HPB

Question 1

What are the pre-op, intra-op and post-op considerations when treating a patient with portal hypertension.

Answer 1

Pre-op
- Is there a non-surgical option?
- Should they be transferred to an HPB unit?
- Consult and involve a gastroenterologist
- Manage any ascites – usually with spironolactone and frusemide.
- Optimise coagulation status
- TEG is a much better marker of coagulation in patients with CLF.
- Manage electrolytes.
- Manage nutrition – both macro and micronutrient deficiencies
- Consider cross sectional imaging to identify varices.
- Consider gastroscopy to assess and eradicate varices pre-operatively - these are more likely to bleeding the post-op period.
- Have a bail out strategy - shunt or surgeon.

Intra-op
- Give prophylactic antibiotics
- Avoid enlarged abdominal wall veins - use an energy device.
- Avoid transverse abdominal incisions.
- Drain ascites
* Intermittently aspirate ascites as opposed to leaving a drain.
- Make sure you close the peritoneum and all the layers of the abdominal wall.

Post-op
- Have a risk of developing decompensated liver failure.
- This is because of the stress response to the condition and surgery, anaesthetic medications, and the fluid and electrolyte shifts a/w surgery.
- Constipation, dehydration, post-operative bleeding and infections can all cause decompensation.
- Closely monitor there blood tests including bilirubin, INR, and platelet function.
- Monitor for hepatorenal syndrome

Management of ascites
- Diuretics.
- Restricting fluid and salt intake.
- Correcting electrolyte disturbances.
- Keeping a high index of suspicion for SBP

Hepatic encephalopathy treatment
- Lactulose – aiming for 2-3 bowel motions per day.
Lactulose – acidifies the colon and promotes the conversion of ammonia to ammonium in the bowel, which means it is not absorbed

Question 2

What is the sequelae of chronic liver disease

Answer 2

Chronic liver failure sequale
- Can be thought of as :
* Problems with the function of the liver
* Portal hypertension

Problems with liver function.
- Carbohydrate metabolism – liver converts lactate to glucose. Glucose is used in skeletal muscle, and converted to lactate which goes back to the liver and is converted to glucose. In liver failure, this process is interrupted and you end up with lactic acidosis and hypoglycaemia.
- Protein metabolism – liver breaks down protein and amino acids and clears nitrogen. Ammonia is produced as biproduct of enterocyte metabolism. Normally liver converts ammonia to urea which allows urinary excretion. In liver failure ammonia builds up – hepatic encephalopathy. Treatment is lactulose (lactulose reduces the absorption of ammonia in the gut)
- Coagulation – liver makes coagulation factors and fibrinolytic proteins – increased risk of bleeding AND thrombosis. Impaired bile salt excretion impairs absorption of Vitamin K – Vitamin dependent factors are reduced – 10, 9, 7 and 2. Liver also makes protein C and S which are antithrombotic factors (thus you have a tendency to clotting)
- Immune function – creates acute phase proteins (i.e. CRP), plays an important role in the innate immune cells (produces Kupfer cells which is part of the reticuloendothelial system). Also produces opsonin’s which allows phagocytosis.
Metabolism – liver metabolises a lot of medications – this will be impaired in liver failure.

Question 3

What is the normal portal vein pressure and what is defined as portal hypertension?

Answer 3

• Normal portal vein pressure is between 2-5mmHg
• Portal hypertension when > 5mmHg and complications occur when it is >10mmHg.

Question 4

What is the pathophysiology of portal hypertension?

Answer 4

Main factors which drive portal hypertension

• Increased vascular resistance to portal flow - in cirrhosis is driven by increased resistance of the hepatic microcirculation.
• Increase in the portal flow – due to the hyperdynamic circulation triggered from splanchnic vasodilatation - cause by release of NO

Question 5

How is portal hypertension diagnosed?

Answer 5

Non-invasive modalities
* CT and USS
○ Splenomegaly
○ Re-canalized umbilical vein
○ Ascites
○ Dilated portal vein >13mm or SMV > 11mm
○ Heterogenous and nodular liver.
○ Collateral veins in retroperitoneum and abdominal wall.
○ Caudate hypertrophy.
* USS specific
○ Reduced portal vein flow velocity.
○ Reversal of portal vein flow - hepato-fugal flow.

Invasive modalities
* Hepatic venous pressure gradient measurement.
○ Catheter is inserted into middle hepatic vein via internal jug.
○ Middle hepatic venous pressure is measured - free hepatic venous pressure
○ Vein is occluded then wedge pressure is measured - this will allow an estimate between the portal vein and IVC.
○ Difference diagnosis portal hypertension
>12mmHg is considered significant.

Question 6

What is the pathophysiology of cirrhosis?

Answer 6

• Pathophysiology
  1. There is an initiating injury resulting in inflammation - damaged hepatocytes release ROS and cytokines.

    2. Hepatic stellate cells are activated - which transform into myofibroblasts 
        i. This results in deposition of excessive collagen
  
    3. Sinusoidal remodelling occurs which increases the vascular resistance. 
  
    4. Collagen bands form bridges between portal tracts and central veins - isolating hepatocytes into regenerative nodules. 
        i. Results in cycles of necrosis, fibrosis, scarring and regeneration

5. Leading to a distortion of the microcirculation of the liver - resulting in portal hypertension

Question 7

What is the Child pugh score and what does it tell you?

Answer 7

Child-Pugh Score
- 5 Factors – bilirubin, albumin, INR, presence of encephalopathy, presence of ascites
- Remember as 2 clinical and 3 biochemical
- A - mild liver disease – 10% mortality after major surgery
- B – moderate liver disease – 30% mortality after major surgery
C – severe liver disease – 70% mortality after major surgery

Question 8

What is the MELD score? What does it tell you?

Answer 8

MELD – model for end stage liver disease
- Primarily used to prioritise patients awaiting liver transplant
- Log formula which takes into account serum bilirubin, INR, creatinine - remember it as 3 biochemical
- MELD-Na has the addition of sodium - thus 4 biochemical

• MELD 6-9 = 90 day mortality following abdominal surgery is 10%
• MELD 10-19 = 90 day mortality following abdominal surgery is 30%
• MELD 20-29 = 90 day mortality following abdominal surgery is 70%

MELD 30-40 = 90%.

Question 9

What are the sites of porto-systemic shunting?

Answer 9

• Porto-systemic collateral shunt develops (varices) develop which can divert up to 80% of portal flow
  
  • Sites are
    ○ Lower oesophagus.
    ○ Upper end of anal canal
    ○ Bare area of the liver - can anastomose with phrenic vessels.
    ○ Periumbilical region
    ○ Retroperitoneum
    Sites of previous surgery

Question 10

How are oesophageal varices graded?

Answer 10

Grading
- Grade 1
* Small and straight cushions which compress with insufflation

* Grade II varices are raised above the mucosa and do not compress with insufflation, occupy 1/3 of the oesophageal lumen.

• Grade III varices are raised above the mucosa and do not compress with insufflation, occupy 2/3 of the oesophageal lumen

Question 11

What is the medical management of gastro-oesophageal varices?

Answer 11

• Propranolol is a non-selective beta blocker – dose is as high as the patient can tolerate.
• Propranolol causes peripheral vessels dilatation and splanchnic vasoconstriction which reduces the portal pressures.
• The arterial blood pressure is also lowered which can exacerbate hepato-renal syndrome
• Hyponatraemia is CI to betablockers (because hyponatraemia is a sign of already reduced renal blood flow which will only get worst if given i.e. RAAS compensatory mechanism is not enough to maintain sodium levels).

Question 13

How do you insert a Sengstaken-Blakemore tube

Answer 13

How to insert
1. Position the patient supine
2. Advance the tube through the mouth into the stomach (like you would an orogastric tube).
3. Inflate the gastric balloon with 50mls of air initially and verify placement with a chest xray
4. If confirmed - continue inflating the gastric balloon to the recommended volume - usually 200-300mls of air
5. Apply gentle traction to seat the balloon against the GOJ
If bleeding persists - inflate the oesophageal balloon - do not exceed 40mmHg

Question 14

What are the indications for TIPS?

Answer 14

• Indications
  
  • Emergency
    ○ Acute variceal bleeding when all treatment options have failed
  • Non-emergency
    ○ Recurrent variceal bleeding
    ○ Refractory tense ascites
    ○ Hepatic hydrothroax
    ○ Portal hypertensive gastropathy
    ○ Hepato-renal syndrome
    ○ Malignant compression of portal veins.
    Budd-Chiari syndrome

Question 15

CI to TIPS?

Answer 15

The main issue with TIPS is the onset or exacerbation of encephalopathy - thus should be avoided in these patients

Other CI
- unrelieved biliary obstruction
- sepsis
- PV thrombosis

Question 16

What are the different types of surgical shunts?

Answer 16

• Non-selective
  
  • Decompression entire portal tree and divert all flow away from portal vein.
  • Very effective for treatment of varices BUT result in encephalopathy and accelerate hepatic failure.
  • Methods include
    ○ End-to-side portocaval (aka Eck fistula) - don’t get hepatic decompression
    ○ Side-to-side portocaval - get both intestinal and hepatic decompression.
• Selective
  
  • Distal splenorenal aka Warren shunt - will decompression gastrosplenic veins.
    
    • Partial shunting i.e. PTFE graft between portal vein and IVC using 10mm graft - results in less encephalopathy but patient still has some degree of portal hypertension.

Question 17

What is the nerve supply of the biliary tract?

