A 46-year-old with right upper quadrant pain

• Symptomatic cholelithiasis: RUQ pain radiating to the right back after fatty meals, resolves after a few hours, multigravid, obese
• Acute cholecystitis: Persistent (> 4h) severe RUQ pain, fever, Murphy’s sign
• Acute cholangitis: Persistent RUQ pain, fever, jaundice (Charcot’s triad)
• Acute pancreatitis: Severe epigastric pain radiating straight through the back, due to cholelithiasis (gallstone pancreatitis) or alcohol abuse
• Acute gastritis: Gnawing epigastric pain, aspirin, NSAIDs, Steroids
• Peptic ulcer disease: Intermittent burning epigastric pain that improves (duodenal) or worsens (gastric) with food intake, due to H. pylori, NSAIDs, Steroids
• Malignancy (gastric, pancreatic, biliary): Chronic pain, weight loss, fatigue
• Fitz-Hugh-Curtis syndrome: RUQ pain, H/O pelvic inflammatory disease (Chlamydia or Neisseria gonorrhea), fever, “violin string” adhesions between the liver and diaphragm
• Myocardial infarction: Epigastric pain (referred), diabetes, cardiovascular disease, hypercholesterolemia
• Acute hepatitis: Recent travel, intravenous drug use, unprotected sexual contact
• Hepatic abscess: RUQ pain, high fever, hepatomegaly (bacterial or amoebic)
• Acute pyelonephritis: Costovertebral angle tenderness, dysuria, hematuria

• • Suggests a biliary origin of the pain
  Fatty foods trigger the release of cholecystokinin (CCK) which leads to contraction of the gallbladder. Gallstones may obstruct the cystic duct such that the gallbladder is unable to empty. The gallbladder is distended stretching the visceral peritoneum that surrounds it. This leads to right upper quadrant or epigastric pain that is vague and mild-to moderate in severity

• The gallbladder and scapula share the same cutaneous dermatome from the same spinal level.

The gallbladder is innervated by the phrenic nerve

The scapula is innervated by the supraclavicular nerve

• Female gender
• Parity
• Age > 40 years
• Obesity
• Parity
• High-fat diet

Patients with biliary disease often have the 4 Fs – female, fat, forty, fertile

Other risk factors include heredity (hispanics, pima indians), crohn’s disease, terminal ileal resection, and rapid weight loss after bariatric surgery

A high-fat diet increases cholesterol in bile

High estrogen (female, pregnancy, and oral contraceptive use) leads to higher cholesterol in bile and reduced gallbladder motility

In obesity there is a decrease in bile salts

In Cronhn’s disease and terminal ileal resection enterohepatic circulation is impaired leading to loss of bile salts as less is reabsorbed

Rapid weight loss after bariatric surgery is associated with impaired gallbladder emptying

• Symptomatic cholelithiasis is a constant, dull right upper quadrant or epigastric abdominal pain that is caused by transient blockage of the cystic duct or common bile duct by stones

Biliary colic is a misnomer. The pain from gallstones is not technically colicky. Colicky pain typically waxes and wanes with periods of intense pain e.g. ureter intermittently contracting in the presence of a stone. The pain from gallstones is constant and may last from minutes to hours before dissipating

Symptomatic cholelithiasis is a better term to use

Every year 3-5% of patients with symptomatic cholelithiasis develop complications. These include acute cholecystitis, chronic cholecystitis, choledocholithiasis, cholangitis, gallstone pancreatitis, fistula with gallstone ileus, and rarely gallbladder cancer

• Smoking
• Parity

• Escherichia coli
• Bacteroides fragilis
• Klebsiella
• Enterobacter
• Enterococcus
• Pseudomonas

Gram negative rods and anaerobes

• Bile salts
• Cholesterol
• Lecitihin

• Admirand’s triangle describes the physiochemical basis of formation of cholesterol gallstones based on the concentration of cholesterol, lecithin, and bile salts. If there is an imbalance of these components, cholesterol or bilirubin may precipitate out forming stones
• Cholesterol gallstones form when its concentration increases and overwhelms the dissolving capability of bile salts, or when there is a reduction in the concentration of lecithin and bile salts.
• Supersaturation of bile with calcium bilirubinate (in hemolysis) gives rise to pigmented stones

The major organic solutes in bile are bilirubin, cholesterol, bile salts and phospholipids (lecithin).

