Upper gastrointestinal bleeding

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Aditya Ganti M.B.B.S. [2]

Upper gastrointestinal bleeding (UGIB) is defined as bleeding from the gastrointestinal tract that originates proximal to the ligament of Treitz. The most common causes of UGIB are peptic ulcer disease and esophageal varices. Clinical presentation includes overt bleeding from the gastrointestinal tract, rapid or slow, either manifested by hematemesis of fresh (blood-streaked to frankly bloody) or old (‘coffee ground’) vomitus, and/or melena. Initial management of UGIB includes an assessment of the patient’s hemodynamic status and repletion of lost intravascular volume, if needed. Diagnosis is most often made during upper endoscopy, which is usually performed within 24 hours of presentation,; sooner in patients who may be actively bleeding or who are hemodynamically unstable. Treatment is most often a combination of medical and endoscopic therapy. Prognosis depends on the cause of bleeding and the patient’s overall condition. Mortality from nonvariceal bleeding is 10%; Mortality from variceal bleeding is 20%. Despite advances in gastric acid suppression and endoscopic diagnosis and therapy, mortality rates have remained stable.

Alessandro Benedetti was the first to give a detalied description of stomach in 1947. In 1543, Vesalius, a Belgian anatomist was the first to describe the anatomy of the esophagus. In 1682, D Zollikofer was the first to perform sclerotherapy by injecting an acid into a vein to induce thrombus formation. Asklepios was the first to describe association between GI bleeding and peptic ulcer disease.

According to the American Gastroenterological Association, upper GI bleeding can be classified based on the rate of blood loss into overt(acute), occult or obscure(chronic) forms.

The main inciting event in the pathogenesis of upper GI bleeding is damage to mucosal injury. This mucosal injury can occur at various levels of GI tract. If the damage and bleeding is confined upto ligament Treitz, it is defined as upper GI bleeding. Regardless of etiology, if the balance of gastric acid secretion and mucosal defenses is disrupted, acid interacts with the epithelium to cause damage leading to hemorrhage.

There are many causes of upper GI hemorrhage. Causes are usually anatomically divided into their location in the upper gastrointestinal tract, which could either be esophageal (esophageal varices) or gastric (gastric ulcer) or duodenal e.g. duodenal ulcer. Patients are also usually stratified into having either variceal or non-variceal sources of upper GI hemorrhage, as the two have different treatment algorithms and prognosis. Other causes could be from infectious diseases, medication side effects, trauma or malignancy.

The various causes responsible for UGIB include peptic ulcer disease, esophagitis, gastritis/gastropathy, esophagogastric varices, ectopic varices, portal hypertensive gastropathy, angiodysplasia, dieulafoy’s lesion, gastric antral vascular ectasia, Mallory-Weiss syndrome and upper GI tumors and must be differentiated from one another.

About 75% of patients presenting to the emergency room with GI bleeding have an upper source. The diagnosis is easier when the patient has hematemesis. In the absence of hematemesis, 40% to 50% of patients in the emergency room with GI bleeding have an upper source. The incidence of acute UGIB is approximately 50 to 100 per 100,000 individuals worldwide. Patients of all age groups may develop upper gastrointestinal bleeding. Males are more commonly affected by UGIB than females.

Common risk factors in the development of upper gastrointestinal bleeding include advancing age, previous history of gastrointestinal bleed, chronic kidney disease, underlying cardiovascular disease, cirrhosis and portal hypertension, presence of H.pylori infection, NSAID’s or aspirin use in patients with a history of ulcer disease, patients on dual antiplatelet therapy and patients of 60 years or older.

There is insufficient evidence to recommend routine screening for upper GI bleeding.

If left untreated upper gastrointestinal bleeding can become life-threatening. Massive blood loss can result in a severe drop in blood pressure resulting in decreased blood supply to organ systems leading to death. Complications of UGIB include end-organ damage and iron-deficiency anemia. Prognosis is generally good with prompt treatment, and the 1-year mortality rate of patients with nonvariceal UGIB is approximately 10%.

Upper GI Endoscopy is the gold standard test for the diagnosis of upper gastrointestinal bleeding. The American Society for Gastrointestinal Endoscopy guidelines recommends that upper gastrointestinal endoscopy is performed within 24 hours of presentation in all patients with UGIB. Endoscopy serves not only as a diagnostic tool in the localization of bleeding but also enables the use of therapeutic options, which include embolization or vasopressin infusion.

Patients with upper GI hemorrhage often present with hematemesis, coffee ground vomiting, melena, maroon stool, or hematochezia if the hemorrhage is severe. The presentation of bleeding depends on the amount and location of hemorrhage. Patients may also present with complications of anemia, including chest pain, syncope, fatigue and shortness of breath. Obtaining the history is the most important aspect of making a diagnosis of upper GI bleed. It provides insight into the cause, precipitating factors and associated comorbid conditions and also helps in determining the severity of the bleed as well as in identifying the potential source of bleed.

Patients with chronic upper GI bleeding usually appear fatigue, on contrast depending upon the amount of blood loss, patient appear in distress and shock in acute upper GI bleeding.

In patients with acute Upper GI bleeding who are unstable rapid assessment and resuscitation should be initiated even before diagnostic evaluation. Once hemodynamic stability is achieved, a proper clinical history, physical examination, and initial laboratory findings are crucial not only in determining the likely sources of bleeding but also in directing the appropriate intervention. In acute GI bleeding, initial hematocrit level measured will not accurately reflect the amount of blood loss. Laboratory findings of chronic upper GI bleeding include anemia, coagulopathy, and an elevated BUN-to-creatinine ratio.

