Massive upper gastrointestinal bleeding is a common clinical condition, primarily characterized by hematemesis and melena. The rate of misdiagnosis and mortality remains relatively high, necessitating careful attention. Although there are dozens of causes for upper gastrointestinal bleeding, five conditions are most commonly associated with severe bleeding requiring surgical intervention.
Gastric and Duodenal Ulcers
These account for approximately 40% to 50% of cases, with three-quarters attributed to duodenal ulcers. Severe bleeding ulcers are typically located in the posterior wall of the duodenal bulb or along the lesser curvature of the stomach. The bleeding is often caused by erosion and rupture of the blood vessels at the ulcer base, most commonly involving arterial hemorrhage. Chronic ulcers accompanied by significant scar tissue frequently exhibit arterial rupture with reduced contraction ability, leading to pulsing, spurting hemorrhage that is resistant to hemostatic medications administered intravenously or orally. For patients aged 50 and older, the presence of arteriosclerosis in small arterial walls makes bleeding particularly difficult to resolve spontaneously.
Two specific scenarios warrant attention in gastric and duodenal ulcers:
- Drug-induced ulcers: Medications such as aspirin and indomethacin can increase gastric acid secretion or damage the gastric mucosal barrier, inducing acute ulcers or activating existing ulcers, which may result in severe bleeding.
- Anastomotic ulcers: These are commonly observed in patients who underwent partial gastrectomy with gastrojejunostomy or simple gastrojejunal bypass surgery. The incidence is about 1% to 3% for the former and as high as 15% to 30% for the latter. Most cases occur within two years post-surgery, although early onset after surgery is also possible. A minority of patients may experience severe bleeding that warrants surgical or interventional treatment.
Portal Hypertension
Accounting for roughly 20% to 25% of cases, cirrhosis-related portal hypertension is frequently associated with esophageal and gastric varices in the submucosa of the lower esophagus and gastric fundus. Thin mucosa resulting from varices is susceptible to injury from rough food or erosion by gastric acid reflux. In addition, elevated pressure in the portal venous system increases the likelihood of variceal rupture, leading to uncontrolled massive hemorrhage.
Primary liver cancer with cancerous thrombus in the main trunk of the portal vein may induce acute portal hypertension, causing rupture of esophageal and gastric fundus varices with severe bleeding. Clinically, this manifests as significant hematemesis, often resulting in hypovolemic shock. The condition is highly dangerous and associated with poor prognosis.
Stress Ulcers or Acute Erosive Gastritis
These conditions account for approximately 20% of cases. They are frequently related to shock, complex trauma, severe infections, extensive burns (Curling ulcers), traumatic brain injuries (Cushing ulcers), or major surgeries. Under these circumstances, sympathetic excitation and increased catecholamine secretion from the adrenal medulla lead to spasmodic contraction of submucosal blood vessels in the stomach. This results in mucosal ischemia and hypoxia, leading to the formation of superficial ulcers (not penetrating the muscularis mucosa) or multiple erosive lesions of varying sizes.
These ulcers or erosions are predominantly located in the stomach and less commonly in the duodenum, often leading to significant bleeding.
Gastric Cancer
Massive bleeding frequently occurs in advanced or late-stage gastric cancer. Necrotic tissue sloughing or ulceration on the surface of ischemic tumor tissues may erode blood vessels, resulting in severe bleeding.
Hemobilia
Localized chronic infections within the liver can cause the expansion of intrahepatic bile ducts, combined with single or multiple abscesses. Bleeding resulting from vascular erosion at the site of infection or abscess may drain into the intestinal tract through extrahepatic bile ducts, leading to hematemesis or melena. This condition is referred to as hemobilia. Liver cancer, hepatic hemangioma, or trauma-induced rupture of central hepatic parenchyma may also result in massive intrahepatic biliary bleeding.
Other less common causes include vascular malformations of the upper gastrointestinal tract, upper gastrointestinal injuries, Mallory-Weiss syndrome (mucosal tears at the gastroesophageal junction), acute gastric dilatation, internal hernias, and others.
Clinical Analysis
For patients with massive upper gastrointestinal bleeding, unless in a state of shock requiring immediate resuscitation, essential steps such as taking a detailed medical history, performing physical examinations, and conducting laboratory tests should be completed within a short period in a targeted and focused manner. Through analysis, an initial determination can be made regarding the amount, rate, cause, and location of the bleeding, allowing timely and effective treatment interventions.
