Profuse bleeding of the g.i. tract may be life-threatening and constitutes a medical emergency that requires prompt treatment in a hospital environment. In the past, most situations like this required emergency surgery and removal of part of the stomach. Now with our newer technology, many bleeding ulcers can be cauterized which stops the bleeding. In many cases, surgery can now be avoided.
Acute gastrointestinal (GI) bleeding is a potentially life-threatening abdominal emergency that remains a common cause of hospitalization. The incidence of upper gastrointestinal bleeding
is defined as bleeding derived from a source proximal to the ligament of Treitz. Hematemesis and melena are the most common presentations of acute UGIB, and patients may present with both symptoms. Occasionally, a brisk UGIB manifests as hematochezia.
The history and physical examination provide crucial information for the initial evaluation of a patient presenting with a GI tract hemorrhage. The history findings can be extremely helpful in determining the location of the GI hemorrhage. Alcohol abuse or a history of cirrhosis should elicit consideration of portal gastropathy or esophageal varices as sources for the bleeding. A history of recent nonsteroidal anti-inflammatory drug (NSAID) abuse should elicit concern about bleeding from a gastric ulcer.
Causes of bleeding are many, and some of the more important ones are listed below:
CAUSES OF HEMORRHAGE OF THE UPPER G.I. TRACT
1. Hemorrhagic esophagitis
2. Esophago-Gstric varices
3. Cancer of the esophagus
4. Mallory-Weiss syndrome
5. Erosive gastritis
6. Gastric ulcer.
7. Stomach cancer
8. Duodenal ulcer
9. Arterio-venous malformation.
10. Gastric or duodenal polyps
11.Dieulafoy´s Lesion (Exulceratio Simplex)
12. Angiodysplasia
13. Aortoenteric fistula
14. Hemobilia.

Mallory-Weiss Syndrome. 34-year-old male physician who had been ingesting alcoholic beverages, presented with bleeding of the g.i. tract.

Mallory-Weiss Syndrome. 43-year-old male who presented with vomiting after ingestion of alcoholic beverages. Also note the signs of reflux esophagitis as well as a blood clot from a gastro esophageal tear.

Dieulafoy´s Lesion (Exulceratio Simplex). You must see the video clip. Here, you can observe in the video clip an active arterial bleeding. We recommend seeing it in full screen mode. 79-year-old female patient which had a bifemoral-aortic surgery (prosthesis) 25 days ago; a week before this procedure, she initiates with upper intestinal bleeding, with hematemesis, melenic stools, paleness and hypotension. She was hospitalized and a emergency endoscopy practiced by another college was performed after a series of ice cold gastric lavage. Due to the active bleeding, it was impossible to diagnose during this Endoscopy. 5 days later, after, the bleeding re-started and she received 4 blood transfusions. We then performed a new Endoscopy a day later and being more aggressive, we used the Therapeutic endoscope, with double channel and a more suction power. After a successful aspiration of the blood and good maneuvering, we were able to see the source of the bleeding. Download the video clip by clicking on the endoscopic image. Dieulafoy´s Lesion is a vascular abnormality found almost exclusively in the proximal stomach that presents dramatically as acute and rapidly recurrent massive upper gastrointestinal hemorrhage when a small sub mucosal artery ruptures into the gastric lumen. Hemorrhage is caused by thrombosis and perforation of an abnormally large, tortuous sub mucosal artery in the center of a solitary 2- to 5-mm gastric mucosal erosion, surrounded by normal-appearing mucosa. Although reports from the pre-endoscopic era suggested a mortality rate of up to 80% more recent series report mortality in less than 30% of cases.

Frequent causes of hemorrhage of the lower digestive tract:
1. Anorectal diseases
2. Polyps of the colon
3. Diverticular disease of the colon.
4. Colon and rectal cancer.
5. Intestinal amebiasis.
6. Ulcerative Colitis
7. Regional enteritis
8. Arterio-venous malformation

Multiple diverticulae of the colon. This frequent cause of rectal bleeding is associated with hemorrhage which is dark red in color.
Please click on the image to download the video clip , wait to be downloaded
complete and press Alt and Enter to appreciate in full screen.

Unspecific ulcerative colitis. Multiple serpentine ulcers, exudate, and edema are seen. Note the presence of pseudo-polyps and the diminished vascular markings.
Please click on the image to download the video clip , wait to be downloaded
complete and press Alt and Enter to appreciate in full screen.

Bleeding of the upper g.i. tract due to gastric ulcer and hipertensive gastropathy.

Active bleeding due to esophageal varices. Note the gastric fundus with bright red hemorrhage.

Same case as above. Observe the site of the hemorrhage with endoscope in retroflection maneuver.

Endoscopic image of same case.




Sclerotherapy for active bleeding due to esophageal varices.