There are no specific ECG findings associated with upper gastrointestinal bleeding. However, an electrocardiogram is be performed in order to exclude arrhythmia and cardiac causes of hypotension (following acute MI).

There are no abdominal x-ray findings associated with upper gastrointestinal bleeding. However, an x-ray may be helpful in the diagnosing the complications of underlying disease. Findings of abdominal X-ray in perforated viscus associated with UGIB include free air under the diaphragm.

There are no echocardiography/ultrasound findings associated with upper gastrointestinal bleeding. However, ultrasound can be helpful in establishing portal vein patency prior to transjugular intrahepatic portosystemic shunt (TIPS) placement in patients with variceal bleeding.

Abdominal CT is not the study of choice in the evaluation of acute upper gastrointestinal bleeding. However, a CT can be helpful in the detection of UGIB from pseudoaneurysms of the mesenteric vessels, branches of the celiac axis and masses of the upper GI system or liver tumors.

There are no MRI findings associated with upper gastrointestinal bleeding. Similar to CT, MRI has no real role in the assessment of acute upper gastrointestinal bleeding. MRI can be only helpful in depicting small visceral pseudoaneurysms or masses.

In cases where the source of bleeding is unidentified after upper endoscopy, the utilization of subsequent diagnostic modalities depends upon the hemodynamic stability of the patient. Other imaging studies include CT angiography, catheter angiography, radionuclide imaging.

Nasogastric lavage and UpperGI endoscopy are other diagnostic studies that are helpful in the diagnosis of upper gastrointestinal bleeding. Evidence of old (brown colored or ‘coffee grounds’) or fresh blood documents on nasogastric lavage indicates the presence of UGIB.

In patients with acute Upper GI bleeding who are unstable rapid assessment and resuscitation should be initiated even before diagnostic evaluation. The initial steps in the management of a patient with UGIB is to assess the severity of bleeding, and then institute fluid and blood resuscitation as needed. Once hemodynamic stability is achieved, a proper clinical history, physical examination, and initial laboratory findings are crucial not only in determining the likely sources of bleeding but also in directing the appropriate intervention. Equilibration between the intravascular and extravascular spaces is not complete until 24 to 72 hours after bleeding has occurred. Nasogastric lavage should be performed if the presence or source of bleeding is unknown. Upper gastrointestinal endoscopy is the primary diagnostic tool, performed for both diagnosis and treatment of active bleeding. The American Society for Gastrointestinal Endoscopy guidelines recommends upper endoscopy within 24 hours of presentation in all patients with UGIB. Angiography and tagged erythrocyte scan are rarely needed but may be used to diagnose active UGIB, particularly in patients where EGD is contraindicated. Also, upper gastrointestinal tract radiographic studies using barium are generally not advised, as they may obscure visualization during EGD. Upper gastrointestinal bleeding is a medical emergency and requires prompt treatment. According to the American Society of Gastroenterology guidelines, the recommended medications include PPI’s, octreotide and antibiotics. Pharmacotherapy is only used as an adjuvant therapy for all patients with UGIB.

Surgery is the last resort in the management of upper GI bleeding. Surgical options include TIPS, balloon tamponade, and emergency laparotomy. In UGIB, diagnostic and therapeutic endoscopy is be performed simultaneously. Therapeutic upper gastrointestinal endoscopy should be performed in all patients with suspected UGIB to evaluate and possibly treat the source of bleeding. The urgency of endoscopy depends on the anticipated source of bleeding, rapidity of blood loss, and hemodynamic stability of the patient. The common procedures used to manage upper GI bleeding caused by the peptic ulcer disease and esophageal varices are sclerotherapy (EIS), coagulation (thermal, electric, and argon plasma), hemostatic clips and variceal band ligation.

Effective measures for the primary prevention of upper GI bleeding include administration of PPI in patients with an increased risk due to critical illness or use of NSAIDs or aspirin. In patients with cirrhosis and suspected portal hypertension, who found to have esophageal varices patients are given prophylactic treatment with a nonselective β-blocker or undergo endoscopic variceal ligation (EVL) with surveillance endoscopy.

Effective measures for the secondary prevention of UGIB include discouraging the use of NSAIDS in all patients with a history of UGIB. For patients who are at high risk for rebleeding (elderly patients; those taking anticoagulant and antiplatelet medications), indefinite use of a PPI may be recommended. A combination of nonselective β-blockers plus EVL is the best option for secondary prophylaxis of UGIB from varices.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Aditya Ganti M.B.B.S. [2]

Alessandro Benedetti was the first to give a detalied description of stomach in 1947. In 1543, Vesalius, a Belgian anatomist was the first to describe the anatomy of the esophagus. In 1682, D Zollikofer was the first to perform sclerotherapy by injecting an acid into a vein to induce thrombus formation. Asklepios was the first to describe association between GI bleeding and peptic ulcer disease.

• In 1497, Alessandro Benedetti was the first to give a detailed description of stomach and its anatomy.
• In 1543, Vesalius, a Belgian anatomist was the first to describe the anatomy of the esophagus.^[1]
• In 1682, D Zollikofer was the first to perform sclerotherapy by injecting an acid into a vein to induce thrombus formation.^[2]
• In 1853, Debout and Cassaignaic reported success in treating varicose veins by injecting perchlorate of iron.^[3]
• Endoscopic injection of bleeding peptic ulcers with adrenaline has been practiced since the 1970s.^[3]
• In 1982: D. Fleischer was the first to use an endoscopic laser as palliative therapy for esophageal carcinoma.
• In 1929, Coppleson was the first to advocate the use of sodium salicylate or quinine as the best choices of sclerosant.^[2]
• In 1982: D. Fleischer was the first to use an endoscopic laser as palliative therapy for esophageal carcinoma.
• Prof. Sicard developed the use of sodium carbonate and then sodium salicylate during and after the First World War as a sclerosant.
• Asklepios was the first to describe association between GI bleeding and peptic ulcer disease.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Aditya Ganti M.B.B.S. [2]

According to the American Gastroenterological Association, upper GI bleeding can be classified based on the rate of blood loss into overt(acute), occult or obscure(chronic) forms.

