Transcript Gastroenterology Cases - Dr. Nav Saloojee_compressed

Gastroenterology Cases
Nav Saloojee MD
April 2008
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.
Filling defects on barium study.
Esophageal plaques on EGD
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
• ~80% will develop esophageal symptoms but some
asymptomatic
• 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
•Ampho B if neutropenic
Daignosis?
l
squamocolumnar junction is
located in the tubular
esophagus proximal to the
anatomic GE 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
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
ALT 105
Bilirubin normal
Albumin 34
CXR / 3V Abdo normal
IV Fluid, Thiamine started
Next Step?
ALP 103
GGT 620
INR 1.1
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 ( jaundice,
coagulopathy)
– Encephalopathy
Risk Factors for Acetaminophen
Hepatotoxicity
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Older Age
Dose
Blood Level of Acetaminophen
Chronic Alcohol Ingestion
• Fasting
• Concomitant Medication
• Late Presentation
Lower threshold for injury as
ETOH depletes GSH / 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 )
• Acetaminophen level should be determined at presentation
• Recognize that levels within 4 hours of ingestion are unreliable due to
delayed gastric emptying
• After 4 hours, levels are a reliable indicator of the risk of liver injury
• 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 )
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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
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Rising INR
Acidosis
Renal Failure
Encephalopathy
– Remember that the early signs are subtle
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
Level
U/S
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 )
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
Bulging flanks. Rectal reveals melena
• Hb 110 MCV 99 Platelets 125
Urea 15 Creatinine 89
•Normal AST/ ALT /ALP Bili 88 INR 1.5 Albumin 24
palpable.
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 wary 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
• Several trials show octreotide alone to be comparable to
endoscopy alone in control of variceal hemorrhage
• RCTs show beneficial effect in control of 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
• Banding or Sclerotherapy
• Both 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
•Sedatives
•Metabolic alkalosis
• Treatment : Treat underlying cause
Lactulose
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Secondary Prophylaxis
• Both B Blockade and Banding reduce risk of rebleed
• Which is better is open to debate
• No proof for using both
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 of mild chronic renal failure due to 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 17. Creatinine 210. 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
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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
Case 6
• 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 6
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 7
• 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
•Sigmoidoscopy as shown below