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ACUTE GI BLEEDING

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ACUTE GI BLEEDING

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ACUTE GI BLEEDING

  1. 1. 1 Prepared by
  2. 2. OUTLINE 2  Introduction  Definition  Epidemology  classificationCause and risk factors  Aproach to patients with acute GI bleeding  Management
  3. 3. Introduction 3 Figure 23.2 The principal function of GIT is to provide the body with a continuous supply of nutrients, water and electrolytes.
  4. 4. Introduction…. Histology of the Alimentary Canal  From esophagus to the anal canal the walls of the GIT 4 have the same four layers From the lumen outward they are the 1. Mucosa, 2. Submucosa, 3. Muscularis externa, and 4. Serosa  Each layer has a predominant tissue type and a specific digestive function
  5. 5. Introduction…Blood Supply to Digestive System  The blood vessels of the GI-system are part of a more extensive system 5 called the splanchric circulation.  splanchnic BF =1000 ml/min  It includes the blood flow through the GIT itself plus through the spleen, pancreas and the liver.  All of the blood that courses through the gut, spleen and pancreas then flows immediately into the liver by way of the portal vein.  In the liver, blood passes through million of liver sinusoids and finally leaver the liver by way of the hepatic veins that empty into the inferior venacava of the general circulation.
  6. 6. Blood Supply to GIT (cont’d) 6
  7. 7. Gastrointestinal Bleeding: 7 Bleeding from the gastrointestinal (GI) tract may present in five ways.  Hematemesis is vomitus of red blood or "coffee-grounds" material.  Melena is black, tarry, foul-smelling stool.  Hematochezia is the passage of bright red or maroon blood from the rectum.  Occult GI bleeding (GIB) may be identified in the absence of overt bleeding by a fecal occult blood test or the presence of iron deficiency.  Finally, patients may present only with symptoms of blood loss or anemia such as lightheadedness, syncope, angina, or dyspnea.
  8. 8. Classification of GI Bleeding 8  UGIB  blood loss proximal to ligament of Treitz(DJ flexure)  LGIB blood loss distal to ligament of Treitz (DJ flexure)  Ligament of treize….  Upper GI bleeding 4x more common than lower GI bleeding
  9. 9. Suspencery ligament of doudenum or ligament of tertz 9
  10. 10. UGIB 10  Upper GI bleeding refers to bleeding from oesophagus, stomach, duodenum.  Can be: Variceal bleeding Non-variceal bleeding
  11. 11. Sources of Gastrointestinal Bleeding 11 Upper Gastrointestinal Sources of Bleeding  The annual incidence of hospital admissions for upper GIB (UGIB) in the United States and Europe is 0.1%, with a mortality rate of 5–10%.  Patients rarely die from exsanguination; rather, they die due to decompensation from other underlying illnesses.  The mortality rate for patients <60 years in the absence of major concurrent illness is <1%.  Independent predictors of rebleeding and death in patients hospitalized with UGIB include increasing age, comorbidities, and hemodynamic compromise (tachycardia or hypotension).
  12. 12. Sources of bleeding in patients hospitalized for upper gi bleeding 12 Sources of Bleeding Proportion of Patients, % Ulcers 31–67 Varices 6–39 Mallory-Weiss tears 2–8 Gastroduodenal erosions 2–18 Erosive esophagitis 1–13 Neoplasm 2–8 Vascular ectasias 0–6
  13. 13. 13  Peptic ulcers are the most common cause of UGIB, accounting for up to 50% of cases; an increasing proportion is due to nonsteroidal anti-inflammatory drugs (NSAIDs), with the prevalence of Helicobacter pylori decreasing.  Mallory-Weiss tears account for 5–10% of cases.  The proportion of patients bleeding from varices varies widely from 5 to 40%, depending on the population.  Hemorrhagic or erosive gastropathy (e.g., due to NSAIDs or alcohol) and erosive esophagitis often cause mild UGIB, but major bleeding is rare.