According to the American Gastroenterological Association (AGA), upper gastrointestinal bleeding can be classified based on the rate of blood loss into overt(acute), occult or obscure(chronic) forms.^[1][2][3][4]

• Overt GI bleeding: Overt GI bleeding is defined as acute bleeding which is visible and can present in the form of hematemesis, “coffee-ground” emesis, melena, or hematochezia.
  

• Occult or chronic GI bleeding: Occult GI bleeding is defined as a microscopic hemorrhage which can present as hemoccult-positive stools with or without iron deficiency anemia. It is the initial presentation in patients with no evidence of visible blood loss and is positive on fecal occult blood test(FOBT).

• Obscure GI bleeding: Obscure GI bleeding is defined as recurrent bleeding in which a source is not identified after upper endoscopy and colonoscopy. It can be either overt or occult.

Upper GI bleeding

Based on blood loss

Overt

Occult

Obscure

Hematemesis Coffee-ground emesis Melena Hematochezia

Microscopic hemorrhage Heme-occult positive stools

Source is not identified

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Aditya Ganti M.B.B.S. [2]

The main inciting event in the pathogenesis of upper gastrointestinal (GI) bleeding is damage to mucosal injury. This mucosal injury can occur at various levels of GI tract. If the damage and bleeding is confined up to ligament of Treitz, it is defined as upper GI bleeding. Regardless of etiology, if the balance of gastric acid secretion and mucosal defenses is disrupted, acid interacts with the epithelium to cause damage.

The digestive system is supplied by the celiac artery. The celiac artery is the first major branch from the abdominal aorta, and is the only major artery that supplies the digestive organs.^{[1][2][3][4][5][6][7]}

Foregut		Blood supply
Esophagus	Upper esophageal sphincter Cervical esophagus	Inferior thyroid artery
	Thoracic esophagus	Aortic esophageal arteries or branches of the bronchial arteries
	Distal esophagus Lower esophageal sphincter	Left gastric artery and left phrenic artery
Stomach	Lesser curvature	Right and left gastric arteries
	Greater curvature	Right and left gastroepiploic arteries
	Gastric fundus	Short gastric arteries
Duodenum	First and second parts	Gastroduodenal artery (GDA) and Superior pancreaticoduodenal artery
	Third and fourth parts	Inferior pancreaticoduodenal artery

• The gastric mucosa is protected from the acidic environment by mucus, bicarbonate, prostaglandins, and blood flow.^[8][9][10]
• This mucosal barrier consists of three protective components which include:
  • Layer of epithelial cell lining.
  • Layer of mucus, secreted by surface epithelial cells and foveolar cells.
  • Layer of bicarbonate ions, secreted by the surface epithelial cells.

The following table demonstrates the defense mechanisms of gastric mucosal barrier:^[11]

Defense mechanisms of gastric mucosal barrier
Mucus layer	Forms a protective gel-like coating over the entire gastric mucosal surface
Epithelial layer	Epithelial cell layer are bound by tight junctions that repel fluids
Bicarbonate ions	Neutralize acids

The main inciting event in the pathogeneis of upper GI bleeding is damage to mucosal injury. This mucosal injury can occur at various levels of GI tract. If the damage and bleeding is confined up to ligament of Treitz, it is defined as upper GI bleeding.^[12][13]

Etiology	Frequency of occurance
Peptic ulcer disease	50%
Variceal bleeding	20%
Esophagitis, gastritis, and duodenitis	10-15%
Mallory-Weiss tear	15%
Malignancy	3-5%
Arteriovenous malformation	<3%
Gastric antral vascular ectasia	<1%
Dieulafoy lesion	<1%

• Regardless of etiology, if the balance of gastric acid secretion and mucosal defenses is disrupted, acid interacts with the epithelium to cause damage.^[14][15][16]
  • Varices are large, tortuous veins and protrude into the lumen, rupturing.^[17]
  • Helicobacter pylori disrupts the mucosal barrier and causes inflammation of the mucosa of the stomach and duodenum.^[18][19]
  • As the ulcer progresses beyond the mucosa to the submucosa the inflammation causes weakening and necrosis of arterial walls, leading to pseudoaneurysm formation followed by rupture and hemorrhage.^[20]
  • NSAIDs inhibit cyclooxygenase, leading to impaired mucosal defenses by decreasing mucosal prostaglandin synthesis.^[21]
  • During stress, there is acid hypersecretion; therefore, the breakdown of mucosal defenses leads to injury of the mucosa and subsequent bleeding.
  • Mucosal defects along with dilated and tortuous vessels in dieulafoy lesion put them at risk for rupture because of necrosis of the arterial wall from exposure to gastric acid.^{[22][23][24][25]}

