1. ACUTE GASTRO INTESTINAL BLEEDING
Dr. Pratyusha Alamuri FELLOW IN CRITICAL CARE AWARE GLOBAL HOSPITAL

2. Introduction Acute GI bleeding is a common admission to the ICU
Also a major cause of morbidity & mortality

3. Classified accordingly UGI BLEED: Above ligament of treitz LOWER GI BLEED: Below ligament of treitz

4. Causes of UGI bleed 1.Peptic ulcers(DU:GU 3:1) 2.Varices(EV:GV 9:1)
3.Portal hypertensive gastropathy
4.Mallory weiss tears
5.Gastritis,duodenitis & esophagitis
6.Hemobilia:Bleed from biliary tree
7.Hemosuccus pancreaticus:Bleed from PD
Dieulafoy lesion

5. PUD-accounts for 75% of UGI bleeding
Bleeding from varices, esophagitis, duodenitis, mallory weiss tear-Each account for between 5% & 15%

6. CLINICAL PRESENTATION
Hematemesis & melena are the most common presentations of acute UGI bleed Hematochezia:Passage of bright red to maroon blood from the rectum-usually represents a lower GI bleed.Also can be feature of massive upper GI bleed Vomiting & retching preceding hematemesis suggests mallory weiss tears

8. Other symptoms include:
1.Pain epigastrium or diffuse abdominal pain 2.Burning type of epigastric pain 3.Heart burn,retching 4.Giddiness

9. Signs include:
Pallor
Icterus-in case of CLD
Signs of hypovolemic shock:
Hypotension,tachycardia,cold extremities
Mental confusion,oliguria

10. HIGH RISK PATIENT Hematemesis Syncope SBP <100mmHg
Postural hypotension
Blood transfusion requirement of more than 4 units of blood in 12 hours to maintain blood pressure
Age over 60 years
Multiple comorbidities

11. MANAGEMENT OF NON VARICEAL BLEEDING
1.Initial resuscitation is important Blood & plasma expanders should be given through large bore IV cannulae Vital signs should be closely monitored Observe central venous pressure & hourly urine out put in case of hypovolemic shock Consider endoscopy after resuscitation

12. UGI ENDOSCOPY
Allows identification of the site,nature of bleeding & appropriate treatment
Source of bleeding like ulcers,varices,mallory weiss tears & other lesions with bleeding are identified
Peptic ulcers that are actively bleeding or have bleed recently may show stigmata of hemorrhage on endoscopy

13. Stigmata of hemorrhage HIGH RISK ULCERS
1.Spurter or oozer: % recurrent bleeding 85-90% 2.Protuberant vessel % recurrent bleeding 35-55% 3.Adherent clot % recurrent bleeding 30-40% 4.Flat spot % recurrent bleeding 5-10% 5.None % recurrent bleeding 5%

14. Stigmata of hemorrhage

15. HIGH RISK ULCERS
Proximal postero-inferior wall of duodenal bulb-(Gastro duodenal artery)
High lesser curvature of the stomach-(Left gastric artery)
These are the sites for severe recurrent bleeding

16. TREATMENT
Patients at high risk of recurrent bleeding pharmacological control without endoscopic haemostasis is inadequate thus combination offers best therapy for ulcer bleeding
Pharmacological+Endoscopic therapy is best

17. ENDOSCOPIC THERAPY
Endoscopic haemostasis should be used in patients with a high risk of persistent or recurrent bleeding
1.Epinephrine(adrenaline)injection-1:10,000 dilution
2.Coaptive coagulation:Uses direct pressure & heat energy(heater probe)—limits view of lesser curve & posterior wall of duodenal bulb
3.Hemoclips:Clipping of bleeding vessel
Lesser curve,gastric fundus & posterior wall of duodenum technically difficult

18. PHARMACOLOGICAL CONTROL
High dose,constant infusion of IV PPI will sustain intragastric pH >6 & enhance clot stability(80mg IV bolus & 8mg/hour infusion)
Example:IV Pantoprazole as mentioned
To prevent acidic environment
Given after endoscopic therapy

19. SURGERY
Indications:
1.Arterial bleeding that cant be controlled by endoscopic haemostasis
2.Massive transfusion(ie total of 6-8 units of blood required to maintain BP
3.Recurrent clinical bleeding after initial success in endoscopic haemostasis
4.Evidence suggestive of GI perforation
*Surgical procedures include various types of gastrectomy
How ever morbidity is significantly high in surgical patients

20. Variceal Bleeding
Serious complication of portal HTN with a high mortality
Child pugh’s classification is most important prognostic factor for early rebleeding & survival

21. Treatment-Variceal bleeding
Initial resuscitation is again important
Fresh frozen plasma & platelet transfusion may be indicated
Lactulose via ryles tube(15-30ml every 4-6 hours should be given)to prevent or correct hepatic encephalopathy
Prevent overt transfusions-may increase portal pressurerebleed
Close hemodynamic monitoring is required

22. PHARMACOLOGICAL CONTROL OF VARICEAL BLEEDING
Infusion of octreotide(somatostatin analogue)
reduces portal blood pressure—50mcg bolus followed by 50mcg/hour for 2-5 days
safe & effective vasoactive agents used in acute varcieal bleeding
Effective when used in combination with endoscopic therapy
Terlipressin(vasopressin analouge) also used in variceal bleed.Given at a dose of 2mg IV every four hours during the first 48 hours reducing to 1 mg every 4 hours for another 3 days.Also improves renal perfusion in HRS.But limited in ischemic heart disease.

