Hepatobiliary Flashcards
What is the epidemiology of gallstones?
- About 8% of the over 40s population
- Incidence increasing over the last 20 years; western diet
- Slightly increased incidence in females
- 90% gallstones are asymptomatic
What are the possible constituents of gallstones?
- Phospholipids: lecithin
- Bile pigments (broken down Hb)
- Choelsterol: principle constituent of most
What is the aetiology of gallstones?
- Lithogenic bile: Admirang’s triangle
- Biliary sepsis
- Gallbladder hypomotility -> stasis
- Pregnancy, OCP
- TPN, fasting
What is the difference in appearance and number between cholesterol gallstones, mixed and pigment stones?
- Cholesterol
- Large
- Often solitary
- Pigment
- Small, black, gritty, fragile
- Mixed
- Often multiple
What % of gallstones are cholesterol, pigment, or mixed?
- Cholesterol - 20%
- Pigment - 5%
- Mixed - 75% (but cholesterol is major component)
What determines the formation of cholesterol gallstones?
Admirand’s triangle:
- Low bile salts
- Low lecithin
- High cholesterol
What are the risk factors for cholesterol gallstones?
- Female
- OCP, pregnancy
- Old
- High fat diet and obesity
- Racial e.g. American Indian tribes
- Loss of terminal ileum (reduced bile salts)
What makes up pigment gallstones and what are they associated with?
Calcium bilirubinate; associated with haemolysis
What are the complications of gallstones?
- In the gallbladder:
- Biliary colic
- Acute cholecystitis ± empyema
- Chronic cholecystitis
- Mucocele
- Carcinoma
- Mirizzi’s syndrome (gallstone impacted in cystic duct or neck of gallbladder causing compression of CBD -> obstruction and jaundice)
- In the CBD
- Obstructive jaundice
- Pancreatitis
- Cholangitis
- In the gut
- Gallstone ileus
What is the pathogenesis of biliary colic?
Gallbladder spasm against a stone impacted in the neck of the gallbladder (Hartmann’s pouch) or less commonly the CBD
How does biliary colic present?
- RUQ pain radiating to the back (scapular region
- Associated with sweating, pallor, nausea and vomiting
- No fever
- Attacks can be precipitated by fatty food (stimulates release of CCK) and last <6hours or as little as a few minutes but pain is constant for that time
- May be tenderness in right hypochondrium o/e
- ± jaundice if stone passes into CBD
- Settles if stone becomes disimpacted/passess to CBD
What are the differentials for biliary colic?
- Cholecystitis/other gallstone disease
- Pancreatitis
- Bowel perforation
How should you investigate suspected biliary colic?
- Same work up as cholecystitis - difficult to distinguish clinically
- Urine: bilirubin, urobilinogen, Hb
- Bloods: FBC, U+E, amylase, LFTs, G+S, clotting, CRP
- Amylase, WCC and CRP usually normal
- Imaging
- AXR: 10% stones are radioopaque
- Erect CXR to look for perf
- US detects 98% of stones (less reliable if in bile duct)
- Stones: acoustic shadow
- Dilated ducts >6mm
- Inflamed GB: wall oedema
- If uncertain after US do HIDA cholescintigraphy which shows failure of GB filling (requires functioning liver)
- If dilated ducts seen on US do MRCP
How is biliary colic managed?
- Conservative
- Rehydrate and NBM
- Opioid analgesia: morphine 5-10mg/2h max
- High recurrence rate therefore surgery favoured
- Surgical
- As for conservative with either:
- Urgent lap chole (same admission)
- Elective lap chole at 6-12 weeks
- As for conservative with either:
What is the pathogenesis in acute cholecystitis?
- Stone or sludge impaction in Hartmann’s pouch
- Leads to chemical and/or bacterial inflammation
- 5% are acalculous due to sepsis, burns, DM
What are the possible sequelae of acute cholecystitis?
- Resolution ± recurrence
- Gangrene and rarely perforation
- Chronic cholecystitis
- Empyema
How does acute cholecystitis present?
- Similar to biliary colic but pain is more severe and persistent
- Severe RUQ pain that radiates to the right scapula and epigastrium
- Fever
- Vomiting
What are the examination findings in acute cholecystitis?
- Local peritonism in RUQ
- Tachycardia with shallow breathing
- ± jaundice
- Murphy’s sign
- 2 fingers over the gallbladder and ask the patient to breath in
- Causes pain and breath catch - must be negative on the left
- Phlegmon may be palpable (mass of adherent omentum and bowel)
- Boas’ sign - hyperaesthesia below the right scapula (ribs 9-11 posteriorly)
How should you investigate suspected acute cholecystitis?
