A gastrointestinal (GI) bleed is defined as blood loss occurring anywhere along the GI tract, from the oropharynx to the anus. Blood loss originating from any GI source above the ligament of Treitz, the suspensory ligament of the duodenum, is classified as an upper GI bleed (Nassar et al., 2021). An upper GI bleed is five times more likely than a lower GI bleed and, depending on its severity, carries a high risk of morbidity and mortality (Gibson, Scaturo, & Allen, 2018).

Upper GI Bleed Classification

An upper GI bleed can be classified as either variceal or nonvariceal. A variceal bleed occurs due to rupture of varices (i.e., dilated veins) in the esophagus or stomach. A nonvariceal bleed occurs due to an imbalance between gastric acid, pepsin secretion, and the body's mucosal defense barriers. Over time, this imbalance can cause erosion and ulceration of the gastric or esophageal mucosa.

Variceal Bleed

Variceal hemorrhage causes 70% of upper GI bleeds in patients with cirrhosis or portal hypertension (Mallet, Rudler, & Thabut, 2017). Varices are superficial, dilated veins that form collaterals in the GI tract to decompress the portal circulation in patients with cirrhosis. They develop when the hepatic vein pressure gradient rises above 12 mmHg (Sanyal & Bajaj, 2021). As cirrhosis progresses and the liver becomes more fibrotic, the increase in portal pressure and influx of portal flow to these veins causes them to swell and enlarge, making them more prone to rupture and bleeding (Alqahtani & Jang, 2021).

Nonvariceal Bleed

Peptic Ulcer Disease

The most common cause of a nonvariceal upper GI bleed is peptic ulcer disease (PUD), which leads to gastric or duodenal ulcers. Helicobacter pylori (H. pylori) infection and the use of nonsteroidal anti-inflammatory drugs (NSAIDs) account for 80% of PUD and PUD-associated bleeding (Wilkins, Wheeler, & Carpenter, 2020). H. pylori is a gram-negative bacterium that expresses adhesions that promote its attachment to the gastric epithelium. Once attached, it penetrates and colonizes the gastric mucosa, inducing inflammation and gastric or duodenal injury. H. pylori produces bacterial urease, an enzyme that breaks down gastric urea to ammonia, thereby neutralizing the stomach's acidic environment to allow the organism to survive (Lanas & Chan, 2017). The use of NSAIDs induces damage to the gastric mucosa through prostaglandin inhibition, which impairs mucus and bicarbonate secretion in the stomach. This increases the risk of gastric injury (Lanas & Chan, 2017).

Mallory-Weiss Syndrome

Mallory-Weiss syndrome is another cause of upper GI bleeding, occurring in 8%-15% of patients who present with an upper GI bleed (Guelrud, 2020). Although the exact mechanism of this syndrome is unknown, it is believed that an acute increase in abdominal pressure from forceful vomiting, coughing, or straining produces longitudinal mucosal lacerations in the distal esophagus or proximal stomach (Rawla & Devasahayam, 2021). Heavy alcohol use is a major risk factor in the development of these tears. The bleeding severity is increased in patients who drink alcohol and have a history of portal hypertension or esophageal varices (Guelrud, 2020). Mallory-Weiss syndrome can also be iatrogenic, occurring due to trauma from transesophageal echocardiograms, esophagogastroduodenoscopy (EGD), or nasogastric tube placement. These procedures all involve esophageal manipulation and can inadvertently cause mucosal lacerations. Although relatively uncommon, they are linked to Mallory-Weiss syndrome (Rawla & Devasahayam, 2021).

Erosive Disorders of the Esophagus and Stomach

Erosive disorders of the esophagus or stomach can also lead to upper GI bleeding. Erosive esophagitis is caused by the backflow of acid from the stomach through the lower esophageal sphincter. Decreased tone and increased relaxation of the lower esophageal sphincter leads to antegrade acid flow and esophageal injury (Antunes & Sharma, 2021). Immunosuppressed patients are at increased risk for developing infectious esophagitis, and infections with Candida albicans, cytomegalovirus, or herpes simplex virus can also facilitate esophageal injury. In the case of esophageal candidiasis, an impaired host immune response allows the fungus to proliferate and colonize the esophageal mucosa forming large white plaques throughout the esophagus. This infection is rare, but a serious complication can be an upper GI bleed (Antunes & Sharma, 2021). Other causes of erosive esophagitis include pill-induced esophageal damage from tetracycline antibiotics, chronic NSAID or aspirin use, and bisphosphonates. Acute erosive gastropathy occurs when the gastric mucosa is exposed to injurious substances such as alcohol, NSAIDs, and cocaine, disrupting the gastrum's protective mucosal barrier, thereby allowing pepsin and acid to penetrate the epithelium. Stress and critical illness can also be factors in the development of acute erosive gastropathy (Jensen & Feldman, 2020).

