy’s sign is negative
  • Liver function tests are normal

• Choledocholithiasis
  • Blockage of the common bile duct
  • Associated with ‘colicky’ pain
  • Obstructive jaundice
  • Liver function tests – increase in serum bilirubin, high conjugated bilirubin, raised GGT and ALP

• Cholangitis
  • An infection of entire biliary tract.
  • It may involve pathogens of distal bowels and is also known as ‘ascending cholangitis.
  • The classical sign of cholangitis is Charcot’s triad – which is right upper quadrant pain, fever and jaundice.
  • Liver function tests – increase if enzymes (AST, ALT, ALP, GGT) with raised bilirubin.
  • Bile is an extremely favorable growth medium for bacteria and infections develop rapidly and become quite severe.

Chronic cholecystitis must be differentiated from the following diseases on the basis of right upper quadrant pain:

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 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

References

1. ↑ Bluth, Edward I.; Benson, Carol B.; Ralls, Philip W.; Siegel, Marilyn J. (2008). “1: Right Upper Quadrant Pain”. doi:10.1055/b-0034-71418.
2. ↑ Knab LM, Boller AM, Mahvi DM (2014). “Cholecystitis”. Surg. Clin. North Am. 94 (2): 455–70. doi:10.1016/j.suc.2014.01.005. PMID 24679431.
3. ↑ Sung JY; Costerton JW; Shaffer EA (1992). “Defense system in the biliary tract against bacterial infection”. World J. Gastroenterol. 37 (5): 689–96. doi:10.1007/BF01296423. PMID 1563308.CS1 maint: Multiple names: authors list (link)

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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], Aditya Govindavarjhulla, M.B.B.S. [3]

It is estimated that 20 to 25 million Americans (10%–15% of the population) have gallstones. However, only 1-4% experience symptomatic gallstone diseases. Gallstone disease 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. Females are more commonly affected by gallstone diseases than males for calculous cholecystitis. Males are at increased risk compared to females for acalculous cholecystitis following trauma and burns.

The epidemiology and demographics of chronic cholecystitis is given bellow:

• It is estimated that 20 to 25 million Americans (10%–15% of the population) have gallstones. However, only 1000 to 4000 per 100, 000 (1-4%) individuals experience symptomatic gallstone diseases.^[1][2][3][4]

• It is estimated that 12000 to 13000 (12% to 13%) per 100,000 individuals with chronic cholecystitis have no demonstrable stones.^[1]

• The risk of gallstone diseases increases with age.^[5]

• 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.^[2][6]

• Females are more commonly affected by gallstone diseases than males for calculous cholecystitis.^[2][6]
• Males are at increased risk compared to females for acalculous cholecystitis following trauma and burns.^[7]

Gallstone diseases are comparatively less prevalent in the developing countries.^[2]

• Gallstone disease accounts for 700,000 cholecystectomies and costs of ∼$6.5 billion annually only in the United States.^[2]
  • 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.^[2]
  • 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], Aditya Govindavarjhulla, M.B.B.S. [3]

Common risk factors in the development of calculous cholecystitis (cholelithiasis) include female gender, increasing age, obesity, pregnancy, family history, genetic factors, and oral contraceptive use. Common risk factors in the development of acalculous cholecystitis include AIDS, diabetes mellitus, major surgery, burns, sepsis, and long term total parenteral nutrition use.

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.^[1][2][3][4]

• Common risk factors in the development of chronic calculous cholecystitis are:
  • Advancing age
  • Female gender
  • Obesity
  • Multi parity
  • Family history
  • Genetic factors
  • Oral contraceptives
  • Diabetes
• Common risk factors in the development of acalculous cholecystitis are:^[5]
  • Long lasting fasting
  • Total parenteral nutrition (TPN)
  • Weight loss
  • Severe burns
  • Sepsis
  • Diabetes Mellitus
  • Major surgery

• Less common risk factors in the development of acute cholecystitis include:^[6]
  • Infections
    • Bacterial
    • Protozoal
  • AIDS

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] ; Associate Editor(s)-in-Chief: Aditya Govindavarjhulla, M.B.B.S. [2], Furqan M M. M.B.B.S[3]

There is insufficient evidence to recommend routine screening for chronic cholecystitis. However, screening ultrasound can be used in children presenting with abdominal pain. Bile amylase concentration may also be a useful screening tool for chronic cholecystitis.

There is insufficient evidence to recommend routine screening for chronic cholecystitis. However, screening may be considered in the following scenarios:^[1][2][3]

• Point of care ultrasound can be used as a screening tool in pediatric cholecystitis, where children present with abdominal pain.
• In critically ill patients, ultrasound has insufficient evidence to be a sensitive screening test for acalculous cholecystitis.
• For chronic cholecystits due to pancreatic biliary reflux, bile amylase concentrations may be a useful screening tool.

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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]

Cholecystitis presents with abdominal pain, which is not relieved by antacids and postural changes and lasts longer than 6 hours. It is sometimes preceded by attacks of biliary pain (due to gallstones). Untreated cholecystitis resolves spontaneously in half of the uncomplicated cases without surgery in a span of 7 – 10 days. The complications of chronic cholecystitis include gangrenous cholecystitis, perforation of the gallbladder, Mirizzi syndrome, gallstone ileus, and gallbladder malignancies.

The natural history of chronic cholecystitis is as under:

• Cholecystitis presents with abdominal pain, which is not relieved by antacids and postural changes and lasts longer than 6 hours.
• It is sometimes preceded by attacks of biliary pain (due to gallstones).
• Fever may not be a prominent symptom at the time of presentation but can be seen if untreated or complicated by infections.
• Untreated cholecystitis resolves spontaneously in half of the uncomplicated cases without surgery in a span of 7 – 10 days.
• The remaining cases can progress to complications and cause severe morbidity and mortality.^[1]

The complications of chronic cholecystitis include:

Mirizzi syndrome is due to the partial obstruction of the common hepatic bile duct. This can be secondary to stone impaction or chronic inflammation in the adjacent gallbladder Hartman pouch.^[1]

• Gangrenous cholecystitis may occur following severe inflammation that interrupts the blood flow to the gallbladder. It is potentially more life-threatening because the dead tissues are vulnerable to secondary severe infections, which can spread to become sepsis.^[2][3]
  • The known risk factors are:
    • Male gender
    • Age above 50 years
    • Leukocytosis
    • Diabetes
    • Cardiovascular diseases

• CT scan is a better tool in the evaluation of gangrenous cholecystitis. The mortality rate of gangrenous cholecystitis is as high as 22% since it can lead to gallbladder perforation, abscess formation and peritonitis. So once suspected, an emergency cholecystectomy is done to reduce the morbidity and mortality due to its life threatening complications^[4].

Gallbladder perforation (GBP) is a rare but life-threatening complication of cholecystitis. The early diagnosis and treatment of GBP are crucial to patient morbidity and mortality.^[2][3][5][6]

Gallstone ileus is the result of mechanical obstruction of the small bowel due to the gallstones. Gallstones reach the bowel through a fistulous channel between gallbladder and the small intestine.^[1][6]

• The following growths may arise in chronic gallbladder infection:^[3][6]
  • Benign
    • Papilloma
  • Malignant
    • Adenocarcinoma
    • Papillary carcinoma
    • Squamous cell carcinoma

Uncomplicated cholecystitis has a favorable prognosis. Complicated cases can be treated successfully with surgery and they usually do well.^[7]

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