1. Presenter: Dr. Thaha Rashid P T Moderator: Dr. Gyan Singh
UPPER GI HEMORRAGE
Presenter: Dr. Thaha Rashid P T
Moderator: Dr. Gyan Singh

2. Introduction
Acute gastrointestinal (GI) hemorrhage is a significant cause of morbidity and mortality in the emergency setting.
The source of GI bleeding can range from the esophagus through to the colon and is classified into upper or lower GI bleeding depending on the site of bleeding relative to the ligament of Treitz.
Hemorrhage persisting or recurring after negative endoscopy is termed obscure bleeding
Occult bleeding is when there are no signs of overt bleeding, but the presenting symptoms are due to chronic blood loss and anemia
Mortality from upper GI bleeding is 5–14%

3. Approach to the patient

4. Initial assessment and resuscitation
Initial evaluation should focus on rapid assessment of the magnitude haemorrhage
Less than 20% - Postural changes in BP & pulse
20–30% - Tachycardia (>100 beats/min) and a reduced pulse pressure
Greater than 40% - impairment of conscious level (obtundation /agitation), cool, clammy peripheries, & systolic BP less than 90 mm Hg
Fluid resuscitation in unstable patients should be commenced with a 2-L bolus of crystalloid

5. Supplemental oxygen will maximize oxygen delivery to tissues
Success of fluid resuscitation should be monitored using parameters such as heart rate, blood pressure, and urine output
Supplemental oxygen will maximize oxygen delivery to tissues
Blood test – CBC, LFT, KFT, Coagulation profile, Grouping and cross matching
Blood transfusion
Decreased response to fluid resuscitation
Presence ongoing bleeding
Cardiopulmonary comorbidities
Old age- hematocrit below 30%
Young age- hematocrit below 20%
Suspected likelihood of rebleeding - esophageal varices
Packed red cells are the optimal form of transfusion

6. History and examination
Time of onset, volume, and frequency of bleeding are key aspects of the history in determining amount of blood loss
Hematemesis may be bright red when fresh, but older blood will resemble coffee grounds
Melena is passage of offensive, black, tarry stool (60 ml of UGI bleeding)
Hematochezia usually results from bleeding from the left side of the colon
Syncope, angina - end-organ symptoms suggestive of reduced oxygen delivery

7. Antecedent vomiting - Mallory-Weiss tear
Recent weight loss or loss of appetite – malignancy
Recent epigastric pain - peptic ulceration
Alcohol intake or liver disease - variceal bleeding
Previous aortic surgery - Aortoenteric fistula
Drug history – NSAIDs, SSRIs - peptic ulceration
Use of anticoagulants
Physical examination
Nasopharynx and oropharynx
Pigmented lesions in the oral mucosa - Peutz-Jeghers disease
Tender epigastrium - Peptic ulceration
Lymphadenopathy – malignancy
Splenomegaly, ascites, jaundice, palmar erythema – Variceal
Rectal examination – Melena, rectal cancer, hemorrhoids

8. Identification of source of bleeding
Nasogastric Aspiration
Confrm upper GI bleeding
Assesses the rate of bleeding
Removal of blood from the stomach – Better visualisation in Endoscopy
EGD
Gold standard investigation for UGI bleeding
Should be performed within 24 hours of presentation
Identification of the source of bleeding
Determine the underlying etiology
Achieving hemostasis
Provides prognostic information
Colonoscopy or Flexible sigmoidoscopy

10. Capsule Enteroscopy Endoscopic access to the small bowel is difficult
Capsules measure 11 ×26 mm
Contain a lens
White LED for illumination
Silver oxide batteries
Radio transmitter

11. Deep enteroscopy Double-balloon enteroscopy Single-balloon enteroscopy
Balloons grip the intestinal wall, allowing advancement of the endoscope forward
Spiral enteroscopy - special overtube with helices
Advantage – Biopsy, Execute therapeutic measures
Disadvantage – Higher rates of perforation

