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Similar to gastrointestinal bleeding
gastrointestinal bleeding
- 1.
- 2. Gastrointestinal bleeding or gastrointestinal hemorrhage describes every form of hemorrhage (loss of blood) in the gastrointestinal tract, from the pharynx to the rectum.
- 7. A. UPPER GIBLEEDING B. PEPTIC ULCER DISEASE C. LOWER GI BLEEDING D. HAEMORROIDS
- 9. Upper gastrointestinal bleeding refers to bleeding in the upper gastrointestinal tract, commonly defined as bleeding arising from the oesophagus, stomach, or duodenum (part above the ligament of treitz).
- 10. ESOPHAGEAL CAUSES ESOPHAGEAL VARICES ESOPHAGITIS ESOPHAGEAL CANCER ESOPHAGEAL ULCERS MALLORY WEISS TEAR
- 11. GASTRIC CAUSES 1.GASTRIC ULCER 2. GASSTRIC CANCER 3. GASTRITIS 4. GASTRIC VARICES 5. GASTRIC ANTRAL VASCULAR ECTASIA 6. DIEULAFOY’S LESIONS
- 12. DUODENAL CAUSES DUODENALULCERS AORTO-ENTERIC FISTULAE OTHER CAUSES HEMATOBILIA HEMOSUCCUS PANCREATICUS SUPERIOR MESENTERIC ARTERY SYNDROME PROVOKING DRUGS NSAIDS ASPIRIN SSRIs
- 13. Etiology (drugs/injury/stress) Injuryin mucosa layer Untreated , unhealed injury grows towards the submucosa layer Injury of the vessels going through this submucosal layer bleeding occurs blood mixes with the gastric juices & content
- 14. comes out ofbody either with vomiting / with stools blood loss anemia, palpitation, hypovolemic shock death
- 16. 1. ORTHOSTATIC HYPOTENSION 2. DECREASE HEMOGLOBIN LEVEL 3. BASIC METABOLIC PROFILE – BUN & COAGULATION PROFILE 4. ENDOSCOPY 5. NASOGASTRIC LAVAGE 6. ANGIOGRAPHY 7. BARRIUM CONTRAST STUDY 8. CT SCAN 9. ULTRASONOGRAPHY
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- 18. Acute hemorrhage Forrest I a (Spurting hemorrhage) Forrest I b (Oozing hemorrhage) Signs of recent hemorrhage Forrest II a (Visible vessel) Forrest II b (Adherent clot) Forrest II c (Flat pigmented haematin on ulcer base) Lesions without active bleeding Forrest III (Lesions without signs of recent hemorrhage or fibrin-covered clean ulcer base)
- 19. VARIABLE SCORE 0SCORE 1 SCORE 2 SCORE 3 Age <60 60-79 >80 Shock No shock Pulse >100 SBP>100 SBP<100 Co-morbidity Nil major CHF, IHD, major morbidity Renal failure , liver failure, metastatic cancer Diagnosis Mallory weiss tear All other diagnoses GI malignancy Evidence of bleeding None Blood , adherent clot, spurting vessels
- 20. ADMISSION RISK MARKERSCORE BLOOD UREA- 6.5<8 8<10 10<25 >25 2 3 4 6 HB(g/L)- 120<130 100<120 <100 1(men) 3(men) & 1(women) 6(men & women) SBP(mmHg)- 100-109 90-99 <90 1 2 3 Other markers- Pulse >100/min 1 melena 1 syncope 1 Hepatic disease 2 cardiac failure 2
- 21. In thevalidation group, scores of 6 or more were associated with a greater than 50% risk of needing an intervention. Score: Score is equal to "0" if the following are all present: Hemoglobin level >12.9 g/dL (men) or >11.9 g/dL (women) Systolic blood pressure >109mm Hg Pulse <100/minute Blood urea nitrogen level <18.2mg/dL NOMELENA OR SYNCOPE No past or present liver disease or heart failure
- 22. ◦ Assess forairway , breathing , circulation first ◦ If not present/ or compromised activate rapid response team & restore the abc first ◦ Fluid resuscitation by IV colloids / crystalloid transfusion ◦ Maitainence of vital signs ◦ Hemodynamic monitoring can be needed ◦ Blood transfusion depending on blood reports ◦ Pain management , but analgesics should be used cautiously ◦ Sedatives can be used, but after determining level of consciousness ◦ Do an endoscopy to rule out the actual problem.