Answer 17

Nerve supply of the biliary tract

• Efferent
  
  • Parasympathetic - hepatic branch of anterior vagal trunk (crosses lesser omentum)
    ○ Causes gallbladder contraction and sphincter relaxation
  • Sympathetic
    ○ Coeliac plexus ganglion - inhibits gallbladder contraction
• Afferent
  Pain fibers - runs with sympathetic - T7-T9

Question 18

What is the embyrology of the liver? How does the embyrology relate to the ligaments?

Answer 18

• Starts as a liver bud at 3 weeks gestation as an outgrowth from the endoderm of the foregut.
• Grows into the ventral mesogastrium and the septum transversum which is part of the mesoderm layer
• The septum transversum is of mesodermal origin thus will contribute the Kuppfer cells and endothelial cells.
• By 4 weeks gestation, the connection from the liver to the duodenum narrows which forms the bile duct. The gallbladder grows off this bile duct.
• Vitelline veins fuse which forms the portal veins, SMV and splenic veins.
• Paired umbilical veins carry oxygenated blood to the fetus through the umbilicus. These drain into the ductus venosus which is a connection between the portal vein and the IVC which allows the blood to bypass the liver and then drain into the heart.
• The left umbilical vein will regress and become the ligamentum teres which runs in the free edge of the falciform ligament.
  The ductus venosum eventually becomes the ligamentum venosum – there is a corresponding fissure in the liver from this remnant.

Question 19

Explain the anatomy of the caudate lobe?

Answer 19

• Segment 1 is the caudate lobe – medially, the ligamentum venosum borders the caudate lobe.
• Inferior to the caudate lobe is the inflow to the liver (portal vein etc) and superiorly to the caudate lobe is the hepatic vein confluence.
• Has mixed inflow (both left and right)
• Has direct venous drainage into the IVC via smaller veins.

Question 20

What is the embryology of the pancreas? Explain pancreatic divisum?

Answer 20

• Develops at 2 separate buds.
• Each of them are an outgrowth of the endoderm at the junction of the foregut and midgut.
• The dorsal bud (larger) grows into the dorsal mesogastrium.
• The ventral bud (smaller) grows into the ventral mesogastrium.
• As the duodenum develops and rotates, both buds rotate clockwise (dorsal 90 degrees and ventral 270 degrees).
• The ventral bud makes up the uncinate process and the inferior part of the pancreatic head.
• Ducts then fuse to create a common duct
• The accessory pancreatic duct which drains into the minor papilla will only drain dorsal bud (head body and tail)
• Pancreatic divisum is where there is no communication between the two ducts (thus ventral bud drains via major papilla and dorsal bud via minor papilla)
  Annular pancreas – complete ring of pancreatic tissue around the duodenum. The duct will also circle around the duodenum. Can cause compression of the duodenum requiring surgical intervention.

Question 21

Wha is the gastro-colic trunk of Henle and what is its importance?

Answer 21

• Gastro-colic trunk of Henle sits adjacent to the SMV (on the right) over the head of the pancreas.
• Serves as a confluence point for veins draining the stomach, pancreas and right colon.
• Has very variable anatomy but will often receive a right superior colic vein, right gastroepiploic vein, and anterior superior pancreaticoduodenal vein.
  The right superior colic vein drains the hepatic flexure and this can be torn when mobilising the hepatic flexure (registrar vein) .

Question 22

What is the pathophysiology of ascites in portal hypertension?

Answer 22

• Triad of portal hypertension, arterial vasodilatation and neurohormonal activation, leading to sodium and water retention.
  
  • Portal hypertension plays a major role - ascites usually develops in patients with a hepatic venous pressure gradient of greater than 12mmHg.
  • Portal HTN - results in shearing stress of the mesenteric vasculature - result in NO release - splanchnic vasodilatation - decreased renal blood flow - activation of RAAS - salt retention.
  • Portal HTN also causes sympathetic over-activity which stimulates Na re-absorption in PT, loop of Henle, distal tubule.
  • This excess sodium retention - hypervolemia - increased capillary hydrostatic pressures - fluid leaks into peritoneal cavity.

Contrary to earlier theories, decreased plasma oncotic pressure from low albumin does not cause ascites

RAAS system
- renin secreted by renal juxto-glomerular apparatus in the kidney in a response to reduced renal blood flow - renin converts Angiotensinogen to Ang I which goes to the lung. Ang I is converted into Angiotensin II - Angiotensin II stimulates release of aldosterone from the adrenals - Aldosterone stimulates sodium re-absorption in the distal tubule (H+/K+ swap)

Question 23

What is the utility of an ascitic tap with a serum albumin ascites gradient?

Answer 23

SAAG > 11 predicts the patient will have portal hypertension. SAAG < 11 will predict they do not (this reflects that ascitic albumin is very low because it is just water leaking)

Question 24

What is the treatment of ascites in portal hypertension ?

Answer 24

Medical
- salt and fluid restriction.
- diuretics - frusemide and spironolactone).
Interventional
- paracentesis - often given with an albumin infusion.

Refeactory ascites
- TIPS
- transplant
- median survival in a patient with refractory ascites is 6 months.

Question 25

What are the risk factors for cholangiocarcinoma?

Answer 25

Situations which cause chronic inflammation - PSC - Recurrent cholangitis and choledocholithiasis - Choledochal cysts. - Hepatolithiasis - Chronic hepatitis, HIV, EBV, Cirrhosis, heavy ETOH use, T2DM, smoking, biliary enteric anastomosis.

Question 26

What are the different ways cholangiocarcinoma can be classified?

Answer 26

Classification location - Intrahepatic - Hilar - Distal Classification – type of growth - Mass forming – exophytic mass or nodule - Peri-ductal infiltrating – tumour which infiltrates along the duct itself. Often associated with a stricture - Intra-ductal – abrupt caliber change with or without a visible mass. Classification - histological subtype - Nodular sclerosing * Obliterates duct * Spreads along the wall * Associated with a desmoplastic reaction - Papillary * Intraductal variant * Often located in the distal CBD * Often on a stalk More favourable prognosis.

Question 27

What are the CT findings seen with intra-hepatic cholangiocarcinoma?

Answer 27

Capsular retraction - due to desmoplastic reaction. Slow centripetal enhancement (unlike HCC which is rapid centripetal)

Question 28

Describe the Bismuth-Corlette staging for hilar cholangiocarcinoma

Answer 28

1. Limited to CHD distal to confluence 2cm distal to confluence 2. Involves confluence of R and L hepatic ducts but does not extend into the intrahepatic ducts. 3. 3a – tumour spreads from confluence to origin of right hepatic duct (affecting the right posterior and anterior sectoral ducts) 3b. Tumour spreads from confluence to origin of left hepatic duct (involving segment 2, 3, or 4) 4. Tumour invades the origin of both the right and left hepatic ducts.

Question 29

Explain the Blumgart clinical staging of cholangiocarcinoma

Answer 29

Stratifies on the basis of 3 factors. This allows an assessment of both resectability and the likelihood of distant metastatic disease. 1. Second order biliary radical involvement 2. Portal vein involvement 3. Hepatic lobar atrophy.

Question 30

How do you assess resectability for a patient with cholangiocarcinoma?

Answer 30

A - anatomy - looking at portal vein involvement, involvement of second order biliary radical, hepatic artery involvement, and lobar atrophy. Once there is evidence of disease on both sides then a tumour becomes unresectable, hepatic artery proper involvement means tumours is unresectable (NB: you can resect the portal vein) B - tumour biology - if there is evidence of metastasis or very high CA 19-9 C - co-morbidities - is the patient fit for major surgery or a cirrhotic.

Question 31

T staging of intra-hepatic cholangiocarcinoma?

Answer 31

T1 - solitary tumour without vascular invasion. T1a - < 5cm T1b - >5cm T2 - solitary tumour with intrahepatic vascular invasion, or multiple tumours without vascular invasion. T3 - Tumours perforated the visceral peritoneum. T4 0 tumours involving the extrahepatic structures by direct invasion.

Question 32

T staging of extrahepatic cholangiocarcinoma?

Answer 32

T1 - depth of invasion < 5mm T2 - depth of invasion 5-12mm T3 - depth of invasion >12mm T4 - Tumour involves coeliac axis or SMA.

Question 33

What are the pros and cons of pre-operative biliary decompression in patients with cholangitis? What are the indications?

Answer 33

- Pro’s – likely improves patients nutrition pre-operatively, and the function of the liver remnant - Con’s – can introduce infection to the biliary tree – increases pre-operative risk of cholangitis. May cause tumour seeding which increases the risk of recurrence. Is indicated in patients with * Cholangitis * Severe jaundice * Borderline FLR

Question 34

What chemotherapy agents are used for patients with cholangiocarcinoma?

Answer 34

- Due to how rare this tumour is there is limited data. - Adjuvant treatment - capecitabine - this is based on the BILCAP 2019 study which showed an improved overall survival. * Indications for adjuvant chemotherapy ○ T3/4 tumours ○ LVI ○ Lymph node involvement. ○ Positive resection margins. - Palliative treatment - gemcitabine + cisplatin - based on ABC-02 trial NB: Radiotherapy is sometimes given adjuvantly to patients with positive margins.

Question 35

What are the advantages of CT and MRI when evaluating a patient with colorectal liver metastasis?

Answer 35

CT Highly specific and sensitive. Low cost. Vascular mapping Liver volume estimation. Therapy monitoring. Extrahepatic spread evaluation. MRI Good at detecting lesion < 1cm, and lesions after chemo induced steatosis. Good for lesion characterization, treatment planning, treatment response monitoring. Primovist is used because it is not taken up by Primovist.

Question 36

How should patients with synchronous colorectal cancer be managed?

