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DDx, Manangement, Treatment Upper GI Bleeding. Introduction Definition: bleeding originating proximal to the ligament of Treitz (suspensory muscle of.

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Presentation on theme: "DDx, Manangement, Treatment Upper GI Bleeding. Introduction Definition: bleeding originating proximal to the ligament of Treitz (suspensory muscle of."— Presentation transcript:

1 DDx, Manangement, Treatment Upper GI Bleeding

2 Introduction Definition: bleeding originating proximal to the ligament of Treitz (suspensory muscle of duodenum) Incidence: 47 per 100,000 bleeding stops spontaneously in 75% of cases More common in males and the elderly

3 Look for signs of shock  massive digestive hemorrhage pallor, prostration, perspiration, pulselessness and pulmonary insufficiency Prevent aspiration of blood Provide definitive airway management Stabilize the circulatory dynamic state intravenous injection of extracellular fluid Administer oxygen Institute cardiac monitoring. Give gastric acid secretion inhibitors gastric acid inhibits blood coagulation Replace volume with crystalloids. Emergency Care

4 If coagulopathy is present, transfusion is necessary. Transfusions should be based on the clinical findings of volume depletion or continued bleeding rather than initial hematocrit values. General guidelines for initiation of blood transfusion continued active bleeding failure to improve perfusion and vital signs after the infusion of 2 L of crystalloid. The threshold for blood transfusion should be lower in the elderly. Coagulation factors should be replaced, as needed. When the circulatory dynamic state is stable and UGIH has been judged as cause of shock, urgent endoscopy is performed. Transfusion

5 Medical History Hx of GI bleeding, esophageal varices, alcohol use, medications recent weight loss, change in stools, abdo pain, abdo aneurysm repair, liver disease, or abdo surgery. Vomiting/retching suggestss Mallory–Weiss tears Hx of hemorrhoids, anal fissures, or rectal trauma In AIDS/ immunocompromised patients, bleeding may be related to Kaposi sarcoma, lymphoma, or cytomegalovirus ulcerations.

6 Physical Examinations Vital signs: hypotension, tachycardia, decreased pulse pressure or tachypnea. Spider angiomata, palmar erythema, jaundice, and gynecomastia suggest liver disease. Petechiae and purpura suggest an underlying coagulopathy. Skin findings may be suggestive of the Peutz-Jeghers, Rendu- Osler-Weber, or Gardner syndromes. An ENT examination can reveal an occult bleeding source that has resulted in swallowed blood and subsequent coffee-ground emesis or melena. The abdominal examination may disclose tenderness, masses, ascites, or organomegaly. A rectal examination is indicated to detect the presence of blood and its appearance (bright red, maroon, or melanotic).

7 Diagnostic Studies Endoscopy: gold standard tool for Dx of UGI bleeding Locates source of bleed 75-95% of time If actively bleeding, performed ASAP If not, and patient is stable, performed within 24 hrs Angiography: 1% of patients with upper GI bleeding may be useful if endoscopy cannot identify a bleeding source even when active bleeding is suspected Exploratory laparoscopy: a group of operations that are performed with the aid of a camera placed in the abdomen

8 Treatment Endoscopic hemostasis Mechanical Hemoclip, balloon tamponade, ligation Physically stops the bleeding Injection Ethanol, epinephrine, monoethanolamine oleate Induces: thrombosis, vasoconstriction, vascular tamponade, sclerosis Thermocoagulation APC, laser, hemostatic forceps, microwaves Triggers blood coagulation upon contact Hemostyptic spray/Tissue adhesives Thrombin, fibrin glue, sodium alginate Physically stops bleeding by formation of a solid plastic cast

9 Laboratory Tests Type and cross-match blood. FBC, BUN, creatinine, electrolyte, glucose, coagulation, and liver function studies should be considered Elevated BUN levels due to digestion and absorption of hemoglobin, and a BUN:creatinine ratio 30 is suggestive of a UGI source of bleeding. Coagulation studies: INR, PTT, and platelet count

