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CBL 1 A CASE OF ACUTE CHOLECYSTITIS

Question 1 this patient had DISTRESSING PAIN; for this case, the doctor should have enquired about
RADIATION OF THE PAIN. E.g. gall bladder inflammation may also manifest as the radiation of pain to the
RIGHT SHOULDER due to phrenic nerve contribution at the levels of C3,4,5 / diaphragmatic irritation due
to proximity of gall bladder+ Boas sign [pain/hyperesthesia beneath or behind the scapula]

Acute cholecystitis Murphys sign positive strongly indicative for cholecystitis; RUQ pain and fever
jaundice is relatively less in cholecystitis

Acute [ascending] cholangitis possibly because she resembled Charcots

Choledocholithiasis [general description only not an actual dx commonest S/S is asymptomatic
/cholelithiasis silent too [not a stand alone dx]

Acute pancreatitis acute pain, nausea, fever, jaundice [in advanced disease where inflammation ascends
to liver via accumulation of bile; compression of Vater leads to transient jaundice due to swelling,
edematous inflame pancreas in AP], tachypnea and tachycardia, dyspnea on slight/moderate exertion;
pain is piercing and very acute [radiates through the back; eg chronic pain is mild, constant pain,
hemorrhagic pain is the piercing type]

Acute viral hepatitis

AMI [should be placed higher up the differential since this is more dangerous and should be ruled out first]

PUD

***
Murphys sign differentiates between the various cholangitis, phyelonephritis, pancreatitis, appendicitis etc
- Not the same as Guarding of abdomen, since guarding of the abdomen involves the inflammation
of the parietal peritoneum underlying abdominal muscles [self protective mechanism]; guarding is
not a necessary accompanying sign for gall bladder dsx
- Pathophysiology of Murphys sign inflamed parietal peritoneum due to proximity of the inflamed
gall bladder is stretched upon inspiration

Question 2
Lab investigation interpretation:
Note: the range given in the case was for Men
Her Hb, Hc and MCV were normal.
WBC was elevated due to inflammation and a shift to the left for Neutrophils [acute inflammation]
Note: CRP above 50 could imply sepsis.
Slight elevation in urea is a common founding in patients who are dehydrated, malnourished, nauseas and
LOA
Pre-renal uremia reduced blood volume and hence reduced filtration in kidneys this is readily
correctable and reversible.

Total bilirubin high due to duct obstruction; increase in GGT/Alk Phos indicates stasis of bile in the duct
rising up to the liver and irritating the epithelial lining of the ducts

Professors comment on the lab results:
- GGT/ALKPHOS elevated in cholestasis due to obstruction
- ALT if there is hepatocellular damage in this case, due to rising bile/inflammation in
cholangitis/cholecystitis
- Best tests in liver fx for prognosis is albumin in an acute situation of such short term, we do not
expect a drop in albumin
- If this was acute hepatitis, the ALT should be in the THOUSANDS
- If in long standing liver dsx you can get abnormalities of albumin and clotting factors
- In this case, 24 hours is too short a time to see such abnormalities.

Question 3
Interpretation of the AXR:
This is an abdominal XR of Miss AR AP film in supine view patient is lying down where fluids levels are
not visible only bowel gases

Good coverage from top of lier to the pubic symphysis

We can see the lumbar spine clearly this means the axis is good and symmetrical

Levels L2 to sacrum, no fractured ribs pelvic inlet are normal

Psoas muscles are visible

Lateral to psoas muscle outline of kidneys [normal, 3 vertebrae in length liver is not enlarged and
appears normal]

Pathology visible: calcified gallstones

Not possible to be renal stones bc anatomical not possible right kidney should be lower down, and the
shape is wrong. Urinary and renal stones

Urovesical junction commonest site of urinary stones [see XR on the right side of UV junction at the
tip of ischial spine landmark of UVJ/ medial to the tip of acetabulum] could also be fecoliths/ and
multiple stones in such areas should bring up suspicion of parathyroid disorders

Note: Just because this is a single dimension we cannot say confidently the exact location of the stone

Do not confuse the gallstones with upper pole of kidney stones to confirm, take LATERAL XR behind
vertebra renal, anterior to vertebrae gallstone

Explanation for picture of jaundice:
Scleral icterus and some xanthelasma [yellow deposits around her deposits due to hypercholesterolemia
and family history of DM]; however, no lipid profile test was not done.

The hyperbilirubinemia of 170 is very high, and exceeds the threshold for which ocular icterus manifests.

Note; if the albumin was LOW and the dsx was CHRONIC what other things would you look for?
Gynecomastia, testicular trophy, superimposed acute and prolonged liver condition, spider nevi, asterixis
Also ask for medical history and drug history
Look for stigmata of chronic liver dsx if hypoalbuminemia

What other physical exams would you look for?
Pruritus indicates obstructive jaundice [excoriations on skin all over body ind bile acids accumulating in
blood circulation -accumulates in connective tissue beneath skin]
Shifting dullness ascites [one of the complications of gallstone dsx is perforation leading to peritonitis]
rule out long standing liver disease and its sequelae such as portal HPT
AAA rule this out since Abdominal pains worst outcome is AAA [rule this out as this is mainly without
specific symptoms and is fatal]
Middle aged/elderly patients tend to have rather insignificant PE results
Splenomegaly - rules out portal HPT [usually done with ascites]

Why was an US demanded for?
Gallstones, pericholecystic fluid [esp in acute cholecystitis] and gall wall thickening , patency of hepatic
and portal veins
CBD visualization, pericystic [fluid around GB fundus] and pericholecystic [around superior part of fundus
of GB esp at area of cystic duct entering GB if there is fluid accumulation there, most probably due to
acute cholecystitis] is clearer on US, esp EUS.
Dilated CBD more than 10cm
Abnormal GB wall - more than 4 mm
Good overview of focal liver/pancreatic disx such as tumours and pseudocysts, hamartomas, hematomas,
infectious foci.