Answer 36

Synchronous colorectal liver metastasis - Most difficult and will change patient to patient. - Depends on the below factors * Is the colon/rectal cancer symptomatic. * Do they need neoadjuvant treatment of there rectal cancer? - The recent evidence suggests treatment of the hepatic disease first is favorable - as patients die of their metastatic disease. - Another debate is whether or not patients with upfront resectable liver disease should be given neoadjuvant chemotherapy. - With regards to combined liver + colon resection * Can be considered if one of the procedures is "small" i.e. anterior resection + non-anatomical resection of 1 segment. For the exam: "There is evidence to suggest that a liver first approach as an improve OS compared to bowel surgery first - thus should be recommended in patients with synchronous colorectal cancer. Most patients are given neoadjuvant chemotherapy prior to liver resection (but there are exceptions)".

Question 37

What are the requirements to consider a patient for liver resection with colorectal liver metastasis?

Answer 37

Liver resection for colorectal liver metastasis - The Americas HPB expert consensus statement says that there are 4 requirements needed to consider a patient for liver surgery 1. Tumour can be removed completely 2. FLR is adequate to prevent post-operative liver failure. 3. Extra-hepatic disease sites are controllable Primary can be resected for a cure.

Question 38

How do you determine if a patient has resectable liver metastasis?

Answer 38

- Ability to achieve and Ro resection - Vascular inflow and outflow - hepatic artery, portal vein, hepatic vein - Biliary drainage - Leaving 2 perfused adjacent segments.

Question 39

What is an adequate FLR?

Answer 39

- Depends on quantity and quality. - If a patient has normal liver function – can leave 20-30% of normal liver behind. - If patient has underlying liver disease or has had chemotherapy – need more i.e. 30-40%. - If a patient has cirrhosis – 40-50%. How do you assess the volume of liver which is being left behind? Liver volumetrics which can be done with either CT or MRI.

Question 40

How is post-operative liver failure diagnosed?

Answer 40

- The definition of post-operative liver failure is an acquired deterioration in the ability of the liver to maintain its synthetic, excretory, and detoxifying functions. - Is found if the INR is increased, or elevated bilirubin on post-operative day 5. - Associated with a high risk of mortality - 70% - "50-50" criteria a/w increased risk of mortality * Bilirubin > 50 INR < 50% (greater than 1.7)

Question 41

What can be done pre-op, intra-op, and post-op to prevent post-op liver failure

Answer 41

Pre-op - Avoid fasting pre-operative. Intra-op - Oxidative stress – reduce Pringle time and also intermittently give breaks. - Minimizing blood loss. - Minimizing blood transfusions. Post-op - Early recognition and treatment of post-operative haemorrhage. - Early recognition of biliary obstruction of leak. - Early recognition of intra-abdominal sepsis. - Maintaining hydration post-operative. - Adequate nutrition and the use of TPN.

Question 42

Risk factors for HCC?

Answer 42

- Cirrhosis (90% of HCC arise in cirrhotic livers) * Hep B, Hep C * Alcoholic liver disease * NAFLD * PBC and PSC * Haemochromatosis, Wilsons disease, Alpha-1 antitrypsin - Metabolic and lifestyle factors * Obesity * T2dm * Smoking - Exposure for alflatoxins

Question 43

What is the pathogenesis of HCC?

Answer 43

- 90% of patients with HCC have underlying cirrhosis – repeated cellular injury – chronic inflammation – regeneration – fibrosis – cirrhosis – dysplasia – carcinoma. - Pathway from microscopic dysplastic foci, nodules with low grade dysplasia, to nodules with high grade dysplasia, to early HCC(<2cm in size) and then HCC. - Chronic Hep B confers an additional risk * HBV DNA integrates into host genome - is an oncogene. The aetiology for non-cirrhotic HCC are less well understood - although the risk factors for non-cirrhotic HCC have been identified (and are generally the same risk factors for cirrhosis i.e. viral, autoimmune, genetic, and environmental)

Question 44

What is the histopathology of HCC?

Answer 44

- Typically are well vascularized tumours with most of the blood supply from the hepatic artery. - Wide trabecula, prominent acinar pattern, preponderance for vascular invasion. - As HCC progress, lose normal portal tracts and develop non-triad related vessels – this angiogenesis is the hallmark of an HCC. - HCC has a surrounding capsule (up to 80% of the time).

Question 45

How is HCC graded?

Answer 45

Edmonson grading Edmonson grades 1-4 are used - Grade 1 and 2 are well differentiated. - Grade 3 is moderately differentiated. - Grade 4 is poorly differentiated.

Question 46

What are the hallmarks of fibrolamaller HCC?

Answer 46

- These tumours are often found in young people who don’t have history of cirrhosis - Are encapsulated with a central scar thus can be mistaken for focal nodular hypoplasia - Are often very large at diagnosis - i.e. 10cm. - On T2 imaging, the central scar is hypointense. - Fibrolamaller HCC will not take up Primivist on MRI unlike FNH. This test is used to distinguish between between the two. - The central scar in fibrolamellar HCC is due to central necrosis (whereas in FNH the central scar is due to fibrosis associated with numerous vascular channels). - DOES NOT MAKE AFP - Do have a better prognosis than a normal HCC if they can be resected.

Question 47

What are the CT findings of an HCC?

Answer 47

- Typically hypodense on non-con phase. - Brisk enhancement on arterial phase due to aberrant blood vessels from hepatic artery. * HCC blood supply comes primarily from the hepatic artery - Evidence of rapid washout in PV and delayed phase (as has no portal inflow - thus no enhancement on portal phase). - Often associated with a hyperenhancing capsule - which enhances on portal venous and delayed phase. If you see evidence of ‘washout’ then you are saying this is an HCC.

Question 48

What is the role of biopsy for HCC's?

Answer 48

- Diagnosis of HCC is generally made of radiology - Circumstances where you may consider biopsy are - diagnostic uncertainty (i.e. LIRADS 4 or elevated CA 19-9), patient is not a cirrhotic, non-surgical therapy is being considered. There is a concern that biopsying a lesion can result in tract seeding.

Question 49

What are the different treatment options for HCC?

Answer 49

Look at notes

Question 50

What is the Milan criteria and USCF criteria?

Answer 50

- Milan criteria * Criteria which is trying to select patients which have > 70% 5-year survival after liver transplant * Solitary tumour, less than 5cm in size or £ 3 tumours which are £ 3cm in size, no extrahepatic manifestations, no vascular invasion. * Patients beyond Milan criteria may still be offered surgery if they can downstage into an accepted criteria. - UCSF criteria * Single tumour < 6.5cm or 2-3 tumours <4.5cm. * With tumour diameter <8cm. * No vascular invasion. 0 No extra-hepatic spread.

Question 51

What is Primovist and how is it used in liver imaging?

Answer 51

- Also known as gadoxetate disodium is a hepatobiliary-specific contrast MRI agent. - Is captured using T1-weighted images (not T2) - It helps characterize liver lesions, as well as determine if they are malignant or benign. - MOA 1. Extracellular phase a. Early dynamic phase b. Enhances vascular structures and is important for assessing arterial enhancement of liver lesions. 2. Hepato-biliary phase/delayed phase. a. Taken up by functional hepatocytes and excreted into the bile duct. Thus will provided delayed enhancement of normal liver tissue but not take up in malignant lesions (like HCC or metastasis) due to impaired hepatocyte function.

Question 52

What is the aetiology, natural history, and histology of FNH?

Answer 52

Focal nodular hyperplasia - Benign condition of the liver with no malignant potential. Risk of rupture is very low (unlike hepatic adenoma) Aetiology - Hyperplastic process arising from an arterial malformation causing hyper-perfusion - Main risk factor is female sex 9:1 preponderance - Because FNH occurs commonly in woman between the ages of 20-40 a relationship with the OCP has been suggested but not confirmed. Natural history - Most don’t change in size. - 20% of patients will have more than 1 area. Histology - Well circumscribed, non-encapsulated, focal area of hepatocytes with a central fibrous scar. - Central scar consists of collagen, aberrant arteries and veins. - Proliferation of hepatocytes with cirrhotic like architecture. - Fibrous septa replace bile ducts. Arteries show intimal fibrosis and media hypertrophy.

Question 53

What are the CT and MRI findings of FNH?

Answer 53

CT - Characterized by a central scar - Hypo or isodense liver lesions. - On arterial phase will get homogenous arterial enhancement apart from the central scar. - The lesion remains enhanced on PV phase (as has portal flow) - On the delayed phase the scar can enhance depending on the vascularity of the scar MRI - Typically is done with Primivist contrast - On non-enhanced T1 image will look isointense (same as surrounding liver) with central scar looking hypointense - On arterial phase FNH will enhance and the scar will remain hypointense. - On the PV phase you will get an isointense lesion with an enhancing scar. - On T2 will you have an isointense lesion but the scar will be hypertense. - When using Primovist, there will be uptake with Primovist contrast on the hepatobiliary phase - this is unlike hepatic adenomas or hepatocellular carcinomas. The key thing with using Primivist (Gadoxetic acid) is that an FNH lesion will take up Primivist in the T1 hepatobiliary phase (which is the delayed phase) due to the presence of normal hepatocytes. This is different to a hepatic metastasis, or hepatic adenoma which will not take up Primivist contrast during the hepatobiliary phase. **The hepatobiliary phase is a delayed phase thus an HCC will appear to “washout”**

Question 54

How should FNH be managed

Answer 54

- Benign non-malignant lesion so if asymptomatic and confident with diagnosis then does not require treatment. - If symptomatic treatment options include * Resection * TACE/RFA/MWA

Question 55

Risk factors for hepatic adenomas?

