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Eamc endoscopic radiologic conference 2014

  1. CASE 1 EP, 34 Female CC: Fever 1 month PTA Fever Tmax 38.9 Non-productive cough Epigastric pain Worked up - normal 2 weeks PTA Increased severity of epigastric pain, with associated vomiting, no diarrhea Persistence of fever Admission
  2. PMHx: IgA nephropathy 2009 - on Prednisone Bronchial asthma 2012 Persistent chronic epigastric pain x~1year- s/p EGD 2013: Gastritis (-) HPN, DM, PTB FHx: Unremarkable PSHx: Non-smoker Non-alcoholic beverage drinker Denies illicit drug use
  3. PE: Conscious, coherent, not in CP distress BP 120/80 CR 90 RR 18 Temp 38.9C Pink palpebral conjunctiva, anicteric sclerae Supple neck, cervical lymphadenopathies Symmetrical chest expansion, no retractions, clear breath sounds Adynamic precordium, AB 5th ICS L MCL, no murmurs Globular abdomen, NABS, soft, tenderness at the epigastric and RUQ area, no organomegaly, no mass Pulses full and equal, no edema DRE: no mass, no melena
  4. Course in the ward • Managed as a case of fever of unknown origin • Laboratory work ups: CBC Chest CT scan Blood CS Whole abd CT scan Typhidot Serum Galactomanan 2D echo Amylase, Lipase Urinalysis
  5. CBC: HGB 10.2 HCT 0.31 WBC 16.83 NEUTRO 85.6 LYMPHO 4.6 MONO 8.6 PLT 385 Urinalysis: Yellow Clear SG 1.020 PH 6.0 Protein +2 Glucose Neg WBC 2/hpf RBC 2/hpf Epith cells 2/hpf Bacteria 5/hpf CC: Na 134 K 4.8 Cl 97.0 Crea 176.8 Amylase 66 Lipase 18
  6. • Blood CS: no growth • Typhidot – IgG, IgM: Negative
  7. Interpret whole abdominal CT scan
  8. What is your impression? What are your differential diagnoses? What is your next diagnostic plan? Interpret EGD
  9. What is your impression? Interpret colonoscopy
  10. What would be your next diagnostic plan? Interpret upper GI series
  11. What is your final impression? What would be your plan of management?
  12. What is the ideal management in dealing with fistula?
  13. • Colonic-duodenal fistulas are rare, and may be secondary to benign or malignant conditions • Most common lesion - carcinoma of the transverse colon Xenos E S, Halverson J D. Duodenocolic fistula: case report and review of the literature. J Postgrad Med 1999;45:87
  14. • Of the reported cases of benign duodenocolic fistula, 30 have followed disease primarily in the duodenum - peptic ulcer, diverticulum and as a sequel to gastrectomy • Colonic disease - regional enteritis, ulcerative c olitis, appendicitis, diverticulosis coli and typhoid fever accounted for 20
  15. • Gallbladder - cholecystitis and biliary tract surgery for 17 • The origin was uncertain in 23 cases- developmental, tuberculosis, foreign body, etc. J. R. McQuaide. G. Naidoo. Benign Duodenocolic Fistula, A Report of 3 Cases. South African Medical Journal. 1979.600-604
  16. Clinical Presentation • Diarrhea - occasionally bloody and often intermittent • Weight loss • Upper abdominal colicky pain • Vomiting or foul eructations
  17. • Symptoms tend to be episodic, with short exacerbations and long remissions. • Emaciation follows, with electrolyte imbalance • Superimposed on these basic features may be other signs and symptoms due to the primary condition
  18. Treatment • Current therapeutic options include medical treatment and surgical management. • Spontaneous healing of fistulas without treatment is rare. • Various placebo-controlled clinical trials of medical treatment have shown a fistula self- closure rate of only 6% to 13%.
  19. • For symptomatic internal fistulas, surgical resection of the affected bowel segments was required. • Small fistulas can be occluded with fibrin glue or clipping by endoscopy whereas in large fistulas, endoscopic therapy with a detached endoloop and hemoclips is an alternative bridging method until final surgical repair.
  20. • A review of the English literature showed only sixty-three cases of CD with coloduodenal fistula. Surgery remains the mainstay of therapy. Meng-Tzu Weng, Shu-Chen Wei, Yu-Wen Tien, I-Lun Shih, Jau-Min Wong. Crohn’s Disease Complicated with Duodenocolic Fistula: A Case Report
  21. • Case series have described the successful use of cyanoacrylate glues for the endoscopic treatment of refractory bile leaks, pancreatic fistulae and a variety of other GI tract fistulae; however, there are no controlled trials. Seewald S. Endoscopic treatment of biliary leakage with n-butyl-2-cyanoacrylate. Gastroint Endosc 2002; 56:916-9
  22. • A recent randomized trial comparing fibrin glue with observation only for Crohn’s patients with anal fistulae found higher closure rates in the glue patients (38% vs 16%, P Z.04) • Numerous case series report achieving prompt closure with the use of fibrin glue for enterocutaneous fistulae, including persistent gastrocutaneous fistulae after gastrostomy tube removal.
