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CB - Soft Tissue - Digestive System > 95 - Liver and Biliary Surgery > Flashcards

95 - Liver and Biliary Surgery Flashcards

1
Q

What is the proportion of the liver
right to left?

A

3:2
Right: Left

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2
Q

Name the liver lobes

A

Quadrate
Right medial
Right lateral
Caudate (Caudate and Papillary Processes)
Left lateral
Left medial

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3
Q

Which lobe has substantial attachment to the quadrate?

A

Right medial

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4
Q

Which lobe is fused to the base of the caudate lobe?

A

Right lateral

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5
Q

What is the most caudal part of the liver?
Where does it extend to?

A

Caudate process of caudate lobe

Extends to 12th intercostal space

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6
Q

What are the attachments of the liver?

A

Vena cava = Firmly attached
Coronary ligament = Liver to diaphragm (continuation of peritonium, covers all liver except for porta hepatis)
Triangular ligaments = 2 x right (larger to right lateral, other to right medial) and 1 x left (to left lateral) come from the coronary ligaments and attach the liver lobes to the diagragm
Hepatorenal ligament = Caudate process to right kidney
Hepatogastric ligament = Papillary process to Lesser curvature
Hepatoduodenal ligament= Papillary process to proximal duodenum

Hepatogastric and hepatoduodenum are part of the lesser omental attachment from the papillary process to the lesser curvature of

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7
Q

What are the boundaries of the epiploic foramen?

A

Cranial = Liver
Caudal = Mesoduodenum
Dorsal = Caudal vena cava
Ventral = Hepatic artery and portal vein

Temporary inflow occlusion = Pringle manouvre

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8
Q

Which blood vessel is not occluded during the pringle manouvre?

A

The pringle manouvre does NOT prevent bleeding from reverse blood flow via the Gastroduodenal Artery (GDA)

However, positioning the finger more cranially prevents portal VENOUS bleeding from the gastroduodenal vein

Fingers should be placed more cranially to prevent reverse flow from this.

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9
Q

How long can the pringle manouvre be perormed for?

A

10-15 minutes

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10
Q

Which two blood vessels supply to the liver?
How much does each contribute to
a) blood flow
b) oxygen supply

A

Hepatic artery (branch from celiac artery)
- 20% blood supply
- 50% O2

Portal vein (Arterialised)
- 80% blood supply
- 50% O2

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11
Q

The portal vein is a confluence of which vessels?

A

Cranial mesenteric
Caudal mesenteric
Splenic vein
Gastroduodenal vein (in dogs)

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12
Q

How does branching of the within the liver portal vein differ between dogs and cats

A

Dogs – 2 branches
* Right => Supplies caudate and right lateral
* Left => Divides into central => right medial and papillary process and left => left medial, left lateral and quadrate

Cat – 3 branches
* Right => Caudate and right lateral
* Central => Right medial and quadrate
* Left => Left medial and left lateral

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13
Q

In to which vessel do the hepatic veins drain?

In which order (caudal to cranial do they enter?)

Which are completely covered by parenchyma?

A

Hepatic veins drain into caudal vena cava

Caudate, right lat, right med, quadrate, left division and papillary join together

Each lobe has it’s own hepatic vein

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14
Q

Which hepatic veins are completely covered by parenchyma?

A

Right division = completely covered

Central = variably covered

Left =1/2 to 1/3 circumference surrounded by parenchyma

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15
Q

How many hepatic arterial branches are generally present?

Which is the largest?

A

Hepatic artery = 3-5 branches

Left = Largest

Right lateral => Caudate and right lateral

Right middle => Right medial, dorsal quadrate, left medial (if more vessels, this one is likely split)

Left => Part of quadrate, left lateral, left medial, cystic artery

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16
Q

Which hepatic arterial branch supplies the cystic artery of the gall bladder?

A

Left

Medial branch of the left hepatic branch

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17
Q

Describe the flow of the blood within the liver

A

Portal vein & Hepatic Arteries enter the liver

Blood mixes within the sinusoids

Collect within the central vein

Emerge into the hepatic vein

Insert into the caudal vena cava

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18
Q

Describe the course which bile takes from production by hepatic cells to reach the duodenum

A

Bile produced by sheets of liver cells surrounding sinusoids

Discharged between cells into BILE CANALICULI

Canaliculi unite to form BILIARY DUCTULES

Ductules form INTERLOBULAR DUCTULES in centre of portal triads with hepatic artery and portal vein branches

Anastomose to form INTER LOBAR BILE DUCTS

Anastomes to form INTRAHEPATIC DUCTS

Emergy from the liver as HEPATIC DUCTS

Each hepatic duct enters the COMMON BILE DUCT which drains into the duodenum

The gallbladder is present for storage and communicates with the common bile duct via the CYSTIC DUCT

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19
Q

When does the cystic duct become the common bile duct?

