Hepatobiliary Surgery Flashcards
Epidemiology of gallstones?
8% of population >40 yrs.
Incidence increased over last 20yrs.
Incidence increased over last 20yrs: western diet
Slightly increased incidence in females
90% of gallstones remain asymptomatic
Formation of gallstones?
General composition
- Phospholipid: Lecithin
- Bile pigments (broken down Hb)
- Cholesterol
Aetiology of gallstones?
- Lithogenic bile: Admirand’s Triangle?
- Biliary sepsis
- gallbladder hypomobility –> - Stasis
- Pregnancy, OCP
- TPN, fasting
- Sudden weight loss (Obesity surgery)
- Loss of bile salts - Terminal ileitis
- Diabetes - metabolic syndrome
What are cholesterol stones?
Large Often Solitary Formation increased according to Admirand's triangle: - decreased bile salts - Decreased lecithin - Increased cholesterol
Risk factors for cholesterol stones?
- Female
- OCP, Pregnancy
- Increase Age
- High fat diet and obesity
- Racial: E.g American indian tribes
- Loss of terminal ileum (decreased bile salts)
What are pigment stones?
- Small, black, gritty, fragile
- Calcium bilirubinate
- Associated with haemolysis
Mixed stones: 75%
Often multiple
Cholesterol is the major component
Complication of gallstones in the gallbladder?
- Biliary Colic
- Acute cholecystitis + empyema (RUQ + Fever)
- Chronic cholecystitis
- Mucocele
- Carcinoma
- Mirizzi’s syndrome (deranged LFT)
Complications of gallstones in the CBD?
Obstructive jaundice
Pancreatitis
Cholangitis
Complications of gallstones in the gut?
Gallstone ileus
What is the pathogenesis of biliary colic?
- Gallbladder spasm against a stone impacted in the neck of the gallbladder
- Less commonly the stone may be in the CBD.
Presentation of biliary colic?
Biliary colic
- RUQ pain radiating –> back (scapular region)
- Associated with sweating, pallor, n/v.
- Attacks may be ppted by fatty food and last 6hr.
- Tenderness in the right hypochondrium
- ± jaundice if stones passes into the CBD.
RUQ pain- colic
RUQ pain plus fever- cholecystitis
RUQ pain plus fever plus jaundice (charcot triad)- cholangitis
epigastric pain- more likely pancreatitis
What are the differentials for biliary colic?
- Cholecystitis/other gallstone disease
- Pancreatitis
- Bowel perforation
Investigations in biliary colic?
Same work up as cholecystitis as may be difficult to differentiate clinically
- Urine: bilirubin, urobilinogen, Hb
- Bloods: FBC, U+E, Amylase, LFTs, G+S, Clotting, CRP.
- Imaging
AXR: 10% of gallstones are radio-opaque
Erect CXR: looking for perforation
US:
- Stones: acoustic shadow
- Dilated ducts >6mm
- Inflamed GB: wall oedema
- If dilated ducts seen on US –> MRCP
If diagnosis uncertain after US
- HIDA cholescintigraphy:
shows failure of GB filling
Management of Biliary Colic?
Conservative
- Rehydrate + NBM
- Opioid analgesia: morphine 5-10mg/2hr max
- High recurrence rate therefore surgical management favoured
Surgical management
- As for conservative + either:
Urgent lap chole (same admission)
- Elective lap chole @ 6-12 weeks.
What is acute cholecystitis?
Path
- Stone or sludge impaction in Hartmann’s pouch
- -> Chemical and/or bacterial inflammation
- 5% are acalculous: sepsis, burns, DM.
Sequelae of disease of acute cholecystitis?
- Resolution ± recurrence
- Gangrene and rarely perforation
- Chronic cholecystitis
- Empyema
Presentation of acute cholecystitis?
Severe RUQ pain
- Continous
- Radiates to right scapula and epigastrium
Fever
Vomiting
Examination of acute cholecystitis?
- Local peritonism im RUQ
- Tachycardia with shallow breathing
± jaundice - Murphy’s sign. 2 fingers over the GB and ask pt to breath in –> Pain and breath catch. Must be -ve on the L.
- Phlegmom may be palpable
Mass of adherent omentum nad bowel - Boas’ sign
Hyperaesthesia below the right scapula.
What are the investigations of acute cholecystitis?
- Urine: bilirubin, urobilinogen
- Blood:
FBC: Increased WCC,
U+E: dehydration from vomiting
Amylase, LFTs, G+S, clotting, CRP
Imaging - AXR: gallstones, porcelain gallbladder - Erect CXR: look for perforation - US Stones: acoustic shadow Dilated ducts (>6mm) Inflamed GB: wall oedema
If diagnosis uncertain after US
- HIDA cholescintigraphy: shows failure of GB filling
MRCP if dilated ducts seen on US.
