Teaching Clinic - Investigations in Gastroenterology & Hepatology Flashcards
F/48:
o Recurrent epigastric discomfort for many years
o OGD: mild antral gastritis
o Urea breath test performed
How do you interpret the findings?
False negative
Triple therapy: clarithromycin, amoxicillin, PPI
Assume negative result is falsely negative
Discrepancy in H. pylori results (causes for false negative)
False negative results
- Drugs in past 2 weeks: PPI (H. pylori moves proximally to body / fundus), Bismuth, Antibiotics
- Acute upper GI bleeding (rapid urease test)
- Technical issue
- Bleeding during testing = Blood will have interaction with rapid urease test
- Rapid urease test (technical issue, i.e. patient doesn’t know how to breath into the test)
M/53:
o Chronic heavy drinker
o Admitted for haemetemesis
o INR 1.8 platelet 87x109/L
o Emergency OGD performed
What is the grading? What is the treatment?
- Esophageal varices
- Three grades by visualization = Grade 3: as big as whole lumen
Band ligation
Medical treatment:
- Terlipressin (acute setting) = constrict splanchnic circulation
- Somatostatin analogue
- Antibiotics to prevent superimposed infection
Restrictive transfusion (excessive transfusion will lead to excessive bleeding) = only transfuse if Hb <7 g/dL (only transfuse one pack cells)
Long-term: non-selective beta blockers
Reassessment OGD 4 weeks later. What is seen here?
Red wale sign (red patches or strips on the varices): stigmata of recent bleeding
Need rebanding (commonly required)
What is the management in this case?
Prominent varices but no red wale sign = no re-banding needed
M/72:
o Chronic hepatitis B cirrhosis on entecavir
o Recent decompensation
o Admitted for haemetemesis
o INR 1.6 platelet 110x109/L
o Where is the gastroscope?
- J view for cardia
- Gastric varix with red wale sign (DO NOT BIOPSY = bleeding)
How is this gastric varix with red wale sign managed? What is this procedure?
Poke needle into varix and apply tissue glue [Cyanoacrylate] (1-2 minutes)
Needle needs to be in varix for short period of time. If glue is not properly adminstered and needle is dislodged, there will be torrential bleeding
Gastric varices treatment
Medical treatment:
- Terlipressin
- Antibiotics
- Other supportive measures (e.g. correct coagulopathy)
Restrictive transfusion
Cyanoacrylate (tissue glue) injection
Long-term: non-selective beta blocker
TIPS: transjugular intrahepatic portosystemic shunt
F/91:
o Advanced dementia
o Old-age home resident
o Noted with refusal of oral intake
What is this?
Foreign body ingestion (wedding ring)
What is this?
Fish bone: infection, ulceration, haemorrhage, perforation
What is this?
Metal ingestion
What is this? How do we treat?
Gastric bezoar
Tx: drink coca cola (original form!)
Shrink after 1/7
How do we manage this?
Nail clipper
Emergency gastrectomy
M/72:
o Intermittent burning chest pain
o Each episode lasting for hours
o Negative CT coronary angiogram
o Globus sensation+
What is the abnormality? What is the diagnosis?
What is the management?
What is the gold standard diagnosis for this patient?
- Mucosal break at 2 and 5 o’clock (LA Grade A) - Esophagitis as a complication of GERD (majority has no esophagitis)
- PPI x 8/52
- 24H pH test
When must we perform a 24h pH test?
24 hour pH: when considering antireflux surgery
Confirm diagnosis before surgery
If patient has reflux symptoms, it doesn’t always mean GERD
It could be functional reflux, if you do a surgery (fundoplication) for these patients, his symptoms will still remain
GERD
- OGD indications
- Treatment
OGD indications:
- Unclear diagnosis
- “Alarm” symptoms
Majority have normal OGD (no esophagitis)
Empirical acid suppresion >8 weeks
Lifestyle modification
What are “alarming” symptoms of GERD?
- Obstructive symptoms (dysphagia, odynophagia, repeated vomiting)
- GI bleeding
- New onset of symptoms in >55 y/o
M/69:
o History of PCI 4 months ago
o On aspirin and clopidogrel
o Admitted for melaena
o OGD performed
What is the lesion?
Where is the lesion?
What should be done?
- Duodenal ulcer (Forest IIA: visible non-bleeding vessels)
- D1/2 junction
- Endoscopic haemostasis (needed for Forest IIA and above)
- Combination therapy: endoscopic adrenaline injection (stop the bleeding) + electrocoagulation / hemoclip
Depends on preference of endoscopist and location of bleeding site
What is being performed?
