Download back to basics Gastroenterology Dr Saloojee 2015

Gastroenterology Cases
Nav Saloojee MD
2015
MCC Objectives : Gastroenterology
• Have an approach to abdominal mass/pelvic mass
• Have an approach to hepatomegaly
• Beable to examine the liver
• Have an approach to abdominal distension.
Beable to separate bowel obstruction from ascites
• Have an approach to anorectal pain
• Have an approach to acute /chronic abdominal pain
• Have an approach to liver enzymes
• Have an approach to UGIB / LGIB
MCC Objectives : Gastroenterology
• Have an approach to constipation
• Have an approach to acute and chronic diarrhea
• Have an approach to dysphagia
• Have an approach to fecal incontinence
• Have an approach to jaundice
• Have an approach to nausea / vomiting
Realize that many of the causes are not GI in origin
• Have an approach to weight loss
Case 1 ODYNOPHAGIA
• 35 y.o homosexual male presents with odynophagia.
• HIV for about 5 years. CD4 100. VL 5000.
• Hep C from IV drug use
• No AIDS defining illnesses and has been
noncompliant with antiretrovirals therapies.
•Physical exam is unremarkable except for the presence
of oral thrush.
Esophageal plaques on EGD
Filling defects on barium study
Odynophagia
•Infection
•Candida
•CMV
•HIV ulcers
•HSV
•Pill esophagitis
•Tetracycline/doxycycline
•NSAIDS
•Slow K
•Iron
•Others
•Inflammatory
• ( Severe GERD, Crohn’s, Behcet’s, Pemphigoid,
•Chemo / radiation )
•Toxic ingestion
•Lye
Esophageal Disease In HIV
• Esophageal candidiasis
• most frequent AIDS defining illness
• CD4 generally <200
• colonization by oral flora
• occurs in combination with other pathology in ~25% ( CMV, HIV
ulcer, HSV)
• Common in other immunocompromised states
•CRF, steroid use, hematologic malignancy, radiation, chemotherapy,
etc.
Treatment
•Nystatin ( topical therapy ) for oral thrush
•Fluconazole 100mg for 14 days for esophageal candidiasis
•Amphotericin B if neutropenic
Diagnosis?
l
squamocolumnar junction is
located in the tubular
esophagus, proximal to the
anatomic gastroesophageal
junction
Biopsy shows specialized
intestinal metaplasia. Mucosa
resembles intestine in that it is
villiform , numerous goblet
cells are present and
epithelium is columnar
Barrett’s Esophagus
• Barrett’s is premalignant
• In a 5 year follow up of 50 patients with Barrett’s and High
Grade Dysplasia, 32 % developed adenocarcinoma
• PPI probably does not reverse changes but is recommended as
lifelong treatment of the underlying reflux
• The length of Barrett’s is important.
• There is a recommendation for once in a lifetime endoscopy
for a patient with longstanding reflux symptoms to exclude
Barrett’s
Dysphagia
•Distinguish esophageal dysphagia from oropharyngeal dysphagia
( inability to initiate swallow, nasal regurgitation, coughing and
choking)
• Esophageal dysphagia : Key questions to distinguish mechanical (
reflux stricture, esophageal cancer) from motility ( achalasia and others
)
• Solids only or both solids / liquids?
• Intermittent or progressive?
• Is there a history of reflux?
• Is there weight loss?
Reflux Stricture
Dysphagia
• Investigations : EGD, Ba Swallow, Manometry
Barium swallow and
EGD for a patient
with intermittent,
nonprogressive
dysphagia to solids.
No weight loss
Diagnosis?
Ba swallow and EGD
for a patient with
progressive dysphagia
to both solids and
liquids. Weight loss.
Diagnosis?
What would
manometry show?
EGD is important in suspected Achalasia. This
patient had manometry consistent with achalasia (
Hypertensive LES that does not relax with swallow
and aperistalsis of lower esophagus ). Gastric
Adenocarcinoma.
