Acute and chronic bleeding from the upper gastrointestinal tract is a common indication for endoscopy and hospitalization and is associated with significant morbidity and mortality. The causes of upper gastrointestinal bleeding are numerous and can result in both acute and chronic hemorrhage. The aim of this article is to examine the pathologic features of various diseases associated with upper gastrointestinal tract bleeding.
Upper gastrointestinal tract bleeding leads to approximately 250,000 to 300,000 hospitalizations and results in 15,000 to 30,000 deaths in the United States per year. Defined as bleeding due to disorders located proximal to the ligament of Treitz, upper gastrointestinal tract bleeding occurs in numerous clinical settings and is associated with unique risk factors. The most common causes of upper gastrointestinal bleeding, in order of frequency, include peptic ulcer disease (eg, due to use of nonsteroidal anti-inflammatory drugs [NSAIDs]), varices, acute erosions/ulcers (including esophagitis, gastritis, and duodenitis), Mallory-Weiss tears, and malignant tumors ( Table 1 ). Other less common causes of upper gastrointestinal tract bleeding include vascular abnormalities, such as arteriovenous malformation, Dieulafoy lesion, and gastric antral vascular ectasia (GAVE). Several factors are associated with an increased risk of upper gastrointestinal bleeding, such as use of NSAIDs, Helicobacter pylori , and alcohol consumption. Upper gastrointestinal bleeding may occur both acutely, with life-threatening hemorrhage, and/or chronically, in which case patients may present with iron deficiency anemia and other associated symptoms. This review focuses on the anatomic and pathologic findings of the common diseases associated with upper gastrointestinal tract bleeding.
| Diagnosis | Frequency (Percentage) |
|---|---|
| Peptic ulcer disease, including duodenal and gastric ulcer | 28–59 |
| Variceal bleeding | 4–14 |
| Mucosal erosive disease, including esophagitis, gastritis, and duodenitis | 1–31 |
| Mallory-Weiss tear | 4–8 |
| Malignancy | 2–4 |
| Arteriovenous malformation | 3 |
| Gastric antral vascular ectasia | ∼1 |
| Dieulafoy lesion | ∼1 |
Vascular anatomy of the upper gastrointestinal tract
The vascular supply of the esophagus is segmental. The upper esophagus is supplied by branches of the superior and inferior thyroid arteries, the mid esophagus by branches of the bronchial and right intercostal arteries and descending aorta, and the distal esophagus by branches of the left gastric, left inferior phrenic, and splenic arteries. The venous drainage of the esophagus is also segmental. The upper esophagus is drained via the superior vena cava, the mid esophagus via the azygos veins, and the distal esophagus via the portal vein from the left and short gastric veins. In addition, the esophagus has a dense submucosal vascular anastomotic network, which helps render the organ resistant to ischemic injury. This anastomotic network is involved by varices in the distal esophagus of patients with portal hypertension.
The arterial supply of the stomach consists of branches from the celiac artery, which include the common hepatic, left gastric, and splenic arteries. The venous drainage of the stomach follows the arterial supply. Blood empties into the portal vein or one of its tributaries: the splenic or superior mesenteric veins. Branches from these vessels form two vascular arcades in the lesser and greater curvatures of the stomach. Similar to the esophagus, the presence of a complex anastomotic network decreases the risk of ischemia in this organ.
The duodenum is supplied by vessels according to the embryonic origin of its parts. The foregut-derived proximal duodenum is supplied by branches of the celiac artery, whereas the midgut-derived distal duodenum is supplied by branches of the superior mesenteric artery. Venous drainage of the proximal duodenum occurs via the superior pancreaticoduodenal vein, which empties into the portal vein, and drainage of the distal duodenum occurs via the anterior and posterior inferior pancreaticoduodenal veins, which empty either into a jejunal vein, or directly into the superior mesenteric vein.
