Hepatobiliary Flashcards
- What is biliary colic?
Biliary colic is an acute abdominal pain caused by a transient obstruction of the gallbladder (usually by a gallstone in Hartmann’s pouch or the cystic duct and rarely due to a stricture or tumor.)
The pain presents severely in the RUQ or epigastric region and is not a true colic due to the typical pain pattern of rising to a plateau and then being continuous in nature.
It typically radiates as a band across the upper abdomen and to the inferior angle of the right scapula and it is associated with nausea, vomitting and sweating.
The pain occurs when the gall bladder attempts to contract against the obstruction and this contraction is stimulated further by CholeCystoKinin from the duodenum post prandially, especially with fatty food.
Investigations and Management:
• Blood tests (FBC, UEC, CRP, LFTs, Lipase)
• Abdominal USS – stones or sludge
• Analgesia (opioid drugs e.g. morphine or fentanyl)
• Nil by mouth
• NSAIDs and antispasmodics may also be helpful
• IV fluid resuscitation
• Cholecystectomy should be considered
Complications:
• Acute cholecystitis or chronic cholecystitis
• Acute pancreatitis
• Ascending cholangitis
• Mucocoele or empyema formation
• Carcinoma of the gallbladder
• Rarely – perforation or fistula formation
- What causes cholangitis?
Cholangitisis an infection of the biliary tract. It is caused by obstruction of the biliary tree, which may lead to bile stasis and subsequent bacterial infection. Clinically it is characterized by the Charcot triad, which consists of abdominal pain, fever, and jaundice, although jaundice is not always present. Sepsis and septic shock may develop as a complication of acute cholangitis.
• Cholangitis can be caused by - E coli, Klebsiella, Proteus, Enterobacter, Citrobacter infecting the biliary tract in cases of: o Choledocholithiasis o Surgical injury causing strictures o ERCP introduced gut bacteria o Biliary tumours o Radiation induced biliary injury
- What are the clinical features of cholangitis?
Charcots triad- RUQ pain, jaundice and fevers with rigors.
Reynolds pentad- charcots triad + shock (tachy and hypotension) + altered mental status.
Other clinical features include pale stool and pruritus.
Dx: - Requires evidence of inflammation + bile duct obstruction o Inflammation: Fever, leucocytosis, elevated CRP o Obstruction: Elevated liver enzymes USS/CT – dilation of CBD, gallstones
Mx:
- Initial resuscitation
o NBM, IV Fluids, Indwelling catheter (input/output),
Analgesia (opiates, NSAIDs)
- Initiate sepsis pathway as required
- Mx Infection:
o IV Abx – Ampicillin and Gentamicin - Mx obstruction:
o Urgent decompression
ERCP (within 24-48h) +/- sphincterotomy +/- biliary stone removal
Percutaneous transhepatic cholangiography (PTC)
Endoscopic ultrasound guided (EUS) drainage
Open surgical drainage
- Mx underlying cause:
o E.g. cholecystectomy, biliary stent
- What is cholecystitis?
Cholecystitis is inflammation of the gallbladder that most commonly occurs after cystic duct obstruction from cholelithiasis. This is known as calculous cholecystitis.
Acalculous cholecystitis is less common and seen primarily in critically ill patients.
The acute inflammation in cholecystitis is due to the increased intraluminal pressure and irritation from supersaturated bile.
Acute cholecystitis is suspected based on symptoms and signs.
The pain of cholecystitis is similar in quality and location to biliary colic but lasts longer (ie, > 6 h) and is more severe.
Vomiting is common, as is right subcostal tenderness. Within a few hours, the Murphy sign (deep inspiration exacerbates the pain during palpation of the right upper quadrant and halts inspiration) develops along with involuntary guarding of upper abdominal muscles on the right side. Fever, usually low grade, is common.
INVESTIGATIONS?
Transabdominal ultrasonography is the best test to detect gallstones. The test may also elicit local abdominal tenderness over the gallbladder (ultrasonographic Murphy sign). Pericholecystic fluid or thickening of the gallbladder wall indicates acute inflammation.