Transaminase Elevation
What is the differential diagnosis for a patient with elevated
transaminases ?
What is the differential if transaminase levels >1000?
What tests should one do in a patient with elevated
transaminases?
Transaminase Elevation ( ie
hepatocellular injury)
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Drugs
Acetominophen, etc
Alcohol
NAFLD
Viral Hepatitis
Ischemic Liver Injury
Hemochromatosis
Wilson’s disease
Autoimmune hepatitis
Alpha one antitrypsin deficiency
Common Bile Duct Stone
Marked Transaminase Elevation
Few Causes of Transaminase Elevation >1000
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Drugs
Viral Hepatitis
Ischemic Liver Injury
Autoimmune hepatitis
Common Bile Duct Stone ( Not much more than 1000 )
Transaminase Elevation : Tests
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Drugs
Alcohol
NAFLD
Viral Hepatitis
Ischemic Liver Injury
Hemochromatosis
Wilson’s disease
Autoimmune hepatitis
Alpha one antitrypsin deficiency
Common Bile Duct Stone
Clinical, levels
Clinical, GGT, AST>ALT
U/S. Exclude other Dx
Serology
Clinical
Ferritin, % sat, gene test
Ceruloplasmin
ANA, Anti Smooth m
A1AT level
U/S
Cholestasis
Extrahepatic Cholestasis
• CBD Stone
• Pancreatic Cancer
• Primary Sclerosing Cholangitis : MRCP
• Extrinsic CBD Compression
Intrahepatic Cholestasis
• Meds
• Primary Biliary Cirrhosis : Antimitochondrial antibody
• Sepsis
• TPN
• Pregnancy
PSC
Approach Abnormal Liver Enzymes
Abnormal Liver enzymes
Increased ALP, GGT
Cholestatic Pattern
Increased AST, ALT
Hepatocellular Pattern
Ultrasound shows CBD dilatation
Y
Extrahepatic Cholestasis
N
Intrahepatic Cholestasis
Approach to Abnormal Liver Enzymes
Q. What are the stigmata of chronic liver disease?
Approach to Abnormal Liver Enzymes
• Palmar Erythema
• Dupuytren’s Contarcture
• Gynecomastia
• Telangiectasia
• Parotid enlargement
• Caput Medusae
• Testicular Atrophy
• Ascites
• Splenomegaly
• Asterixis
Case 2
45 year old woman
History of alcohol abuse
Presents to Emergency with intoxication, nausea and vomiting
No other history available
Physical examination
VSS. Afebrile.
Mucous membranes dry
Abdomen soft. Non tender. No mass. No HSM.
No stigmata of chronic liver disease
Remainder of exam normal
Case 2
Lab
CBC, Lytes, Glucose, Urea, Creatinine normal. Anion Gap normal.
AST 210 ( increased )
ALT 105 ( increased )
Bilirubin normal
Albumin 34 ( normal )
CXR / 3V Abdo normal
IV Fluid, Thiamine started
Next Step?
ALP 103 ( normal)
GGT 620 ( increased)
INR 1.1 ( normal )
Acetaminophen Hepatotoxicity
Acetaminophen level 150 ug/mL ( 1000uM/ L)
ETOH level positive
Remainder of tox screen negative
Acetaminophen Hepatotoxicity
Acetaminophen
P-450
Acetaminophen-Sulphate
Acetaminophen-glucuronide
Urine
Toxic intermediate metabolite
( ? NAPQI )
Glutathione Conjugation
Hepatocyte Protein
conjugation
Cell Death
Metabolism of toxic doses of Acetaminophen depletes glutathione and
saturates glucuronide and sulphate conjugation pathways
Hepatotoxicity produces necrosis. Inflammation is minimal.
Recovery is associated with complete resolution without fibrosis
Acetaminophen Hepatotoxicity
• Safe in doses of 1 to 4 grams /day
• Single doses greater than 10 g can result in liver injury
• Severe Liver injury ( ALT > 1000) or fatality associated with doses of
15 –25 g.
