Hematemesis
Hematemesis is the medical term for the vomiting of blood or blood-containing material from the upper gastrointestinal tract, typically appearing as bright red blood or dark, coffee-ground-like material due to partial digestion by stomach acid.[1] It is a hallmark symptom of upper gastrointestinal bleeding (UGIB), which originates proximal to the ligament of Treitz in the esophagus, stomach, or duodenum, and often accompanies other signs such as melena (black, tarry stools) or systemic symptoms like orthostasis and fatigue.[2] The condition arises from various underlying etiologies, with peptic ulcer disease accounting for 32-36% of cases, followed by esophagitis (24%), gastritis (18-22%), duodenitis (13%), and esophageal varices (11%).[2] Other notable causes include Mallory-Weiss tears from prolonged vomiting (5-15%), vascular anomalies like Dieulafoy lesions, neoplasms such as esophageal or gastric cancer, and erosive conditions exacerbated by nonsteroidal anti-inflammatory drugs (NSAIDs), aspirin, or Helicobacter pylori infection.[3] In patients with liver disease, portal hypertension can lead to varices, while less common triggers encompass clotting disorders, pancreatitis, or swallowed blood from epistaxis.[4] Epidemiologically, UGIB has an annual incidence of 80-150 cases per 100,000 people, predominantly affecting men and increasing with age; it represents about 75% of acute gastrointestinal hemorrhages, though U.S. hospitalization rates declined by 21% from 2002 to 2012.[2] Mortality ranges from 2-10%, underscoring the need for prompt intervention, as significant blood loss can result in shock, organ damage, or death if untreated.[4] Diagnosis typically involves urgent evaluation with blood tests (e.g., complete blood count, coagulation studies, liver function), nasogastric lavage to confirm upper GI origin, and esophagogastroduodenoscopy (EGD) as the gold standard for identifying the bleeding source.[4] Treatment focuses on hemodynamic stabilization through intravenous fluids, blood transfusions, and acid-suppressive therapy (e.g., proton pump inhibitors), with endoscopic interventions like clipping, banding, or sclerotherapy for active bleeding; surgery is reserved for refractory cases.[2] The prognosis depends on the etiology and timeliness of care, with many episodes resolving spontaneously but requiring long-term management of underlying conditions to prevent recurrence.[4]Overview
Definition
Hematemesis is defined as the vomiting of blood that originates from the upper gastrointestinal tract, specifically the esophagus, stomach, or duodenum.[2] This condition involves the regurgitation of fresh blood or blood mixed with gastric contents, which can appear bright red if recent or altered due to exposure to gastric acid.[5] A key feature distinguishing hematemesis from similar presentations is its source: bleeding must arise proximal to the ligament of Treitz, the anatomical boundary marking the transition from the duodenum to the jejunum.[6] In contrast, coffee-ground emesis refers to the vomiting of partially oxidized blood, presenting as dark, granular material resembling coffee grounds, which indicates slower or older bleeding within the upper tract.[7] Hematemesis must also be differentiated from hemoptysis, the coughing up of blood from the lower respiratory tract, as well as from the vomiting of swallowed blood due to epistaxis (nasal bleeding) or hematochezia, which is the passage of bright red blood per rectum from lower gastrointestinal sources.[5][7] Clinically, hematemesis signals active or recent hemorrhage from the upper gastrointestinal tract and is frequently considered a medical emergency due to the risk of significant blood loss and hemodynamic instability.[1] It is often associated with underlying conditions such as peptic ulcers.[2]Epidemiology
