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Question 1

Infection

Answer 1

The invasion of normally sterile tissue by organisms resulting in infectious pathology

Question 2

Bacteraemia

Answer 2

Presence of viable bacteria in the blood

Question 3

Sepsis

Answer 3

A life-threatening organ dysfunction caused by a dysregulated host response to infection (Sepsis-3 - 2016), as evidenced by organ dysfunction and infection.

Organ dysfunction = defined as an increase in 2 or more points in SOFA score - predicted mortality of 10% or more. NB SOFA score is an organ dysfunction score - not diagnostic of sepsis nor does it identify those whose organ dysfunction is truly due to infection but rather helps identify pts who potentially have a high risk of dying from infection.

Infection: no clear guidelines to help clinician identify the presence of infection or to causally link an identified organisms with sepsis.

So all sepsis has organ dysfunction by definition; SIRS as a term has fallen out of fashion and is no longer included in the definition of sepsis as it is not always caused by infection.

Question 4

Septic shock

Answer 4

A subsect of sepsis in which underlying circulatory, cellular and metabolic abnormalities are profound enough to substantially increase mortality (is assoc w hosp mortality >40%).

Defined by patients who fulfill criteria for sepsis as above (have infection and increase in SOFA score of 2 or more) and also, despite adequate fluid resuscitation, require vasopressors to maintain a MAP of 65mmHg or more and have a lactate of over 2.

Question 5

MODS

Answer 5

Multiple organ dysfunction syndrome = progressive organ dysfunction in an acutely ill pt, such that homeostasis can’t be maintained w/o intervention. Is at severe end of severity of illness spectrum of both infectious (sepsis, septic shock) and noninfectious conditions (eg SIRS from pancreatitis).

Can be classed as primary or secondary.
Primary = the result of a well-defined insult in which organ dysfunction occurs early & can be directly attributable to the insult itself (eg renal failure due to rhabdomyolysis)
Secondary = organ failure that’s not in direct response to the insult itself, but is a consequence of the host’s response (eg ARDS in pts w pancreatitis).

No universally accepted criteria for individual organ dysfunction in MODS, however the organ-specific parameters used in SOFA are commonly used to diagnose MODS.

In general, the greater the number of organ failures, the higher the mortality, w the greatest risk being associated w resp failure requiring mechanical ventilation.

Question 6

SIRS

Answer 6

SIRS criteria is no longer used to identify those with sepsis since it is present in many hospitalised pts who don’t develop infection (e.g. autoimmune disorders, pancreatitis, vasculitis, thromboembolism, burns or surgery) & their ability to predict death is poor when compared w other scores e.g. SOFA score.

Is considered a clinical syndrome that is a form of dysregulated inflammation. Previously defined as 2 or more abnormalities in temp, HR, respiration or WCC.

Question 7

qSOFA

Answer 7

Modified version of SOFA score. Identifies patients with suspected infection at risk of poor outcomes typical of sepsis (prolonged LOS, or in-hospital mortality) based on the presence of 2/3 of any of RR>22, SBP<100, altered mentation. Mortality risk of 10% in these patients in general hospital population. I.e. three components, each of which scores 1, and a score of 2 or more is associated with poor outcomes due to sepsis.

Question 8

SOFA score

Answer 8

Sequential organ failure assessment score. Scores 6 organ systems from 0-4 - resp (PaO2, FiO2), coag (plts), liver (bili), cardio (hypotension, inotrope requirement), CNS (GCS), renal (creatinine). Score of 2 or more suggests presence of organ dysfunction. Dysfunction in 2 or more systems = MODS.

I.e. MODS is quantified by the SOFA score

Question 9

Intra-abdominal hypertension & ACS

Answer 9

Normal intra-abdo pressure = 5-7mmHg
IAH = sustained or repeated pathological elevation in IAP ≥12mmHg
ACS = organ dysfunction caused by intra-abdominal hypertension (sustained IAP >20mmHg (w or w/o APP <60mmHg) that is assoc w new organ dysfunction/failure)
APP = MAP-IAP (target APP of ≥60mmHg is correlated w survival from IAH and ACS

Classification
IAH: grade 1 (12-15mmHg); grade 2 (16-20mmHg); grade 3 (21-25mmHg); grade 4 (>25mmHg)
ACS: primary or secondary

Question 10

Classification of oeosphagitis

Answer 10

LA Classification
Grade A - one or more mucosal breaks, confined to mucosal folds, each not >5mm in max length
Grade B - one or more mucosal breaks >5mm in length, but not continuous between mucosal folds
Grade C - mucosal breaks that are continuous between the tops of 2 or more mucosal folds, but which involve <75% of the oesophageal circumference
Grade D - mucosal breaks which involve ≥75% of oesophageal circumference