A

After the last hepatic duct enters the cystic duct => Common bile duct

Double cystic and bile ducts reported in dogs

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20
Q

Describe the anatomy of the major and minor duodenal papillae in DOGS

A

Located on mesenteric margin

Major duodenal papilla
- CBD and pancreatic duct adjacent not combined
- 3-6 cm aborad to pylorus
- Intramural portion runs 1-2cm orad to papilla

Minor duodenal papilla
- 1-2 cm aborad to major
- Entry of accessory pancreatic duct (which is the main pancreatic duct in dogs)

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21
Q

Describe the anatomy of the major and minor duodenal papillae in CATS

A

CBD and pancreatic duct combine prior to entry into the major duodenal papilla

Accessory pancreatic duct is only present in 20% of cats (and is much smaller)

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22
Q

Name the major functions of the liver
(7)

A
  • Modify immune function
  • Synthesis of clotting factors
  • Maintenance and metabolism of carbohydrates and lipids
  • Synthesis and clearance of proteins
  • Synthesis of bile and gastrin
  • Storage of Vitamins, fat, glycogen, zinc and copper
  • Clearance of toxic metabolites
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23
Q

What is the principle hepatic retricuoendothelial system cell?

A

Kupffer cells = Hepatic macrophages
Large reticuoendothelial system reserve

  • Responsible for phagocytosis of endogenous and foreign substances
  • Remove endotoxin, GA agents, drug metabolistes, particulate matter
  • Dysfunction impacts clearance => Endotoxaemia, sepsis, sensitivity drugs
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24
Q

Which clotting factors are NOT produced by the liver?

A

Factor VIII
Von willebrands factor

Suspected to be associated with the vascular endothelium

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25
Q

Which are the vitamin K dependent factors?

A

II, VII, IX ,X

2/7/9/10

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26
Q

Why are vitamin K dependent factors depleted in hepatic disease?

A

The liver is responsible for carboxylation of these vitamin K depenent factors

Vitamin K is fat soluble, it requires emulsification with bile salts to be re-absorbed
- Biliary obstruction => Deficiency

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27
Q

Which other important factors associated with haemostasis are produced by the liver? (5)

A

Protein C
Plasminogen
Antithrombin III
Alpha macroglobulin
Alpha antiplasmin

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28
Q

At what level of clotting factor deficiency does coagulopathy become evident?

What % of cases with liver disease will spontaneously haemorrhage?

A

< 15% of normal concentrations => Clinical signs of coagulopathy

< 2% of cases will spontaneously haemorrhage

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29
Q

At what % hepatic dysfunction is hypoglycaemia expected?

A

Loss of functional mass > 70-80%

Responsible for gluconeogenesis and glycogenolysis

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30
Q

What is expected to happen to cholesterol levels in hepatic dysfunction?

A

Liver Dysfunction => Hypocholesterolaemia

Cholesterol is synthesised in the liver

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31
Q

Which important plasma proteins are synthesised by the liver?

A

Albumin
alpha, beta, gamma globulins
Acute phase proteins

Liver synthesises ~ 20 % of all proteins in the body

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32
Q

At what level of liver dysfunction is hypoalbuminaemia expected?

A

Loss of functional mass > 70-80%

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33
Q

What is bile composed of

A

Bile acids
Bilirubin (80% from Hb, the rest myoglobin)
Cholesterol
Phospholipids
Water
Bicarbonate

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34
Q

What triggers bile release from the gall bladder?

A

Cholecystokinin
(secreted by the duodenual mucosa)

triggers =>
Gall bladder contraction
Sphincter of Oddi relaxation

CCK released in reponse to ingesta entering duodenum

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35
Q

What is the function of bile acids?

How are bile acids synthesied and conjugated

A

Emulsification and absorption of fats
Endotoxin binding

Bile acids are synthesised in the liver from cholesterol
Conjugated with taurine in cats, taurine or glycine in dogs

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36
Q

How much bile is excreted vs recycled?

