Hepatobiliary Disease
Content
Advisor : dr dr. Sjaiful Bachri, SpB SpB Melissa L. Thenata Fakultas Kedokteran Universitas Tarumanag Tarumanagara ara
Liver Structure
Largestt gland in the body Larges (1.5 Kg)
Under the diaphragm, within the rib cage in the upper right quadrant of the
abdomen
Liver Structure
4 lobes: major (left and right), minor (caudate and quadrate)
Ducts: common hepatic, cystic from gall bladder, common bile – choledochus (join ( join pancreatic
duct at hepatopancrea hepatopancreatic tic ampulla)
Liver Structure
Liver lobules – hexagonal structures consisting consisting of hepatocytes
Hepatocytes radiate radiate outward from a central c entral vein
At each of the six corners of a lobule is a portal triad
Liver sinusoids
Liver Structure
Hepatocytes produce bile
Bile flows through canals called bile canaliculi to a bile duct
Bile ducts leave the liver via the common hepatic duct
Liver Function
Regulating Regula ting homeostasis of carbohyd carbohydrate, rate, lipid and amino acid metabolism.
Storing nutrients such as glyc glycogen, ogen, fats and vitamin B 12, A and K.
Producing and secreting plasma proteins and lipoproteins, including clotting factors factors and acute phase proteins.
Liver Function
Synthesizing and secreting bile salts for lipid digestion.
Detoxifying Detoxi fying and ex excreting creting bilirubin, other endogenous waste products and exogenous metal ions, drugs and toxins (xenobiotics).
Clearing toxins and infective agents from the portal venous blood whilst maintain systemic immune tolerance to antigens in the portal circulation.
Gall Bladder Structure
Thin-walled green muscular sac
On the inferior surface of the liver
Stores bile that is not immediately needed for digestion
When the muscular m uscular wall of the gallbladder contracts contracts bile is expelled into the bile duct
Gall Bladder Structure
Gall Bladder Function
Stores ± 60 mL of bile, released when food containing fat fat enters the digestive tract.
The bile, produced in the liver liver,, emulsifies (breaks down) fats and neutralizes acids in partly digested food.
Biliary Atresia
Obliteration or discontinuity of the extrahepatic biliary system, resulting in obstruction to bile flow, in the first few weeks of life.
Inflammatory process process from an unknown cause affects affects the bile duct in the newborn infant.
Destruction of the extrahepa extrahepatic tic bile ducts, causing obstructive jaundice and liver failure. failure.
Kasai procedure, surgical surgical correction of this abnormality before 8 weeks of age produces the best outcome.
Choledochal Cyst
Cystic dilatation of the intra- or extrahep extrahepatic atic ducts is a rare condition, usually presenting presenting before the age of 16 years.
Symptoms : cholangitis, c holangitis, pancreatitis, stone formation and jaundice. Infants may occasionally present present with an abdominal mass.
The cause of this condition is debated.
Choledochal Cyst
Cysts are classified according to their site and shape, although 80% are fusiform abnormalities of the extrahepatic bile duct. Type II cysts are extremely rare.
Choledochal Cyst
Treated by surgical excision of the cyst with the formation of a roux-en-Y anastomosis to the biliary duct.
Hepatobiliary Trauma
The liver is the most commonly injured solid abdominal organ, despite its relative protected location.
Treatment of traumatic liver injuries is based on patient physiology, mechanism and degree of injury, associated abdominal and extra-abdominal injuries and local expertise.