TREATMENTS?
Conservative Tx= NBM, IV fluids, analgesia (opiates, NSAIDs), IV ABx= ampicilin and gentamicin. ongoing low fat diet.
Surgical Tx= cholecystectomy, OR percutaneous cholecystectomy if pt has contraindications.
COMPLICATIONS?
- gangrenous cholecystitis (2-30%)- fundus as vascular supply compromised
- perforation (10%)- most common @ fundus. transient relief followed by peritonitis.
- cholecysto-enteric fistulas- most common to duodenum and hepatic flexure
- gallstone ileus- obstruction of distal ileum due to gallstone that has passed via a fistula- occurs more in elderly and presents as unexplained intermittent small bowel obs. AXR will show pneumobilia, intestinal obs and gallstone in unusual site.
- What techniques are available for treating common bile duct stones? Describe the technique briefly.
The techniques used to treat choledocolithiasis include:
- Endoscopic Retrograde Cholangio-Pancreatography (ERCP)
- LAPAROSCOPIC CBD EXPLORATION
- OPEN CBD EXPLORATION
ERCP involves sedating the patient and inserting a side viewing endoscope that is able to visualise the duodenal papilla. A small canula is then introduced into the biliary system and radiographic contrast is used to visualise the anatomy with fluoroscopy.
Interventions such as sphincterotomy, papillary balloon dilation, lithotripsy and stone collection via balloon and basket retrieval can also be done as part of ERCP to remove the stone.
In the laparoscopic approach basket retrieval can be done in 2 ways. trans cystic which is via the cystic duct and the transductal which is done via a choledochotomy.Unlike the transcystic approach, however, the choledochotomy allows the choledochoscope to be inserted retrograde into the common hepatic duct and right/left hepatic ducts, as well as anterograde into the common bile duct. A wire basket can be deployed via the operating channel of the choledochoscope to retrieve any stone in the entire biliary tree.
Open stone retrieval involves manual manipulation of the CBD. If this is not successful, balloon extraction can be performed and if this is unsuccessful choledochoscopy with wire basket retrieval is performed.
- What are the potential complications of ERCP?
The General complications include;
- anesthetic complications
- contrast allergy
- cardio respiratory issues (aspirations, pneumonia,MI)
- post operative nausea and vomitting
- pain
Complications specific to ERCP include:
- pancreatitis- can be due to injection of contrast up pancreatic duct and/or irritation of mucosa at the ampulla causing edema and obstruction.
- bleeding- from sphincterotomy or injury from instruments
- perforation- of oesophagus/stomach/duodenu/jejunum from endoscope OR CBD perforation from instrument.
- Infection- more specifically cholangitis- this can be due to the introduction of gut bacteria
- stricture formation due to inflammatory fibrosis and future stone recurrence
- What are the symptoms of biliary colic?
How can it be differentiated from acute cholecystitis clinically?
Symptoms of bilary colic include;
- RUQ/epigastric pain
- radiation to the right back inferior scapular
- diaphoresis
- N&V
- lasts less than 6 hours with no fever and peritoneal signs
- pain increases but plateaus
Acute cholecystitis can be differentiate clinically from biliary colic as it presents with :
- a fever
- peritoneal signs such as involuntary guarding
- positive murphys sign as opposed to biliary colic where there is no murphys sign because there is no gall bladder inflammation
- leukocytosis
- What are the common causes of painless obstructive jaundice in a 65yo person?
Painless obstructive jaundice is a hallmark of pancreatic cancer, yet several clinical and diagnostic features must be kept in mind. This is a cancer of the head of the pancreas that compresses on the CBD and causes obstructive jaundice.
Other differentials can include:
- choledocolithiasis that can present with a history of biliary colic but non tender gall bladder and progressive jaundice if the stone is impacted or fluctuant if the stone is mobile.