Generally, bleeding above the pylorus tends to lead to hematemesis. However, if the bleeding volume is small and does not induce nausea or vomiting, the blood is typically discharged through the intestines. Conversely, if the bleeding is rapid and massive, blood below the pylorus can reflux into the stomach, also resulting in hematemesis. Similarly, when the bleeding volume is small and blood remains in the stomach for a prolonged period, the action of gastric acid converts hemoglobin into methemoglobin, causing the vomited blood to appear coffee-ground or dark brown. In contrast, if the bleeding is rapid and large in volume, the blood remains in the stomach for a shorter duration, and the vomited blood will appear dark red or even bright red.
When blood is discharged through the intestines, the action of intestinal fluids converts hemoglobin iron into ferric sulfide, resulting in stool that appears tarry or purplish-black. However, in cases of sudden, heavy bleeding where intestinal peristalsis is heightened, the stool may appear dark red or even bright red, potentially leading to a misdiagnosis of lower gastrointestinal bleeding.
In summary, whether a patient exhibits hematemesis or melena, as well as the color of the blood, is primarily determined by the rate and volume of bleeding, while the anatomical location of the bleeding plays a secondary role. Patients with hematemesis generally experience greater blood loss than those with melena alone. An increased frequency of defecation with thin, black stools typically indicates greater blood loss than normal defecation frequency with well-formed black stools. Patients with melena may lack hematemesis, while those with hematemesis often also have melena.
Different bleeding locations are still associated with distinctive clinical features. Recognizing these characteristics is important for diagnosing the cause and identifying the location of the bleeding.
Bleeding from ruptured esophageal or gastric fundal varices is typically characterized by large-volume bleeding, with a single episode often exceeding 500–1,000 ml, potentially causing shock. Clinically, hematemesis is the primary manifestation, while isolated melena is less common. Even with aggressive nonsurgical hemostatic therapy, recurrent hematemesis is common.
Bleeding from ulcers, erosive gastritis, or gastric cancer in the stomach or duodenal bulb can also present acutely, but a single episode usually involves less than 500 ml of blood, and shock is less frequent. Clinically, bleeding may manifest as hematemesis, melena, or both. Nonsurgical interventions are often effective for hemostasis, but untreated underlying conditions may result in recurrent bleeding.
Biliary bleeding is typically mild, with single episodes involving 200–300 ml, and rarely causes shock. Clinically, melena is the predominant symptom. While bleeding may temporarily cease with nonsurgical treatments, it often recurs cyclically, with intervals typically lasting 1–2 weeks.
Relying solely on the initial presentation of upper gastrointestinal bleeding to determine its cause and location is often insufficient. A comprehensive diagnosis requires the integration of medical history, physical examination, laboratory tests, and imaging studies.
Patients with gastric and duodenal ulcers often report a history of typical epigastric pain that is relieved with antacids or antispasmodic medications, and previous diagnostic tests such as barium meal X-rays or endoscopy frequently confirm the presence of peptic ulcers. For patients who have undergone partial gastrectomy, the possibility of anastomotic ulcers should be considered. Individuals with portal hypertension often have a history of hepatitis or schistosomiasis, with previous barium meal X-rays or endoscopy documenting esophageal varices. For such patients, the diagnosis of massive upper gastrointestinal bleeding is typically straightforward.
However, some individuals may not experience any conscious symptoms prior to bleeding. For example, 10–15% of patients with bleeding from gastric or duodenal ulcers lack a history of typical ulcer symptoms. Therefore, identifying the cause and location of bleeding depends on objective clinical diagnostic findings.
A thorough and detailed physical examination is essential. Findings such as spider nevi, palmar erythema, subcutaneous abdominal varices, hepatosplenomegaly, ascites, and scleral jaundice are often indicative of bleeding from ruptured esophageal or gastric fundal varices. Biliary bleeding is often preceded by severe colicky abdominal pain similar to biliary colic, with tenderness in the right upper quadrant, possibly including an enlarged gallbladder. These symptoms are typically accompanied by chills, high fever, and jaundice, which together strongly indicate a diagnosis. In the absence of severe biliary colic, high fever, or jaundice, distinguishing biliary bleeding from gastric or duodenal ulcer bleeding becomes more challenging.