Hepatobiliary Trauma Liver Organ Injury Scale Grade
I
II
III
Description
Hematoma
Subcapsular Subcapsu lar,, <10% surface area
Laceration
Capsular tear tear,, <1 cm parenchym parenchymal al depth
Hematoma
Subcapsu lar,, <10% - 50% surface area; Subcapsular intraparenchymali, intraparench ymali, <10 cm in length
Laceration
1-3 cm parenchymal depth, <10 cm in length
Hematoma
Subcapsular, >50% surface area or expanding; ruptured subcapsular or parenchymal hematoma
Laceration
<3 cm parenchymal depth
Hepatobiliary Trauma Liver Organ Injury Scale Grade
Description
IV
Hematoma
Parenchymal disruption involving 25% - 75% of Parenchymal hepatic lobe or 1-3 Couinaud segments within a single lobe
V
Laceration
Parenchymal disruption involving >75% of hepatic Parenchymal lobe >3 Couinaud segments within a single lobe
Vascular
Juxtahepatic venous injuries; ie. Retr Retrohepatic ohepatic vena cava/central major hepatic vein
VI
Hepatic avulsion
Management of o f Hepatic Hepatic Trauma Trauma
Gall Bladder Cancer
Highly aggressive malignancy, usually presents at an advanced, incurable stage, 5th most common gastrointestinal tumor
The median survival is less than 6 months after diagnosis
Women : Men = 2 – 6 : 1
The incidence steadily increases with age
Risk factor : obesity, a high-carbohydrate diet, smoking, and alcohol use
Gall Bladder Cancer
Gall bladder cancer arises in the setting of chronic inflammation. In the vast majority of patients (>75%), the source of this chronic inflammation is cholesterol gallstones. gallstones. 10-25% is caused caused by calcifica calcification tion of the gallbladder gallbladder (porcelain (porcelain gallbladder)
Most common type of gallbladde gallbladderr cancer is adenocarcinoma.
Gallbladder cancer can spread by direct invasion invasion through the gallbladder wall into the liver or peritoneal cavity.
Gall Bladder Cancer
The symptoms of gallbladder cancer overlap with the symptoms of gallstones and biliary colic. Abdominal pain may be of a more diffuse and persisten persistentt nature than the classic right upper quadrant pain of galls gallstone tone disease.
Jaundice, anorexia, and weight loss often indicate more advanced disease.
Gall Bladder Cancer Table 2. Summary of the Tumor-NodeTumor-Node-Metastasis Metastasis (TNM) Staging System* Stage
Description
1
Mucosal or muscular invasion (T1N0M0)
2
Perimuscular-tissue invasion (T2N0M0)
3
Transmural invasion, liver invasion < 2 cm; lymph node metastasis to hepatoduodenal ligament (T3N0M0, T1 –3 N1M0)
4A
Liver invasion invasion > 2 cm (T4N0M0, T4N1M0)
4B
Distant nodal (outside porta hepatis) or hematogenous metastasis (TxN2M0, TxNxM1)
Gall Bladder Cancer
The work-up for right-upper-quadrant pain or biliary colic generally starts with an ultrasound examination examination of the gallbladder.
Laboratory Laborat ory tests should include liver function tests and hematocrit. Advanced cases may demonstrate anemia and elevated eleva ted alkaline phosphatase and bilirubin.
Tumor markers, CEA and CA 19-9, 19 -9, may be of help and should be considered if gallbladder cancer is suspected.
Gall Bladder Cancer
Further radiologic work-up such as CT-scan, MRI, or needle biopsy are indicated if gallbladder gallbladder cancer is suspected.
The most common and most mo st effective effective treatment is surgical removal remov al of the gallbladder (cholecystectomy) (cholecystectomy) with part of liver and lymph node dissection.
Chemotherapy has not shown significant activity in gallbladder carcinoma. Typically, 5-fluorouracil (5-FU) has been used with response rates of 10-24% in advanced disease.
Gall Bladder Cancer
Gemcitabine has shown activity in gallbladder cancer. There is an increased response rate with gemcitabine combination with cisplatinum and capecitabine.
Currently, no clearly defined standard exists for chemotherapy in gallbladder cancer. Patients should be encouraged to participate in clinical trials.
Cholangiocarcinoma
Cholangiocarcinomas are malignancies of the biliary duct system that may originate in the liver and extrahepatic bile ducts, which terminate at the ampulla of Vater. Vater.
The etiology of most bile duct cancers remains undetermined. However, one of the most commonly recognized risk factors is primary sclerosing cholangitis.
Cholangiocarcinoma arises from the intrahepatic or extrahepatic biliary epithelium. More than 90% are adenocarcinomas.
Cholangiocarcinoma
Cholangiocarcinomas tend to grow slowly and to infiltrate the walls of the ducts, dissecting along tissue t issue planes.
Local extension occurs into the liver, porta hepatis, and regional lymph nodes of the celiac and pancrea pancreaticoduodenal ticoduodenal chains.
Symptoms of cholangiocarcinoma include jaundice, clay-colored stools, bilirubinuria (dark urine), pruritus, weight loss, and abdominal pain.
Cholangiocarcinoma
The diagnosis and staging of cholangiocarcinoma require require a multimodality approach involving laboratory, radiologic, endoscopic, and pathologic analysis.