How is it degraded?

What clinical sign is evident due to lack of bile excretion in the intestine?

A

Bilirubin degraded to urobiliniogen by intestinal bacteria

Urobilinogen => Urobiliin and stercobilin

90% excreted in faeces

Stercobilin gives faeces it’s brown colour

If obstructed => Acholic (white) faeces

10% resorbed into portal circulation where it is transorted to the liver to be re-excreted in bile

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37
Q

What % liver resection can be tolerated?

A

65-70%

(Only 28% survival after 80% resection)

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38
Q

Why is excessive resection of the liver not tolerated?

A

Inability of the remaining parenchyma to accomodate total portal blood flow without developing portal hypertension

Portal pressure > 16 mmHg after hepatectomy associated with lower survival and lower regeneration

(Better survival if have portocaval shunts)

39
Q

When does liver regeneration start/peak?

A

Starts within hours
Peaks within 3 days

Near complete hypertrophy/hyperplasia by 6 days after 70% hepatectomy

40
Q

What is the hepatic arterial buffer response?

What is the proposed cause?

A

Reduced portal perfusion
=> Increased hepatic arterial perfusion

Due to reduced adenosine washout from the portal circulation

Adenosine is a potent vasodilator
Triggers compensatory increase in arterial perfusion

41
Q

How can the hepatic arterial buffer response be used to the surgeons advantage?

A

For massive hepatectomies
Ipsilateral Portal vein embolisation preoperatively => Hypertrophy of contralateral liver which will remain after transection

Liver volume increased by 25-35% after portal vein embolisation

42
Q

Which mediators are involved in hepatic proliferation and regeneration? (9)

A

Cytokines
- IL-6, TNFa

Growth factors
- Hepatocyte GF, Epidermal GF, TGFb

Vasoregulators
- NO, PGE2

Hormones
- Insulin, oestrogen

43
Q

Name 6 factors that reduce hepatic regeneration

A

Biliary obstruction (reduces portal flow)
Diabetes Mellitus (reduced insulin)
Hepatectomy with pancreatectomy
Malnutrition
Older age
Males

44
Q

What detrimental effects can bile salts have during bile peritonitis?

A

Inflammation
Haemolysis
Tissue Necrosis
Hyperosmolality => Third spacing and hypovolaemia

Worse prognosis if bacterbilia = septic bile peritonitis

45
Q

What are the most common causes of bile peritonitis

A

Trauma
Necrotising cholecystitis
Ruptured GBM

46
Q

What are the most common locations for biliary rupture due to trauma?

A

Body of the common bile duct
Cystic duct
Avulsion of the CBD from the duodenum
Avulsion of the hepatic duct from the CBD

(Rarely GB)

Short, wide cystic duct => acute compression => rapid emptying of GB rupture
Simultaneous shearing forces => Avulsion due to fixed position of duodenum and mobile position of liver

47
Q

Causes of EHBTO

A

Pancreatitis
Neoplasia
GBM
Cholangitis/Cholangiohepatitis
Cholelithiasis
Migrating FB
Diaphragmatic hernia
Parasitic disease

48
Q

How long does it take for changes to develop following bilary obstruction?

A

CBD dilation & Serum bilirubin elevation within 24-48 hours

Dilation of lobular ducts takes 4-6 days

49
Q

What physiological responses are seen with EHBTO?

A
  • Hypotension with poor response to vasopressors
  • Decreased contractility
  • Acute renal failure (endotoxin causes acute tubular necrosis)
  • Coagulopathies/DIC
  • GI haemorrhage (endotoxin mediated damage and increased gastric secretions)
  • Delayed wound healing (reduced fibroplasia and angiogenesis)

High mortality rate

50
Q

What % of choleliths are radiopaque?

A

50% in dogs
80% in cats

Calcification of the IH and IH biliary tracts can be rarely seen

51
Q

What is the diameter of the normal common bile duct?

A

3-4 mm

Distended 24-48 hours after obstruction
Dilation of intrahepatic ducts is delayed - don’t over intepret lack of intrahepatic distension
Consider serial measurements

52
Q

How can biliary flow be further interogated on US?

A

IV Injection of Cholecystokinin (Sincalide)

Normal dogs empty GB by > 40% within 1 hour of injection

** < 20% reduction in GB volume if obstructed**

53
Q

Give two methods of performing a contrast study of the biliary tract

A
  • Percutaneous US guided cholecystography
  • Endoscopic retrograde cholnagiopancreatography
    (injected via major duodenal papilla)
54
Q

Which radionuclide is used for hepatic scintigraphy?

