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Conferences and Medical Updates

Mercy September 2016

Mercy Conference 2017 september update

Hepatitis C  Dr Eugene Schiff

  • Fatigue is related to HCV viremia
  • Hepatitis C Ag is on the horizon – ELISA test
  • Resurgence of HCV.- the prevalence dropped in 2004 and now in 2014 the incidence is back to 2/1000,000.  This is due to heroin on the street
  • Heroin is cheaper than oxycontin
  • 80% of people were born between 45 to 65.  (in the past)
  • NS3/4A meds are simeprevir, partaprevir, grazoprevir.  Future asunaprevir, vedroprevir sovaprevir.
  • NS5A meds Ledipasvir, Ombitasvir, Daclatasvir, Elbasvir.  Future Velpatasvir, Odalasvir, PPI-668
  • NS5B inhibitor Sofosbuvir
  • Non nucleoside NS5B inhibitor Dasabuvir
  • Cyclophilin Inhibitor SCY-635
  • HCV treatment Path App
  • Hardest to treat is cirrhotic GT3 that has relapsed or failed treatment
  • Fibroscan : can be misleading in CHF patients

Alcoholic hepatitis Paul Thuluvath

  • 3.3 million people die from alcohol related problems
  • Increased risk when intake is more than 30 grams/day.  1% if they drink 30-60 grams and 6% if intake is more than 120 gm.
  • 1 drink is 14 grams – 360 ml of beer, 150 ml of wine,
  • Obesity, female viral hepatitis, genetic predisposition are more likely to develop alcohol liver disease
  • 90% of alcoholic develop fatty liver and 20% alcoholic hepatitis and 15% cirrhosis
  • Two types – fast acetylation or slow acetylation.
  • ADH and ALDH enzymes  in acetylation
  • Adiponutrin on chromosome 22 increases risk
  • Alcohol macrocytosis is from alcotohol toxicity, B 12 def, and increased lipid on RBC
  • Other features besides macrocytosis are AST:ALT more than 2, increased INR, increased WBC, decreased lymphocytosis, high ESR, low plt and Hb
  • Liver biopsy can show fatty liver, hepatitis, fibrosis or cirrhosis
  • Symptoms of alcohol hepatitis – low grade fever, anorexia, RUQ pain, abdominal distension, proximal muscle weakness or confusion.  Signs are jaundice, hepatomegaly, ascites, proximal myopathy or asterxis.  Rarely malnutrition
  • Prevent recevidism by using baclofen, gabapentin, naltrexone, acamprosate
  • 50% of patients with alcohol hepatitis will have cirrhosis
  • Recidivism is 70%
  • Scores for outcome – DF more than 32,(30% 30 day mortality) MELD score more than 21 has 20% 90 day mortality and Lille score after 7 days of prednisolone
  • Lille score is based on bilirubin – if after 7 days it does not improve after prednisone, they wont get better
  • Lille score mortality if more than 0.45 is 75% at 6 months and if less than 0.45 mortality is 15%
  • Alcoholic hepatitis Histologic Score (AHHS).  0-3, 4-5, 6-9 score has mortality of 3, 19 and 55% at 90 days
  • 20% misdiagnosis in Alcohol hepatitis.  So if in doubt consider liver biopsy
  • Cause of death in alcoholic hepatitis liver failure 55%, GI bleed 21%, sepsis 7% and others
  • Dose of prednisone is 40 mg a day.  Encourage good nutrition, high protein .1.5 g/kg, high calories 35-40Kcal/kg, thiamine, folate, magnesium, phosphate and pyridoxine supplement.
  • Rule out sepsis
  • Pentoxyfylline is not helpful except if they have hepatorenal syndrome.
  • Prednisone only had a 28 day mortality benefit.
  • Steroid and pentoxyfylline is not helpful.
  • Unproven benefit with GCSF or metadoxine (anti oxidant)
  • Severe AH – prednisone  for 28 days plus NAC for 5 days. Dose of NAC is  Day 1 150 mg/kg in 30 min followed by 50/kg in 4 hours and then 100 mg/kgfor 16 hours
  • Day 2-5 100 mg/kg.  All is in D5W
  • If lille score more than0.56 stop treatment and if Lille score more than 0.45 consider OLT