The most studied serum tumor markers are the CA 19-9, 19 -9, is currently the most commonly used tumor marker for cholangiocarcinoma.
Surgical resection with curative intent is the treatment of choice for extrahepa extrahepatic tic cholangiocar cholangiocarcinoma. cinoma.
Gallstones
Two major types of gallstones: cholesterol and pigment stones. Cholesterol gallstones contain50% cholesterol monohydrate. Pigment stones have 20% cholesterol cholester ol and are composed primarily of calcium bilirubinate.
Predisposing factors include demographic/ demographic/genetics, genetics, obesity, weight loss, female sex hormones, age, ileal disease, pregnancy, type IV hyperlipidemia, and cirrhosis.
Gallstones
Many gallstones are “silent”.. Symptoms occur “silent”
when stones produce inflammation or obstruction of the cystic or common bile ducts.
Gallstones
Major symptoms: (1) biliary colic —a severe steady ache in the RUQ or epigastrium that begins suddenly; often occurs 30 –90 min after meals, lasts for several hours, and occasionally radiates radiat es to the right scapula or back; (2) nausea, vomiting. Physical Physic al exam may be normal or show epigastric or RUQ tenderness.
Mild and transient elevations elevations in bilirubin [85 mol/L (5 mg/dL)] mg /dL)] accompany biliary colic.
Gallstones
Only 10% of cholesterol gallstones are radiopaque. USG is best diagnostic test.
Elective cholecystectomy should be reserved for: (1) symptomatic patients; (2) persons with previous complications of cholelithiasis; and (3) presence of an underlying condition predisposing to an increased increas ed risk of complications (calcified or porcelain gallbladder).
Gallstones
Patients with gallstones 3 cm or with an anomalous gallbladder containing stones should be considered for surgery.
Laparoscopic cholecystectomy is minimally invasive and is the procedure of choice for most patients undergoing elective cholecystectomy.
Oral dissolution agents (ursodeoxycholic (ursodeoxycholic acid) partially or completely dissolve small radiolucent stones in 50% of selected pts within 6 –24 months.
Gallstones
Extracorporeal Extracorpor eal shockwav shockwave e lithotripsy followed by medical litholytic therapy is effective in selected patients with solitary radiolucent gallstones. gallstones. Because of the frequency of stone recurrence and the effectiveness of laparoscopic surgery, the role of oral dissolution therapy and lithotripsy has been reduced to selected patients who are not candidates for for elective cholecystectomy.
Acute Cholecystitis
Acute inflammation of the gallbladder usually caused by cystic duct obstruction by an impacted stone.
90% calculous; 10% acalculous.
Acalculous cholecystitis associated with higher complication rate and associated with acute illness (i.e., burns, trauma, major surgery), fasting, hyperalimentation leading to gallbladder stasis, vasculitis, carcinoma of gallbladder or common bile duct, some gallbladder infections but in > 50% of cases an underlying explanation is not found.
Acute Cholecystitis Signs and symptoms :
Attack At tack of bilary colic (RUQ or epigastric pain), progressively worsens worsens
Nausea, vomiting, anorexia
Fever
Examination typically reveals RUQ tenderness
Palpable RUQ mass found in 20% of patients
Murphy’s sign is present when deep inspira inspiration tion or cough during
palpation of the RUQ R UQ produces increased pain or inspirat inspiratory ory arrest.
Acute Cholecystitis
Laboratory Laborat ory : Mild leukocytosis; serum bilirubin, alkaline phosphatase, and AST may be mildly elevated. elevated.
Imaging : Ultrasonography is useful for demonstra demo nstrating ting gallstones galls tones and occasionally a phlegmonous mass surrounding the gallbladder. Radionuclide scans may identify cystic duct obstruction.
Acute Cholecystitis
No oral intake, nasogastric nasogastric suction, IV fluids and electrolytes, analgesia (meperidine or NSAIDS), and antibiotics (ureidopenicillins, ampicillin sulbactam, third-genera third-generation tion cephalosporins; anaerobic coverage coverage should be added if gangrenous gangr enous or emphysemat emphysematous ous cholecystitis is suspected; consider combination with aminoglycosides in diabetic patient or others with signs of gram-negative gram-negative sepsis).
Acute Cholecystitis
Acute symptoms will resolve in 70% of o f patient.
Optimal timing of surgery depends on patient stabilization and should be performed as soon as feasible.