Question 4
The justification for P/T empirical tx:
Biliary sepsis involves polymicrobial infection.
Piperacillin is ESBL - antipseudomonal action, tazobactam is beta lactamase inhibitor
Cover G+ [Enterococcus, Streptococcus], G- [E Coli, Klebsiella]
Or Cefotaxime
If need to cover Psd Ceftriaxone
And to include Clostridia, Bacteroides [anerobes] metronidazole.

Anerobes GNB in mouth is penicillin sensitive unless not nave
Beneath diaphragm, anerobes mainly beta lactamase producers

Hence: either P/T + M or CEF + M

Picture interpretation:
Gram + cocci in pairs and lengthy chains
Gamma haemolytic
And lactose fermenting on MCC [to culture GNB which ferment lactose]; on the agar, the colonies look
small [smaller than that on blood agar, meaning they are very fastidious; magenta color colonies on MCC
indicate ENTEROCOCCI until proven otherwise]
Hence, most probably E. fecium/ E. fecalis [G+ FACULTATIVE AEROBE]; MCC has bile salts and crystal
violet inhibits non-gut G+; the bile salts are selective for the gut flora such as gut strep, gut staph, gut
enterococci. Not suitably for anerobes unless environment provided. Enterococci are generally aerobic and
do not need specific aeration.
Organisms of the gut are bile-resistant, hence they can survive on MCC media.
MCC selective and differential functions
Differential bc it has an indicator and lactose to differentiate the lactose and non lactose fermenters.

P/T was used instead of co-amox. This is because PT is wider coverage bile cultures usually manifest one
dominant organism but in reality, infections of the gut are polymicrobila hence the need for a wider
spectrum. This also prevents selection of Clostridia.

Diagnosis biliary sepsis secondary to acute cholecystitis [or acute cholangitis]
Bacteria proliferates in stagnant bile
Elevated biliary pressure leads to bacteremia increased intrabiliary pressure causes reflux of bacteria into
intrahepatic and perihepatic circulation to cause bacteremia.

Most signs of sepsis were met raised WBC, CRP, NF, tachyp, tachycardia, chills, rigors

Biliary sepsis is merely an umbrella term to describe an array of manifestations due to biliary problem.

Dilatation of duct is not compulsory for diagnosis for acute cholecystitis.

Profs answer: It is a combination of ACUTE CHOLECYSTITIS and ACUTE CHOLANGITIS [acute cholangitis
is an emergency which needs prompt attention]

Note: Gallstones are more commonly formed in Hartmanns pouch of GB. CBD is rarely a site for stone
formation.

Acute cholangitis is ASSOCIATED WITH DILATED CBD due to a complicated choledocholithiasis. Cholangitis
is present, remove the stone and then remove the GB to prevent recurrence.

Less likely to be perforated/emphymatous patient will come in with more toxic manifestation such as
generalized peritonitis.

This is NOT an acute sepsis because cardinal point is hypotension. However, she has to be tackled as an
emergency patient given that she has MOST of the septic symptoms, esp with a dilated CBD and
cholangitis.

Question 5
Short term strategy for AC: ERCP is needed in this case of sepsis emergency to relieve sepsis.
ERCP is not to be confused with OGS.
Side note: The furthest for OGS is 3
rd
duodenum. Done by surgeon.
ERCP radiative hence handed by the radiologist. ERCPs scope is at the side, OGS is the tip.
OGS is diagnostic; MRCP diagnostic.
ERCP is mainly for therapeutic and diagnostic
ERCP can cause irritation of Vater and damage peripheral parenchyma of pancreas
ERCP aim for posteromedial aspect of duodenum and enter Vater.

In this case, to do sphincterotomy we need to do cannulation of ERCP into Vater and up the biliary tract.
Possible reasons for failure of ERCP cannulation into ampulla: stone too big/riding too high in CBD
Hence, we just drain the bile out if we cannot remove the stone. This is to treat the sepsis due to
obstruction of CBD by relieving the increased biliary HPT.
We can remove it another day via choledochotomy.

In a sick patient like this one, the ERCP is indicated to either relieve the intra-ductal HPT or the stone.

An alternative to the removal of the stone is to stent the duct, to allow a larger lumen to drain the bile.
And also, increase chance for the stone to exit the duct via the now enlarged lumen.

Differentiate primary and secondary cholangitis. Secondary is due to stones.

Note: Post sphincterotomy bleeding is a real danger.

Question 6
Fistulas of the biliary tract is most common in the third or second part of duodenum.
Two places of narrow lumen duodenal jejual at ligment of Trietz due to anatomical narrowness; stone
also easily stuck at ileocecal junction where both narrow and low pressure. gallstone ileus.

Note: pericholangitis/pericholecystitis and chornic states such as chronic cholecystitis you may see a
rare condition called Rokitansky Aschoff sinuses.

Strictures [permanent damages to the bile duct terminus] - choledocho-duodenalstomy is to redirect to
duodenum by circumventing the stricture part of the duct.

Removal of stone often reverses dilated CBD hence strictures tend to be rare.

Note: dual purpose of drainage via ERCP save sepsis, and reverse LFT by saving liver function. Doing
any surgery on a pt with normal LFT has good prognosis.

Note: dyspnea in gallstone dsx is due to:
NOT hepatorenal syndx [bc NOT chronic liver dsx]
Probably due to localized peritonitis/pain upon breathing