Management of acute cholecystits?
Conservative
- NBM
- Fluid resus
- Analgesia: paracetamol, diclofenac, codeine
- Abx: cefuroxime and metronidazole
- 80%-90% settle over 24-48hrs
- Deterioration: perforation, empyema
Surgical
- May be elective surgery @ 6-12 weeks (decreased inflammation)
- If <72hrs, may perform lap chole in acute phase.
- Empyema
High fever
RUQ mass
Percutaneous drainage: cholecystostomy.
What is chronic cholecystitis?
Flatulent dyspepsia - Vague upper abdominal discomfort - Distension, bloating - Nausea - Flatulence, burping - Symptoms exacerbated by fatty foods CCK release stimulated gallbladder (cholecystokinin)
Differential for chronic cholecystitis?
PUD
IBS
Hiatus Hernia
Chronic pancreatitis
Investigations for chronic cholecystitis?
AXR: porcelain gallbladder
US: stones, fibrotic, shrunken gallbladder
MRCP
Management of chronic cholecystitis?
Medical
- Bile salts (not very effective)
Surgical
- Elective cholecystectomy
- ERCP first if US shows dilated ducts and stones.
What is a mucocele?
- Neck of gallbladder blocked by stone but contents remain sterile
- Can be very large –> palpable mass
- May become infected –> empyema
Gallbladder carcinoma?
- Rare
- Associated with gallstones and gallbladder polyps
- Calcification of gallbladder –> Porcelain GB
- Incidental Ca found in 0.5-1% of lap choles.
Mirizzi’s syndrome?
- Rare
- Large stone in GB presses on the common hepatic duct –> obstructive jaundice
- Stones may erode through into the ducts.
Gallstone Ileus?
Large stone erodes from GB –> duodenum through a cholecysto-duodenal fistula 2nd to chronic inflammation
May impact in distal ileum –> obstruction
Rigler’s Triad
- Pneumobilia (air in bile duct)
- Small bowel obstruction
- Gallstone in the RLQ
Stone removal via enterotomy
Acute pancreatitis pathophysiology?
Pancreatic enzyme released and activated in vicious circle
1. Oedema + fluid shift + vomiting –> Hypovolaemic shock while enzymes –> autodigestion and fat necrosis.
- Vessel autodigestion –> retroperitoneal haemorrhage
- Inflammation –> Pancreatic necrosis
- Super-added infection: 50% of pts with necrosis
Epidemiology of acute pancreatitis?
1% of surgical admissions
4th and 5th decade
10% mortality
Aetiology of acute pancreatitis? Common
Gallstones (45%)
Ethanol (25%)
Idiopathic (20%): microstones?
Trauma Steroids Mumps (Coxsackie B) Autoimmune, Ascaris Infection Scorpion venom Hypertriglyceridaemia, Hypercholymicronaemia, Hypercalcaemia, hypothermia ERCP Drugs
More rare causes of acute pancreatitis?
Trauma Steroids Mumps/Coxsackie B Autoimmune e.g PAN Scorpion venom ERCP Drugs: thiazides, azathioprine, sodium valproate, furosemide, bendoflumethiazide)
Symptoms of acute pancreatitis?
Severe epigastric pain –> back pain
- May be relieved by sitting forward
- Vomiting
Signs of acute pancreatitis?
Increased HR Increased RR Fever Hypovolaemia --> shock Epigastric tenderness Jaundice Ileus --> absent bowel sounds Ecchymoses - Grey Turners: Flank - Cullens: periumbilical (tracks up Falciform)
Differential for Acute Pancreatitis?
Perforated DU
Mesenteric infarction
MI
Modified Glasgow Criteria?
- Valid for EtOH and Gallstones
- Assess severity and predict mortality
- Ranson’s criteria are only applicable to EtOH and can only be fully applied after 48hrs.
What is PANCREAS used to measure?
PaO2 <8 (hypoxia) Age >55 Neutrophils >15 x 10 Ca2+ <2mM (hypocalcaemia) Renal function U >16 mM Enzymes LDH >600, AST >200 Albumin <32 Sugar >10mM (hyperglycaemia)
Investigations for acute pancreatitis?
Bloods - FBC: Increased WCC - Increased amylase (>1000/3x ULN) and increased lipase Increased in 80% Returns to normal by 5-7d.
- U+E: dehydration and renal failure
- LFTs: cholestatic picture, increased AST, increased LDH.