NSAIDS

Inhibits cyclooxygenase pathway

COX-1

COX-2

Reduced mucosal blood flow

Reduced mucosal and bicarbonate secreation

Impaired platelet aggregation

Reduced angiogenesis

Increased leucocyte adherence

Impaired defence Impaired healing

Mucosal Injury

		Gross Pathology	Microscopic Pathology
Varices		Large and tortuous veins that protrude into the lumen	Varices may be difficult to demonstrate in surgical specimens
Mallory-Weiss Tear[26]		Isolated or multiple cleft like mucosal defects	Defects in the esophageal squamous mucosa Cells of acute inflammation Multiple ruptured blood vessels in the lamina propria or submucosa Prior lacerations may show various degrees of healing Granulation tissue Fibrosis[26] Epithelial regeneration
Esophagitis[27]	Herpes esophagitis	Shallow ulcers Sharp and raised edges Normal intervening erythematous mucosa	Ground glass inclusion bodies
	Cytomegalovirus esophagitis	Superficial ulcers Well-circumscribed	Intranuclear inclusions CMV infects mesenchymal cells in the lamina propria and submucosa
	Fungal esophagitis	Erythematous Hyperemic Friable Discrete and raised white plaque	Neutrophils within the squamous epithelium
	Pill esophagitis	Discrete ulcers	Not specific and include: Necrosis Eosinophilic infiltrate
	Toxic esophagitis	Mucosal erythema Edema Hemorrhage Necrosis	Acid injury: Coagulative necrosis Eschar Alkaline injury: Liquefactive necrosis Cells of acute inflammation Abundant granulation tissue
Gastroesophageal Reflux Disease[28]		Mucosal erythema Edema	Basal cell hyperplasia Elongation of the lamina propria papillae Mixed intraepithelial inflammation Neutrophils, eosinophils, and lymphocytes Squamous cell degeneration
Barrett Esophagus[29]		Mucosal erythema Edema	Columnar metaplasia Mucinous columnar cells Goblet cells, and enterocyte-like cells, among others. Cells of acute inflammation
Acute Gastritis		Mucosal hyperemia associated with: Bleeding Erosions Ulcers	Dilation and congestion of mucosal capillaries, edema, and hemorrhage in the lamina propria Ischemic-type changes such as Degenerated and necrotic epithelium Fibrinoid necrosis Adherent fibrinopurulent debris
Gastric Ulcers[30]		Solitary, typically less than 2 cm in diameter, and have sharply defined borders. The ulcer edges are usually flat, and the base of the ulcer usually appears smooth. The presence of a radiating pattern of rugal folds is characteristic of peptic ulcers	Fibrinopurulent debris Necrosis Granulation tissue
Portal Hypertensive Gastropathy[31]		Mosaic pattern of congestion Most commonly involves the fundus	Dilation, tortuosity, and thickening of small submucosal arteries and veins. Mucosal capillaries may also show congestion, dilation, and proliferation.
Gastric Antral Vascular Ectasia[31]		Linear pattern of mucosal congestion in the antrum termed “watermelon stomach	Antral biopsies show: Congestion Dilated mucosal capillaries Vascular microthrombi The mucosa also shows: Foveolar hyperplasia Fibromuscular hyperplasia Edema and regenerative changes
Reactive (Chemical) Gastropathy		Edema Surface erosions Polypoid changes, and friability	The mucosa shows: Congestion Edema Fibromuscular hyperplasia Foveolar hyperplasia
Peptic Disease		Normal/slightly edematous mucosa Increased friability, erosions, and ulcers	Increased plasma cells Neutrophilic infiltrate Villous blunting The surface epithelium usually shows mucous cell (pseudopyloric) metaplasia
Ischemia		Hypoperfused ulcers	Acute ischemia Mucosal edema Congestion Coagulative necrosis Chronic ischemia Fibrosis Strictures
Structural Abnormalities of Blood Vessels[32]		Large-caliber artery within the submucosa	Dilated venules and arteriole in direct communication with each other
Inflammatory Bowel Disease		—	Lymphoplasmacytic infiltrate with numerous neutrophils

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Ogheneochuko Ajari, MB.BS, MS [2]

There are many causes for upper gastrointestinal (GI) hemorrhage. Causes are usually anatomically divided into their location in the upper gastrointestinal tract, which could either be esophageal (for example esophageal varices) or gastric (an example is gastric ulcer) or duodenal e.g. duodenal ulcer. Patients are also usually stratified into having either variceal or non-variceal sources of upper GI hemorrhage, as the two have different treatment algorithms and prognosis. Other causes could be from infectious diseases, medication side effects, trauma or malignancy and e.t.c.

Life-threatening causes include conditions which may result in death or permanent disability within 24 hours if left untreated.

• Anthrax
• Ebola virus

The most common causes of upper gastrointestinal bleeding include:^[1][2][3]

• Duodenal ulcer
• Esophagitis
• Esophageal varices
• Gastric tumors
• Gastric ulcer
• Gastritis
• Mallory-Weiss syndrome
• Peptic ulcer

Other less common causes of upper gastrointestinal bleeding include:^[4][5][6]

• Neoplasms
  • Gastric cancer
  • Esophageal tumors
• Esophagitis
• Gastric erosions/gastropathy
  • Acute erosive gastritis caused by drugs, radiation, infection, or direct trauma
  • Reactive gastropathy, which may be due to bile reflux, particularly after partial gastrectomy
  • Portal hypertensive gastropathy, which results in increased friability of gastric mucosa in patients with cirrhosis
• Dieulafoy lesions
  • Dilated aberrant submucosal vessels that erode the overlying epithelium in the absence of an ulcer
• Gastric varices
• Gastric antral vascular ectasia
  • Dilated gastric vessels of unknown etiology that cause chronic UGIB and iron-deficiency anemia

