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4th year everything > Hepatobiliary Surgery > Flashcards

Hepatobiliary Surgery Flashcards

1
Q

Epidemiology of gallstones?

A

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

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2
Q

Formation of gallstones?

A

General composition

  • Phospholipid: Lecithin
  • Bile pigments (broken down Hb)
  • Cholesterol
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3
Q

Aetiology of gallstones?

A
  • 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
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4
Q

What are cholesterol stones?

A 
Large
Often Solitary 
Formation increased according to Admirand's triangle: 
- decreased bile salts 
- Decreased lecithin 
- Increased cholesterol
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5
Q

Risk factors for cholesterol stones?

A
  • Female
  • OCP, Pregnancy
  • Increase Age
  • High fat diet and obesity
  • Racial: E.g American indian tribes
  • Loss of terminal ileum (decreased bile salts)
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6
Q

What are pigment stones?

A
  • Small, black, gritty, fragile
  • Calcium bilirubinate
  • Associated with haemolysis
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7
Q

Mixed stones: 75%

A

Often multiple

Cholesterol is the major component

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8
Q

Complication of gallstones in the gallbladder?

A
  • Biliary Colic
  • Acute cholecystitis + empyema (RUQ + Fever)
  • Chronic cholecystitis
  • Mucocele
  • Carcinoma
  • Mirizzi’s syndrome (deranged LFT)
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9
Q

Complications of gallstones in the CBD?

A

Obstructive jaundice
Pancreatitis
Cholangitis

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10
Q

Complications of gallstones in the gut?

A

Gallstone ileus

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11
Q

What is the pathogenesis of biliary colic?

A
  • Gallbladder spasm against a stone impacted in the neck of the gallbladder
  • Less commonly the stone may be in the CBD.
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12
Q

Presentation of biliary colic?

A

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

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13
Q

What are the differentials for biliary colic?

A
  • Cholecystitis/other gallstone disease
  • Pancreatitis
  • Bowel perforation
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14
Q

Investigations in biliary colic?

A

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

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15
Q

Management of Biliary Colic?

A

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.

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16
Q

What is acute cholecystitis?

A

Path

  • Stone or sludge impaction in Hartmann’s pouch
  • -> Chemical and/or bacterial inflammation
  • 5% are acalculous: sepsis, burns, DM.
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17
Q

Sequelae of disease of acute cholecystitis?

A
  • Resolution ± recurrence
  • Gangrene and rarely perforation
  • Chronic cholecystitis
  • Empyema
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18
Q

Presentation of acute cholecystitis?

A

Severe RUQ pain

  • Continous
  • Radiates to right scapula and epigastrium

Fever
Vomiting

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19
Q

Examination of acute cholecystitis?

A
  • 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.
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20
Q

What are the investigations of acute cholecystitis?

A
  • 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.

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21
Q

Management of acute cholecystits?

A

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.
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22
Q

What is chronic cholecystitis?

A 
Flatulent dyspepsia
- Vague upper abdominal discomfort
- Distension, bloating 
- Nausea 
- Flatulence, burping 
- Symptoms exacerbated by fatty foods 
CCK release stimulated gallbladder (cholecystokinin)
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23
Q

Differential for chronic cholecystitis?

A

PUD
IBS
Hiatus Hernia
Chronic pancreatitis

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24
Q

Investigations for chronic cholecystitis?

A

AXR: porcelain gallbladder
US: stones, fibrotic, shrunken gallbladder
MRCP

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25
Q

Management of chronic cholecystitis?

A

Medical
- Bile salts (not very effective)

Surgical

  • Elective cholecystectomy
  • ERCP first if US shows dilated ducts and stones.
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26
Q

What is a mucocele?

A
  • Neck of gallbladder blocked by stone but contents remain sterile
  • Can be very large –> palpable mass
  • May become infected –> empyema
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27
Q

Gallbladder carcinoma?

A
  • Rare
  • Associated with gallstones and gallbladder polyps
  • Calcification of gallbladder –> Porcelain GB
  • Incidental Ca found in 0.5-1% of lap choles.
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28
Q

Mirizzi’s syndrome?