- Ca down
- Glucose up
- CRP: monitor progress > 150 after 48hrs = severe
- ABG: decreased O2 suggests ARDS
Urine: glucose, increased conjugated bilirubin, decreased urobilinogen
Imaging
- CXR: ARDS, perf DU
- AXR: sentinel loop, pancreatic calcification
- US: Gallstones, dilated ducts, inflammation
- Contrast CT: Balthazar Severity Score
Conservative management of acute pancreatitis?
Manage @ ITU if severe
- Constant reassessment is key
- Hrly TPR, UO
- Daily FBC, U+E, Ca2+, Glucose, amylase ABG. Serum lipase is more sensitive and specific
Fluid resus
- Aggressive fluid resus: keep UO >30ml/h
- Catheter ± CVP
Pancreatic Rest
- NBM
- NGT if vomiting
- TPN may be required if severe to prevent catabolism
Analgesia
- Pethidine via PCa
- Or morphine 5-10 mg/2hr max
Antibiotics
- Not routinely given if mild
- Use if suspicion of infection or before ERCP
- Penems often used meropenem, imipenem
Management of complications of acute pancreatitis?
ARDS: o2 therapy or ventilation
Increased glucose: insulin sliding scale
- Increased/decreased Ca
- EToH withdrawal: chlordiazepoxide
Intervention management is pancreatitis with dilated ducts 2nd to gallstones
ECRP + sphincterotomy –>
If due to just gallstones - undergo early cholecystectomy
Surgical management of acute pancreatitis?
Surgical management - Indications Infected pancreatic necrosis - Pseudocyst or abscess - Unsure diagnosis
Operations
- Laparotomy + necrosectomy (pancreatic debridement)
- Laparotomy + peritoneal lavage
- Laparostomy: abdomen let open with sterile packs in ITU
What are the early systemic complications of Acute Pancreatitis?
Respiratory: ARDS, pleural effusion Shock: hypovolaemic or septic Renal failure DIC Metabolic - Decreased Ca - increased glucose - metabolic acidosis
What are the late >1 weeks complication of acute pancreatitis?
Pancreatic necrosis Pancreatic infection Pancreatic abscess - May form in pseudocyst or in pancreas - Open or percutaneous drainage
Bleeding: from splenic artery
May require embolisation
Thrombosis
- Splenic A, GDA or colic branches of SMA
- May –> bowel necrosis
- Portal vein –> portal HTN
Fistula formation
- Pancreato-cutaneous –> skin breakdown
What is a pancreatic pseudocyst (late complication)
- Collection of pancreatic fluid in the lesser sac surrounded by granulation tissue
- Occurs in 20% (esp in EToH pancreatitis)
- Presentation
4-6 weeks after acute attack
Persisting abdominal pain
Epigastric mass –> early satiety
Complications
- Infection –> abscess
- Obstruction of duodenum or CBG
Invx - persistently increased amylase ± LFTs
- US/CT
management
- <6cm - Spontaneous resolution
- > 6cm = endoscopic cyst-gastrostomy
- Percutaneous drainage under US/CT.
What is chronic pancreatitis caused by?
AGITS
- Alcohol
- Genetic
CF
HH - Immune
Lymphoplasmacytic sclerosing pancreatitis (Increased IgG4) - triglycerides increased
- Structural
Obstruction by tumour
Pancreas divisum
Presentation of chronic pancreatitis?
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
- Epigastric mass; Pseudocyst
Investigations for chronic pancreatitis?
Increased Glucose
Decreased faecal elastase: decreased exocrine function
US: pseudocyst
AXR: speckled pancreatitis calcifications
CT: pancreatic calcifications. With IV contrast. Look for pancreatic calcification
Management of chronic pancreatitis?
Diet
- No alcohol
- Low fat, increased carbs
Drugs
- Analgesia
- Enzyme supplements: pancreatin (creon)
- ADEK vitamins
- DM management
Surgery
- Indications (unremitting pain, weight loss, duct blockage)
- Can do a Whipple’s, pancreaticojejunostomy; drainage
- Endoscopic stenting
Complications of chronic pancreatitis?
Pseudocyst DM Pancreatic Ca Pancreatic swelling --> biliary obstruction Splenic vein thrombosis
Pancreatic Endocrine neoplasia types?
Insulinoma Gastrinoma -.> Zollinger-Ellison Glucagonoma VIPoma Somatostatinoma
What is an insulinoma?
- Fasting/exercise-induced hypoglycaemia
- Confusion, stupor, LOC
- Increased insulin + increased c-peptide + decreased glucose
Gastrinoma (ZE syndrome)
Hypergastrinaemia –> hyperchlorhydia –> PUD + chronic diarrhoea
Glucagonoma
Increased glucagon –> Mild DM
Characteristic blistering rash
- Necrolytic migratory erythema
VIPoma?
