GI Flashcards
Pattern of Liver Enzyme Elevation
Hepatocellular (ALT, AST)
1000’s: Toxins/Drugs (acetaminophen)
Viral (acute Hep A, B, D, or E)
Vascular: Shock, Budd Chiari
Acute stone w/ in 24 hours
Autoimmune hepatitis
Wilson’s (rare)
100’s: Viral (Hep B, C), CMV, EBV
Alcoholic Hepatitis AST > ALT
<100’s: Autoimmune (Celiac), NASH
Hemochromatosis, Wilson’s, A1AT
Cholestatic (ALP, GGT)
Obtain U/S / MRCP
Extrahepatic (biliary duct dilatation):
- Painful - Stones
- Painless - Strictures (PSC), benign obstruction
(IgG4/AIP, AIDS cholangiopathy), malignant
obstruction
Intrahepatic (no duct dilatation):
Drugs (antibiotics, TPN, estrogens, MTX), PBC,
infections, cholestasis of pregnancy, infiltrative
disease
Workup:
- U/S, CT, MRCP, EUS (for stones)
- ERCP NOT for diagnosis, generally only for
therapeutic intervention
- Liver biopsy
Hepatitis A- diagnosis and treatment
- Self-limited infection
- Fecal-oral transmission
- Diagnosis: Anti-HAV IgM
- Treatment is supportive, transplant for fulminant hepatitis
- You can immunize against it
– Who? - Travelers to Hep A Endemic countries, chronic liver disease, MSM, PWID,
recurrent plasma derived clotting factors, zoo-keepers or vets handling non-
human primates
- Post exposure prophylaxis: Household contacts of Hep A infected
individuals, co-workers and clients of infected food handlers, contacts in
childcare or JK/SK
Acute Hepatitis B- diagnosis and treatment
- Diagnosis
– Hepatitis B surface antigen (HBsAg) and core IgM are positive - Natural history
– <5% of adults progress to chronic HBV
– <1% of adults develop liver failure - Treatment
– Treatment is mainly supportive
– Consider antiviral therapy (knowing they may become surface Ag negative and
not require this long term)
– Ensure household and sexual contacts are immune and provide hepatitis B
vaccine if they are not immune - No need for Hep B Immunoglobulin per CDC for household contacts.
- Sexual contacts and those with percutaneous exposure to high risk source are
recommended for Hep B immunoglobulin within 48h ideally if their immune status is
unknown (or low titre)
Following Chronic Hep B
Baseline work-up for Hep B sAg+
* Physical exam
* ALT, CBC, Cr, HBV DNA, HBe serology, fibroscan
* HIV, Hep D in high risk groups (PWID, from endemic area)
Follow-up for Hep B sAg+
* ALT, HBV DNA q 6-12mos, and repeat fibroscan if persistent elevated ALT and HBV DNA
* US (not AFP) every 6 mos for HCC surveillance if:
– All cirrhotics
– Asian M > 40, Asian F > 50
– African > 20
– Family History HCC (in first degree relatives)
– All HIV co-infected starting age 40
Chronic Hep B: Who and Why to treat?
Why treat?
– Prevent cirrhosis
– Prevent HCC
- Goals of treatment
– Suppress viral replication
(decrease HBV DNA level)
– eAg seroconvert
(eAg+/eAb- à eAg-/eAb+)
– sAg seroconvert
(sAg+/sAb- à sAg-/sAb+)
Who to treat?
– Cirrhosis
* Liver transplant workup if decompensated (MELD >15)
* If Fibrosis > stage 1, regardless of ALT or HBeAg status, with
HBV DNA>2000, treatment is case by case decision
– Extra-hepatic manifestations
– HBeAg positive, ↑ ALT, HBV DNA ≥ 2,000 IU/ml (CASL)
– HBeAg negative,↑ ALT, HBV DNA ≥ 2,000 IU/ml
– Pregnancy
* End 2nd/ Start of 3rd trimester + high DNA levels (HBV DNA
>200,000 IU/ml i.e. 5 logs, 2x105) - treat to prevent fetal transmission [tenofovir]
* Baby should also get HBIG + HBV vaccine after birth
- Do not treat
– Immune-tolerant phase or inactive CHB phase (normal ALT)
– Acute infection is generally managed supportively
Treatment of Chronic HBV
Nucleotide Analogues
(tenofovir, entecavir, lamivudine)
*Pros
– Tenofovir/Entecavir very high barrier to
resistance, considered 1st line
– Potent viral suppression
– Well tolerated
* Cons
– Many years of therapy, and can be life
long (especially in eAg negative disease)
– (Getting less) expensive
– Unlikely to convert to seroconvert sAg
Peg-Interferon
*Pros
– Finite therapy (typically 48w)
– Generally more durable response
* Cons
– Side effects (lots)
– Only specific patients benefit
* Low DNA, high ALT
* Non cirrhotic HBeAg+ CHB (CASL2018,
though practically not used anymore)
– Cannot use in decompensated cirrhosis
Hepatitis C- diagnosis and work-up
Diagnosis -
Prior exposure (and immune cleared, or cured by therapy) = Anti-HCV
Chronic Hepatitis =Anti-HCV HCV RNA
Work-up at diagnosis:
* HCV Genotype testing, HCV RNA level, HIV, HBV
* Liver enzymes, liver function testing
* Abdominal ultrasound
* Fibrosis assessment, prognostication:
– TE/FibroScan, FibroTest, AST: Platelet ratio index (APRI), or biopsy
Extrahepatic manifestations of hepatitis C:
o Autoimmune: Autoimmune thyroid disease, myasthenia gravis, Sjogren’s
o Renal: MPGN > membranous glomerulopathy
o Derm: Porphyria cutanea tarda, leukocytoclastic vasculitis
o Heme: lymphoma (NHL), autoimmune hemolytic anemia, ITP, Cryoglobulinemia
o Other: Insulin resistance / Diabetes mellitus
Approach to HCV Treatment
1) Treat ALL patients with chronic hep C EXCEPT those with short life expectancy due to comorbidities
2) Check HCV RNA (and genotype, especially if cirrhosis), check for co-infections (Hep B, HIV)
3) Fibrosis Assessment
– Can use APRI score/ FIB-4 score to exclude clinically significant fibrosis. If > F2 fibrosis à proceed to fibroscan.
– Fibroscan > 12.5 kPa = cirrhosis.
– Ultrasound is insensitive for cirrhosis. Only needed IF cirrhotic, to exclude HCC.
– If cirrhosis, consider transplant assessment (MELD ≥ 15).