- 23. 1. FLUID REPLACEMENT 2. OCTREOTIDE/VASOPRESSIN & NITROGLYCERINE 3. ENDOSCOPIC BANDING+SCLEROTHERAPY(WITH BETA BLOCKERS & NITRATES TO STOP REBLEED) 4. BALLON TAMPONADE WITH A SENGSTAKEN BLAKEMORE TUBE/MINNESOTA TUBE) + TRANSJUGULAR INTRAHEPATIC PORTOSYSTEMIC SHUNT(TIPS)
- 25. APC involvesthe use of a jet of ionized argon gas (plasma) that is directed through a probe passed through the endoscope. The probe is placed at some distance from the bleeding lesion, and argon gas is emitted then ionized by a high voltage discharge (approx 6kV). High-frequency electrical current is then conducted through the jet of gas, resulting in coagulation of the bleeding lesion on the other end of the jet.
- 26. Persistent hypotension Failure of medical treatment or endoscopic homeostasis Coexisting condition ( perforation, obstruction, malignancy) Transfusion requirement (4 units in 24 hr) Recurrent hospitalizations
- 28. Endoscopy: ◦Aspirationpneumonia ◦ Perforation Complications from coagulation, laser treatments Surgery: ◦ Ileus ◦ Sepsis ◦Wound
- 29.
- 30. Peptic ulcer diseaseis a condition characterised by erosion of GI mucosa resulting from digestive action of HCL acid & pepsin. Any portion of the GI tract that comes into contact with the gastric secretions is susceptible to ulcer development, including the lower esophagus, stomach , duodenum, & margin of gastrojejunal anastomosis after surgical procedures.
- 31. Age- peakage for gastric ulcer is 50-60 yrs & for duodenal ulcers 35-45 yrs. Sex – gastric ulcer greater in women whereas duodenal ulcer greater in men & postmenopausal women.
- 32. ACIDS DRUGS ALCOHOL H.PYLORI INFECTION ISCHEMIA
- 33. ETIOLOGYCAL FACTORS BREAKDOWNOF GASTRIC MUCOSA ACID BACK DIFFUSION INTO MUCOSA DESTRUCTION OF MUCOSAL CELLS INCREASE ACID & PEPSIN RELEASE NEXT SLIDE HISTAMINE
- 34. 1. FURTHER MUCOSAL EROSION 2. DESTRUCTION OF BLOOD VESSELS 3. BLEEDING HISTAMINE INCREASED VASODILATION & CAPILLARY PERMEABILITY ULCERATION LOSS OF PLASMA PROTEINS INTO GASTRIC LUMEN & MUCOSAL EDEMA
- 35. Duodenum (calledduodenal ulcer) Esophagus (called esophageal ulcer) Stomach (called gastric ulcer) Meckel's diverticulum (called Meckel's diverticulum ulcer; is very tender with palpation)
- 36. Type I:Ulcer along the body of the stomach, most often along the lesser curve at incisura angularis along the locus minoris resistantiae. Not associated with acid hypersecretion. Type II: Ulcer in the body in combination with duodenal ulcers. Associated with acid oversecretion. Type III: In the pyloric channel within 3 cm of pylorus. Associated with acid oversecretion. Type IV: Proximal gastroesophageal ulcer Type V: Can occur throughout the stomach. Associated with chronic use of NSAIDs (such as aspirin)
- 38. GI BLEEDING PERFORATIONPENETRATION GASTRIC OUTLET OBSTRUCTION CANCER
- 39. XRAY EGD GASTRIN LEVEL DIAGNOSIS OF H.PYLORI 1.UREA BREATH TEST 2. EGD BIOPSY 3. RAPID URASE TEST 4. ANTIBODY LEVEL 5. STOOL ANTIGEN TEST USG
- 40. A. Conservative therapy- Adequate rest Bland diet Cessation of smoking Drug therapy Stress management
- 41. B. Acute exacerbationwithout complications- NPO NG suction Adequate rest Cessation of smoking IVF replacement Drug therapy
- 42. C. Acute exacerbationwith complications (haemorrhage ,perforation, obstruction) NPO NG suction Bed rest IVF replacement Blood transfusion Stomch lavage
- 43. antacids orH2 antagonists antibiotics (e.g. Clarithromycin, Amoxicillin, Tetracycline, Metronidazole) proton pump inhibitor (PPI) Cytoprotective (eg. sucralfate, bismuth subsalicylate) Anticholinergics Others- sedatives, TCAs
