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Surgery > Hepatobiliary Surgery > Flashcards

Hepatobiliary Surgery Flashcards

1
Q

How does Acute Cholecystitis Classically Present?

A

[Gallstone obstruct cystic duct]

  • HPI – RUQ pain, Fever, N&V
  • PMH – Gallstone disease
  • PE – Murphy’s+, TGR+, Distended GB [30%]
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2
Q

How does Acute Cholangitis Classically Present?

A

[Gallstone/Stricture/MBO → stasis → infection → CBD inflammation]

HPI

  • Charcot’s Triad [RUQ pain, Fever, Jaundice]
  • Obstructive Jaundice [Tea-coloured urine, Pale stool, Pruritus]
  • Infection [Fever, Chills & Rigors]
  • N&V

PMH – Gallstone disease, Biliary surgery, Known CA

PE – Reynald’s Pentad [Hypotension, Confusion], Murphy’s-, TG+R-

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3
Q

What are features of biliary colic?

A
  • Biliary colic is NOT a true colic – instead of waxing/waning, it is constant RUQ pain
  • Radiation → R Scapula/Shoulder
  • Associated → N&V, Abdominal distension
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4
Q

Define Murphy’s Sign

A

Inspiratory arrest during deep palpation of the RUQ

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5
Q

What is the Courvoisier’s Law?

A

If the gallbladder is palpable in patient with painless jaundice, the cause is unlikely to be gallstone disease

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6
Q

What investigations would you order in suspected cholecystitis/cholangitis?

A
  • Bloods – CBC, Septic workup, LFT, Amylase, RFT [dehydration & pre-surgical baseline], PT/APTT
  • Urine – Bilirubin and Urobilinogen
  • Imaging – AXR [IO, aerobilia, pigmented stones], Biliary US, ERCP/PTC
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7
Q

Is bilirubin in urine conjugated or unconjugated?

A
  • All bilirubin in urine is CONJUGATED
  • Unconjugated bilirubin is bound to albumin ∴not filtered in kidney
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8
Q

How would you manage a patient with Acute cholecystitis?

A
  1. Fluid resuscitation – correct electrolyte imbalance, hydration, NBM
  2. Empirical antibiotics
  3. Analgesics prn
  4. Definitive treatment – Cholecystectomy / Cholecystostomy + Elective -ectomy
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9
Q

How would you manage a patient with Acute cholangitis?

A
  1. Fluid resuscitation – correct electrolyte imbalance, hydration, NBM
  2. Empirical antibiotics
  3. Analgesics prn
  4. Biliary Decompression
  • 24-48h after stabilisation
  • Methods
    • ERCP Sphincterotomy/Sphincteroplasty + Extraction + Stenting
    • Nasobiliary Drain [external drain]
    • PTBD or Surgery [ECBD] if ERCP fails
  1. Definitive Treatment – Elective Cholecystectomy + ECBD
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10
Q

Endoscopic Sphincterotomy vs Sphincteroplasty

A

Sphincterotomy – Dis = Risk of bleeding & perforation, Sphincter function los

Sphincteroplasty

  • Adv – Preserves sphincter function
  • Dis – X extract large stones, ↑risk of pancreatitis
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11
Q

What are the commonest organisms causing Cholangitis and Treatment?

A

Bacteria

  • Gram-ve bacteria – Klebsiella, Enterococcus, E. coli
  • Anaerobes [Bacteroides]
  • Tx – 3rd gen Cephalosporin [Ceftriaxone] + Metronidazole
    • Augmentin also acceptable

Parasites

  • Endemic in Asian countries
  • Transmission by ingesting raw fish
  • Organisms - Clonorchis sinensis, Ascaris
  • May cause cholangitis, IHD stone, pancreatitis, CC
  • Dx - stool exam
  • Tx - Praziquantel [CS] and Mebendazole [A]
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12
Q

Boundaries of the Calot’s Triangle and Significance

A
  • Superior – Inferior border of the liver
  • Lateral – Cystic duct
  • Medial – Common hepatic duct
  • Significance
    • Centre of triangle contains Lund’s LN
    • Cystic artery traverses the triangle; both cystic artery & duct clipped before proceeding with cholecystectomy
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13
Q

Cholecystectomy – Laparoscopic or Open?