- cholangiocarcinoma- adenocarcinoma of biliary duct
- mets from another GIT cancer
some uncommon causes include;
- pancreatitis
- Mirizzi syndrome- gallstone in hartmanns pouch causing inflammation of gallbladder and extrinsic compression of an extrahepatic biliary duct
- peri-ampullary malignant tumors
- strictures of the common bile duct
- How might a person with pancreatic cancer present to their GP?
Common presenting features include;
- an age of onset between 60-80
- presence of risk factors (smoking, chronic pancreatitis, high alcohol consumption, obesity, T2D)
- belt shaped epigastric pain which radiates to the back
- Courvoisier sign- enlarged gall bladder and painless jaundice
- diarrhea (possible steatorrhea secondary to exocrine pancreatic insufficiency)
- thrombosis of unknown origin
- weight loss and anorexia
- fatigue and weakness
- nausea and vomiting
- Why does a tumour of the head of the pancreas cause jaundice? AND
What are the haematological consequences of biliary obstruction?
The common bile duct (CBD) passes through the head of the pancreas to join with the pancreatic duct before entering the duodenum.
A tumour of the head of the pancreas will cause extrinsic compression of the CBD, leading to obstruction of flow into the duodenum, backflow into the biliary system and leakage of conjugated bilirubin through tight junction between hepatocytes into the blood. Alternatively metastatic lymphadenopathy of the porta hepatis may also result in biliary obstruction. Jaundice is caused by elevated levels of bilirubin in the blood – for jaundice to be visible serum bilirubin needs to be > 30μmol/L (normal range is 3-17μmol/L)
Haematological consequences:
- Elevated conjugated bilirubin (>50%)
- Obstructive LFT pattern (elevated ALP and GGT, with smaller elevation of AST and ALT, GGT increase occurs earlier and persists longer)
- Hypercholesterolaemia (normally excreted in bile but now back flows into serum level)
- Prolonged Prothrombin Time (PT) due to malabsorption of vitamin K and other fat soluble vitamins (ADEK)
- Why or how do gallstones cause pancreatitis?
Small gallstones (<5mm) have the propensity to pass through the cystic duct and CBD and get lodged at the ampulla of Vater.
This leads to obstruction of the pancreatinc duct and prevents exocrine pancreatic excretion into the duodenum and also allows for reflux of bile into the pancreatic duct.
The onset of pancreatitis is due to inappropriate activation of pancreatic enzymes and autodigestion of the pancreas.
There are many pancreatic enzymes secreted but trypsinogen triggers a cascade of activation when it is activated by enterokinase in the duodenum to become trypsin. In the case of obstruction there is failure of the normal inhibitory processes that prevents trypsinogen from spontaneously activating to trypsin and this leads to activation of all the enzymes and subsequently autodigestion of the pancreas.
Once the autodigestion process is initiated the inflammatory process leads to:
- oedema, haemorrhage and eventually necrosis if left untreated
- cytokine production which leads to systemic inflammatory response syndrome (SIRS) and potentially acute respiratory distress syndrome (ARDS) and disseminated intravascular coagulation (DIC).
- the third space fluid losses can lead to renal failure if left untreated.
- What are the common causes of pancreatitis?
I- idiopathic (10-20%0
G- gallstones (35-40%)
E- ethanol (30%)
T- trauma
S- steroids
M- mumps and malignancy and other viruses
A- autoimmune (rare)
S- scorpion venom (rare)
H- hypertriglyceridaemia (1-4%) MORE SO PREGNANCY hypercalcemia, hyperlipidemia, hypothermia
E- ERCP (2-3%)
D- drugs (<1.5%) - FANS- frusemide, azathioprine, NSAIDs, steroids
- How do you assess the severity of an episode of pancreatitis when the patient is first being admitted to hospital?
Severity is an important indicator of mortality and facilitates management decisions.
There are several scoring systems available to predict which patients will develop severe disease, including the Ranson criteria, modified Glasgow scores, Balthazar system and the Revised Atlanta severity criteria.
These scoring system rely on clinical and laboratory findings to provide early warning of severity and indicate prognosis.
