Upper gastrointestinal hemorrhage refers to bleeding in the digestive tract above the ligament of Treitz, including the esophagus, stomach, duodenum, pancreas, bile ducts, and other areas. Its clinical manifestations include varying degrees of hematemesis and melena.

Massive upper gastrointestinal hemorrhage is defined as a blood loss exceeding 1000ml or more than 20% of the circulating blood volume within a few hours, accompanied by varying degrees of peripheral circulatory dysfunction. It is one of the common clinical emergencies and requires timely diagnosis and active, rational treatment.

bubble_chart Etiology

Upper gastrointestinal bleeding has many disease causes, with the most common being peptic ulcers and esophageal or gastric variceal rupture caused by cirrhosis. Common disease causes are listed as follows:

1. Esophageal diseases
   1. Esophagitis: In cases of reflux esophagitis, esophageal diverticulitis, and other esophageal inflammations, patients often experience retrosternal pain and acid reflux, with relatively minor bleeding.
   2. Esophageal cancer: Mainly manifests as dysphagia and other esophageal obstruction symptoms, possibly accompanied by minor bleeding.
   3. Esophageal and gastric cardia mucosal tear syndrome (Mallory-Weiss syndrome): Caused by severe nausea and vomiting, a sudden increase in intra-abdominal pressure, or excessive gastric pressure forcefully impacting the esophagogastric junction, leading to local mucosal tearing. Its main symptoms include severe vomiting, initially of gastric contents, followed by hematemesis and melena.
2. Portal hypertension leading to esophageal and gastric variceal rupture
   1. Cirrhosis: Nodular cirrhosis, schistosomiasis-induced hepatic fibrosis, and biliary cirrhosis are relatively common. In China, esophageal and gastric variceal rupture bleeding due to cirrhotic portal hypertension is quite prevalent, accounting for about 10–20% of upper gastrointestinal bleeding, ranking second among all upper gastrointestinal bleeding cases. Due to the thickening of esophageal varices, high portal venous pressure, and lack of surrounding supportive tissue, the bleeding is often severe, difficult to stop, and may rapidly lead to shock. Rebleeding is common even after the initial bleeding stops, resulting in a poor prognosis.
   2. Portal vein obstruction: Portal vein thrombosis, portal vein inflammation, or compression of the portal vein by intra-abdominal masses.
   3. Hepatic vein obstruction: Hepatic vein obstruction syndrome (Budd-Chiari syndrome).
3. Gastric and duodenal diseases
   1. Peptic ulcer: Gastric and duodenal ulcers with bleeding are the leading cause of upper gastrointestinal bleeding in China, accounting for about 50–80%. Bleeding occurs during the active phase of the ulcer due to erosion of blood vessels. If accompanied by arteriosclerosis, bleeding is less likely to stop spontaneously. Peptic ulcer bleeding is closely related to excessive gastric acid secretion, so duodenal ulcers with bleeding are more common. Patients often have a history of chronic, periodic, and rhythmic epigastric pain, followed by hematemesis and melena. Post-gastrectomy anastomotic ulcer bleeding still falls under the category of peptic ulcer bleeding.
   2. Inflammations include acute simple gastritis, acute erosive gastritis, chronic gastritis, remnant gastritis, duodenitis, and duodenal diverticulitis.
   3. Acute gastric mucosal lesions include acute hemorrhagic gastritis and stress ulcers. The former is often caused by medications such as aspirin, phenylbutazone, and indomethacin. The latter is usually triggered by severe acute infections, burns, cerebrovascular accidents, shock, poisoning, or pulmonary encephalopathy.
   4. Tumors: Common cases include gastric cancer bleeding. Gastric cancer usually causes minor bleeding, and patients often have no history of ulcers but present with short-term epigastric pain, poor appetite, weight loss, and upper gastrointestinal bleeding with no other identifiable cause. Other tumors such as lymphoma, leiomyoma, remnant gastric cancer, and periampullary cancer can also cause bleeding.
   5. Other upper gastrointestinal diseases: Gastric mucosal prolapse, gastric schistosomiasis, gastric and duodenal tuberculosis, gastric and duodenal Crohn’s disease, hiatal hernia, hemangioma, polyps, gastric volvulus, etc.
4. Diseases of adjacent organs or tissues to the upper gastrointestinal tract
   1. Biliary tract bleeding: Gallbladder or bile duct stones, gallbladder or bile duct cancer, biliary ascariasis, etc.
   2. Pancreatic diseases: Such as pancreatic cancer or acute pancreatitis complicated by abscess rupture.
5. Systemic diseases
   1. Hematologic diseases: Leukemia, aplastic anemia, thrombocytopenic purpura, hemophilia, etc., can all present with gastrointestinal bleeding as a primary symptom.
6. Vascular diseases: Allergic purpura, arteriosclerosis, hereditary hemorrhagic telangiectasia.
7. Chronic nephritis, uremia, etc.