23. ENDOSCOPIC VARICEAL THERAPY
1.Endoscopic sclerotherapy:sclerosants used(ethanolamine oleate,sodium tetradecyl sulphate 1-3%,polidocanol Mainstay of treatment-controls 80-90% of acute variceal bleeding Complications:ulcer formation,fever,chest pain,mediastinitis 2.Endoscopic variceal ligation:Mechanical method-strangulate varices Less complications-coz no chemical irritation More preferred in many centers

24. BALLOON TAMPONADE-VARICEAL BLEEDING
Balloon tamponade:Exert pressure directly on the bleeding point
Sengstaken blackmore tube has been replaced by the four lumen minnesota tube which allows aspiration of gastric & esophageal contents
Limited to 24 hours to avoid tissue pressure necrosis
Used in exceptional cases when therapies fail to control bleeding

25. TIPS-In variceal bleed
Transjugular Intrahepatic Portosystemic Shunt
In good hands success can be achieved in over 90% of cases
Strongly considered in child’s pugh class C with score with in 1-2 days of hospitalization
Complications:Intra-abdominal hemorrahage & stent occlusion

26. SURGERY-In variceal bleed
Include direct devascularization of the lower esophagus plus the proximal stomach & a variety of surgical shunts
But role of surgery has diminished since the advent of endoscopic therapy & TIPS
Is now 2nd line treatment when bleeding continues or recurs after two sessions of sclerotherapy or EVL

27. EV & EVL

28. Mallory Weiss Tear

29. Mallory weiss tear VS Boerhaaves
Mallory weiss tear:Linear mucosal tears at gastroesophageal junction Boerhaaves syndrome: Complete transmural(full thickness) laceration or perforation of esophagus at GE junction

30. Dieulafoy’s lesion -Aberrant vessel in sub mucosa bleeds from a pinpoint mucosal defect

31. UGI Bleed management algorithm

32. LOWER GI BLEEDING
About 20% of GI bleeding arises from the lower GI tract
Bleeding source distal to ligament of treitz

33. Causes of LGI bleed Diverticular hemorrhage Angiodysplasia
Both occur on right colon
Colonic polyps
Carcinoma
IBD

34. CLINICAL PRESENTATION
Hematochezia-most common presentation of lower GI bleed
Small intestinal bleed & right colon bleed present as melena
Abdominal pain preceding a massive bleeding episode suggests ischemia or IBD
Diverticulosis,angiodysplasia,mekels diverticulumpresents painless bleeding
PTN hemorrhoids present with massive hematochezia

35. Diverticular bleeding

36. Colonic Angiodysplasia

37. Colon carcinoma

38. IBD-UC

39. INVESTIGATIONS Plan after initial resuscitation/hemodynamic stability
Always exclude UGI bleed before colonoscopy
Proctosigmoidoscopy-helps to identify hemorrhoids & rectal tumors
If proctosigmoidoscopy & gastro-duodenoscopy are negative than lower GI tract should be examined by colonoscopy,angiography or radionucleotide scan

40. COLONOSCOPY Difficult in actively bleeding patient
Risk of perforation high
Poor visualization due to blood
Bowel preparationyields better results
once bleeding has stopped

41. Angiography or radionuclide scan
Diagnostic angiography:
Helpful when colonoscopic view is completely obscured by active hemorrhage
Helpful in defining abnormal vasculature(angiodysplasia,arteriovenous malformations & inherited vascular anomalies like rendu-osler-weber syndrome,pseudoxanthoma elasticum & Ehlers danlos syndrome)
Angiography localize the site of bleeding in 80-85% of patients when bleeding rate is more than 0.5ml/min
*99m technetium labelling of RBCs has been reported to detect the source of active bleeding
More sensitive than angiography detects bleeding as low as 0.1ml/min

42. Angiography-localizing site of bleed to ascending colon

43. 99m technetium labeled red blood cell scan localizing the source of bleed in proximal sigmoid colon

44. Management/Treatment
Colonoscopic :Bleeding from vascular anamolies can be treated by electrocoagulation,heater probe & laser photocoagulation unless the anamolies are too large or diffuse
Angiographic:Intra-arterial infusion of vasopressin or occlusion of the bleeding artery with embolic agents such as absorbable gelatin sponge used in lower GI bleed
Surgical:Diverticular bleeding usually arises from larger vessel may be difficult to control with colonoscopic or angiographic therapy-require surgery
Surgery also indicated in vascular anamolies when endoscopic treatment fails
Surgeries done are immediate laparotomy to perform colectomy(segmental)

45. Algorithm for lower GI bleed management

46. THANK YOU