Question 11

Classification of gastric ulcers

Answer 11

Historically classified using the Johnson classification, which was anatomically based and related to acidic states:

• type I - lesser curve at incisura; low to normal acid state
• type II - two ulcers; gastric body and duo; high acid state
• type III - pre-pyloric; high acid state
• type IV - high on lesser curve - normal acid state
• type V - anywhere - NSAID related

Question 12

UGI bleeding scores

Answer 12

• The Rockall scoring system places emphasis on a correlation between M&M and advancing age, shock or significant co-morbidity; score <3 good prognosis, >8 poor prognosis
  
  • derived based on 5 significant risk factors for mortality form a National UK audit
  • consists of an initial score from clinical parameters (age, shock, comorbidities) & a complete composite score after endoscopic assessment
  • initial score of zero (ie age <60, no tachycardia, no hypotension, no comorbidity): v low mortality
  • composite score, incorporating endoscopic info incl cause of bleeding & stigmata of haemorrhage has been validated in prospective studies, but more accurate in predicting mortality than risk of rebleeding
• The Glasgow-Blatchford score (Hb, urea, melaena, SBP, HR, sex, recent syncope, hepatic disease hx, heart failure) predicts likelihood of requiring endoscopic intervention rather than risk of death
  
  • may be able to identify people who don’t need to be admitted to hospital after a UGIB (score of ≤1 are v low risk for rebleeding or mortality)
  • advantages over Rockall score, which assesses risk of death, include a lack of subjective variables e.g. severity of systemci diseases, and lack of a need for OGD to complete the score, so can be calculated when first presents
  • a simpler version of the score (modified GBS) = calculated using only the BUN, Hb, SBP and HR; score ranges from 0-16
    
    • prospective study of modified score found it performed as well as the full GBS and outperformed Rockall score w regard to predicting need for clinical intervention, rebleeding and morality

Question 13

How is acid reflux diagnosed and scored objectively

Answer 13

DeMeester score

• acomposite score of the acid exposure during 24 or 48hr ambulatory pH monitoring
• 6 parameters
  
  • percent total time pH <4
  • percent upright time pH <4
  • percent supine time pH <4
  • number of reflux episodes
  • number of reflux episodes lasting ≥5mins
  • longest reflux episode (minutes)
• composite score >14.72 indicates reflux

Question 14

Macroscopic appearance of gastric carcinoma - classification

Answer 14

• early gastric cancers: Paris system
  
  • type 0-I = polypoid (protruded or pedunculated)
  • type 0-II = nonpolypoid
    
    • type 0-IIa - slightly elevated
    • type 0-IIb - flat
    • type 0-IIc - flightly depressed
  • type 0-III = excavated
• advanced gastric cancers: Borrman classification
  
  • type 1 = protruded
  • type 2 = ulcerated w elevated borders
  • type 3 = ulcerated w infiltrative margins
  • type 4 = diffusely infiltrating
  • type 5 = not fitting other types (unclassifiable)

Question 15

Aberrant biliary anatomy

Answer 15

• aberrant hepatic duct = defined as a duct draining a normal portion of the liver that joins the biliary tree outside of the liver
• normally RHD is divided into a right anterior (medial) and a right posterior (lateral) branch which joins to form a short right bile duct which joins with the left to form a CHD
• variations in 30-40%
• most common variations relate to right posterior sectoral duct which may drain into:
  
  • left hepatic duct - 15%
  • directly into CBD - 10%
  • trifurcation w right ASD and LHD 11%
• anatomy of left hepatic duct more constant

Question 16

Aberrant hepatic arterial anatomy

Answer 16

• either of the right or left hepatic arteries may be replaced or accessory
• 10-15% RHA is replaced or has an accessory coming from SMA
  
  • artery typically runs from right to left behind CHD and PV
  • may be at risk during pancreatectomy
  • typically, RHA gives off cystic artery & if RHA is aberrant or replaced it tends to give off a cystic artery that is more lateral to the cystic duct (ie in free edge & may be mistaken for CD)
• 6-10% LHA is replaced or has an accessory from the left gastric artery where it runs in the gastrohepatic ligament
  
  • may be at risk in oesophagogastric surgery and usu divided in oeosphagectomy in order to create an anastomosis within the chest

Question 17

Aberrant portal vein anatomy

Answer 17

• variations relatively uncommon
• most common = trifurcation - division into left, right anterior and right posterior branches
• other variations include right anterior or posterior arising from portal vein early, or off the left portal vein

