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Upper gastrointestinal bleeding: What medics should know

In patients with UGI tract hemorrhage, initiate early transport and, if the patient needs to be supine, use a lateral position to decrease the risk of aspiration

It's a long haul from the mouth to the anus and a lot goes on during the trip to extract the nutrients we need to survive and dispose of the non-nutritional leftovers. Obviously, this system requires an extensive blood supply to accomplish its mission, but sometimes that blood flow gets diverted.

Brief anatomy
The gastrointestinal system is mostly one long tube with an opening at each end, with a variable internal tube diameter depending on function. The system follows a somewhat winding path so that most of it can be contained within the abdominal cavity. The tube is divided into an upper and a lower gastrointestinal (GI) tract. The division point is at the ligament of Treitz, a band of muscle and connective tissue that secures the last section of the duodenum to the diaphragm.1 Anything north of the ligament is upper GI: the duodenum, stomach, esophagus and mouth. Anything south of the ligament is lower GI: the rest of the small intestine (jejunum, ileum), cecum, colon and rectum. The upper GI tract is largely responsible for intake and digestion and the lower GI tract for absorption and excretion.

Upper gastrointestinal bleeding is divided into variceal and non-variceal sources. Variceal bleeding is from dilated and over distended veins (varices) in the esophagus and stomach that can produce excessive vessel wall tension and potentially tear thru the vein and bleed. The elevated pressure in these veins is from portal hypertension. The portal venous system moves nutrient rich blood from the GI tract to the liver for processing.2 If the liver is damaged by excessive alcohol use or disease like hepatitis, scarring occurs that can produce cirrhosis of the liver. This causes the hepatic veins to narrow and increase the back pressure in the portal system which produces the portal hypertension that over distends the veins in the esophagus and stomach that may tear and bleed.3

The diseased liver may provide a second threat to life by producing inadequate amounts of clotting factors, thus impeding the formation of blood clots. These patients may require replacement of clotting factors via the transfusion of whole blood or by infusing fresh frozen plasma when packed red blood cells are utilized. Additionally, if excessive alcohol intake is involved, platelets counts can be abnormally decreased and add a third life threat from bleeding.

Non-variceal upper gastrointestinal bleeding or NVUGIB is most frequently from gastric ulcers which are often caused by infection with the bacteria H. Pylori or from overuse of non-steroidal anti-inflamatory drugs, NSAIDSs, such as aspirin, ibuprofen, naproxen, etc. Less common causes of NVUGIB are esophageal ulcers, Mallory-Weiss tears that occur around the gastro-esophageal junction from forceful vomiting, gastric or esophageal erosions from excessive alcohol use or from NSAIDS.4

Prehospital treatment
Field treatment for UGI bleeding is the same as the treatment for any internal bleeding or for external bleeding that cannot be controlled with pressure, hemostatic dressings/pads/gauze, or a tourniquet. Treatment includes: timely transport, supplemental oxygen, judicious fluid therapy and frequent reassessment. If you can provide an anti-emetic, then less vomiting may prevent the disruption of formed clots.

Initial facility care
The receiving facility will reassess the patient for signs and symptoms of inadequate perfusion and determine if a blood transfusion is required. Inserting a nasogastric or NG tube will provide a visual of the bleeding activity. A bright red blood NG tube aspirate (or emesis) from NVUGIB or a dark venous blood aspirate (or emesis) from variceal hemorrhage would suggest recent bleeding. If the suction canister for the NG tube continues to fill with either shade of blood, then active bleeding is in progress. If the tube aspirate (or emesis) looks like coffee grounds, then bleeding has occurred in the recent past and become partially digested.

On occasion, patients with UGIB may exhibit copious rectal bleeding from profuse UGI hemorrhage that pushes the blood through the bowel too fast to be broken down or mixed with stool. Fortunately, this does not occur very often. Most cases of rectal bleeding are mild and due to non-life threatening problems like hemorrhoids. Melena is a black, tarry, sticky, smelly stool that is formed as blood moves at a normal pace through the bowel allowing the blood to be digested and well mixed in the stool prior to hitting the end of the line. But all that is black is not blood. Ingested iron, bismuth or black licorice may produce a black stool, although it doesn't tend to be as tenacious and odorous as its cousin melena.

For the patient with suspected NVUGIB, the use of proton pump inhibitors (PPIs) such as omeprazol, pantoprazol or lansoprazol can help slow the bleeding by decreasing the acid production of the stomach and the damage the acid inflicts on exposed blood vessels.4 PPIs may also prevent excess acid from disassembling blood clots already formed in the stomach.5

The patient with suspected variceal bleeding will often have signs and symptoms associated with severe liver damage such as ascites, edema, jaundice, and bruising. Octreotide, a commercial form of the hormone somatostatin, is administered intravenously to produce vasoconstriction of the arterial blood supply to the GI tract. This decreases the venous blood flow in the portal system, which decreases the back pressure in the gastroesophageal varices, which decreases the potential for bleeding.3 It is not clear if octreotide is effective in NVUGIB, but if the bleeding source is unknown the initial facility provider may opt to administer octreotide after the PPI.

Specialty care
Ultimately, patients with UGI bleeding will need the care of a gastroenterologist and, on occasion, a surgeon. Gastroenterologists utilize esophagogastroduodenoscopy (EGD) to view the UGI tract. This is accomplished with a long flexible fiberoptic tube about the diameter of your little finger that is connected to a video camera and provides direct visualization of the esophagus, stomach and first part of the duodenum. Obviously, being able to visualize the upper GI tract generally makes the diagnosis. If active blood flow is noted, a variety of therapeutic attacks on the source of bleeding can be made via the EGD scope. Various devices can be inserted through extra channels built into the EGD tube to reach the esophagus, stomach and duodenum. The business end of these long handled instruments can provide cauterization of bleeding sites, or the ability to band or clip bleeding vessels, or inject areas of hemorrhage with vasoconstrictors such as epinephrine or vasopressin, or inject sclerosing agents (irritants) into varices to cause clotting and scarring to plug the leak.

The need for surgery to control UGIB is infrequently necessary and generally required only after EGD interventions are unable to control hemorrhage.

In patients with UGI tract hemorrhage, initiate early transport and, if the patient needs to be supine, use a lateral position to decrease the risk of aspiration. Make sure you have your gown, mask and face shield in place as these patients tend to vomit and, in the back of the ambulance, they may be pointed in your direction. Obtain intravenous or intraosseous access en route and maintain systolic blood pressure in the 80-90 mmHg range to keep the vital organs alive without increasing blood loss. And notify the receiving facility early — forewarned is forearmed.


1. Gray H, Lewis WH. Gray's Anatomy of the Human Body. 20th Ed. New York, NY: Bartleby; 2000
2. Witmer LM. Clinical Anatomy of the Portal System in the Context of Portal Hypertension. Available at http://www.oucom.ohiou.edu/dbms-witmer/downloads/portal.pdf. Accessed September 23, 2011
3. Garcia-Tsao G, Sanyal AJ, Grace ND, Carey W. Prevention and Management for Gastroesophageal Varices and Variceal Hemorrhage in Cirrhosis. Hepatology 2007; 46(3):922-937.
4. Cappell MS, Friedel D. Initial Management of Acute Upper Gastrointestinal Bleeding: From Initial Evaluation up to Endoscopy. Med Clin N Am 2008; 92:491-509
5. Green FW, Kaplan MM, Curtis LE, Levine PH. Effect of acid and pepsin on blood coagulation and platelet aggregation. A possible contributor to prolonged gastroduodenal mucosal hemorrhage. Gastroenterology. 1978; 74(1):38-43

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