4) If simple HCV (no cirrhosis, co-infection), choose one of 2 pan-genotypic regimens:
– Sofosbuvir/ Velpatasvir (Epclusa; 1 pill once daily x 12 wks) or Glecaprevir/ Pibrentasvir (Maviret; 3 pills once daily x 8 wks)
5) Check viral load 12-weeks post treatment completion. If negative, the patient is likely CURED
(termed SVR12, sustained virological response)
Alcohol-associated Hepatitis- definition and tx
- Acute onset hepa//s associated with ongoing alcohol intake (within 8 wks)
- AST > 50, AST/ALT > 1.5-2, and both values < 400, Tbili > 51
- Clinical diagnosis; Biopsy rarely needed (consider if AST/ALT > 400, other Dx suspected)
- Treatment
– Assess eligibility for steroids: Severe AH i.e. Maddrey Discriminant Funcaon≥ 32 (or MELD >20)
or presence of encephalopathy à Prednisolone 40mg PO daily (⬆28d mortality; max benefit
at MELD 25-39) - If Lille score at 4 or 7 days < 0.45 à continue pred x 28d then taper; if ≥ 0.45 à stop; consider early
liver transplantation (no longer requirement for minimum period of abstinence; case-by-case)
– Assess for contraindications to steroids: Uncontrolled infection, uncontrolled GI bleed, AKI
– EtOH cessation and nutrition (high calorie, high protein diet) are vital
– NAC can be considered in addition to steroids – “may improve 30 d survival in severe AH”
– NO role for pentoxifylline in addition to steroids per ACG/AASLD; trend toward benefit in HRS
– No mortality benefit for prophylactaic antibiotics in Alc hep (Louvet et al. JAMA. 2023)
Metabolic-Associated Fatty Liver Fast Facts
NEW terminology faiy liver disease:
* MASLD (NAFLD): Faiy liver with no
hepatocellular injury
* MASH (NASH): + hepatocellular injury
* Met-ALD: MASLD + increased EtOH intake
MASLD Diagnosis - 1) evidence of steatosis,
2) rule out 2° causes (i.e. EtOH)
– MASH can only by diagnosed definiatively on Bx
– Associated with T2DM (most imp RF), ↑lipids,
HTN, obesity, metabolic syndrome, OSA
– Most common cause of death in MASLD is ♥
– Many cases of cryptogenic cirrhosis are likely
“burned out” MASLD
Screen for clinically significant fibrosis:
– T2DM, medically comorbid obesity, 1st degree relative
with MASH cirrhosis, pts with alcohol use
– FIB-4 score for everyone à if > 1.3 à fibroscan
– Treatment
* Weight loss (diet + moderate intensity exercise)
≥ 3-5% ↓ to improve steatosis, 7-10% to improve fibrosis
* Identify + manage CV risk factors
– Statins are safe in MASLD/MASH, including
compensated cirrhosis
* Pharmacotherapy
– Semaglutide for MASH + T2DM/ obesity
* Bariatric surgery if obese
Approach to Cirrhosis: Causes
Determine etiology
– (1) Viral (2) Fatty liver [EtOH, NASH], (3) Autoimmune/ cholestatic
[AIH, PBC, PSC], (4) Genetic [Wilson, HH, A1AT], (5) Chronic biliary
disease, (6) Vascular [R CHF, Budd Chiari]
– Labs, abdominal imaging (+ doppler), and consider biopsy if
indeterminate cause
* Assess severity
– Child-Pugh score – predicts perioperative mortality for open
abdominal surgery (based on old data, likely overestimates risk):
– CP A (score 5-6) – 10%
– CP B (score 7-9) – 30%
– CP C (score 10-15) – 80%
– MELD ≥ 15 – refer for liver transplant assessment
* 6 mo of EtOH abstinence no longer a rule in Ontario (case by case)
Approach to Cirrhosis:
Complications + Counseling
Assess for complications:
– Varices à EGD at diagnosis, then interval based on findings
– Ascites/SBP à Paracentesis at diagnosis, any inpatient presentation, and if concern for SBP
– Hepatic encephalopathy à History/ exam
– Hepato-renal syndrome, Hep-pulmonary Syndrome/porto-pulmonary hypertension à History/exam/labs
– HCC à Abdominal U/S at diagnosis and q6mo
– Screen for FRAILTY, MALNUTRITION in clinic (new – ACG 2021 Guideline on Frailty, Sarcopenia and
Malnutrition in Cirrhosis)
* Counseling:
– Abstinence from alcohol, adequate nutrition, weight loss for NAFLD
– Limit acetaminophen to ≤ 2g/day
– Avoid sedatives, NSAIDs, ACEI/ARBs
– HAV, HBV, COVID 19, TdAP, Pneumococcal, flu vaccinations (+zoster if age >50, MMR and Varicella where
applicable)
– Refer to multidisciplinary team if frailty, sarcopenia or malnutrition (ACG 2021 Guidelines)
– Refer to palliative care team if decompensated cirrhosis at any point in journey (AASLD 2022 Guidance
statement -improves symptoms, quality of life, caregiver stress)
Approach to Varices
Primary prophylaxis (never bled)
– Screen every patient at diagnosis of cirrhosis or at time of decompensation
– Patients receive: NSBB OR EVL
– Detailed algorithm on next slide
* Secondary prophylaxis (after bleed)
– Patients receive: NSBB AND EVL
NSBB: non selective beta blocker ex. nadolol, propranolol; OR carvedilol | titrate to HR 55-60 and
maintain SBP>90
EVL: endoscopic variceal ligation
(see table in notes)
Ascites- etiology and management
Etiology
– SAAG >11 = ‘transudative’ (e.g., portal HTN)
– SAAG < 11 = ‘exudative’ (e.g., malignancy, pancreatitis, infection (TB), nephrotic syndrome)
* For ascites related to portal HTN
– Initial management
* Treat underlying liver disease (stop alcohol, treat HCV, etc.)
* Salt restriction (< 2 g or 88 mmol/day)
– Water restriction not necessary unless [Na] < 125
* Diuretics (start with Spironolactone 100mg and Lasix 40mg daily, titrate as needed – monitor for :
hypotension, AKI, electrolyte imbalance)
– Failing medical therapy
* Serial therapeutic paracentesis; give albumin 6-8 g/L of fluid removed for taps > 4L
* TIPS if no contraindications (encephalopathy, HCC)
– Liver transplant
10mmol/day of non-urinary Na loss; therefore:
1) For patients not on diuretics, do 24-hour urine Na collection
* 24-hr urine Na <78 mmol - COMPLIANT w diet
* 24-hr urine Na >78 mmol -NON-COMPLIANT
2) Start diuretics if ongoing ascites or unable to comply
3) For patients on diuretics, do 24-hour urine Na collection
* 24-hr uNa <78 mmol -DIURETIC-RESISTANT at current doses à increase diuretic
dose until limited by AKI, electrolyte abN, BP, etc.
* 24-hr uNa >78 mmol AND patient not losing weight -NON-COMPLIANT with Na
restriction - reinforce Na restriction
* 24-hr uNa >78 mmol AND weight loss à patient is adherent to sodium restriction
and diuretic sensitive -stay the course
Spontaneous Bacterial Peritonitis Diagnosis
Perform diagnostic paracentesis in every patient with new ascites AND in every
cirrhotic with ascites who presents to hospital
- SBP classically presents with abdominal pain and fever (can also present with
encephalopathy, hypotension, AKI, or worsening liver function) - Diagnosis of SBP
– Neutrophils in ascitic fluid > 250 cells/mm3 OR culture-positive ascitic fluid - culture-negative ascites still requires complete course of treatment
– Rule out secondary cause of peritonitis (e.g., bowel perforation or recent
surgery)
Spontaneous Bacterial Peritonitis- treatment
Treatment of confirmed SBP
– Ceftriaxone (or Fluoroquinolone if Pen allergic) x 5 days
– HRS prophylaxis - Day 1: Albumin 1.5g/kg; Day 3: Albumin 1 g/kg
* In practice almost everyone gets albumin, but guidelines suggest only if Cr > 88,
BUN > 10.7, or bili > 68
* Post SBP: lifelong prophylaxis with Norfloxacin, Septra DS, or Cipro.