NAFLD Dr. Younoussi

  • Treatment options are
    • Weight loss
    • Statins and fibrates
    • Antioxidants
      • Vitamin E/C
      • Betaine
      • NAC
      • Lecithin
      • Silymarin
      • Beta carotene
      • EPA
    • Treatment of IR
    • PPRA agonist (perixosome proliferator-activated receptor agonist
    • Anti TNF like pentoxyfylline
    • ACE or ARB
    • Caspase inhibitors
    • Bile acid Ursodeoxcyholic acid
  • NAFLD is a phenotype (a diverse pathologic process from multiple other diseases)
  • NASH is fat, liver injury and inflammation. Must exclude HCV and alcohol
  • Middle east has highest incidence
  • Obesity,, DM, metabolic syndrome, increased lipid or TG
  • Lean NAFLD : 3.7 % had NASH even if BMI less than 25  They  have insulin resistance and DM
  • NASH is an independent risk factor for cardiac disease
  • NASH and HCC.  If NASH is present, higher mortality for HCC
  • Highest mortality for NASH is in age and DM
  • New NAFLD regimens are
    • OCA (famesoid X recept agonist)  Used for PBC.  FLINT study fibrosis improvement and caused increased lipid profile.
    • Simtuzumab (anti lysyl oxidase like 2 monoclonal Ab)
    • Fatty acid / bile acid conjugate – Aramchol
    • Dual inhibitor of CCR2 and CCR5 – cenicriviroc
    • Dual peroxisome proliferator activated receptor – GFT 505  Elafibrinor
    • Probiotics – VSL #3 Probably not helpful
  • Ballooning and portal inflammation  and fibrosis will develop cirrhosis. This is the advantage of liver biopsy.  Fibrosis was the most significant indicator
  • Cost of NAFLD is 100 billion dollars per year for USA
  • Obesity, insulin resistance (IR) or T2D with second hit (oxidative stress from mitochondria and CYP 450 OR adipokines) leads to inflammation and necrosis. BOTH PATHWAYS NEEDED.
  • Fibroscan and MR elastography are very helpful
  • APRI score, Fib -4, bARD, BAAT, fibrotest, NAFLD fibrosis score.
  • HAIR, NASH test, NPI
  • Fibrosure is not good.  NASH – CK-18 is another score
  • Fib-4 – http://gihep.com/calculators/hepatology/fibrosis-4-score/
  • BARD score http://gihep.com/calculators/hepatology/bard/
  • NAFLD score – http://nafldscore.com
  • HOMA score for insulin resistance
  • DM plus morbidly obese – restrictive surgery
  • Vitamin E helps in non diabetic NASH.  Start with 400 , monitor LFT.  Vitamin E – cardiovascular disease
  • DM is an independent risk factor for HCC

HCC and surgery Dr. Hanish

  • Sorafenib – no difference
  • Resection – If normal liver, resect.  But 80% of patients have cirrhosis or advanced fibrosis and plt less than 150,000 makes resection unsafe.  Must have at least 50% functional liver reserve .  In other words, plt more than 150, MELD less than 10, portal pressure less than 10 and 50% functional liver – RESECTION if lesion is solitary and less than 5 cm BUT 67 % tumor resection at 5 years and 83% recurrence at 10 years
  • Local therapy – DEB-TACE, Y90, cryoablation, RFA, microwave, Ire
  • Transplant
  • Chemical ablation
  • RFA improved survival benefit if lesion more than 2 cm, Not helpful if 5 cm lesion.
  • RFA works by heating tumor to more than 100 celcsius.  Sometimes it can cause rupture
  • Microwave heats it up too but there is NO HEAT sink.  There is no renal failure which occurs with RFA
  • Bland ablation shows 2 year survival benefit.
  • TACE 2 year survival is 63%.  Drug eluting beads has improved outcomes.
  • Y90 radioembolization – beta emitors and downsizes tumor.  Have to wait for 6 weeks after Y90.  It is most effective for portal vein thrombosis.

HPylori  Dr Lisa Pichai

  • Flagyl, tetracycline, Rifabutin, Furzolidone, Levofloxacin, Chlarithromycin, Amoxicillin
  • Standard treatment in the past was triple therapy
  • Hp has 2 states replicating and non replicating states
  • Easier to kill when it is replicating and pH is 6-8. In non replicating, pH is less than 6.  Most drugs break down in acidic environment
  • 5 strains of Hp
  • In USA flagyl resistance is common
  • There is a lot of point mutation in Hp
  • Changes in Hp forms – spiral to coccoid forms. Coccoid forms are resistant.
  • They have plasmid mediated resistance
  • India high flagyl resitance and some tetracycline
  • In USA Biaxin resistance is 17%
  • MUST TREAT 14 days.
  • MUST CONSIDER REGIONAL RESISTANCE INFORMATION
  • PBMT is option for first line  OR PAMC either option.
  • RESTRICT triple therapy.- PAC, PMC, PAM
  • Against use of levofloxacin as first level.  PAL is second line
  • DO NOT — — USE SEQUENTIAL THERAPY
  • FAILED TREAT – PBMT with higher dose of tetra OR PAL.
  • IF THEY have failed levo or amoxicillin in either regimen  failed first time
  • RIFABUTIN causes myelotoxicity. — — USE ONLY IF THEY FAILED 3 other regimens and check Hp for sensitivity
  • ADJUVANT – add probiotics.