Hematemesis represents a prominent manifestation of upper gastrointestinal bleeding (UGIB), with global incidence rates for UGIB varying widely from 15 to 172 cases per 100,000 person-years, reflecting differences in diagnostic access and underlying etiologies.[8] In high-income countries, the annual incidence of UGIB is approximately 80 to 150 per 100,000 population, while rates are higher in low- and middle-income countries due to factors such as untreated peptic ulcers and limited healthcare resources.[2][9] Hematemesis accounts for approximately 30% to 50% of UGIB presentations in adults, often indicating more active or voluminous bleeding compared to melena alone.[2] Mortality rates for acute UGIB range from 2% to 10% overall, with case-fatality proportions of 0.7% to 4.8%; these figures are higher in low-resource settings, where delays in intervention contribute to poorer outcomes.[2][8][9] Patients presenting with hematemesis experience worse short-term outcomes, including a 10-fold higher likelihood of requiring emergency blood transfusions and extended hospital stays averaging 6 additional days, though all-cause mortality differences compared to non-hematemesis UGIB remain statistically imprecise in smaller cohorts.[10] Demographically, hematemesis and UGIB occur more frequently in males, with a male-to-female ratio of about 2:1, attributed to higher rates of risk behaviors and comorbidities in men.[2] The condition peaks in incidence during ages 50 to 70 years, with over 70% of cases affecting individuals aged 60 or older, as age-related physiological changes and cumulative exposures amplify vulnerability.[2][11] Major population-level risk factors for hematemesis include a history of prior GI bleeding, which elevates recurrence risk; anticoagulant and antiplatelet therapy, such as warfarin or aspirin, increasing odds by 2- to 3-fold; high-dose nonsteroidal anti-inflammatory drugs (NSAIDs); chronic alcohol abuse; Helicobacter pylori infection; and liver cirrhosis, particularly for variceal sources.[2][12] In elderly populations, polypharmacy—defined as five or more concurrent medications—further heightens susceptibility through drug interactions and cumulative gastrointestinal toxicity.[11] Epidemiological trends show stable or declining UGIB incidence in high-income regions over the past two decades, driven by effective Helicobacter pylori eradication and proton pump inhibitor use, alongside a 21% reduction in hospitalizations from 2002 to 2012. Recent data from 2019 show UGIB incidence increasing to 116.2 per 100,000 after a decline, particularly among the elderly owing to expanded antithrombotic prescriptions and polypharmacy prevalence exceeding 70% in those over 60.[2][13] Mortality has improved concurrently due to widespread endoscopic therapies, dropping case-fatality rates from 2.6% to 1.9% in monitored cohorts.[14] However, as of 2025, cases are rising among the elderly owing to expanded antithrombotic prescriptions and polypharmacy prevalence exceeding 70% in those over 60, underscoring ongoing public health challenges in aging populations.[11][15]Etiology and Pathophysiology
Causes
The prevalence of causes for hematemesis varies by geographic region and population, with peptic ulcer disease more dominant in Western settings and variceal bleeding higher in areas with prevalent liver disease such as parts of Asia and Africa.[16] Hematemesis, the vomiting of blood, most commonly arises from upper gastrointestinal bleeding (UGIB), with peptic ulcer disease representing the leading etiology in adults, accounting for approximately 32% to 50% of cases based on endoscopic evaluations. This includes both gastric and duodenal ulcers, frequently associated with Helicobacter pylori infection, nonsteroidal anti-inflammatory drug (NSAID) use, or stress-related factors in critically ill patients.[2][17] Esophageal varices are a major cause of UGIB, comprising 6% to 30% of episodes and ranking as the second most frequent in populations with high rates of liver cirrhosis and portal hypertension, where ruptured varices lead to significant hemorrhage.[2][18] Mallory-Weiss syndrome, characterized by mucosal tears at the gastroesophageal junction due to forceful retching or vomiting, accounts for 4% to 15% of cases and is often linked to alcohol abuse or severe nausea.[2][17] Erosive conditions such as gastritis (18-22%), esophagitis (24%), and duodenitis (13%) collectively contribute significantly to hematemesis instances, typically resulting from mucosal inflammation due to irritants like NSAIDs, alcohol, or acid reflux.[2] Vascular malformations, including Dieulafoy lesions (aberrant submucosal arteries) and angiodysplasia, are responsible for about 5% of cases, presenting as sudden, massive bleeding without prior ulceration.