• Bleeding from the hepatobiliary tract
• Aortoenteric fistulas
  • Most commonly involves the lower duodenum.
  • Common causes include aortic aneurysms or prosthetic vascular grafts, syphilis and tuberculosis
• Crohn’s disease involving the upper gastrointestinal tract
• Metastatic malignancy involving the upper gastrointestinal tract, such as melanoma or renal cell carcinoma
• Hemosuccus pancreaticus
  • Pancreatic inflammation or cancer may result in bleeding into the pancreatic duct, which connects to the duodenum

Causes of Acute Upper GI bleeding
Esophagus	Esophagitis Mallory–Weiss tear Esophageal varices Esophageal ulcers Esophageal cancer
Gastric	Gastric ulcer Gastric cancer Gastritis Gastric varices Portal hypertensive gastropathy Gastric antral vascular ectasia Dielafuoy lesions
Duodenal	Duodenal ulcer Vascular malformations, including aorto-enteric Fistulae Bleeding from the bile duct due to Liver biopsy Trauma Arteriovenous malformations Liver tumors

Cardiovascular	Cholesterol embolism, mesenteric vascular occlusion, vasculitis
Chemical/Poisoning	Arsenic trioxide, arsenicals, caustic ingestion, ethylene glycol, mercury
Dental	No underlying causes
Dermatologic	Craniomandibular dermatodysostosis, Degos disease, dermatomyositis, hereditary haemorrhagic telangiectasia, Osler-Weber-Rendu syndrome, vasculitis
Drug Side Effect	Alendronate, alosetron, anticoagulants, aspirin, bevacizumab, clopidogrel, colchicine, dicoumarol, Fluorouracil, indomethacin, iron compounds, melarsoprol, NSAIDS, phenprocoumon, phenylbutazone, polyethylene glycol-electrolyte solution (PEG-ES), potassium chloride, quinidine, tetracycline, warfarin, zinc, ziv-aflibercept
Ear Nose Throat	Hereditary haemorrhagic telangiectasia, Osler-Weber-Rendu syndrome
Endocrine	Carcinoid
Environmental	No underlying causes
Gastroenterologic	Alcoholic cirrhosis, alcoholic fatty liver, anal fissure, angiodysplasia, aortoenteric fistula, Banti’s syndrome, biliary atresia, bowel ischemia, bowel obstruction, bowel strangulation, Budd-Chiari syndrome, chronic portal vein thrombosis, coats plus syndrome, colitis, colitis cystica profunda, colonic diverticulosis, colonic tubular adenomata, colonic villous adenomata, colonoscopy, colorectal cancer, Crohn’s disease, Degos disease, Dieulafoy’s ulcer, duodenal polypectomy, duodenal ulcer, duodenal webs, duplication cysts, esophageal cancer, esophageal cyst, esophageal varices, esophagitis, familial adenomatous polyposis, Gardner syndrome, gastric antral vascular ectasia, Gastric cancer, gastric polyps, gastric ulcer, gastric varices, gastric volvulus, gastric webs, gastritis, gastroduodenal ulcers, gastrointestinal duplications, hemobilia, hemorrhoids, hemosuccus pancreaticus, hepatic arterioportal fistula, intussusception, liver cirrhosis, Mallory-Weiss syndrome, Mallory-Weiss tear, Meckel’s diverticulum, mesenteric vascular occlusion, Ménétrier’s disease, peptic ulcer, Peutz-Jeghers syndrome, pneumatosis cystoides intestinalis, portal hypertension, portal hypertensive gastropathy, proctitis, ruptured esophageal varices, solitary rectal ulcer syndrome, stomach cancer, stress gastritis, stress ulcer, superior mesenteric artery occlusion, ulcerative colitis, watermelon stomach, Zollinger-Ellison syndrome
Genetic	Banti’s syndrome, carbamoylphosphate synthetase deficiency, coats plus syndrome, Crohn’s disease, Ehlers-Danlos syndrome, familial adenomatous polyposis, Gardner syndrome, hepatorenal tyrosinemia, Kasabach-Merritt syndrome, neurofibromatosis type I, Peutz-Jeghers syndrome, pseudoxanthoma elasticum, Wiskott-Aldrich syndrome
Hematologic	Blood clotting disorders, carcinoid, coagulopathy, essential thrombocytosis, hemophilia, haemorrhagic disease of the newborn, hemorrhagic thrombocythemia, Henoch-Schoenlein purpura, iron deficiency anemia, Kasabach-Merritt syndrome, systemic mastocytosis, thrombocytopenia, Wiskott-Aldrich syndrome
Iatrogenic	Parenteral nutrition-induced liver disease, post-surgical anastomosis, radiation-induced telangiectasia
Infectious Disease	Acanthocephaliasis, ancylostoma duodenale, angiostrongyliasis, anthrax, bacillary dysentery, balantidiasis, candida albicans, cytomegalovirus, ebola virus, entamoeba histolytica, giardiasis, helicobacter pylori, herpes simplex virus, Katayama fever , necator americanus (hookworm), parasites, schistosoma mansoni, strongyloidiasis, trichuriasis, typhoid fever, yellow fever
Musculoskeletal/Orthopedic	Craniomandibular dermatodysostosis, Ehlers-Danlos syndrome, pelvic fracture
Neurologic	Degos disease, hereditary haemorrhagic telangiectasia, Labrune syndrome, neurofibromatosis type I, Osler-Weber-Rendu syndrome
Nutritional/Metabolic	Carbamoylphosphate synthetase deficiency, hepatorenal tyrosinemia, milk protein intolerance
Obstetric/Gynecologic	Choriocarcinoma, endometriosis, leiomyoma
Oncologic	Adenocarcinoma, anal cancer, blue rubber bleb nevus syndrome, carcinoid, cecal carcinoma, choriocarcinoma, colorectal cancer, esophageal cancer, familial adenomatous polyposis, Gardner syndrome, gastric cancer, hemangiomas, kaposi sarcoma, lipoma, lymphoma, malignancy, melanoma, mesenchymal neoplasm, metastatic tumor, Peutz-Jeghers syndrome, small bowel cancer, small bowel lymphoma, small bowel tumors, stomach cancer, systemic mastocytosis, tumors
Ophthalmologic	Coats plus syndrome
Overdose/Toxicity	Drug overdose
Psychiatric	No underlying causes
Pulmonary	No underlying causes
Renal/Electrolyte	Cholesterol embolism, chronic renal failure, craniomandibular dermatodysostosis, Henoch-Schoenlein purpura
Rheumatology/Immunology/Allergy	Crohn’s disease, dermatomyositis, food allergy, food protein-induced enterocolitis syndrome (FPIES), Henoch-Schoenlein purpura, microscopic polyangiitis, polyarteritis nodosa, systemic mastocytosis, vasculitis, Wiskott-Aldrich syndrome
Sexual	No underlying causes
Trauma	Trauma
Urologic	No underlying causes
Miscellaneous	Foreign body, swallowed maternal blood

