UPPER GIT BLEEDING HEMATEMESIS

1. AlyaaAlmuhammad BasmaAlmujadidi UPPER GIT BLEEDINGHEMATEMESIS

2. OBJECTIVES • History & Examination & portal system • Definition & Related terms • Clinical presentation • Differential Diagnosis • Hematemesis VS Hemoptysis • Management

3. History

4. About a third of patients with peptic ulcers do not have symptoms before they bleed. Almost half of the patients who bleed have no symptoms to suggest the cause of the bleeding.

9. Definition • Bleeding derived from any source proximal to the Ligament of Treitz 1 in 1000 in us who experienced upper GI bleeding Men :women 2 : 1 Mortality rate 10%

10. Where is it from? GI TRACTRESPIRATORY TRACTDark red or brown Bright red In clumps Foamy, runny & bubbly Mixed with food mixed with mucous Acidic pH alkaline pH Stomachache, abdominal discomfort chest pain, warmth Nausea, retching before and after episode persistent cough

11. Differentiation mild bleeding severe bleeding Normal Pulse Weak & Rapid Normal BP BP>10Hg Normal breathing Deep & Tach Mucosa slightly dry Parched Slightly Urine OP Anuris Conscious Fainting <15% >15%

12. Surgical opinion is usually sought in case the source of bleeding cannot be identified endoscopically, and laparotomy is necessary.

13. Related Terms • Hematemesis? • Vomiting of blood • Red or Brown Dark ??? Coffee ground • Hematochezia Upper OR Lower? • Blood in the stool • Melena Upper Or Lower? • Black, tarry, smelly stool

14. Upper Gastrointestinal Bleeding Etiology

17. Esophageal varices

18. Clinical Presentation • Hematemesis - 40-50% • Melena - 70-80% • Hematochezia - 15-20% • Syncope - 14.4% • Presyncope - 43.2% • Dyspepsia - 18% • Epigastric pain - 41% • Heartburn - 21% • Diffuse abdominal pain - 10% • Dysphagia - 5% • Weight loss - 12% • Jaundice - 5.2%

19. Hepatic Portal System • system of veins that comprises the hepatic portal veinand its tributaries • Hepatic portal vein • Splenic vein • celiac trunk • superior mesenteric vein • inferior mesenteric vein

20. HPS • Portal Hypertension • Pressure difference between the portal vein and the hepatic veins=< 5 mm Hg • Portacaval Anastomosis portal circulation systemic circulation left gastric veinAzygos vein Esophageal Varices UGIB

21. Peptic Ulcer • A break in the epithelial surface (i.e. ulceration) of the oesophagus, stomach or duodenum . • PU includes Duodenal ulcer. (commonest) Gastric ulcer. Esophageal ulcer. Meckel’s ulcer .

22. Common causes of PU • Infection with H.pylori. • NSAID and the usual suspects (Alcohol ,smoking, stress) • Imbalance between the aggressive and protective mechanisms. • Acid hypersecretion due to increase number of parital cells or as seen in (Zollinger-Ellison syndrome).

23. Clinical Features (PU) • M > F ,20-50 yrs. • Epigastric pain during fasting (hunger pain), relieved by food and Antacids. • Back pain if ulcer is penetrating posteriorly. • Hematemesis from ulcer penetrating GD artery posteriorly. • Can lead to peritonitis if ulcer occurs anteriorly. • Can lead to pyloric stenosis.how?

24. The Forrest classification of PU Bleeding • F-IActive bleeding: F-I/a. Spurting arterial bleeding F-I/b. Oozing bleeding • F-IISigns of recent haemorrhage : F-II/a. Visible vessel on the base of ulcer F-II/b. Coagulum in the ulcer F-II/c. Coffee ground ulcer base • F-III No sign of bleeeding

25. Class Appearance Rebleeding rate(%) I active bleeding 55 II visible vessel 43 III adherent clot 22 IV flat spot 10 V clean base 5

26. Beheviour of PU Bleeding • Spontaneous stoping: 70-80 % • Probability of rebleeding: 30-50 % • Rebleeding within 24-48 hours: 70-80 % • Mortality among patients operated because of rebleeding: 20-30 %

27. Erosive inflammation in the upper GIT • Regular or incidental alcohol intake • Side effect of a medicine NSAID Salycil containing drugs Steroids • Other illnesses • cardio-respiratory, cardio-vascular, trauma, burning & postoperative conditions

28. Duodenal ulcers •Commonest PUD • • >95 % in the first part of duodenum • • more benign • •More associated with H.pylori

29. Gastric ulcer types

30. Different pathogenessis •Type I - body of stomach on lesser curvature, normal to low acid secretion. • Type II – Two ulcers present - body of stomach on lesser curvature, hypersecretion of acid. • Type III – pre pyloric , hypersecretion of acid. • Type IV – lesser curvature , near EGJ, normal to low acid secretion. • Type V – anywhere, NSAIDs related.