What changes are detected in EHBTO?

A

Technitium 99m iminodiacetic acid
(Mebrofenin or disofenin)

Radionuclide accumulates in bile
If obstructed, cannot be seen within the intestine within 3 hours

Dose not DDx functional vs mechanical obstruction or cause

55
Q

Which imaging modality has 100% specificity for differentiating benign vs malignant hepatic lesions?

A

MRI

CT is not superior to US for detecting mass lesions
CT or MRI cholangiopancreatography can be useful to DDx leakage from extrahepatic ducts or EHBTO

56
Q

Which bacteria are most commonly implicated in hepatic abscesses?

A

E.coli
Staph
Enterococcus
Klebsiella
Clostridium

57
Q

Which factors predispose to hepatic abscess?

Disease/drugs

A

Diabetes Mellitus
UTI
Pancreatitis
Pneumonia
Gall Bladder Rupture
Phenobarbitone
Glucocorticoids

Dickerson vet surg 2023 - 30% had underlying hepatic neoplasia

58
Q

Treatment options for hepatic abscesses

A

Antibioitcs alone
Percutaneous drainage and ethanol injection
Surgical debridement/omentalisation

59
Q

How do hepatic abscesses in cats differ to dogs?

A

Multifocal

~70% septic on presentation

~80% mortality rate

May have underlying neoplasia

60
Q

Which lobe is most commonly affected by liver lobe torsion?

Give 4 suggestions why?

A

LEFT LATERAL
- Large size
- Mobile
- Separated anatomy
- Laxity in hepatogastric ligament?

Middle aged/old, large breed dogs with non-specific signs
Non-septic and demonstrate mature neutrophilia

61
Q

Treatment of liver lobe torsion

A

Emergent surgery
Liver lobectomy
Prophylactic gastropexy

Excellent Px with prompt surgery

62
Q

What are the most common choleliths?

A
  • Calcium carbonate
  • Calcium bilirubinate
  • Cholesterol
  • Bilirubin

Calcium carbonate most common in cats
Calcium carbonate and bilirubinate in dogs

63
Q

What causes cholelithiasis?

A

Cholestasis
Infection
Mucin over production

64
Q

What % of dogs with choleliths have a positive culture?
Which bacteria are most common?

A

70% aerobic culture
55% anaerobic culture

E.coli, staph, enterococcus, Kleb

65
Q

What do bacteria produce which can precipitate out calcium bicarbonate?

A

Beta- Glucoronidase

Enzyme deconjugates soluble bilirubin glucuronide to insoluble unconjungated bilirubin

Precipitates out calcium bicarbonate

66
Q

How do cats with choleliths present?

A

EHBTO

or
Triaditis
- IBD
- Pancreatitis
- Cholecystitis

25% asymptomatic
Triaditis => Non-specific GI signs

67
Q

Treatment for cholelithiasis

A

Duodenostomy => Flush into gall bladder => Confirm CBD patency => Cholecystectomy

OR

Choledochotomy
Sphicterotomy
Cholecystoenterostomy

68
Q

Mortality rate with cholelithiasis?

A

10%

Increased to 25% if present with EHBTO

Reduced to 3% if unobstructed

69
Q

What breeds are predisposed to Gall bladder muocoele?

A

Shepland Sheepdogs

70
Q

What genetic mutation is associated with GBM?

A

Deficiency in ABCB4 gene

(Amy Banks Charlotte Banks family of 4)

71
Q

What underlying conditions are associated with GBM?

A

Hyperadrenocorticism (29 x)
Hypothyroidism (3 x)

21% of dogs with GBM have HAC
14% of dogs with GBM have HypoT4

72
Q

Diagnostic findings in GBM

Bloods, imaging

A

Haem
- Leukocytosis (~50%)

Chem
- ALP, ALT, AST elevated
- Tbil elevated later in process

Rads
- Non-specific
- Hepatomegaly, GB enlargement/mineralisation

US
- Stellate, finely striated
- Kiwifruit
- GB discontinuity in rupture

Abdominocentesis
- 86% sensitive for rupture
- Biliary crystals?

73
Q

Which bacteria are most commonly isolated with GBM?

A

E.coli
Enterococcus

74
Q

Medical treatment for GBM

Indication for medical?