gastric lesions – dr. kantsevoy

  • MUST DO ENDOSCOPIC LIFT.  This is 100% sensitive and 99% specific
  • ANY LN THAT IS POSITIVE SHOULD BE CONSIDERED MALIGNANT

Gluten sensitivity – Richard desi

  • Gluten is a mixture of protein found in barley, rye, oat, spelt, kamut, triticale and wheat
  • Prevalence 1:70 to 1:300 in most countries
  • Neurological symptoms, osteoporosis, arthritis and rash
  • Signs are vitamin def, osteoporosis, iron def, anemia
  • Oral glutenase is being studied
  • 1 in 5 is on a gluten free diet
  • NCGS : people believe it can cause brain fog? Fatigue? Depression? Numbness in the hand, eczema and fatigue
  • Gluten sensitivity maybe an immune mechanism

Opportunistic infection dr. harris

  • HSV – type 1 or 2.
    • Crusted lesions not infectious
    • Acute phase – painful ulcers
    • Stress, sun exposure reactivates hsv virus. Usual outbreaks are 3-4/year
    • It can spread from one part of the body by auto touching.  Ophthalmic involvement is worrisome
    • Rx famciclovoir and acylovoir.
    • Amino acid lysine can be helpful
  • Varicella zoster
    • Dermatological infection
    • Often Trigeminnal involvement
    • Use attenuated zoster immunization.
    • It is live attenuated virus
    • Give immunization – 3 weeks before biologic.  Or must be off immunomodulater for 6 months before giving the live virus
    • Look up paper on opportunistic diseasesin IBD review by Manish
  • CMV can occur in immunocompetent patients also
  • EBV – causes infectious mono, nasopharyngeal ca, burkitts lymphoma and B cell lymphoma
  • HPV : 99% cervical ca have HPV DNA (type 16 or 18)
  • HPV can occur in mouth also (tonsillar cancer)
  • TB :
  • Listeriosis _ occurs from contaminated food. Young, elderly and pregnant.    S/S are headache, stiff neck, meningitits.  Contaminated vegatables, milk, Incubation periodis 1 month
  • Histoplasmosis and Apergillosis : Endemic here
  • Anisayakasis (sushi )

Biologics in IBD in 2016 – Dr. Ray Cross

  • Biologics modify the natural history of IBD
  • Early biologic gives endoscopic healing at 2 years – higher rates (80% at 2 years ) and those who heal remain  healed for 2 more years and just on azathioprine after that
  • SONIC trial (combination is better for both UC or CD)
  • AGA pathway – care pathway  2 steps  Low risk versus high risk
  • High risk are those with deep ulcers, extensive involvement, age less than 30, perianal disease, rectal disease, complicated behavior and prior surgery (for CD)
  • High risk give anti TNF
  • Low risk use budesonide or AZA or both
  • UC – High risk – young age, deep ulcers, high CRP, steroid at time of diagnosis, C diff or CMV infection or extensive colitis.
  • Low risk oral 5 ASA, budesonide or rectal steroids.
  • High risk – entyvio or anti TNF
  • Non responders are due to – IBS, psychiatric disease, look for stricture, bile salt diarrhea, bacterial overgrowth, celiac, short bowel, deep seated or intractable disease, smoking and other drugs
  • Stricture is the biggest reason in non responders
  • Stricture score – mass or abscess, mesenteric stranding, prox dilatation of colon more than 3 cm, SBO, fistula.  If 1-5 score, most of them will need surgery.  1 point for each of the above points
  • Anti drug Ab are bad
  • Immunosuppresants improved outcome
  • High baseline TNF better outcome
  • Low albumin, worse outcome faster clearance
  • High CRP drug clears faster
  • Body size – higher BMI clears drug faster,
  • Males have a faster clearance
  • Switch to different anti TNF if antibody present. If Ab present 20% response. Change medicine 90% medicine
  • Do drug level twice a year
  • TAILORIX study :
  • Entyvio : Alpha 4 beta 7 and madcam-1 blocked.  Give at 0,2, 6
  • Vedolizumab every 4-8 weeks
  • 1/3 patients need it every 4 weeks per Dr. Cross in his practice
  • Ustekinumab : Stelara   Approved for Psoriasis  IL-23 inhibitor.  Study is UNITI-1.  Treatment refractory group..  50% had failed 2 different regimens.  6 mg/kg
  • Response rate is 21% healing and response is 40%
  • IM-UNITI study : dose is 90 q 8
  • Monotherapy is reasonable for some patients
  • Age more than 60 avoid 6 MP.
  • Recent malignancy, avoid combination therapy
  • Drug level is part of practice guidelines
  • Entyvio onset is slow 6-8 weeks, no drug level and costlier.  So second line