Indications for SBP prophylaxis
1) Patients who have previously had SBP -Indefinite SBP prophylaxis
2) Patients with cirrhosis who present with upper or lower GI bleeding (don’t need to
have ascites) à SBP prophylaxis x 7 days
3) Cirrhotic with ascitic fluid protein is <15 g/L and at least one of:
- Impaired renal function (Cr ≥ 106, BUN ≥ 8.9, Na ≤ 130)
- Impaired liver function (Child-Pugh ≥ 9 and Bili ≥ 51 umol/L)
Hereditary Hemochromatosis (HH) definition
ACG Clinical Guideline: Hereditary Hemochromatosis (2019)
* Autosomal recessive disorder causing ↑ intestinal absorption of iron à iron overload
* More common in Northern European descent;
* Most HH is due to mutation of HFE gene at C282Y, H63D, or S65C
– Type 1A hemochromatosis: C282Y homozygous = confirms diagnosis of HH
– Type 1B hemochromatosis: C282Y/H63D heterozygous = less likely (but possible) to
have iron overload
– Genotypes that do not lead to clinically significant iron overload = C282Y/ wildtype,
H63D/ wildtype, H63D homozygote, S65C mutation (type 1C hemochromatosis)
Hereditary Hemochromatosis Clinical Manifestations
- Iron deposition in end-organs:
– Liver: Cirrhosis, elevated liver enzymes
– Skin: ‘Bronze’ hyperpigmentation
– Endocrine: Hypopituitarism (impotence,
amenorrhea), diabetes (islet cell destruction).
– MSK: Arthropathy (2nd/3rd MCP ‘hooked
osteophytes’) - Fatigue
- Increased risk of infection: Listeria monocytogenes,
Yersinia enterocolitica, E. Coli, Vibrio vulnificus. - DDx Iron Overload (secondary iron overload)
– Dyserythropoeisis (sickle cell, thalassemia)
– Chronic transfusions
– Other chronic liver diseases: - MASLD *RC favorite
- Alcohol-related liver disease
- Hep C
Hereditary Hemochromatosis Treatment
Who + when to treat:
– C282Y homozygotes if ferritin > 300 (men) or > 200 (women) AND Tsat > 45%
– C282Y/H63D heterozygotes/ other à Evaluate for other causes of iron overload/ liver dz + consider
MRI/ Bx to estimate hepatic iron concentration (HIC) à Treat other causes 1st, then, if high HIC à treat
* Treatment:
– 1st-line = phlebotomy targeting ferritin 50 – 100
– 2nd- line (when patient refractory to phlebotomy e.g. anemia, high output CHF) = chelation (i.e.
desferoxamine, deferiprone, deferasirox)
* Risks of retinal/auditory toxicity (desferoxamine), agranulocytosis (deferiprone), liver/renal toxicity (deferasirox).
– No need to limit red meat/dietary iron if undergoing phlebotomy
– Avoid consuming vitamin C supplements (↑iron absorption)
– Avoid uncooked seafood (Listeria, Yersinia, and Vibrio ♥ Fe)
– Liver transplantation for decompensated cirrhosis/focal HCC
* HCC screening: Only if cirrhosis. ACG recommends against screening if fibrosis ≤ stage 3.
* Other Heterozygotes: Monitor iron indices annually + assess for organ damage, no treatment needed
Celiac Disease- diagnosis
Symptoms & Signs:
– Diarrhea/ steatorrhea, abdo pain, bloadng, weight loss, anemia, osteoporosis, enamel defects, elevated
transaminases (mild), inferdlity
– Vitamin + mineral deficiencies – A, D, E, B12, Fe, Ca
– Dermadds herpedformis
* Diagnosis:
– And-TTG IgA & quandtadve immunoglobulins (r/o ↓ IgA) +/- and-deamidated gliadin pepdde [DGP] IgG (if ↓
IgA) +/- and-endomysial andbody [EMA]
– Upper endoscopy with small-bowel biopsy – Marsh Classificadon [High risk, posidve serology]
Celiac Disease tx
Treatment: Lifelong gluten-free diet
* Follow-up – Ensure adherence
– Diet history
– ↓ antibody titres +/- improvement of histology
– Follow-up serology 6 and 12 months post
diagnosis, then annually*
* Patients with persistent symptoms despite
negative serology should undergo repeat biopsy
to determine healing*
HLA DQ2/DQ8 Testing
– Should NOT be routinely ordered (poor PPV)
– Consider if…
* Equivocal histology in seronegative patients
* Evaluation in patients on a gluten-free diet where testing can be falsely negative
* Discordant serology and histology
* Suspicion of refractory Celiac or when Diagnosis in question
* Patients with Down’s syndrome
* Patients with a history diagnosis of Celiac (especially as very young children before
introduction of TTG-IgA testing)
Crohn’s Disease- definition and diagnosis
Inflammatory bowel disease characterised by transmural inflamma/on, strictures and
fistulas, that can affect anywhere in the GI tract from ‘gum to bum’.
* Common disease loca0ons:
– Small bowel - terminal ileal involvement is most common
– Ileocolids
– Colonic
– Mouth + upper GI tract
* Clinical Manifesta0ons:
– Abdominal pain, diarrhea, weight loss, fever, peri-anal symptoms
– ↑ CRP, anemia, ↓ Albumin, ↓ Fe, ↓ B12, ↑ fecal calprotecdn
* Diagnosis:
– Ileocolonoscopy & biopsy
* Patchy inflammation, skip lesions, aphthous ulcers, cobble-stone mucosa
* Rectal involvement + circumferential continuous inflammation less common in CD vs UC
– Small bowel imaging (CT/MR-enterography, capsule endoscopy) +/- EGD
– No role for serology in diagnosis of IBD (e.g. ANCA/ ASCA)
Crohn’s Treatment Options
Induction
– Mild
* 5-ASA (Guidelines recommend AGAINST
this, but still used for mild colonic Crohn’s)
* Budesonide (Entocort, Cortimet)
– Moderate to Severe
* Budesonide
* Prednisone/methylpred
* MTX
* Anti-TNF – Infliximab (Remicade),
Adalimumab (Humira)
* Anti-Integrin – Vedolizumab (Entyvio)
* Anti-IL12/23 – Ustekinumab (Stelara)
Maintenance
– Mild
* Thiopurine (AZP, 6-MP)
– Moderate to Severe
* MTX
* Thiopurine (AZP, 6-MP)
* Anti-TNF – Infliximab, Adalimumab
* Anti-integrin – Vedolizumab
* Anti-IL-12/23 – Ustekinumab
* Anti-IL 23 – Risankizumab (FDA approved
Jun 2022; not yet in Canada)
General Patterns in CD Treatment
– Sulfasalazine can be considered only for mild colonic Crohn’s disease. 5-ASAs are NOT effective for
Crohn’s ileitis, fistulizing or moderate-severe disease.