- Urine: bilirubin, urobilinogen, Hb
- Bloods: FBC (raised WCC), U+E (dehydration from vomiting), amylase (raised but not as much as pancreatitis), LFTs (may be raised), G+S, clotting, CRP
- Imaging
- AXR: gallstone, porcelain gallbladder
- Erect CXR to look for perf
- US
- Stones: acoustic shadow
- Dilated ducts >6mm
- Inflamed GB: wall oedema
- If uncertain after US do HIDA cholescintigraphy which shows failure of GB filling (requires functioning liver)
- If dilated ducts seen on US do MRCP
How is acute cholecystitis managed?
- Conservative
- NBM
- Fluid resus
- Analgesia: paracetamol, diclofenac, codeine
- Antibiotics: cefuroxime and metronidazole
- 80-90% settle over 24-48 hours
- Deterioration: perforation, empyema
- Surgical:
- Used to do lots of interval surgery after 6 weeks; less common now because doesn’t have an advantage
- Lap chole especially if mucocoele
- Empyema (high fever and RUQ mass)
- Percutaneous drainage: cholecystostomy
How does chronic cholecystitis present?
- Flatulent dyspepsia
- Vague upper abdominal discomfort
- Distension, bloating
- Nausea
- Flatulence, burping
- Symptoms exacerbated by fatty foods (CCK release stimulates gallbladder)
What are the differentials for chronic cholecystitis?
- PUD
- IBS
- Hiatus hernia
- Chronic pancreatitis
What investigations should you do in suspected chronic cholecystitis?
- AXR: porcelain gallbladder
- US: stones, fibrotic, shrunken gallbladder
- MRCP
How do you manage chronic cholecystitis?
- Medical
- Bile salts
- Not very effective
- Surgical
- Elective cholecystectomy
- ERCP first if US shows dilated ducts and stones
What is a gallbladder mucocoele and what is the concern with it?
Where the neck of the gallbladder gets blocked by a stone but its contents remain sterile; can be very large and create a palpable mass. Can become infected (empyema)
How common is gallbladder carcinoma and what is it associated with?
- Rare - incidentally found in 0.5-1% of lap choles
- Associated with gallstones and gallbladder polyps
- Calcification of gallbladder -> porcelain gallbladder
- Adenoma or cholangiocarcinoma
What is Mirizzi’s syndrome?
- Rare
- Large stone in the gallbladder presses on the common hepatic duct leading to obstructive jaundice
- Stone may erode through into the ducts
What is a gallstone ileus?
Where a large stone (>2.5cm) erodes from the gallbladder into the duodenum through a cholecysto-duodenal fistula secondary to chronic inflammation. May impact in the distal ileum leading to obstruction
Which triad is seen in gallstone ileus?
Rigler’s triad:
- Pneumobilia
- Small bowel obstruction
- Gallstone in RLQ
What is the treatment for gallstone ileus?
Stone removal via enterotomy
What is Bouveret’s syndrome?
Like gallstone ileus but duodenal obstruction
What are the causes of obstructive jaundice?
- 30% stones
- 30% Ca head of pancreas
- 30% other:
- LNs at porta hepatis: TB, cancer
- Inflammatory: PBC, PSC
- Drugs: OCP, sulfonylureas, fluclox
- Neoplastic: cholangiocarcinoma
- Mirizzi’s syndrome
What are the clinical features of obstructive jaundice?
- Jaundice
- Noticeable at 50mM
- Seen at tongue frenulum first
- Dark urine
- Pale stools
- Itch (bile salts) - specific to obstructive jaundice
What investigations should be done in obstructive jaundice?
- Urine
- Dark
- High bilirubin, low urobilinogen
- Bloods
- FBC: raised WCC in cholangitis
- U+E: hepatorenal syndrome
- LFT: raised cBR, very high ALP, high AST/ALT
- Clotting: low vitamin K -> high INR
- G+S as may need ERCP
- Immune: AMA, ANCA, ANA
- Imaging:
- AXR: may visualise stone, pneumobilia suggests gas forming infection
- US:
- Dilated ducts >6mm
- Stones (95% accurate)
- Tumour
- MRCP or ERCP
- Percutaneous transhepatic cholangiography
How should obstructive jaundice from stones be managed?