Esophageal disorders
Varices
Esophageal varices are an important cause of hematemesis, which typically occur in patients with portal hypertension and portosystemic shunting. Cirrhosis due to alcohol is the most common cause of portal hypertension and varices, although other causes of liver cirrhosis may also cause varices. Varices are most common in the distal esophagus and are typically asymptomatic until they rupture, which results in acute bleeding. Endoscopically they appear as large and tortuous veins that protrude into the lumen. Endoscopic biopsies of varices are usually not performed because of the high risk of bleeding, unless there is an alternative indication for biopsies. Varices may be difficult to demonstrate in surgical specimens or at the time of autopsy, because the dilated vessels tend to collapse. When a surgical specimen from a patient with varices is examined histologically, the main finding is the presence of enlarged and dilated vessels within the lamina propria or submucosa. Associated hemorrhage or organizing thrombi within vessels may be present as well. Secondary findings, such as ulceration, necrosis, and inflammation, may also be present in the esophagus, particularly if the patient has been previously treated with ligation or sclerotherapy.
Mallory-Weiss Tear
Mallory-Weiss tears are longitudinal mucosal lacerations most commonly located in the distal esophagus, but may also involve the lesser curvature of the stomach. Mallory-Weiss tears clinically are associated with forceful retching and/or vomiting, and occur more commonly in patients with chronic alcoholism, aspirin use, and/or a hiatal hernia. Bleeding due to a Mallory-Weiss tear is usually acute, but some patients may present with chronic low-grade blood loss and iron deficiency anemia. Rarely, Mallory-Weiss tears may occur as a complication of upper endoscopy. In addition, Mallory-Weiss tears are associated with Boerhaave syndrome (acute rupture of the esophagus). Mallory-Weiss tears appear grossly as isolated or multiple cleftlike mucosal defects oriented along the long axis of the distal esophagus and proximal stomach, most commonly on the right lateral side of the organ. Adherent blood clots may be present. Microscopically, recent Mallory-Weiss tears reveal defects in the esophageal squamous mucosa, which sometimes extend into the submucosa. The tissue surrounding the defect may show acute inflammation and multiple ruptured blood vessels in the lamina propria or submucosa. Associated hemorrhage, or a hematoma, may be present as well. Prior lacerations may show various degrees of healing, such as granulation tissue, fibrosis, and epithelial regeneration.
Boerhaave Syndrome
Boerhaave syndrome is defined as a spontaneous complete transmural rupture of the esophagus that occurs when a sudden pressure gradient between the esophagus and thoracic supporting structures develops. The pressure gradient may develop when the esophagus becomes overdistended because of food, liquid, or gas. Patients present with a history of forced vomiting and may have a history of hiatal hernia, reflux esophagitis, and/or gastritis. The esophagus in patients with Boerhaave syndrome is rarely examined pathologically, except in fatal cases at the time of autopsy. On gross examination perforations of the esophagus appear as linear, longitudinal defects most often in the left lateral position, 1 to 3 cm above the gastroesophageal junction. The microscopic findings are nonspecific. Acute inflammation and tissue hemorrhage may be present, adjacent to the area of perforation.
Esophagitis and Esophageal Ulcers
Bleeding caused by esophagitis or ulcers is usually occult. Patients typically present with anemia or melena. However, the severity of bleeding depends, in part, on the underlying cause and extent of the esophageal injury; acute bleeding may also occur. The most common causes of esophagitis and ulcers include gastroesophageal reflux disease, infection (eg, due to Candida , herpesvirus, or cytomegalovirus [CMV]), and chemical or physical injury (eg, due to drugs, ingested toxins, or foreign bodies).
Infectious esophagitis
Infectious esophagitis is most often caused by fungi or viruses. In general, infections occur in immunocompromised patients, although immunocompetent patients may also be affected. Infectious esophagitis typically causes odynophagia, fever, and retrosternal pain, but in severe cases bleeding may occur. Herpes simplex virus and CMV are the most important viral causes of esophagitis, whereas Candida is the most common cause of fungal esophagitis.
