The presentatin is about Upper Gastro Intestinal Bleeding, its causes, approach to the patients with GI Haemorrhage, initial assessment, resuscitation, history and physical examination, localisation, specific causes of GI Haemorrhage, investigations and managements.

1. UPPER G.I. BLEEDING
Dr. Manotosh Biswas
SR, General Surgery
AIIMSK

2. INTRODUCTION
 Acute G.I. hemorrhage is a common clinical problem with diverse manifestations.
 Trivial to massive/from virtually any region
 Classified by the location relative to the ligament of Treitz
 Obscure bleeding: hemorrhage that persists/recurs after negative evaluation with
endoscopy
 Occult bleeding: not apparent to the patient until symptoms related to the anemia
are manifested
 Management of these patients is frequently multidisciplinary

3. APPROACH TO THE PATIENT WITH GI HEMORRHAGE

4. INITIAL ASSESSMENT
 Patient’s airway and breathing take first priority
 Patient’s hemodynamic status becomes the dominant concern
 The preexisting deficits and ongoing hemorrhage
 Continuous reassessment of the patient’s circulatory status  aggressiveness of
subsequent evaluation and intervention
 Determination of severity
 >40% loss : Obtundation, agitation, & hypotension (SBP <90 mm Hg in the supine position)
associated with cool, clammy extremities
 20% to 40% loss: resting HR >100 beats/min with a decreased pulse pressure
 20% at least: postural changes - ↓ in BP of >10 mm Hg or ↑ of the pulse of >20 beats/min

5. RESUSCITATION
 More severe the bleeding, the more aggressive the resuscitation
 two large-bore IV lines, preferably in the antecubital fossae
 Unstable patients  2-liter bolus of crystalloid solution, usually RL
 Blood typing & cross matching, CBC, Coagulation profile, LFT
 Foley catheter
 Administering supplemental oxygen
 Blood transfusion  packed RBCs are the preferred form
 high-volume transfusion  empirically receive both FFP & platelets & calcium

6. HISTORY AND PHYSICAL EXAMINATION
 Preliminary assessment of the site & cause of bleeding & comorbidities
 Characteristics of the bleeding:
 Hematemesis: vomiting of blood
 Melena: passage of black, tarry, and foul-smelling stool
 Hematochezia: bright red blood from the rectum
 Demographic data
 Elderly – angiodysplasias, diverticula, ischemic colitis, and cancer
 Younger – peptic ulcers, varices, and Meckel’s diverticula

7. HISTORY AND PHYSICAL EXAMINATION
 Medical history
 Antecedent epigastric distress – peptic ulcer
 Antecedent vomiting – Mallory-Weiss tear
 Weight loss – malignant disease
 Liver disease – variceal bleeding
 Previous aortic surgery – aortoenteric fistula
 Medication (NSAIDs, SSRIs, warfarin, LMWH) - GI mucosal erosions
 Physical examination
 Oropharynx and nose – Local source
 Abdominal examination – to exclude masses, splenomegaly, and adenopathy
 Epigastric tenderness – gastritis or peptic ulceration
 Stigmata of liver disease - jaundice, ascites, palmar erythema, and caput medusae

8. LOCALIZATION

9. RISK STRATIFICATION

10. ACUTE UPPER GASTROINTESTINAL
HEMORRHAGE
 Bleeding that arises from the GI tract
proximal to the ligament of Treitz
 Accounts for nearly 80% of significant
GI hemorrhage
 The foundation for the diagnosis and
management: EGD
 Angiography
 Operative intervention
 Tagged RBC scan is seldom necessary
 contrast studies usually contraindicated

11. SPECIFIC CAUSES OF
UPPER GASTROINTESTINAL
HEMORRHAGE
Nonvariceal Bleeding

12. PEPTIC ULCER DISEASE
 Most frequent cause of upper GI hemorrhage (~40% of all)
 10% to 15% of patients with peptic ulcer disease develop bleeding at some point
 Bleeding develops as a consequence of acid-peptic erosion of the mucosal surface
 Chronic blood loss is common
 Significant bleeding typically results when there is involvement of an vessel
 Gastroduodenal artery or left gastric arteries

14. PEPTIC ULCER DISEASE
 Medical management
 PPI
 The association between H. pylori
infection & bleeding is less strong
 Ulcerogenic medications should be
stopped
 Endoscopic management
 Epinephrine injection (usually addition
of thermal therapy to the injection)
 Heater probes
 Coagulation
 Application of clips
 Surgical management
 10% of patients with bleeding ulcers
still require surgical intervention
 Indications (traditionally): blood
transfusion requirements, excess of 6
units

15. MALLORY-WEISS TEARS
 mucosal and submucosal tears that occur near the gastroesophageal junction
 alcoholic patients after a intense retching & vomiting following binge drinking
 forceful contraction of the abdominal wall against an unrelaxed cardia
 5% to 10% of cases of upper GI Bleeding
 diagnosed on the basis of history
 Endoscopy  retroflexion maneuver and to view the area just below the
gastroesophageal junction
 Most tears occur along the lesser curvature
 Supportive therapy  90% of bleeding episodes are self-limited
 severe ongoing bleeding  endoscopic, embolization, gastrotomy and suturing