Tests for hemoglobin levels, red blood cell counts, and hematocrit values may show no changes during the early stages of bleeding. After bleeding has occurred, interstitial fluid is absorbed into the bloodstream, diluting the blood. It typically takes more than 3–4 hours for these values to reliably reflect the degree of blood loss. Liver function tests and serum ammonia levels can help differentiate between bleeding caused by gastric or duodenal ulcers and bleeding due to portal hypertension. Liver function is generally normal and ammonia levels are not elevated in the former, whereas liver function is often significantly impaired and serum ammonia is elevated in the latter. Coagulation function tests also provide important reference data.
It is important to note that even when one of the five common conditions mentioned above is clearly diagnosed, it is not necessarily the direct cause of the bleeding. For instance, in patients with cirrhosis and portal hypertension, 20–30% of massive bleeding cases may be caused by portal hypertensive gastropathy, and 10–15% may result from concomitant gastric or duodenal ulcers. If clinical analysis fails to establish the cause of the bleeding, rarer conditions should be considered, including esophageal hiatal hernia, multiple gastric polyps, benign tumors of the stomach or duodenum, Mallory-Weiss syndrome, and hematological disorders. Additional diagnostic tests can assist in distinguishing these potential causes.
Auxiliary Examinations
Examination with the Sengstaken-Blakemore Tube
This method has some significance in distinguishing the location of bleeding. The procedure is simple and straightforward. Given that the use of a Sengstaken-Blakemore tube for treatment may lead to rebleeding and severe complications such as esophageal rupture and aspiration pneumonia, it is currently only utilized as a temporary measure for managing esophagogastric variceal bleeding that cannot be controlled by endoscopy.
X-ray barium swallow examination
Performing a barium swallow examination during the acute phase of upper gastrointestinal bleeding is not recommended. After the patient’s shock status has improved, barium swallow examination can be employed for diagnostic purposes. Using a non-compression technique for double-contrast imaging, approximately 80% of bleeding sites can be identified, and the procedure is relatively safe.
Endoscopic examination
Endoscopy can assist in identifying the location and nature of the bleeding while also facilitating hemostasis. Endoscopy should be performed early, ideally within 24 hours of bleeding onset, yielding a positive diagnostic rate of approximately 95%. For patients whose hemodynamics remain unstable despite active resuscitation, urgent endoscopy should be performed. Given the large bleeding volume associated with variceal bleeding, where the rate of transfusion and fluid replacement is often much lower than the bleeding rate, endoscopy should be conducted within 12 hours for suspected cases of variceal bleeding.
For patients with negative findings from gastroscopy or duodenoscopy who continue to exhibit active bleeding, capsule endoscopy or double-balloon enteroscopy can be used for further examination to detect potential bleeding lesions in the small intestine.
Abdominal CT angiography (CTA) and digital subtraction angiography (DSA)
For severe or active bleeding, if endoscopy is not feasible or inconclusive in identifying the cause of bleeding, abdominal CTA can be employed to determine the bleeding source and its cause. Abdominal CTA is capable of detecting bleeding rates of ≥0.3 ml/min, making it highly sensitive to both arterial and venous sources of bleeding. Additionally, CTA can provide insights into intestinal wall abnormalities, such as vascular malformations and masses.
CTA is not a therapeutic measure; in situations where treatment delay poses a high risk, DSA can be directly pursued for diagnostic and therapeutic purposes. For patients with acute non-variceal upper gastrointestinal bleeding, selective angiography can be performed to locate the bleeding source and simultaneously administer treatments such as intra-arterial injection of vasoconstrictive agents or transcatheter arterial embolization. Contrast extravasation is a direct indicator of the bleeding site; at least 0.5 ml of blood containing the contrast agent must leak per minute from the vascular rupture to visualize the bleeding site. Detection rates significantly decrease when the bleeding rate is below 0.5 ml/min.
Radionuclide scintigraphy
Abdominal γ-scintigraphy with red blood cells labeled with 99mTc can detect radioactive concentration zones at the site of bleeding when the bleeding volume exceeds 5 ml. Positive results can often be obtained within one hour of scanning, particularly for intermittent bleeding, where the positive localization rate exceeds 90%. This method is suited for chronic recurrent bleeding with rates of 0.1–0.5 ml/min but is not applicable for cases of massive bleeding.