- Conservative
- Monitor LFTs: passage of stone may lead to resolution
- Vitamins ADEK
- Analgesia
- Cholestyramine
- Interventional
- If: no resolution, worsening LFTs or cholangitis
- ERCP with sphincterotomy and stone extraction
- Surgical:
- Open/lap stone removal with T tube placement
- T tube cholangiogram 8 days later to confirm stone removal
- Delayed cholecystectomy to prevent recurrence
- Open/lap stone removal with T tube placement
What are the features of ascending cholangitis/its associated triad and pentad?
- May complicate CBD obstruction
- Charcot’s triad: fever/rigors, RUQ pain, jaundice
- Reynolds pentad: Charcot’s triad + shock + confusion
How is ascending cholangitis managed?
- Cef and met
- 1st: ERCP
- 2nd: open or lap stone removal with T tube drain
What are the risk factors for pancreatic carcinoma?
- Smoking
- Inflammation: chronic pancreatitis
- Nutrition (high fat diet/Western)
- EtOH
- Diabetes
- Family history
What is the pathology in pancreatic carcinoma?
- 95% ductal adenocarcinomas
- Present late and metastasise early
- Direct extension to local structures
- Lymphatics
- Blood -> liver and lungs
- Within peritoneum: transcoelomic spread
- 70% head, then body, then tail
How does pancreatic carcinoma present?
- Typically males >60
- Painless obstructive jaundice: dark urine, pale stools, itching
- Epigastric pain which radiates to the back, relieved by sitting forward
- Anorexia, weight loss and malabsorption
- Acute pancreatitis
- Sudden onset DM in the elderly
What are the signs associated with pancreatic carcinoma?
- Palpable gallbladder
- Jaundice
- Epigastric mass (occasionally)
- Thrombophlebitis migrans (Trousseau sign)
- Splenomegaly: PV thrombosis -> portal hypertension
- Ascites
- Virchow’s node (L supraclavicular)
What is Courvoisier’s law?
In the presence of painless obstructive jaundice, a palpable gallbladder is unlikely to be due to stones
What investigations should be done in suspected pancreatic carcinoma?
- Bloods: cholestatic LFTs, raised CA19-9 (90% sensitivity), raised calcium, PT prolonged with obstructive jaundice
- Imaging:
- US: pancreatic mass, dilated ducts, hepatic mets, guide biopsy
- EUS: better than CT/MRI for staging
- CXR: mets
- Laparoscopy: mets, staging
- ERCP
- Shows anatomy
- Allows stenting
- Biopsy of peri-ampullary lesions
How is pancreatic carcinoma managed?
- Surgery
- Fit, no mets, tumour ≤3cm (≤20% patients)
- Whipple’s pancreaticoduodenectomy
- Distal pancreatectomy
- Post op chemo delays progression
- 5 year survival 5-14%
- Palliation
- Endoscopic/percutaneous stenting of CBD
- Palliative bypass surgery: cholecystojejunostomy and gastrojejunostomy
- Pain relief: may need coeliac plexus block
What is the prognosis in pancreatic carcinoma?
Mean survival is <6 months, and 5 year survival is <2%
What is the pathophysiology in acute pancreatitis?
Pancreatic enzymes are released and activated in a vicious circle; multi stage process:
- Oedema + fluid shift + vomiting -> hypovolaemic shock while enzymes -> autodigestion and fat necrosis
- Vessel autodigestion -> retroperitoneal haemorrhage
- Inflammation -> pancreatic necrosis
- Superadded infection: 50% of patients with necrosis
How common is pancreatitis, what is the mortality and what age group gets it?
4th and 5th decades. 1% of surgical admissions with a 10% mortality
What are the causes of pancreatitis?
- Gallstones (45%)
- Ethanol (25%)
- Idiopathic (20%) - maybe microstones
- Trauma
- Steroids
- Mumps and other infections e.g. coxsackie B
- Autoimmune e.g. PAN
- Scorpion (Trinidadian)
- Hyperlipidaemia (I and V), hypercalcaemia, hypothermia
- ERCP: 5% Risk
- Drugs e.g. thiazides, azathioprine
What are the clinical features of acute pancreatitis?
- Symptoms:
- Severe epigastric pain radiating to the back and relieved by sitting forward in some cases
- Vomiting
- Signs
- Acutely unwell with circulatory insufficiency
- High HR and RR
- Fever
- Hypovolaemia -> shock
- Epigastric tenderness
- Jaundice
- Ileus -> absent bowel sounds
- Ecchymoses
- Grey Turners: flank
- Cullens: periumbilical (tracks up falciform)
What are the differentials for acute pancreatitis?
