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Gastroenterology Cases

Gastroenterology Cases. Nav Saloojee MD April 2011. 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.

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Gastroenterology Cases

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  1. Gastroenterology Cases Nav Saloojee MD April 2011

  2. 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.

  3. Filling defects on barium study. Esophageal plaques on EGD

  4. 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

  5. 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.

  6. Treatment • Nystatin ( topical therapy ) for oral thrush • Fluconazole 100mg for 14 days for esophageal candidiasis • Ampho B if neutropenic

  7. 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

  8. 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

  9. Dysphagia • Distinguish esophageal dysphagia from oropharyngeal dysphagia ( inability to initiate swallow, nasal regurgitation, coughing and choking) • Key questions in esophageal dysphagia to distinguish mechanical ( reflux stricture, schatzki’s ring, 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

  10. Dysphagia • Investigations : EGD, Ba Swallow, Manometry Barium swallow and EGD on a patient with intermittent, nonprogressive dysphagia to solids with no weight loss Diagnosis? Ba swallow and EGD on a patient with progressive dysphagia to both solids and liquids. Weight loss. Diagnosis? What would manometry show?

  11. 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.

  12. 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?

  13. Transaminase Elevation ( ie hepatocellular injury) • Drugs Acetominophen, etc • Alcohol • NAFLD • Viral Hepatitis • Ischemic Liver Injury • Hemochromatosis • Wilson’s disease • Autoimmune hepatitis • Alpha one antitrypsin deficiency • Common Bile Duct Stone

  14. Marked Transaminase Elevation Few Causes of Transaminase Elevation >1000 • Drugs • Viral Hepatitis • Ischemic Liver Injury • Autoimmune hepatitis • Common Bile Duct Stone ( Not much more than 1000 )

  15. Transaminase Elevation : Tests • Drugs Clinical, levels • Alcohol Clinical, GGT, AST>ALT • NAFLD U/S. Exclude other Dx • Viral Hepatitis Serology • Ischemic Liver Injury Clinical • Hemochromatosis Ferritin, % sat, gene test • Wilson’s disease Ceruloplasmin • Autoimmune hepatitis ANA, Anti Smooth m • Alpha one antitrypsin deficiency Level • Common Bile Duct Stone U/S

  16. 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

  17. PSC

  18. Approach Abnormal Liver Enzymes Abnormal Liver enzymes Increased ALP, GGT Cholestatic Pattern Increased AST, ALT Hepatocellular Pattern Ultrasound shows CBD dilatation Y N Extrahepatic Cholestasis IntrahepatisCholestasis

  19. Approach to Abnormal Liver Enzymes Q. What are the stigmata of chronic liver disease?

  20. Approach to Abnormal Liver Enzymes • Palmar Erythema • Dupuytren’s Contarcture • Gynecomastia • Telangiectasia • Parotid enlargement • Caput Medusae • Testicular Atrophy • Ascites • Splenomegaly • Asterixis

  21. 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

  22. Case 2 Lab CBC, Lytes, Glucose, Urea, Creatinine normal. Anion Gap normal. AST 210 ALP 103 ALT 105 GGT 620 Bilirubin normal INR 1.1 Albumin 34 CXR / 3V Abdo normal IV Fluid, Thiamine started Next Step?

  23. Acetaminophen Hepatotoxicity Acetaminophen level 150 ug/mL ( 1000uM/ L) ETOH level positive Remainder of tox screen negative

  24. Acetaminophen Hepatotoxicity Acetaminophen P-450 Acetaminophen-Sulphate Toxic intermediate metabolite ( ? NAPQI ) Acetaminophen-glucuronide Urine Glutathione Conjugation Hepatocyte Protein conjugation Cell Death Metabolism of toxic doses of Acetaminophen depletes glutathione and saturates glucuronide and sulphate conjugation pathways

  25. Hepatotoxicity produces necrosis. Inflammation is minimal. Recovery is associated with complete resolution without fibrosis

  26. 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

  27. Risk Factors for Acetaminophen Hepatotoxicity • Older Age • Dose • Blood Level of Acetaminophen • Chronic Alcohol Ingestion Lower threshold for injury as ETOH depletes GSH / induces p450 • Fasting • Concomitant Medication p450 induction ( Barbituates, INH, Dilantin) • Late Presentation Best outcome if Rx within 12 hours

  28. 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

  29. Therapy N- Acetylcysteine ( NAC ) • Severe liver injury virtually abolished if NAC given within 12 hours for patients with a toxic Acetominophen level: Hepatotoxicity Death NAC within 12 hours <8% 1% NAC 12-16 hours 34% 2-3%

  30. 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

  31. Acetaminophen Hepatotoxicity Contact Transplant Centre • Rising INR • Acidosis • Renal Failure • Encephalopathy • Remember that the early signs are subtle

  32. 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?

  33. 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.

  34. 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?

  35. 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 )

  36. 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?

  37. GI Bleeding Clinical presentation Hematochezia Passage of bright red blood from rectum Occult Slow GI bleeding . Not apparent to patient (Iron Deficient / Fecal Occult Blood positive) Obscure Bleeding of any sort which is not easily pinpointed by usual diagnostic techniques

  38. Approach to the Bleeding Patient Assess the severity of bleeding Hemodynamics % Intravascular Severity of Bleed Volume Loss Shock ( resting hypotension) 20-25 Massive Postural Change 10-20 Moderate Normal <10 Minor Resuscitation IV Access Monitor vitals Transfuse when necessary Correct Coagulopathy ie platelets, fresh frozen plasma, Vitamin K

  39. Take a History 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!

  40. Tests Hb Platelets MCV + / - Ferritin INR Urea Localize bleed ( Endoscopy, Angiography) Treat bleed ( pharmacologic, endoscopic, angiographic, surgery)

  41. 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 MCV 99 Platelets 125 Urea 15 Creatinine 89 • Normal AST/ ALT /ALP Bili 88 INR 1.5 Albumin24

  42. Case 4 What is the cause of bleeding? What is the differential diagnosis? What are the indicators for urgent endoscopy?

  43. Causes of Upper GI Bleeding Jutabha et al. Med Clin North Am 1996 UCLA. Prospective series of 1000 patients.

  44. 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

  45. 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

  46. Causes of Portal Hypertension Be wary of Splenic Vein Thrombosis

  47. Case 4 What is the management of variceal bleeding?

  48. 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

  49. 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

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