  23. • Fibrin glue has been used to close esophageal perforations in case reports. • A single case report exists with successful closure of a duodenal perforation with fibrin glue.
  24. • A case report in which a covered colonic stent was used successfully to close the fistula by using an anooral guide wire (”body floss” technique). Shubhang Kulkarni, Covered Stent Placement for Duodenocolic Fistula: A Novel Use of the ”Body Floss” Technique. Journal of Vascular and Interventional Radiology.Pages 729–730, May 2011
  25. End of first case
  26. Case 2 EB, 38 Male CC: Jaundice and melena 7 years PTA: Jaundice Local hospital: SGPT = 177 SGOT = 151 ALP= 441 HBsAG = NR UTZ: • enlarged left liver lobe • low normal sized right liver lobe with several parenchymal calcification • left intrahepatic duct calculi • Intrahepatic ducts are mildly dilated • 4.6x3.8 cm hyperechogenic focus at region of porta hepatis Hepatobiliary TB TB-DOTS x 6months Lost to follow-up
  27. 5 years PTA: Persistence of jaundice Hematochezia EGD: Unremarkable Colonoscopy: Not consented CT SCAN whole abdomen: • enlarged left liver lobe • atrophied right liver lobe with several parenchymal calcifications • segmental narrowing over D1-D3 and sigmoid area Treated with anti-koch’s for 6 months but lost to follow up
  28. 2 days PTA: Melena 2x/day ~ 50ml per episode Epigastric pain 8/10 no radiation to the back No hematochezia Still with jaundice At the ER: Hematochezia ~400mL BP 80/50 mmHg, CR 110/min Admission
  29. PPMHx: (+) Hepatobiliary TB – treated x 6 months 2007 (-) HPN, DM, dyslipidemia, hepatitis (-) renal disease (-) allergies, asthma (-) cancer, stroke, heart attack (-) trauma and surgery PSHx: Non-smoker Non-alcoholic beverage-drinker Previous use of illicit drugs – stopped 4 years ago FHx: No liver disease, cancer, stroke, DM (+) HPN
  30. ROS: (-) cough (-) dyspnea, chest pain, palpitations (-) constipation, diarrhea (-) dysuria PE: Awake, alert, coherent BP= 80/50, CR= 110/min, RR= 18 Temp= 37; BMI= 22 Pale palpebral conjunctiva, icteric sclera, no active dermatoses Non-hyperemic PPW, supple neck, no cervical LAD Symmetrical chest expansion, clear breath sounds Adynamic precordium, AB 5th LICS MCL, (-) murmurs Abdomen flabby, normoactive, soft, no masses and tenderness. liver span 10 cm from MCL, traube’s space obliterated, no caput, no spider angioma Pulses poor and equal, no edema and cyanosis DRE: red stool tactating finger
  31. CBC: 6/27 7/4 HGB 86 66 HCT 269 197 WBC 7.9 10.8 NEUTROPHILS 64 80 LYMPHOCYTES 30 17 PLT 191 298 CC: 6/27 7/4 NA 134 135 K 3.8 3.9 BUN 5.8 CREA 122 88 6/27 PT INR TB 5 mg/dl DB 3 mg/dl IB 1.1mg/dl albumin 25.47 AST 114 ALT 113 ALP 620 HBsAg NR Anti-HBS NR Anti-HCV NR
  32. What are your differential diagnoses? What is your diagnosis? What is your next diagnostic plan? Interpret the endoscopy
  33. What is your next diagnostic plan? Interpret duodenoscopy
  34. What is your diagnosis? What is your next diagnostic plan? Interpret CT angiogram
  35. CT ANGIOGRAPHY • Lobulated vascular structure within dilated CHD • ( consider a vascular malformation or pseudoaneursym from a branch of right hepatic artery) • Mildly dilated IHD, CBD, distended GB & cystic duct secondary to iso to hyperdense foci in CHD & CBD (most likely blood clots) • Contracted right liver lobe and enlarged left liver lobe with chronic liver parenchymal disease and calcifications • Distented GB with thickened walls and soft calculi • Tiny CHD calculus • Prominent spleen • Paraesopahgeal,perigastric,peripancreatuc and perisplenic varices
  36. HEPATIC ARTERY ANEURSYM • 12% of visceral aneurysm • 20% Intrahepatic • 30% right hepatic artery – 2nd to common hepatic artery • Tuberculosis incidence? Abbas J Vasc Surg 2003 Taylor Postgrad Med J 1986