Urgentt cholecystectomy is appropriate in most patients with a Urgen suspected or confirmed complication.
Delayed surgery surgery is reserved for patients with high risk of emergent surgery surgery and where the diagnosis is in doubt.
Chronic Cholecystitis
Chronic inflammation of the gallbladd gallbladder; er; almost alwa always ys associated with gallst gallstones. ones. Results from repeated acute/subacute acute/suba cute cholecystitis or prolonged mechanical irritation of gallbladder wall.
May be asymptomatic for years, may progress to symptomatic gallbladder gallbladd er disease or to acute cholecystitis, or present with complications.
Chronic Cholecystitis
Laboratory Laborat ory tests are usually normal.
Ultrasonography preferred; usually shows gallstones within a contracted gallbladder gallbladder..
Surgery indicated if patient is symptoma symptomatic. tic.
Liver Infections – Pyogenic Abscess
Pyogenic or bacterial abscess may be caused by several factors. Infections may arise from the biliary tract, portal vein and hepatic artery or by direct extension.
Symptoms : pyrexia and rigours associated with right upper quadrant pain, general malaise and anorexia.
Examination may reveal tender hepatomegaly. A pleural effusion may be present. Occasionally, hypotension and cardiovascular collapse may be the presenting symptoms.
Liver Infections – Pyogenic Abscess
Laboratory tests : hyperbilirubinemia, raised alkaline phosphatase and transaminase levels, blood cultures are frequently positive, leucocytosis.
USG / CT scan abdomen : to determine the size, characteristics, number and anatomical location of the liver abscesses.
Chest X-ray : elevated hemidiaphragm or a pleural effusion.
ERCP or a colonoscopy : to determine the cause of pyogenic liver abscesses.
Liver Infections – Pyogenic Abscess Treatment :
Analgesics and attention to adequate nutrition and hydration
Antimicrobial therapy
Drainage Drainag e of the abscess
Frequent clinical, biochemical, microbial and radiologic radiological al follow-up is required to assess progress and detect relapses
Liver Infections – Amoebic Liver Abscess
Amoebic infestation infestation is caused by the organism Entamoeba histolytica .
Transmission is by passage of cysts in the stool, the cysts then being ingested orally as a result of poor hyg hygienic ienic practices.
Risk factors include malnutrition, depressed immunity and low socioeconomic status.
Complications of amoebic abscess include rupture into the peritoneal cavity cavity or hollow viscus such as colon or stomach.
Liver Infections – Amoebic Liver Abscess
The onset of the disease may be sudden or gradual.
The most common symptoms : right upper quadrant pain, general malaise, weight loss, pyrexia and sweating.
Signs : tender hepatomegaly and, occasionally, jaundice.
Full blood examination : leukocytosis and eosinophilia.
Amoebic serology and stool cultures are usually positive.
The antibiotic of choice is metronidazole.
Benign Liver Tumors - Adenoma
Hepatocellular adenomas occur most commonly in women in the third or fourth decades who take birth control pills.
The major concern is their tendency to rupture with massive haemorrhage; therefore, therefore, this condition must be considered in young women presenting with abdominal pain, signs of hypovolaemic hypov olaemic shock and fea features tures of haemoperitoneum.
After resuscitation, the treatment is resection of the aff affected ected liver segment.
Benign Liver Tumors – Focal Nodular Hyperplasia
Focal nodular hyperplasia (FNH) (FNH) is not a true neoplasm but is probably due to a fibrous reaction to vessel ingrowth.
It is most common in young women.
It appears as a nodular firm vascular mass.
There may be symptoms of right upper quadrant pain.
No specific treatment is required and the main purpose of management is to distinguish the lesion from neoplasms.
Hepatocellular Cancer (Hepatoma)
Worldwide’s most common tumor.
Male : female female = 4 : 1; tumor usually usually develops develops in cirrhotic liver liver in persons in fifth or sixth decade.
High incidence in Asia and Africa is related to etiologic relationship between between this cancer and hepatitis B and C infections.
Hepatocellular Cancer (Hepatoma)
Aflatoxin exposure exposure contributes to etiology and leaves a molecular signature, a mutation in codon 249 of the gene for p53.
Surgical resection or liver transplant transplantation ation is therapeutic option but rarely successful.
Hepatitis B vaccine prevents prevents the disease. Interf Interferon eron may prevent prevent liver cancer in persons with chronic active hepatitis C disease and possibly in those with hepatitis B.