- Perforated DU
- Mesenteric infarction
- MI
What is the scoring system for acute pancreatitis that allows you to assess severity and predict mortality that is valid for EtOH and gallstones?
Modified Glasgow Criteria: PANCREAS
- PaO2 <8kPa
- Age >55 years
- Neutrophils >15x109/L
- Ca2+ <2mM
- Renal function U>16mM
- Enzymes: LDH >600iu/L, AST >200iu/L
- Albumin <32g/L
- Sugar >10mM
- 1 = mild, 2 = moderate, 3 = severe
What are Ranson’s criteria?
Scoring system for acute pancreatitis that is only applicable to EtOH and can only be fully applied after 48h
What investigations should be done in suspected acute pancreatitis?
- Bloods:
- FBC (raised WCC)
- Amylase >1000/3xULN but don’t rely on this; rised in 80% and returns to normal in 5-7 days
- Elevated lipase (elevation lasts longer than amylase
- Cholestatic LFTs with raised AST and LDH
- Low calcium
- High glucose
- CRP to monitor progress: severe if >150 after 48 hours
- ABG: low O2 suggests ARDS
- Urine: glucose, raised cBR, low urobilinogen
- Imaging:
- CXR: ARDS, exclude perfed DU
- AXR: sentinel loop, pancreatic calcification
- US: gallstone and dilated ducts, inflammation
- Contrast CT: Balthazar severity score
Describe the medical/conservative management of acute pancreatitis
- Manage at appropriate level e.g. ITU, constant reassessment with hourly TPR and UO and daily FBC, U+E, calcium, glucose, amylase and ABG
- Fluid resus: aggressive to keep UO >30ml/hour, catheter ±CVP
- Pancreatic rest: NBM, NGT if vomiting, TPN may be needed if severe to prevent catabolism
- Analgesia: pethidine via PCA or morphine 5-10mg/2h max ± epidural
- Antibiotics: not routinely given if mild, but use if suspicion of infection or before ERCP; penems often used e.g. meropenem, imipenem
- Manage complications: ARDS (O2, ventilation), high glucose (insulin sliding scale), high/low calcium, EtOH (chlordiazepoxide), renal support
Describe the interventional management of acute pancreatitis
- ERCP
- If pancreatitis with dilated ducts secondary to gallstones
- ERCP + Sphincterotomy - decreases complications
Describe the surgical management of acute pancreatitis
- Indications:
- Infected pancreatic necrosis
- Pseudocyst or abscess
- Unsure diagnosis
- Operations
- Laparotomy + necrosectomy (pancreatic debridement)
- Laparotomy + peritoneal lavage
- Laparostomy: abdomen left open with sterile packs in ITU
What are the early complications of acute pancreatitis?
- Respiratory: ARDS, pleural effusion
- Shock: hypovolaemic or septic
- Renal failure
- DIC
- Metabolic
- Low calcium
- High glucose
- Metabolic acidosis
What are the late complications of acute pancreatitis (>1 week)?
- Pancreatic necrosis
- Pancreatic infection
- Pancreatic abscess
- May form in pseudocyst or in pancreas
- Open or percutaneous drainage
- Bleeding e.g. from splenic artery (may need embolisation)
- Thrombosis
- Splenic artery, GDA or colic branches of SMA
- May lead to bowel necrosis
- Portal vein -> portal hypertension
- Splenic artery, GDA or colic branches of SMA
- Fistula formation
- Pancreato-cutaneous - skin breakdown
What is a pancreatic pseudocyst and how common are they?
Collection of pancreatic fluid in the lesser sac surrounded by granulation tissue that occur in 20%, especially EtOH pancreatitis
How does a pancreatic pseudocyst present?
- 4-6 weeks after the acute attack
- Persisting abdominal pain
- Epigastric mass -> early satiety
What are the complications of a pancreatic pseudocyst?
Infection -> abscess, obstruction of duodenum or CBD
What investigations should you do in a suspected pancreatic pseudocyst?
Persistently raised amylase ± LFTs
US/CT
How do you treat a pancreatic pseudocyst?
- <6cm: spontaneous resolution
- >6cm:
- Endoscopic cyst-gastrostomy
- Percutaneous drainage under US/CT
What are the causes of chronic pancreatitis?
- Alcohol (70%)
- Genetic (CF)
- Immune (lymphoplasmacytic sclerosing pancreatitis - raised IgG4)
- Raised triglycerides
- Structural
- Obstruction by tumour
- Pancreas divisum
How does chronic pancreatitis present?