• Chronic ingestions of 4-6/ g day can lead to injury
• Among heavy drinkers fatal doses of 6 g have been described
• Most common cause of drug induced liver injury
• An important cause of Fulminant Hepatic Failure
– Rapid development of hepatocellular dysfunction (coagulopathy,
encephalopathy )
Risk Factors for Acetaminophen
Hepatotoxicity
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Older Age
Dose of acetominophen
Blood level of acetaminophen
Chronic Alcohol Ingestion
• Fasting
• Concomitant Medication
• Late Presentation
Lower threshold for injury as
ETOH depletes glutathione
ETOH induces p450
p450 induction ( Barbituates, INH,
Dilantin)
Best outcome if Rx within 12 hours
Therapy
Activated Charcoal may be useful in first 4 hours
N- Acetylcysteine ( NAC ) : If in doubt, Give NAC
• Acetaminophen level should be determined at presentation
• Recognize that levels within 4 hours of ingestion are unreliable due to
delayed gastric emptying
• NAC given orally in U.S., given IV in Canada
• NAC stimulates hepatic synthesis of GSH, may bind NAPQI, may be
a sulphate precursor
• Side Effects of NAC : GI upset and Allergic reactions
• If a patient has known NAC hypersensitivity, Methionine can be used
as an antidote
Therapy
N- Acetylcysteine ( NAC )
•
Severe liver injury virtually abolished if NAC given within 12 hours
for patients with a toxic Acetominophen level:
NAC within 12 hours
NAC 12-16 hours
Hepatotoxicity
Death
<8%
34%
1%
2-3%
Therapy
N- Acetylcysteine ( NAC )
• After 16 hours, NAC less likely to affect liver necrosis
• Nevertheless, late presenters should receive NAC as studies have
shown decreased mortality when given in this group
• Remember, the nomogram is only useful in an acute ingestion
• Also, the nomogram was developed for nonalcoholic patients
• NAC should be given in a chronic ingestion if hepatotoxicity is
suspected
• If an acetaminophen level can not be done quickly, NAC should be
given
• Follow Enzymes, INR, Mental Status, Acetominophen level
• Consider prolonged NAC until acetominophen levels fall
Acetaminophen Hepatotoxicity
Contact Transplant Centre
• Rising INR
• Encephalopathy
– Remember that the early signs are subtle
• Acidosis
• Renal Failure
Case 3
• 40 year old woman presents to Emergency
• For 2 years, intermittent RUQ/ epigastric discomfort.
• Episodes last 2 or 3 hours and then resolve.
• No previous investigation
• Now presents with RUQ pain that is not resolving
• No significant past history. No meds.
• Afebrile. Physical exam is normal aside from mild RUQ
tenderness
• AST and ALT 1.5 times normal. Alkaline Phosphatase and
GGT three times normal. Bilirubin 1.5 times normal. Normal INR
and Albumin
•She is admitted
Diagnosis?
Case 3
•Choledocholithiasis. History of biliary colic.
•Ultrasound confirms CBD dilation and intrahepatic
duct dilation. Stones seen in gallbladder.
•ERCP below shows filling defects due to stones which
are removed.
Case 3
• Post ERCP she feels well and liver enzymes
normalize.
• Cholecystectomy is suggested but she declines.
• Three months later she presents with fever, jaundice,
and RUQ pain
• She looks unwell. Marked tenderness in RUQ
• WBC 18. Liver enzymes show cholestatic picture and
increased bilirubin
•Diagnosis?
Ascending Cholangitis
• CBD obstruction with bile stasis and bacterial infection in
biliary tree
• Pus under pressure in the bile ducts leads to sepsis
• 85% of cases due to CBD obstruction from stone
• RUQ pain, fever and jaundice are Charcot’s triad.
