HPB Surgery

Question 1

What is Mirizzi syndrome?

Answer 1

• A stone located in Hartmanns pouch (an out-pouching of the gallbladder wall at the junction with the cystic duct) or in the cystic duct itself can cause compression on the adjacent common hepatic duct.
• Causes obstructive jaundice

Question 2

How is Mirizzi’s syndrome diagnosed and managed?

Answer 2

Diagnosis: MRCP

Laparoscopic cholecystectomy

Question 3

What tests/ investigations would you do for jaundice?

Answer 3

• Bloods: FBC, UE, CRP clotting, film, reticulocyte count, Coombs’ test and haptoglobins for haemolysis, malaria parasites, u&e, LFT, γ‎-gt, total protein, albumin. Paracetamol levels. Hep A,B,C
• USS
• ERCP: If bile ducts are dilated and lft not improving
• MRCP: Or endoscopic ultrasound (eus) if conventional ultrasound shows gallstones but no definite common bile duct stones.
• Liver biopsy
• CT/ MRI

Question 4

Why does jaundice result in dark urine?

Answer 4

• As conjugated bilirubin is water-soluble, it is excreted in urine, making it dark.
• Less conjugated bilirubin enters the gut and the faeces become pale.

Question 5

Briefly describe the process of bilirubin metabolism?

Answer 5

• Bilirubin is conjugated with glucuronic acid by hepatocytes, making it water-soluble.
• Conjugated bilirubin is secreted in bile and passes into the gut.
• Some is taken up again by the liver (via the enterohepatic circulation) and the rest is converted to urobilinogen by gut bacteria.
• Urobilinogen is either reabsorbed and excreted by the kidneys, or converted to stercobilin, which colours faeces brown

Question 6

How would pre hepatic, hepatic and post hepatic jaundice appear?

Answer 6

• Pre hepatic - no changes to stool or to urine
• Hepatic - dark urine, no stool changes
• Post hepatic - pale stools, dark urine

Question 7

What are some of the causes of jaundice?

Answer 7

• Pre hepatic:
  
  • Haemolysis
  • Drugs/ contrast
  • Rifampacin
  • Gilbert’s syndrome
  • Malaria
• Hepatic: cholangiocarcinoma, hepatitis ABC, EBV, budd chiaria, haemachromatosis, cirrhosis, A1 anti trypsin deficiency
  
  • ​Drugs: anti malarials, RIP of TB, paracetemol, alcohol
• Post hepatic: PBC, PSC, gallstones, acute cholesytitis, ascending cholangitis, mirrizzi syndrome, pancreatic cancer
  
  • Drugs: flucloxacillin, prochloperazine, steroids, fusidic acid, steroids, sulphonylurea

Question 8

What drugs can induce jaundice?

Answer 8

• Haemolysis: antimalarials
• Hepatitis: Paracetemol, Isoniazid, rifamipicin, pyrazinamide, monoamine oxidase inhibitors, sodium valproate, statins
• Cholestasis: flucloxacillin, fusidic acid, co amox, nitrofuranton, steroids, sulphonylureas, chlorapromazine

Question 9

What are some of the signs of chronic liver disease?

Answer 9

• Hepatic encephalopathy
• Lymphadenopathy
• Hepatomegaly
• Splenomegaly
• Ascites
• Palpable gallbladder

Question 10

What is biliary colic?

Answer 10

• Biliary colic occurs when the gallbladder neck becomes impacted by a gallstone. Gallbladder contracts against the stone → pain

Question 11

How does Biliary Colic present?

Answer 11

• RUQ pain (radiates → back): sudden, dull, colicky
• ± Jaundice
• +/- Nausea or vomiting
• Pain is usually worse on eating fatty foods

Question 12

How would you manage BC?

Answer 12

• Conservative: lifestyle, diet, lose weight
• Pharmacological
  
  • IV fluids
  • Analgesia: morphine
  • Anti emetic: ondansetron
• Sugery:
  
  • Elective lap. cholecystectomy within 6 weeks of first presentation

Question 13

How does acute cholecystitis arise?

How does it present?

Answer 13

• Follows stone or sludge impaction in the neck of the gallbladder
• May cause continuous epigastric or RUQ pain (referred to the right shoulder)
• Vomiting, fever, local peritonism, or a GB mass.
• Inflammatory component: local peritonism, fever, wcc↑
• Positive Murphy’s sign

Question 14

How would you investigate acute cholecystitis?

Answer 14

• Bedside: urinalysis and pregnancy test
• Bloods: FBC (↑WCC),UE, CRP, amylase, lipase, LFT, gamma GT
• US: a thick-walled, shrunken gb (also seen in chronic disease), pericholecystic fluid, stones, cbd (dilated if >6mm).
• MRCP: use if US has not detected common bile duct stones but the bile duct is dilated and/or

LFTs are abnormal.

• Plain AXR: shows ~10% of gallstones; it may identify a ‘porcelain’ gb (associated risk of cancer).

