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
2
Q
How is Mirizzi’s syndrome diagnosed and managed?
A
Diagnosis: MRCP
Laparoscopic cholecystectomy
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
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.
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
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
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
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
9
Q
What are some of the signs of chronic liver disease?
A
- Hepatic encephalopathy
- Lymphadenopathy
- Hepatomegaly
- Splenomegaly
- Ascites
- Palpable gallbladder
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
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
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
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
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).
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.
16
Q
What are the complications of gall stones?
A
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
