Upper Gastro-Intestinal Bleeding Case Discussion.pptx
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Nov 02, 2025
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About This Presentation
UGIB case
Size: 862.4 KB
Language: en
Added: Nov 02, 2025
Slides: 50 pages
Slide Content
Case Discussion on Upper GI Bleeding Presenter- Bethlehem Alemayehu (IMR3) Moderator- Dr. Rezene Berhe (Consultant Internist, Gastroenterologist and Hepatologist )
History C.C- bloody vomiting of 4 days HPI 23 year old male patient who presented to the ER with a history of 01 episode of bloody vomiting which was massive h as also had complaints of easy fatigability, tinnitus and light headedness had history of black, tarry stool prior to that
History Cont’d had frequent complaint of epigastric pain for which he was taking OTC medications lives in west Harerge & has hx of river water contact chews chat on a regular basis
Otherwise… n o hx of regurgitation No history of other medication use no hx of alcohol use, binge drinking or retching n o cough, chest pain or weight loss no hx of yellowish discoloration of eye , n o constipation or straining no hx body swelling no personal or family hx of liver disease n o previous surgical history
Physical Examination GA - acutely s ick l ooking v/s BP- 100/60 PR- 110 RR- 20 HEENT- pale conjuctivae , NIS LGS- no significant lymphadenopathy Chest- clear CVS- S1 & S2 well heard, no murmur or gallop Abdomen- flat, moves with respiration, no organomegally Msk - no edema or rash CNS- GCS-15/15
Investigation Cont’d Abdominal ultrasound- Liver is 12cm in size but has irregular border and coarse echotexture. No focal lesion seen. The portal veins are dilated main portal vein measuring 18mm with decreased velocity measuring 12cm/sec. Hepatic veins are normal. Spleen is enlarged measuring 15cm normal in echo. Conclusion: Splenomegaly , minimal ascites, coarse liver with irregular border, portal vein dilated and decreased velocity. (Signs of portal hypertension with features of early cirrhosis)
Rx Omeprazole 40mg IV BID Plasil 10mg IV TID Transfused with 03 units of packed RBCs EGD planned
Differential Diagnoses UGIB 2ry to Bleeding Peptic Ulcer UGIB 2ry to Mallory-Weiss Tear UGIB 2ry to Esophagitis
1. PUD a defect in the gastric or duodenal mucosa that extends through the muscularis mucosa into the deeper layers of the wall Major risks: NSAID use , H.pylori infection , or both rates have been steadily falling over the past several decades the prevalence of ulcer disease in young people has declined NSAID-related ulcers in older adults have increased due both to increased
2. Erosive Esophagitis growing in proportion to peptic ulcer disease as a cause of UGIB p atients often have a history of GERD Hematemesis appears to be more common compared to melena often have a more benign course, with shorter hospital stays, lower rebleeding rates, and lower mortality rate compared to other causes
3 . Mallory Weiss Tears longitudinal mucosal lacerations (intramural dissections) in the distal esophagus and proximal stomach usually associated with forceful retching bleeding is often from submucosal arteries amount of blood loss is usually small and self-limited
Our Patient… EGD There are columns of long tortuous esophageal varices involving more than third of the distal esophageal lumen. Four bands were applied starting from the most distal part of the in spiral fashion and the proximal part of the varices collapsed subsequently. There is no significant post band bleeding. The pt was transferred to ER with stable v/s . plan was to continue supportive care, to identify & treat the underlying cause of portal hypertension, to start & optimize NSBB, unfortunately the pt disappeared from the ER
Final Assessment Acutely decompensated cirrhosis 2ry to ? with UGIB 2ry to Esophageal Varices with severe anemia
Varices develop as a consequence of portal hypertension in approximately 50 percent of patients with cirrhosis variceal hemorrhage occurs at an annual rate of 5 to 15 percent onset of UGIB from varices usually signifies significant portal hypertension developing bleeding while being treated with a beta blocker is a poor prognostic sign differentiating variceal from nonvariceal bleeding clinically, even in patients with known cirrhosis, could be difficult Risk factors for variceal hemorrhage include increasing severity of liver disease, increasing Child-Pugh class, variceal size, and the presence of red wale markings on varices
Approach to Upper GI Bleeding
Intraluminal bleeding from an intestinal source originating proximal to the ligament of Treitz . esophagus, stomach, and duodenum Overt bleeding Hematemesis (red blood/ coffee ground emesis), Melena, Hematochezia (passage of red or maroon blood per rectum) Occult bleeding Anemia Obscure bleeding Recurrent/persistent GI bleeding from a source that can not be identified using upper or lower endoscopy
Severe GI bleeding Shock or orthostatic hypotension A drop in hematocrit by 6% or hemoglobin by 2gm/dl Transfusion of at least 2 units of packed RBC
80% GI bleed is self limited 20% continue to bleed 30-40% mortality Benefit most from acute medical, endoscopic or surgical interventions Mortality rate of 5%-10% for Severe UGI bleeding has not changed since the 1970s Increase in the proportion of older patients increase in the number of patients with cirrhosis and variceal bleeding.