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Aditya Ganti M.B.B.S. [2]

The various causes responsible for UGIB include peptic ulcer disease, esophagitis, gastritis/gastropathy, esophagogastric varices, ectopic varices, portal hypertensive gastropathy, angiodysplasia, dieulafoy’s lesion, gastric antral vascular ectasia, Mallory-Weiss syndrome and upper GI tumors and must be differentiated from one another.

Several diseases can present with UGIB, and hence must be differentiated from one another.^{[1][2][3][4][5][6][7]}

Disease/Cause	Bleeding manifestations				Symptoms				Risk factors	Endoscopic findings
	Hematemesis	Melena	Hematochezia	Occult blood	Abdominal pain	Dysphagia	Dyspepsia	Weighloss
Ulcerative or erosive
Peptic ulcer disease	+	+	+	+	+	–	+	+/-	NSAIDs Infections: Helicobacter pylori CMV HSV Stress ulcer ZES	Ulcer with smooth, regular, rounded edges Ulcer base often filled with exudate Examination of the ulcer may reveal: Active bleeding Nonbleeding visible vessel Adherent clot Flat pigmented spot Clean ulcer base
Esophagitis	+	+	–	+	–	+	–	–	Gastroesophageal reflux disease Medications: Tetracycline Doxycycline Clindamycin Trimethoprim-sulfamethoxazole NSAIDs Bisphosphonates Potassium chloride Quinidine Iron supplements  Infections: HSV CMV Candida albicans HIV	Peptic esophagitis The ulcerations are usually irregularly shaped or linear, multiple, and distal. Pill-induced Ulcerations are usually singular and deep, occurring at points of stasis (especially near the carina), with sparing of the distal esophagus Infectious esophagitis: HSV – Discrete, superficial ulcers, with well-demarcated borders that tend to involve the upper or mid-esophagus; vesicles may be seen CMV – Ulcers range from small and shallow to large (>1 cm) and deep; most patients have multiple lesions Candida – Diffuse white plaques HIV – Tends to involve the mid to distal esophagus, ulcers may be shallow or deep, and may be large
Gastritis/gastropathy	+	+	–	+	+	–	+	–	Risk factors: H. pylori NSAIDs Excessive alcohol consumption Radiation injury Physiologic stress Weight loss surgery Bile reflux Risk factors for bleeding: Anticoagulant use	Erythematous mucosa Superficial erosions Nodularity Diffuse oozing
Complications of portal hypertension
Esophagogastric varices	+	+	+	–	+	–	–	–	Portal hypertension from: Cirrhosis Portal vein thrombosis	Vascular structures that protrude into the esophageal and/or gastric lumen Findings associated with an increased risk of hemorrhage: Longitudinal red streaks on the varices (red wale marks) Cherry-colored spots that are flat and overlie varices Raised, discrete red spots
Ectopic varices	+	+	+	–	–	–	–	–		Vascular structures that protrude into areas of the gastrointestinal tract lumen other than the esophagus or stomach (eg, small bowel, rectum)
Portal hypertensive gastropathy	+	+	+	+	+	–	–	–		Mosaic-like pattern that gives the gastric mucosa a “snakeskin” appearance
Vascular lesions
Angiodysplasia	+	+	+	+	–	–	–	–	End-stage renal disease Aortic stenosis Hereditary hemorrhagic telangiectasia Von Willebrand disease Radiation therapy	Small (5 to 10 mm), flat, cherry-red lesions, often with a fern-like pattern of arborizing, ectatic blood vessels radiating from a central vessel.
Dieulafoy’s lesion	+	+	+	–	+	–	–	–	Bleeding may be associated with NSAIDs use Hypertension Chronic kidney disease Diabetes Alcohol abuse	Usually located in the proximal stomach May have active arterial spurting from the mucosa without an associated ulcer or mass If the bleeding has stopped, there may be a raised nipple or visible vessel without an associated ulcer
Gastric antral vascular ectasia	+	+	+	+	+	–	–	–	Cirrhosis with portal hypertension Chronic kidney disease Diabetes mellitus Scleroderma Bone marrow transplantation	Longitudinal rows of flat, reddish stripes radiating from the pylorus into the antrum.
Traumatic or iatrogenic
Mallory-Weiss syndrome	+	+	+	–	–	–	–	–	Vomiting/retching (often related to alcohol consumption) Straining at stool or lifting Coughing Seizures Blunt abdominal trauma Hiatal hernia	Tear in the esophagogastric junction. Usually singular and longitudinal, but may be multiple. The tear may be covered by an adherent clot.
Foreign body ingestion	+	+	+	+	–	+	–	–	Psychiatric disorders Dementia Loose dentures	Visualization of the foreign body endoscopically.
Post-surgical anastomotic hemorrhage (marginal ulcers)	+	+	+	+	+	–	+	–	Gastric bypass surgery NSAID use H. pylori infection Smoking	Ulceration/friable mucosa at an anastomotic site.
Aortoenteric fistula	+	+	+	–	+	–	–	–	Infectious aortitis Prosthetic aortic graft Atherosclerotic aortic aneurysm Penetrating ulcers Tumor invasion Trauma Radiation injury Foreign body perforation	Endoscopy may reveal a graft, an ulcer or erosion at the site Adherent clot, or an extrinsic pulsatile mass in the distal duodenum or esophagus.
Tumors
Upper GI tumors	+	+	+	+	+	+	+	+	History of alcoholism, smoking	Ulcerated mass in the esophagus, stomach, or duodenum. In gastric malignancies: The folds surrounding the ulcer crater may be nodular, clubbed, fused, or stop short of the ulcer margin The margins may be overhanging, irregular, or thickened Bleeding lymphoma may appear as An ulcerated mass Polypoid lesion As a gastric ulcer
Miscellaneous
Hemobilia	+	+	+	–	+	–	–	–	History of: Cholecystectomy Endoscopic biliary biopsies or stenting TIPS placement Angioembolization Blunt or penetrating abdominal trauma Gallstones Cholecystitis Hepatic or bile duct tumors Intrahepatic stents Hepatic artery aneurysms Hepatic abscesses	Blood or clot emanating from the ampulla. ERCP may reveal a filling defect in the bile duct
Hemosuccus pancreaticus	+	+	+	–	+	–	+	–	Chronic pancreatitis Pancreatic pseudocysts Pancreatic tumors Pancreatic pseudoaneurysm Therapeutic endoscopy of the pancreas or pancreatic duct: Pancreatic stone removal Pancreatic duct sphincterotomy Pseudocyst drainage Pancreatic duct stenting	Blood or clot emanating from the ampulla. Cross-sectional imaging or angiography is often required to confirm the diagnosis.