Electrocoagulation – thermal energy to ablate the lesion (Cx: perforation)
Patient has PCI 4 months ago. Since patient is on aspirin and clopidogrel with duodenal ulcer bleeding. Can we continue aspirin and clopidogrel?
- If there is life-threatening bleeding (usu. GI bleeding or brain bleeding) : stop both anti-platelets
- Control bleeding ASAP
Resume anti-platelet ONCE bleeding is controlled - When resume aspirin / clopidogrel, need PPI coverage long-term
Peptic ulcer bleeding
- Endoscopic therapy
- Medical therapy
Endoscopic therapy:
- Adrenaline injection + electrocoagulation / hemoclips
Medical therapy:
- Intravenous PPI infusion
Supportive transfusion
Forrest classification
What do we do when endoscopy fails?
Angiogram & Embolisation
Any contrast out of the blood vessel is extravasation
If you embolise too proximally, you will increase the chance of ischaemic bowel
F/47:
o Noted gradual darkening of skin for a few months
o Prescribed topical medication by GP, no improvement
- What is the diagnosis?
- Vague epigastric mass on palpation?
- Acanthosis nigricans = suspect GI malignancy
- Forest III (clean base, no need haemostasis)
- Non-bleeding gastric ulcer
Clean based ulcer
What should we do?
Biopsy gastric ulcers whenever possible
- May be deceptively benign-looking
- Consider reassessment OGD to document ulcer healing (6-8 weeks)
‘Poorly-differentiated’
‘Diffuse’
Involvement of H. pylori for intestinal
What are the two main types of gastric cancer
Intestinal
Diffuse-type gastric cancer
- maybe H pylori -ve
- May not follow inflammation / atrophy / metaplasia / dysplasia casdacde
- Involvement can be submucosal
- Worse prognosis
M/37:
o Insidious increase in dysphagia (>3 years)
o Both liquids and solids
o Recurrent choking
o Admitted for aspiration pneumonia
o OGD: Tight gastroesophageal junction
o What is this investigation?
o Diagnosis?
o What is this investigation?
- Barium swallow
- Bird beak appearance = achalasia (DDx: CA esophagus)
- Manometry (x-axis = time; y-axis = pressure along esophagus; result: no peristalsis after swallowing)
- What is achalasia?
- What will be seen on Barium swallow and manometry?
- What FU Ix do we need to order?
- How do we manage achalasia?
- Failure of releaxation of lower esophgeal sphincter
- Barium swallow: ‘Bird-beak’ appearance
- Manometry: Aperistalsis
OGD needed to exclude pseudoachalasia - Management:
– Endoscopic dilatation
– Surgical myotomy
– POEM (Peroral endoscopic myotomy)
Dissect all the muscle down to OGJ
M/64:
o Admitted for high fever
o Bilirubin 125 umol/L ALP 335 U/L
What are we suspecting?
- Suspect acute cholangitis
- ERCP: duodenoscope = insert cannula into ampulla of Vater and inject dye (cholangiogram)
Goal: provide endoscopic drainage
What procedure is shown? Why is it performed?
Duodenoscope (looking sideway): the bulging mass = ampulla of vater → sphincterotomy (enlarge ampulla of vater) for stenting, stones Cholangiogram (after injection of contrast to CBD) Plastic stent: biliary drainage
What does CT show? Medical therapy?
- Cholangitic liver abscess (the other hypodense structure = gallbladder)
- Empirical 3rd generation cephalosporin as first line for biliary infection [4-6 weeks] – lifesaving so give before culture is back
How do you interpret the results? What is your recommendation? What else is needed?
- If responding to empirical 3rd cephalosporin and haemodynamically stable
- can step down to Augmentin for 4-6 wks (if patient is deteriorating, DO NOT DE-ESCALATE ABx)
- If admission to ICU = step up to big gun antibiotics
Biliary infection and liver abscess:
- Treatment of cholangitis
- Treatment of liver abscess
Cholangitis:
- Biliary drainage (ERCP or PTBD)
- Need subsequent stone extraction and ductal clearance
- Cholecystectomy
- Empirical antibiotics targeting gram -ve bacilli
Liver abscess
- May need drainage
- Prolonged course of antibiotics
- Need to delineate cause
M/52:
o Referred for known chronic hepatitis B
o Serum ALT all along <40 U/L
o Normal albumin and bilirubin
o No HBV DNA level or HBeAg status available
o Ultrasound: fatty liver changes, no ascites
What is ‘LSM’ and ‘CAP’?