Medical therapy:
Initial management
Resuscitation of a hemodynamically unstable patient begins with assessing and addressing the
ABCs (ie, airway, breathing, circulation) of initial management. Patients presenting with
severe blood loss and hemorrhagic shock present with mental status changes and confusion. In
such circumstances, patients cannot protect their airway, especially when hematemesis is
present. In these cases, patients are at increased risk for aspiration, which is a potentially
avoidable complication that can significantly affect morbidity and mortality. This situation must
be recognized early, and patients must be electively, not emergently, intubated in a controlled
setting using cricoid pressure.
Once the airway is secured, the next step in evaluation is assessing the patient’s circulation. Intravenous access must be obtained. Bilateral 16-gauge (minimum) upper extremity peripheral intravenous lines are adequate for volume resuscitative efforts. Poiseuille law states that the rate of flow through a tube is proportional to the fourth power of the radius of the cannula and is inversely related to its length (Corson, 2001). Thus, short, large-bore peripheral intravenous lines are adequate for rapid fluid infusion. A rough guideline for the total amount of crystalloid fluid volume needed to correct the hypovolemia is the 3-for-1 rule. Replace each milliliter of blood loss with 3 mL of crystalloid fluid. This restores the lost plasma volume. Patients with severe coexisting medical illnesses, such as cardiovascular and pulmonary diseases, may require pulmonary artery catheter insertion to closely monitor hemodynamic cardiac performance profiles during the early resuscitative phase.
Once the ABCs have been addressed, assess the patient’s response to resuscitation based on evidence of end organ perfusion and oxygen delivery. An interesting study published by Kaplan et al evaluated whether the physical examination findings alone or in combination with biochemical markers (arterial lactate levels) can help accurately diagnose hypoperfusion. Their study revealed that skin temperature upon physical examination in combination with serum bicarbonate levels correlated well with the level of systemic perfusion. The patients identified as being hypoperfused based on clinical parameters were confirmed by following the serum lactate or mixed venous oxygen saturation (SvO2) and cardiac index. Pulmonary artery catheters may be helpful to guide therapy. Foley catheter placement is mandatory to allow a continuous evaluation of the urinary output as a guide to renal perfusion. This labor-intensive management should be performed only in an ICU setting.
Once the maneuvers to resuscitate are underway, insert a nasogastric tube (NGT) and perform an aspirate and lavage procedure. This should be the first procedure performed to determine whether the GI bleeding is emanating from above or below the ligament of Treitz. If the stomach contains bile but no blood, UGIB is less likely. If the aspirate reveals clear gastric fluid, a duodenal site of bleeding may still be possible. In a retrospective review of 1190 patients, Luk et al found that positive NGT aspirate findings were 93% predictive of an upper GI source of bleeding.

Various techniques currently available for achieving hemostasis

Injection of vasoactive agents

Injection of sclerosing agents

Bipolar electrocoagulation

Band ligation

Thermal probe coagulation

Constant probe pressure tamponade

Argon plasma coagulator

Laser photocoagulation

Rubber band ligation

Application of hemostatic materials, including biologic glue.

The 3 most popular methods of hemostasis are injection therapy, coaptive coagulation, and laser phototherapy.

Injection therapy involves the use of several different solutions injected into and around the bleeding lesion. The different solutions available for injection are epinephrine, sclerosants, and clot-producing materials such as fibrin glue. The epinephrine used for injection is diluted (1:10,000) and injected as 0.5- to 1-mL aliquots. Epinephrine is a vasoactive agent that works by inducing vasoconstriction and decreasing blood flow to the area. This allows for increased platelet function and clot formation to attain hemostasis. Debate continues over whether the hemostatic effect of epinephrine is due to the induced vessel vasoconstriction and subsequent platelet aggregation or to the tamponade effect produced by injecting the volume of drug into the tissue surrounding the bleeding lesion.

Injecting a volume of sterile isotonic sodium chloride solution and providing a tamponade effect also leads to hemostasis, although not as effectively as epinephrine. Although the injected epinephrine is absorbed into the systemic circulation, this does not appear to have any adverse effects on hemodynamic status. The sclerosant solutions used today include ethanol, polidocanol, and sodium tetradecyl sulfate.

The sclerosants create hemostasis by inducing thrombosis, tissue necrosis, and inflammation at the site of injection. When large volumes are injected, the area of tissue necrosis can produce an increased risk of local complications such as perforation. Combining the various agents into a single injection has not been shown to be more beneficial than single-agent therapy alone. Combining epinephrine injections with human thrombin (600-1000 IU) reduces the risk of bleeding . The use of fibrin glue has been shown to be successful, with results similar to that of epinephrine injections.
Coaptive coagulation uses direct pressure and thermal therapy to achieve hemostasis. Thermal therapy includes monopolar and bipolar electrocoagulation and heater-probe application. The bleeding vessel is isolated, compressed, and tamponaded prior to coagulation therapy. By using both maneuvers, the depth of tissue injury is minimized. Coaptive coagulation is as effective as injection therapy in achieving hemostasis.

Laser phototherapy uses an Nd:YAG laser to create hemostasis by generating heat and direct vessel coagulation. This is a noncontact thermal method. It is not as effective as coaptive coagulation because it lacks the use of compression to create a tamponade effect . An additional deterrent to its use is expense.