Other imaging modalities
Ultrasound and plain CT scans are helpful in identifying and diagnosing conditions such as liver, biliary, or pancreatic stones, abscesses, or tumors. Magnetic resonance imaging with portal vein and biliary tract reconstruction can assist in assessing the diameter of the portal vein, the presence of thrombi or cancerous thrombi, and abnormalities in the biliary tract.
Through the aforementioned clinical examinations, physical assessments, and auxiliary tests, the cause and location of massive upper gastrointestinal bleeding can generally be determined. This allows targeted and effective hemostatic measures to be implemented based on the specific circumstances.
Management
Initial Management
Initially, 1–2 sufficiently large intravenous routes should be established, such as central venous catheterization via the internal jugular vein or subclavian vein, to ensure rapid restoration of blood volume. Simultaneous tests for blood typing, cross-matching, complete blood count, and hematocrit should be conducted. For patients in shock, an indwelling urinary catheter is needed to monitor hourly urine output. Central venous pressure measurement is advisable if resources allow. Blood pressure and pulse dynamics are monitored to estimate the volume of gastrointestinal bleeding, while hemoglobin, red blood cell count, and hematocrit results are used to gauge the degree of blood loss.
When blood loss is less than 10% of the total blood volume (<400 ml), compensatory changes in blood volume are minimal, with limited fluctuations in pulse and blood pressure, and no significant clinical symptoms are expected. Blood loss exceeding 10% of the total volume, occurring over a short period, may result in symptoms such as dizziness, fatigue, dry mouth, increased heart rate, or tachycardia, with a pulse rate of 90–100 beats/min, while systolic blood pressure remains normal but pulse pressure narrows. Blood loss exceeding 25% of the total volume (>1,000 ml) can lead to symptoms such as syncope, cold extremities, oliguria, and restlessness, with a pulse rate exceeding 120 beats/min and systolic blood pressure dropping to 70–80 mmHg. If blood loss continues to 2,000 ml or more, systolic blood pressure may fall to 50 mmHg or lower, accompanied by severe hypovolemic shock symptoms, including dyspnea, anuria or oliguria, and rapid thready pulse, which may become unpalpable.
The shock index (pulse rate/systolic blood pressure) can assist in estimating blood loss. A normal value is 0.5. An index of 1 corresponds to blood loss of approximately 800–1,000 ml (20–30% of total blood volume), while an index greater than 1.5 correlates with blood loss of 1,200–2,000 ml (30–50% of total blood volume). Urine output and central venous pressure serve as important reference points for guiding the rate and volume of fluid and blood transfusions. Indicators such as blood pressure returning to baseline levels, pulse rate below 100 beats/min, urine output exceeding 0.5 ml/(kg·h), clear consciousness, absence of significant dehydration, and normalization of arterial blood lactate levels suggest adequate volume resuscitation.
Hemostatic medications include intravenous administration of vitamin K1, fibrinogen, and thrombin. For severe acute upper gastrointestinal bleeding of unknown etiology, proton pump inhibitors combined with somatostatin or its analogs are administered intravenously, with adjustments made following the identification of the cause. Vasopressin, which promotes constriction of visceral arterioles, may be used to achieve hemostasis but is contraindicated in patients with hypertension or coronary artery insufficiency. Vasoactive drugs may be considered for severe and persistent hypotension resulting from hypovolemic shock.
Etiological Management
Massive Bleeding from Gastric and Duodenal Ulcers
For patients younger than 30 years, the bleeding is often due to acute ulcers, and hemostasis can frequently be achieved following initial management. However, bleeding in patients older than 50 years, those with a longer history, or those with chronic ulcers is less likely to resolve spontaneously. After stabilization of blood pressure and pulse, partial gastrectomy should be performed early. Resection of the ulcer-prone site and the bleeding ulcer is the most reliable method to prevent rebleeding. When duodenal ulcers are located low and near the bile duct or have already penetrated into the pancreatic head, resection of the ulcer may damage the bile duct or pancreatic head. In such cases, the anterior wall of the duodenum can be incised, and the ulcer surface sutured with silk. The gastroduodenal and pancreaticoduodenal arteries are ligated, leaving the ulcer in place, followed by partial gastrectomy.