- Epigastric pain
- Bores through to back
- Relieved by sitting back or hot water bottle -> erythema ab igne
- Exacerbated by fatty food or EtOH
- Steatorrhoea and weight loss
- DM: polyuria, polydipsia
- Epigastic mass: pseudocyst
What investigations should you do in suspected chronic pancreatitis?
- Hyperglycaemia
- Low faecal elastase: decreased exocrine function
- US: pseudocyst
- AXR: speckled pancreatic calcifications
- CT: pancreatic calcifications
How do you treat chronic pancreatitis?
- Diet
- No alcohol
- Low fat, high carb
- Drugs:
- Analgesia: opiates, may need coeliac plexus block
- Enzyme supplements: pancreatin (Creon)
- ADEK vitamins
- DM treatment - insulin requirements are often greater than idiopathic diabetes because of a lack of glucagon (?)
- Surgery
- Distal pancreatectomy, Whipple’s
- Pancreaticojejunostomy: drainage
- Endoscopic stenting
What are the indications for surgery in chronic pancreatitis?
- Unremitting pain
- Obstructive jaundice
- Duct blockage
- Malignancy
- Correctable anatomical complications
What are the possible complications of chronic pancreatitis?
- Pseudocyst
- DM
- Pancreatic cancer
- Pancreatic swelling -> biliary obstruction
- Splenic vein thrombosis -> splenomegaly
- Ascites (rare): usually due to alcoholic pancreatitis with communication between the pancreatic duct and peritoneal cavity
What is the epidemiology of pancreatic endocrine neoplasias?
30-60 years, ~15% associated with MEN1
What are the features of insulinoma?
- Fasting/exercise-induced hypoglycaemia
- Confusion, stupor, LOC
- High insulin and C-peptide, low glucose
What is the pathophysiology of gastinoma/Zollinger-Ellison?
Hypergastrinaemia -> hyperchlorhydria -> PUD and chronic diarrhoea (inactivation of pancreatic enzymes)
What are the features of a glucagonoma?
- Rise in glucagon -> mild DM
- Characteristic blistering rash - necrolytic migratory erythema
What are the features of VIPoma/Verner-Morrison?
- Watery diarrhoea
- Hypokalaemia
- Achlorhydria
- Acidosis
- (also called WDHA syndrome)
What are the features of a somatostatinoma and why?
- Somatostatin inhibits glucagon and insulin release, and inhibits pancreatic enzyme secretion
- Features:
- DM
- Steatorrhoea
- Gallstones
- Usually very malignant with a poor prognosis
Where are the 2 commonest sites for an ectopic pancreas?
Meckel’s, small bowel
What is a pancreas divisum and is it significant?
- Failure of fusion of the dorsal and ventral buds
- Bulk of pancreas then drains through a smaller accessory duct
- Usually asymptomatic but can lead to chronic pancreatitis
What is an annular pancreas and how may it present?
- Fusion of dorsal and ventral buds around duodenum
- May present with infantile duodenal obstruction
What is the pathology seen in cholangiocarcinoma?
Rare bile duct tumour - adenocarcinoma. Typically occurs at the confluence of the right and left hepatic ducts (‘Klatskin’ tumour)
What are the risk factors for cholangiocarcinoma?
- PSC
- Ulcerative colitis
- Choledocholithiasis
- Hep B/C
- Choledochal cysts
- Lynch 2
- Flukes
How does cholangiocarcinoma present?
- Progressive painless obstructive jaundice
- Gallbladder not palpable
- Steatorrhoea
- Weight loss
What investigations are key in cholangiocarcinoma?
CA 19-9 and cholestatic LFTs
How is cholangiocarcinoma managed?
- Poor prognosis so no curative treatment
- Palliative stenting by ERCP
What is the pathophysiology of a hydatid cyst?
- Zoonotic infection by Echinococcus granulosus
- Occurs in sheep-rearing communities
- Parasite penetrates the portal system and infects the liver -> calcified cyst
How does a hydatid cyst present?
- Mostly asymptomatic
- Pressure effects
- Non specific pain
- Abdominal fullness
- Obstructive jaundice
- Rupture
- Biliary colic
- Jaundice
- Urticaria
- Anaphylaxis
- Secondary infection
What investigations are key in a hydatid cyst?
CT and eosinophilia
How is a hydatid cyst treated?
- Medical: albendazole
- Surgical cystectomy - indicated for large cysts