31. Gasrtric ulcer distribution • • Most within 2cm from the junction of the antral-fundic mucosa. • • 60% - lesser curvature proximal to the incisuraangularis • • 20-25% prepyloric • • 10% lesser curvature distal to EGJ • • 5-10% greater curvature

32. Mallory-Weiss syndrome (tear) • The cause:the sudden increase of intragastric pressure • Alcohol intoxication • Pathology: Rupture of the mucosa in the cardia • Treatment:Conservative treatment usually sufficient, no need of operation

33. MWS

34. Management: • Initial assessment of the patient : • Patient resuscitation and hemodynamic stabilization • Brief history and examination

35. Patient resuscitation and stabilization:- Check vital signs Assess airway and breathing Assess circulatory status (postural hypotension) Obtain intravenous access ( 2 large bore Ivs 14-18 gauge) Replace volume ( Ringers lactate or normal saline) obtain blood for grouping, cross-match(4-6 unit), haemoglobin, urea, prothrombin time, electrolytes, LFT's. Transfuse blood (if necessary) Catheterization to measure urine output ( >30 ml/hr) Correct any Coagulopathy ( vit k , FFP)

36. Risk assessment : • Mild to Moderate Upper GI Bleeding • The patient is < 60 years of age, and has no chronic medical illness. • There is no sign of hemodynamic instability. • Hematocrit is > 30%. • Severe Upper GI Bleeding • The patient is > 60 years old. • There are signs of hemodynamic instability (Pulse >100/min, SBP < 100 or postural hypotension). • There is active bleeding (bright red hematemesis, bright red blood in NG tube or hematochezia with hypotension). • Drop in hematocrit of 6% or more. • There is severe co morbid disease (liver, cardiac, pulmonary or renal)

37. Keep NPO- incase of sudden repeat bleed , may need urgent endoscopy or NG intubation. ECG – for signs of ischemia or infarct IV PPI ( omperazole – pantoprazole) endoscopy to identify source of bleeding within 24h and type of management afterwards.

38. Medical Therapy; 1-Non-variceal bleeds: • IV H2 receptor antagonists (ranitidine) • IV PPI (pantoprazole) • reduce rebleeding rates, need for surgery and transfusion req. • Dose: IV pantoprazole 80 mg bolus then 8 mg/hr 2- Variceal bleeding • Octreotide – prior to endoscopy in case of active bleeding to help reduce portal venous pressure by splanchnic arterial constriction. • Dose: 250 μg bolus IV then 250 μg/hr. • Long- term non-selective beta-blocker (oral propranolol). *it is the treatment of choice *it is as effective as sclerotherapy and ligation.

39. Indications for intervention are the following : Massive uncontrolled bleeding Rebleeding especially if bleeding vessel or clot on ulcer has been seen at endoscopy More than 4-6 units of blood in 24 hrs

40. Interventional options : Non- operative and Operative

41. Non-operative ( Endoscopic) • The three chief methods of endoscopic therapy are: • Topical treatment • Injection treatment • Mechanical treatment • Thermal treatment

43. 1- In ulcers: injection of adrenaline or vessel coagulated with the heater probe. (H.pylori eradication, stop NSAIDs). 2-In varecis: It is urgent to confirm the diagnosis. Varices injected with sclerosing agent that arrest bleeding by producing vessel thrombosis. Variceal banding. Balloon tamponade (Sengstaken-blakemore tube )

45. Operative ( Surgical) Peptic ulcer: • Suture-Stiching of ulcer • vagotomy • resection type operation Acute erosions: Vagotomy and drainage or partial gastrectomy Oesophagealvarices : oesophagealtransection , portocaval or distal splenorenal shunting Carcinoma: partial or total gastrectomy

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