biomarkers in ibd.  dr matilda hagan

  • CRP.  It is produced by hepatocytes from IL-6, TNF-alpha, IL-1B and mesenteric adipocytes in CD pt. Half life is19 hours
  • Fecal calprotectin  S 1008A8 protein and calcium and zinc binding
  • Fecal lactoferrin
  • Fecal calprotectin is more sensitive than CRP and suggests mucosal healing
  • IBD versus non IBD tesing : no fecal marker can do it.
  • Low crp (less than 0.5) and low calprotectin less than 1 % of IBD
  • FC predicts disease relapse
  • Clinical endpoint should be FC less than 50, which shows mucosal relapse
  • If FC less than 50, after anti TNF 84% remained disease free
  • ASCA and ANCA markers –
  • ASCA is present in normal upto 5% 60^ of CD and 10% UC
  • ASCA + and ANCA neg CD
  • ANCA + – UC
  • Anti-CBir1 is associated with development of CD of the pouch after IPAA
  • Anti-Omp C in UC associated with colectomy
  • CD with ANCA + are less likely to have complications
  • Novel markers are anti Flagellin Ab, ALCA and ACCA
  • Monitoring of IBD
  • If 6 TGN is more than 235 more likely to respond
  • Infliximab level should be more than 3-4 mcg/ml
  • TAXIT – get therapeutic levels

Mucosal healing dr. harris

Deep remission : clinical, histological and biomarker resolution
UC use Mayo score :  0-3.  Normal, to mild erythema
Scores : Rutgeerts score : 0 ulcers, less than 5 ulcers, more than 5 ulcers, ulcers without intervening normal structure and last is cobblestone with stricture.  This is for Crohns
In clinical studies – for CD is looking for transmural healing now

Microscopic colitis
MC is LC and CC.  Only histological differences
Female predominance
Age usually more than 65
Theory is related bile acids, increased NO and Pg, impaired electrolyte absorbtion and autoimmune from luminal Ag all lead to MC
Chronic diarrhea, dehydration, weight loss and abd. Pain
PPI, NSAIDs, ASA, ranitidine, SSRi, ticlid, ascarbose and statins.  Other factors are smoking and auto immune disease
9 mg uceris for 8 weeks – Budesonide  First line of therapy now
Follow up colon is not needed
Budesonide superior to Mesalamine
Maintenance for  budesonide 6 mg for 6 months
Boswellia serrata for MC
Probiotics no difference with placebo
Mesalamine plus questran is same as Mesalamine
Azathioprine can be used but only 28% remission rate . This is for resistant patients. Other option is methotrexate
Get right side cold bx
Other use includes BSS and bile acid resins  (bismuth sub salicylase) BSS – 2-3 tablets 3 or 4 times a day 262 mg each
Lomotil
eosinophilic esophagitis dr. richard desi

EoE 15 per HPF but not been validated
Diseases associated with Eosinophilia of esophagus,  PPI- EE, CD, infection, achalasia, drugs hypersensitivity, vasculitis etc
Blood eos may or may not be present
Male 3:1
More in urban setting
Higher in cold and arid zones
EoE decreased after 45
Feline esophagus, strictures in 21%, whitish papules, linear furrows 48%, whitish papules 27% (microabscess)
PPI for 8 weeks repeat bx. If no eos, then probably not EoE
Budesonide / fluticasone trial if EoE
Six week elimination diet
If all fails, elemental diet
Allergiest referral

noac in endoscopy – dr. maheshwari

  • neuroendocrine tumors dr. vadim guschinh. This is rare and is associated with high mortality
  • Type 1 resect antrum
  • Type 2 sandostatin and surgery for large tumors
  • Type 3 gastrectomy with LN dissection

SB NET

  • Frequent liver and LN meds, subcm tumors
  • Multiple
  • Severe desmoplastic reaction
  • Abdominal pain, diarrhea and carcinoid
  • Simultaneous liver resection
  • Survival 65% 5 year disease and 50% if metastatic

(NET)

Neuroendocrine – second most common after colo rectal cancer
1000,000 patients in US
Increasing incidence
Tumor sites GI tract, then adrenal and then lung, merkle, medullary
Ki-67 index – less than 3, 3-20 and more than 20 is well differentiated moderately differentiated and poorly differentiated
Non functioning tumors can cause pain, weight loss,
Rectum neuroendocrine present with bleeding and local problems
68 Ga Octreotide or use 68 Ga octreotide with PET/CT scan
Debulking is beneficial
Primary tumor can be occult
3 types of hypergastrinemia

  • Type 1 is auto immune gastritis

Rectal NET

  • Small 1-2 cm good prognosis
  • Larger than 2 cm have 60% node positivity and 25% liver mets.  N. Multiple small tumors throughtout stomach
  • Type 2 ZE
  • Type 3 similar to adenoca of stomach. This is rare and is associated with high mortality
  • Type 1 resect antrum
  • Type 2 sandostatin and surgery for large tumors
  • Type 3 gastrectomy with LN dissection
  • eeds APR.  Poor prognosis if conservative management