Answer 55

- Occurs mainly in young to middle aged woman. - ARE associated with use of the OCP and anabolic steroid (were relatively uncommon before the advent of the OCP) - Are associated with obesity, glycogen storage disease, diabetes, galactosaemia, iron overload, occur in woman in the 3rd to 5th decade of life. Increased risk in pregnancy.

Question 55

How to hepatic adenomas present?

Answer 55

- Asymptomatic. - Present with abnormal LFTs and pain - Have a risk of spontaneous haemorrhage thus can present acutely. Have a risk of malignant transformation.

Question 55

What are the macroscopic and microscopic features of hepatic adenomas?

Answer 55

Macroscopically - Usually solitary – nodular appearance - Pale yellow macroscopically, sometimes with areas of haemorrhage, congestion, necrosis or fibrosis. Microscopically Uniform cords of bland appearing hepatocytes with intracellular fat. Generally ecnapsulated. Have a purly arterial blood supply

Question 56

How are hepatic adenomas classified?

Answer 56

- Hepatocyte nuclear factor alpha (HNF1a) germline mutated adenomas – 30-35%. Low risk of progression to malignancy. More common in young woman and a/w OCP. - Inflammatory – 30% of adenomas. more common in obese patients or NAFLD, more likely to be associate with haemorrhage. - b-catenin mutated adenomas - 10% of adenomas - much higher incidence of malignancy Sonic hedgehog adenomas – rare.

Question 57

What are the CT and MRI findings of hepatic adenomas?

Answer 57

CT - Due to mixed composition of cells, fat and haemorrhage these lesions often look heterogenous. - Unenhanced CT – hypodense - Arterial phase – enhance (centripetal) - Portal venous phase – may show washout and become isodense but less intense than HCC. Mainly has an arterial blood supply (unlike benign lesions) MRI - T1 imaging – hyperintense and heterogenous - T2 imaging – hyperintense and heterogenous - Won't take up primovist

Question 58

What are the indications for resection of hepatic adenomas?

Answer 58

All adenomas in men. Adenomas >5cm after cessation of the pill in woman. B-catenin mutated tumours (if biopsy has been taken). So when can you observe? - Woman with hepatic adenomas <5cm

Question 59

What are the CT and MRI findings of haemangioma?

Answer 59

CT - Hypodense on non-contrast phase - Arterial phase – nodular peripheral enhancement - PV – enhancement continues towards the centre of the lesion (centripetal filling). - Delayed phase – ongoing enhancement of the lesion MRI - Looks very bright (lightbulb sign) on T2 imaging (because haemangiomas are fluid filled) - Looks hypointense on T1 imaging compared to surrounding liver. When given with Primovist contrast - have nodular enhancement with progressive centripetal filling.

Question 60

What are the indications for intervention of a haemangioma?

Answer 60

Indications for intervention - Majority are observed - Symptoms * Compressive * Kasselbach-Merrit syndrome ○ Severe thrombocytopenia and DIC due to consumption of platelets, clotting factors and fibrinogen by the tumour - Diagnostic doubt Relative indications - Growth on interval imaging - Tumours which are greater than 10cm (not 5cm like hepatic adenomas) - Patients who play contact sport.

Question 61

What is the treatment of pyogenic liver abscess?

Answer 61

- Give the patient antibiotics - Abscess < 5cm - needle guided aspiration. - Abscess > 5cm - needle guided aspiration and placement of catheter. - Percutaneous drainage can be repeated if necessary. - For abscesses < 3cm and not easily drainage - reasonable likelihood of success with antibiotics alone. - Total course of antibiotics should be 6 weeks. - Important to identify and treat any underlying cause. Patients with who have failed percutaneous approach. - Open or laparoscopic surgical drainage Follow up - Some people would advocate for repeat imaging to ensure resolution. Colonoscopy should be performed to rule out an underlying malignancy.

Question 62

What is the lifecycle of the echinoccocus tapeworm?

Answer 62

- The echinococcus tapeworm spends its life in the small bowel of dogs (definitive host) - The dog then sheds the eggs in the faeces which infect an intermediate host such as sheep - Eggs are ingested sheep and larvae are released due to digestion from enzymes in the upper GI tract in humans - Larvae penetrate jejunum and travel to the liver. - Cyst is usually present after 3 weeks. - Dogs come and eat the dead sheep which results in infection of the definitive host. Humans are accidental intermediate hosts.

Question 63

What are the layers of an echinoccocus cyst?

Answer 63

- Inner layer – endocyst (germinal layer) – fluid filled, responsible for the production of Hydatid fluid, also contains protoscolices (potential worm heads). - Next layer is the ectocyst (laminated layer) – acelluar hylar membrane around the inner layer. - Pericyst – host derived fibrous capsule

Question 64

How to patients with echinococcus liver cysts present?

Answer 64

- Typically are asymptomatic small cysts - If the cyst ruptures – can result in dissemination of echinococcus in the peritoneum and blood stream which can cause an acute anaphylactic reaction. - Can put pressure on the biliary tree causing jaundice and cholangitis. - Can present with RUQ pain if they are large or irritating parietal peritoneum. - Can rupture causing acute pain. - Can get secondarily infected causing hepatic abscesses. Rarely the cyst can cause pressure on the hepatic veins causing a Budd-Chiari type syndrome.

Question 65

How are echinococcus cysts classified?

Answer 65

CE1 - simple, unilocular cyst CE2 - cyst with well defined septations. CE3a - cyst with detached membrances (water-lilly sign) or poorly defined septations. CE3b - cyst with daughter vesicles within a solid matrix. CE4 - cyst with heterogenous content and no daughter vesicles. CE5 - cyst with a calcified wall.

Question 66

How do you perform and open cyst drainage of an echinococcus cyst?

Answer 66

- This may be an option where you are worried about damaging major structures nearby. - Patients should be given 3 months of albendazole. - A laparotomy is performed. - Packs soaked in hypotonic saline are placed around the liver cutting off the remaining peritoneum. - The cyst is punctured at its most accessible part. - The contents of the cyst are drained. - The cavity is flushed with a scolicidal agent. - The germinal layer is removed (endocyst) as well as the ectocyst The cavity is filled with omentum.

Question 67

What is the pathophysiology of Amoebic liver abscess?

Answer 67

- Faecal-oral spread route (human to human) - Cystic form of parasite is ingested by humans. - Trophocytes are released in human GI tract and multiply in the colon. - Trophocytes then reach liver through PV and lymph circulation. Can also be through direct extension through colon wall!

Question 68

What is the treatment of an amoebic liver abscess?

Answer 68

Treatment - You need both a luminal agent and a tissue agent. - Tissue agent is metronidazole for 7-10 days. - Luminal agent is Paromycin (to remove any cysts within the bowel) Perc drainage is only recommended when medical therapy has failed or if cyst is at high risk of rupture.

Question 69

What does Schistosomiasis cause?

Answer 69

- Liver fluke which is endemic in Latin America, Africa and asia. - Water-borne infection. - Important cause of liver fibrosis – causes a granulomatous infection in the pre-sinusoidal peri-portal spaces. - Often will get minimal symptoms with early infection. - Chronic infection leads to liver fibrosis which is not reversible. Diagnosed by detection of parasitic eggs within the stool.

Question 70

What is the liver injury grading system?

Answer 70

Liver injury grading - The American Association for the Surgery of Trauma Organ injury Scan (AAST-OIS) is commonly used. - Looks at the presence of haematoma, laceration, and active bleeding. AAST I - Subcapsular haematoma < 10% surface area - Parenchyma laceration <1cm in depth. AAST II - Subcapsular haematoma 10-50% of surface area: - Intraparenchymal haematoma <10cm in diameter - Laceration 1-3cm in depth and < 10cm in length. AAST III - Subcapsular haematoma > 50% of surface area, intraparenchymal haematoma > 10cm, - Laceration >3cm in depth - Active bleeding contained within the liver parenchyma AAST IV - Parenchymal disruption involving 25-75% of a hepatic lobe - Active bleeding extending beyond the liver parenchyma into the peritoneum. AAST V - Parenchymal disruption > 75% of a hepatic lobe. - Venous injury including vena cava or central hepatic veins.

Question 71

Risk factors for gallstone formation?

Answer 71

- Family history - More common and white European and American populations. - Least common in Black Africans. - Female sex (10:1), previous pregnancy (on the basis that oestrogen stimulates hepatic cholesterol excretion and reduces bile sale secretion, thus promoting stone formation), and pregnancy (results in reduced gallbladder motility, which promotes stone formation). - Obesity – due to increased biliary secretion of cholesterol causing supersaturation in the bile. - Ileal Crohn's - due to decreased bile acid enterohepatic absorption leading to cholesterol supersaturation in bile (and thus cholesterol stones) - Rapid weight loss (excess hepatic cholesterol excretion into bile)

Question 72

What are the different types of gallstones and how do they form?

Answer 72

Pathogenesis of gallstone formation - Bile is composed of bilirubin, cholesterol, fatty acids, and minerals. - If one of the major components is present in excess - supersaturation occurs (bilirubin excess = pigments stones, cholesterol excess = cholesterol stones. - For stones to form - need a nidus. Mucin, acts as a nidus. - Biliary stasis also contributes - which can occur in pregnancy, obesity and diabetics. Cholesterol stones - Most common type of gallstone. - Can be light yellow, dark green, or chalk white - Primarily made of cholesterol - Normally, cholesterol is transported in the bile in Micelles (cholesterol, bile salts, and lecthicin) - When bile becomes supersaturated with cholesterol - it precipitates out as crystals. - Factors which drive this are obesity, high-fat diet. Pigment stones (Black stones) - Account for 10% of all gallstones. - Gallstones are composed mainly of calcium bilirubinate. - Excess of unconjugated bilirubin as a result of increased RBC breakdown - Most common in patients with chronic haemolytic anaemia – hereditary spherocytosis, sickle cell disease, B thalassemia. - Also seen in patients with pernicious anaemia and liver cirrhosis. Brown stones - Composed of calcium bilirubinate mixed with calcium soaps and cholesterol - Form due to infect bile - Bacteria produced enzymes (Beta-glucuronidase) which deconjugate bilirubin - calcium binds - becomes supersaturated forming stones. More common in Asian population and people with biliary tract strictures/recurrent infection.