bubble_chart Clinical Manifestations

The clinical manifestations of upper gastrointestinal bleeding depend on the nature of the lesion, location, amount of bleeding, bleeding speed, and the body's compensatory status. In chronic bleeding, even with a significant amount of blood loss, there may be no obvious changes in pulse or blood pressure due to gradual compensation by the body. In acute bleeding, even if the amount of blood loss is not very large, rapid bleeding can lead to increased pulse, decreased blood pressure, fainting, and in severe cases, shock.

The main clinical manifestations of upper gastrointestinal bleeding are as follows:

1. Hematemesis and Melena

Upper gastrointestinal bleeding proximal to the pylorus often presents with hematemesis. However, if the bleeding distal to the pylorus is large in volume and rapid in speed, blood refluxing into the stomach can also manifest as hematemesis. In esophageal lesions, the hematemesis is often bright red. In cases of esophageal variceal rupture, the bleeding is typically massive and may be projectile. Gastric bleeding or bleeding from other sites that enters the stomach and is vomited often appears as coffee-ground-like material due to the formation of methemoglobin by the action of gastric acid on the blood. If gastric bleeding is large in volume and rapid in speed, the blood may remain in the stomach for a short time, resulting in the vomiting of bright red blood, possibly with clots. Bleeding in the duodenal bulb primarily manifests as melena but may also be accompanied by hematemesis. Bleeding distal to the duodenum usually presents only as melena, with rare instances of hematemesis.

Minor upper gastrointestinal bleeding may only result in a positive fecal occult blood test without visible melena. Melena appears when the bleeding exceeds 60ml. Generally, bleeding distal to the pylorus primarily manifests as melena, while bleeding proximal to the pylorus often includes hematemesis. Typical melena is tarry, black, and shiny, caused by the formation of iron sulfide from the iron in hemoglobin reacting with intestinal sulfides. If upper gastrointestinal bleeding is massive and rapid, with strong intestinal peristalsis and short transit time, the stool may appear purple-red or bright red, resembling lower gastrointestinal bleeding. Conversely, if lower gastrointestinal bleeding is minor and the blood remains in the intestine for a long time, it may also produce tarry stools. Therefore, careful differentiation between the two is necessary.

Massive upper gastrointestinal bleeding is often accompanied by hemorrhagic peripheral circulatory failure. In cases of large-volume, rapid bleeding, the rapid reduction in circulating blood volume can lead to symptoms such as dizziness, weakness, palpitations, thirst, sweating, blurred vision, and syncope upon standing after defecation. Physical examination may reveal pallor of the skin, lips, and nail beds, restlessness, cold extremities, cold sweating, thready and rapid pulse, decreased blood pressure, and even shock. In severe cases, there may be confusion, tachycardia, oliguria, or anuria.

3. Fever

Most patients experience fever, typically low-grade or moderate, with temperatures not exceeding 38.5°C, lasting 3–5 days. The mechanism of fever is not entirely clear but may be related to reduced circulating blood volume, peripheral circulatory failure, and anemia.

After upper gastrointestinal bleeding, the protein digestion products from the blood entering the intestine are largely absorbed. The bleeding-induced peripheral circulatory failure, low blood pressure, and reduced cardiac output decrease renal blood flow and glomerular filtration rate, leading to elevated blood urea nitrogen levels and resulting in enterogenic azotemia, which may also be accompanied by acidosis. In upper gastrointestinal bleeding, azotemia typically begins to rise within hours of bleeding, peaking at 24–48 hours, with plasma levels not exceeding 6.7mmol/L (40mg/dl). If there is no further bleeding, levels return to normal within 2–4 days.