Drugs are MIBG, PRRT, cheomotherapy

liver imaging. dr. ankur gupta

US – increased echogenicity meaSB NET

  • Frequent liver and LN meds, subcm tumors
  • Multiple
  • Severe desmoplastic reaction
  • Abdominal pain, diarrhea and carcinoid

ns fatty liver

US – increased echogenicity means fatty liver, cirrhosis

  • DD is iron deposition, cirrhosis, infiltrative neoSimultaneous liver resection
  • Survival 65% 5 year disease and 50% if metastatic
  • plasm, sarcoidosis, wilsons disease, glycogent storage and infection

US can prRectal NET

  • ove if it iSmall 1-2 cm good prognosis
  • Larger than 2 cm have 60% node positivity and 25% liver mets.  Needs APR.  Poor prognosis if conservative management

s cyst or not a cyst.   Looks black
Hemangioma on US shows posterior acoustic enhancement, no color flow
Hemangioma on US shows posterior acoustiDrugs are MIBG, PRRT, cheomotherapy
c
liver imaging. dr. ankur gupta

enhancement, no color flow, hypoechoic center with hyperechoic periphery
The DUS – increased echogenicity means fatty liver, cirrhosis

  • DD is iron deposition, cirrhosis, infiltrative neoplasm, sarcoidosis, wilsons disease, glycogent storage and infection
  • D includes FNH, adenoma etc

HCC – Stage 0 to stage C
Milan criteria
US sensitivity is 65%
US sensitivity is 65%
4 phase CT – no conUS can prove if it is cyst or not a cyst.   Looks black
trast, early arterial and late arterial, portal venous and then equilibirium 3 min plus
MRI T2 weighted sequences and diffusHemangioma on US shows posterior acoustic enhancement, no color flow, hypoechoic center with hyperechoic periphery

  • The DD includes FNH, adenoma etc

ion DWI

HCC nodules.  If less tIf adenoma more than 5 cm, surgical MRI DO NOT — — USE GAD.  It can cause developmental anomaly in lung or GI tract of fetus
resection since it grows in pregnancy
Unique diseases are hyperemesis gravidarum, IntPropofol is cat B, meperidine is Cat C, benzo is cat D and small doses midazolam is ok.  Defer till secondaHyperecohic lesions are metastatic or malignant
HCC – Stage 0 to stage C
Milan criteria
n 1 cm, repeat MRI in 3 months.
If between 1-2, get CT or MRI
US sensitivity is 65%
4 phase CT – no First through 20 weeks,  IHCP in second and third, AFLP in third and the eclampsia and HELLP in 20  to 22 weeks onwards

  • ICHP, 5 % pruritis, abnormal LFT, unconjugated hyperbilirubinemia,
  • Eclampsia upto 7.5%, HTN proteinuria, peripheral edema and seizures. Liver abnormality is uncommon and non specific.  RUQ pain due to swelling of liver,striking transaminases, hematoma below glissons capsule.  Cause is  ischemia, .  Maternal mortality is 1%, Hypertensive crisis, renal damage, neuro complications
  • HELLP : 0.5% of all pregnancyies It is advanced form of pre eclampsia.
  • Advanced age, nulliparous and multiparity.  RUQ pain, hemolysis, TTP, low platelet, microangiopathic hemolytic syndrome.  Mortality for mother is 1-3 %, hepatic infarction subcapsular hematoma, intra parenchymal hemorrhage.  Fibrin deposition causes infarction.. If less than 34 weeks consider glucocorticoids.  Missippi protocol, use Mg sulfate, BP control and use steroids.  Recurrence with subsequent 3-27%
  • AFLP : autosomal recessive – faty acid oxidation disorder in fetus and it crosses placenta and then causes fatty liver in mother.  This causes fatty liver.  Needs abnormal genetic in both mother and father.   Occurs in 1.1000, third trimester, nausea, vomiting, abd. Pain, anorexia, jaundice. Fetal def of LCHAD.  High complication rate.  Rx delivery.  Use Swansea diagnostic criteria for AFLP  6 or more present.
  • HSV – high mortality rate in 74% . Rx empiric acyclovoir
  • HBV high mother to child transmission – Tenofovir or telbivudine use in 3rd trimester. Esp if high viral load.  Cat B drug
  • No HCV treatment a few months before conception
  • Cirrhosis in Pregnancy,  Get rid of varices.  Do EGD.