Question 18

Classification of bile duct injuries

Answer 18

Strasberg classification (modified from Bismuth)

A = bile leak from cystic duct stump or minor biliary radical in GB fossa

B = occlusion of part of biliary tree, usu aberrant RHD

C = transection but not occlusion of part of biliary tree, usu aberrant RHD

D = bile leak from main bile duct w/o major tissue loss (/lateral injury to biliary tree)

E1 = transection/stricture of main duct >2cm from confluence

E2 = transection/stricture of main duct <2cm from confluence

E3 = transection/stricture at confluence w R and L ducts in continuity

E4 = transection/stricture at confluence w separation of R and L ducts

E5 = combined injury to main duct and RPSD (involve aberrant RHD anatomy)

Question 19

Classification of biliary SOD

Answer 19

Milwaukee (or Hogan-Geenan) classification

• type I: biliary type pain + abnormal LFTs + dilated CBD
  
  • if delayed drainage at ERCP, do sphincterotomy (generally considered to have sphincter stenosis)
• type II: biliary type pain + abnormal LFTs or dilated CBD
  
  • do sphincter manometry and sphincterotomy if that’s abnormal
• type III: pain only w/o abnormal LFTs or dilated CBD
  
  • unlikely to benefit from sphincterotomy

Question 20

Classification of cholangiocarcinoma

Answer 20

• intrahepatic (10%)
• hilar/perihilar (65%) - extends from distal to cystic duct up to and including confluence of right and left bile ducts; further classified by Bismuth-Corlette classification
  
  • type I = involves CHD below biliary confluence
  • type II = involves biliary confluence
  • type IIIa = involves biliary confluence extending into RHD
  • type IIIb = involves biliary confluence extending into LHD
  • type IV = involves confluence & extends into both L& RHDs
• distal extrahepatic (25%) - excludes GB & ampulla of Vater

Question 21

Classification of choledochal cysts and their treatment

Answer 21

Todani classification

• type I (50%) = fusiform dilatation of extrahepatic bile duct
  
  • cyst resection, cholecystectomy, REYHJ
• type II (2%) = saccular diverticulum of extrahepatic bile duct
  
  • cyst resection & if APBJ, REYHJ
• type III = bile duct dilatation wihtin duodenal wall (choledochocoele)
  
  • type IIIA: BD & PD enter cyst, which then drains into duo at a separate orifice (usu present as cystic bulges of the intra-ampullary CBD)
    
    • often amenable to sphincterotomy & bc malignancy rarely been reported, should do endoscopic biopsies of cyst epithelium to determine what the cyst is lined with; biliary mucosa increased risk cf duodenal mucosa); can also do endoscopic snare resection of these
  • type IIIB: a diverticulum of the intraduodenal CBD or intra-ampullary common channel; typically present as a penduous fluid-filled mass within duo lumen, distal to and arising from major papilla
    
    • can be resected surgically or endoscopically
  • ??or Whipple’s now recommended
• type IV = multiple cysts w involvement of both extrahepatic and intrahepatic ducts (IVa) or extrahepatic only (IVb) - second most common
  
  • IVb - REYHJ
  • IVa - if only one lobe can be treated w partial hepatectomy & recon though controversial if liver resection adds benefit
• type V = multiple cysts involving intrahepatic ducts only / Caroli’s disease
  
  • lobectomy if confined to noe lobe or transplant if diffuse disease

?Treat complications first. Then excise affected disease removing all cyst epithelium and therefore malignant potential. Cholecystectomy and REY hepatico-jejunostomy.

Complications: cholangitis, primary duct stones (both choledocholithiasis and cystolithiasis), hepatolithiasis, secondary biliary cirrhosis due to prolonged biliary obstruction & recurrent cholangitis, CA (10-30%), intraperitoneal cyst rupture, acute and chronic pancreatitis, bleeding due to erosion of cyst into adjacent vessels or as a result of portal hypertension, often presenting as GI haemorrhage due to haemobilia, GOO from obstruction of duo lumen

Pathogenesis of malignancy = field change - entire biliary tree at risk, even nondilated portions & complete excision of a benign choledochal cyst doesn’t eliminate risk of subsequent cholangiocarcinoma development

Question 22

Mirizzi classification

Answer 22

Mirizzi syndrome = CHD obstruction caused by a gallbladder impacted in cystic duct or Hartmann’s pouch

type I (11%) = no fistula (type IA = cystic duct present; type IB = cystic duct obliterated)

type II (41%) = fistula involving <1/3 CBD width

type III (44%) = fistula involving 1/3-2/3 CBD width

type IV (1%) = fistula involving >2/3 CBD width / destruction of wall of CBD