  14. 14. 14 PUD (DU & GU)  Are break in the gastric or duodenal mucosa that arises when the normal factors are impaired or overwhelmed by acid or pepsin Erosive Gastritis  Because this process is superficial, it is a relatively unusual cause of severe gastrointestinal bleeding (< 5% of cases).
  15. 15. MW TEAR (LACERATION) 15  Classically, Mallory-Weiss tears are mucosal lacerations at the GEJ or in the cardia of the stomach  associated with repeated retching or vomiting  another important cause of nonvariceal UGIB.  acute UGIB secondary to Mallory-Weiss tears bleeding episodes are self-limited.
  16. 16. ESOPHAGITIS 16  Is a common medical condition,  usually caused by gastroesophageal reflux.  Less frequent causes include  infectious esophagitis (in patients whoare immunocompromised),  radiation esophagitis, and  esophagitis from direct erosive effects of medication or corrosive agents.
  17. 17. VASCULAR ECTASIAS 17  Vascular ectasias, also referred to as “angiomas,” “arteriovenous malformations,” and “angiodysplasia,” are another source of acute and chronic nonvariceal UGIB  Abnormal communication  The severity of bleeding can also range from trivial to severe  Vascular ectasias are associated with chronic renal insufficiency or failure; valvular heart disease, specifically aortic stenosis; and congestive heart failure.
  18. 18. Varices 18  There is communication between the intra-abdominal splanchnic circulation and the systemic venous circulation through the esophagus.  When portal venous blood flow into the liver is impeded by cirrhosis or other causes, the resultant portal hypertension induces the formation of collateral bypass channels.  The increased pressure in the esophageal plexus produces dilated tortuous vessels called varices.  Variceal rupture produces massive hemorrhage into the lumen.  produce no symptoms until they rupture
  19. 19. LGIB 19  Lower GI bleed refers to bleeding arising distal to the ligament of Treitz (DJ flexure)  Although this includes jejunum and ileum bleeding from these sites is rare.  Vast majority of lower GI bleeding arises from colon/rectum/anus  over 90% of cases arise from the colon
  20. 20. CAUSES OF Acute LGIB Majorcauses  Diverticulosis(40%)  Colitis  IBD  Ischemia  Infection  Angiodysplasia (avm)(30%)  Neoplasia  Anorectal  Hemorrhoids  Fissure 20
  21. 21. Causes... 21 Causes of Colon bleeding Causes of Rectal bleeding Causes of Anal bleeding Diverticular Disease Polyps Haemorrhoids Polyps Malignancy Fissure Malignancy Proctitis Malignancy Colitis
  22. 22. IBD 22  Chronic inflammation of the colon.  ulcerative colitis & Crohn disease  is characterized by severe inflammation and ulceration of the colon and rectum  Patients with inflammatory bowel disease (especially ulcerative colitis) often have diarrhea with variable amounts of hematochezia
  23. 23. Differentiation of Upper from Lower Gib  Hematemesis indicates an upper GI source of bleeding 23 (above the ligament of Treitz).  Melena indicates that blood has been present in the GI tract for at least 14 h (and as long as 3–5 days).  The more proximal the bleeding site, the more likely melena will occur.  Hematochezia usually represents a lower GI source of bleeding, although an upper GI lesion may bleed so briskly that blood does not remain in the bowel long enough for melena to develop.  When hematochezia is the presenting symptom of UGIB, it is associated with hemodynamic instability and dropping hemoglobin.
  24. 24. 24  Bleeding lesions of the small bowel may present as melena or hematochezia.  Other clues to UGIB include hyperactive bowel sounds and an elevated blood urea nitrogen level (due to volume depletion and blood proteins absorbed in the small intestine).  A nonbloody nasogastric aspirate may be seen in up to 18% of patients with UGIB—usually from a duodenal source.  Even a bile-stained appearance does not exclude a bleeding postpyloric lesion because reports of bile in the aspirate are incorrect in 50% of cases.  Testing of aspirates that are not grossly bloody for occult blood is not useful.