A
  • Rare
  • Large stone in GB presses on the common hepatic duct –> obstructive jaundice
  • Stones may erode through into the ducts.
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29
Q

Gallstone Ileus?

A

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

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30
Q

Acute pancreatitis pathophysiology?

A

Pancreatic enzyme released and activated in vicious circle
1. Oedema + fluid shift + vomiting –> Hypovolaemic shock while enzymes –> autodigestion and fat necrosis.

  1. Vessel autodigestion –> retroperitoneal haemorrhage
  2. Inflammation –> Pancreatic necrosis
  3. Super-added infection: 50% of pts with necrosis
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31
Q

Epidemiology of acute pancreatitis?

A

1% of surgical admissions
4th and 5th decade
10% mortality

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32
Q

Aetiology of acute pancreatitis? Common

A

Gallstones (45%)
Ethanol (25%)
Idiopathic (20%): microstones?

Trauma 
Steroids 
Mumps (Coxsackie B) 
Autoimmune, Ascaris Infection 
Scorpion venom 
Hypertriglyceridaemia, Hypercholymicronaemia, Hypercalcaemia, hypothermia 
ERCP
Drugs
33
Q

More rare causes of acute pancreatitis?

A 
Trauma 
Steroids 
Mumps/Coxsackie B
Autoimmune e.g PAN 
Scorpion venom 
ERCP 
Drugs: thiazides, azathioprine, sodium valproate, furosemide, bendoflumethiazide)
34
Q

Symptoms of acute pancreatitis?

A

Severe epigastric pain –> back pain
- May be relieved by sitting forward

  • Vomiting
35
Q

Signs of acute pancreatitis?

A 
Increased HR
Increased RR
Fever
Hypovolaemia --> shock
Epigastric tenderness
Jaundice
Ileus --> absent bowel sounds 
Ecchymoses 
- Grey Turners: Flank 
- Cullens: periumbilical (tracks up Falciform)
36
Q

Differential for Acute Pancreatitis?

A

Perforated DU
Mesenteric infarction
MI

37
Q

Modified Glasgow Criteria?

A
  • 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.
38
Q

What is PANCREAS used to measure?

A 
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)
39
Q

Investigations for acute pancreatitis?

A 
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
40
Q

Conservative management of acute pancreatitis?

A

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
41
Q

Management of complications of acute pancreatitis?

A

ARDS: o2 therapy or ventilation
Increased glucose: insulin sliding scale
- Increased/decreased Ca
- EToH withdrawal: chlordiazepoxide

42
Q

Intervention management is pancreatitis with dilated ducts 2nd to gallstones

A

ECRP + sphincterotomy –>

If due to just gallstones - undergo early cholecystectomy

43
Q

Surgical management of acute pancreatitis?

A 
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
44
Q

What are the early systemic complications of Acute Pancreatitis?

A 
Respiratory: ARDS, pleural effusion
Shock: hypovolaemic or septic 
Renal failure 
DIC 
Metabolic 
- Decreased Ca
- increased glucose 
- metabolic acidosis
45
Q

What are the late >1 weeks complication of acute pancreatitis?

A 
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

46
Q

What is a pancreatic pseudocyst (late complication)

A
  • 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.
47
Q

What is chronic pancreatitis caused by?

A

AGITS
- Alcohol

  • Genetic
    CF
    HH
  • Immune
    Lymphoplasmacytic sclerosing pancreatitis (Increased IgG4)
  • triglycerides increased
  • Structural
    Obstruction by tumour
    Pancreas divisum
48
Q

Presentation of chronic pancreatitis?

A

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
49
Q

Investigations for chronic pancreatitis?

A

Increased Glucose
Decreased faecal elastase: decreased exocrine function
US: pseudocyst
AXR: speckled pancreatitis calcifications

CT: pancreatic calcifications. With IV contrast. Look for pancreatic calcification

50
Q

Management of chronic pancreatitis?

A

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
51
Q

Complications of chronic pancreatitis?

A 
Pseudocyst
DM
Pancreatic Ca
Pancreatic swelling --> biliary obstruction 
Splenic vein thrombosis
52
Q

Pancreatic Endocrine neoplasia types?