16. STRESS GASTRITIS
 Appearance of multiple superficial erosions of the entire stomach
 Result from the combination of acid and pepsin injury in the context of ischemia
 Acid suppressive therapy is often successful in controlling the hemorrhage
 When this fails, consideration should be given to administration of octreotide or
vasopressin, endoscopic therapy, or even angiographic embolization
 The surgical choices included vagotomy and pyloroplasty with oversewing of the
hemorrhage or near-total gastrectomy

17. ESOPHAGITIS
 infrequently the source for significant
hemorrhage
 GERD  Esophageal inflammation 
chronic blood loss
 Other causes  medications, Crohn’s
disease, and radiation
 suppressive therapy, Endoscopic
control
 Surgery is seldom necessary

18. DIEULAFOY LESION
 vascular malformations, primarily along
the lesser curve of the stomach within 6
cm of the gastroesophageal junction
 rupture of unusually large vessels (1 to
3 mm)
 Erosion of the gastric mucosa overlying
these vessels
 mucosal defect is usually small (2 to 5
mm)  difficult to identify
 endoscopic control, embolization,
surgical intervention

19. GASTRIC ANTRAL VASCULAR
ECTASIA(GAVE)/WATERMELON STOMACH
 collection of dilated venules appearing
as linear red streaks converging on the
antrum
 Acute severe hemorrhage is rare
 persistent, iron deficiency anemia from
continued occult blood loss
 Endoscopic therapy is indicated for
persistent, transfusion-dependent
bleeding
 antrectomy.

20. MALIGNANCY
 Associated with chronic anemia
 Hemoccult-positive stool rather than episodes of significant hemorrhage
 Ulcerative lesions that may bleed persistently
 GIST, leiomyomas, lymphomas.
 Surgical resection is indicated rather than endoscopic therapy

21. AORTOENTERIC FISTULA
 Primary aortoduodenal fistulas are rare
 The more common entity seen clinically is a graft-enteric erosion
 the median interval is about 3 years
 pseudoaneurysm at the proximal anastomotic suture line in the
setting of an infection  subsequent fistulization
 often massive and fatal
 present first with a “sentinel bleed.”
 Any evidence of bleeding in the distal duodenum (3rd
/4th
portion)
on EGD should be considered diagnostic
 Therapy includes ligation of the aorta proximal to the graft,
removal of the infected prosthesis, and extra-anatomic bypass

22. HEMOBILIA
 typically associated with trauma, recent instrumentation of the biliary tree, or
hepatic neoplasms
 suspected in anyone who presents with hemorrhage, right upper quadrant pain,
and jaundice (Quincke's triad)
 Endoscopy can be helpful by demonstrating blood at the ampulla
 Angiography is the diagnostic procedure of choice.
 If diagnosis is confirmed, angiographic embolization is the preferred treatment

23. OTHERS
Hemosuccus pancreaticus
 Bleeding is bleeding from the
pancreatic duct
 Erosion of a pancreatic pseudocyst
into the splenic artery
 Abdominal pain and hematochezia
 Angiography is diagnostic and
permits embolization, which is often
therapeutic
Iatrogenic bleeding
 follow therapeutic or diagnostic
procedures
 percutaneous transhepatic procedures
 Endoscopic sphincterotomy
 upper GI surgery
 resection and anastomosis

24. SPECIFIC CAUSES OF
UPPER GASTROINTESTINAL
HEMORRHAGE
Bleeding Related to Portal Hypertension

25. PORTAL HYPERTENSION
 Most often in the setting of cirrhosis
 Result of bleeding from varices
 Collateral pathway for decompression
of the portal system into the systemic
venous circulation
 Most common in the distal esophagus

26. MANAGEMENT
 Fluid resuscitation in patients with cirrhosis is a delicate balance
 Early admission to an ICU setting
 Low threshold for intubation
 Defects in coagulation are common
 Underlying sepsis

27. MANAGEMENT
 Medical management
 Pharmacologic therapy to reduce portal hypertension
 Vasopressin produces splanchnic vasoconstriction
(cardiac vasoconstriction)
 somatostatin or its synthetic analogue, octreotide
 Terlipressin is a newer vasopressin
 Temporary control of bleeding and allows time for
resuscitation
 Endoscopic management
 varices are identified, sclerotherapy and variceal banding
 Banding seems to have a lower complication rate and,
when expertise is available, should be the therapy of
choice

28. MANAGEMENT
 Other management
 Balloon tamponade – sengstaken-blakemore tube, the minnesota tube
 Self-expanding esophageal stents
 Emergent portal decompression – TIPS and surgical shunting
 Isolated gastric varices  due to left sided hypertension  splenectomy
 Prevention of rebleeding
 Nonselective beta blocker, such as nadolol, and an antiulcer agent, such as a PPI or
sucralfate
 Endoscopic band ligation repeated every 10 to 14 days until all varices have been
eradicated
 Elective portal decompression
 The preferred elective shunt is a selective distal splenorenal shunt

29. THANK
YOU