A
  • Laparoscopic preferred – Shorter hospital stay, less pain, better cosmesis
  • Conversion to open [5% risk] due to
    • Previous upper abdominal surgery [adhesions ++]
    • Cholecystitis [on-going infection]
    • Complicated anatomy
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14
Q

Cholecystectomy – Early or Delayed?

A
  • Urgent [immediate; in patients not responding to treatment]
  • Early [within 48-72h]
    • Adv – ↓Hospital Stay; Avoid readmission
    • Dis – ↑Chance of operative & septic complications
  • Delayed [conservative management → interval surgery in 8-12wks]
    • Adv – Avoid misdiagnosis
    • Dis – Risk of interval complications requiring readmission
  • [NO significant differences in early vs delayed in mortality, conversion rates, bile duct injury]
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15
Q

Indications for Cholecystostomy

A
  • Approach – Percutaneous or Open; Catheter under US guidance → drain GB
  • Followed by elective cholecystectomy 4-6wks later
  • Indications
    • Unfit for surgery [haemodynamically unstable, moribund]
    • Early surgery difficult/risky [extensive GB inflammation]
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16
Q

Non-surgical means of stone treatment

A
  • Shockwave lithotripsy
  • Medical – UDCA [9mo intensive tx → lifelong maintenance]
  • Liver diet

[All treatments retaining GB = 50% recurrence in 5yrs]

17
Q

Pros and Cons of Hepatobiliary Ultrasound

A

Pros

  • No ionising radiation
  • Cheap and Portable
  • Sensitive and accurate for detecting
    • Bile duct (intra & extra-hepatic) dilatation [>0.6cm diameter]
    • Gallstones [>95% accuracy for stones >0.1cm]
  • US guided intervention can be performed

Cons

  • Operator dependent
  • Visualisation can be impeded
    • Pneumobilia
    • Previous Operations [Abdominal scar, Surgical clips, Ileus]
18
Q

US Features of Cholecystitis

A
  1. Pericholecystic Fluid
  2. Thickened Gallbladder Wall [>3mm; ∵oedema]
  3. Sonographic Murphy’s Sign
  4. Gallstones with Acoustic Shadowing [mobile & echogenic]
19
Q

What are the modalities of Cholangiography?

A
  1. ERCP – Endoscopic Retrograde Cholangiopancreatography
    * Complications – Pancreatitis, Perforation
  2. MRCP - Magnetic Resonance CP
  3. PTC – Percutaneous Transhepatic Cholangiography
  • Gradually replaced by MRCP
  • Complications – Bleeding, Hepatic injury
  1. T-Tube Cholangiogram – after Cholecystectomy + ECBD → look for residual stone
20
Q

When is CT indicated for acute cholecystitis?

A
  1. Suboptimal Ultrasound [e.g. obscured by scar]
  2. Complications [GB perforation, Pericholecystic abscess, Empyema]
21
Q

What parameters are in Child-Pugh Score?

A
  • Albumin – N= 35-50; 1+ = >35; 2+ = 28-35; 3+ = <28
  • Bilirubin – N= >20; 1+ = <34; 2+ = 34-51; 3+ = >51
  • Clotting [INR] – N=<1.5; 1+ = <1.7; 2+ = 1.7-2.2; 3+ = >2.2
  • Distension – 1+ = None; 2+ = Mild; 3+ = Moderate
  • Encephalopathy – 1+ = None; 2+ = Grade 1-2; 3+ = Grade 3-4
  • Interpretation
  • Child A – 5-6pts; 1/2yr Mort = 100%; 85%
  • Child B – 7-9pts; 1/2yr Mort = 80; 57%
  • Child C – 10-15pts; 1/2yr Mort = 45%; 35%
22
Q

What is the underlying pathophysiology of cirrhosis-induced portal hypertension?