A 
Insulinoma
Gastrinoma -.> Zollinger-Ellison
Glucagonoma 
VIPoma 
Somatostatinoma
53
Q

What is an insulinoma?

A
  • Fasting/exercise-induced hypoglycaemia
  • Confusion, stupor, LOC
  • Increased insulin + increased c-peptide + decreased glucose
54
Q

Gastrinoma (ZE syndrome)

A

Hypergastrinaemia –> hyperchlorhydia –> PUD + chronic diarrhoea

55
Q

Glucagonoma

A

Increased glucagon –> Mild DM
Characteristic blistering rash
- Necrolytic migratory erythema

56
Q

VIPoma?

A

Watery diarrhoea
Hypokalaemai
- Achlorhydria
- Acidosis

57
Q

Somatostatinoma

A

Somatostatin

  • Inhibits glucagon + insulin release
  • Inhibits pancreatic enzyme secretion

Features

  • DM
  • Steatorrhoea
  • Gall stones
58
Q

Cholangiocarcinoma patholgy?

A

Pathology

  • Rare bile duct tumour
  • Adenocarcinoma
  • Typically occur @ confluence of right and left hepatic ducts: called Klatskin tumours.
59
Q

Cholangiocarcinoma risk factors?

A 
PSC
Ulcerative colitis 
Choledocholithiasis (bile stones in duct) 
Hep B/C
Choledochal cysts
Lynch 2
Flukes
60
Q

Presentation of cholangiocarcinoma

A

Progressive painless obstructive jaundice
- Gallbladder not palpable

Steatorrhoea
Weight loss

61
Q

Investigations of Cholangiocarcinoma ?

A

Cholestatic LFTs

Ca 19-9

62
Q

Management of cholangiocarcinoma ?

A

Poor prognosis: no curative management

Palliative stenting by ERCP

63
Q

Causes of Obstructive Jaundice?

A 
- 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
64
Q

Clinical features of obstructive jaundice?

A
  • Noticeable @ ~50mM
    Seen @tongue frenulum first
  • Dark urine, pale stools.
  • Itch (bile salts)
65
Q

Investigations for obstructive jaundice?

A

Urine

  • Dark
  • Increased bilirubin
  • Decreased urobilinogen
66
Q

Bloods for obstructive jaundice?

A
  • 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
67
Q

Imaging for obstructive jaundice?

A

AXR

  • May visualise stone
  • Pneumobilia suggest gast forming infection

US

  • Dilated ducts >6mm
  • Stones (95% accurate)
  • Tumours

MRCP or ERCP
Percutaneous Transhepatic Cholangiography

68
Q

Management of the stones? Conservative

A

Monitor LFTs: passage of stones may –> resolution
Vitamin ADEK
Analgesia
Cholestyramine

69
Q

Interventional management of stones?

A

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
70
Q

Ascending cholangitis?

A

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
71
Q

Risk factors for a pancreatic carcinoma?

A 
Smoking 
Inflammation: chronic pancreatitis 
Nutrition: increased fat diet
EtOH 
DM
72
Q

Pathology of pancreatic carcinoma?

A 
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

73
Q

Presentation of pancreatic carcinoma?

A
  • 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
74
Q

Signs of pancreatic carcinoma?

A
  • Palpable gallbladder
  • Jaundice
  • Epigastric mass
  • Thrombophlebitis migrans (Trousseau Sign)
    Splenomegaly: PV thrombosis –> Portal HTN
  • Ascites
75
Q

What is courvoisier’s law?

A

IN the presence of painless obstructive jaundice, a palpable gallbladder is unlikely to be due to stones.

76
Q

Investigations of pancreatic carcinoma?

A

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
77
Q

Management of pancreatic cancer?

A

Surgery

  • Fit, not mets, tumour <3cm (<10% of patients)
  • Whipple’s pancreaticoduodenectomy
  • DIstal pancreatectomy
  • Post-op chemo delays progression
  • 5yrs = 5-14%/
78
Q

Palliation of pancreatic cancer?

A

Endoscopic/percutaneous stenting of CBD
Palliative bypass surgery
- Cholecystojejunostomy + gastrojejunostomy
- Pain relief - coeliac plexus block

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