  37. TUBERCULOSIS • Most – saccular, pseudoaneurysm and rapid growth • Mechanism – Erosion of vessel wall by contiguous focus of TB – Direct seeding of the intima, adventitia or media via vasa vasorum TSURUTANI Int. Med 2000 Husen annals Saudi Med 1997
  38. HEPATIC ARTERY ANEURSYM • Quincke’s triad of hemobilia (jaundice, right upper quadrant pain, bleeding) – 1/3 of cases • Risk of rupture 14% • Rupture biliary tree 41% • Mortality – 40% • Angiography – gold standard Trauman – Mays Surg Clinics of N.A. 1977 Harlaftis Amer Journal of Surg 1977 Singh world Journal of Gastroenterology 2006
  39. HEPATIC ARTERY ANEURSYM - TREATMENT • Endovascular technique (preferred) (Lumsden 1996) – Coils (large feeding vessel), particular embolics, glue, or Onyx ) – Complications (Abbas 2003) • Short term – hepatic ischemia, abcess and cholecystitis • Long term- recanalization • Surgery – risk of hepatic necrosis – small – 26 collaterals liver (Michles 1966) – Ligation, excision, endoaneurysmorrhaphy, wrapping. Wiring, hepatic lobectomy, suture of aneurysm to liver (Ariyan 1975) – High risk post operative complications (Ikeda 2010)
  40. End of second case
  41. NW, 47 Male 7 days: Epigastric pain 3 days: Fever Anorexia Malaise 2 days: Melena Dizziness SEHx: Non-smoker 1 bottle of gin daily x 10 years Marijuana use Garbage collector, fruit sorter Case 3 CC: Melena PPMHx: (-) HPN, DM, TB, CVA, CAD (-) previous surgery (-) intake of NSAID, ASA, steroid
  42. Awake, coherent, cooperative, weak-looking, not in CP distress 100/60, 100-110/min, 37-38.6’C Pale palpebral conjunctivae, anicteric sclerae Clear breath sounds, no spider angioma Flat abdomen, NABS,, direct tenderness at the epigastric area, hepatomegaly 14cm, (+) obliterated traube’s space, no ascites, no caput medusa, no spider angioma Good sphincteric tone, no mass, melena CBC Hgb 62 g/L Hct 0.190 WBC 15.4 x109/L Neutro 84% Lympho 12% Mono 4% Platelets 401 CC Crea 63umol/L BUN 6.7umol/L Na 132 K 3.3
  43. What is your impression? What is your next diagnostic plan? What are your differential diagnoses? Interpret endoscopy
  44. During endoscopy, what would you do next?
  45. Would you revise your impression? What would be your next diagnostic examination?
  46. What is your final impression? What is your next diagnostic examination?
  47. Endoscopic drainage
  48. Ultrasound-guided aspiration of the right liver lobe abscess How would you manage the right liver lobe abscess?
  49. Gastric ulcer perforating to liver Pyogenic liver abscess penetrating to stomach incidenc e 6 case reports 3 case reports presenta tion Melena +/- epigastric pain, then fever, +/- jaundice Fever, +/- jaundice, +/- epigastric pain, then melena Diagnost ics Chronic looking ulcer Multiple ulcers Treatme nt Surgical medical Spontaneous fistulization o S. Leite, A. P. Silva, et al. Unusual cases and technica Liver Abscess Complicated Eun-Sun Kim, et al Journal of gastroenterology Hepatogastric fistula: a rare Gandham VS, Pottakkat B, P BMJ Case Rep.2014 Jul 17;2 micking . Caletti penetrating subcapsular g into the liver. y 0
  50. Follow-up EGD before after
  51. End of third case
  52. Post-ERC

Notas del editor

  1. Benign Duodenocolic Fistula A Report of 3 Cases J. R. McQUAIDE. G. NAIDOO South African Medical Journal p600-604. Apr 7 1979
  2. 1. The diarrhoea, which is a constant feature, was originally attributed to the direct passage of duodenal contents to the colon, thus bypassing the small bowel. Most evidence now favours the theory that retrograde passage of colonic contents into the duodenum with inevitable bacterial contamination causes jejunitis and intestinal hurry. (The diminution of symptoms after proximal colostomy, or after the use of antibiotics capable of controlling colonic bacteria, supports this theory.)