update on barretts dr. greenwald

  • Norman Barrett from Australia first discovered it
  • Do not biopsy less than 1 cm of z line variability
  • Prague classification – C and M and location of diaphragm and GEJ
  • Even if no intestinal metaplasia. Repeat EGD in 1-2 years
  • 17% intestinal metaplasia of GEJ / cardia. Risk of cancer is same as general population.
  • Partially deflate stomach and then get GEJ location.
  • Screening for Barretts if reflux for more than 5 cm,age more than50, Caucasian, central obesity, tobacco use, FH of BE/eso cancer
  • Don’t screen women.
  • Don’t screen with short life expectancy
  • Consider unsedated trans nasal endoscopy.
  • If dysplasia then change to 4 quad in 1 cm.
  • Don’t biopsy esophagitis
  • Offer EMR
  • Maximum 8 specimens in 1 jar
  • Risk of cancer progression is lower than we were taught.  It is 0.2% per patient per year
  • Most patients of Barretts die from something else
  • ? role of aspirin for prevention.  PPI once a day unless bid for reflux control
  • RFA is treatment of choice
  • Nodules – remove with EMR
  • HGD risk of cancer is 6%/patient/year
  • Ablation helps prevent LGD from going to cancer
  • RFA success rate is 91%  RFA treated versus control 1% cancer versus 9% in untreated
  • Even after RFA, needs repeat EGD and survellience
  • Rigorous seattle protocol must be followed
  • WATS 3D brushings
  • Volume Laser endomicroscopy – – VLE.
  • Liquid cryotherapy – Patient on Coumadin and needs nodule resection
  • NO cryotherapy.  –  Mimi Canto from Hopkins uses it

acute pancreatitis from mayo clinic dr santhi vege

  • 1% mortality of Pancreatitis – IN mayo mortality is 2-3% mortality
  • Interstitial or mild and Severe.
  • In Mayo – three types, Mild, moderate and severe
    • Moderate is local complications
    • Mild just interstitial edema
    • Severe is necrotizing with organ failure – cardiac, renal and respiratory
  • Revised atlantic 2012 classification
  • Now 2 phase is First phase 1-2 weeks.  Here there is systemic complications from inflammation.  People die usually in first 2 weeks.    Second phase at week 3-4 week usually causes morbitity but no death
  • SIRS defined by pulse more than 90,
  • Type of necrosis   Two types.  Pure pancreatic necrosis is extremely.  Peripancreatic necrosis is second.  Third the worst is necrosis both in pancreas and peripancreatic
  • Acute necrotic collections or acute peri-pancreatic fluid collections
  • Pseudocyst is rare.  Most often is walled off necrotic collection.
  • Critical pancreatits – infected necrosis plus persistent organ failure
  • Day 1 US.
  • MRI or EUS is rarely
  • Perfusion CT – lesser volume
  • Subtraction color map CT.   Less radiation and easier procedure compared to perfusion CT
  • Etiology : gallstones and microlithiasis.  If ALT is more than 3 x UNL 90% PPV for biliary case.  (stones or microlithiasis)
  • If ALT is less than 3 UNL, and gallstones – get cholecystectomy is ok
  • Badalov class 1 -4 for drug induced pancreatitis.
  • Usually drug started in 6 months of pancreatitis
  • TG has to be more than 1000
  • AIP is rare cause of AP
  • Main duct and side branch of IPMN
  • Younger patients with idiopathic AP – genes

Systemic Inflammatory Response Syndrome (SIRS) Score
• SIRSdefinedby≥2ofthefollowing: Pulse > 90 /min
Resp > 20 / min or PaCO2 < 32 mm Hg Temp > 38 or < 36° C
WBC count > 12,000 or < 4,000 / mm3
Fenagles Law

  • CRP more than 150, necrosis on CT, age, comorbidity, increased BMI, persistent SIRS at 48 hours, persistant organ failure at 48 hours are poor predictors
  • PPV for severity is only 50%
  • Rx.  Most important is IVF.  250 ml – 350 ml/hour, use lactated ringer.  No strong evidence of using more than 4.5 liters
  • Compartment syndrome with too much fluid
  • No role of prophylactic antibiotics.  Maybe helpful in necrosis involved organ failure
  • Urgent ERCP is only if patient has cholangitis
  • Oral intake early
  • Enteral nutrition is better than TPN. Usually between 3-5 days
  • NO TPN, NO TPN NO TPN uncles he cannot tolerate enteral supplement
  • Infected necrosis usually at 1 week
  • Walled off necrosis (WON)
  • Necrotizing pancreatitis – preferably do it at 4 weeks and not before otherwise high mortality.  Intervention is needed only infected. Sterile if SBO etc.
  • WON – antibiotics, catheter drainage,..10 different management.  Look up on slide
  • Percutaneous drainage is the best, then endoscopic drainage and then laproscopic. OPEN not done. Hybrid is becoming popular
  • Portal vein thrombosis – anticoagulants for 3 months
  • Pseudoaneurysms needs embolization
  • Pentoxifylline may be helpful.
  • Chronic pancreatitis – genetic, alcohol and smoking.  50% idiopathic. The 1 % of alcoholics who develop pancreatitis have abnormal gene
  • Hyper lipase syndrome – chronically goes up and down.  Study in asymptomatic in Italy. Also elevated lipase occurs in CKD, bililary, intestinal issues etc. It is NON SPECIFIC.