bubble_chart Auxiliary Examination

1. Laboratory tests:
   1. Blood count and hematocrit: Upper gastrointestinal bleeding often leads to acute post-hemorrhagic anemia. Within 6–12 hours after bleeding, red blood cell count, hemoglobin levels, and hematocrit decrease, while white blood cell count increases, reaching 10×10⁹–20×10⁹/L. White blood cell count returns to normal 2–3 days after hemostasis. In cases of cirrhosis with esophageal or gastric variceal bleeding, leukocytosis may not occur due to concurrent hypersplenism, and leukopenia may even be observed.
   2. Urine and stool routine tests, as well as fecal occult blood test.
   3. Liver function tests: Abnormal liver function tests aid in the diagnosis of cirrhosis. Elevated serum bilirubin levels suggest biliary tract diseases, cirrhosis, or ampullary tumors. If necessary, albumin/globulin ratio and enzymatic tests may be performed.
2. Gastroduodenoscopy: This is highly useful for identifying the cause and location of upper gastrointestinal bleeding. For timely diagnosis, emergency endoscopy within 24–48 hours of bleeding is often recommended. To further clarify the nature of the lesion, biopsies can be taken under direct endoscopic visualization for pathological diagnosis. Some patients may also undergo endoscopic hemostasis.
3. X-ray examinations:
   1. Barium meal study: This can detect certain digestive system lesions, particularly peptic ulcers. However, performing this test during active bleeding may exacerbate hemorrhage. If delayed too long, minor lesions such as shallow peptic ulcers or acute gastric mucosal lesions may heal and go undetected. Therefore, the timing should be carefully chosen, ideally a few days after bleeding stops or the condition stabilizes. Double-contrast upper gastrointestinal radiography can visualize mucosal patterns and detect subtle lesions.
   2. Selective angiography: For upper gastrointestinal bleeding with no abnormalities found on gastroduodenoscopy but persistent active bleeding, superior mesenteric angiography can confirm the diagnosis. Vasopressin may also be administered via the angiographic catheter for hemostasis.
   3. Endoscopic retrograde cholangiopancreatography (ERCP): Helpful for diagnosing biliary or pancreatic bleeding.
   4. Percutaneous transhepatic portography: This can demonstrate the extent of left gastric vein and esophageal varices caused by portal hypertension and may be combined with embolization therapy.
4. B-mode ultrasound: Useful for diagnosing hepatic, pancreatic, or biliary tract bleeding.

bubble_chart Diagnosis

1. Identify whether it is upper gastrointestinal bleeding
   1. Hematemesis should be differentiated from hemoptysis.
   2. Melena should be distinguished from black stools caused by food or medications. Consuming foods such as pork liver, poultry, or animal blood, iron-rich vegetables, or taking medications like activated charcoal, iron supplements, or bismuth preparations can all result in black stools, and differentiation is necessary.
   3. Upper gastrointestinal bleeding should also be differentiated from nasal or oral bleeding such as epistaxis or gingival bleeding.
   4. Upper gastrointestinal bleeding sometimes needs to be distinguished from lower gastrointestinal bleeding.
2. Estimate the severity of bleeding: A positive fecal occult blood test indicates a daily blood loss of more than 5ml. The appearance of melena suggests a daily blood loss of over 60ml. Hematemesis may occur when the stomach accumulates 250–300ml of blood. A single blood loss of less than 400ml may not cause systemic symptoms. Acute circulatory volume reduction may occur in cases of large or rapid bleeding. Therefore, the severity of bleeding can be estimated based on symptoms of cardiac or cerebral ischemia, pulse, blood pressure, and hemoglobin levels.
   1. Grade I bleeding patients may experience dizziness and lack of strength, but their pulse, blood pressure, and hemoglobin levels remain unchanged. The blood loss accounts for less than 10% of the total blood volume, i.e., less than 500ml.
   2. Grade II bleeding patients may exhibit dysphoria, palpitation, thirst, and oliguria, with a pulse rate of around 100 beats per minute, a slight drop in blood pressure, and hemoglobin levels of 70–100g/L. The estimated blood loss is about 20% of the total blood volume, or approximately 1000ml.
   3. Grade III bleeding patients may present with pale complexion, rapid and thready pulse, cold sweating, or even anuria, indicating hemorrhagic shock. The pulse rate exceeds 120 beats per minute, systolic blood pressure falls below 10.67kPa (80mmHg), and hemoglobin levels are below 70g/L. The estimated blood loss exceeds 30% of the total blood volume, i.e., more than 1500ml.
3. Determine whether bleeding continues: The following signs suggest ongoing or recurrent bleeding:
   1. Frequent hematemesis with bright red blood, increased frequency of melena, loose and dark red stools, accompanied by hyperactive borborygmi.
   2. Despite adequate blood transfusion or fluid replacement, peripheral circulatory failure shows no significant improvement, or central venous pressure remains unstable.
   3. Continued decline in red blood cell count, hemoglobin, and hematocrit levels. However, in the early stages of bleeding, due to hemoconcentration, these values may appear normal and only decline after 6–12 hours.
   4. In cases of adequate fluid replacement and normal renal function, persistent elevation of blood urea nitrogen (BUN).
4. Determine the cause and location of bleeding: Based on medical history, symptoms, and signs, along with appropriate laboratory and auxiliary tests, over 90% of patients can have the cause and location of bleeding identified, facilitating further treatment.
   1. Medical history and physical examination are crucial and should be conducted briefly and promptly during emergency care. Peptic ulcer bleeding often presents with chronic, periodic, and rhythmic epigastric pain, which can be relieved by alkaline medications. Pain may intensify and its rhythm may change before bleeding, then subside afterward. Physical examination may reveal localized tenderness in the upper abdomen, either to the left or right of the xiphoid process, with few other signs. Patients with cirrhosis and esophageal-gastric variceal bleeding often have a history of viral hepatitis or chronic alcoholism, with portal hypertension, particularly splenomegaly before bleeding, spleen shrinkage after bleeding, and gradual spleen enlargement again after bleeding stops. Those with a history of taking gastric mucosa-damaging drugs like acetylsalicylic acid, alcoholism, or being in a stress state such as unconsciousness or burns may have acute gastric mucosal lesions. Middle-aged or older individuals with recent irregular epigastric pain accompanied by anorexia and weight loss should be alert to stomach cancer. If severe vomiting precedes hematemesis and melena, Mallory-Weiss syndrome (esophageal-gastric mucosal tear syndrome) should be considered.
   2. Laboratory and ancillary examinations: Rational selection of necessary laboratory and other ancillary tests is extremely helpful in determining the disease cause and location of upper consumptive thirst gastrointestinal bleeding.

