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Year 3 - Surgery > HPB Surgery > Flashcards

HPB Surgery Flashcards

1
Q

What is Mirizzi syndrome?

A
  • 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
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2
Q

How is Mirizzi’s syndrome diagnosed and managed?

A

Diagnosis: MRCP

Laparoscopic cholecystectomy

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3
Q

What tests/ investigations would you do for jaundice?

A
  • 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
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4
Q

Why does jaundice result in dark urine?

A
  • 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.
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5
Q

Briefly describe the process of bilirubin metabolism?

A
  • 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
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6
Q

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

A
  • Pre hepatic - no changes to stool or to urine
  • Hepatic - dark urine, no stool changes
  • Post hepatic - pale stools, dark urine
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7
Q

What are some of the causes of jaundice?

A
  • 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
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8
Q

What drugs can induce jaundice?

A
  • Haemolysis: antimalarials
  • Hepatitis: Paracetemol, Isoniazid, rifamipicin, pyrazinamide, monoamine oxidase inhibitors, sodium valproate, statins
  • Cholestasis: flucloxacillin, fusidic acid, co amox, nitrofuranton, steroids, sulphonylureas, chlorapromazine
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9
Q

What are some of the signs of chronic liver disease?

A
  • Hepatic encephalopathy
  • Lymphadenopathy
  • Hepatomegaly
  • Splenomegaly
  • Ascites
  • Palpable gallbladder
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10
Q

What is biliary colic?

A
  • Biliary colic occurs when the gallbladder neck becomes impacted by a gallstone. Gallbladder contracts against the stone → pain
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11
Q

How does Biliary Colic present?

A
  • RUQ pain (radiates → back): sudden, dull, colicky
  • ± Jaundice
  • +/- Nausea or vomiting
  • Pain is usually worse on eating fatty foods
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12
Q

How would you manage BC?

A
  • Conservative: lifestyle, diet, lose weight
  • Pharmacological
    • IV fluids
    • Analgesia: morphine
    • Anti emetic: ondansetron
  • Sugery:
    • Elective lap. cholecystectomy within 6 weeks of first presentation
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13
Q

How does acute cholecystitis arise?

How does it present?

A
  • 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
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14
Q

How would you investigate acute cholecystitis?

A
  • 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).
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15
Q

What is murpheys sign?

A

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.

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16
Q

What are the complications of gall stones?

A
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17
Q

How would you treat manage acute cholecystitis?

A
  • 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.
18
Q

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

A
  • 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)
19
Q

What are the sx of chronic cholescystitis?

A
  • 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)
20
Q

How would you treat obstructive jaundice with CBD stones?

A
  • ERCP with sphincterotomy ± biliary trawl
  • Then cholecystectomy may be needed, or open surgery with CBD exploration
21
Q

What is ascending cholangitis?

A
  • Infection of the biliary tract
  • It is caused by a combination of biliary outflow obstruction* and biliary infection.
22
Q

How does cholangitis present?

A
  • 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
23
Q

What organisms are most commonly implicated in cholangitis?

A
  • Escherichia Coli (27%)
  • Klebsiella species (16%)
  • Enterococcus (15%).
24
Q

What is Gallstone Ileus?

What would you see on imaging?

A
  • 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).
25
Q

What are some of the causes of acute pancreatitis?

A

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

26
Q

What are some of the signs of acute pancreatitis?

A
  • Hypocalcaemia: tetany, chvosek and trousseau sign
  • Cullen’s and grey turner sign: bruising around the umbilicus and the flanks; second to retroperitoneal haemorrhage
27
Q

What is the pathogenesis behind acute pancreatitis?

A
  • 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
28
Q

What are the symptoms of acute pancreatitis?

A
  • 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
29
Q

What are the signs of acute pancreatitis?

A
  • 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
30
Q

How would we investigate acute pancreatitis?

A
  • 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
31
Q

What are some of the complications of acute pancreatitis?

A
  • 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
32
Q

How would we manage acute pancreatitis?

A
  • 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
33
Q

When is ERCP + sphincterotomy performed compared over cholesystectomy?

A
  • Elderly patients
  • If surgery is contraindicated
  • If stones are in the common bile duct
34
Q

What is gallbladder empyema?

A
  • When the gallbladder becomes filled with pus
  • Patients will become unwell, often septic, presenting with a similar clinical picture to acute cholecystitis.
35
Q

How is gallbladder empyema diagnosed and managed?

A

US scan or CT scan.

Laparoscopic cholecystectomy*

36
Q

What investigations are used for diagnosing ascending cholangitis?

A
  • 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)
37
Q

How would you manage ascending cholangitis?

A
  • 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
38
Q

What is Chronic Pancreatitis?

A
  • 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
39
Q

What are some of the causes of chronic pancreatitis?

A
  • Chronic alcohol abuse, idiopathic
  • Metabolic, infection (HIV, mumps), bacterial hereditary, autoimune of congenital (annular pancreas)
  • RF: smoking, alcohol, FH
40
Q

What are the symptoms of chronic pancreatitis?

A
  • 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
41
Q

What investigations do you do for chronic pancreatitis?

A
  • 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
42
Q

How would we manage chronic pancreatitis?

A
  • 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

Year 3 - Surgery (10 decks)

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