What are the implications?
What is your recommendation?
What is the Mx?
- LSM: Liver stiffness measurement; CAP (quantification of liver fat) controlled attenuation for steatosis
- Cirrhotic range, Child’s A compensated cirrhosis
Mx:
- USG for HCC surveillance
- If patient has known cirrhosis, start antiviral regardless of HBV status, 6/12 FU for USG
- OGD to screen for varix
(could be due to hep B + steatosis)
F/56:
o DM on glicazide, hyperlipidemia on simvastatin
o Incidental finding of deranged LFT
o USG: fatty liver changes, no dilated biliary tract
o HAV/ HBV/ HCV/ HEV unremarkable
Interpret the LFT abnormalities?
What is your next step?
- LFT: hepatitic picture
- Underlying NASH cannot cause AST or ALT >400, so look for other causes: drug-induced, autoimmune
- Autoimmune markers, liver biopsy (eosinophils in drug allergy) = ANA, anti-smooth muscle antibody
Eosinophils: drug-allergy
If we see eosinophils in liver biopsy in patient with hepatitic liver function test, what must we think of?
Traditional Chinese Medicine: Drug-induced liver injury
F/56:
o DM on glicazide, hyperlipidemia on simvastatin
o Incidental finding of deranged LFT
o USG: fatty liver changes, no dilated biliary tract
o HAV/ HBV/ HCV/ HEV unremarkable
- Day 20 results: are you worried?
- What is your management
- Not liver failure because INR not high (1.5-1.6)
- Transplant only when INR rises to 2.0 (severe heaptitis, esp. in drug-induced liver injury = prolonged hepatitis [weeks & months for complete biochemical resolution]
- No drugs are needed
- Observe for now: monitor INR, bilirubin
- Drug-induced may require a few months to resolve = no need transplant if downtrend
M/58:
o Chronic hepatitis B, on entecavir for 7 years
o LFT previously normal, HBV DNA undetectable
o Noted ALP 330 U/L, bilirubin 39 umol/L
o Ultrasound: dilated intrahepatic ducts
What Ix is this?
MRCP shows dilatated intrahepatic duct (as thick as CBD) with multiple IHD strictures, slightly dilated CBD
Perform ERCP
What are the DDx of intrahepatic strictures?
Most significant:
- IgG4 related disease
- Primary sclerosing cholangitis (usually concomitant with UC/ IBD = arrange colonoscopy)
Less significant:
- Malignancy (e.g. Klaskin tumour) = but there won’t be strictures everywhere
- Recurrent pyogenic cholangitis (only causes dilatation, not strictures)
- Ketamine-related cholangiopathy (Ketamine is no longer popular)
- HIV cholangiopathy
Don’t say PBC (microscopic disease: bile duct is anatomically normal; AMA +ve)
IgG4-related disease
- Typically occur in 6th decade of life (M > F)
Multi-organ involvement - Open affect biliary tract and pancreas
F/68:
o CRHD with MVR performed at 53 years
o On warfarin
o Noted Fe deficient anaemia 4 years ago
o INR maintained 2-2.5
o OGD/ colonoscopy unremarkable
o Stool OB positive
o Next step?
- Perform a capsule endoscopy
Patient has chronic rheumatic heart disease with MVR performed at 53 years. On warfarin.
What is seen in this capsule endoscopy? What should we order next?
Angiodysplasia (not typical star sign)
Only order capsule endoscopy when we are certain there is possible small bowel bleeding. There is no therapeutic purpose, it is only for investigation.
Small bowel enteroscopy: Management = argon plasma coagulation (white after ablation)
Long-term: intravenous iron
Angiodysplasia has well-known association with valvular heart disease + there is bleeding tendency (cannot stop warfarin) = patient will forever need INR maintained at 2-2.5
Occult GI bleeding
- Stool OB positive with no visible blood loss
- Fe deficiency anaemia (exclude menstrual blood loss)
Many different causes: angiodysplasia/GAVE/GIST/polyp/SB ulcer/lymphoma
First: OGD / colonoscopy
Small bowel evaluation: - Capsule endoscopy: localisatoin
- Small bowel enteroscopy: targeted, therapeutic
Long-term: may need intravenous Fe
Bowel angiodysplasia: Thalidomide )reduce requirement of subsequent transfusion and IVI)
Male 70 years old
- History of advanaced gastric cancer with disseminated mets
- Admitted for repeated vomiting
- What is the cause?