Question 73

How is cholecystitis graded as per the Tokyo Guidelines? How does this influence management decisions?

Answer 73

- Grade 1 * Acute cholecystitis without organ dysfunction and mild inflammatory changes. * Early laparoscopic cholecystectomy - Grade 2 * WCC > 18 * Palpable tender mass * Duration of symptoms > 72 hours. * Marked local inflammation - gangrene, pericholecystic abscess, hepatic abscess etc. * Early laparoscopic cholecystectomy - Grade 3 * Associated with organ dysfunction of at least 1 system. ○ Cardiovascular - hypotension. ○ Neurological - decreased GCS ○ Respiratory - Pa02/Fi02 < 300 (hypoxia) ○ Renal - Oliguria or creatinine >180 ○ Hepatic - INR > 1.5 ○ Hematological - platelets <100 - If organ dysfunction favorable (i.e. renal impairment or cardiovascular) and reversible - can perform laparoscopic cholecystectomy - If organ dysfunction is not favorable (hepatic, neurological, respiratory) or not reversible - biliary drainage.

Question 74

How is Mirizzi syndrome graded?

Answer 74

- Type 1 – external compression of CBD but no fistula present. - Type 2 – stone has eroded into the bile duct resulting in a fistula affecting 1/3 of the CBD circumference - Type 3 – stone has eroded affecting up to 2/3 of the CBD. Type 4 – stone has eroded causing complete destruction of CBD wall.

Question 75

How is a Mirizzi usually managed?

Answer 75

Type 1 Mirizzi syndrome - Can be treated with subtotal cholecystectomy leaving the posterior wall which is usually adherent with the bile duct. - If the cystic duct is present can be ligated but sometimes it cannot be found in which case a drain should be left. If a bile leak develops manage with ERCP. Type 2-4 Mirizzi - Defined as a fistula between the gallbladder and bile duct. Bile duct closure or T-tube insertion rarely works and Roux-en-Y HJ is usually required.

Question 76

What is the pathogenesis of acalculous cholecystitis?

Answer 76

- Found in ICU patients - Cause is multifactorial * Ischaemia - gallbladder has a terminal arterial supply - making it vulnerable to ischaemia * Stasis - results in bile becoming concentrated which promotes inflammation and can become secondarily infected.

Question 77

What are the risk factors for acalculous cholecystitis?

Answer 77

Risk factors include burns, trauma, cardiopulmonary bypass, prolonged fasting, TPN, sepsis, diabetes, atherosclerosis, systemic vasculitis, acute renal failure, and AIDS.

Question 78

How are biles duct injuries classified?

Answer 78

Bile duct injury classification - Was originally just the Bismuth classification but then Strasberg added to it (to include other bile duct injuries other than main duct and confluence injuries) Strasberg classification Classification of bile duct injury - A=injury to duct of Lushka or cystic duct. - B=right posterior sectoral duct has been clipped or occlude. - C=right posterior sectoral duct is leaking - D=injury to CBD with leakage of bile but not circumferential injury - E=full circumferential injury to CBD. Type E injuries (this is the same as the Bismuth classification of strictures) 1. Transection >2cm from confluence 2. Transection < 2cm from confluence 3. Injury to confluence but the confluence still intact 4. Destruction of confluence 5. Injury to the main bile duct and injury to the right posterior sectoral duct.

Question 79

What are the risk factors for a gallbladder polyp harbouring malignancy?

Answer 79

- Patients > 60 years of age. - Indian, Chilean, and Eastern Europe. - Sessile polyp - Multiple polyps - Known PSC – much higher risk of developing gallbladder cancer. - If contains internal vascularity - more likely to be a true adenomatous polyp.

Question 80

What is the management of gallbladder polyps?

Answer 80

Polyps which can be surveilled - Polyps < 6mm in size. - Polyps 6-9mmg in size with no risk factors Polyps which requires cholecystectomy - 6-9mm in size with risk factors – cholecystectomy. - For any polyp under surveillance - if it grows by > 2mm or reaches 1cm – cholecystectomy.

Question 81

What are the risk factors for gallbladder cancer?

Answer 81

Chronic inflammation is the main risk factor - Gallstones - PSC - Anomalous pancreaticobiliary junction - Cholecystoenteric fistula - Typhoid infection - Adenomatous polyps. - Calcified wall/Porcelain gallbladder – incidence of gallbladder cancer is about 10% * Occurs in the setting of a chronically inflamed gallbladder, where calcium salts are deposited in the gallbladder wall - a process known as dystrophic calcification. Calcification typically occurs in the muscularis layer and can extend to the serosal surface.

Question 82

What is the T staging of gallbladder cancer?

Answer 82

T1a - mucosa. T1b - muscularis. T2 - perimuscular connective tissue. No extension beyond serosa or into liver. T3 - perforates serosa OR extends into liver < 2cm, or extension into one adjacent organ. T4 - tumour extends into liver by >2cm OR two or more adjacent organs.

Question 83

What should you do with a post-operative diagnosis of a gallbladder cancer?

Answer 83

- Unless it is a T1a tumour (which is treatment complete), patients should be referred to an HPB centre. T1b + tumours (muscularis) require a cholecystectomy, partial hepatectomy of segment IVb and V, and a portal lymphadenectomy.

Question 83

What treatment is given adjuvantly for gallbladder cancer?

Answer 83

The BILCAP study published in 2019 showed capecitabine had a higher median survival than surveillance.

Question 84

How does a HIDA scan work?

Answer 84

How does a HIDA scan work? - Technitium-99 HIDA is injected - HIDA is a synthetic compound which mimics bile - is taken up by the liver and excreted in the bile. - A gamma probe is used to detect the radiotracer as it moves through the liver, gallbladder and biliary system. - The gallbladders contraction is tested by injecting cholecystokinin (CKK) * The gallbladder ejection fraction can then be calculated A low gallbladder EF suggests chronic cholecystitis or gallbladder dysfunction.

Question 85

How does a HIDA scan help you when evaulating a patient with functional biliary pain?

Answer 85

- Patients with a low gallbladder ejection fraction (<40%) may benefit from lap cholecystectomy although the evidence is controversial. Even patients with a normal gallbladder ejection fraction may benefit - although this is controversial.

Question 86

What are the types of sphincter of oddi dysfunction?

Answer 86

Organic stenosis (formerly type 1) Biliary pain with 1. No bile duct stones 2. Abnormal LFTs AND dilated common bile duct 3. Delayed drainage of ERCP contrast beyond 45 minutes. Functional sphincter of Oddi disorder (formerly type II) Biliary pain with 1. No bile duct stones 2. Elevated LFTS OR dilated duct but not both Functional biliary-type pain (Type III) Biliary pain 1. No bile duct stones. 2. Normal LFTS AND normal ducts Criteria for pancreatic sphincter of Oddi dysfunction 1. Recurrent attacks of acute pancreatitis - with lipasaemia or imaging findings 2. Other causes of pancreatitis excluded. 3. Normal pancreas and endoscopic USS Abnormal sphincter manometry.

Question 87

What is the treatment of spincter of oddi dysfunction?

Answer 87

Treatment - Organic stenosis (Type 1) - endoscopic sphincterotomy - Functional sphincter of Oddi patients (Type 2) - manometry, and those with high pressure sphincters should have a sphincterotomy. - Functional biliary type pain (Type III) - should not be offered sphincterotomy.

Question 88

Wha are the causes of biliary strictures?

Answer 88

Iatrogenic - post gallbladder surgery - post liver transplant - post hepaticojejunostomy - trauma Gallstone related - Mirizzi syndrome Inflammatory related - Recurrent cholangitis - Parasitic infections (liver flukes and Echinococcus) - PSC - HIV/AIDS cholangiopathy - Pancreatitis - IgG4 cholangiopathy Congenital - Choledochal cysts - Biliary atresia

Question 88

Why does HIV cause biliary strictures?

Answer 88

- Thought to develop due to secondary opportunistic infections within the biliary tree and then subsequently cause inflammation, intraductal stones and strictures. - CMV, cryptosporidium are common infections. - Can cause papillary stenosis, and long segment extra-hepatic strictures. Anti-retroviral treatment can be associated with regression.

Question 89

What is the aetiology of choledochal cysts?

Answer 89

- A single mechanism of bile duct cysts is unlikely given there is a spectrum of disease. - Most widely accepted hypothesis is cysts occur due to an abnormal pancreatico-biliary duct junction. - Proteolytic enzymes in pancreatic juice result in a deterioration of the duct wall. - Epithelial damage can lead to mucosal dysplasia and malignant transformation. Some people think that at type II cyst is more likely due to a congenital defect in the wall and thus less likely to be associated with malignancy.

Question 90

What is the Todani classification of choledochal cysts?