•This is a medical emergency
• Treatment
•Blood Cultures
•Antibiotics ( ex Ampicillin / Cefotaxime / Flagyl )
•Decompression of CBD with ERCP or PTC ( percutaneous
transhepatic cholangiography )
GI Bleeding
Clinical presentation
• Hematemesis : Vomiting of fresh red blood. Indicates brisk
upper GI bleed
• Coffee ground emesis : Vomiting of blackish material. Indicates
upper GI bleed
• Melena
Passage of loose, black tarry stool.
Commonly from UGIB. Can be from Right colonic bleed
Other causes of black stool?
GI Bleeding
Clinical presentation
• Hematochezia :Passage of bright red blood from rectum
• Occult : Slow GI bleeding . Not apparent to patient ( Iron
Deficiency / Fecal Occult Blood positive)
• Obscure : Bleeding of any sort which is not easily pinpointed by
usual diagnostic techniques
Approach to the Bleeding Patient
• Assess the severity of bleeding
Hemodynamics
Shock ( resting hypotension)
Postural Change
Normal
% Intravascular
Volume Loss
20-25
10-20
<10
Severity of Bleed
Massive
Moderate
Minor
• Resuscitation
– IV Access
– Monitor vitals
– Transfuse when necessary
– Correct Coagulopathy
ie platelets, fresh frozen plasma, Vitamin K
Take a History
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Age
Known GI disease or previous bleed
Known Liver Disease
Previous surgery
ASA /NSAID /Coumadin
Gastrointestinal symptoms ( pain, dysphagia, vomiting, weight
loss, change in bowel habit )
• Chest Pain , SOB
• Physical may not help, but exclude signs of chronic liver disease
Rectal examination!
Tests
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Hb
Platelets
MCV + / - Ferritin
INR
Urea
• Localize bleed ( Endoscopy, Angiography)
• Treat bleed ( pharmacologic, endoscopic,
angiographic, surgery)
Case 4
•58 year old man presents to the emergency department with
hematemesis. No abdominal pain.
• Long history of alcohol abuse.
• No past medical history. On no medications
• On exam, BP 90/ 50 and HR 130. Postural changes.
• Palmar erythema, dupuytrens contracture, telangiectasia on chest,
gynecomastia. No asterixis.
• Abdomen soft. Non tender. Liver not palpable. Spleen tip palpable.
Bulging flanks. Rectal reveals melena
• Hb 110 (low ) MCV 99 ( high normal ) Platelets 125 (low)
Urea 15 ( high ) Creatinine 89 ( normal )
•Normal AST/ ALT /ALP Bili 88 ( high) INR 1.5 ( high )
Albumin 24 ( low )
Case 4
What is the cause of bleeding?
What is the differential diagnosis?
What are the indicators for urgent endoscopy?
Causes of Upper GI Bleeding
PUD
Varices
Mallory Weiss
Tumour
Vascular
Dieulafoy
Other
Jutabha et al. Med Clin North Am 1996
UCLA. Prospective series of 1000 patients.
Early Endoscopy for Upper GI Bleeding
• Overall, 80 % of UGIB self limited.
• But 8-10% mortality
• Early endoscopy
Suspected variceal bleed ex. Cirrhotic patient
Indicators of Profuse Bleeding
Hemodynamic instability DESPITE resuscitation
Hematemesis
Red Blood per rectum in a suspected UGIB
? Multiple Comorbidities
Natural History of Variceal Bleeding
• Esophageal varices develop in 50 % of patients with cirrhosis
• 30% of patients with varices will have a bleed within 2 years of
diagnosis
• After one variceal bleed, the risk of a second is high. 60 to 70 %
will rebleed within 2 years.
• Variceal bleeding accounts for 20 – 33 % of deaths in cirrhotics
Causes of Portal Hypertension
Be aware of Splenic
Vein Thrombosis
Case 4
What is the management of variceal bleeding?
Management of Variceal Bleed
• Volume Resuscitation
• Correct coagulopathy. Vit K and FFP. +/- platelets
• Pharmacotherapy : IV Octreotide 50 ug bolus and then
50ug /hour
• Antibiotics
• Endoscopic Therapy
• Balloon Tamponade
• TIPS
• Watch for encephalopathy
• Secondary Prophylaxis
Pharmacotherapy.