12. Red Cell Labeling (Nuclear Scintigraphy)
Visceral Angiography
Can detect bleeding of 0.5–1 mL/min
Red Cell Labeling (Nuclear Scintigraphy)
Can detect GI bleeding at a rate of 0.1 mL/min
Tc99 labelled RBCs are injected
Sensitivity 100%
Specificity is less because of intestinal motility

14. THERAPEUTIC OPTIONS Pharmacologic Endoscopic
Preventing recurrence of bleeding
Proton pump inhibitors
H.pylori eradication
Hemostatics
Endoscopic
Thermal coagulation
Injection therapy - Epinephrine
Mechanical devices - metallic clips and band ligation
Argon plasma coagulation – Non contact coagulation
Laser-mediated coagulation

15. Interventional Angiography
Embolization of the bleeding vessel
Microcoils
Gelfoam (gelatin sponge)
Polyvinyl alcohol
May also be coupled with selective infusion of a vasoconstrictor such as vasopressin
Surgery
When all modalities of hemorrhage control have failed
Treatment of choice - Malignancy

16. Causes of Upper GI bleeding
NONVARICEAL BLEEDING – 80%
Peptic ulcer disease 30%-50%
Mallory-Weiss tears 15%-20%
Gastritis or duodenitis 10%-15%
Esophagitis 5%-10%
Arteriovenous malformations 5%
Tumors 2%
PORTAL HYPERTENSIVE BLEEDING – 20%
Gastroesophageal varices >90%
Hypertensive portal gastropathy <5%
Isolated gastric varices

17. Peptic Ulcer Disease Most frequent cause of upper GI hemorrhage
40% of all cases
Bleeding is the principal cause for death in PUD
Bleeding develops as a consequence of peptic acid erosion of the mucosal surface
Usually chronic blood loss
Significant bleeding results when there is involvement of an artery of the submucosa, gastroduodenal artery or left gastric arteries

18. Management Medical Management Stop any causes (Drugs)
Ulcerogenic medications : NSAIDs, Salicylates, SSRI
Non ulcerogenic alternatives : COX-2 inhibitors
Proton pump inhibitors – Control bleeding and reduce rebleeding
Anti H.pylori treatment – 2 antibiotics

19. Endoscopic Management
Endoscopy within 24 hours

20. Endoscopic therapy is recommended in cases of active bleeding as well as those with a visible vessel (Forrest I to IIa)
In case of an adherent clot (Forrest IIb), the clot is removed and the underlying lesion evaluated
Epinephrine injection (1 : 10,000) to all four quadrants of the lesion
Thermal therapy with heater probes, monopolar or bipolar electrocoagulation, or laser or argon plasma coagulation
A combination of injection with thermal therapy achieves hemostasis in 90% of bleeding PUDs
Hemoclips, which is difficult to apply is helpful with a spurting vessel

22. Surgical Management Indications for Surgery
Hemodynamic instability despite vigorous resuscitation (>6 U) transfusion
Failure of endoscopic techniques to arrest hemorrhage
Rebleed after initial stabilization (with up to two attempts at obtaining endoscopic hemostasis)
Shock associated with recurrent hemorrhage
Continued slow bleeding with a transfusion requirement >3 U /day
The first priority - Control of the haemorrhage
Definitive acid-reducing procedure

23. Surgery for duodenal ulcer
Exposure of the bleeding site by longitudinal duodenotomy or duodenopyloromyotomy
Anterior ulcer- four-quadrant suture ligation with nonabsorbable suture
Posterior ulcer eroding into the pancreaticoduodenal or gastroduodenal artery- suture ligation of the vessel proximal and distal to the ulcer + U stich underneath the ulcer to control the pancreatic branches

25. Acid reducing operation
Usefulness has been questioned because simple closure and H. pylori control is sufficient to prevent recurrence
Pyloroplasty, combined with truncal vagotomy, is the most frequently used operation
Antrectomy with truncal vagotomy- In refractory duodenal ulcer disease or who has failed conservative surgery