• Black stones are associated with hemolytic diseases e.g. sickle cell disease. The amount of unconjugated bilirubin increases leading to the formation of black stones.
• Brown stones are larger and softer than brown stones and are associated with bacterial infection and parasite infestation.

Black stones are often found in the gallbladder

Brown stones form in the bile ducts

• Symptomatic cholelithiasis: Transient obstruction of the cystic duct → visceral peritoneum stretches → dull RUQ pain
• Acute cholecystitis: Persistent obstruction of the cystic duct → stretching, inflammation and ischemia of the gallbladder → inflammation of the parietal peritoneum
• Choledocholithiasis: Obstruction of the common bile duct
• Cholangitis: Obstruction of the common bile duct → bacterial overgrowth → inflammation of the entire biliary tree ascending into the liver
• Gallstone pancreatitis: Obstruction of the pancreatic duct and common bile duct → inflammation of the pancreas caused by obstruction of pancreatic enzymes
• Gallstone ileus: Large stone erodes into the duodenum (gallbladder-duodenal fistula) → stone travels in GI tract and is trapped in the ileocecal valve (narrowest part of the GI tract) → small bowel obstruction (misnomer! not an ileus)
• Mirizzi syndrome: Large gallstone impacted in the cystic duct → compression of the common hepatic duct

• The infundibulum (Hartmann’s pouch)

It is the convex, enlarged, redundant and dependent aspect at the neck of the gallbladder

Symptomatic cholelithiasis is managed as outpatient with an elective laparoscopic cholecystectomy

Acute cholecystitis requires admission, IV antibiotics and IV fluids. Urgent cholecystectomy can be planned as indicated.

• These are systemic signs of infection

Fever and tachycardia suggest a more severe biliary disease e.g. acute cholecystitis or acute cholangitis

Symptomatic cholelithiasis does not present with systemic symptoms

• This is called Murphy’s sign.
• It represents localized peritonitis of the right upper quadrant anterior wall parietal peritoneum due to inflammation of the adjacent gallbladder

Increased intrathoracic pressure during inspiration pushes the liver and gallbladder inferiorly to come into contact with the palpating hand. Pain is felt immediately when the fundus of the gallbladder contacts the examiner’s hand causing cessation of breathing from the pain

Murphy’s sign is specific for acute cholecystitis

It is only positive if palpation of the LUQ does not reproduce the pain

A phlegmon (adherent omentum or bowel) may also be palpable in the RUQ

• Complete Blood Count: for leukocytosis and left-shift
• Hepatobiliary (RUQ) ultrasound: Diagnostic test of choice
• Liver Function Test: for total bilirubin, ALP, GGT and AST, ALT
• Amylase and Lipase: to rule out gallstone pancreatitis

• Normal gallbladder wall thickness ranges from 1-2 mm
• Normal CBD diameter ranges from 4 – 6 mm

A CBD > 6mm is considered abnormally dilated and suggests obstruction from either a gallstone or tumor. Diameter increases ~1mm per decade after age 40.

Gallbladder wall thickness > 3mm is abnormal

• Ultrasound is 95% sensitive and 97% specific for gallstones (even as small as 1-2 mm)

It is however poor in detecting gallstones within the CBD (50% sensitivity) since gas from the bowel can interfere with transmission of ultrasound waves

• Thickened gall bladder wall > 3 mm
• Pericholecystic fluid
• Probe tenderness (sonographic Murphy’s sign)

Gallstones appear as hyperechoic structures with distal acoustic shadowing

• Polyps do not change position when the patient moves

Polyps > 1cm are suspiscious for cancer. > 2cm have a high likelihood of cancer

Gallbladder cancer is associated with gallstones. Always take gallbladder specimen for histology and check the final pathology report

• Emphysematous cholecystitis

Occurs when the gallbladder is infected with gas-forming organisms e.g. Clostridium.

Similar to a nectrotizing soft tissue infection. It is common in older men, often with diabetes mellitus.

Emphysematous cholecystitis can progress to gallbladder perforation, intra-abdominal abscess, sepsis and death is emergency cholecystectomy is not performed

Pneumobilia (air in the biliary tree due to gallstone ileus – fistula between the gallbladder and duodenum) can be confused with emphysematous cholecystitis

• Thickened bile

May cause obstruction

• Possibilities
  • False-negative ultrasound (< 5%, rare)
  • Acalculous cholecystitis (mostly in critically ill patients)
  • Other non-biliary causes
• Cholescintigraphy (HIDA scan) is the next diagnostic test of choice

False-negative ultrasound occurs when stones are very small (<1mm) or very few

Long term TPN in critically ill patients can cause acalculous cholecystitis due to sludging. Biliary stasis and ischemia in these patients lead to cholecystitis. Other features of gallbladder inflammation e.g. wall thickening and pericholecystic fluid will be present in this case.