[2] Less common etiologies encompass malignancies, such as gastric or esophageal cancer (2% to 6%), and rare conditions like aortoenteric fistulas, which may occur post-aortic surgery and carry high mortality.[17][18] Iatrogenic causes include post-endoscopic bleeding or medication-induced erosions from anticoagulants, antiplatelets, or corticosteroids, exacerbating underlying lesions.[2] Ingested blood from non-gastrointestinal sources, such as epistaxis or oral bleeding, can mimic hematemesis but is distinguished by history and examination.[12] Although the focus remains on adults, pediatric hematemesis etiologies differ, with peptic ulcers (often H. pylori-related), esophagitis, gastritis, and foreign body ingestion or Meckel's diverticulum being more prevalent, while varices are less common unless cirrhosis is present.[19][20]Pathophysiology
Hematemesis results from the erosion of blood vessels within the mucosal lining of the upper gastrointestinal tract, primarily due to lesions such as peptic ulcers or esophageal varices. In peptic ulcers, gastric acid and pepsin digest the protective mucosal barrier, exposing underlying submucosal arteries or veins and leading to hemorrhage; arterial erosion typically produces high-pressure, brisk bleeding, while venous involvement results in slower blood loss.[2] Esophageal varices, dilated submucosal veins formed in response to portal hypertension, rupture under increased pressure, initiating venous hemorrhage that can rapidly escalate due to the fragile nature of these vessels.[21] Following vessel disruption, blood accumulates in the stomach, where it irritates the gastric mucosa and stimulates the vomiting reflex, expelling the contents as hematemesis. Rapid hemorrhage allows for minimal exposure to gastric secretions, resulting in bright red vomitus, whereas slower bleeding permits partial oxidation and digestion of hemoglobin by stomach acid, yielding the dark, coffee-ground appearance characteristic of altered blood.[2] This propagation is confined to the upper gastrointestinal tract proximal to the ligament of Treitz, distinguishing it from lower sources.[5] Hemodynamically, acute blood loss induces hypovolemia, triggering compensatory tachycardia to maintain cardiac output; severe volume depletion (>15% loss) can progress to orthostatic hypotension and shock. In variceal bleeding, portal hypertension—defined by a hepatic venous pressure gradient exceeding 10-12 mm Hg—amplifies the pressure gradient across ruptured vessels, accelerating hemorrhage and worsening hypovolemia.[21][5] The severity of bleeding is modulated by factors such as vessel caliber, with arterial sources posing greater risk than venous ones due to higher flow rates. Coagulopathy, including thrombocytopenia common in cirrhosis, impairs initial clot formation, while antiplatelet agents like aspirin exacerbate hemorrhage by inhibiting platelet aggregation and prolonging bleeding time.[12] Bleeding may initially be occult, detected only through fecal occult blood testing, before progressing to overt hematemesis; rebleeding risk, affecting 10-20% of cases, is heightened by the acidic gastric milieu, which inhibits platelet function, destabilizes fibrin clots, and promotes fibrinolysis.[2][22]Clinical Presentation
Symptoms and Signs
Hematemesis is characterized by the vomiting of blood from the upper gastrointestinal tract, which may appear as bright red blood indicating fresh, active bleeding or as dark, coffee-ground-like material from partially digested blood. The volume of vomited blood can range from small streaks mixed with gastric contents to massive amounts exceeding 500 mL, often suggesting significant hemorrhage.[2][6] Associated symptoms frequently include epigastric pain, particularly in cases related to peptic ulcers, and retching or vomiting preceding the bleed, as seen in Mallory-Weiss tears. Systemic manifestations of hypovolemia, such as dizziness, syncope, and abdominal distension, may accompany the primary symptom due to blood loss. In slower bleeds, patients often report melena, the passage of black, tarry stools, while brisk upper gastrointestinal bleeding can lead to hematochezia, or bright red blood per rectum.[6][12][7] Signs of severity encompass hemodynamic instability, including pallor, tachycardia, hypotension, and progression to shock, reflecting substantial blood volume depletion. Acute presentations typically involve sudden, massive vomiting of bright red blood, as in esophageal varices, whereas chronic hematemesis manifests as recurrent small-volume episodes, often from gastric erosions or neoplasms.[2][12][7] Red flags signaling high-risk hematemesis include airway compromise from aspiration of blood, altered mental status due to severe anemia or hypovolemia, and profuse bleeding in patients over 60 years or with comorbidities like cirrhosis.[7][6]Differential Diagnosis