Herpes esophagitis
Anatomically, the distal half of the esophagus is most commonly involved by herpes. Lesions are characterized by shallow, sharply defined ulcers, with relatively normal intervening mucosa. The ulcers typically have a white adherent exudate and erythematous raised edges. The characteristic histologic feature of herpes infection is the finding of nuclear inclusions located within superficial squamous cells. The inclusions are most often present at the lateral margins of ulcers, within degenerated, sloughed squamous cells. If the ulcers are not appropriately sampled, nuclear inclusions may be difficult to demonstrate, because the intervening mucosa between ulcers may not reveal infected cells. Immunocompromised patients usually have many more inclusions than do immunocompetent patients. Herpes inclusions are located within the cell nucleus and, morphologically, include two variants. Cowdry A bodies are characterized by the presence of round homogeneous amphophilic or eosinophilic intranuclear bodies surrounded by a clear halo and a thickened nuclear membrane. Ground-glass inclusions are characterized by the presence of a smooth, lightly basophilic homogeneous chromatin pattern. Multinucleation of infected squamous cells is common. In addition to inclusions within squamous cells, other histologic findings include acute and chronic inflammation and exudate. Herpes simplex virus type I is the most common cause of herpes esophagitis, but herpes simplex virus type II or varicella zoster virus show identical morphologic findings. Immunohistochemical stains may be used to confirm the presence of herpes virus.
Cytomegalovirus esophagitis
CMV infection is less common than herpes but also affects mainly immunocompromised patients. CMV esophagitis usually involves the mid or distal esophagus. Grossly, ulcers are well-circumscribed, discrete, and superficial, similar to herpes ulcers. However, in contrast to herpes, CMV infects mesenchymal cells in the lamina propria and submucosa, such as endothelial cells, fibroblasts, or macrophages. Therefore, CMV inclusions are most commonly seen at the base of ulcers, within mesenchymal tissue. Thus if biopsies do not contain subepithelial stromal tissue, CMV inclusions may be missed. CMV inclusions are found in the nucleus and/or cytoplasm of mesenchymal cells, which also typically exhibit enlargement. One type of intranuclear CMV inclusion consists of eosinophilic or basophilic rodlike or round structures, surrounded by a clear halo and a thickened nuclear membrane. This type of inclusion is morphologically similar to Cowdry A herpes inclusion. Similar types of inclusions may also be found within the cytoplasm of infected cells. Other types of inclusions caused by CMV include a stippled and ill-defined cluster of granular, basophilic structures, within either the nucleus or cytoplasm. In contrast to herpes infection, multinucleation is not common in CMV infection. Other common findings include nonspecific acute inflammation and exudate. Immunohistochemical stains may be used to confirm the presence of CMV.
Fungal esophagitis
Fungal esophagitis is most often caused by Candida albicans or Candida tropicalis . Candidal esophagitis is characterized grossly by erythema, hyperemia, and friability of the squamous mucosa. In some cases, a diffuse black membrane may develop. In addition, discrete and raised white plaques may be present, particularly in the distal esophagus. Microscopic examination demonstrates active esophagitis characterized by the presence of neutrophils within the squamous epithelium. Chronic inflammation, characterized by lymphocytes and plasma cells, may also be present, within both the epithelium and the lamina propria. Ulceration, with associated exudate, and sloughed squamous cells may also be present, a finding that corresponds to the grossly visible white plaques. Budding yeast forms and pseudohyphae of Candida organisms are typically located within the exudate, or within inflamed superficial squamous epithelium. Histochemical stains, such as periodic acid-Schiff or silver stains, can be used to help identify the organisms. Culture may be helpful for determining the species and to guide specific therapy, especially in patients who have recurrent candidal esophagitis. Other rare fungal infections of the esophagus include Histoplasma , Aspergillus , Mucor , and coccidiosis.
Pill esophagitis
Esophagitis due to direct mucosal contact of ingested tablets (“pill esophagitis”) occurs commonly, especially in elderly patients or in patients with multiple comorbidities. Medications frequently implicated include ferrous sulfate, doxycycline, alendronate, and potassium chloride, although many other types of medications have been associated with esophagitis. Pill esophagitis typically results in the formation of discrete ulcers at the junction of the proximal and middle third of the esophagus, where the aortic arch compresses the esophagus. Atrial enlargement and tumors may predispose patients to pill esophagitis. Microscopically, the features of pill esophagitis are not specific and include necrosis, prominent eosinophilic infiltrate, spongiosis and, if severe, ulceration. In cases of chronic pill esophagitis, foreign-body giant-cell reaction and fibrosis may develop. Pill fragments may be identified in tissues as polarizable material.