A
  • Portal Hypertension due to 2 main factors
  1. ↑Resistance to portal flow – architectural distortion [fibrosis & regenerative nodules occlude sinusoids in the liver]
  2. ↑Portal blood flow ∵splanchnic vasodilatation [∵↑NO bioavailability in cirrhosis]
23
Q

How can cirrhosis lead to upper GI-bleeding?

A
  1. Gastro-oesophageal varices [∵Portal hypertension]
  2. Peptic Ulcer Disease [∵↓hepatic metabolism of gastrin → ↑Gastrin = ↑HCl]
  3. Portal hypertensive gastropathy
  4. ↑Bleeding tendency [∵↓Production of clotting factors]
24
Q

What are the management modalities for variceal bleeding?

A
  1. Management of ACTIVE variceal bleeding
  2. PROPHYLAXIS to prevent further bleeding
  3. CHRONIC management
25
Q

How would you manage a patient presenting with ACTIVE variceal bleeding?

A
  1. Stabilise – Monitor vital signs + Initiate active fluid resuscitation
  • A – Protect airway if encephalopathy
  • B – Nasal cannula + supplemental O2
  • C – BP & HR + 2x large bore IV catheters → initiate 1L N/S fast
  • D – Decompress
    • NEVER use a NGT in suspected varices
    • Monitor – U/O [Foley’s], CVP [Swan-Ganz]
  • Basic investigations
    • T&S + Transfusions [packed RBC/Platelets/Clotting factors] → target Hb 7g/dL
    • Bloods – CBC, L/RFT, PT/aPTT
  1. Pharmacological treatment [HAPK]
  • Target Bleeding – UGI haemostasis [Omeprazole] + Correct coagulopathy [Vit K]
  • Target Pathophysiology
    • Antibiotic prophylaxis – ↓SBP and re-bleeding risk with Ciprofloxacin or Ceftriaxone
    • Portal pressure – ↓Portal pressure using splanchnic vasoconstrictors [Octreotoide, Somatostatin, Terlipressin]
  1. Temporary measures – Control bleeding while awaiting definitive treatment
  • Sengstaken-Blakemore tube → Balloon tamponade effect
    • Temporary measure in case of uncontrollable bleeding
    • Consists – Gastric and Oesophageal; Balloon and Opening
    • Precautions
      • Must protect airway first
      • Maximum 24hrs – temporarily deflate after 12hrs to prevent pressure necrosis
  1. Definitive treatment
  • Endoscopic
    • Band ligation – preferred as ↑effect and ↓complications
    • Injection sclerotherapy
  • Emergency Shunt Surgeries – X ideal LT preventive measure
    • [ONLY use in refractory bleeding NOT controlled by pharmacological and endoscopic means]
    • TIPS [Transhepatic intrahepatic Porto-systemic Shunt]
    • Splenorenal Shunt [Prox. (splenectomy involved) and Dist.]
    • Portocaval, Mesocaval shunts
26
Q

What are the prognostic factors predicting risk of re-bleeding?

A

[Previous Child Forrest Site Size]

  • Previous – Previous bleeds [70% will re-bleed after first episode; most cases re-bleed within 48hrs]
  • Child – ↑Child-Pugh Score = ↑Risk
  • Forrest – ESRH [longitudinal streaks, discrete (Cherry) red spots, blood blisters (haematocysts), erythema]
  • Site – GEJ ↑commonly bleed ∵fewest supportive tissue
  • Size – ↑Size = ↑Bleed
27
Q

What is the mechanism of action of Lactulose in preventing HE?

A
  1. Osmotic laxative – ↓enteric transit time → ↓time for bacterial production of ammonia
  2. Create Acid Medium – Lactulose → Lactose + Galactose by gut fermenters → Lactose to lactic acid → acid medium → X ammonia absorption by ionising it

Surgery (8 decks)

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