• IV Octreotide has a net impact of splanchnic vasoconstriction
reducing variceal blood flow
• RCTs show beneficial effect in control of the initial bleed
( ie octreotide + endoscopic therapy better than endoscopy alone)
• IV octreotide shown to prevent early in hospital rebleed after
control of initial hemorrhage. Continue for 48-72 hours
Endoscopic Therapy
Endoscopic Therapy
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Banding
Can control acute bleed in about 90%
Banding may be difficult due to poor visualization
Current standard of care is combined endoscopic and
pharmacotherapy (octreotide)
Refractory Bleeding
• Balloon Tamponade.
• Complications : Aspiration Pneumonia, Esophageal ulceration or
perforation
• High rate of rebleed when balloon deflated
Refractory Bleeding
• TIPS ( Transhepatic Intrahepatic Portosystemic Shunt )
• A technically successful TIPS will decompress the portal
circulation and control bleed in almost all patients
• Main complication is encephalopathy
Precipitants of Hepatic encephalopathy
•GI Bleed
•Uremia
•Dehydration
•Hypokalemia
•Constipation
•Excess dietary protein
•Infection ( SBP )
•Sedatives
•Metabolic alkalosis
Treatment : Treat underlying cause
Lactulose
•
Secondary Prophylaxis
B Blockade or Repeated banding ( until varices obliterate )
reduce risk of rebleed
Gastric Varices
Gastric Varices
Case 5 . Lower GI Bleed
• 74 year old woman
• Presents to the Emergency with 4 episodes of passing blood per
rectum that day
• No abdominal pain, or other GI symptoms
• Past history : hypertension
• On an ACE inhibitor. No other medications
• BP 150/90. HR 90. No postural changes
• Physical exam normal except red blood on rectal exam
• Hb 120. MCV normal. Urea 10. Creatinine 100. Other labs
normal.
• Receives appropriate supportive care
Lower GI Bleed
•DDX
• Diverticular Bleed
• Angiodysplasia
• Colon Cancer
• Ischemic Colitis
• Consider a brisk upper GI bleed
• Other causes less common
Lower GI Bleed
Diverticular bleeding
Bleeding spontaneously ceases
in about 80%
Roughly 25 % rebleed
Of these, 50 % bleed again
Angiodysplasia
Mostly right sided
Again, around 80 % subside
spontaneously
Lower GI Bleed
Colon Cancer
Rarely Severe LGIB
Presentation ( R vs L) ?
Endoscopic Management of Acute
Lower GI Bleeding
Approach to Lower GI Bleed
Acute Lower GI Bleed
Resuscitate
EGD if UGIB suspected
Bleeding Stops
Bleeding Persists
Colonoscopy after
bowel preparation
Angiogram to localize bleed
Refer to surgery
Colonic Polyps
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Can be characterized by gross appearance
Sessile vs pedunculated (on a stalk)
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Removal of adenomatous polyps prevents Colorectal
Cancer
CRC : Screening
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Early detection of Colon cancer improves prognosis
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Fecal Occult Blood Testing /Fecal Immunochemistry (FIT)
every 1-2 years
FOBT is inexpensive and non invasive
FOBT testing will reduce CRC mortality
FOBT is not a good test to detect polyps
Many false positives occur. Only 2 % of positive tests due to
cancer
CRC : Screening
FOBT/FIT
Flexible Sigmoidoscopy
DCBE
Colonoscopy
CT Colonography?
CRC : Screening
Screen patients at average risk at age 50 and then every ten years
( with colonoscopy )
Screen patients with first degree relative ten years before index
case and then every 5 years ( with colonoscopy)
If adenomatous polyp found, screen every 5years ( with
colonoscopy )
IBD patients with pancolitis. Colonoscopy 8-10 years after
diagnosis and then q 2 years.