Question 15

What is murpheys sign?

Answer 15

Lay 2 fingers over the RUQ; ask patient to breathe in. This causes pain & arrest of inspiration as an inflamed GB impinges on your fingers.

It is only +ve if the same test in the LUQ does not cause pain.

Question 16

What are the complications of gall stones?

Answer 16

Question 17

How would you treat manage acute cholecystitis?

Answer 17

• Medical:
  
  • NBM, IVI
  • Pain relief (opioids): morphine
  • Abx (based on local guidelines), eg co-amoxiclav 625mg/8h iv
  • Anti emetic: ondansetron
• Surgery:
  
  • Laparoscopic cholecystectomy: within 1 week of presentation, ideally within 72hrs of presentation
  • • Percutaneous cholescystecomy: if not fit for surgery and not responding to antibiotics
  • Open surgery: if there is GB perforation.

Question 18

When looking at gallstones, what things are usually visualised on USS?

Answer 18

• The presence of gallstones or sludge (the start of gallstone formation)
• Gallbladder wall thickness (if thick walled, then inflammation is likely)
• Bile duct dilatation (indicates a possible stone in the distal bile ducts)

Question 19

What are the sx of chronic cholescystitis?

Answer 19

• Chronic inflammation ± colic.
• Ongoing RUQ or epigastric pain
• Nausea and vomiting
• ‘Flatulent dyspepsia’: vague abdominal discomfort, distension, nausea, flatulence, and fat intolerance (fat stimulates CCK release and GB contraction)

Question 20

How would you treat obstructive jaundice with CBD stones?

Answer 20

• ERCP with sphincterotomy ± biliary trawl
• Then cholecystectomy may be needed, or open surgery with CBD exploration

Question 21

What is ascending cholangitis?

Answer 21

• Infection of the biliary tract
• It is caused by a combination of biliary outflow obstruction* and biliary infection.

Question 22

How does cholangitis present?

Answer 22

• Charcot’s triad: RUQ pain, fever and jaundice
• Reynold’s Pentad: Jaundice, Fever, and RUQ Pain, Hypotension, and Confusion
• Other Signs: pale stool with dark urine, pruritus, rigors

Question 23

What organisms are most commonly implicated in cholangitis?

Answer 23

• Escherichia Coli (27%)
• Klebsiella species (16%)
• Enterococcus (15%).

Question 24

What is Gallstone Ileus?

What would you see on imaging?

Answer 24

• A stone erodes through the GB into the duodenum; it may then obstruct the terminal ileum.
• AXR shows: air in CBD (= pneumobilia), small bowel fluid levels, and a stone
• Duodenal obstruction is rarer (Bouveret’s syndrome).

Question 25

What are some of the causes of acute pancreatitis?

Answer 25

‘get smashed‘. Gallstones (~35%), Ethanol (~35%), Trauma (~1.5%), Steroids, Mumps, Autoimmune (pan), Scorpion venom, Hyperlipidaemia, hypothermia, hypercalcaemia, Ercp (~5%) and emboli, Drugs

Question 26

What are some of the signs of acute pancreatitis?

Answer 26

* **Hypocalcaemia**: tetany, chvosek and trousseau sign * **Cullen's and grey turner sign:** bruising around the umbilicus and the flanks; second to retroperitoneal haemorrhage

Question 27

What is the pathogenesis behind acute pancreatitis?

Answer 27

* Premature and exaggerated activity of digestive enzymes in pancreas * Enzyme release -\> autodigestion of fat -\> fat necrosis -\> free fatty acid release + hypocalcaemia * End stage pancreatitis is necrosis of the pancreas

Question 28

What are the symptoms of acute pancreatitis?

Answer 28

* Gradual or sudden severe epigastric or central abdominal pain (radiates to back, sitting forward may relieve) * Nausea and vomiting prominent * Epigastric tenderness and guarding * Signs of hypovolaemia: tachycardia, hypotension, tachypnoea

Question 29

What are the signs of acute pancreatitis?

Answer 29

* Fever * Jaundice * Shock: ↑HR, tachypnoea, hypotensive * Ileus * Rigid abdomen ± local/general tenderness, * Periumbilical bruising (Cullen’s sign) or flanks (Grey Turner’s sign) - blood vessel autodigestion and retroperitoneal haemorrhage * Signs of hypocalcaemia

Question 30

How would we investigate acute pancreatitis?

Answer 30

* Bloods: FBC, UE, LFT, CRP, serum amylase + lipase (diagnostic of acute pancreatitis if 3x the upper limit of normal\*), Ca2+ * Imaging: * **Abdo USS** if cause is unknown * **AXR**: not usually performed routinely: can show a **‘sentinal loop sign’** - dilated proximal bowel loop adjacent to the pancreas, which occurs secondary to localised inflammation * **Contrast-enhanced CT scan**: If performed after **48hrs** from initial presentation, it will often show areas of pancreatic oedema and swelling * **MRCP**

Question 31

What are some of the complications of acute pancreatitis?