Ribivarin / interferon (IFN) is most effective treatment of chronic hepatitis C.
Liver Structure
Largestt gland in the body Larges (1.5 Kg)
Under the diaphragm, within the rib cage in the upper right quadrant of the
abdomen
Liver Structure
4 lobes: major (left and right), minor (caudate and quadrate)
Ducts: common hepatic, cystic from gall bladder, common bile – choledochus (join ( join pancreatic
duct at hepatopancrea hepatopancreatic tic ampulla)
Liver Structure
Liver lobules – hexagonal structures consisting consisting of hepatocytes
Hepatocytes radiate radiate outward from a central c entral vein
At each of the six corners of a lobule is a portal triad
Liver sinusoids
Liver Structure
Hepatocytes produce bile
Bile flows through canals called bile canaliculi to a bile duct
Bile ducts leave the liver via the common hepatic duct
Liver Function
Regulating Regula ting homeostasis of carbohyd carbohydrate, rate, lipid and amino acid metabolism.
Storing nutrients such as glyc glycogen, ogen, fats and vitamin B 12, A and K.
Producing and secreting plasma proteins and lipoproteins, including clotting factors factors and acute phase proteins.
Liver Function
Synthesizing and secreting bile salts for lipid digestion.
Detoxifying Detoxi fying and ex excreting creting bilirubin, other endogenous waste products and exogenous metal ions, drugs and toxins (xenobiotics).
Clearing toxins and infective agents from the portal venous blood whilst maintain systemic immune tolerance to antigens in the portal circulation.
Gall Bladder Structure
Thin-walled green muscular sac
On the inferior surface of the liver
Stores bile that is not immediately needed for digestion
When the muscular m uscular wall of the gallbladder contracts contracts bile is expelled into the bile duct
Gall Bladder Structure
Gall Bladder Function
Stores ± 60 mL of bile, released when food containing fat fat enters the digestive tract.
The bile, produced in the liver liver,, emulsifies (breaks down) fats and neutralizes acids in partly digested food.
Biliary Atresia
Obliteration or discontinuity of the extrahepatic biliary system, resulting in obstruction to bile flow, in the first few weeks of life.
Inflammatory process process from an unknown cause affects affects the bile duct in the newborn infant.
Destruction of the extrahepa extrahepatic tic bile ducts, causing obstructive jaundice and liver failure. failure.
Kasai procedure, surgical surgical correction of this abnormality before 8 weeks of age produces the best outcome.
Choledochal Cyst
Cystic dilatation of the intra- or extrahep extrahepatic atic ducts is a rare condition, usually presenting presenting before the age of 16 years.
Symptoms : cholangitis, c holangitis, pancreatitis, stone formation and jaundice. Infants may occasionally present present with an abdominal mass.
The cause of this condition is debated.
Choledochal Cyst
Cysts are classified according to their site and shape, although 80% are fusiform abnormalities of the extrahepatic bile duct. Type II cysts are extremely rare.
Choledochal Cyst
Treated by surgical excision of the cyst with the formation of a roux-en-Y anastomosis to the biliary duct.
Hepatobiliary Trauma
The liver is the most commonly injured solid abdominal organ, despite its relative protected location.
Treatment of traumatic liver injuries is based on patient physiology, mechanism and degree of injury, associated abdominal and extra-abdominal injuries and local expertise.
Hepatobiliary Trauma Liver Organ Injury Scale Grade
I
II
III
Description
Hematoma
Subcapsular Subcapsu lar,, <10% surface area
Laceration
Capsular tear tear,, <1 cm parenchym parenchymal al depth
Hematoma
Subcapsu lar,, <10% - 50% surface area; Subcapsular intraparenchymali, intraparench ymali, <10 cm in length
Laceration
1-3 cm parenchymal depth, <10 cm in length
Hematoma
Subcapsular, >50% surface area or expanding; ruptured subcapsular or parenchymal hematoma
Laceration
<3 cm parenchymal depth
Hepatobiliary Trauma Liver Organ Injury Scale Grade
Description
IV
Hematoma
Parenchymal disruption involving 25% - 75% of Parenchymal hepatic lobe or 1-3 Couinaud segments within a single lobe
V
Laceration
Parenchymal disruption involving >75% of hepatic Parenchymal lobe >3 Couinaud segments within a single lobe
Vascular
Juxtahepatic venous injuries; ie. Retr Retrohepatic ohepatic vena cava/central major hepatic vein
VI
Hepatic avulsion
Management of o f Hepatic Hepatic Trauma Trauma
Gall Bladder Cancer
Highly aggressive malignancy, usually presents at an advanced, incurable stage, 5th most common gastrointestinal tumor
The median survival is less than 6 months after diagnosis
Women : Men = 2 – 6 : 1
The incidence steadily increases with age
Risk factor : obesity, a high-carbohydrate diet, smoking, and alcohol use
Gall Bladder Cancer
Gall bladder cancer arises in the setting of chronic inflammation. In the vast majority of patients (>75%), the source of this chronic inflammation is cholesterol gallstones. gallstones. 10-25% is caused caused by calcifica calcification tion of the gallbladder gallbladder (porcelain (porcelain gallbladder)
Most common type of gallbladde gallbladderr cancer is adenocarcinoma.