Although injection therapy and thermal therapy are highly successful methods to control a bleeding vessel, rebleeding still occurs in 15-20% of cases. Combining injection therapy with heater-probe coagulation can be used in an attempt to reduce the rebleeding rate in high-risk patients who have spurting arterial bleeding observed during endoscopy. The epinephrine injection stops the bleeding by vasoconstricting the vessel, which then provides a clearer view for the endoscopist to see the lesion, to apply the heater probe to the appropriate area, and to permanently seal the vessel. Chung et al compared single-agent therapy to combined epinephrine injection with heater-probe application. The study revealed a reduction in the incidence of rebleeding and the need for emergent surgical intervention when using combined therapy.

The endoscopic appearance of the bleeding lesion has been used to identify patients at high risk for recurrent bleeding. The indication for endoscopic therapy is based on the size, site, and stigmata of recent bleeding. An actively bleeding vessel is treated because it is a high-risk lesion with a 55% risk for recurrent bleeding. A nonbleeding visible vessel is also a high-risk lesion that is treated because of its 43% risk for rebleeding. Recurrent bleeding occurs most commonly within the first 72 hours.

Treatment of clots adherent to a lesion is based on the patient’s risk factors to withstand and survive another bleeding episode. The risk for rebleeding varies from 14-36%. Low-risk lesions are those that appear as flat, pigmented spots and those that involve a clean ulcer base with no visible vessel. The risk for rebleeding in these lesions is 10% and 5%, respectively. Endoscopic treatment of these low-risk lesions is not usually performed.

Upper gastrointestinal hemorrhage due to esophageal varix. This image displays the exactly site of the bleeding at the cardias, actve variceal bleeding is appreciated. The major challenge for the endoscopist is to determine if the bleeding has been from esophageal, esophagogastric, or isolated gastric varices. In the absence of active bleeding or an obvious adherent or protruding clot, large distal esophageal varices (i.e., within 5 cm of the squamocolumnar junction) with red wale markings should be interpreted as the cause of bleeding. Endoscopic therapy should be initiated and directed at these varices. If the esophageal varices continue into the cardia, that is, are esophagogastric varices, endoscopic therapy should begin on the cardia side of the squamocolumnar junction because the gastric component of these varices usually can be eliminated. Once initiated, endoscopic therapy should most often be pursued with the eventual goal of eradication. After the initial treatment, endoscopic therapy is usually repeated in 5 to 7 days and then every 1 to 2 weeks until the distal esophageal varices are obliterated or reduced to a very small size. The interval between follow-up procedures tends to be longer (i.e., 2 weeks) in patients who have undergone variceal band ligation. Once eradicated, varices are typically reexamined in 6-month periods. About 30% of patients with cirrhosis and portal hypertension bleed from ruptured esophageal varices. 1 with a mortality for the initial bleed that may exceed 50% After a first bleed, untreated patients have a risk of rebleeding as high as 60%. The risk decreases with time, returning to baseline values by the sixth week after the variceal bleeding episode. Although gastric varices also bleed, little information is available on their natural history and their fate after endoscopic sclerotherapy of esophageal varices. The goals of treatment in acute variceal bleeding are: a. Correct hypovolaemia b. Stop bleeding as soon as possible c. Prevent early rebleeding c. Prevent complications e. Prevent deterioration of liver function.

The video displays multiple varices that have been banding. Mortality due to variceal bleeding secondary to portal hypertension has decreased significantly in the past 2 decades. Endoscopic therapy has been the mainstay of treatment for acute variceal bleeding. Variceal banding ligation has superceded injection sclerotherapy as the most popular treatment modality for acute bleeding. Multiple banding ligators are widely used with high success in restoring hemostasis. The combination of banding and sclerotherapy may be useful in preventing the early recurrence of varices and rebleeding after initial obliteration of varices. Click on the image to download the video clip.

Endoscopic sequence 1 of 2. Upper intestinal bleeding deriving from a multiple giant gastric ulcers which provided multiple bleeding sites. The image and video can observe active bleeding at the bottom of a giant Gastric ulcer. The patient received several gastric lavages with ice cold water by the doctor who sent us the patient. During the endoscopy, we suctioned abundant blood.

Endoscopic sequence 2 of 2. 76-year-old female which had a daily dose of aspirin, presents with abundant hematemesis and melenic stools, paleness, and hypotension a ay before the endoscopy. The image and video shows a giant ulcer and a visible vessel at the incisura angularis.

Endoscopic Sequence 2 of 2. Upper gastrointestinal hemorrhage due to duodenal ulcer.

Endoscopic Sequence 2 of 2. The image and the video display a duodenal ulcer at the posterior wall. The ulcer has some vessels that are the etiology of the bleeding.

This image and the video clip display a diverticulosis with active bleeding. Lower GI bleeding from iverticulosis occurs in the form of bright red-colored or wine-colored stools