- 44. E. surgery – perforation –simple closure with omentum graft gastric outlet obstruction-pyloroplasty or vagotomy ulcer removal or reduction-billroth I& II vagotomy & pyloroplasty
- 46. LGIB encompasses awide spectrum of symptoms, ranging from trivial hematochezia to massive hemorrhage with shock. Acute LGIB is defined as bleeding that is of recent duration, originates beyond the ligament of Treitz, results in instability of vital signs, and is associated with signs of anemia with or without need for blood transfusion
- 47. Coagulopathy— specificallya bleeding diathesis Colitis ◦ ischaemic colitis ◦ ulcerative colitis ◦ infectious colitis E. coli Shigella Salmonella Campylobacter jejuni Hemorrhoids
- 48. Angiodysplasia Neoplasm— cancer Diverticular disease— diverticulosis, diverticulitis Anal fissure Crohn's disease Mesenteric ischemia colonic polyps
- 49. MELENA BLOOD PER RECTUM HEMATOCHEZIA FEVER ABDOMINAL CRAMP DEHYDRATION
- 50. MODERATE MASSIVE OCCULT 1.ANY AGE 2.HEMATOCH EZIA/MELENA 3.LONG TERM DISEASE 4. MODERATE AMOUNT ACUTE/CHRO NIC BLEEDING 1.AGE>65YRS+MEDICA L PROBLEM 2. HEMATOCHEZIA 3.SBP=90 4.HR>100 5.LOW URINE OUTPUT 6.HB=6 1.ANY AGE 2. HYPOCHROMI C MICROCYTIC ANEMIA 3.NEOPLASM/ CONGENITAL
- 51. Colonoscopy Radionuclide scans: Angiography complete blood cell (CBC) count Serum electrolytes levels Coagulation profile, including activated partial thromboplastin time (aPTT), prothrombin time (PT), manual platelet count, and bleeding time Helical CT scanning of the abdomen and pelvis can be used when a routine workup fails to determine the cause of active GI bleeding.
- 52. The management ofLGIB has 3 components, as follows: Resuscitation and initial assessment Localization of the bleeding site Therapeutic intervention to stop bleeding at the site
- 53. Hemicolectomy Colectomy Abdomino-perineal resection
- 54. Diverticular bleeding:Colonoscopy with bipolar probe coagulation, epinephrine injection, or metallic clips Recurrent bleeding: Resection of the affected bowel segment Angiodysplasia: Thermal therapy (eg, electrocoagulation, argon plasma coagulation) In patients in whom the bleeding site cannot be determined, vasoconstrictive agents such as vasopressin (Pitressin) can be used. If vasopressin is unsuccessful or contraindicated, superselective embolization is useful.
- 56. Haemorrhoids aredilated haemorrhoidal veins. Haemorrhoids : Haem=blood Rhoos = flowing PILES Pila= swelling The actual term now a days used for this is Haemorrhoidal disease.
- 57. Sex: In hospital based studies Men > women In community based studies men = women Age: Increase with age Socioeconomic status and occupation: > high socioeconomic group > heavy laborer and occupations with prolonged sitting or standing
- 61. Venous obstruction: The principal cause of haemorrhoidal disease seems to be the congestion and hypertrophy of internal anal cushions. Cushions congest because 1. They fail to empty rapidly during the act of defecation. 2. They are abnormally mobile. 3. They are trapped by tight internal sphicter. When the cusions are congested, they bleed and become edematous.oedema causes stretching of the tissue and finally hypertrophy. Fecal mass in the rectum compress the veins. Straining constricts the intermuscular vein so blocks emptying of veins. Predisposing fctors of venous obstruction: Raised intra abdominal pressure during pregnancy,from ascites or pelvic tumor, or raised portal venous pressure with hepatic cirrhosis. Piles of pregnancy: These are not necessorily abnormal.