Watery diarrhoea
Hypokalaemai
- Achlorhydria
- Acidosis
Somatostatinoma
Somatostatin
- Inhibits glucagon + insulin release
- Inhibits pancreatic enzyme secretion
Features
- DM
- Steatorrhoea
- Gall stones
Cholangiocarcinoma patholgy?
Pathology
- Rare bile duct tumour
- Adenocarcinoma
- Typically occur @ confluence of right and left hepatic ducts: called Klatskin tumours.
Cholangiocarcinoma risk factors?
PSC Ulcerative colitis Choledocholithiasis (bile stones in duct) Hep B/C Choledochal cysts Lynch 2 Flukes
Presentation of cholangiocarcinoma
Progressive painless obstructive jaundice
- Gallbladder not palpable
Steatorrhoea
Weight loss
Investigations of Cholangiocarcinoma ?
Cholestatic LFTs
Ca 19-9
Management of cholangiocarcinoma ?
Poor prognosis: no curative management
Palliative stenting by ERCP
Causes of Obstructive Jaundice?
- Causes 30% Stones 30% Ca head of the pancreas 30% - LNs @portal hepatitis: TB, Ca Inflammatory: PBC, PSC Drugs: OCP, sulphonylureas, fluclox Neoplastic: cholangiocarcinoma Mirizzi's syndrome
Clinical features of obstructive jaundice?
- Noticeable @ ~50mM
Seen @tongue frenulum first - Dark urine, pale stools.
- Itch (bile salts)
Investigations for obstructive jaundice?
Urine
- Dark
- Increased bilirubin
- Decreased urobilinogen
Bloods for obstructive jaundice?
- FBC: Increased WCC in cholangitis
- U+E: hepatorenal syndrome
- LFTs: increased cBR, increased ALP a lot, some increase in AST/ALT.
- Clotting: decreased vit K –> Increased INR
- G+S: may need ERCP
Immune: AMA, ANCA, ANA
Imaging for obstructive jaundice?
AXR
- May visualise stone
- Pneumobilia suggest gast forming infection
US
- Dilated ducts >6mm
- Stones (95% accurate)
- Tumours
MRCP or ERCP
Percutaneous Transhepatic Cholangiography
Management of the stones? Conservative
Monitor LFTs: passage of stones may –> resolution
Vitamin ADEK
Analgesia
Cholestyramine
Interventional management of stones?
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 8d later to confirm stone removal
- Delayed cholecystectomy to prevent recurrence
Ascending cholangitis?
May complicate CBD obstruction
- Charcot’s triad: fever/rigors, RUQ pain, jaundice
- Reynold’s pentad: Charcot’s triad + shock + confusion
Management
- Cef and Met
1st: ERCP
2nd: open or lap stone removal with T tube drain
Risk factors for a pancreatic carcinoma?
Smoking Inflammation: chronic pancreatitis Nutrition: increased fat diet EtOH DM
Pathology of pancreatic carcinoma?
90% ductal adenocarcinoma Present late, metastasis early - Direct extension to local structure - Lymphatics - Bloods -- Liver and lungs
60% located in the head, 25% in body, 15% in tail
Presentation of pancreatic carcinoma?
- Typically male >60 yrs
- Painless obstructive jaundice: dark urine, pale stools.
- Epigastric pain: radiates to back, relieved sitting
- Anorexia, weight loss and malabsorption
- Acute pancreatitis
- Sudden onset DM in the elderly
Signs of pancreatic carcinoma?
- Palpable gallbladder
- Jaundice
- Epigastric mass
- Thrombophlebitis migrans (Trousseau Sign)
Splenomegaly: PV thrombosis –> Portal HTN - Ascites
What is courvoisier’s law?
IN the presence of painless obstructive jaundice, a palpable gallbladder is unlikely to be due to stones.
Investigations of pancreatic carcinoma?
Blood: Cholestatic LTFs, increased Ca19-9 (90%) ,increased Ca.
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
Management of pancreatic cancer?
Surgery
- Fit, not mets, tumour <3cm (<10% of patients)
- Whipple’s pancreaticoduodenectomy
- DIstal pancreatectomy
- Post-op chemo delays progression
- 5yrs = 5-14%/
Palliation of pancreatic cancer?
Endoscopic/percutaneous stenting of CBD
Palliative bypass surgery
- Cholecystojejunostomy + gastrojejunostomy
- Pain relief - coeliac plexus block