The revised atlanta score categorises severity into the following groups:
●Mild acute pancreatitis, which is characterized by the absence of organ failure and local or systemic complications
●Moderately severe acute pancreatitis, which is characterized by no organ failure or transient organ failure (<48 hours) and/or local complications
●Severe acute pancreatitis, which is characterized by persistent organ failure (>48 hours) that may involve one or multiple organs
At initial evaluation, the severity of acute pancreatitis should be assessed by clinical examination to assess for early fluid losses, organ failure (particularly cardiovascular, respiratory, or renal compromise), measurement of the systemic inflammatory response syndrome (SIRS) score.
A complete metabolic panel, serum calcium, complete blood count, serum triglycerides and lactate are all useful investigations to assess severity. Although measurement of serum amylase and lipase is useful for diagnosis of pancreatitis, serial measurements in patients with acute pancreatitis are not useful to predict disease severity, prognosis, or for altering management.
- What is the initial management of pancreatitis?
Start by assessing the patient’s need for resuscitation- ABCDE.
If the pt is stable the next step consists of supportive care with aggressive fluid resuscitation and regular assessments, pain control, and nutritional support.
Attention to adequate fluid resuscitation should be the first priority in addressing abdominal pain, as hypovolemia from vascular leak and hemoconcentration can cause ischemic pain and resultant lactic acidosis. Adequate pain control requires the use of intravenous opiates.
Patients with mild pancreatitis can often be managed with intravenous hydration alone since recovery occurs rapidly, allowing patients to resume an oral diet within a week. Nutritional support is often required in patients with moderately severe pancreatitis and almost invariably needed in patients with severe pancreatitis as they are unlikely to resume oral intake within five to seven days.
Nasojejunal tube feeding (using an elemental or semi-elemental formula) is preferred to total parenteral nutrition (TPN).
Prophylactic antibiotics are not recommended in patients with acute pancreatitis, regardless of the type or severity. Abx would only be needed if pt deteriorates and is septic or there is suspicion for infected necrotitis.
Patients with acute pancreatitis should be monitored closely in the first 24 to 48 hours. Patients with organ failure will need ongoing monitoring for other complications that might arise.
Vital signs, especially oxygen saturation should be monitored and supplemental oxygen administered to maintain arterial oxygen saturation of greater than 95 percent.
Urine output, electrolytes, serum glucose levels should all be closely monitored. Patients that are severe should be be managed in the intensive care unit and should be monitored for potential abdominal compartment syndrome with serial measures of urinary bladder pressures. Any further complications that arise should be managed and any appropriate consult with gastroenterolgy, surgery or other specialties should be considered.
- What are the potential late complications of severe, acute pancreatitis, late being 2 or 3 weeks after the start of the episode?
Late complications include:
- pancreatic insufficiency (malabsorption and DM)
- chronic pancreatitis
- pancreatic pseudocyt formation
- splanchnic venous ( unusual manifestation of venous thromboembolism which involves one or more abdominal veins (portal, splenic, mesenteric and supra-hepatic veins)
- enteric fistulas
- intestinal obstructions- (mechanical obstruction by inflamed pancreas, pericolitis or mesenteric throbosis due to inflammatory state.)
- walled off pancreatic necrosis
- pancreatic ascites
Infected pancreatic necrosis, ARDS, DIC and GIT bleeding are complications that can present both early and late.
- What is the investigation/procedure? What does it show? Describe 3 complications of this intervention.
* picture of ERCP*
- Most Likely = Endoscopic Retrograde Cholangiopancreatography (ERCP)
- ERCP shows a side viewing endoscope in the 2nd part of the duodenum, with a catheter injecting contrast into the biliary tree (visualising pancreatic duct, CB, cystic duct, gallbladder, CHD, RHD & LHD) – in the image above there are stones in the gallbladder [filling defects] and ?stones in the cystic duct [may be normal visualisation of the spiral valves of Heister.
The image in the exam might show: dilatation, filling defects, structuring, perforation etc.