  25. 25.  Obscure GIB is defined as persistent or recurrent bleeding for which no source has been identified by routine endoscopic and contrast x-ray studies; it may be overt (melena, hematochezia) or occult (iron-deficiency anemia).  Current guidelines suggest angiography as the initial test for massive obscure bleeding, and video capsule endoscopy, which allows examination of the entire small intestine, for all others. 25 GIB of Obscure Origin
  26. 26. 26  Push enteroscopy, with a specially designed enteroscope or a pediatric colonoscope to inspect the entire duodenum and part of the jejunum, also may be considered as an initial evaluation.  A systematic review of 14 trials comparing push enteroscopy to capsule revealed "clinically significant findings" in 26% and 56% of patients, respectively.  However, in contrast to enteroscopy, lack of control of the capsule prevents its manipulation and full visualization of the intestine; in addition, tissue cannot be sampled and therapy cannot be applied.
  27. 27. Clinical Presantation : 27  Hematemesis  Melena  Hematochezia  Syncope  Dyspepsia  Epigastric pain  Heartburn  Diffuse abdominal pain  Dysphagia  Weight loss  Jaundice
  28. 28. Approach to the Patient: Gastrointestinal Bleeding 28  History  Physical examination  Lab investigation
  29. 29. APROACH TO PATIENT………….. Con’t 29  History: • Abdominal pain • Haematamesis • Haematochezia • Melaena • Features of blood loss: shock, syncope, anemia • Features of underlying cause: dyspepsia, jaundice, weight loss
  30. 30. 30 o Drug history: NSAIDs, Aspirin, anticoagulants, o History of epistaxis or hemoptysis to rule out the GI source of bleeding. o Past medical :previous episodes of upper gastrointestinal bleedin; coronary artery disease; chronic renal or liver disease; o Past surgical: previous abdominal surgery
  31. 31. Approach Cont….. 31 Physical Examination : • General examination and systemic examinations • VITALS: Pulse = Feable pulse BP = Orthostatic Hypotension • SIGNS of shock: Cold extremeties, Tachycardia, Hypotension Chest pain, Confusion, Delirium, Oliguria, and etc.
  32. 32. 32 SKIN changes: Cirrhosis – Palmer erythema, spider nevi Bleeding disorders – Purpura /Echymosis, Haemarthrosis, Muscle hematoma. • Signs of dehydration (dry mucosa, sunken eyes, skin turgor reduced). • Signs of a tumour may be present (nodular liver, abdominal mass, lymphadenopathy, and etc. • DRE : fresh blood, occult blood, bloody diarrhea • Respiratory, CVS, CNS  For comorbid diseases
  33. 33. Lab Diagnosis : 33 CBC with Platelet Count, and Differential  A complete blood count (CBC) is necessary to assess the level of blood loss.  CBC should be checked frequently(q4-6h) during the first day. Hemoglobin Value, Type and Crossmatch Blood  The patient should be crossmatched for 2-6 units, based on the rate of active bleeding.  The hemoglobin level should be monitored serially in order to follow the trend.  An unstable Hb level may signify ongoing hemorrhage requiring further intervention.
  34. 34. 34  LFT- to detect underlying liver disease  The BUN-to- creatinine ratio increases with upper gastrointestinal bleeding (UGIB). A ratio of greater than 36 in a patient without renal insufficiency is suggestive of UGIB.  The patient's prothrombin time (PT), activated partial thromboplastin time, should be checked to document the presence of a coagulopathy
  35. 35. Endoscopy 35 • Initial diagnostic examination for all patients presumed to have UGIB. • Endoscopy should be performed immediately after endotracheal intubation (if indicated), hemodynamic stabilization, and adequate monitoring in an intensive care unit (ICU) setting have been achieved.
  36. 36. 36 Endoscopy
  37. 37. Imaging 37 • CHEST X-RAY-Chest radiographs should be ordered to exclude aspiration pneumonia, effusion, and esophageal perforation. • Abdominal X-RAY- erect and supine films should be ordered to exclude perforated viscous and ileus.