Gallbladder cancer can spread by direct invasion invasion through the gallbladder wall into the liver or peritoneal cavity.
Gall Bladder Cancer
The symptoms of gallbladder cancer overlap with the symptoms of gallstones and biliary colic. Abdominal pain may be of a more diffuse and persisten persistentt nature than the classic right upper quadrant pain of galls gallstone tone disease.
Jaundice, anorexia, and weight loss often indicate more advanced disease.
Gall Bladder Cancer Table 2. Summary of the Tumor-NodeTumor-Node-Metastasis Metastasis (TNM) Staging System* Stage
Description
1
Mucosal or muscular invasion (T1N0M0)
2
Perimuscular-tissue invasion (T2N0M0)
3
Transmural invasion, liver invasion < 2 cm; lymph node metastasis to hepatoduodenal ligament (T3N0M0, T1 –3 N1M0)
4A
Liver invasion invasion > 2 cm (T4N0M0, T4N1M0)
4B
Distant nodal (outside porta hepatis) or hematogenous metastasis (TxN2M0, TxNxM1)
Gall Bladder Cancer
The work-up for right-upper-quadrant pain or biliary colic generally starts with an ultrasound examination examination of the gallbladder.
Laboratory Laborat ory tests should include liver function tests and hematocrit. Advanced cases may demonstrate anemia and elevated eleva ted alkaline phosphatase and bilirubin.
Tumor markers, CEA and CA 19-9, 19 -9, may be of help and should be considered if gallbladder cancer is suspected.
Gall Bladder Cancer
Further radiologic work-up such as CT-scan, MRI, or needle biopsy are indicated if gallbladder gallbladder cancer is suspected.
The most common and most mo st effective effective treatment is surgical removal remov al of the gallbladder (cholecystectomy) (cholecystectomy) with part of liver and lymph node dissection.
Chemotherapy has not shown significant activity in gallbladder carcinoma. Typically, 5-fluorouracil (5-FU) has been used with response rates of 10-24% in advanced disease.
Gall Bladder Cancer
Gemcitabine has shown activity in gallbladder cancer. There is an increased response rate with gemcitabine combination with cisplatinum and capecitabine.
Currently, no clearly defined standard exists for chemotherapy in gallbladder cancer. Patients should be encouraged to participate in clinical trials.
Cholangiocarcinoma
Cholangiocarcinomas are malignancies of the biliary duct system that may originate in the liver and extrahepatic bile ducts, which terminate at the ampulla of Vater. Vater.
The etiology of most bile duct cancers remains undetermined. However, one of the most commonly recognized risk factors is primary sclerosing cholangitis.
Cholangiocarcinoma arises from the intrahepatic or extrahepatic biliary epithelium. More than 90% are adenocarcinomas.
Cholangiocarcinoma
Cholangiocarcinomas tend to grow slowly and to infiltrate the walls of the ducts, dissecting along tissue t issue planes.
Local extension occurs into the liver, porta hepatis, and regional lymph nodes of the celiac and pancrea pancreaticoduodenal ticoduodenal chains.
Symptoms of cholangiocarcinoma include jaundice, clay-colored stools, bilirubinuria (dark urine), pruritus, weight loss, and abdominal pain.
Cholangiocarcinoma
The diagnosis and staging of cholangiocarcinoma require require a multimodality approach involving laboratory, radiologic, endoscopic, and pathologic analysis.
The most studied serum tumor markers are the CA 19-9, 19 -9, is currently the most commonly used tumor marker for cholangiocarcinoma.