Hematemesis, the vomiting of blood from an upper gastrointestinal source, must be differentiated from several mimicking conditions to guide appropriate management. Common mimics include respiratory tract bleeding, nasopharyngeal sources, and non-hemorrhagic discolorations, each distinguished by clinical history, blood characteristics, and associated symptoms. Accurate differentiation relies on a thorough history and physical examination, as misidentification can lead to delayed treatment of the underlying cause.[7] Respiratory mimics primarily involve hemoptysis, the expectoration of blood from the lungs or bronchi, which can resemble hematemesis but arises from pulmonary pathology such as bronchitis, pneumonia, or aspiration pneumonia. Hemoptysis typically presents as bright red, frothy blood mixed with sputum, often accompanied by cough, dyspnea, or chest pain, in contrast to the nausea and abdominal discomfort preceding true hematemesis. Aspiration pneumonia may contribute to hemoptysis through secondary infection and inflammation in the airways, particularly in patients with altered consciousness or swallowing difficulties. Key discriminators include the alkaline pH of hemoptysis (due to lack of gastric acid exposure) versus the acidic pH of hematemesis, as well as the presence of respiratory symptoms over gastrointestinal ones.[23][24] Non-gastrointestinal sources of apparent hematemesis include epistaxis, where posterior nasal bleeding is swallowed and later vomited, mimicking upper GI hemorrhage. This is particularly relevant in patients with a history of nosebleeds, trauma, or coagulopathy, and the blood may appear similar to fresh hematemesis without associated GI symptoms. Oral bleeding from gum disease, dental procedures, or pharyngeal sources can also lead to swallowed blood and subsequent vomiting, distinguishable by examination of the oral cavity and absence of epigastric pain. These mimics account for a small but notable fraction of cases initially presenting as hematemesis, emphasizing the need for nasal and oropharyngeal inspection.[7][25] Non-bleeding mimics often involve ingested substances that discolor vomitus, such as red food dyes, beetroot, or certain medications, creating a false appearance of blood without actual hemorrhage. For instance, consumption of beetroot juice can produce red-tinged emesis due to betalain pigments, leading to unnecessary investigations if dietary history is overlooked. These pseudohematemesis cases are benign but require exclusion through patient inquiry about recent intake, as they lack the systemic signs of true bleeding like hemodynamic instability.[26][20] Gastrointestinal mimics include rare presentations of lower GI bleeding, where massive colonic hemorrhage might reflux into the stomach and be vomited, though this is uncommon and typically accompanied by hematochezia or melena rather than isolated hematemesis. Boerhaave syndrome, a spontaneous esophageal rupture often following forceful vomiting, can present with hematemesis alongside severe chest pain and mediastinitis, but it is distinguished by the acute onset after retching and systemic signs of perforation. These conditions highlight the importance of correlating presentation with overall clinical context to avoid conflation with primary upper GI sources.[5][27]| Feature | Hematemesis | Hemoptysis | Epistaxis (Swallowed) |
|---|---|---|---|
| Presentation | Vomiting of red or coffee-ground blood | Coughing up frothy, bright red blood | Vomiting after swallowing nasal blood |
| Associated Symptoms | Nausea, abdominal pain, melena | Dyspnea, chest pain, cough | History of nosebleed, no GI pain |
| Blood Appearance | Acidic, clotted, mixed with food | Alkaline, foamy, mixed with sputum | Fresh red, no froth or food |
| pH | Acidic (gastric) | Alkaline (respiratory) | Neutral (nasal) |