CBL-1 Acute Cholecystitis

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    CBL 1 A CASE OF ACUTE CHOLECYSTITIS

    Question 1this patient had DISTRESSING PAIN; for this case, the doctor should have enquired aboutRADIATION OF THE PAIN. E.g. gall bladder inflammation may also manifest as the radiation of pain to theRIGHT SHOULDER due to phrenic nerve contribution at the levels of C3,4,5 / diaphragmatic irritation dueto 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] cholangitispossibly because she resembled Charcots

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

    Acute pancreatitisacute pain, nausea, fever, jaundice [in advanced disease where inflammation ascendsto 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 inflammationof the parietal peritoneum underlying abdominal muscles [self protective mechanism]; guarding isnot 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 2Lab investigation interpretation:Note: the range given in the case was for MenHer 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 andLOAPre-renal uremia reduced blood volume and hence reduced filtration in kidneys this is readilycorrectable and reversible.

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

    Professors comment on the lab results:- GGT/ALKPHOSelevated in cholestasis due to obstruction-

    ALT if there is hepatocellular damage in this case, due to rising bile/inflammation incholangitis/cholecystitis

    - Best tests in liver fx for prognosis is albuminin an acute situation of such short term, we do notexpect a drop in albumin

    - If this was acute hepatitis, the ALT should be in the THOUSANDS- If in long standing liver dsxyou can get abnormalities of albumin and clotting factors- In this case, 24 hours is too short a time to see such abnormalities.

    Question 3Interpretation of the AXR:

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    This is an abdominal XR of Miss ARAP film in supine viewpatient is lying down where fluids levels arenot visibleonly bowel gases

    Good coveragefrom top of lier to the pubic symphysis

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

    Levels L2 to sacrum, no fractured ribspelvic inlet are normal

    Psoas muscles are visible

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

    Pathology visible: calcified gallstones

    Not possible to be renal stonesbc anatomical not possibleright kidney should be lower down, and theshape is wrong. Urinary and renal stones

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

    Note: Just because this is a single dimensionwe 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 behindvertebrarenal, anterior to vertebraegallstone

    Explanation for picture of jaundice:Scleral icterus and some xanthelasma [yellow deposits around her deposits due to hypercholesterolemiaand 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 CHRONICwhat 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 historyLook for stigmata of chronic liver dsx if hypoalbuminemia

    What other physical exams would you look for?Pruritusindicates obstructive jaundice [excoriations on skin all over bodyind bile acids accumulating inblood circulation -accumulates in connective tissue beneath skin]Shifting dullnessascites [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

    AAArule 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 resultsSplenomegaly - 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 hepaticand portal veinsCBD visualization, pericystic [fluid around GB fundus] and pericholecystic [around superior part of fundusof GBesp at area of cystic duct entering GB if there is fluid accumulation there, most probably due toacute cholecystitis] is clearer on US, esp EUS.Dilated CBDmore than 10cm

    Abnormal GB wall - more than 4 mmGood overview of focal liver/pancreatic disx such as tumours and pseudocysts, hamartomas, hematomas,infectious foci.

    Question 4The justification for P/T empirical tx:

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    Biliary sepsis involves polymicrobial infection.Piperacillin is ESBL - antipseudomonal action, tazobactam is beta lactamase inhibitorCover G+ [Enterococcus, Streptococcus], G- [E Coli, Klebsiella]Or CefotaximeIf need to cover PsdCeftriaxone

    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 chainsGamma haemolytic

    And lactose fermenting on MCC [to culture GNB which ferment lactose]; on the agar, the colonies looksmall [smaller than that on blood agar, meaning they are very fastidious; magenta color colonies on MCCindicate ENTEROCOCCI until proven otherwise]Hence, most probably E. fecium/ E. fecalis [G+ FACULTATIVE AEROBE]; MCC has bile salts and crystalvioletinhibits non-gut G+; the bile salts are selective for the gut flora such as gut strep, gut staph, gutenterococci. Not suitably for anerobes unless environment provided. Enterococci are generally aerobic anddo not need specific aeration.Organisms of the gut are bile-resistant, hence they can survive on MCC media.MCCselective and differential functionsDifferential 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 coveragebile cultures usually manifest onedominant organism but in reality, infections of the gut are polymicrobila hence the need for a widerspectrum. This also prevents selection of Clostridia.

    Diagnosisbiliary sepsis secondary to acute cholecystitis [or acute cholangitis]Bacteria proliferates in stagnant bileElevated biliary pressure leads to bacteremiaincreased intrabiliary pressure causes reflux of bacteria into

    intrahepatic and perihepatic circulation to cause bacteremia.

    Most signs of sepsis were metraised 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 cholangitisis 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. Cholangitisis 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 asgeneralized peritonitis.

    This is NOT an acute sepsisbecause cardinal point is hypotension. However, she has to be tackled as anemergency patient given that she has MOST of the septic symptoms, esp with a dilated CBD andcholangitis.

    Question 5Short 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 3rdduodenum. Done by surgeon.ERCPradiativehence handed by the radiologist. ERCPs scope is at the side, OGS is the tip.

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    OGS is diagnostic; MRCPdiagnostic.ERCPis mainly for therapeutic and diagnosticERCP can cause irritation of Vater and damage peripheral parenchyma of pancreasERCPaim 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 CBDHence, 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 6Fistulas 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; stonealso 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 arare condition called Rokitansky Aschoff sinuses.

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

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

    Note: dual purpose of drainage via ERCP save sepsis, and reverse LFT by saving liver function. Doingany 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