IBD patients with distal colitis. Colonoscopy 15 years after
diagnosis and then q 2 years.
Case 6
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20 year old university student
3 year history severe, episodic periumbilical pain
Some relief of pain with bowel movement
3 to 6 loose bowel movements/ day. No blood
No weight loss
Past history unremarkable
Meds
Iron supplement
Family history unremarkable
No extraintestinal manifestations of IBD
•
Differential diagnosis?
Case 6
Labs
Hb 106 (low) MCV 73 (low)
Plt 697 (high)
ESR 25 (high)
CRP 45 ( high)
Ferritin 6 (low)
Albumin 20 (low)
Lytes , Urea, Cr, Liver enzymes, TSH Normal
Anti ttg negative. IgA normal
Case 6
Colonoscopy
Colon normal
Ileum. Linear ulcers. Cobblestoned appearance. Erythema.
normal
Crohn’s ileitis
Case 6
Biopsies of ileum
chronic inflammatory cell infiltrate
distortion of architecture
granulomata
Case 6
Inflammatory crohn’s
Response to steroid
Unfortunately steroid dependent
Failed azathioprine ( imuran )
Doing well on infliximab ( remiacade)
What is the difference between Ulcerative colitis and
Crohn’s?
Ulcerative Colitis and Crohn’s Disease
Crohn’s
Ulcerative Colitis
Th2
Th1
Superficial inflammation
Transmural Inflammation
May be granulomata
Bleeding more common
Weight loss and pain more
common
Continuous
Discontinuous
Colon only
Anywhere in GI tract
Predilection for terminal ileum
Inflammatory
Inflammatory
Fibrostenosing
Fistulizing
Better with smoking
Worse with smoking
Surgery curative
Recurs after surgery
The evolution of therapy: toward
optimal treatment of IBD
Objectives of therapy
Less surgery
Surgery
Biologics
:Infliximab /
Adalimumab
Immunosuppressives
(AZA/6-MP, MTX)
Steroids
Proper patient identification:
• Which patients should be treated with IFX?
• Widespread use
• Earlier recognition of failure
• Brief exposure
• Earlier identification of
resistance/dependence
Case 7
• 57-year-old man
• Recently diagnosed as having ulcerative colitis
• Presents with persistent bloody diarrhea
• Abdominal pain
• He had a fever of 38.8 degrees. HR 120. BP 110 / 70
• Decreased bowel sounds, and a tense, mildly distended abdomen.
• WBC 15
Case 7
Diagnosis?
Treatment ?
Toxic Megacolon
• Differentiate from ileus where there is no colonic
inflammation
• Inflammation leads to colonic paralysis
• Can result from IBD / Ischemia / Infectious colitis
• X-ray evidence of colonic distension. > 6 cm in transverse
colon
• Fever, tachycardia, high WBC
• High mortality with perforation
• Remember, perforation can occur in ulcerative colitis ( or
other forms of colitis ) without toxic megacolon
Toxic Megacolon : Treatment
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NPO, F&E, NG
IV Solumedrol 20 mg q8h for 24 hours
Immediate surgical consult
Colectomy if fails to resolve in 24-48 hours or if
peritoneal signs
Case 8
• 69 year old man hospitalized for pneumonia
• After treatment with antibiotics, develops small
volume, non bloody, profuse diarrhea
• Medications noncontributory
• Physical exam noncontributory
• Bloodwork noncontributory
Clostridium Difficile
• Spore forming microorganism distributed widely in the
environment
• Major risk is associated antibiotic use which disrupts
normal colonic flora
• Hospitalized patients particularly at risk in part due to age
and immunodeficiency
• Easily transferable and thus a threat to hospitalized patients
• C. Diff produces toxin A and B which mediate colonic
damage
• Testing stool for toxin forms the basis of diagnosis
• Can perform endoscopy for rapid diagnosis : presence of
pseudomembranes : yellowish adherent plaques
Any
Questions?