AIP auto immune pancreatitis – Dr. Raina

  • IgG4 has limitations
  • Has frequent presentation of obstructive jaundice, with or without mass, lymphocytic infiltrate and responds to steroids
  • Abundant IgG4 laden plasma cells infiltration in other organs also.
  • IgG4 might be a systemic disease
  • IgG4-related sclerosisg disease.  Variable serum IgG4 levels
  • Very rare – 1.4 , 100,000 incidence ins pancreas
  • Two types – Type 1 and Type 2 .  Type 1 is classic.  Type 2 is a gel lesion or idiopathic duct pancreatitis.  Type 1 is called LPSP is part of systemic syndrome.  Lymphoplasmacytic sclerosing pancreatitis.
    • Usually elderly male, systemic disease that can affect nearly any organ system and responds to steroids.
    • Type 2 is IDCP or idiopathic duct centric pancreatitis.  Granulocytic epithelial lesion (GEL) on bx.  No IgG4 elevation and is associated ot UC.  Occurs at 50-60 while type 1 is 70’s
  • No pseudocyst seen with AIP
  • The can have steatorrhea, weight loss, diabetes, obstructive jaundice.
  • Sausage shaped pancreas is mostly poster ! The typical  The head is prominent but duct is not dilated.
  • Focal AIP – Just in head or tail.  IgG4 is more than 280 mg and Ca 19-9 less than 85 probably focal AIP
  • Extra pancreatic manifestation of LPSP – biliary tree, salivary grland, prostate, kidney, retroperitoneum, thyroid,, lymph nodes, colonic pseudotumor.
  • IgG4 cholangiopathy –mostly around central hepatic duct !
  • 6 cardinal things storiform fibrosis is another feature besides the others mentioned above
  • IgG4 level more than 2 ULN is type 1 and 1-2 ULN in type 2.
  • IgG4 gets elevated in skin disorders and parasitic disorders also
  • Severe alcoholic hepatitis and PSC can also increase IgG4
  • IgG4 does not bind to complement.
  • Example bee hive workers IgG4 goes up progressively to attenuate response to bee stings
  • UC subtype – possibly patients with UC and high IgG4 on biopsy possibly have a higher chance of getting PSC

pancreatic cysts dr jagannath

  • Current Guidelines
  • Increasing incidenctal pancreatic cysts lesions IPCL.
  • IPMN – 3 types.  Branc chain, main duct and mixed.
  • Usually in 7 or 8th decade, equal M and F, 70% asymptomatic.
  • If symptomatic cystic lesion with pain is a bad prognostic sign.  More likely to be malignancy
  • Cyst more than 3, solid component, abrupt change in PD, lymphadenopathy, thick cyst wall, dilated main PD more than 5-9 mm

Management of esophageal stricture Dr. michael kochman

  • Dilatation .1 to .3% perforation rate for dilation and 0.2% bleeding
  • Complex stricture – unable to pass endoscope, more than 2 cm and angulation
  • Can use bronchoscopy.
  • Tissue biopsy is not a contraindication to doing dilatation.
  • Can do EGD through the PEG and then do dilatation through it
  • Retrograde dilation and access
  • Wire guided dilation – must have proximal and distal control. Savory or balloon – no difference
  • Cannot use Maloney dilators into complex strictures
  • Balloons preferred for epidermolysis bullosa, trachea-esophageal prostehses, anastomotic strictures, lach of mechanical advantage for savary, planned passage of endoscopy subsequent to dilatation
  • Savary can coil in pharynx – especially in very tight strictures
  • Refractory and recurrent.  14 mm. is target.  Recurrent is if it closes after being patent for 4 weeks.
  • pPeptic and schatzkis ring just one dilation. Schatzkis ring dilate with single dilator 18 mm
  • Post surgical or radiation requires generally at least 3 dilations
  • If length is more than 5 and requires multiple dilatations
  • Kenalog 10 mg/ml in each 4 quadrants with sclera needls in the middle of stricture.  Dilate after injection.  Use for recurrent scar
  • Polyflex – it is not definitive solution. It is only temporizing.  Migration is 52%
  • Off label use of endoprosthesis.   Braided endoprosthesis, fully covered is preferred.  Laser cut SHOULD NOT BE — — USED  Must be removed in a few months
  • Self bouginage is a consideration
  • Can use scissors to cut some strictures
  • Endoprosthesis do not fix transmural process
  • Schatzkis ring savory 18 mm one pass.
  • EoE stricture – probably not safe to dilate.
  • EoE stricture use balloon.  Do not go more than 14 mmg
  • Cricopharyngeal bars – can use 18-20 mm dilator savory. It gives short term relief and botox does not work.  Refer to ENT?
  • After dilatation, air translocation occurs but true perforation is is barium is shown to leak