Acalculous cholecystitis has a high morbidity and mortality. It can be treated emergently by cholecystostomy tube to decompress the gallbladder or cholecystectomy if the patient is a reasonable surgical candidate.

In a HIDA scan, radiolabelled hepatic iminodiacetic acid is given IV and imaging is performed. The compound is absorbed by hepatocytes and excreted into bile and seen within 30-60 minutes in the gallbladder, bile ducts and small bowel in a normal patient.

• No contrast is seen in the gallbladder within 2-4 hours since the cystic duct is obstructed

HIDA scan is also helpful in patients with bile leaks to determine the source of the leak and in patients with impaired gallbladder emptying from non-obstructive causes (biliary dyskinesia)

• Yes

HIDA > Ultrasound > CT-Scan

CT scan is not as sensitive as ultrasound and HIDA. But it can be used to deliniate biliary tree and adjacent structures especially with malignancy.

Lipase has a higher sensitivity for pancreatitis than amylase

• Acute cholecystitis
  • She has a history of severe persistent right upper quadrant and epigastric abdominal pain following ingestion of fatty food, nausea, and vomiting
  • The right upper quadrant and epigastric region show tenderness to palpation
  • She has fever, tachycardia, and an elevated WBC count
  • Murphy sign is positive
  • She also has a history of symptomatic cholelithiasis
  • There are stones in her gallbladder, gallbladder wall thickening and pericholecystic fluid
  The normal total bilirubin and alkaline phosphatase make choledocholithiasis and cholangitis less likely. The diameter of her CBD is also normal. Normal amylase and lipase rule out gallstone pancreatitis

90%

• Patients with unrelenting abdominal pain, high fever, persistent tachycardia, markedly elevated WBC count and/or hyponatremia

Common in elderly men and diabetes mellitus

Acute cholecystitis is part of a clinical spectrum that can progress to gangrenous cholecystitis (gallbladder wall becomes necrotic). This can lead to severe sepsis and gallbladder perforation

Emergency cholecystectomy is required to prevent the increased morbidity associated with delay

• If there is Charcot’s triad
  • Right upper quadrant pain
  • Jaundice
  • Fever

Cholangitis commonly occurs following choledocholithiasis. Combined acute cholecystitis and cholangitis is uncommon but can occur.

Reynold’s pentad (Charcot’s triad + Hypotension + Altered Mental Status) if present represents fulminant septicemia in patients with cholangitis

Cholangitis requires immediate decompression of the biliary tract, often with ERCP, although percutaneous transhepatic cholangiography with drainage ccan be performed if ERCP is not an option

• Admission
• Nil per mouth (NPO)
• Analgesia
• IV fluids
• IV antibiotics targeting gram-negative and anaerobes
• Cholecystectomy ideally within 48 hours

• Antibiotics should cover gram-negatives and aerobes

Second generation cephalosporins e.g. Cefoxitin, Cefuroxime and first generation cephalosporins e.g. Cefazolin

Broad-spectrum penicillin/B-lactamase inhibitors e.g. Piperacillin/Tazobactum or Ampicillin/Sulbactum can be used as an alternative

Third and fourth generation cephalosporins can be used in severe cases

• Tokyo Consensus Guidelines for severity grading of acute cholecystitis

Grade III patients can be managed operatively if their status permits. Percutaneous cholecystostomy can be performed to rapidly relieve symptoms if the patient is not fit for surgery.

• Cholecystostomy (drainage of the gallbladder)
• Cholecystectomy (removal of the gallbladder)
• Intra-operative cholangiogram and common bile duct exploration (to evalute and clear stones from the common bile duct)

Cholecystostomy tube can be placed transperitoneal or transhepatic.