bubble_chart Treatment Measures

1. General Treatment

1. Rest: The patient should be bedridden. Fear and dysphoria can exacerbate bleeding, so the patient should be kept calm, and sedatives may be administered as appropriate. For patients with cirrhosis and esophageal-gastric variceal bleeding, morphine and barbiturates are contraindicated to prevent hepatic encephalopathy.
2. Diet: Except for cases of esophageal-gastric variceal bleeding and frequent hematemesis, fasting is generally unnecessary. Light, easily digestible liquid or semi-liquid foods can be provided.
3. Close Monitoring: Continuously observe hematemesis and melena, as well as changes in consciousness, pulse, blood pressure, respiration, and hourly urine output. Regularly recheck red blood cell count, hemoglobin levels, and hematocrit to assess the occurrence and progression of hemorrhagic shock.

To improve microcirculation and prevent or treat hemorrhagic shock, blood volume should be replenished as quickly as possible. Intravenous fluids should be administered rapidly at first, using normal saline, Ringer's solution, dextran, or other plasma substitutes. If systolic blood pressure falls below 12 kPa (90 mmHg) or hemoglobin drops below 70 g/L, blood transfusion is necessary. For cirrhosis patients, fresh blood is preferred because stored blood contains higher levels of ammonia, which may induce hepatic encephalopathy. If necessary, adjust the infusion rate and volume under central venous pressure monitoring. 3. Hemostatic Measures

(1) Sengstaken-Blakemore Tube Balloon Tamponade

For esophageal-gastric variceal bleeding, balloon tamponade with a Sengstaken-Blakemore tube is the first-line treatment, providing temporary hemostasis and buying time for surgery. The tube is inserted nasally into the stomach, where the gastric balloon is inflated and then pulled outward to compress the varices at the gastric fundus. The esophageal balloon is then inflated to compress the esophageal varices, with an external traction force of 1 kg maintained. This usually achieves satisfactory hemostasis. Prolonged balloon compression may cause mucosal erosion and necrosis, so the balloon should be deflated every 12 hours for 30 minutes before reinflation. After bleeding stops, observe for 24 hours. If no further bleeding occurs, administer 20–30 mL of liquid paraffin or edible vegetable oil orally before removing the tube. Caution is required to prevent blood reflux into the trachea or airway obstruction due to tube displacement. (2) Hemostatic Medications