– Fistulas (any kind) à Biologic (anti-TNF e.g. infliximab have the most evidence, then vedolizumab)
– Perianal disease (abscesses or fistulae) à Anti-TNF (+/- antibiotics if concern for infection)
– Do not use antibiotics alone to induce or maintain remission
– Tofacitinib not approved for CD (only UC)
– Once remission achieved, generally continue the agent that induced remission (except steroids)
– Indications for surgery in Crohn’s disease: Intestinal obstruction, refractory/ fulminant disease, high-
grade dysplasia/ cancer, severe perianal disease/ fistulas/ abscess, perforation.
Crohn’s Disease Complications
– Abscess:
* Drain (IR or I+D or surgery) and antibiotics (Cipro/Flagyl or CTX/ flagyl), prior to immunosuppression
– Fistula:
* Characterize perianal fistulae w/ EUS (endoscopic ultrasound) or MRI pelvis +/- EUA (exam under anesthesia)
* Anti-TNF preferred to induce a symptomatic response and maintain remission
* Other options: Vedolizumab/ ustekinumab or surgery
– Stricture:
* ‘Cold’ stricture:
– Fibrostenotic disease, no active inflammation on imaging or endoscopy
– Conservative mgmt. (i.e. bowel rest, NG tube), endoscopic dilation or surgery
* ’Hot’ stricture
– Active inflammation (may be overlying area of fibrosis/ cold stricture)
– Steroid bridge to maintenance therapy (usually biologics)
Ulcerative Colitis- presentation and diagnosis
Immune-mediated condition of the colon often associated with rectal inflammation,
extending proximally to involve the adjacent colon in a continuous manner.
* Disease Location:
– Proctitis – w/in 18 cm from the anal verge
– Left-sided colitis – sigmoid to splenic flexure
– Extensive/ ‘pan’ colitis – beyond the splenic flexure
* Clinical Manifestations:
– ‘Proctitis’ – small volume + frequent BMs w/ blood,
tenesmus, urgency, crampy abdominal pain
– Fever, fatigue, weight loss
– Inflammatory markers: Anemia, ↓ Albumin, ↑ ESR/CRP,
↑ fecal calprotectin
- Diagnosis:
– Ileocolonoscopy + biopsies - Continuous inflammation from rectum proximally
- Granular, friable mucosa
- Bx – i.e. crypt abscesses, lamina propria cellularity
Ulcerative Colitis Treatment Options
Induction
– Mild
* 5ASA PO (extensive), PR (proctitis)
(suppository < 18cm, enema – to splenic
flexure)
* Budesonide
– Moderate to Severe
* Budesonide
* Prednisone/methylpred
* Anti-TNF – Infliximab, Adalimumab,
Golimumab
* Anti-Integrin – Vedolizumab
* Anti-IL-12/23 – Ustekinumab
* JAK-inhibitor – Tofacitinib, upadacitinib
(Approved 2023)
* Sphingosine 1-phosphate receptor
modulator – Ozanimod (Approved 2022)
Maintenance
– Mild
* 5ASA PO, PR
– Moderate to Severe
* Thiopurine (AZP, 6-MP)
* Anl-TNF – Infliximab, Adalimumab,
Golimumab
* Anl-Integrin – Vedolizumab
* Anl-IL-12/23 – Ustekinumab
* JAK-inhibitor – Tofacilnib, upadacilnib
* Sphingosine 1-phosphate receptor
modulator – Ozanimod
IBD – General Principles
No role for serology (ASCA/ANCA/anti-OmpC etc.) in diagnosis
* Pre-Biologic Work-up:
– HBV, HCV
– TB skin test; If BCG vaccinated à CXR and/ or IGRA
– VZV titres; certain biologics require this
– Strongyloides serology if high pretest probability*
* Before starting AZA/6MP – check TMPT
* Fecal calprotectin used as a marker of disease activity
* Treatment target – Clinical (symptoms, steroid free), biochemical
(inflammatory markers), and endoscopic (mucosal healing) remission
Inpatient IBD
- IBD flares commonly overlap with infection
1. Rule out C. diff/ other infection if worsening diarrhea (even if no recent antibiotics)
2. Rule out abscess in a Crohn’s patient with fever and abdominal/perianal pain - Use appropriate imaging (CT abdo, MR pelvis, EUS, etc.)
3. Withhold immunosuppression until (1+2) are addressed. - If the patient looks septic, cover with antibiotics
4. CMV colitis can co-exist with IBD and requires colonic biopsies to diagnose (CMV blood PCR is not
enough; look for “owl-eye inclusion bodies” on pathology and CMV+ immunohistochem off biopsy) - Don’t stop DVT prophylaxis even if patient having bloody diarrhea
– Risk of thrombosis > risk of life-threatening hemorrhage in hospitalized IBD patients with acute flare - Bile-salt diarrhea – Occurs with ileitis or after ileal resection – ALWAYS assess for (CT or C Scope) and treat active IBD before treating for bile salt diarrhea
- cholestyramine (bile acid sequestrant)
- Work-up:
– Labs – CBC, lytes, extended lytes, Cr, AST/ALT/ALP, bilirubin, INR, albumin, ESR/CRP
– Stool tests – Stool C&S, Stool O&P, C. diff toxin, +/- fecal calprotectin
– Imaging – AXR, +/- CT abdomen, +/- CT/MR enterography (i.e. small bowel imaging)
– Endoscopy – for diagnosis, to assess disease severity, rule out mimics (ischemia,
CMV), can send aspirates for micro - Management:
– IV fluids, bowel rest, VTE prophylaxis
– Minimize narcotics, NSAIDS
– Start IV steroids once infection is ruled out
– If minimal response after ~ 72h IV steroids à Infliximab
– Consider general surgical consultation for treatment refractory colitis, toxic
megacolon, perianal/intra-abdominal abscess, complex fistulizing Crohn’s
UGIB- pre-endoscopy management
Pre-endoscopy (POSSIBLE ORAL SCENARIO)
– ABC’s, monitoring, O2, 2-large bore IV’s, fluids (ABC-MOIF)
– [Apply Glasgow-Blatchford score to identify low-risk patients that can be
discharged with outpatient follow up]
– CBC, urea, Cr, cross and type, INR/PTT, Liver enzyme and function tests
– Transfuse
* Hb > 70; consider higher target (>80) if symptomatic/ active cardiac ischemia, or
unstable
* Plts > 50 if actively bleeding/unstable
– Reverse anticoagulation
* See slide on antithrombotic mgmt. in GI bleed
– PPI therapy (IV bolus + infusion or BID dosing)
UGIB in patient with Cirrhosis- management
UGIB (variceal or not) + Cirrhosis (or suspected non-cirrhoGc portal HTN)
1. Restric]ve transfusion strategy (target 70-90 g/dL)
* No FFP
2. IV vasoac]ve drug (octreobde, somatostabn, terlipressin [not yet in Canada] or
vasopressin) as soon as variceal bleed is suspected; conbnue x 5 days post- endoscopy if variceal bleed
3. IV PPI unbl varices ruled out
4. Endoscopy within 12h of presentabon
5. An]bio]c prophylaxis is indicated for any GI bleed in a pabent with cirrhosis
* Cetriaxone 1g/24h x 5-7 days
* Following variceal bleed + EVL:
– Inibate NSBB when vasoacbve drugs stopped
* NSBB not required if pt had a TIPS placed; TIPS is rescue if bleed despite NSBB+EVL
Non-variceal UGIB- management
Endoscopic management
– Erythromycin 250 mg IV suggested 30 min before endoscopy
– Endoscopy should be performed within 24 hours (or within 12 hours in
high-risk patients, including suspected variceal bleeds)
– Endoscopic therapy only for high-risk ulcers (Forest IA, IB, IIA ulcers)
- If ongoing/ re-bleeding: repeat EGD, consider IR embolization or
surgical management - Consider radiation for tumor bleeds
Post-endoscopy
– High-risk ulcers à IV PPI BID or PPI infusion x 72 hours, then oral PPI BID for at least the first 2
weeks after endoscopy
– Low-risk ulcers à Oral PPI (no guidelines; typically BID x 2-4 weeks then stop)
– Restart anti-platelets and anticoagulation as soon as possible (see ACG-CAG guidelines next slide)
* Restarting OAC or antiplatelets (or both) not associated with increased GI bleed risk compared
to not restarting but IS associated with a reduction in all cause mortality (Witt DM Hematology ASH education
Program 2016:620).
