Peptic ulcers are open sores that develop on the lining of the stomach (gastric ulcer) or the first part of the small intestine (duodenal ulcer). These ulcers can cause a person to vomit blood, a condition medically termed hematemesis. Hematemesis is a severe symptom of internal bleeding and signals an acute medical emergency requiring immediate professional care. Ulcers form when the protective layer of mucus lining the digestive tract is eroded, allowing stomach acid to damage the underlying tissue. When this erosion compromises a blood vessel, significant bleeding occurs, which is then expelled through vomiting.
Peptic Ulcers and the Mechanism of Bleeding
The digestive tract’s inner surface is normally protected by a thick layer of mucus and bicarbonate. A peptic ulcer represents a break in this mucosal barrier that extends deep into the wall of the organ. As the ulcer deepens, it moves past the muscularis mucosa layer and into the submucosa, where larger blood vessels are located. A hemorrhage occurs when continuous acid exposure and erosion eventually penetrate the wall of an artery or a vein.
The volume and speed of the bleed dictate how the blood appears when it is vomited. If the bleeding is rapid and the blood has not been exposed to stomach acid for long, the vomit will appear as bright red blood. This bright red color indicates a fresh, active bleed and suggests an ongoing hemorrhage.
If the blood has pooled in the stomach before being expelled, stomach acid begins to digest the hemoglobin. This partial digestion process changes the color and texture of the vomit. The resulting material looks dark, granular, and brown, resembling wet coffee grounds, which medical professionals refer to as “coffee ground emesis.” While both forms of hematemesis are serious, the coffee-ground appearance suggests the bleeding may have slowed or stopped, whereas bright red blood signals an active hemorrhage.
Recognizing Different Types of Gastrointestinal Bleeding
While hematemesis is the most alarming sign of a bleeding ulcer, internal bleeding can manifest in other ways depending on the location and speed of the hemorrhage. Hematemesis specifically points to a source of bleeding in the upper gastrointestinal tract, including the esophagus, stomach, or duodenum. Blood that travels further down the digestive tract is altered by intestinal bacteria and enzymes, changing its appearance in the stool.
Melena is the medical term for dark, black, and tarry stools, which have a distinct foul odor. This appearance is caused by digested blood and is characteristic of an upper GI bleed, such as a peptic ulcer, where the blood has spent enough time in the intestines to be broken down.
Another presentation is hematochezia, which is the passage of bright red blood from the rectum. While typically associated with bleeding in the lower GI tract, a rapid hemorrhage from an upper GI source can sometimes rush through the system quickly enough to still appear red in the stool.
Systemic signs of blood loss can accompany these symptoms and indicate a significant loss of blood volume. These signs include feeling dizzy or lightheaded, a rapid heart rate, or pale, clammy skin. Confusion and weakness are also symptoms of hypovolemic shock, which occurs when blood loss is severe and the body cannot circulate enough oxygenated blood.
Immediate Steps and Emergency Triage
Vomiting blood is always a medical emergency, and the immediate action is to call emergency services. For the individual experiencing hematemesis, the most important initial step is to remain calm and position themselves to prevent aspiration. If conscious, the person should lie down on their side to protect their airway in case of further vomiting. They should not attempt to eat, drink, or take any oral medications.
Upon arrival at the hospital, the medical team’s first priority is rapid resuscitation and stabilization, focusing on the patient’s airway, breathing, and circulation. This often involves establishing multiple large-bore intravenous (IV) lines to begin fluid resuscitation with crystalloid solutions to restore blood pressure and volume. If significant blood loss has occurred, a transfusion of packed red blood cells may be initiated to replenish lost blood volume and maintain oxygen-carrying capacity.
A high-dose infusion of a Proton Pump Inhibitor (PPI) medication is administered immediately to suppress the production of stomach acid. Reducing the acid level helps stabilize the blood clot attempting to form at the ulcer site, which temporarily controls the bleeding. The definitive treatment is typically an upper endoscopy, a procedure where a flexible tube with a camera is passed down the throat to locate the source of the bleeding. During the endoscopy, the physician can treat the ulcer directly by injecting a vasoconstrictor like epinephrine, using thermal coagulation, or applying endoscopic clips to close the compromised vessel.
Underlying Causes of Peptic Ulcers
Understanding the underlying factors that cause peptic ulcers is important for long-term prevention and management. Most peptic ulcers are caused by two primary factors that disrupt the balance between protective mucosal defense mechanisms and acid secretion. The most common cause worldwide is infection with the bacterium Helicobacter pylori (H. pylori), which colonizes the stomach lining. This bacterium causes chronic inflammation and weakens the mucosal barrier, making the tissue vulnerable to acid damage.
The second major cause is the chronic use of Nonsteroidal Anti-Inflammatory Drugs (NSAIDs), such as ibuprofen, naproxen, and aspirin. These medications damage the stomach lining by inhibiting the production of protective prostaglandins. Prostaglandins are hormone-like substances that stimulate the secretion of protective mucus and bicarbonate, and maintain blood flow to the lining. The prolonged use of NSAIDs removes this protective mechanism, leaving the stomach and duodenal walls exposed to acid.
Secondary factors can further increase the risk of ulcer formation or impede healing. Smoking is known to delay ulcer healing and increase the risk of recurrence. Excessive alcohol consumption is also a contributing factor, as it can irritate and erode the mucosal lining, compounding the damage caused by H. pylori or NSAIDs.