26. Surgery for gastric ulcer
Gastrotomy and suture ligation
Because of a 10% incidence of malignancy, gastric ulcer resection is generally indicated
Simple excision alone is associated with rebleeding in as many as 20% of patients so distal gastrectomy is generally preferred
Ulcers of the proximal stomach-
near-total gastrectomy
distal gastrectomy combined with resection of a tongue of proximal stomach to include the ulcer

28. Mallory-Weiss Tears 15% to 20% of cases
Mucosal and submucosal tears that occur near the gastroesophageal junction
Usually develop in alcoholic patients after a period of intense retching and vomiting following binge drinking
Occur in any patient who has a history of repeated emesis
Forceful contraction of the abdominal wall against an unrelaxed cardia, resulting in mucosal laceration of the cardia as a result of the increase intragastric pressure

29. Usually diagnosed based on history
Endoscopy is frequently used to confirm the diagnosis
Retroflexion maneuver
Most tears occur along the lesser curvature
Supportive therapy- 90% of bleeding episodes are self limited and the mucosa often heals within 72 hours
Severe ongoing bleeding
Endoscopic therapy with injection or electrocoagulation
Angiographic embolization with gelatin sponge
high gastrotomy and suturing of the mucosal tear

30. Stress Gastritis
Commonly encountered lesion in critically ill patients
Multiple superficial erosions of the entire stomach
Combination of acid and pepsin injury in the context of ischemia from hypoperfusion states
Head injury -Cushing’s ulcers
Burns -Curling’s ulcers
Significant hemorrhage from stress ulceration is a common phenomenon

31. Patients with these risk factors should be given prophylactic therapy with antacids, histamine-2 (H2) receptor antagonists, PPIs, or sucralfate
Management of shock and sepsis
Acid suppressive therapy
Endoscopic therapy- Doubtful benefit
Selective infusion of vasopressin into the splanchnic circulation through the left gastric artery
Angiographic embolization of left gastric artery
Surgery- Oversewing with figure-of eight stitches, Total gastrectomy in life threatening refractory cases

32. Esophagitis Esophageal inflammation secondary to GERD
Crohn’s disease, radiation
Various infectious agents may also cause esophagitis, particularly in the immunocompromised
Acid suppressive therapy
Endoscopic control of the hemorrhage, usually with electrocoagulation or a heater probe
Infectious cause- targeted therapy

34. Dieulafoy’s Lesion
Vascular malformations found primarily along the lesser curve of the stomach within 6 cm of the gastroesophageal junction
Unusually large vessels (1 to 3 mm) in the gastric submucosa
Erosion of the gastric mucosa overlying these vessels leads to haemorrhage
Dieulafoy’s lesions appear as reddish-brown protrusions on endoscopy with no ulceration
The mucosal defect is usually small (2 to 5 mm) and may be difficult to identify

35. Endoscopic control- Application of thermal or sclerosant therapy
Angiographic coil embolization
Surgical intervention
Gastrostomy with oversewing of the lesion
Partial gastrectomy- if bleeding point is not identified
Surgical intervention may require prior endoscopic tattooing

36. Gastric Antral Vascular Ectasia
Collection of dilated venules appearing as linear red streaks converging on the antrum in a longitudinal fashion
Watermelon stomach
Acute severe hemorrhage is rare
Patients present with persistent iron deficiency anemia from continued occult blood loss
Endoscopic therapy- APC
Antrectomy

38. Malignancy
Chronic anemia or hemoccult-positive stool rather than episodes of significant hemorrhage
Malignancies that present as ulcerative lesions will bleed persistently
Endoscopic therapy is often successful in controlling these bleeds
As rebleeding rate is high, surgical resection is indicated
Extent of resection is dependent on the specific lesion
Palliative resections for control of bleeding usually entail wedge resections

39. Aortoenteric Fistula Previous abdominal aortic aneurysm repair
May occur as a result of an inflammatory or infectious aortitis
Development of a pseudoaneurysm at the proximal anastomotic suture line in the setting of an infection, with subsequent fistulization into the overlying duodenum
Hemorrhage is often massive and fatal
Typically, patients with bleeding from an aortoenteric fistula will present first with a sentinel bleed, a self-limited episode that heralds the subsequent massive, and often fatal, hemorrhage

40. This should prompt urgent upper endoscopy because diagnosis at this stage can be lifesaving
Evidence of bleeding in the distal duodenum (third or fourth portion) on EGD should be considered diagnostic
Therapy includes ligation of the aorta proximal to graft, removal of the infected prosthesis, and an extra-anatomic bypass.