Initial Evaluation PATIENT ASSESSMENT assess hemodynamic stability and the necessity for fluid resuscitation If there is hemodynamic instability Resuscitation must be commenced immediately Insert at least two large bore IV cannulae (into large peripheral veins) Supplemental oxygen to keep SpO2 >92%
Estimation of blood loss
Draw blood samples urgently Hemoglobin : may be normal initially (12-24 hours) Urea: Elevated urea may indicate severe UGIB Cross match for transfusion Organ function test PT/INR
Resuscitation and Stabilization Optimal fluid resuscitation and stabilization is essential prior to endoscopy Patients with active bleeding should receive intravenous fluids/crystalloids Patients at risk of fluid overload may require intensive monitoring. Intubation for airway protection severe ongoing hematemesis and/or altered mental status
Blood transfusion Blood transfusions must be individualized . Restrictive blood transfusion strategy Transfuse if Hgb g/dl Target Hgb 7-9 g/dl High risk patients ( older adults, coronary artery disease or advanced cirrhosis) Transfuse if Hgb g/dl to maintain a Hgb level of 10 g/dl.
Patients with active bleeding and hypovolemia may require blood transfusion despite normal hemoglobin . Platelet transfusion if platelet count is below 50,000/mm3 FFP, PCC can be given for patients who were taking warfarin/DOACs
NGT Aspiration May be used to clear blood/clots in the stomach before endoscopy Not recommended for diagnostic purpose
Patients on anticoagulation Patients on ASA: do not discontinue. If discontinued, restart in 3-5 days Patients on DAPT: continue aspirin and d/c the other agent. Discuss with cardiologist. Patients on anticoagulants (VKA, DOACS): discontinue all anticoagulants and restart soon once bleeding is controlled.
Risk stratification Used for nonvariceal UGI bleeding at greatest risk for Mortality And Rebleeding to triage patients to a higher level of hospital care or more urgent endoscopy Pre-endoscopic scoring system Glasgow-Blatchford Score Clinical Rockall Score AIMS65 score Post-endoscopic scoring system Complete Rockall , Baylor Scoring System and the Cedars-Sinai Bleeding Index
Glasgow-Blatchford score GBS= 0-1: Out patient management and endoscopy (<1% false negative rate) GBS likely require endoscopic therapy
Need for any intervention 30 day mortality
PPI before endoscopy – recommended Resulted in significantly reduced rates of high-risk stigmata Did not show any statistically significant difference in the outcomes of mortality, rebleeding , or progression to surgery
Prokinetic agents – routine use not recommended Erythromycin or metoclopramide administered 30 to 60 minutes before endoscopy decreased need for a repeat endoscopy no improvement in other clinical outcomes/survival Recommended for patients with a high probability of having fresh blood or a clot in the stomach
ENDOSCOPY Role in Acute UGIB Effective in Diagnosing And Treating most causes of UGIB Timing of Endoscopy Early endoscopy ( within 24 hrs of hospital admission ) Decreased length of hospital stay and requirement for blood transfusion
ENDOSCOPIC TREATMENT MODALITIES Injection methods Normal saline and Dilute Epinephrine Tamponade effect and pharmacologic effect Sclerosants (alcohol, polidocanol ) Thrombin, fibrin, and cyanoacrylate glue Thermal Non-contact: APC, Nd:YAG Laser therapy Contact: Heater probe, Bipolar coagulation Mechanical therapy Clips, band ligation
Repeat Endoscopy Not routinely recommended Recommended for patients with evidence of recurrent bleeding
Pharmacotherapy PPI Increases luminal PH to >4 (often >6) Enhances platelet aggregation & plasma coagulation Can Consistently keep higher gastric PH H2 receptor blockers acute ↑ in PH but tolerance ( tachyphylaxis ) develops fast, hence not preferred in UGIB Significant decrease in Rebleeding Rate Oral high dose vs IV PPI Similar outcomes Oral PPI can be given if IV PPI is not available IV infusion vs divided dosing: comparable outcomes
Somatostatin & Octreotide Proposed mechanism ↓splanchnic & gastroduodenal mucosal blood flow ↓GI motility ↓gastric secretion Compared to placebo & H2 blockers Decreases risk of rebleeding Uncertain benefits in NVUGIB Not recommended for non variceal UGIB
Angiography and Surgery In patients with refractory bleeding: recurrent bleeding despite 2 sessions of endoscopic hemostasis No significant difference between the two Trans angiography embolization (TAE) Surgery Failed TAE Immediate surgical intervention Massive bleeding and those who cannot be medically resuscitated Large or pulsating visible vessel
Variceal Bleeding Acute mortality rate with each bleed is ~ 30% 30% rebleed in 1 year The higher the HVPG, the higher the risk of bleeding HVPG>20mmHg: high risk of EV bleeding GV bleeding not strongly associated with HVPG
Medical management Vascoactive therapy (Somatostatin and octreotide, Terlipressin ) as effective as sclerotherapy for controlling variceal bleeding an adjunct to endoscopic therapy Terlipressin showed mortality benefit Antibiotics to cirrhotic patients with variceal bleeding High risk of SBP and other infections in such patients decreases in the rates of mortality and bacterial infections Ceftriaxone 1gm IV daily for 5-7 days
Endoscopic Sclerotherapy to achieve initial hemostasis and reduce the risk of rebleeding Endoscopic Band Ligation Reduces the rates of rebleeding , and overall mortality, compared with sclerotherapy Technically challenging to perform during active variceal bleeding Balloon Tamponade Stent (SX Ella stent) Transjugular Intrahepatic Portosystemic Shunt Portosystemic Shunt Surgery Esophageal transection
References Harrison’s Principles of Internal Medicine 21 st Edition Sleisenger And Fordtran’s Gastrointestinal And Liver Disease, 11 th Edition UpToDate https://www.nejm.org/doi/full/10.1056/NEJMoa1211801 https://pubmed.ncbi.nlm.nih.gov/28053181 /