10 Monitoring for Rebleeding Gastric lavage: Via nasograstic (GN) tube Reassess with using intermittent low continuous suction Continued bleeding or rebleeding  emergent endoscopy Stool: Record frequency, color, and approximate amount of stool Continued passage of bright red, maroon, or melenic stools  further studies or transfusion Hemoglobin/Hematocrit: Check every 4 hours

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13 Pathophysiology Peptic Ulcer Disease Gastritis Esophageal and Gastric Varices Mallory-Weiss Syndrome Other Causes

14 Peptic Ulcer Disease (PUD) Clinical Findings: epigastric to LU quadrant burning pain, pain can be made worse/better with food depending on location of ulcer Treatment: PPIs Somatostatin: peptide reduce splanchnic blood flow, GI motility, inhibit acid secretion, etc. Disposition: Admit patients with: active bleeding, tachycardia, hypotension, anaemia, >65 yo, significant comorbid disease. Otherwise, a follow up with gastroenterologist and discharged

15 Gastritis Definition: inflammation of the lining of the stomach Clinical Findings: Although gastritis is asymptomatic in many cases, patients may experience anorexia, nausea, dyspepsia, pain, and immediate postprandial emesis. Gastritis rarely results in massive bleeding by itself, but it can occur in the presence of portal hypertension and coagulopathies. Treatment: Continue nasogastric lavage until brisk bleeding has resolved. For nonbleeding, clinically suspected gastritis, a trial of an antacid with viscous lidocaine ("GI cocktail") may provide quick relief. Consider prescribing a proton-pump inhibitor or any of the many over-the-counter histamine H2 antagonists.

16 Esophageal Varices Cause underlying liver disease and portal hypertension are at increased risk for esophageal or gastric variceal bleeding. 40% develop this symptom Mortality 30-50% Alcohol-induced and viral cirrhosis most common in USA Parasite most common in developing countries Clinical: cannot be clinically diagnosed on the basis of signs and symptoms alone. approximately 50% of patients with known varices who present with GI bleeding, the bleeding is from a source other than the varices. Endoscopic verification is mandatory for accurate diagnosis and treatment.

17 Treatment Medical Therapy evacuation of gastric contents including blood. octreotide has been proven effective in controlling bleeding. Octreotide decreases splanchnic and hepatic blood flow as well as transhepatic and variceal pressures. Endoscopic Therapy Endoscopic variceal ligation (EVL)- banding of blood vessels Repeated every 2 weeks until variceals are gone (2-4 sessions) Sclerotherapy involves the injection of various sclerosing agents to promote thrombus formation. Band ligation uses endoscopically placed rubber bands, which block blood flow and promote thrombus formation. Both therapies work well in over 90% of patients, but band ligation is associated with fewer complications. Balloon Tamponade In rare circumstances it may be necessary to insert the Sengstaken–Blakemore tube to tamponade uncontrolled hemorrhage prior to endoscopic confirmation. It compress swollen blood vessels called

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19 Mallory-Weis Syndrome Definition: Tears in the esophageal mucosa and submucosa that usually occur after forceful retching and vomiting. Bleed stops spontaneously. 3% mortality Clinical Findings: retching, vomiting this disorder has been reported following chest compressions, coughing, sneezing, or even straining with bowel movement. Many cases have no discernible predisposing factor. Treatment: Provide emergency management. Nasogastric lavage until clear. For persistent bleeding, consult with an endoscopist for emergent EGD A proton-pump inhibitor may be used to reduce acid or bile that may impair healing of the mucosal tear. Treating precipitating factors such as antiemetics for nausea and vomiting. most patients stop bleeding spontaneously with healing of the mucosal tear in 48–72 hours.

20 Other Causes Stress ulcer arteriovenous malformation malignancy Ear, nose, and throat sources of bleeding can also masquerade as GI hemorrhage.


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