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Discussant_Slides.ppt
- 1. CPC 01.12.10 John O. Clarke,M.D. Assistant Professor of Medicine Director of Esophageal Motility Johns Hopkins University
- 2. Questions to Address (1)Whatwere the patient’s risk factors for bleeding? (2)How does HIV affect the differential? (3)What is the most likely diagnosis?
- 3. Differential Diagnosis ofUpper GI Bleed • Ulcerative or erosive – Idiopathic – Drug-induced – H. pylori – Other Infectious – Stress-induced – Zollinger-Ellison Syndrome • Esophagitis – Peptic – Infectious – Pill-induced • Portal hypertension – Varices – Portal hypertensive gastropathy • Vascular – Idiopathic angiomas – Osler-Weber-Rendu syndrome – Dieulafoy’s lesion – Gastric antral vascular ectasia – Radiation-induced telangectasia – Blue rubber bleb nevus syndrome • Traumatic or post-surgical – Mallory-Weiss tear – Surgical anastomosis – Aortoenteric fistula – Post-polypectomy • Tumors
- 4. DDx of MassiveUpper GI Bleed • Ulcer – Idiopathic – Drug-induced – H. pylori – Other infections • Esophagitis – Infectious • Portal hypertension – Varices • Vascular – Dieulafoy’s lesion • Traumatic – Mallory-Weiss tear – Aortoenteric fistula • Tumors
- 5. What affect doesHIV have? • All items on the prior slide are still possible • Infection and tumors become more likely
- 6. Relationship of CD4Count to Infection & Tumor Wilcox C M. Gut 2008;57:861-870
- 7. What Were ThisPatient’s Risk Factors? (1) Esophageal ulcer (5-6cm but clean-based) (2) Esophageal varices (though small) (3) Gastric polyp (possible neoplasm) (4) Bluish lesion at GEJ (vascular, infection or tumor)
- 8. Esophageal Ulcer “An ulcerwas found in the mid esophagus 5-6cm in length . . . not bleeding” • What is the differential diagnosis? (1) Pill-induced (2) Infectious - HSV (IgG +) - CMV (PCR +) - Primary HIV - Other (no indication from history) (3) Neoplasm - Adenocarcinoma - Squamous cell - Lymphoma - Kaposi’s sarcoma • Unlikely to be the primary source unless it eroded into a varix/artery or rapidly grew in size
- 9. Esophageal Varices “There were2-3 small associated esophageal varices . . . 2 bands were placed” • Esophageal varices are indicative of portal hypertension, either from cirrhosis and/or portal vein thrombosis • The patient clearly had cirrhosis based on history, exam, blood labwork (prothrombin time, albumin, bilirubin, platelets, ammonia), and ascitic fluid analysis • Mortality from variceal hemorrhage remains approximately 35% • On a side note, he should have had antibacterial therapy given an active GI bleed in the context of cirrhosis and known ascites . . . • Could be the source of bleeding but slightly atypical for small varices to result in catastrophic hemorrhage
- 10. Gastric polyp “A 2-cmpolyp was seen near the angularis. This lesion was not biopsied” • DDx – Benign (hyperplastic, fundic gland polyp, adenoma) – Primary cancer • Gastric adenocarcinoma – Metastatic or diffuse • Lymphoma • Kaposi’s sarcoma • Unlikely to be the source of bleeding
- 11. Bluish Lesion atGEJ “A 1.5 cm bluish ‘bean-like’ lesion was seen at the GEJ. This appeared to be a vermiform lesion rather than a visible vessel” • What is this? – Tumor • Kaposi’s sarcoma • Lymphoma • Metastatic – Vascular • Dieulafoy’s lesion (atypical to be at GEJ) • Gastric varix (atypical description) – Infection (atypical) • Unlikely to be primary source of bleeding (unless eroded into a varix)
- 12. Other Factors toConsider (1)The stomach was not cleared during endoscopy (2)Ascitic fluid represents portal hypertension; however, infection/neoplasm could be superimposed (SAAG less accurate) (3) Travel to Asia & Mexico may have led to atypical exposure not listed above (4) Left pleural effusion less common with ascites than right (and may be masking another process)
- 13. Specific Topics ToCover
- 14. Gastrointestinal CMV • Occursin up to 5% of untreated patients with AIDS • Most cases occur when CD4 < 50 • Prior to HAART, universally fatal on diagnosis – Colitis: 4 months – Esophagitis: 8 months • Often complicated by hemorrhage or perforation • Can occur anywhere throughout the GI tract • Multiple large ulcers • Multiple biopsies required to make diagnosis
- 15. Gastrointestinal HSV • Lesscommon than CMV in patients with HIV/AIDS • Occurs in 3-5% of HIV patients with esophagitis • Rarely causes ulcers larger than 2cm • Usually causes multiple ulcers
- 16. Primary HIV Ulcers •Mechanism poorly understood • May occur in 4-12% of patient with HIV/AIDS with esophageal symptoms • Typically very large in size; often solitary • Can be associated with bleeding or perforation • Biopsies are routinely non-diagnostic • Responds to prednisone or thalidomide
- 17. Kaposi’s Sarcoma • Low-gradevascular tumor a/w HHV-8 • 20,000 times more frequent in AIDS patients than general population • GI involvement in 40% of patients • Appear as hemorrhagic nodules on endoscopy • Usually associated with skin findings (not reported in this case) • HH8 also associated with primary effusion lymphoma (theoretically possible in this case but less likely)
- 18. Non-Hodgkin Lymphoma • 25-40%of HIV patients eventually develop malignancy; 10% are NHL • Risk of NHL 60-165 fold greater if HIV • CD4 count usually < 100 • Can present as esophageal ulcers, polyps or nodules in the GI tract • Can be associated with hemorrhage (although not classic)
- 19. What Remains OnThe Differential? • Esophageal varices related to HBV/Cirrhosis • Gastrointestinal CMV • Possible malignancy (Kaposi’s Sarcoma > NHL) • Possible primary HIV ulcer
- 20. Clinical Diagnosis • Kaposi’sSarcoma • Gastrointestinal CMV • Cirrhosis re: HBV with esophageal varices • HIV/AIDS