Vascular Etiologies

Various vascular causes of an upper GI bleed include angiodysplasias, Dieulafoy lesions, gastric antral vascular ectasia (GAVE), and aortoenteric fistula (AEF).

Angiodysplasias

Angiodysplasias are an acquired vascular defect that results in the development of abnormal, tortuous, dilated blood vessels in the mucosal and submucosal layers within the GI tract (Aghighi, Taherian, & Sharma, 2021). Over time, these vessels dilate and erode through the mucosa leading to a GI bleed. Upon examination with an endoscope, an angiodysplasia will appear as a 5- to 10-mm flat, red, projecting vessel (Aghighi et al., 2021). Although typically found in the small bowel and colon, angiodysplasia can also be found in the stomach and duodenum, causing either overt or occult blood loss in approximately 4%-7% of patients (Salztman, 2022).

Some risk factors for developing angiodysplasia include age over 60 years, end-stage renal disease (ESRD), von Willebrand disease, left ventricular assist device usage, and cardiovascular disease, particularly aortic stenosis (Costable & Greenwald, 2020). Nearly 40%-60% of patients with angiodysplasia have more than one present, and they are usually found in the same region of the GI tract (Saltzman, 2022). Although some angiodysplasias are found incidentally, those with bleeding angiodysplasias typically present with signs of anemia without associated abdominal pain. If bleeding does occur, it is usually chronic and recurrent (Salztman, 2022).

Dieulafoy Lesion

Although typically acute, another type of vascular GI bleed is a Dieulafoy lesion. This lesion is a vascular malformation in the GI tract of a tortuous submucosal blood vessel, not caused by an ulcer or erosion (Ali et al., 2022). It is a rare but life-threatening cause of an upper GI bleed given the potential for massive hemorrhage, and accounts for 6.5% of all nonvariceal upper GI bleeds (Malik & Anjum, 2021). A minor vessel wall defect leads to fibrinoid necrosis at the base of the lesion, causing it to bleed. In addition, thrombus formation in the gastric mucosal lining or gastric mucosal atrophy not caused by ulceration can lead to these abnormal lesions. Nearly 70% of all Dieulafoy lesions are found in the lesser curvature of the stomach or within 6 mm of the gastroesophageal junction (Malik & Anjum, 2021).

Gastric Antral Vascular Ectasia

Gastric antral vascular ectasia (GAVE) is another vascular etiology of upper GI bleeding. This disorder is relatively uncommon, accounting for only 4% of nonvariceal upper GI bleeds (Hsu et al., 2018). Endoscopic examination of the gastric mucosa will reveal the characteristic sign of this disorder: parallel raised or flat longitudinal erythematous stripes giving rise to its commonly referred to name "watermelon stomach" (Figure 1). It can also present as a diffuse "honeycomb" pattern of dilated and tortuous blood vessels known as angiodysplasias. A third variant of GAVE can present as nodules in the gastric antrum, known as nodular antral gastropathy (Smith, Davis, & Caldwell, 2018).

FIGURE 1. Gastric antral vascular ectasia: "watermelon stomach." Used with permission from "Watermelon Stomach," by S.

GAVE is associated with autoimmune diseases such as systemic sclerosis, liver cirrhosis, portal hypertension, metabolic syndrome, cardiovascular disease, and chronic kidney disease. Metabolic syndromes such as nonalcoholic steatohepatitis, hyperlipidemia, diabetes, and hypertension are also correlated with GAVE. Although the pathogenesis is unclear, these diseases promote a pro-inflammatory, pro-thrombotic, and oxidative state, which can precipitate microvascular injury leading to neoangiogenesis through vascular endothelial growth factor upregulation (Smith et al., 2018). This can cause vascular ectasia.

Mechanical stress is also believed to play a role in the development of GAVE. The pressures in the stomach's antrum, or lower region before the pylorus, are higher than in other stomach sections. Strong peristalsis through this region may cause antral mucosa prolapse leading to intermittent obstruction of the gastric vasculature, fibromuscular hyperplasia, and vascular ectasia, as dilated vessels are prone to rupture and bleed (Alkhormi, Memon, & Alqarawi, 2018). Hormonal factors are also believed to play a role. Several reported case series illustrate a connection between hypergastrinemia and GAVE and describe the successful use of octreotide, a gastrin inhibitor, in patients with GAVE-associated bleeding (Smith et al., 2018).