41. Hemobilia
Associated with trauma, recent instrumentation of the biliary tree, or hepatic neoplasms.
Should be suspected in anyone who presents with hemorrhage, right upper quadrant pain, and jaundice
Endoscopy- blood at the ampulla
Angiography- diagnostic procedure of choice
Angiographic embolization is the preferred treatment

42. Hemosuccus Pancreaticus
Erosion of a pancreatic pseudocyst into the splenic artery
Bleeding from the pancreatic duct
Diagnosis requires a high index of suspicion in patients with abdominal pain, blood loss, and a past history of pancreatitis
Angiography is diagnostic and permits embolization, which is often therapeutic
Distal pancreatectomy, often results in cure

43. Bleeding Related to Portal Hypertension
Usually the result of bleeding from varices
Dilated submucosal veins develop in response to the portal hypertension, providing a collateral pathway for decompression of the portal system into the systemic circulation
They are most common in the distal esophagus and can reach sizes of 1 to 2 cm
Overlying mucosa becomes increasingly tenuous, excoriating with minimal trauma

44. May also develop in the stomach and hemorrhoidal plexus of the rectum
Gastroesophageal varices develop in approximately 30% of patients with cirrhosis and portal hypertension
Compared with nonvariceal bleeding, variceal hemorrhage is associated with an increased risk of rebleeding & mortality
Hemorrhage is frequently massive, accompanied by hematemesis and hemodynamic instability

46. Medical Management
Vasopressin produces splanchnic vasoconstriction and has been shown to reduce bleeding significantly
Octreotide, is the vasoactive agent of choice
Continuous IV infusion of these agents results in temporary control of bleeding and allows time for resuscitation and appropriate diagnostic and therapeutic maneuvers.

47. Endoscopic Management
Early EGD is critical to evaluate the source of bleeding because more than 50% of bleeding is caused by nonvariceal sources
If bleeding esophageal varices are identified, sclerotherapy and variceal banding have been shown to control hemorrhage effectively
Sclerotherapy-perforation, mediastinitis, and stricture
Banding- Need for expertise

49. Other Management Balloon tamponade
Sengstaken-Blakemore tube consists of a gastric tube with esophageal and gastric balloons
Inflation of the balloons compresses the esophagogastric venous plexus, arresting bleeding
Deflation can be associated with recurrent bleeding in 50% of patients
Hence this technique is reserved as a temporizing measure

51. Prevention of Rebleeding
Approximately 70% of patients will have a rebleed within 2 months without further definitive therapy
Medical therapy
Non-selective beta blocker, such as nadolol
Antiulcer agent, such as a PPI or sucralfate
Endoscopic band ligation repeated every 10 to 14 days until all varices have been eradicated

52. Radiologic or Surgical Portal Decompression
In 10% of cases of when endoscopic management is unsuccessful
TIPS
Artifcial anastomosis between the hepatic and portal veins
Under fluoroscopic guidance, using a covered stent
Control bleeding in 95% of cases
Disadvantage- hepatic encephalopathy from diversion of blood away from the liver parenchyma
Surgical shunting- More morbidity and mortality than TIPS

54. Shunt surgery Non selective Selective Partial Shunts
End to side portacaval
Side to side portacaval
Conventional splenorenal
Selective
Left gastric vena caval shunt
Distal splenorenal shunt
Partial Shunts
Portacaval shunt using small diameter PTFE graft (10mm)

55. Non selective

56. Distal spleno renal shunt

57. Partial Shunts

58. Gastric varices are managed much the same way as esophageal varices
Isolated gastric varices – Splenic vein thrombosis – Splenectomy
Portal hypertensive gastropathy
Diffuse dilation of the mucosal, and submucosal venous plexus
Snake-skin appearance with cherry-red spots

59. Thank you