Toxic esophagitis
Corrosive or caustic injury may occur as a result of either alkaline (eg, lye) or acid (eg, nitric acid) ingestion. The typical clinical settings are accidental ingestion by a child or purposeful ingestion during a suicide attempt in adults. Grossly the esophagus may show mucosal erythema, edema, hemorrhage, and necrosis, depending on the severity of the injury. Histologically the pathologic features are nonspecific. Acid injury tends to cause coagulative necrosis and the formation of an eschar. The eschar prevents deep tissue from undergoing further injury. By contrast, alkaline injury causes liquefactive necrosis, with fat and protein digestion, which can lead to extensive tissue loss. Alkaline injury has more potential for deep tissue penetration; esophageal rupture may occur in severe cases. Early in the injury course, the esophagus typically shows marked acute inflammation and abundant granulation tissue. When healed, strictures may develop, which are formed of dense submucosal fibrosis.
Gastroesophageal Reflux Disease
Gastroesophageal reflux typically affects the distal 8 to 10 cm of esophagus. Microscopic features include basal cell hyperplasia, elongation of the lamina propria papillae, mixed intraepithelial inflammation (including neutrophils, eosinophils, and lymphocytes), and squamous cell degeneration. In severe cases ulceration may be present, characterized by loss of squamous epithelium, granulation tissue, and acute inflammation. However, none of the histologic findings of gastroesophageal reflux are pathognomonic. Although gastroesophageal reflux disease is a common cause of esophageal ulceration, overall it is not a common cause of esophageal bleeding.
Barrett Esophagus
Barrett esophagus is defined as endoscopically recognizable columnar epithelium in the esophagus, which microscopically shows columnar epithelium with goblet cells. Barrett esophagus is the result of chronic gastroesophageal reflux disease. Microscopically, Barrett’s esophagus shows replacement of the squamous epithelium by columnar epithelium. The columnar epithelium is composed of a mixture of mucinous columnar cells, goblet cells, and enterocyte-like cells, among others. Acute inflammation, hyperplastic and regenerative features of the epithelium characterized by mucin depletion, nuclear hyperchromasia, and increased mitoses may be present. Ulceration is associated with an increased risk of bleeding.
Esophageal disorders
Varices
Esophageal varices are an important cause of hematemesis, which typically occur in patients with portal hypertension and portosystemic shunting. Cirrhosis due to alcohol is the most common cause of portal hypertension and varices, although other causes of liver cirrhosis may also cause varices. Varices are most common in the distal esophagus and are typically asymptomatic until they rupture, which results in acute bleeding. Endoscopically they appear as large and tortuous veins that protrude into the lumen. Endoscopic biopsies of varices are usually not performed because of the high risk of bleeding, unless there is an alternative indication for biopsies. Varices may be difficult to demonstrate in surgical specimens or at the time of autopsy, because the dilated vessels tend to collapse. When a surgical specimen from a patient with varices is examined histologically, the main finding is the presence of enlarged and dilated vessels within the lamina propria or submucosa. Associated hemorrhage or organizing thrombi within vessels may be present as well. Secondary findings, such as ulceration, necrosis, and inflammation, may also be present in the esophagus, particularly if the patient has been previously treated with ligation or sclerotherapy.
Mallory-Weiss Tear
Mallory-Weiss tears are longitudinal mucosal lacerations most commonly located in the distal esophagus, but may also involve the lesser curvature of the stomach. Mallory-Weiss tears clinically are associated with forceful retching and/or vomiting, and occur more commonly in patients with chronic alcoholism, aspirin use, and/or a hiatal hernia. Bleeding due to a Mallory-Weiss tear is usually acute, but some patients may present with chronic low-grade blood loss and iron deficiency anemia. Rarely, Mallory-Weiss tears may occur as a complication of upper endoscopy. In addition, Mallory-Weiss tears are associated with Boerhaave syndrome (acute rupture of the esophagus). Mallory-Weiss tears appear grossly as isolated or multiple cleftlike mucosal defects oriented along the long axis of the distal esophagus and proximal stomach, most commonly on the right lateral side of the organ. Adherent blood clots may be present. Microscopically, recent Mallory-Weiss tears reveal defects in the esophageal squamous mucosa, which sometimes extend into the submucosa. The tissue surrounding the defect may show acute inflammation and multiple ruptured blood vessels in the lamina propria or submucosa. Associated hemorrhage, or a hematoma, may be present as well. Prior lacerations may show various degrees of healing, such as granulation tissue, fibrosis, and epithelial regeneration.