Answer 90

- Type I – solitary cyst of the extrahepatic biliary tree – fusiform dilation – most common. - Type II – diverticulum of the bile duct (can look like a duplication of the gallbladder). - Type III – dilatation of the distal CBD within the duodenal wall (choledochocele) - Type IVa – multiple extrahepatic cysts and intrahepatic cysts - Type IVb – multiple extrahepatic cysts only. Type V – multiple intrahepatic cysts, but no extrahepatic cysts (also known as Caroli disease)

Question 91

Why do we treat choledochal cysts?

Answer 91

To reduce the risk of malignancy, episodes of cholangitis, pancreatitis

Question 92

What is the treatment for each type of choledochal cyst?

Answer 92

Type I - resection of entire extrahepatic biliary tree with bilioenteric anastomosis (can either be a hepaticoduodenostomy or hepaticojejunostomy) - This includes resection of the intra-pancreatic duct segment - this segment can get dysplastic change associated with a "field defect". Type II - cholecystectomy + cyst excision is the treatment of choice. - In 50% of cases, patients require a more extensive procedure due to the associated inflammatory reaction - this includes a bile duct resection. Type III - malignant transformation is very rare and is generally managed with an endoscopic sphincterotomy (as opposed to Whipple’s!!!) Type IVa - The extra-hepatic component as a type I cyst. - The management of the intra-hepatic component will depend on the degree of disease, associated stones, strictures etc. If there is localized disease a segmental resection can be performed. Type IVb Same approach as a type I cyst (entire extra-hepatic excision of the bile duct) .

Question 93

What is primary biliary stenosis?

Answer 93

- Is more accurately called primary biliary cholangitis - Is a chronic, progressive autoimmune liver disease primarily affecting the intra-hepatic bile ducts, leading to cholestasis, fibrosis and potentially cirrhosis if left untreated. - Pathophysiology * Autoimmune destruction of small intrahepatic bile ducts. * Impaired bile flow (cholestasis) - accumulation of bile acids - hepatocellular damage and fibrosis. - Management * Ursodeoxycholic acid - improves bile flow and delays disease progression. * Cholesyramine - Complications * Portal hypertension. * Cirrhosis and liver failure * ADEK deficiency. - HCC

Question 94

What is the pathophysiology of pancreatitis?

Answer 94

- Three pathways thought to precipitate pancreatitis - ductal obstruction, direct damage to acinar cells leading to pancreatic enzyme leak, or defective intracellular transport of pro-enzymes - Pancreatic duct obstruction – raises duct pressure, causes accumulation of pancreatic fluid within the gland. - Alcohol increases protein viscosity within the small ducts leading to segmental obstruction. - There is leak of intracellular lysosomal enzymes which mix with pancreatic pro-enzymes resulting into autodigestion. - The other pathway is primary injury to acinar cells – causes from viruses, drugs, shock, ischaemia. - Damaged acini leak pancreatic enzymes. - Last pathway is defective intracellular transport of pro-enzymes – as in cystic fibrosis. - Cellular injury leads to mixing of zymogen granules with trypsin - which results in autodigestion within the pancreas gland. - Leads to local damage with swelling, necrosis etc. - Lipase breaks down TAGS to Fatty acids - which results in the formation of calcium soaps - can drive hypocalcaemia. - Inflammation activates neutrophils and macrophages, which release inflammatory cytokines such as IL-1, 6, 8, and TNF-alpha which increase local response and also cause a SIRS response - Complement pathway and coagulation pathway is also activated – can cause small vessel thrombosis and necrosis. - Cytokines causes endothelial dysfunction/leaky capillaries systemically – thus peripheral oedema and respiratory interstitial oedema, renal failure etc.

Question 95

What is the modified GLASGOW score?

Answer 95

P - Pa02 < 80mmHg A - Age > 55 years N - Neutrophils > 15 C - calcium < 2 R - creatinine - urea > 16 E - Enzymes - LDH > 600 A - albumin < 32 S - sugar > 10

Question 96

What is the ATLANTA classification for acute pancreatitis?

Answer 96

Revised ATLANTA classification 2012 - Divides pancreatitis into 3 groups – mild acute pancreatitis, moderately severe acute pancreatitis and severe acute pancreatitis. Mild acute pancreatitis - No organ failure - OR local complications - OR systemic complications. Moderately-severe pancreatitis - Transient organ failure which lasts < 48 hours - OR local complications such as peri-pancreatic fluid collections or necrosis - OR systemic complications such as an exacerbation of pre-existing disease. Severe acute pancreatitis - Persistent organ failure after 48 hours. NB: Organ failure is renal, cardiovascular, or respiratory and is determined using the Modified Marshall scoring system.

Question 97

What are some early and late complications of pancreatitis?

Answer 97

Early complications of pancreatitis - Splenic artery pseudoaneurysms and haemorrhage - PV thrombosis and occlusion. - Stomach/duodenal ulceration - Gastric outlet obstruction (can be due to oedema or pancreatic collections) - Bile duct stricture or duodenal stricture. - Infarction of transverse colon due to thrombosis of middle colic. - Disconnected duct syndrome – leads to disruption of the pancreatic duct. Late complications of pancreatitis - Development of pseudocysts or walled off necrosis. - Pancreatic ascites - Pancreatico-duodenal fistulas - Pancreatic insufficiency – exocrine or endocrine. - Adenocarcinoma.

Question 98

Why is delayed feeding contra-indicated in the management of acute pancreatitis?

Answer 98

Delaying feeding increases the risk of infective peri-pancreatic necrosis and increases need for interventions for necrotizing pancreatitis

Question 99

What is the step up approach for treatment of pancreatitis?

Answer 99

‘Step up’ approach - Perc drainage followed by upsizing drains followed by minimally invasive retroperitoneal necrosectomy. - Proven to be superior than open necrosectomy in NEJM 2010 (PANTER trial) · Reduction in major complications · Other studies have shown it to have a lower risk of mortality - Minimally invasive approach reduced rate of complications and death. - By using the most minimally invasive technique, you are avoiding the SIRS response associated with major surgery. Endoscopic step-up approach - Endoscopic approach has been compared to surgical step up approach · Same mortality and morbidity outcomes. Endoscopic found to have shorter length of hospital stay without the risk of pancreatico-cutaneous fistula.

Question 100

What is the pathogenesis of chronic pancreatitis?

Answer 100

- Two hit theory– initial hit which initiates acute pancreatitis followed by an abnormal response which leads to inflammation becoming chronic and chronic pancreatitis. - Toxic metabolite theory – alcohol and tobacco and other environmental factors damage acinar cells which result in chronic obstruction - Ductal blockade theory – protein plugs form within pancreatic ducts. Protein plugs cause an increase in the ductal pressure which leads to acinar cell autodigestion and inflammation. Alcohol is through this pathway as it makes the ductal system liquid “thicker”. Oxidative stress theory – oxidative stress causes free radical production within the acinar cells which leads to activation of inflammatory pathways.

Question 101

Why do patients with chronic pancreatitis get bad pain?

Answer 101

- Chronic pain – likely due to increased pressure within the ductal system – there has been a demonstrated relationship between the intra-pancreatic ductal system and pain. There is inflammatory involvement of the intra-pancreatic nerve fibers – inflammatory cells infiltrate around the nerves. There is an increase in the amount of nerve fibers within the pancreas and there is also an increased in neuro-transmitters such as substance

Question 102

How is Chronic pancreatitis diagnosed?

Answer 102

If diagnosed on history, evidence of pancreatic insufficiency, evidence of endocrine dysfunction, risk factors, and imaging findings

Question 103

What are the USS and CT findings consistent with chronic pancreatitis?

Answer 103

- USS – may show intraductal calcifications and parenchymal calcifications. Pancreatic duct dilatation and irregularities. Evidence of previous AP such as pseudocysts and splenic vein thrombosis. CT with IV contrast – helpful to diagnose CP and look for complications of AP and CP. Will see loss of pancreatic volume, inflammation around the pancreas, fibrosis, and ductal findings including beading and irregularities, dilated side-branch radicals, enlargement of the main pancreatic duct, calcifications within the pancreatic parenchyma.

Question 104

What are the complications of chronic pancreatitis?

Answer 104

- Chronic pancreatitis is associated with pancreatic adenocarcinoma - Biliary stricture – distal aspect of CBD - Duodenal stenosis and gastric outlet obstruction. - Pseudocyst formation - False aneurysms of visceral vessels. - Portal and splenic vein occlusion – had lead to extrahepatic portal hypotension – which can present with haematemesis and melena. Pancreatic ascites and fistula

Question 105

How is pancreatic exocrine insufficiency diagnosed? How do you treat it?

Answer 105

- Test using faecal elastase. >200 units/gram is normal. <100 units/gram is severe exocrine insufficiency. * The faecal elastase result will not change with Creon administration. - Creon is used as replacement therapy. - Creon can be based on clinical suspicion alone. - Dietician needs to be involved in the setting of steatorrhoea. * To monitor response of Creon - should be done on the basis of symptoms ○ Diarrhoea - Nutrition status.

Question 105

What are the goals of treatment for a patient with chronic pancreatitis?

Answer 105

* Modify exacerbating behaviors. * Detect and treat pancreatic insufficiency (exocrine and endocrine(. * Determine contributing factors to abdominal pain and manage pain. - Enable the pancreas to heal itself.

Question 106

What are the non-surgical treatments for chronic pancreatitis?

Answer 106

Treat pancreatic exocrine insufficiency with Creon. Manage pain - can use neuromodulators like gabapentin. Can also consider a coeliac plexus block.

Question 107

What are the endoscopic and surgical treatment options for chronic pancreatitis?