Surgical resection with curative intent is the treatment of choice for extrahepa extrahepatic tic cholangiocar cholangiocarcinoma. cinoma.
Gallstones
Two major types of gallstones: cholesterol and pigment stones. Cholesterol gallstones contain50% cholesterol monohydrate. Pigment stones have 20% cholesterol cholester ol and are composed primarily of calcium bilirubinate.
Predisposing factors include demographic/ demographic/genetics, genetics, obesity, weight loss, female sex hormones, age, ileal disease, pregnancy, type IV hyperlipidemia, and cirrhosis.
Gallstones
Many gallstones are “silent”.. Symptoms occur “silent”
when stones produce inflammation or obstruction of the cystic or common bile ducts.
Gallstones
Major symptoms: (1) biliary colic —a severe steady ache in the RUQ or epigastrium that begins suddenly; often occurs 30 –90 min after meals, lasts for several hours, and occasionally radiates radiat es to the right scapula or back; (2) nausea, vomiting. Physical Physic al exam may be normal or show epigastric or RUQ tenderness.
Mild and transient elevations elevations in bilirubin [85 mol/L (5 mg/dL)] mg /dL)] accompany biliary colic.
Gallstones
Only 10% of cholesterol gallstones are radiopaque. USG is best diagnostic test.
Elective cholecystectomy should be reserved for: (1) symptomatic patients; (2) persons with previous complications of cholelithiasis; and (3) presence of an underlying condition predisposing to an increased increas ed risk of complications (calcified or porcelain gallbladder).
Gallstones
Patients with gallstones 3 cm or with an anomalous gallbladder containing stones should be considered for surgery.
Laparoscopic cholecystectomy is minimally invasive and is the procedure of choice for most patients undergoing elective cholecystectomy.
Oral dissolution agents (ursodeoxycholic (ursodeoxycholic acid) partially or completely dissolve small radiolucent stones in 50% of selected pts within 6 –24 months.
Gallstones
Extracorporeal Extracorpor eal shockwav shockwave e lithotripsy followed by medical litholytic therapy is effective in selected patients with solitary radiolucent gallstones. gallstones. Because of the frequency of stone recurrence and the effectiveness of laparoscopic surgery, the role of oral dissolution therapy and lithotripsy has been reduced to selected patients who are not candidates for for elective cholecystectomy.
Acute Cholecystitis
Acute inflammation of the gallbladder usually caused by cystic duct obstruction by an impacted stone.
90% calculous; 10% acalculous.
Acalculous cholecystitis associated with higher complication rate and associated with acute illness (i.e., burns, trauma, major surgery), fasting, hyperalimentation leading to gallbladder stasis, vasculitis, carcinoma of gallbladder or common bile duct, some gallbladder infections but in > 50% of cases an underlying explanation is not found.
Acute Cholecystitis Signs and symptoms :
Attack At tack of bilary colic (RUQ or epigastric pain), progressively worsens worsens
Nausea, vomiting, anorexia
Fever
Examination typically reveals RUQ tenderness
Palpable RUQ mass found in 20% of patients
Murphy’s sign is present when deep inspira inspiration tion or cough during
palpation of the RUQ R UQ produces increased pain or inspirat inspiratory ory arrest.
Acute Cholecystitis
Laboratory Laborat ory : Mild leukocytosis; serum bilirubin, alkaline phosphatase, and AST may be mildly elevated. elevated.
Imaging : Ultrasonography is useful for demonstra demo nstrating ting gallstones galls tones and occasionally a phlegmonous mass surrounding the gallbladder. Radionuclide scans may identify cystic duct obstruction.
Acute Cholecystitis
No oral intake, nasogastric nasogastric suction, IV fluids and electrolytes, analgesia (meperidine or NSAIDS), and antibiotics (ureidopenicillins, ampicillin sulbactam, third-genera third-generation tion cephalosporins; anaerobic coverage coverage should be added if gangrenous gangr enous or emphysemat emphysematous ous cholecystitis is suspected; consider combination with aminoglycosides in diabetic patient or others with signs of gram-negative gram-negative sepsis).
Acute Cholecystitis
Acute symptoms will resolve in 70% of o f patient.
Optimal timing of surgery depends on patient stabilization and should be performed as soon as feasible.
Urgentt cholecystectomy is appropriate in most patients with a Urgen suspected or confirmed complication.