Boerhaave Syndrome
Boerhaave syndrome is defined as a spontaneous complete transmural rupture of the esophagus that occurs when a sudden pressure gradient between the esophagus and thoracic supporting structures develops. The pressure gradient may develop when the esophagus becomes overdistended because of food, liquid, or gas. Patients present with a history of forced vomiting and may have a history of hiatal hernia, reflux esophagitis, and/or gastritis. The esophagus in patients with Boerhaave syndrome is rarely examined pathologically, except in fatal cases at the time of autopsy. On gross examination perforations of the esophagus appear as linear, longitudinal defects most often in the left lateral position, 1 to 3 cm above the gastroesophageal junction. The microscopic findings are nonspecific. Acute inflammation and tissue hemorrhage may be present, adjacent to the area of perforation.
Esophagitis and Esophageal Ulcers
Bleeding caused by esophagitis or ulcers is usually occult. Patients typically present with anemia or melena. However, the severity of bleeding depends, in part, on the underlying cause and extent of the esophageal injury; acute bleeding may also occur. The most common causes of esophagitis and ulcers include gastroesophageal reflux disease, infection (eg, due to Candida , herpesvirus, or cytomegalovirus [CMV]), and chemical or physical injury (eg, due to drugs, ingested toxins, or foreign bodies).
Infectious esophagitis
Infectious esophagitis is most often caused by fungi or viruses. In general, infections occur in immunocompromised patients, although immunocompetent patients may also be affected. Infectious esophagitis typically causes odynophagia, fever, and retrosternal pain, but in severe cases bleeding may occur. Herpes simplex virus and CMV are the most important viral causes of esophagitis, whereas Candida is the most common cause of fungal esophagitis.
Herpes esophagitis
Anatomically, the distal half of the esophagus is most commonly involved by herpes. Lesions are characterized by shallow, sharply defined ulcers, with relatively normal intervening mucosa. The ulcers typically have a white adherent exudate and erythematous raised edges. The characteristic histologic feature of herpes infection is the finding of nuclear inclusions located within superficial squamous cells. The inclusions are most often present at the lateral margins of ulcers, within degenerated, sloughed squamous cells. If the ulcers are not appropriately sampled, nuclear inclusions may be difficult to demonstrate, because the intervening mucosa between ulcers may not reveal infected cells. Immunocompromised patients usually have many more inclusions than do immunocompetent patients. Herpes inclusions are located within the cell nucleus and, morphologically, include two variants. Cowdry A bodies are characterized by the presence of round homogeneous amphophilic or eosinophilic intranuclear bodies surrounded by a clear halo and a thickened nuclear membrane. Ground-glass inclusions are characterized by the presence of a smooth, lightly basophilic homogeneous chromatin pattern. Multinucleation of infected squamous cells is common. In addition to inclusions within squamous cells, other histologic findings include acute and chronic inflammation and exudate. Herpes simplex virus type I is the most common cause of herpes esophagitis, but herpes simplex virus type II or varicella zoster virus show identical morphologic findings. Immunohistochemical stains may be used to confirm the presence of herpes virus.
Cytomegalovirus esophagitis
CMV infection is less common than herpes but also affects mainly immunocompromised patients. CMV esophagitis usually involves the mid or distal esophagus. Grossly, ulcers are well-circumscribed, discrete, and superficial, similar to herpes ulcers. However, in contrast to herpes, CMV infects mesenchymal cells in the lamina propria and submucosa, such as endothelial cells, fibroblasts, or macrophages. Therefore, CMV inclusions are most commonly seen at the base of ulcers, within mesenchymal tissue. Thus if biopsies do not contain subepithelial stromal tissue, CMV inclusions may be missed. CMV inclusions are found in the nucleus and/or cytoplasm of mesenchymal cells, which also typically exhibit enlargement. One type of intranuclear CMV inclusion consists of eosinophilic or basophilic rodlike or round structures, surrounded by a clear halo and a thickened nuclear membrane. This type of inclusion is morphologically similar to Cowdry A herpes inclusion. Similar types of inclusions may also be found within the cytoplasm of infected cells. Other types of inclusions caused by CMV include a stippled and ill-defined cluster of granular, basophilic structures, within either the nucleus or cytoplasm. In contrast to herpes infection, multinucleation is not common in CMV infection. Other common findings include nonspecific acute inflammation and exudate. Immunohistochemical stains may be used to confirm the presence of CMV.
