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Upper GIT Haemorrhage

Upper GIT Haemorrhage. Prof/ Walid Elshazly. A prof of surgery. Acute Gastrointestinal Bleeding. Prof/ Walid Elshazly. GI Bleeding. Clinical Presentation Acute Upper GI Bleed Acute Lower GI Bleed. Clinical Presentation. Hematemesis: bloody vomitus (bright red or coffee-grounds)

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Upper GIT Haemorrhage

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  1. Upper GIT Haemorrhage Prof/ Walid Elshazly A prof of surgery

  2. Acute Gastrointestinal Bleeding Prof/ Walid Elshazly

  3. GI Bleeding • Clinical Presentation • Acute Upper GI Bleed • Acute Lower GI Bleed

  4. Clinical Presentation Hematemesis: bloody vomitus (bright red or coffee-grounds) Melena: black, tarry, foul-smelling stool Hematochezia: bright red or maroon blood per rectum Occult: positive guaiac test Symptoms of anemia: angina, dyspnea, or lightheadedness

  5. Patient Assessment • Hemodynamic status • Localization of bleeding source • CBC, PT, and T & C • Risk factors • Prior h/o PUD or bleeding • Cirrhosis • Coagulopathy • ASA or NSAID’s

  6. Resuscitation • 2 large bore peripheral IV’s • Normal saline or LR • Packed RBCs • Correct coagulopathy

  7. Location of Bleeding • Upper • Proximal to Ligament of Treitz • Melena (100-200 cc of blood) • Nasogatric aspirate • Lower • Distal to Ligament of Treitz • Hematochezia

  8. Acute UGIBDemographics • 10,000 - 20,000 deaths annually • Mortality stable at 10% • 80% self-limited • Continued or recurrent bleeding - mortality 30-40%

  9. Acute UGIBPrognostic Indicators • Cause of bleeding • Severity of initial bleed • Age of the patient • Comorbid conditions • Onset of bleeding during hospitalization

  10. Acute UGIBPrognostic Indicators Tedesco et al. ASGE Bleeding Survey. Gastro Endo. 1981.

  11. Acute UGIBDifferential Diagnosis

  12. Peptic ulcer disease Gastric ulcer Duodenal ulcer Portal hypertension Esophagogastric varices Gastropathy Esophagitis Mallory-Weiss tear Dieulafoy’s lesion Vascular anomalies Hemobilia Hemorrhagic gastropathy Aortoenteric fistula Neoplasms Gastric cancer Kaposi’s sarcoma Acute UGIBDifferential Diagnosis

  13. Acute UGIBFinal Diagnoses of the Cause in 2225 Patients Tedesco et al. ASGE Bleeding Survey. Gastro Endo. 1981.

  14. Acute UGIBCauses in CURE Hemostasis Studies (n=948) Savides et al. Endoscopy 1996;28:244-8.

  15. Endoscopic Appearanceof Ulcers

  16. Thermal Bipolar probe Monopolar probe Argon plasma coagulator Heater probe Mechanical Hemoclips Band ligation Injection Epinephrine Alcohol Ethanolamine Polidocal Endoscopic Therapy

  17. Endoscopic Therapy Laine and Peterson New Eng J Med 1994;331:717-27.

  18. Adjuvant Medical Therapy • Acid suppression (intragastric pH > 4) • Histamine 2 Receptor Antagonists (H2RAs) • Ranitidine (Zantac) • Famotidine (Pepcid) • Proton Pump Inhibitors (PPIs) • Pantoprazole (Protonix) • Lansoprazole (Prevacid) • Esomeprazole (Nexium)

  19. Mallory-Weiss Tear

  20. Esophageal Varices

  21. Variceal Band Ligation

  22. Variceal Band Ligation

  23. MEDICAL THERAPYAcute Variceal Bleeding • Vasopressin/Glypressin • Nonselective vasoconstrictor • 50% efficacy in controlling bleeding • 25% vasospastic side effects • Octreotide • Cyclic octapeptide analog of somatostatin • Longer acting than somatostatin • Equivalent to sclerotherapy and improves endoscopic results

  24. TIPS Coronary Vein IVC Splenic Vein Portal Vein

  25. Aortoduodenal Fistula Aorta Duodenum Fistula Graft

  26. Lower GIT Haemorrhage Prof/ Walid Elshazly A prof of surgery

  27. Lower gastrointestinal hemorrhage Lower gastrointestinal hemorrhage refers to a spectrum of intestinal bleeding that arises distal to the ligament of Treitz. Incidence rate: 20/100,000/ year Disease of the elderly 200 fold increase from the 3rd to 9th decades of life Mortality 2-4 % 80 – 85 % bleeding stop spontaneously

  28. BLEEDING FRANK OCCULT SMALL BLEED MASSIVE BLEED (rare) ANAEMIA ٍٍٍSELF LIMITED ٍٍٍNON-SELF LIMITED

  29. Degrees of hemorrhage Lower gastrointestinal bleeding presents with varying degrees of hemorrhage. Minor and self-limited, patient describe the passage of 100–250 mL of blood, possibly a few clots, and often mixed with mucous. 2) Major and self-limited Patients experiencebrisk, copious bleeding 3) Major and ongoing ? Patients present with massive and continuous hemorrhage associated with hypovolemia.