Anastomotic ulcers, often occurring after gastrojejunostomy, are typically difficult to manage conservatively, necessitating early surgery. Surgical resection of the anastomosis, repeat gastrojejunostomy, and vagotomy are required. It is equally important to explore the residual duodenal stump. If the residual stump is excessively long and contains remaining antral mucosa, resection of the residual stump is necessary to achieve long-term efficacy. Drug-induced acute ulcers usually stop bleeding following discontinuation of the offending drug and initial management.
Bleeding from Ruptured Esophageal or Gastric Fundal Varices caused by Portal Hypertension
Management decisions depend on the patient's liver function. For patients with poor liver function (e.g., jaundice, ascites, or prehepatic encephalopathy), initial measures may include hemostasis via three-lumen, two-balloon tube compression or sclerotherapy/ligation under endoscopy. Emergency transjugular intrahepatic portosystemic shunting (TIPS) may be necessary. For patients with good liver function, surgical hemostasis can be performed to prevent rebleeding and reduce the risk of hepatic encephalopathy. A commonly used method is pericardial devascularization, which involves completely severing the abnormal blood flow of the esophageal and gastric fundal varices to achieve definitive hemostasis.
Stress Ulcers or Acute Erosive Gastritis
Intravenous administration of H2-receptor antagonists or proton pump inhibitors is used to suppress gastric acid secretion, promoting lesion healing and hemostasis. Somatostatin and its analogs reduce visceral blood flow while suppressing the secretion of gastrin, effectively inhibiting gastric acid production and achieving significant hemostasis. When these measures fail, partial gastrectomy or selective vagotomy combined with pyloroplasty may be necessary.
Massive Bleeding caused by Gastric Cancer
Once massive bleeding due to gastric cancer is confirmed, early surgery is required. For tumors without distant metastases, radical partial or total gastrectomy can be performed. For advanced gastric cancer, palliative resection may be considered to control bleeding.
Biliary Bleeding
Most cases involve mild bleeding, which often resolves with non-surgical measures such as antibiotics and hemostatic agents. For recurrent massive bleeding, super-selective hepatic artery angiography may be used to identify the cause and location, while simultaneously performing embolization hemostasis. If bleeding persists, surgery is required. Once the localized intrahepatic lesion is confirmed, hepatic lobectomy can be performed. Ligation of branches of the hepatic artery or the hepatic proper artery on the affected side may also halt the bleeding. If the bleeding site remains ambiguous, the common bile duct is incised with small catheters inserted into the left and right hepatic ducts to detect bloodstained bile and identify the bleeding side. Intraoperative cholangiography or choledochoscopy, if available, aids in locating the bleeding site and determining the extent of liver resection.
Unexplained Upper Gastrointestinal Bleeding
For patients with unclear diagnoses who remain hemodynamically unstable after initial aggressive management, exploratory laparotomy should be considered early to identify the cause and stop bleeding.
An upper midline incision or right rectus abdominis incision is typically used for exploratory laparotomy. The stomach and duodenum are examined first. If no abnormalities are found, the liver and spleen are inspected for cirrhosis or splenomegaly, and the gallbladder and common bile duct are closely assessed. Biliary bleeding is often accompanied by an enlarged gallbladder that appears dark blue due to bloodstained bile; diagnostic aspiration of the gallbladder or common bile duct may be performed if necessary.
If the liver, spleen, gallbladder, and common bile duct appear normal, the gastroduodenal ligament is divided to inspect the posterior wall of the stomach and duodenal bulb. The gastric fundus and cardia should be carefully examined.
Next, the transverse colon and mesocolon are lifted to sequentially examine the jejunum from its origin. If no lesions are identified but blood is present in the stomach or duodenum, a longitudinal incision is made along the anterior wall of the gastric antrum between the lesser and greater curvatures, where blood vessels are sparse, for internal examination.
The incision should be large enough, extending up to 10 cm if needed, to ensure a thorough investigation of the gastric mucosa. Submucosal vessels should be ligated, or ultrasonic scalpels used to minimize bleeding from the incision. Small superficial bleeding ulcers, often located in the gastric fundus and hidden beneath adhered clots or pseudoaneurysmal arterial remnants, may be overlooked without careful inspection.
If no abnormalities are identified within the stomach, the duodenum is manually explored via the pylorus or by incising the pylorus longitudinally to inspect the posterior wall of the duodenal bulb near the pancreatic head. This systematic exploration often reveals the cause and location of bleeding.