Fungal esophagitis
Fungal esophagitis is most often caused by Candida albicans or Candida tropicalis . Candidal esophagitis is characterized grossly by erythema, hyperemia, and friability of the squamous mucosa. In some cases, a diffuse black membrane may develop. In addition, discrete and raised white plaques may be present, particularly in the distal esophagus. Microscopic examination demonstrates active esophagitis characterized by the presence of neutrophils within the squamous epithelium. Chronic inflammation, characterized by lymphocytes and plasma cells, may also be present, within both the epithelium and the lamina propria. Ulceration, with associated exudate, and sloughed squamous cells may also be present, a finding that corresponds to the grossly visible white plaques. Budding yeast forms and pseudohyphae of Candida organisms are typically located within the exudate, or within inflamed superficial squamous epithelium. Histochemical stains, such as periodic acid-Schiff or silver stains, can be used to help identify the organisms. Culture may be helpful for determining the species and to guide specific therapy, especially in patients who have recurrent candidal esophagitis. Other rare fungal infections of the esophagus include Histoplasma , Aspergillus , Mucor , and coccidiosis.
Pill esophagitis
Esophagitis due to direct mucosal contact of ingested tablets (“pill esophagitis”) occurs commonly, especially in elderly patients or in patients with multiple comorbidities. Medications frequently implicated include ferrous sulfate, doxycycline, alendronate, and potassium chloride, although many other types of medications have been associated with esophagitis. Pill esophagitis typically results in the formation of discrete ulcers at the junction of the proximal and middle third of the esophagus, where the aortic arch compresses the esophagus. Atrial enlargement and tumors may predispose patients to pill esophagitis. Microscopically, the features of pill esophagitis are not specific and include necrosis, prominent eosinophilic infiltrate, spongiosis and, if severe, ulceration. In cases of chronic pill esophagitis, foreign-body giant-cell reaction and fibrosis may develop. Pill fragments may be identified in tissues as polarizable material.
Toxic esophagitis
Corrosive or caustic injury may occur as a result of either alkaline (eg, lye) or acid (eg, nitric acid) ingestion. The typical clinical settings are accidental ingestion by a child or purposeful ingestion during a suicide attempt in adults. Grossly the esophagus may show mucosal erythema, edema, hemorrhage, and necrosis, depending on the severity of the injury. Histologically the pathologic features are nonspecific. Acid injury tends to cause coagulative necrosis and the formation of an eschar. The eschar prevents deep tissue from undergoing further injury. By contrast, alkaline injury causes liquefactive necrosis, with fat and protein digestion, which can lead to extensive tissue loss. Alkaline injury has more potential for deep tissue penetration; esophageal rupture may occur in severe cases. Early in the injury course, the esophagus typically shows marked acute inflammation and abundant granulation tissue. When healed, strictures may develop, which are formed of dense submucosal fibrosis.
Gastroesophageal Reflux Disease
Gastroesophageal reflux typically affects the distal 8 to 10 cm of esophagus. Microscopic features include basal cell hyperplasia, elongation of the lamina propria papillae, mixed intraepithelial inflammation (including neutrophils, eosinophils, and lymphocytes), and squamous cell degeneration. In severe cases ulceration may be present, characterized by loss of squamous epithelium, granulation tissue, and acute inflammation. However, none of the histologic findings of gastroesophageal reflux are pathognomonic. Although gastroesophageal reflux disease is a common cause of esophageal ulceration, overall it is not a common cause of esophageal bleeding.
Barrett Esophagus
Barrett esophagus is defined as endoscopically recognizable columnar epithelium in the esophagus, which microscopically shows columnar epithelium with goblet cells. Barrett esophagus is the result of chronic gastroesophageal reflux disease. Microscopically, Barrett’s esophagus shows replacement of the squamous epithelium by columnar epithelium. The columnar epithelium is composed of a mixture of mucinous columnar cells, goblet cells, and enterocyte-like cells, among others. Acute inflammation, hyperplastic and regenerative features of the epithelium characterized by mucin depletion, nuclear hyperchromasia, and increased mitoses may be present. Ulceration is associated with an increased risk of bleeding.
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