* Timing – variable decision incorporating patient factors and endoscopic findings (Forrest class)
- Consider risk factors
– Test all patients with PUD or gastritis for H. pylori – can biopsy at time of EGD or check serology - Treat with quadruple therapy if positive
- After treatment and confirmation of eradication, PPI therapy can be stopped
– Stop all unnecessary NSAIDs, stop ASA for primary prophylaxis
– For CV patients requiring ongoing ASA and/or Plavix, consider indefinite PPI prophylaxis
– Indefinite PPI if unclear cause of PUD (conditional recommendation)
Anti-thrombotic management- UGIB
Acute GI Bleeding – All guidance “suggest” due to low level of evidence à use your clinical judgement!
i) Patient stable, “hospitalized or under observation for GI Bleed [upper or lower]”
* ASA 81-325 mg for 2o cardiovascular prevention à Suggest no interruption; if interrupted à re-start on the day that
hemostasis is endoscopically confirmed.
* Anticoagulation reversal?
– Warfarin à Suggest AGAINST vitamin K and FFP use. No recommendation for/ against PCC.
* Do not routinely give Vitamin K unless low dose to correct supratherapeutic INR
– DOAC - Suggest AGAINST reversal with PCC/ idarucizumab/ andaxnet alpha
ii) Life threatening hemorrhage, “major clinically overt or apparent bleeding, resulting in hypovolemic shock, or
severe hypotension requiring pressors or surgery”, ↓Hgb >50, transfusion ≥5u PRBC, or causing death”
– Warfarin - PCC “could be considered” (or in patients in whom massive transfusion is undesirable)
* Uncertain re use of vitamin K – see above, conditional recommendation to not use if INR in target range and intervention planned
– DOAC - selective use of PCC (for anti-Xa DOAC) or idarucizumab (for Dabigatran) for those who took DOAC within 24h who have life
threatening bleed “may be appropriate”
– No Platelet transfusions to reverse effect of antiplatelet
H. pylori - who to test
H. Pylori ↑ risk of gastric cancer
* Controversial whether to treat patients solely to prevent cancer, but most recent ACG
guidelines (2017) seem to err on the side of offering treatment to everyone testing positive
– Who to test?
* PUD, MALT lymphoma, resected early gastric cancer, uninvestigated dyspepsia*, long-term
NSAIDs/ASA, otherwise unexplained iron deficiency, ITP
* Do not test those with GERD without dyspepsia or PUD
Treatment of H. Pylori will generally not improve (and can worsen) symptoms of GERD
– MALT lymphoma – treatment of HP alone will cure most cases!
– *Only a minority of patients with dyspepsia and H. Pylori will have symptomatic improvement with eradication
H. pylori Diagnosis
Testing to detect current infection
* Stool Antigen (SN 94% / SP 92%)
* Histology (SN 96% / SP 99%)
* Biopsy Culture (SN 88-95% / SP 95-100%)
* Urea Breath Test (SN 90-95% / SP 95-100%)
– Testing to detect current or prior infection
* Serology i.e. serum IgG (SN 85% / SP 80%)
– If negative in a patient with bleeding ulcer, repeat testing is recommended when acute
bleeding episode resolves
H. pylori Treatment
Suggested treatment:
– First line: PBMT or PAMC x 14 days
* PPI/Bismuth/Metronidazole/Tetracycline (PBMT)
* PPI/Amoxicillin/Metronidazole/Clarithromycin (PAMC)
– Treatment failure:
* PBMT (if prior triple-therapy) x 14 days OR
* PPI/Amoxicillin/Levofloxacin (PAL) x 14 days
* Confirm eradication in all treated patients
– Urea breath test, stool antigen test, or repeat gastric biopsy
Wait ≥ 4 weeks a{er compledng
andbiodc therapy and ≥ 1-2 weeks
a{er PPI therapy before tesdng for H.
pylori to improve test accuracy!
GERD- management
Alarm symptoms (dysphagia, weight loss, GI bleed) à EGD
– Recommend against barium studies – poor SN/SP for GERD and miss mucosal lesions w alarm symptoms
* No alarm symptoms?
– Non pharm mgmt. (weight loss, avoid trigger foods, quit smoking, elevate HOB, etc)
– Trial PPI once daily 30-60min before a meal x 8 weeks
* Symptoms improve? Try to wean PPI, if unable: lowest dose PPI
* Symptoms refractory? à Ensure optimization of PPI therapyà Sx refractory despite optimizationà EGD off
PPI, if normal à reflux monitoring à if negative, discontinue PPI, consider other causes
– Recommend AGAINST other medical therapies (prokinetics, sucralfate, baclofen, H2RA) in PPI
nonresponders (Exception: sucralfate in pregnancy OK, H2RA prn at night if objective nocturnal acid reflux
on pH monitoring despite PPI)
* Extra-esophageal symptoms (cough, asthma, chest pain) need usual workup (PFT, cardiac w/u)
– Can consider BID PPI x 8-12 weeks for typical GERD w/ extraesophageal symptoms; failing this
àendoscopy off PPI
* Surgery – only for objective evidence of GERD
– Fundoplication, Roux en Y bypass for eligible obese patients
– Transesophageal incisionless fundoplication if unwilling to undergo classic lap fundo
Barrett’s Esophagus- diagnosis
Diagnosis:
– Metaplasia of normal squamous epithelium to salmon-colored
columnar epithelium ≥ 1 cm proximal to the gastroesophageal junction.
– Biopsy confirmation of columnar intestinal metaplasia, +/- goblet cells.