- 62. Prolapse ofvascular cushions: Submucosal vascular cushions are supported by Pectin bands(ligaments of park) Muscularis submucosa In normal defecation internal sphicter relaxes and there is outward rotation of vascular tissue and pectin bands. In haemorrhoidal disease this normal rotation is disturbed due to the decrease in elastic tissue caused by; Increased Age Constipation Prolonged straining Endocrine reasons
- 63. BLEEDING SIGNS& SYMPTOMSOF HAEMORRHOIDS PAIN & DISCOMFORT PRURITIS PROLAPSE &LUMP
- 64.
- 65. B:First-degree bleeding withoutprolapse C:Second-degree Prolapsed, reduced spontaneously D:Third-degree prolapsed, requiring manual reduction E:Fourth-degree fibrosed permanently prolapsed
- 66. 1. Thrombosis and infection of internal cushions 2. Anemia 3. Perianal dermatitis 4. Thrombosis of external vascular channels
- 67. Conservative; Medical Sitz bath Invasive therapy Injection sclerotherapy Rubber band ligation Surgical; Excision haemorrhoidectomy Stapled haemorrhoidectomy Doppler guided artery lagation
- 68. A number ofpreventative measures are recommended, including avoiding straining while attempting to defecate avoiding constipation and diarrhea either by eating a high-fiber diet and drinking plenty of fluid or by taking fiber supplements getting sufficient exercise. Stop spending less time attempting to defecate losing weight for overweight persons avoiding heavy lifting are also recommended.
- 69. History taking: Duration Episodes of hematemesis Quantity Color(coffee ground appearance) Blood in stools (maroon colored stools can be present in acute severe upper GI bleeding) History of jaundice(cirrhosis) History of epigastric pain (peptic ulcer, esophagitis, erosive gastritis) Weight loss (carcinoma stomach)
- 70. General examinationand systemic examinations VITALS: Pulse = Thready pulse BP = Orthostatic Hypotension SIGNS of shock: Cold extremeties, Tachycardia, Hypotension Chest pain, Confusion, Delirium, Oliguria, and etc. SKIN changes: Cirrhosis – Palmer erythema, spider nevi Bleeding disorders – Purpura /Echymosis Coagulation disorders – Haemarthrosis, Muscle hematoma.
- 71. Signs ofdehydration (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
- 72. Assess forfeatures of shock Start intravenous fluid replacement Give inj adrenaline Check hemoglobin & start transfusion as soon as possible Send blood for electrolytes Start electrolyte correction as soon as possible Start inj. noradrenaline to maintain B.P. Maintain nutrition by nasogastric or parenteral nutrition Nasogastric suction if requried
- 73. Give preoperative teaching Assess anxiety & provide mental support Explain different treatment modalities & help to choose the best one Explain need of keep in NPM Preoperative medications given
- 74. Provide properposition to maintain airway & prevent choking Give intravenous painkillers Provide oxygen Give IVF Give antiemetics Wound care Assess the vital signs & consciousness frequently
- 75. 1. Fluid electrolyteimbalance r/t blood loss possibly evidenced by hematemesis, melena, dehydration. 2. Hypovolemic / haemorragic shock r/t severe blood loss possibly evidenced by low blood pressure, pallor. 3. Pain in abdomen r/t gastrointestinal tarct mucosa trauma or ulcer possibly evidenced by verbalization, facial expression. 4. Activity intolerance r/t weakness & imbalance between oxygen supply / demand, low haemoglobin possibly evidenced by tachypnea, sortness of breath on activity.
- 76. 5. Ineffective managementof therapeutic regimen r/t lack of knowledge about appropriate nutrition & medication regimen possibly evidenced by frequentverbalization. 6. Imbalanced nutritional status : less than body requirements r/t inadequate nutritional intake & anorexia, dietary restriction possibly evidenced by anorexia, fatigue, weakness. 7. Ineffective tissue perfusion r/t poor oxygenation possibly evidenced by oxygen saturation level, capillary refill.
- 77. T H AN K Y O U