• Perforation:
o Of oesophagus/ stomach/ duodenum/ jejunum from the endoscope
o CBD perforation from instruments/ catheter
• Infection (i.e. cholangitis):
o Due to manipulation and irritation of pancreaticobiliary system
o May occur from introducing contaminated equipment
• Pancreatitis:
o Injection of contrast up the pancreatic duct
o Irritation of mucosa at the ampulla causing oedema and obstruction
- What are the potential early complications of severe, acute pancreatitis, early being in the first 24 to 72 hours of the episode?
The inflammation leads to tissue breakdown and as a result you can get:
- pancreatic necrosis
- pancreatic abscess
- rhabdomyolysis
- haemorrhage
- 3rd space loss of fluid
- Acute Peripancreatic fluid collection
- Abdominal Compartment Syndrome
The hemorrhage and 3rd space fluid loss can lead to shock which can lead to:
- multiple organ dysfn syndrome (MODS)
- ARDS
- and AKI
- This patient is having an operation about 1 week after an episode of acute pancreatitis. What does the patches of white on the fat represent? (examiner needs to point to the area on the right of the picture). What is the mechanism of this? What effect does this have on the serum calcium during the acute phase?
- The patches of white represent= Fat necrosis and saponification.
- • The inflammation of acute pancreatitis leads to release of enzymes, including pancreatic lipase, and this damages adipocytes which leads to necrosis of the pancreatic and peripancreatic fat.
• The free fatty acids released in this process complex with salts (including calcium) to form soaps (a process called fat saponification) – this is what the chalky white deposits are. - • Acutely this is sequestering calcium from the serum and therefore causes a lowering of serum calcium and so you get hypocalcaemia.
This would present clinically as:
o Paraesthesia’s around mouth, fingers, toes
o Muscle cramps
o Tetany (involuntary contractions)
Chvostek’s sign
• Twitching of the facial muscles in response to tapping over the area of the facial nerve)
Trousseau’s sign
• Carpopedal spasm caused by inflating the BP cuff to level above systolic pressure for 3 minutes
- This patient presents with painless jaundice, dark urine and itch.
“Q1. What organ is the surgeon palpating for in this photo?
Q2. What is the significance of being able to palpate this organ which is not normally palpable?
Q3. Explain why this is so?
Q4. What is the name of this sign? “
Q1
- Gallbladder
o Palpated by placing right hand on abdomen perpendicularly and lateral to the abdominal rectus
o Ask patient to take a deep breath and try to feel the liver edge as it descends
Q2
- • Courvoisier’s ‘law’ states that obstructive jaundice in the presence of a palpable gallbladder is not due to stone (and therefore likely to be caused by tumour).
Q3
The theory is that gallstones cause chronic inflammation leading to gallbladder fibrosis or intermittent stone obstruction leads to hypertrophy of the gallbladder wall, either of which will prevent its distension.
In malignancy, progressive obstruction occurs over a short period and the non-thickened gall bladder distends easily.
Q4
- Courvoisier’s Sign
o Non-tender palpably enlarged gallbladder + painless jaundice
o Malignancy until proven otherwise
- This patient is having a liver biopsy.
“Q1. What can you see?
Q2. What is the purpose of a liver biopsy?
Q3. What are the complications?”
- This may be an image of a jaundiced pt, a laporoscopic view of a fibrotic liver or imaging such as USS.
2.Histopathological examination of biopsy tissue can provide otherwise unobtainable qualitative information regarding the structural integrity of the liver and type and degree of injury and/ or fibrosis.
It is usually performed only after thorough non-invasive clinical evaluation
Indications include;
o Histopathological diagnosis, staging and prognosis of liver parenchymal disease
o Focal/ diffuse abnormalities on imaging
o Abnormal LFTs of unknown aetiology
o Fever of unknown origin AND to
o Monitoring progress
3. Complications can include: • Pain • Bleeding • Bile Peritonitis • Transient bacteraemia • Perforation • Subcutaneous emphysema • Pneumoperitoneum • Subphrenic abscess • Carcinoid crisis- overwhelming amount of biologically active compounds from the tumor that may be triggered by tumor manipulation (biopsy or surgery) • Anaphylaxis after biopsy of Echinococcus cyst
- This is an ERCP on a patient who has had a bile duct injury at laparoscopic cholecystectomy.