Answer 31

* **DIC** * **Acute respiratory distress syndrome** * **Pancreatic necrosis:** persistent systemic inflammatio from 7-10 days. Requires CT imaging and FNA * **Pancreatic pseudocyst:** collection of fluid. Treatment: surgical debridement or endoscopic drainage (often into the stomach) (if persistent for \> 6wks) * **Hyperglycaemia**: destruction of islets of langerhans -\> insulin disturbance -\> glucose rises * **Hypocalcaemia**: release lipases -\> fat necrosis -\> formation of free fatty acids, which react with serum calcium to form chalky deposits in fatty tissue

Question 32

How would we manage acute pancreatitis?

Answer 32

* NBM, NG tube, IVI + **saline** * Cathetarise + UO * Give 02 * NICE states: severe acute pancreatitis should be managed in **ITU** * Analgesia: **morphine** - good but may cause Sphincter of Oddi to contract more * Antiemetic: **ondansetron** * Abx: **imipenem IV** * Other: calcium and magnesium replacement * If gallstone pancreatitis with cholangitis: **ERCP** + **gallstone removal** * If with gallstone + bile duct obstruction: **early laparoscopic cholecystectomy​** * If with cholangitis: **ERCP with sphincterotomy**

Question 33

When is ERCP + sphincterotomy performed compared over cholesystectomy?

Answer 33

* Elderly patients * If surgery is contraindicated * If stones are in the common bile duct

Question 34

What is gallbladder empyema?

Answer 34

* When the gallbladder becomes filled with pus * Patients will become unwell, often septic, presenting with a similar clinical picture to acute cholecystitis.

Question 35

How is gallbladder empyema diagnosed and managed?

Answer 35

US scan or CT scan. ## Footnote **Laparoscopic cholecystectomy\***

Question 36

What investigations are used for diagnosing ascending cholangitis?

Answer 36

* **Bloods:** FBC (leucocytosis); LFTs (showing a raised ALP ± GGT + raised bilirubin). * **Blood cultures** * **Imaging**: USS: bile duct dilation \>6cm (CBD) * **Gold standard:** ERCP (diagnostic and therapeutic)

Question 37

How would you manage ascending cholangitis?

Answer 37

* Manage sepsis * **IVI** + fluid resuscitation, routine bloods, and blood cultures taken early * Broad spectrum abx: **co-amoxiclav + metronidazole** * Surgical * 1st: **Endoscopic biliary decompression** - removing the cause of the blocked biliary tree * If gallstones: **ERCP +/- sphincterotomy + stenting** * 2nd: **Percutaneous transhepatic cholangiograpy (PTC)**: For patients who may be too sick to tolerate ERCP * Long term: patients may require **cholecystectomy** if gallstones were the underlying cause

Question 38

What is Chronic Pancreatitis?

Answer 38

* Chronic **fibro-inflammatory** disease of the pancreas * **Progressive** + **irreversible** damage * Characterised by **recurrent** or **persistent** **abdominal pain** and progressive injury to the pancreas and surrounding structures, resulting in scarring and loss of function

Question 39

What are some of the causes of chronic pancreatitis?

Answer 39

* Chronic alcohol abuse, idiopathic * Metabolic, infection (HIV, mumps), bacterial hereditary, autoimune of congenital (annular pancreas) * RF: smoking, alcohol, FH

Question 40

What are the symptoms of chronic pancreatitis?

Answer 40

* **Pain**: epigastric, dull, radiating to the back, post prandial (30 mins), relieved by sitting forwards * Endocrine insufficiency: **hyperglycaemia** and **DM** * **Steattorhoa** (reduced digestive enzymes) * **Nausea** and **vomiting** * **Malnutrition and weight loss** * **Jaundice**

Question 41

What investigations do you do for chronic pancreatitis?

Answer 41

* **Bedside**: urine dip * **Bloods**: FBC, UE, LFT, serum amylase + lipase (will not be elevated the way they are in acute pancreatitis), glucose (↑) * **\*\*Faecal elastase** * **Imaging**: * **\*\*CT scan:** pancreatic atrophy + calcifation, pseudocysts * USS/ MRI: visualises the anatomy of the biliary tree * Abdominal X ray - if disease is severe - calfication * **Specialist**: secretin stimulation, endoscopic USS

Question 42

How would we manage chronic pancreatitis?

Answer 42

* **Analgesia**: ibuprofen +/- paractemol, tramadol * **Pancreatic enzyme replacement** (including lipases), such as **Creon + PPI**: pancreatin + omeprazole * **Fat soluble vitamins** DEAK * Dietary modifications: reduce dietary fat if steatorrhoae persists * **Octreotide** - rarely used: synthetic analogue of somatostatin that may relieve pain through inhibition of neurogenic inflammation and/or inhibition of CCK release and pancreatic secretion * **Diabetes** management: **insulin** * **Endoscopic management:** * ERCP * Pseudocyst drainag * ESWL - pain management * Extreme distal pancreatomy