Abbreviations: RUQ= Right upper quadrant of the abdomen, LUQ= Left upper quadrant, LLQ= Left lower quadrant, RLQ= Right lower quadrant, LFT= Liver function test, SIRS= Systemic inflammatory response syndrome, ERCP= Endoscopic retrograde cholangiopancreatography, IV= Intravenous, N= Normal, AMA= Anti mitochondrial antibodies, LDH= Lactate dehydrogenase, GI= Gastrointestinal, CXR= Chest X ray, IgA= Immunoglobulin A, IgG= Immunoglobulin G, IgM= Immunoglobulin M, CT= Computed tomography, PMN= Polymorphonuclear cells, ESR= Erythrocyte sedimentation rate, CRP= C-reactive protein, TS= Transferrin saturation, SF= Serum Ferritin, SMA= Superior mesenteric artery, SMV= Superior mesenteric vein, ECG= Electrocardiogram

Disease Clinical manifestations Diagnosis Comments Symptoms Signs Abdominal Pain Fever Rigors and chills Nausea or vomiting Jaundice Constipation Diarrhea Weight loss GI bleeding Hypo- tension Guarding Rebound Tenderness Bowel sounds Lab Findings Imaging Peptic ulcer disease Diffuse ± − + − − − + Gastric ulcer- melena and hematemesis Duodenal ulcer- melena and hematochezia Positive if perforated Positive if perforated Positive if perforated N Ascitic fluid LDH > serum LDH Glucose < 50mg/dl Total protein > 1g/dl Air under diaphragm in upright CXR Upper GI endoscopy for diagnosis Gastritis Epigastric ± − + − − − Positive in chronic gastritis + − − − N H.pylori infection diagnostic tests Endoscopy H.pylori gastritis guideline recommendation Gastrointestinal perforation Diffuse + ± – ± − − − + + + ± Hyperactive/hypoactive WBC> 10,000 Air under diaphragm in upright CXR Hamman’s sign Budd-Chiari syndrome RUQ ± − − ± − − − Positive in liver failure leading to varices − − − N Elevated serum aspartate aminotransferase and alanine aminotransferase levels may be more than five times the upper limit of the normal range. Elevated serum alkaline phosphatase and bilirubin levels, decreased serum albumin level. Findings on CT scan suggestive of Budd-Chiari syndrome include: Early enhancement of the caudate lobe and central liver around the inferior vena cava Delayed enhancement of the peripheral liver with accompanying central low density (flip-flop appearance) Peripheral zones of the liver show reversed portal venous blood flow In the chronic phase, there is caudate lobe enlargement and atrophy of the peripheral liver in affected areas Ascitic fluid examination shows: Total protein more than 2.5 g per deciliter White blood cells are usually less than 500/μL. Cirrhosis RUQ − − − + − − + + + − − N Hypoalbuminemia Prolonged PT Abnormal LFTs Hyponatremia Thrombocytopenia US Nodular, shrunken liver Ascites Stigmata of liver disease Cruveilhier- Baumgarten murmur Hemochromatosis RUQ − − − − − − − Positive in cirrhotic patients − − − N >60% TS >240 μg/L SF Raised LFT Hyperglycemia Ultrasound shows evidence of cirrhosis Extra intestinal findings: Hyperpigmentation Diabetes mellitus Arthralgia Impotence in males Cardiomyopathy Atherosclerosis Hypopituitarism Hypothyroidism Extrahepatic cancer Prone to specific infections Inflammatory bowel disease Diffuse ± − − ± − + + + − − − Normal or hyperactive Anti-neutrophil cytoplasmic antibody (P-ANCA) in Ulcerative colitis Anti saccharomyces cerevisiae antibodies (ASCA) in Crohn’s disease String sign on abdominal x-ray in Crohn’s disease Extra intestinal findings: Uveitis Arthritis Ruptured abdominal aortic aneurysm Diffuse ± − + − − − + + + − − N Fibrinogen D-dimer Focused Assessment with Sonography in Trauma (FAST)  Unstable hemodynamics Intra-abdominal or retroperitoneal hemorrhage Diffuse ± − ± − − − − + + − − N ↓ Hb ↓ Hct CT scan History of trauma