* Malignant potential:
– 30 fold ↑ risk of esophageal adenocarcinoma vs average population
– Low overall annual risk (0.1% – 3%)
– Dysplastic > Non-dysplastic; long segment > short segment
Risk Factors:
1. Chronic GERD (weekly symptoms for ≥ 5 years)
2. Age > 50
3. Male gender
4. Tobacco use
5. Central obesity
6. Caucasian
7. Family history of Barrett’s esophagus/ esophageal adenocarcinoma
Screening for Barrett’s Esophagus
Canadian Task Force 2020:
“We recommend not screening adults (≥ 18 years) with chronic GERD for esophageal
adenocarcinoma or precursor conditions (Barrett esophagus or dysplasia) (strong
recommendation; very low-certainty evidence”
Management of Barrett’s Esophagus
Obtain ≥8 biopsies if >1cm salmon mucosa extending from GE jxn
- INTESTINAL METAPLASIA:
- No Dysplasia = EGD in 3y if >3cm segement, otherwise in 5 yrs
- Indefinite Dysplasia = PPI BID*, repeat EGD w biopsy in 6 mos
- Dysplasia = Get Expert Path Review, see next slide
- No metaplasia – Repeat endo w biopsy in 1-2 yrs
Low Grade Dysplasia – discuss risk/benefit of surveillance vs EET
* Surveillance endoscopy q6mos x 2 then annually
* Endoscopic eradication therapy à complete eradication à surveillance endo 1 year then q2y after
High Grade Dysplasia or intramucosal carcinoma (T1a)
* Endoscopic eradication therapy à complete eradication à surveillance endo 3, 6, 12mo then q1y
Submucosal cancer (T1b)
* Surgical referral for esophagectomy
* ”consider” Endoscopic eradication only if low risk features (<2cm, no LVI, well differentiated…)
Approach to Dysphagia
Step 1 History & Physical
1. Oropharyngeal vs esophageal?
* Oropharyngeal – Choking, regurgitation, drooling, symptoms above sternal notch, predisposing neuromuscular
condition, surgery/rads to head and neck
* Esophageal – Regurgitation, sensation of material getting ‘stuck’ below sternal notch
2. Structural vs motility disorder?
* Structural – Primarily solids (may progress to liquids)
* Motility disorder – Solids and liquids
3. Progressive vs intermittent?
* Intermittent symptoms: primary esophageal motility disorders, esophageal ring (Schatzki ring)
4. Alarm features?
* Onset > 50 yo, odynophagia, vomiting, bleeding, weight loss
Step 2 Imaging and/or Endoscopy
– Oropharyngeal à Video fluoroscopy swallowing study
– Esophageal
* Alarm symptoms? à Endoscopy
– Weight loss
– Anemia
– Vomilng
* No alarm symptoms and age < 50, Sx GERD, à Trial of PPI
- Key Concepts from CAG 2018 Guideline
– EGD is recommended > barium swallow for inveskgakon of esophageal
dysphagia. *Can biopsy for EoE on endoscopy!
– Manometry is recommended > barium swallow for inveskgakon of esophageal
moklity disorders
Achalasia- definition and diagnosis
Esophageal motility disorder defined by loss of esophageal peristalsis and incomplete
relaxation of lower esophageal sphincter
* Signs & Symptoms:
– Progressive solid and liquid dysphagia
– Regurgitation + reflux symptoms
– Chest pain
– Weight loss
– Symptoms refractory to PPI therapy
Diagnosis:
– Step 1 – EGD
* Rule out pseudoachalasia + obstruction
* ‘Puckered’ GE juncdon
* Dilated, fluid filled esophagus as disease progresses
– Step 2 - High resoluUon manometry +/- barium swallow
* Manometry
– Gold standard test for achalasia
– Measures pressures and peristaljc waveform throughout esophagus
– Impaired relaxation of LES and abnormal peristalsis are diagnostic
- Barium Swallow – ‘Bird’s beak esophagus’
Achalasia- management
*NB – Achalasia ↑ risk of
esophageal SCC. Poor esophageal
emptying - stasis of food/liquid
à inflammation à dysplasia à
malignancy.
However, current guidelines do
not recommend routine
endoscopic surveillance for SCC.
Poor surgical candidates
– Endoscopic botox injection – 1st line
– Smooth muscle relaxants – CCB, nitrates
* Ex. Nifedipine 10-30mg SL TID, ISDN 5mg SL TID
* *Least effective therapy
Good surgical candidates
– Pneumatic dilatation
* 1st line option
* Risk of tear/perforation
– Laparoscopic Heller Myotomy
* 1st line option
* Often performed with fundoplication (anti-reflux surgery)
– Peroral endoscopic myotomy (POEM)
* 1st line option (especially type 3 achalasia)
* Often complicated by GERD – patients need lifelong acid suppression
– Esophagectomy
* For patients with megaesophagus, sigmoid esophagus, failure of above treatments
Eosinophilic Esophagitis (EoE)- diagnosis and management
Immune-mediated disease characterized by esophageal symptoms and eosinophilic infiltration
(>15 eos/hpf) of the esophageal mucosa in absence of secondary causes of eosinophilia**.
* Risk factors:
– M > F (3:1). Peak incidence at 30-44 yo.
– History of atopy (asthma, eczema, allergic rhinits), food allergies, autoimmune disease
- Clinical presentation: Intermittent solid food dysphagia, food bolus obstruction
- Endoscopic findings: ‘Trachealization’ of the esophagus (‘Feline Esophagus’), linear furrows, white
exudates/ papules, ‘Crate-paper’ esophagus, strictures - Treatment goal = Symptomatic and histologic improvement
– Non-pharmacologic Rx: 6 food elimination diet (eggs, soy, cow’s milk, wheat, tree nuts, seafood).
New evidence that animal milk elimination equivalent to 6 food elimination.
– Pharmacologic Rx:
* 1st line: PPI, topical steroids (swallowed fluDcasone/budesonide, or orodispersible
budesonide [Jorveza])
* 2nd line: Prednisone
* Approved by Health Canada Fall 2022: Dupilumab (anD-IL 4 and IL13)
– Endoscopic treatment for symptomatic strictures: Dilatation
**Secondary causes of
esophageal eosinophilia:
GERD, achalasia, connective
tissue diseases,
hypermobility syndromes,
pill esophagitis, pemphigus,
hyper IgE syndrome
Acute Pancreatitis- definition and etiology
- Definition (need 2/3 criteria for diagnosis):
1. Abdominal pain consistent with disease (acute severe epigastric/ LUQ, radiates to
back, better leaning forward)
2. Lipase and/or amylase ≥ 3x ULN
3. Characteristic findings on imaging - Etiology:
#1: Gall stones - always order U/S to rule out gallstones (Endoscopic ultrasound [EUS] or
MRCP if high clinical suspicion and U/S negative)
#2: EtOH
#3: Other – triglycerides (> 11 mmol/L), hypercalcemia, drugs (GLP1 Rc agonists, 5-ASA,
thiazides, azathioprine), autoimmune, post-ERCP, trauma, viruses, malignancy,
hereditary, smoking, scorpion bite, vasculitis
Acute Pancreatitis - management
Severity: (APACHE II and SIRS are the best)
– Useful to assess adequacy of resuscitation and disposition (ward vs. ICU)
– CT scan NOT required for diagnosis or prognosis (early CT can be misleading)
* Management:
– IV fluids are the only effective therapy for pancreatitis in the first 24-48h
* IV fluids within the first 12-24h are associated with reduced mortality
* Current evidence favors moderate fluid resuscitation (1.5 mL/kg/hour with a 10 mL/kg bolus in patients with
hypovolemia) over aggressive fluid resuscitation
Generally Ringer’s Lactate (trials ongoing), but avoid in hypercalcemic patients
– Analgesia
– Nutrition
* Start clear fluids or low fat diet early (within 24h), advance as able
* If unable to take PO, enteral nutrition preferred (NG=NJ)
– Empiric/ prophylactic antibiotics are not recommended (unless evidence of cholangitis or sepsis)
- Gallstone pancreatitis
– Role of urgent ERCP (<24 hours) is for cholangitis, persistent biliary obstruction, or
severe ongoing pancreatitis (small stones often pass on their own without intervention)
– ERCP can be considered >48 hours if not clinically improving with evidence of persistent
stone
– Ideally, cholecystectomy before discharge - Hypertriglyceridemia-induced pancreatitis
– Generally only if TG very high (> 11)
– If sick à IV insulin, strict NPO +/- plasmapheresis
– Long term à Fibrates, restrict dietary fat, treat secondary causes of hyperTG (diabetes,
ETOH)
Classification and Complications of Acute Pancreatitis
The Atlanta Classification
Early (<4 weeks)
* Interstitial edematous pancreatitis (IEP)
– Most patients with pancreatitis
– Diffuse pancreatic edema
* Acute peripancreatic fluid collection
* Pancreatic necrosis
– 5-10% patients
– ↑ morbidity vs IEP
* Acute necrotic collection
* Infected pancreatic necrosis
– Usually develops after 1 week
Late (≥ 4 weeks)
* Pseudocysts
– Walled-off collection of pancreatic juices
enclosed by fibrous tissue
– ‘Pseudo’cyst as no true epithelial lining
– Can cause biliary or GI obstruction
– Develop after ~4 weeks
– Can become infected, requiring
endoscopic/surgical drainage
* Pancreatic abscess
– Circumscribed collection of pus w/o
pancreatic necrosis
– No longer recognized in the current Atlanta
Classification
* Walled-off pancreatic necrosis
IgG4/Autoimmune Pancreatitis
There are 2 types of AIP
– Type I part of IgG4 RD which also has biliary, salivary, pulmonary, renal, thyroid, LN involvement *Mostly older men (> 60 yo )
– Type II isolated to pancreas and associated with IBD * M = F; > 40 yo
It can mimic pancreatic cancer – But unlike cancer, it responds to steroids!