Answer 107

Endoscopic stent to pancreatic duct - can be used for a dilated pancreatic duct with stones. Duval procedure - Distal pancreatectomy and splenectomy followed by a PJ anastomosis - won't be efffective for proximal pancreatic disease. Peuwstow procedure - longitudinal panreaticojejunostomy Frey procedure - longitudinal pancreaticojejunostomy with a pancreatic head resection. Berger procedure - Duodenum preserving pancreatic head resection

Question 108

What is the pathogensis of pancreatic cancer?

Answer 108

- Stepwise progression of pancreatic ductal intraepithelial neoplasia to pancreatic cancer - this is the most common cause of pancreatic cancer. Note the mutation are similar to the ones in the conventional colorectal cancer pathway i.e. KRAS, TP53, SMAD4. * Generally a KRAS mutation is the first mutation which activates the process. - Conversion of an IPMN - Development of a malignancy from a mucinous cystic adenoma.

Question 109

CA19-9

Answer 109

- Both correlates with prognosis and helps assess response to treatment. - Is indicative of occult metastatic disease. - Usually CA-19-9 levels > 100 suggests unresectable disease or metastatic disease. - Can be elevated in patients with biliary obstruction thus needs to be rechecked once obstruction is relieved. - About 10% of patients don’t secrete CA19-9.

Question 110

What are the CT findings of a pancreatic cancer? What things should you look for

Answer 110

- Double duct signs is suggestive. - Usually present as a hypodense poorly defined mass. - Pancreatic atrophy, loss of glandular contour are other signs. - Often don’t enhance well on arterial imaging and then will become isodense on delayed imaging. Things to comment on when looking at a pancreatic tumour You should assess SMA, coeliac axis, SMV, PV, SMV/PV confluence, Regional lymph nodes, Any evidence of distant disease - hepatic or peritoneal. Any ascites.

Question 111

What is the role of pre-operative ERCP and stenting for patients with pancreatic cancer?

Answer 111

- Like cholangiocarcinoma, this is a topic of ongoing debate. - Jaundiced patients often have poor nutrition and coagulopathy. - Pre-op decompression is associated with procedure specific complications such as cholangitis and pancreatitis. - Opening up the ampulla may contaminate the biliary tree - increasing the risk of post-operative infectious complications.

Question 112

What is the staging of pancreatic cancer?

Answer 112

T1 - tumour < 2cm T2 - tumour 2-4cm T3 - tumour >4cm T4 - tumour involving coeliac axis or SMA N1 - metastasis in 1-3 regional nodes. · CHA, Proximal coeliac, pancreaticoduodenal vessels, SMV, portal vein and SMA nodes. N2- metastasis in 4+ nodes.

Question 113

How is resectability assessed for pancreatic cancer?

Answer 113

A – anatomy of the tumour, which vessels involved etc. B – biology of the tumour i.e. levels of CA 19-9, evidence of lymphadenopathy C – condition of the patient – performance status and co-morbidities. Resectable - No abutment, distortion, encasement or occlusion of SMV or PV - No direct distortion to SMA or coeliac or CHA – need to see a clear fat plane around these vessels. - No lymphadenopathy. Borderline resectable - Can have distortion, narrowing, and even occlusion of SMV or PV as long as they are reconstructable - Can have focal abutment (less than 180 degrees) or SMA or coeliac. - If adjacent organs are involved - they need to be resectable. Locally advanced unresectable tumours. - Encasement of arteries (>180 degrees) - Occlusion of vein with no option of reconstruction.

Question 114

What is the utility of neoadjuvant chemotherapy for pancreatic cancer?

Answer 114

Neoadjuvant chemotherapy - Benefits: · Treats early micro metastatic disease · Patients are more likely to receive the full surgery-chemotherapy "package" if chemotherapy is given upfront. · Allows tumour biology assessment, and thus select patients which are going to have the most benefit from surgery. Thus will avoid doing a highly morbid operation on a patient with limited survival. · There have been some studies which have shown an increased R0 resection rate. - Arguments against. · There is no proven survival benefit for neoadjuvant chemotherapy for patients with pancreatic cancer (compared with adjuvant) · Patients can progress while on chemotherapy ○ This can be looked on as a good or bad thing. When should neoadjuvant chemotherapy be considered? - It is very institution dependent but is generally used for "bad tumours" i.e. · Large · Associated with lymphadenopathy. · Arterial abutment or vein invasion. · High CA19-9

Question 115

What are the complications which can occur after a Whipples.

Answer 115

- Pancreatic leak/pancreatic fistula. If patient is unwell, associated with a poor outcome. Risk factors include having a soft pancreas, narrow duct, or significant intra-operative blood loss. - Bleeding and pseudoaneurysm - Often associated with a pancreatic leaks - Bile leak - Delayed gastric emptying – there is controversy on whether you should preserve or remove the pylorus – a Cochrane review showed no difference. - Diabetes - Exocrine dysfunction. - Dumping syndrome. Risk of mortality after a pancreatic resection is 1-2%.

Question 116

Who do you diagnose, classify, and manage a pancreatic leak?

Answer 116

- Definition * Drain amylase > 3x upper limit of normal n POD3 after pancreatic surgery - Classification * Grade A: asymptomatic - resolves with minimal intervention * Grade B: Symptomatic, requiring persistent drains, nutritional support (TPN), and possible percutaneous drainage. * Grade C: Severe, requiring ICU care, surgical re-exploration, often with sepsis. - Management * Supportive - NPO, octreotide, TPN * Drain management - Surgical intervention - rare - only for uncontrolled leaks.

Question 117

What are the risk factors for an IPMN?

Answer 117

- Occur equally in men and woman. - More common in elderly patients. - More common in patients with a history of pancreatitis - Most common location is the head - Associated with smoking, chronic pancreatitis Associated with colon, breast and prostate cancer.

Question 118

What are the high risk stigmata of an IPMN?

Answer 118

Remember as - x1 clinical - x2 imaging - x1 FNA Obstructive jaundice. Enhancing mural nodule >5mm Main pancreatic duct dilatation > 10mm. Suspicious or positive results of cytology.

Question 119

What are the worrisome features?

Answer 119

x3 clinical and x6 imaging. Clinical - acute pancreatitis. - elevated CA19-9 - New onset or exacerbation of diabetes. Imaging - cyst >30mm - Enhancing mural nodule <5mm. - thickened/enhanced cyst wall. - MPD dilatation 5-9mm. - lymphadenopathy. - cystic growth rate >2.5mm/year.

Question 120

When performing an FNA of a mucinous neoplasm - what should you be testing for?

Answer 120

NA If you are doing an FNA of a IPMN you would expect - High CEA level (because of mucin component) - Mucin containing columnar cells with variable atypia. - FNA isn't sensitive at picking up dysplastic cells but if it does then it is highly specific for HGD/IC (which is why it’s a high risk stigmata) FNA with DNA analysis - This is an emerging technology. - Cyst fluid can be DNA evaluated - this can help determine what type of lesion it is AND can help predict the likelihood of advanced neoplasia. - VHL mutation present = serous cystadenoma. - KRAS mutation - more likely to be an IPMN or MCN. TP53, SMAD4 - more likely to be associated with advanced neoplasia

Question 121

What are mucinous cystic neoplasms of the pancreas? Who gets them? What are the CT findings? What are the histology findings?

Answer 121

- The risk of harboring malignancy is 30% (usually non-invasive) - 10:1 female preponderance. - Average age at diagnosis – 45 years old. - More commonly found in the body and the tail of the pancreas - any macrocystic lesion in the distal pancreas of a female should be considered a MCN until proven otherwise CT findings - Well circumscribed cystic lesion with peripheral calcifications (egg shell sign) Histology findings - Have a lining of columnar epithelium which secretes mucin as well as an ovarian like stroma staining positive for oestrogen and progesterone receptors. FNA – will have a high CEA level (>192) given that it is a mucin secreting tumour.

Question 122

What is the treatment of MCNs?

Answer 122

- Guidelines differ! - The IAP recommend resection for all MCN's regardless of size whereas the European guidelines recommend MCN's < 4cm can be surveilled if there are no high risk features. - European indications for resection * >4cm * <4cm with high risk features - main duct dilatation, enhancing mural nodules, or symptoms related to the cyst. If a patient does not proceed to a resection and is surgically fit, they should be offered life long surveillance (6 monthly to 1 year intervals)

Question 123

What are serous cystadenomas?

Answer 123

- Always benign - Non-mucinous lesion - Account for ¼ of cystic tumours of the pancreas - Grow very slowly - Can be associated with Von-Hippel-Lindau disease - Have a female:male preponderance. More likely in the elderly.

Question 124

What is the histological and radiological findings of serous cystadenomas?

Answer 124

Histology - Can be found anywhere in the pancreas. - Have a honeycomb appearance and calcified central scar without haemorrhage. The honeycomb appearance is due to septations with thick fibrous with innumerable small cysts containing clear fluid. - Benign neoplasms with cuboidal cells lining their cysts which originate from the pancreatic entero-acinar cells. Radiology - On radiology look like a bunch of grapes or honeycomb appearance. - Can have a central calcification in a starburst pattern - If unclear – EUS and FNA – because it is a non-mucinous lesion will have a low CEA, low amylase, and stain positive for periodic acid-schiff (PAS)

Question 125

What are solid pseudopapillary neoplasms and how do they present?

Answer 125

- Non-mucinous neoplastic lesion - Solid tumour which gets cystic degeneration - Much more common in woman than men 10:1. Often found in young woman. - Very rare tumour. - Associated with B-catenin mutation. - Also have a malignancy risk – 15% risk. - Also have a local infiltrating capacity. - Often found very large at diagnosis with a median size of 8cm. Most commonly found in the body and tail of the pancreas Can sometimes present with rupture causing haemoperitoneum.