- Gastric outlet obstruction
- Stent will cover ampulla of vater (ERCP will not be possible)
Gastric Outlet Obstruction: Non-surgical approaches
Causes: Malignant or benign (PUD/post-pancreatitis/caustic injury)
Endoscopy therapy
- Balloon dilatation
- Metallic stent
- EUS-guided gastrojejunostomy (look at photo/mushroom thing = more long-lasting)
Endoscopic ultrasound in GI: applications
- Visualise submucosal / extramural lesions, e.g. GIST
- Fine needle aspiration (pancreatic biopsy & more)
- Drainage of cyst (e.g. pancreatic pseudocyst, usually just behind stomach)
M/61:
o Unremarkable past health
o Participated in government colorectal cancer screening
o Faecal immunochemical test positive
- Pedunculated polyp in sigmoid
- Do a polypectomy to resect the whole polyp and send for histology
What is the most important findings in this histology report?
- High-grade dysplasia
- Tubulovillous adenoma
- Size
How common are colonic adenomas? When is risk of progression increased? What should be done for advanced adenomas?
Colonic adenoma:
- Two-thirds of all colonic polyps
- Variable disease course
- Risk of progression increased in advanced adenoma:
1. High-grade dysplasia
2. Villous histology
3. ≥ 1 cm
- Advanced adenoma: earlier surveillance colonoscopy
M/45:
o Recurrent intermittent blood-stained stool for past 2 years
o Colonoscopy done
o Right colon/ terminal ileum normal
Diagnosis? Management?
- Ulcerative colitis (chronicity, uniformly erythematous mucosa, superficial, rectum most involved)
- 5ASA or mesalazine (oral or topical suppository) only, no need steroid
12 years later:
- Frequent disease relapse over last 2-3 years
- Recurrent course of steroids
- Azathioprine/ mesalazine enema
- Now admitted for bloody diarrhoea x15 per day
Impression? How do we manage him?
Pseudopolyps everywhere = very bad ulcerative colitis + pancolitis
Refractory to current management
Ulcerative colitis
- Areas of involvement
- What to watch out for in acute flare up?
- How do we Ix?
- How do we follow-up patient?
Pancolitis / L-sided colitis / Proctitis
Acute flare up:
- Exclude other causes of colitis / bloody diarrhoea
- Watch out for toxic megacolon
- Perform sigmoidoscopy
- Avoid full colonoscopy due to risk of bowel perforation
Diagnosis >10 years for pancolitis / L-sided colitits
- Need surveillance colonoscopy
F/56:
o History of renal transplantation 4 years ago (IgA nephropathy)
o On tacrolimus, MMF, prednisolone
o Admitted for multilobar pneumonia needing ICU care (antibiotics)
o Developed bloody diarrhoea x8 per day at D4
o Differential diagnosis?
C. difficile colitis
What is seen on endoscopy? How do we confirm the diagnosis? What is the management?
Pseudomembranous colitis (endoscopic appearance)
Could be plain, simple colitis
Stool x PCR C. difficile cytotoxin (C. difficile culture may just be normal coloniser, but cytotoxin is what cause the disease) = disease-causing C. difficile
Management: Oral metronidazole (mild cases), vancomycin (severe)
Clostridiodes difficile infection
- Antibiotic-related diarrhoea =/= C. difficile infection
- Prior antibiotic usage (hospital, long-term care facility)
- Less reported in Asia
- Colonisation vs. genuine infection
- Bacterial culture vs. cytotoxin detection
- Pseudomembranous colitis
- Treatment: metronidazole / vancomycin / faecal transplant via NGT (if there is aspiration, very dangerous)
F/23:
o Recurrent watery diarrhoea and weight loss for >6 months
o Colonoscopy performed
Possible diagnosis
What else to ask in history?
- Crohn’s disease (patchy inflammation instead of uniform) = all 4 layers affected = fistula formation
- Ileo-colonic involvement most common
- UC does not affect small bowel (backwash ileitis is not a true inflammation)
Ask about perianal abscess and anal fistula, 漏管
2y later:
- Symptoms worsen despite treatment
- Anal discharge noted
What imaging was performed? What biological therapy can be considered?
MR-enterography
Anti-TNF side effects:
- TB reactivation
- HBV reactivation
- Allergic reactions
Must do Interferon-Gamme Release Assay to rule out TB