Delayed surgery surgery is reserved for patients with high risk of emergent surgery surgery and where the diagnosis is in doubt.
Chronic Cholecystitis
Chronic inflammation of the gallbladd gallbladder; er; almost alwa always ys associated with gallst gallstones. ones. Results from repeated acute/subacute acute/suba cute cholecystitis or prolonged mechanical irritation of gallbladder wall.
May be asymptomatic for years, may progress to symptomatic gallbladder gallbladd er disease or to acute cholecystitis, or present with complications.
Chronic Cholecystitis
Laboratory Laborat ory tests are usually normal.
Ultrasonography preferred; usually shows gallstones within a contracted gallbladder gallbladder..
Surgery indicated if patient is symptoma symptomatic. tic.
Liver Infections – Pyogenic Abscess
Pyogenic or bacterial abscess may be caused by several factors. Infections may arise from the biliary tract, portal vein and hepatic artery or by direct extension.
Symptoms : pyrexia and rigours associated with right upper quadrant pain, general malaise and anorexia.
Examination may reveal tender hepatomegaly. A pleural effusion may be present. Occasionally, hypotension and cardiovascular collapse may be the presenting symptoms.
Liver Infections – Pyogenic Abscess
Laboratory tests : hyperbilirubinemia, raised alkaline phosphatase and transaminase levels, blood cultures are frequently positive, leucocytosis.
USG / CT scan abdomen : to determine the size, characteristics, number and anatomical location of the liver abscesses.
Chest X-ray : elevated hemidiaphragm or a pleural effusion.
ERCP or a colonoscopy : to determine the cause of pyogenic liver abscesses.
Liver Infections – Pyogenic Abscess Treatment :
Analgesics and attention to adequate nutrition and hydration
Antimicrobial therapy
Drainage Drainag e of the abscess
Frequent clinical, biochemical, microbial and radiologic radiological al follow-up is required to assess progress and detect relapses
Liver Infections – Amoebic Liver Abscess
Amoebic infestation infestation is caused by the organism Entamoeba histolytica .
Transmission is by passage of cysts in the stool, the cysts then being ingested orally as a result of poor hyg hygienic ienic practices.
Risk factors include malnutrition, depressed immunity and low socioeconomic status.
Complications of amoebic abscess include rupture into the peritoneal cavity cavity or hollow viscus such as colon or stomach.
Liver Infections – Amoebic Liver Abscess
The onset of the disease may be sudden or gradual.
The most common symptoms : right upper quadrant pain, general malaise, weight loss, pyrexia and sweating.
Signs : tender hepatomegaly and, occasionally, jaundice.
Full blood examination : leukocytosis and eosinophilia.
Amoebic serology and stool cultures are usually positive.
The antibiotic of choice is metronidazole.
Benign Liver Tumors - Adenoma
Hepatocellular adenomas occur most commonly in women in the third or fourth decades who take birth control pills.
The major concern is their tendency to rupture with massive haemorrhage; therefore, therefore, this condition must be considered in young women presenting with abdominal pain, signs of hypovolaemic hypov olaemic shock and fea features tures of haemoperitoneum.
After resuscitation, the treatment is resection of the aff affected ected liver segment.
Benign Liver Tumors – Focal Nodular Hyperplasia
Focal nodular hyperplasia (FNH) (FNH) is not a true neoplasm but is probably due to a fibrous reaction to vessel ingrowth.
It is most common in young women.
It appears as a nodular firm vascular mass.
There may be symptoms of right upper quadrant pain.
No specific treatment is required and the main purpose of management is to distinguish the lesion from neoplasms.
Hepatocellular Cancer (Hepatoma)
Worldwide’s most common tumor.
Male : female female = 4 : 1; tumor usually usually develops develops in cirrhotic liver liver in persons in fifth or sixth decade.
High incidence in Asia and Africa is related to etiologic relationship between between this cancer and hepatitis B and C infections.
Hepatocellular Cancer (Hepatoma)
Aflatoxin exposure exposure contributes to etiology and leaves a molecular signature, a mutation in codon 249 of the gene for p53.
Surgical resection or liver transplant transplantation ation is therapeutic option but rarely successful.
Hepatitis B vaccine prevents prevents the disease. Interf Interferon eron may prevent prevent liver cancer in persons with chronic active hepatitis C disease and possibly in those with hepatitis B.
Ribivarin / interferon (IFN) is most effective treatment of chronic hepatitis C.