  38. 38. Angiography : 38  Angiography may be useful if bleeding persists and endoscopy fails to identify a bleeding site.  Angiography along with transcatheter arterial embolization (TAE) should be considered for all patients with a known source of arterial UGIB that does not respond to endoscopic management, with active bleeding and a negative endoscopy.  In cases of aortoenteric fistula, angiography requires active bleeding (1 mL/min) to be diagnostic.
  39. 39. Nasogastric Lavage 39  A nasogastric tube is an important diagnostic tool.  This procedure may confirm recent bleeding (coffee ground appearance), possible active bleeding (red blood in the aspirate that does not clear), or a lack of blood in the stomach (active bleeding less likely but does not exclude an upper GI lesion).
  40. 40. 40
  41. 41. 41 BENEFITS OF LAVAGE : 1. Better visualization during endoscopy 2. Give crude estimation of rapidity of bleeding 3. Prevent the development of Porto systemic encephalopathy in cirrhosis 4. Increases PH of stomach, and hence, decreases clot desolation due to gastric acid dilution 5. Tube placement can reduce the patient's need to vomit  During gastric lavage use saline and not use large volume of to avoid water intoxication.  Gastric lavage should be done in alert and cooperative patient to avoid bronco-pulmonary aspiration
  42. 42. Risk Stratification: Rockall Score  Identifies patients at risk of adverse outcome following acute upper GI bleed Variable Score 0 Score 1 Score 2 Score 3 Age <60 60-79 >80 - Shock Nil HR >100 SBP <100 - Co-morbidity Nil major - IHD/CCF/major morbidity Renal failure/liver failure Diagnosis Mallory Weiss tear All other diagnoses GI malignancy - Endoscopic Findings None - Blood, adherent clot, spurting vessel  Score <3 carries good prognosis  Score >8 carries high risk of mortality -
  43. 43. Management 43 Priorities are: 1. Stabilize the patient: protect airway, restore circulation. 2. Identify the source of bleeding. 3. Definitive treatment of the cause.
  44. 44. Emegency Resuscitation Takes priority over determining the diagnosis/cause  ABC (main focus is ‘C’)  Oxygen: 15L Non-rebreath mask  2 large bore cannulae into both ante-cubital fossae Take bloods at same time for FBC, U&E, LFT, Clotting, X match 6Units  Catheterise
  45. 45. 45  IVF initially then blood as soon as available (depending on urgency: O-, Group specific, fully X-matched)  Monitor response to resuscitation frequently (HR, BP, urine output, level of consciousness, peripheral temperature, CRT)  Stop anti-coagulants and correct any clotting derrangement  NG tube and aspiration (will help differentiate upper from lower GI bleed)  Organise definitive treatment (endoscopic/radiological/surgical)
  46. 46. Management (Non-variceal)  Emergency resuscitation as already described  Endoscopy Urgent (within 24hrs) – diagnostic and therepeutic Treatment administered if active bleeding, visible vessel, adherent blood clot Treatment options include injection (adrenaline), coagulation, clipping If re-bleeds then arrange urgent repeat endoscopy.