1. Vasopressin reduces portal venous pressure and is primarily used for esophageal-gastric variceal bleeding. Administer 10 units of vasopressin in 500 mL of 5% glucose solution via continuous IV drip over 4–8 hours, repeating as needed. Avoid rapid infusion to prevent arrhythmias. Contraindicated in patients with coronary artery disease, hypertension, or heart failure. H2-receptor antagonists are effective for peptic ulcers and acute gastric mucosal bleeding. Common options include: - Cimetidine: 600 mg in 500 mL of 5% glucose solution, IV drip over 4–8 hours, twice daily. - Ranitidine: 50 mg IV drip every 6–8 hours. - Famotidine: 20 mg IM or IV in glucose solution, twice daily. - Propranolol: Reduces cardiac output, splanchnic blood volume, and portal pressure, preventing bleeding. Dosage: 20–40 mg three times daily. Other options include adrenochrome, 6-aminocaproic acid, and tranexamic acid. (3) Endoscopic Hemostasis
   1. Sclerotherapy is used for esophageal variceal bleeding. Under endoscopy, a sclerosing agent (e.g., ethanolamine oleate, sodium morrhuate, absolute ethanol, or polidocanol) is injected into the varices.High-frequency electrocoagulation and laser hemostasis are used for hemostasis in peptic ulcers.
      (1) Electrocoagulation hemostasis: Under endoscopy, high-frequency electrocoagulation is performed using a high-frequency generator, high-frequency electrodes, and hot biopsy forceps under direct vision.
      (2) Laser hemostasis: Laser irradiation is applied to the bleeding tissue, causing tissue protein coagulation, vasoconstriction and occlusion, thrombus formation, and cessation of bleeding. Commonly used lasers for photocoagulation hemostasis include argon and neodymium-doped yttrium aluminum garnet (Nd:YAG) lasers.
   2. 5% Monsell's solution (Monsell's liquid, i.e., basic ferric sulfate solution) can induce local gastric wall spasms, constrict blood vessels at the bleeding site, and promote blood coagulation. The drug is sprayed onto the bleeding area via endoscopy to achieve hemostasis.
   (4) Topical Medication

   Oral administration, gastric tube infusion, or endoscopic spraying of drugs directly to the bleeding site can achieve good hemostatic effects. This method is generally used for peptic ulcer bleeding.

   1. Norepinephrine 8mg, added to 100ml of cold saline, administered orally or via gastric tube in divided doses.
   2. Thrombin can be administered orally or sprayed locally under fiber endoscopy. For minor bleeding, the initial dose is 2000 units, dissolved in 50–100ml of saline for oral administration or local spraying, followed by oral administration every 4–6 hours. For significant bleeding, the initial dose is 2000–4000 units orally or sprayed locally, followed by oral administration every 2–4 hours. After oral administration, the patient should slowly change positions to ensure the medicinal solution fully contacts the wound surface for hemostasis. If bleeding stops, medication can be continued until stools normalize and occult blood tests turn negative. This treatment can also be used for esophageal and gastric variceal bleeding.
   3. Oral administration of Sanqi powder or Yunnan Baiyao also has certain hemostatic effects.

   IV. Surgical Treatment

   For upper gastrointestinal massive bleeding that persists despite medical treatment, emergency surgery may be performed. Indications for surgery include:

   1. A history of multiple bleeding episodes, with recent recurrent massive bleeding.
   2. Persistent massive bleeding, with transfusion of 600–800ml within 6–8 hours, yet blood pressure and pulse remain unstable.
   3. Age over 45, with bleeding persisting for 24 hours despite treatment.
   4. Massive bleeding accompanied by pyloric obstruction, acute perforation, or acute diffuse peritonitis.
   5. Liver cirrhosis and esophageal-gastric variceal bleeding that fails to respond to treatments such as Sengstaken-Blakemore tube compression or sclerotherapy.

   bubble_chart Prevention

   Actively treat the primary disease causing upper gastrointestinal bleeding and eliminate the factors leading to bleeding. For example, stopping vomiting can prevent hematemesis caused by esophageal-cardia mucosal tear syndrome. Patients should abstain from alcohol and avoid rough, hard, and irritating foods. Those who meet surgical indications should undergo timely surgical treatment.

   bubble_chart Differentiation

   1. Hematemesis should be differentiated from hemoptysis.
   2. Melena should be distinguished from black stools caused by food or drugs. Consuming foods such as pork liver, poultry or animal blood, iron-rich vegetables, or taking medications like activated charcoal, iron supplements, or bismuth preparations can all lead to black stools, and differentiation should be noted.
   3. Upper gastrointestinal bleeding should also be differentiated from nasal or oral bleeding such as epistaxis or gingival bleeding.
   4. Upper gastrointestinal bleeding sometimes needs to be distinguished from lower gastrointestinal bleeding.