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] ; Associate Editor(s)-in-Chief: Aditya Ganti M.B.B.S. [2]

About 75% of patients presenting to the emergency room with upper gastrointestinal bleeding (UGIB) have an upper source. The diagnosis is easier when the patient has hematemesis. In the absence of hematemesis, 40% to 50% of patients in the emergency room with GI bleeding have an upper source. The incidence of acute UGIB is approximately 50 to 100 per 100,000 individuals worldwide. Patients of all age groups may develop upper gastrointestinal bleeding. Males are more commonly affected by UGIB than females.

• The incidence of acute upper gastrointestinal bleeding (UGIB) is approximately 50 to 100 per 100,000 individuals worldwide.^[1][2]
• Approximately 100,000 patients are admitted to US hospitals for therapy for UGIB.

• The prevalence of UGIB is almost the same as incidence, as it is a medical emergency and is not a chronic disease.

• Patients of all age groups may develop upper gastrointestinal bleeding.
• The population with UGIB has become progressively older, with a concurrent increase in significant comorbidities that increase mortality.
• Mortality increases with older age (>60 y), in both males and females.

There is no racial predilection to upper gastrointestinal bleeding.

• Upper gastrointestinal bleeding is more common in males than females.
• The males to female ratio is approximately 2 to 1.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Arzu Kalayci, M.D. [2] ; Aditya Ganti M.B.B.S. [3]

Common risk factors in the development of upper gastrointestinal bleeding include advancing age, previous history of gastrointestinal bleed, chronic kidney disease, underlying cardiovascular disease, cirrhosis and portal hypertension, presence of H.pylori infection, NSAID’s or aspirin use in patients with a history of ulcer disease, patients on dual antiplatelet therapy and patients of 60 years or older.

Common risk factors in the development of upper gastrointestinal bleeding include:

• Advancing age^[1][2][3][4]
• Previous history of gastrointestinal bleed
• Chronic kidney disease
• Underlying cardiovascular disease
• Cirrhosis and portal hypertension
• Presence of H.pylori infection
• NSAID’s or aspirin use in patients with a history of ulcer disease
• Patients on dual antiplatelet therapy
• Age 60 years or older
• Patients taking glucocorticoids
• Dyspepsia
• Gastroesophageal reflux disease
• Nosocomial stress ulcers due the to the use of mechanical ventilation for more than 48 hours, and coagulopathy.
• Rare conditions associated with gastric acid hypersecretion, such as Zollinger-Ellison syndrome, mastocytosis, or a retained antrum following partial gastrectomy.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Aditya Ganti M.B.B.S. [2]

There is insufficient evidence to recommend routine screening for upper gastrointestinal bleeding.

There is insufficient evidence to recommend routine screening for upper gastrointestinal bleeding.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Aditya Ganti M.B.B.S. [2]

If left untreated upper gastrointestinal bleeding can become life-threatening. Massive blood loss can result in a severe drop in blood pressure resulting in decreased blood supply to organ systems leading to death. Complications of UGIB include end-organ damage and iron-deficiency anemia. Prognosis is generally good with prompt treatment, and the 1-year mortality rate of patients with nonvariceal UGIB is approximately 10%.

If left untreated upper gastrointestinal bleeding can become life-threatening. Massive blood loss can result in severe drop in blood pressure resulting in decreased blood supply to organ systems leading to death. Chronic blood loss if left untreated results in anemia.

Complications of UGIB include:^[1]

• End-organ damage
  • Cardiac ischemia
  • Renal failure
  • Ischemic hepatitis
  • Anoxic brain injury
• Iron-deficiency anemia

• Prognosis is generally good with appropriate treatment, and the 1-year mortality rate of patients with nonvariceal UGIB is approximately 10%.^[2][3][4][5]
• In UGIB, the prognosis doesn’t depend on the severity of bleeding but depends upon patien’ts age and comorbid conditions.
• The majority of patients with UGIB will stop bleeding spontaneously.
• A clean ulcer base has less than a 3% chance of rebleeding; therefore, these lesions are not usually treated or scoped again.
• In otherwise stable patients, patients with a clean ulcer base has less than a 3% chance of rebleeding and are good candidates for early discharge.

Risk of recurrent bleeding without endoscopic therapy versus with endoscopic therapy
Active arterial (spurting) bleeding	55% versus 20%
Nonbleeding visible vessel	43% versus 15%
Adherent clot	22% versus 15%

• Despite advances in gastric acid suppression as well as improved endoscopic diagnostic and therapeutic techniques, the mortality rate from UGIB has remained stable.

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