  47. 47. 47  Pharmacology PPI (infusion) – pH >6 stabilises clots and reduces risk of re-bleeding following endoscopic haemostasis If H pylori positive then for eradication therapy Stop NSAIDs/aspirin/clopidogrel/warfarin/steroids if safe to do so (risk:benefit analysis)
  48. 48. Management (Non-variceal)  Surgery  Reserved for patients with failed medical management (ongoing bleeding despite 2x endoscopy)  Nature of operation depends on cause of bleeding (most commonly performed in context of bleeding peptic ulcer: DU>GU)  E.g. Under-running of ulcer (bleeding DU), wedge excision of bleeding lesion (e.g. GU), partial/total gastrectomy (malignancy)
  49. 49. Variceal Bleeds  Suspect if upper GI bleed in patient with history of chronic liver disease/cirrhosis or stigmata on clinical examination  Liver Cirrhosis results in portal hypertension and development of porto-systemic anastamosis (opening or dilatation of pre-existing vascular channels connecting portal and systemic circulations)
  50. 50. 50  Sites of porto-systemic anastamosis include:  Oesophagus (P= eosophageal branch of L gastric v, S= oesophageal branch of azygous v) Umbilicus (P= para-umbilical v, S= infeior epigastric v)  Retroperitoneal (P= right/middle/left colic v, S= renal/supra-renal/gonadal v)  Rectal  (P= superior rectal v, S= middle/inferior rectal v)  Furthermore, clotting derrangement in those with chronic liver disease can worsen bleeding
  51. 51. Management of Variceal bleeds Emergency resuscitation as already described  Drugs Somatostatin/octreotide – vasoconstricts splanchnic circulation and reduces pressure in portal system Terlipressin – vasoconstricts splanchnic circulation and reduces pressure in portal system Propanolol – used only in context of primary prevention (in those found to have varices to reduce risk of first bleed)  Endoscopy Band ligation  Injection sclerotherapy
  52. 52. 52  Balloon tamponade – sengstaken-blakemore tube  Rarely used now and usually only as temporary measure if failed endoscopic management  Radiological procedure – used if failed medical/endoscopic Mx  Selective catheterisation and embolisation of vessels feeding the varices  TIPSS procedure: transjugular intrahepatic porto-systemic shunt  shunt between hepatic vein and portal vein branch to reduce portal pressure and bleeding from varices): performed if failed medical and endoscopic management  Can worsen hepatic encephalopathy  Surgical  Surgical porto-systemic shunts (often spleno-renal)  Liver transplantation (patients often given TIPP/surgical shunt whilst awaiting this)
  53. 53. Sengstaken-Blakemore Tube TIPSS
  54. 54. Variceal Bleed: Prognosis  Prognosis closely related to severity of underlying chronic liver disease (Childs-Pugh grading)  Child-Pugh classification grades severity of liver disease into A,B,C based on degree of ascites, encephalopathy, bilirubin, albumin, INR  Mortality 32% Childs A, 46% Childs B, 79% Childs C
  55. 55. Management-lower GI BLEEDING  Emergency resuscitation as already described  Pharmacological  Stop NSAIDS/anti-platelets/anti-coagulants if safe  Endoscopic  15% of patients with severe acute PR bleeding will have an upper GI source!)  Colonoscopy – diagnostic and therepeutic (injection, diathermy, clipping)
  56. 56. Management  Radiological  CT angiogram – diagnostic only (non-invasive)  Determines site and cause of bleeding  Mesenteric Angiogram – diagnostic and therepeutic (but invasive)  Determines site of bleeding and allows embolisation of bleeding vessel  Can result in colonic ischaemia
  57. 57. Management  Surgical – Last resort in management as very difficult to determine bleeding point at laparotomy  Segmental colectomy – where site of bleeding is known  Subtotal colectomy – where site of bleeding unclear  Beware of small bowel bleeding – always embarassing when bleeding continues after large bowel removed!
  58. 58. Management Flow Chart for Severe lower GI bleeding Resuscitate Endoscopy (to exclude upper GI cause for severe PR bleeding) Colonoscopy (to identify site and cause of bleeding and to treat bleeding by injection/diathermy/clipping) – often unsuccesful as blood obscures views CT angiogram (to identify site and cause of bleeding) Mesenteric angiogram (to identify site of bleeding and treat bleeding by embolisation of vessel) Surgery
  59. 59. Management  As 85% of lower GI bleeds will settle spontaneously the interventions mentioned on previous slide are reserved for:  Severe/Life threatening bleeds  In the 85% where bleeding settles spontaneously OPD investigation is required to determine underlying cause:  Endoscopy: flexible sigmoidoscopy, colonoscopy  Barium enema
  60. 60. REFERENCE 60  Harrison principles of intrnal medicine 18th edi.  Kumar .clinical medicine 8th edit.  On line search
  61. 61. 61 10Q

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