  30. Lower gastrointestinal hemorrhage Massive lower intestinal hemorrhage is difficult to define. Patients often describe massive bleeding into their commode even when a small amount of blood discolors the water. True massive intestinal hemorrhage typically include Hematocrit less than 30%, Transfusion requirements (up to 3–5 units of blood/blood products), or Orthostasis requiring resuscitation.

  31. Lower gastrointestinal hemorrhage The hemorrhage may present as melena or hematochezia. Melena typically suggests bleeding from a more proximal source in the colon or small intestine. Hematochezia suggests left colonic, rectal, or anal sources. It is wise to note that upper gastrointestinal hemorrhage may present with the rectal bleeding given blood’s cathartic effect and rapid intestinal transit.

  32. Etiologies Common causes for lower gastrointestinal hemorrhage include Diverticulosis (30 - 50%) Angiodysplasia (20 - 30%) Neoplastic (10- 15%) cancer, polyp Inflammatory (15 - 20%) Inflammatory bowel disease. Ischemic colitis, and Anorectal diseases (5-10 %) Unusual causes include Hemorrhage also stems from intestinal tumors or malignancies. Nonsteroidal antiinflammatory drug (NSAID)-related nonspecific colitis, Meckel’s diverticulum, and

  33. LGIBDiverticulosis(30 - 50%) Sac-like protrusions of the colonic mucosa, particularly at locations where blood vessels (vasa recta) enter the colon. LGIB (ARTERIAL) when the diverticula blood supply is damaged Trauma, Ischemia, or Poor clotting).

  34. Diverticulosis

  35. LGIBDiverticulosis(30 - 50%) 5 – 15 % of people with diverticula will have LGIB. Bleeding is PAINLESS. The bleeding In most cases, bleeding ceases spontaneously In 10 to 20 %of cases, the bleeding continues unabated in the absence of intervention

  36. Diverticular Bleeding

  37. LGIBDiverticulosis(30 - 50%) The risk of rebleeding After an episode of bleeding is approximately 25% Increases to 50% among patients who have had two or more prior episodes of diverticular bleeding. Diverticulitis- not a cause of GIT bleeding

  38. LGIB Angiodysplasia (20 - 30%) Angiodysplasia (20 - 30%) (or AVM, or Vascular Ectasias) Composed of ectatic, dilated, thin-walled arteriovenous communications located within the submucosa and mucosa of the intestine. lined by endothelium alone.

  39. LGIB Angiodysplasia (20 - 30%) No one is quite certain precisely why angiodysplasias occur. Current hypotheses suggest a loss of vascular integrity related to loss of transforming growth factor (TGF) β signaling cascade or a deficiency in mucosal type IV collagen.

  40. Adults Angiodysplasia (20 - 30%) Risk Factors Older (65 y.o.) > Younger End stage renal disease Von Willebrand's disease Aortic stenosis? (Heyde’s syndrome), Hereditary hemorrhagic telangiectasias (Osler-Weber-Rendu) Low fiber diet Obesity

  41. LGIB Angiodysplasia (20 - 30%) LGIB (VENOUS) is usually occult and PAINLESS. Located within Cecum 37%, Sigmoid 18%, Ascending 17%, Rectum 14%, Transverse and Descending 7%.

  42. LGIB Angiodysplasia (20 - 30%) Angiography remains the gold standard for the diagnosis of angiodysplasia. After injection of contrast, a series of images are collected in three phases. Early venous filling which normally occurs in later phases. During the next phase, capillary phase, small, tortuous tufts are seen entangled and filled with contrast. Finally, the late phase study demonstrates a persistent of this arteriovenous tuft and a persistent of a slow, emptying vein.

  43. LGIB Angiodysplasia (20 - 30%) When angiography identifies a bleeding angiodysplasia, treatment with Embolization therapy or Directed infusion of vasopressin will decrease or stop the bleeding.

  44. LGIB Angiodysplasia (20 - 30%) The colonoscopic criteria in describing these lesions. The mucosal surface contains a cherry red lesion that is typically flat. The lesions are greater than 2 mm in size and have a “fern-like” appearance. A central feeding vessel is not always visible.

  45. LGIBNeoplastic (10- 15%) Polyps Cancer

  46. LGIBInflammatory (15 - 20%) Radiation Intestinal damage due to fibrosis and ischemia. IBD Ulcerative Crohn’s Disease Radiation colitis Sever Crohn’s Disease Ulcerative colitis

  47. LGIBInflammatory (15 - 20%) Infectious (E. Coli, C. Difficile, C. Jejuni …) Ischemic (Hypoperfusion and Vasoconstriction) Hypotension, Heart Failure, Arrhythmia Vasculitis Infective colitis Ischemic colitis

  48. LGIBInflammatory (15 - 20%) Pseudomembransous Colitis Complication of antibiotic therapy that causes severe inflammation, irritation and swelling of the colon mucosa. Almost any antibiotic can cause this condition. Clostridium difficile, which occurs normally in the intestine, overgrows when antibiotics are taken. This bacterium releases a powerful toxin which causes the symptoms.

  49. LGIBInflammatory (15 - 20%) Pseudomembransous Colitis Ampicillin is the most common cause of this condition in children. Stopping the antibiotic with rehydration therapy and metronidazole is usually used to treat the disorder.

  50. LGIBAno-rectal causes (5 – 10%) Hemorrhoids (< 50 y.o. most common) Anal fissures (most common in child) Anal fistulas Proctitis Gonorrheal or mycoplasmal infections Rectal trauma Foreign objects Rectal CA Rectal polyp

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