Workup
* CT/MRCP + EUS – “Sausage pancreas”
– Biopsy (EUS + FNA or CT-guided Bx of retroperitoneal mass); histology = lymphoplasmacytic infiltrate + fibrosis – Biliary strictures (IgG4-associated cholangitis) * Serum IgG4 > 2x ULN suggestive of Type I AIP (but can be negative!)
Treatment
* Prednisone 40mg daily x 4-6 weeks, then taper – If relapse - retrial steroids or AZA or Rituximab
Chronic Pancreatitis- etiology and diagnosis
- Etiology: “TIGAR-O”
– Toxic/metabolic: CHRONIC alcohol use, hyperTG,
Smoking, hyper Ca, Medications, Toxins…Cystic
Fibrosis
– Idiopathic
– Genetic – CF, and others PRSS1, CTRC…
– Autoimmune pancreatitis
– Recurrent Acute Pancreatitis (RAP)
– Obstructive: i.e. pancreatic divisum (2 distinct
pancreatic ducts, not one), stricture, stone, tumor - Clinical Manifestations:
– Severe abdominal pain
– Fat-soluble vitamin deficiency (ADEK)
– Exocrine pancreatic insufficiency - steatorrhea,
maldigestion, weight loss
– Endocrine pancreatic insufficiency - Diabetes
Diagnosis:
– 1st line – cross-sectional imaging (CT or MRI) à
EUS if uncertain
– Role of pancreatic exocrine function testing (eg
72h fecal fat) unclear in diagnosis of CP.
* Work-up:
– Ca2+, Triglycerides (≥ 5.6 mmol/L)
– Med review – i.e. AZA, cyclosporine
– IgG subclass – IgG4 disease
– Recurrent acute:
* Consider MRCP – r/o divisum, stricture,
tumor, stone
* Consider genetics workup “if etiology
unclear, especially in younger patients” –
PRSS1, CFTR, CTRC, SPINK1
Chronic Pancreatitis - Treatment
- Lifestyle Modification:
– Alcohol and smoking cessation for all - Pancreatic enzymes
– No evidence for relieving pain
– Use for patients with exocrine pancreatic insufficiency
– ↑ weight, ↑ fat-soluble vitamin absorption - Pain management
– Antioxidants (limited benefit) i.e. selenium, ascorbic acid, methionine
– Opioids – if other pain control methods exhausted
– Celiac plexus block - ↓ pain x 3-6 mo. - Obstructive cause – trial of ERCP, EUS. If patient has chronic pain failing endoscopic therapy,
“surgical intervention for long term pain relief”
– CAVEAT: “Performing procedures on individuals using alcohol should be considered cautiously” - Total pancreatectomy + islet cell autotransplant – highly select pts.
Lower GI Bleeding
- Rule out brisk UGIB or other source of bleeding
- DDx of rectal bleeding
– Painless - Diverticular bleed (most common), hemorrhoids, angiodysplasia, polyp/ post-polypectomy, cancer,
ulcers (NSAIDs, stercoral), radiation proctitis, Meckel’s diverticulum
– Painful
* Ischemic colitis (sudden, cramping abdo pain followed by bloody bowel movement)
– Work-up cause: Cardio-embolic? (AFIB? Endocarditis? LV Thrombus) ATHERO-embolic (?AAA,
dissection…), Shock/low flow, Segmental – think vasculitis / PAN
– Mgmt: Most resolve with supportive care (IV fluids, analgesia), empiric antibiotics if moderate-
severe (strong recommendation, low quality evidence), Gen Sx if pancolitis or isolated right-sided
- Hemorrhoid (if thrombosed)
- Anal fissure
– Other (may be associated with cramping) - Inflammatory (IBD), Infectious
Small Bowel Bleeding- inv and tx
Suspect in patients with ongoing overt GI bleeding with normal EGD and colonoscopy
* Diagnostic algorithm if ongoing bleed despite negative EGD/ colonoscopy (in this order):
- Second-look EGD +/- push enteroscopy (to look up to proximal jejunum) +/-colonoscopy
- Video capsule endoscopy (VCE); must have regular CT/ AXR to r/o obstruction
- CT enterography (CTE)
* CTE before VCE if concern for tumors, SB IBD, strictures or other obstructive process that the
capsule would get stuck in
4.CTA if brisk, active bleeding; tagged RBC scan if slow bleed (>0.1 mL/minute)
5.Conventional angiography in IR suite for massive, unstable bleeding
6.Intraoperative enteroscopy (invasive; rarely done)
Treatment options:
– Double-balloon enteroscopy, surgery, IR embolization
– Supportive management with transfusions and iron replacement
Acute Cholangitis- presentation
Bacterial infection of biliary tree usually due to partial/complete obstruction
* Etiology of obstruction
– Stones (choledocholithiasis, Mirizzi syndrome)
– Strictures (malignant/benign)
– Clot
– Masses/tumors (i.e. pancreatic head, Klatskin tumor, metastases)
– PSC, HIV cholangiopathy
– Biliary stent obstruction (stones/sludge)
– Worms (Ascaris lumbricoides, tapeworm)
- Clinical Presentation – ‘Charcot’s Triad, Reynaud’s Pentad’
– Fever, abdominal pain + jaundice +/- hypotension and confusion
– Labs:
* WBC > 10 or < 4
* ALP/GGT > 1.5x ULN, ALT > 1.5x ULN
* Bilirubin > 34
– Imaging:
* Biliary dilatation +/- stones - U/S, CT, MRCP or EUS (↑ sensitivity, respectively)
– Predisposition – PSC, stricture, stent, recent ERCP, etc…
↑ bilirubin + ALP are NOT
common in acute cholecystitis.