“Q1: What does this show?
Q2: What might this patient present with?
Q3: What are the clinical features of this condition?”
1) The ERCP could show a contrast leak, stones, obstruction (stenosis) or a surgical clip on the bile duct resulting in non-filling of intrahepatic ducts.
2) The patient could present with:
- jaundice
- N/V
- fevers/chills
- abdo pain- progression from epigastric pain to biliary peritonitis.
- biles ascites or peritonism
3) cholangitis would present as: • Charcot’s Triad: o RUQ pain/ tenderness o Jaundice o Fevers and Rigors Could also present with added hypotension and altered mental status. Known as Reynolds pentad.
- This woman presented with some upper abdominal fullness and early satiety.
“Q1. What is the lesion and what modalities have been used for its investigation?
Q2. What kind of hepatic cysts do you know?
This lesion is much bigger than most hepatic cysts.
Q3. What complications do you know of large hepatic cysts?”
- Most likely a cystic lesion of the liver.
On USS this would appear round or ovoid, hypoattenuated (anechoic) and well marginated with a thin wall.
On CT it would appear hypoattenuated with no contrast enhancement.
On MRI hepatic cyst follows the signal intensity of water. - • Simple Cysts:
o Simple hepatic cyst (Solitary Cyst)- does not communicate with the intrahepatic biliary tree.
o Adult Polycystic liver disease
o Choledochal Cysts- bile duct cysts due to congenital malformations
o Caroli’s Disease- cystic dilatation of the intrahepatic biliary tree
• Infectious:
o Hydatid Cyst (Echinococcosis)
o Hepatic Abscess
• Neoplastic:
o hepatic Cystadenoma (non invasive mucinous cystic neoplasm)
o Cystadenocarcinoma (invasive mucinous cystic neoplasm)
o Cystic Hepatic Metastasis- cystic nature of metastases is due to the rapid growth beyond hepatic arterial blood supply of the lesion
- In terms of complications of larger cysts they are:
• More likely to be symptomatic (upper abdominal pain and early satiety)
• Spontaneous Haemorrhage
• Rupture into peritoneal cavity or biliary tress
• Infection
• Compression of biliary tree (jaundice, cholangitis, pancreatitis)
• IVC compression
• Portal HTN
• Malignant transformation (cystadenoma to cystadenocarcinoma)
• Anaphylaxis from hydatid cysts (IgE response to Echinococcus antigen)
- This x-ray shows the right upper quadrant of a patient who has had cancer of the pancreas.
“Q1. What does it show?
This patient initially presented with obstructive jaundice and had an endoscopic procedure to relieve that.
Q2. What was the procedure and which stent relates to that?
A second procedure was needed 3 months later because of repeated vomiting.
Q3. What was that and outline the stent?”
- It shows a biliary and duodental stent
- This procedure is ERCP with stent placement - most likely a plastic stent because they are inexpensive, effective and can easily be removed or exchanged
o The negatives include the development of occlusions from sludge and/or bacterial biofilm, which requires repeat ERCP
o Metal stents we introduced to alleviate this issue, however they have significant higher cost and may not be removable - This patient most likely developed malignant duodenal obstruction (AKA gastric outlet obstruction). This is an alternative to gastric bypass to relieve the obstruction.
- This 40 year-old female underwent laparascopic cholecystectomy. During the operation this XRay was taken.
Q1. What is this Xray?
Q2. What does it show?
- This shows an intraoperative cholangiogram. It involves placing dye in the cystic duct and taking an XRAY intraoperatively to assess the transport of dye down the CBD and the contrast empties into the duodenum. The bile ducts are assessed to see if they are of normal size and whether there are any intraluminal filling defects.
- It shows the structures of the biliary tree= intrahepatic ducts, L&R hepatic ducts, CBD, cystic duct, ampulla of vater.
It can also show other abnormalities such as: Dilated biliary tree Strictures Perforations Space occupying lesions