Question 126

What is the treatment of solid pseudopapillary neoplasms?

Answer 126

Resection based on a 15% risk of malignancy. Are often large at diagnosis - thus may get mass associated symptoms.

Question 127

What is Whipple triad?

Answer 127

Refers to the presentation of an insulinoma - Fasting hypoglycaemia symptoms. - Low fasting blood sugar level. - Blood sugar level rises if IV glucose is given.

Question 128

Insulinomas, are they usually: - solitary or multiple? - benign or malignant? - common or uncommon PNET? - avid on Dotatate-PET?

Answer 128

Solitary Benign Most common PNET Usually not avid on Dotatate-PET

Question 129

What percentage of insulinoma's and gastrinoma's are associated with MEN1?

Answer 129

10% and 25%

Question 130

What percentage of gastrinomas are malignant?

Answer 130

90%

Question 131

How does a Gastrinoma cause Zollinger-Ellison syndrome?

Answer 131

Gastrin acts on the parietal cells to release HCl - this can result in ulcers as well as diarrhoea.

Question 132

When should you suspect Zollinger-Ellison syndrome?

Answer 132

Patients with peptic ulcer disease and no risk factors Peptic ulcer disease which is resistant to treatment Peptic ulcer disease in patients with diarrhoea Peptic ulcers in unusual locations.

Question 133

How do you diagnose a Gastrinoma?

Answer 133

Fasting gastrin levels - 10x upper limit of normal. WITH a gastric pH of < 2. Imaging - are usually avid on Dotatate-PET

Question 134

What are the 4 H's of VIPoma?

Answer 134

High volume watery diarrhoea Hypokalaemia. Hypochlorhydria. Hypovolaemia. Diagnose with a fasting VIP level.

Question 135

What are the 4 D's of a Glucagonoma?

Answer 135

Dermatitis - necrolytic migratory erythema. Diabetes DVT Depression. Diagnose with a fasting glucagon level.

Question 136

What are the imaging characteristics of PNETs on CT, MRI, EUS, and Dotatate PET?

Answer 136

USS - Often performed but views often poor. CT - Good for PNETs at least 2cm in size - Sensitivity of 70-90% - Lesion is hyperattenuating compared to surround pancreatic parenchyma. Bright enhancement on arterial phase MRI - On T1 will have a low signal and high on T2 - Sensitivity of 80-90% EUS - This is the most sensitive test for small tumours (i.e. insulinomas) - Sensitivity 90%. - Also allows for FNA of non-functioning tumours. Dotatate-PET - Dotatate is a radiolabeled analogue thus is useful for localisation of PNETs. Insulinomas generally don't express somatostatin receptors thus are less sensitive

Question 137

How is angiography used to localise a PNET?

Answer 137

Selective angiography - This involves hepatic vein sampling after the administration of a stimulus to a feeding artery (as a proxy for portal vein sampling) to localise a PNET - The arterial tree is accessed by a femoral arterial puncture and a catheter sent up which will stimulate the: * Coeliac * Common hepatic. * Splenic. * GDA - For insulinomas - calcium gluconate is given to each of the above locations - then a hepatic vein samples are taken for insulin - will be high in the area of stimulation. For gastrinoma's - secretin is administered - this will stimulate gastrin release.

Question 138

What are the indications for resection of a non-functional pNET

Answer 138

Treatment of non-functional pNETs - <1cm - observed - every 6-12 months for 5 years. - 1-2cm - controversial * Observe if no high risk features i.e. pancreatic duct dilatation, irregular margin. * Might consider EUS and FNA to aid decision making i.e. if Ki67 > 3% or mitotic rate >2/10HPF might consider resection. * Also need to way up location - I.e. Whipple's versus distal pancreatectomy - Surgical resection for tumour > 2cm - have to perform an oncological resection due to he higher risk of malignancy.

Question 139

What is the treatment of a functional pNET?

Answer 139

- Insulinoma - can enucleate - due to their low risk of malignancy. - Gastrinoma - generally oncological resection with lymphadenectomy due to their higher malignant risk - although this is debatable.

Question 140

What is the surgical management of metastatic hepatic disease?

Answer 140

Metastatic liver disease - For well differentiated neuroendocrine tumours - liver based treatments including resection should be offered. * Resectability is the same as for colorectal metastasis i.e. adequate inflow, outflow, biliary drainage, and FLR. * Ablation and TACE can also be used - This is thought improve survival and aid in symptom control Generally for NECS – you avoid debulking or metastectomy procedures as the prognosis is so poor.

Question 141

What medications are used for metastatic non-resectable NETs?

Answer 141

- First line medical options are somatostatin analogues such as lantreotide and octreotide. Slow down the growth of the tumour and also decrease the production of serotonin. - Peptide-receptor radionuclide therapy (PRRT) - radio-nuclide binds to somatostatin receptors * Promotes gallstone formation thus if this is to be given - should have a cholecystectomy. - Everolimus (m-TOR inhibitor). A form of protein kinase inhibitor. - Interferon-alpha Tyrosine-kinase inhibitors such as sunitinib.

Question 142

What surgery should you offer a patient with an insulinoma? What about a gastrinoma?

Answer 142

Insulinoma - can enucleate as very rarely malignant Gastrinoma - much more likely to be malignant thus need formal resection and lymphadenectomy.

Question 143

What is the histological structure of the spleen?

Answer 143

Red pulp - Consists of sinusoids - allows for the removal of old, damaged red blood cells. Is a site for platelet storage and in certain conditions haematopoiesis. - Acts as a blood filter. White pulp - Lymphoid component of the spleen which surrounds splenic arterioles. - Rich in T cells and B cells. - This area is important in immune cells production. Marginal zone - Transition area between the red and white pulp - Contains macrophages, antigen presenting cells, as specialised B cells. - This area is important in trapping and presenting antigens from the blood.

Question 144

What is the function of the spleen?

Answer 144

- Haematopoietic function – during foetal life, red cells and white cells are produced in the spleen. The spleen can also return to this function in the setting of myelofibrosis. - Immune function – fights infection - both innate and acquired immune systems. - Filter function – system in the red pulp helps to clear old and dead red cells. Also clears pathogens.

Question 145

What is the most common aetiology of a splenic abscess? What are the risk factors? What are the common organisms?

Answer 145

- Most common source is haematogenous spread. * Associated with endocarditis, IVDU, osteomyelitis. - Risk factors * Cancer, immunocompromised, IVDU, AIDS. Most common organisms include gram positive cocci – Staph, strep, enterococcus and gram negative enteric organisms (i.e. E coli and Klebsiella).

Question 146

How are Hydatid cysts of the spleen treated?

Answer 146

- First line treatment is generally mebendazole and if refractory - splenectomy - Unlike liver Hydatid disease - PAIR is rarely used.

Question 147

What is splenomegaly?

Answer 147

- Splenomegaly is defined as * A spleen which is >13cm length on USS * >300 grams * Palpable below the costal margin. Massive splenomegaly is > 1kg in size.

Question 148

What are the causes of splenomegaly?

Answer 148

- Infective * Viral - EBV, CMV * Bacterial - salmonella, abscesses. * Parasitic infection - malaria, schistosomiasis. * Hydatid cyst - Benign haematological * Haemolytic anaemia - sickle cell, thalasaemia. * Polycythaemia rubra vera * Myelofibrosis - Malignant haematological * Leukaemia. * Lymphoma. - Metabolic * Amyloidosis * Neimann-Pick - Congestive * Liver cirrhosis. * Portal vein thrombosis - Solid tumour * Metastatic tumours Haemangiomas.

Question 149

What causes ITP?

Answer 149

- Mediated by auto-antibodies to the platelet membrane glycoproteins. - Theses autoantibodies opsonize platelets - leading to phagocytosis within the spleen.

Question 150

What are the indications for surgery in ITP?

Answer 150

- Persistent or recurrent disease which is not able to be managed medically. - Can be offered to patients who would prefer splenectomy over taking long term medication such as Rituximab or a TPO agonist (Romiplostim)

Question 151

What is heretidary spherocytosis?

Answer 151

- This is an autosomally dominant inherited abnormality of the red cell membrane proteins which leads to an increase in its permeability causing it to be rigid and spherical. - These cells become more prone to destruction in the spleen. - Often cause problems in childhood – anaemia, jaundice, splenomegaly and gallstones.

Question 151

What is the treatment of hereditary spherocytosis?

Answer 151

- Splenectomy - Delayed until patients are at least 6 years old (to reduce risk of OPSI) - Goals are to treat anaemia, prevent development of biliary pathology, prevent crisis events, prevent later haemochromatosis. - At time of splenectomy, if gallstones are present then you will perform a lap chole at the same time.

Question 152

What vaccinations should be given to prevent OPSI? What pathogens can cause OPSI?

Answer 152

- Haemophilius influenzae - Flu (every year) - Pneumococcal vaccine - Meningococcal vaccine - Tetanus - Diphtheria. - Pertussis Common pathogens include streptococcus pneumoniae, H influenzae, N meningitis, E coli, Staph Aureus, Strep Pyogenes, and malaria.

Question 153

What are the indications for angioembolisation in splenic trauma?

Answer 153

Can be performed prophylactically or therapeutically. ▪ Therapeutic embolization □ Evidence of ongoing bleeding. ® Significant Hb drop ® Tachycardia. ® Blush on CTA ® Pseudoaneurysm ▪ Prophylactic embolization □ Severe injury without evidence of bleeding ® Grade 4 or grade 5 injuries with haemodynamic stability and no blush. Reduces the likelihood of these patients failing non-operative management and needing a splenectomy