Have a high index of suspicion
for cholangitis!
Acute Cholangitis - Management
Investigations:
– CBC, lytes, creatinine, INR/PTT
– AST, ALT, ALP, GGT, total + direct bilirubin
– Blood cultures
- Empiric Antibiotics:
– Cover common biliary pathogens – CTX/flagyl, piptazo, cipro/flagyl, carbapenem - ‘Source control’
– ERCP + stone removal +/- sphincterotomy (*↑ bleeding risk! Ensure INR < 1.5, PLT >50,
anticoagulants held) +/- stent placement
– Percutaneous transhepatic biliary drainage – IR-guided, if failed ERCP or ++
comorbidities, bleeding risk etc.
– Surgical biliary drainage – rarely required
Microscopic colitis- dx and tx
Two types: lymphocybc or collagenous colibs
* Epidemiology, risk factors
– Older women (mean age 65)
– Comorbid autoimmune diseases – thyroid, celiac, RA
– Associated medicaaons: NSAIDs, PPIs (specifically lansoprazole), SSRIs, pembrolizumab, others
- Symptoms
– Relapsing/remi{ng watery, non-bloody diarrhea; may be severe
– Weight loss, abdominal pain are common - Diagnosis
– Normal-appearing colonoscopy, biopsies confirm diagnosis - Treatment
– Imodium, stop NSAIDs/ other offending meds
– 1st line: Budesonide PO, 2nd line: 5-ASA PO
Primary Sclerosing Cholangitis (PSC)
- Chronic, cholestatic, immune-mediated disease of intra & extrahepatic bile ducts (radiologic diagnosis)
- Clinical presentation:
– M»_space; F, 2/3rd of patients have IBD (most have ulcerative colitis phenotype).
– Up to 50% asymptomatic at presentation. Symptoms include abdominal pain, pruritus, fatigue. - Diagnosis:
– (1) Elevated ALP, (2) multifocal biliary strictures “beads on a string” (usually on MRCP), (3) exclude secondary sclerosing cholangitis, (4) liver Bx if PSC-AIH overlap of small duct PSD suspected. - Differential diagnosis:
– IgG4 related disease (exclude since this entity is steroid-responsive)
– PSC-autoimmune overlap syndrome (respond partially to immunosuppressants) - Treatment:
– ERCP as needed for symptomatic strictures
– MRCP +/- CA 19-9 q1 year to screen for GB cancer and cholangiocarcinoma
– Colonoscopy with surveillance biopsies at diagnosis and q1-2 years
– If cirrhotic, screen for HCC/EoV
– Ursodeoxycholic acid has NO evidence but frequently used; liver transplant for liver failure
Primary Biliary Cholangitis (PBC)
Disease of intrahepatic biliary tree
- Clinical presentation
– Usually middle-aged women (>95% of cases)
– Present with jaundice, pruritus, fatigue, elevated ALP (usually get imaging – either U/S or MRCP to
rule out obstruction)
– Associated with Sjogren’s, celiac disease, and autoimmune thyroid disease - Diagnosis requires 2 of 3:
1. Persistent ALP elevation > 6 months
2. Positive AMA >1:40 (95% sensitive, 98% specific) or specific ANAs (e.g. gp 210/sp 100)
3. Liver biopsy (only needed when diagnosis unclear) - Treatment
– Bone density testing, lipid profile derangements, monitor for cirrhosis
– Ursodeoxycholic acid 15mg/kg has benefit; liver transplant for liver failure
Paracentesis
- Diagnostic
– cell count, culture and sensitivity, biochemistry including albumin (to calculate SAAG),
cytology, AFB, etc.
– Risks: bleeding, infection, perforation, organ injury - Therapeutic
– Purpose is to reduce ascites for symptomatic patients
– Can take off unlimited amount of fluid as one time (suggest replace with 100cc of 25%
albumin for each 4L of fluid removed)
– Avoid therapeutic paracentesis for patients with SBP, UGIB, active infection, or acute kidney
injury (may worsen renal function)
– Risks are same as diagnostic paracentesis AND risk of hypotension, AKI, encephalopathy
Hepatic Encephalopathy (HE)- dx and tx
- Etiology
– Accumulation of glutamine from increased ammonia levels
– Patients can present with day-night sleep reversal, drowsiness, agitation, confusion - Diagnosis
- Clinical diagnosis! (no role for ammonia levels)
- Look for precipitating causes (SBP, infection, GI bleeding, alcohol, drugs, HCC, stroke,
constipation, dehydration, portal or hepatic vein thrombus, electrolyte abnormalities, TIPS ) - Treatment
– Treat underlying cause (stop benzos, opioids, anti-chol)
– Lactulose +/- Rifaximin (typically added if patient had episode of HE while on lactulose)
– Ensure high-calorie, high-protein diet
– Recurrent intractable HE, together with liver failure, is an indication for liver transplant
Hepatorenal Syndrome
- HRS: Functional renal injury in pts with portal HTN 2o cirrhosis/ acute cause (alc hep, fulminant liver failure)
- Pathophysiology: Portal HTN à splanchnic arterial vasodilation à AKI
- HRS classification (based on the rapidity of renal impairment):
– HRS-AKI (formerly type 1 HRS): more severe; Abrupt (< 48h) ↑ Cr ≥ 0.3 mg/dl (~ 26 umol/L) or ↑ Cr ≥ 50% (from b/l in past 3 mo) or urine output < 0.5 ml/kg/h for ≥ 6h.
– HRS-NAKI [non-AKI] (formerly type 2 HRS): less severe; gradual decline in kidney function assoc. w/ refractory ascites - HRS-AKD (HRS-acute kidney disease) if eGFR < 60 mL/min/1.73m2 for < 3 months
- HRS-CKD (HRS-chronic kidney disease) if eGFR < 60 mL/ min/1.73m2 for > 3 months
- HRS-AKI Diagnostic criteria:
1. Cirrhosis/ acute portal HTN with ascites
2. ↑ Cr ≥ 0.3 mg/dl (~ 26 umol/L) or ↑ Cr ≥ 50% (from b/l within past 3 mo) or UO < 0.5 ml/kg/h for ≥ 6h.
3. Other causes ruled out (ATN, shock, drugs, obstructive)
4. No improvement with diuretic withdrawal + 1g/kg IV albumin x 2 days
5. Suggestion of renal vasoconstriction with a FENa < 0.2% (with levels < 0.1% being highly predictive) - Treatment
– Definitive = liver transplant
– ICU = Norepinephrine and IV albumin
– Ward = terlipressin + albumin > octreotide + midodrine + albumin
Hepatopulmonary Syndrome
Etiology
– Patients with cirrhosis or portal hypertension can get hypoxemia from
intrapulmonary vasodilation
– Classic presentation: dyspnea, platypnea, hypoxemia
- Diagnosis:
– Suspect HPS if ABG reveals PaO2 < 80, A-a gradient ≥15
– TT Echo with agitated saline (i.e. bubble study) demonstrates evidence of
intrapulmonary shunting
– Need to exclude other causes - Treatment
– Supplemental oxygen, liver transplant reverses HPS