• Ideally should be performed within 48 hours of admisssion

Early cholecystectomy during acute cholecystitis is safe and shortens total hospital stay

Current opinion recognizes that a lengthy waiting period before operating on acute cholecystitis is unnecessary. It prolongs hospital stay and makes laparoscopic cholecystectomy difficult since the gallbladder becomes scarred, distorting its anatomy, increasing the risk of CBD injury and conversion to open cholecystectomy

• Ongoing coagulopathy
• End-stage liver disease
• Hemodynamic instability
• Inability to tolerate general anaesthesia

• Congestive heart failure (with poor ejection fraction)
• COPD where pneumoperitonum may not be tolerated

• No

Every year 3-5% of patients with symptomatic cholelithiasis develop complications.

These include acute cholecystitis, chronic cholecystitis, choledocholithiasis, cholangitis, gallstone pancreatitis, fistula with gallstone ileus, and rarely gallbladder cancer

• In critically ill patients with acute cholecystitis
• In patients with an unacceptable amount of operative risk (high-risk surgical patients)

A percutaneously placed cholecystostomy tube can be used to decompress the inflamed gallbladder. It can represent a permanent solution (when the gallbladder becomes fibrotic afterwards), or can be followed by interval cholecystectomy depending on clinical status

• Calot’s (Hepatocystic) triangle

Should be visualized during laparoscopic cholecystectomy before dividing any structures

The critical view of safety (including the cystic duct and cystic artery dissected from surrounding fat and fibrous tissue) should be identified, called out, and confirmed before ligating the cystic artery and cystic duct. They should be the only two structures attached to the gallbladder and the liver should be visible behind with no other structures in the field

• This is when the right hepatic artery originates from a vessel other than the common hepatic artery and is the sole blood supply to the right lobe of the liver

Commonly arises from the superior mesenteric artery. About 10-15% of patients have a replaced right hepatic artery.

A replaced right hepatic artery is more prone to injury because of its orientation and proximity to the cystic duct

• Common Bile Duct injury

The most feared complication of laparoscopic cholecystectomy. There is a higher risk of CBD injury during surgery for acute cholecystitis compared to symptomatic cholelithiasis

The injury is often made is the CBD is mistaken for the cystic duct and inadvertently divided

• Primary repair over a T-tube that acts as a secondary stent (if injury involves less than 50% of the bile duct wall and is not due to cautery)
• Roux-en-Y hepaticojejunostomy if more than 50% of the circumference of the bile duct has been injured

Bile duct injury is uncommonly identified at operation. More than half of patient present within the first pos-operative month

Intra-operative cholangiogram can be performed to rule out injury. It must show the right and left hepatic ducts and common hepatic duct, cystic duct, common bile duct and flow of contrast into the duodenum in order to adequately rule out injury or bile duct stone

Attempting primary repair in large injuries will inevitably form a strictures. Strictures cause recurrent cholangitis and eventually cirrhosis which ultimately requires trasnplant

• Presents post-operatively with abdominal pain, bloating, anorexia and elevated LFTs
• Ultrasound or CT-scan of the abdomen/pelvis shows large intraperitoneal fluid collection which can either be blood (from liver injury or cystic artery bleed) or bile leak (bilioma)

If the patient presents with sepsis a drain should be placed

HIDA scan can be obtained to see if bile is leaking or flowing to the duodenum. ERCP can be performed if bile is leaking or if there is no bile entering the duodenum.

• Liver injury
• Cystic duct stump leak
• Common hepatic duct injury
• CBD injury

Bile leaks tend to present before biliary strictures. Late presentation of strictures can occur months or years after the procedure with recurrent cholangitis or cirrhosis

If the cystic duct stump is leaking a stent can be placed in the sphicter of Oddi to create a path of less resistance for bile flow. A cystic duct leak generally resolves with this treatment.

If the CBD or common hepatic duct is injured the patient will most likely require a hepaticojejunostomy

• • Infection
  • Bleeding
  • Vascular injury
  • Retained bile duct stones
  • injury to surrounding structures including the colon, duodenum, or liver
  • Inability to complete cholecystectomy or partial cholecystectomy
  • Need for drain placement
  • Poor wound healing
  • Hernia
  • Pain
  • Myocardial infarction
  • Stroke
  • Deep Venous thrombosis or pulmonary embolism
  • Death
  Similar risks for bot open and laparoscopic cholecystectomy. But the risk of bile duct injury is higher in laparoscopic cholecystectomy and there is a risk of conversion to an open procedure.

• Post-cholecystectomy syndrome (PCS)

Investigations should include CBC, LFTs, and RUQ ultrasound. If an ongoing pathology in the biliary tree is suspected ERCP can be performed.