Recurrent CDAD  Dr.Jagannath

  • Stool is a biologically active complex mixture of living organisms
  • Human : mammalian and microbial cells.  We have more microbials than mammalian cells  Ratio is 10:1
  • 3.3 million microbial genes
  • Archae –Is the link between single cell and eukaryocytes
  • 36,000 bacterial species are in our GI tract.  Most of them are anaerobic.
  • 4 major phyla Bacteroiodetes, Fermecitis,(these 2 or 90%) then  actinobacteria, proteobacteria.
  • Functions are – metabolism of polysacherides, vitamins, development of immune system, protect against pathological organisms
  • B and F – increase in pro-inflammatory bacteria. . Gut dysbiosis – more yeasts, parasites
  • C diff is a world wide epidemic.
  • At risk population is IBD, peri-partum, antibiotics, compromised immune systems,
  • NAP1/B1/027 produces toxin A, B and binary toxin.  Binary toxin makes A and B toxins more virulent
  • Phylogenetic diversity is lost when patients become C diff positive.
  • 20% recurrent rate
  • After each recurrent, your recurrence goes up by 20%
  • Severe C diff DO NOT flagyl.
  • Fulminant C diff – low bp, ileus, Vancomycin 500 m qid
  • Fidaxomicin 88% cure rate.  Lower recurrence rate
  • Third recurrence, consider FMT
  • After 3rd recurrence use FMT.  ACG guidelines
  • Use non toxin C diff to prevent toxin C diff (NTCD)
  • Recurrence rate is lower in patients who have CDA1 and CDB1 antibodies
  • Modify 1 and 2 trials for Zinplava  – Actoxumab and bezlotoxumab (antibody to toxin A and B respectively)
  • Only antibody to toxin b works.
  • Vaccine for C diff.  Partially purified toxoid A and B.  Phase 3 trials underway.
  • FMT capsule G 3 and Rebiotix are two different capsules
  • Could do cecostomy and deposit stool 60 cc at a time

HCV relapse Dr. Paul Thuluvath

  • RAS –Q80K for GT1a with cirrhosis  If mutation cure rate is 10% lower
  • NS5A –RAS mutation if you use grazoprevir/elbasvir combination for GT1a
  • Q80K mutation is 13% incidence
  • If you fail viekera or harvoni – will have NS5A mutations
  • Drug resistant mutations are Q30H/R with ledipasvir, L31M is 4%,Y93H is 2 percent multiple is 5%
  • NS5B no mutations noted with sofosbuvir
  • Viekira pack – does not impact mutation since there are 3 drugs
  • Zepetier (grazoprevir/elbasvir) NS5A RAS but no effect on NS3 RAS
  • Harvoni failures Sofosbuvir plus simeprevir plus ribavirin for 12 weeks or 24 weeks for cirrhosis
  • Sofosbuvir plus zepetier for viekira pack failures

post ercp pancreatitis. dr. kochman

  • If  amylase is less than 1.5 ULN in 4 hours of ERCP, unlikely to develop pancreatitis
  • Modifiable risk –
  • PEP (post ercp pancreatitis)
  • Things we cannot modify are gender, age, prior PEP, ercp
  • Prior PEP  8.7 odds ratio for developing pancreatitis
  • Difficult cannulation – cannulate within 10 min or change technique
  • Risk is 3, 8 and 15 percent based on cannulation attempts less than 5, more than 6 or more than 15 attempts
  • Balloon sphincteroplasty should NOT be done unless sphincterotomy was done first
  • PD stent may decrease risk
  • Failure to place PD stent will cause pancreatitis if you try it and fail
  • Needs 100 cases per year and 1000 cases in training
  • Indocin or diclofenac to decrease pancreatitis
  • 20 cc/kg bolus and then 3 cc/kg/hour for 8 hours with LR
  • 100 mg indomethacin dose rectally

Cirrhosis check list dr. anurag maheshwari

  • 1 out of 3 patients with cirrhosis will be readmitted after initial discharge in 1 month
  • Ascites :Low albumin, is an indicator for SBP prophylaxis
  • Lactulose every 2 hours till he wakes up.  Use NGT even if varices present
  • Use Rifaximin – universal use for all HE patients
  • DVT prophylaxis – SQ lovenox and use of heparin should be used because cirrhosis is a risk factor for DVT x 2 normal population   THERE IS NO SUCH THING AS AUTO ANTICOAGULATION
  • Coreg 3.125 in primary prophylaxis or 6.25 bid for secondary prophylaxis to titrate to HR of 55.
  • FFP prior to procedure is not needed if INR is upto 1.9

ppi in 2016

  • CKD 11.8% versus 8.5 % in patients on PPI
  • Tell patients – the information is retrospective.  It is an association and not cause and effect.  Impossible to adjust confounding factors
  • Increased CV mortality is 2.2 compared to no use of PPI. 4000 use of PPI one has MI
  • B 12 or iron def. anemia – no clear data