A

S-adenosylmethionine (sAME)
Famotidine
Ursidiol

Early cases, Poor GA candidates

75
Q

Surgical treatment for GBM

A
  • Laparoscopic if early in disease process
  • Ensure CBD patency
  • Catheterisation and flushing via duodenostomy if distended
  • Cholecystectomy
  • Closed suction drainage if bile peritonitis

Cholecystoduodenostomy contraindicated- GB wall not viable => Progressive necrosis

Hernon, Vet surg 2023
NO SIGNIFICANT DIFFERENCE in complications - 53% for Flush and 63% for Non-flush
90% survived to discharge

76
Q

What types are neoplasia are most common?

A

Metastatic > Primary

- Haematopoetic
- Lymphoid
- Epithelial
- Mesencymal
- MCT

77
Q

Clin path changes in hepatic neoplasia

A

Hypoalbuminaemia
Elevated liver enzymes
Elevated BAST
Hypoglycaemia
Anaemia
Leukocytosis
Thrombocytosis (~45%)
Hypocoagulability (~20%)

78
Q

Which imaging modalities were highly sensitive and specific for differentiating benign from malignant hepatic neoplasms?

A

Contrast enhanced ultrasound
* 100% sens and 94% spec

MRI
* 100% sens and 86% spec

Contrast for US. - Sonazoid (Perflubutate - Microbubbles)

79
Q

What is the % concordance between open biopsy and FNA/needle core biopsies for hepatic neoplasia

A

70%

80
Q

What are the 4 primary hepatobiliary neoplasms

A

Hepatocellular
Cholangiocellular
Neuroendocrine
Mesenchymal

81
Q

What are the 3 types of hepatocellular carcinoma?

A

Massive (61%)
Nodular (29%
Diffuse (10%)

Note 30% of hepatocellular tumours are adenomas
and 70% carcinomas

82
Q

What is the rate of metastasis of hepaticellular carcinoma?

Where do they met to?

A

Depends on the type

Massive = 36%
Nodular = 93%

LN and lung mets predominate
Renal, adrenal, GI tract, pancreas, marrow, bone, heart, spleen

83
Q

Which lobes are most commonly affected by massive hepatocellular carcinoma

A

Left lobes = 67%

Right lobes ~13-19%, Central lobes ~10-20%

84
Q

MST for massive hepatocellular carcinoma treated surgically vs medically ?

A

Sx = 1460 days

Medical = 270 days

Px worse for right due to incomplete excision

85
Q

What % of massive hepatocellular carcinomas were resected with incomplete margins?

A

~10%

86
Q

Give an alternative treatment modality for hepatocellular carcinoma

A

Chemoembolisation

87
Q

Which primary mesenchmyal cell tumours are seen in the liver

A

Haemangiosarcoma
Leiomyosarcoma
Osteosarcoma
Fibrosarcoma
Mesenchymoma
Chondrosarcoma

Poor Px
Better Px for primary HSA cf metastatic

88
Q

Which location is most common for cholangiocellular tumours in dogs?

A

Intrahepatic = 80-90%

5-20% extrahepatic
and
1-4% Gall bladder

Carcinomas > Adenomas in dogs
Massive (~50%) and nodular (30-50%) types more common than diffuse (~20%)

89
Q

What underlying condition has been implicated in cholangiocellular tumours?

A

Liver Fluke

90
Q

What is your primary differential diagnosis for a thin walled liver mass in cats?

A

Biliary cystadenoma
Good Px with Sx
(More common than carcinoma)

(100% mortality for malignant lesions with mets in 70% at presentation)

91
Q

What were hepatic neuroendocrine tumour referred to as previously?

How do they present?

Prognosis

A

Carcinoids or APUD call tumours
(More common in GI/respiratory tracts)

Diffuse hepatic involvement in 100%
Peritoneal carcinomatosis and LN mets in 93%

Very poor prognosis
Consider surgery only if focal/extrahepatic

More commonly extrahepatic in cats

92
Q

Prognosis for visceral MCTs?

A

Poor Px due to disseminated disease
MST < 2 months
Even with lomustine/toceranib

93
Q

Which cell type does histiocytic sarcoma come from?
Treatment?
Prognosis?

A

Dendritic cell tumours

Can be focal or disseminated

46% respond to lomustine

MST ~100 days

CB - Soft Tissue - Digestive System (12 decks)

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