Aortoenteric Fistula

Finally, an AEF is a rare but severe cause of upper GI bleeding. An AEF occurs when the aortic wall erodes into the GI system and is associated with rapid hemodynamic instability and a high mortality rate. Primary and secondary etiologies exist in the development of AEFs (Dorosh & Lin, 2022). These fistulas primarily arise in the third and fourth duodenal segments due to the proximity of the two structures.

Primary fistulas arise spontaneously due to aortic inflammation or due to mechanical shearing forces on the aorta from a developing aneurysm. As the aortic wall bulges and thins out, it rubs against the enteral wall. The interacting forces of cardiac pulsation and gastric peristalsis contribute to erosion of the aortic wall into the GI tract leading to fistula formation (Dorosh & Lin, 2022).

Secondary fistulas are more common and usually occur after endovascular or open surgical aortic interventions involving a stent-graft placement. The graft can rub against the enteral wall leading to erosion. Furthermore, bacterial translocation into the bloodstream due to wall erosion can seed the synthetic graft, further accelerating fistula development (Dorosh & Lin, 2022).

Infection plays a role in the development of both primary and secondary AEFs. Klebsiella, Salmonella, tuberculosis, and syphilis have been associated with development of primary AEFs, whereas S. aureus, group B Streptococcus, and Veillonella have been cultured in those with secondary AEFs. Two-thirds of those with secondary AEFs have grown Candida species. However, it is difficult to determine the primary infection associated with AEF formation given bowel contamination (Chung, 2018).

Gastric Malignancy

Gastric cancer can also present as an upper GI bleed. Gastric cancer is the fifth most diagnosed cancer worldwide and carries a high mortality rate, as diagnosis usually occurs during the advanced stages of the disease (Smyth, Nilsson, Grabsch, van Grieken, & Lordick, 2020). H. pylori infection remains an important risk factor in developing noncardia gastric cancer. Chronic inflammation and erosion of the gastric epithelium lead to intestinal metaplasia, dysplasia, and eventual malignancy (Smyth et al., 2020). There is also a genetic predisposition to developing gastric cancer, as 10% of all gastric cancers have a familial component. Gastric malignancy is associated with diseases such as familial adenomatous polyposis, Lynch syndrome, juvenile polyposis, Li-Fraumeni syndrome, and Peutz-Jeghers syndrome (Smyth et al., 2020). Table 1 presents an exhaustive list of differential diagnoses for a patient presenting with an upper GI bleed.

TABLE 1. Exhaustive Differential Diagnosis List

History of Present Illness

Bleeding

As part of a complete history, clinicians need to determine the onset, type, and duration of bleeding, and the estimated quantity of blood loss. Signs of overt bleeding include hematemesis, coffee-ground emesis, melena, or hematochezia if the bleed is rapid and severe. Hematemesis is vomiting of bright red blood or clots. Coffee-ground emesis is vomiting of blood mixed with gastric contents. Melena is the passage of dark-tarry stools. Hematochezia is the passage of fresh blood, usually seen in patients with a lower GI bleed but can be indicative of a brisk upper GI bleed (Antunes & Copelin, 2022). However, some bleeding may not be evident on examination and is defined as an occult bleed (Perencevich & Saltzman, 2023).

The degree of bleeding may help to distinguish between diseases. Although any upper GI bleed can present acutely with severe hemodynamic instability, certain diseases are more likely to present with massive hemorrhage. These include an AEF, Dieulafoy lesions, and ruptured varices. Dieulafoy lesions may also present with overt signs of bleeding. On the other hand, occult bleeding is commonly seen with erosive gastropathy, PUD, GAVE, angiodysplasia, and gastric cancer (Perencevich & Saltzman, 2023). Erosive gastritis can be distinguished from other bleeds, as oftentimes bleeding does not begin until 3-7 days after a stressful event or insult to the gastric mucosal lining (Jensen & Feldman, 2020).

Risk Factors

Obtaining a thorough medical history can reveal risk factors for an upper GI bleed. A history of GI bleeding may indicate recurrent bleeding from a prior lesion in 60% of patients (Saltzman, 2022). A known history of cirrhosis or portal hypertension and chronic alcohol use may point to a variceal bleed (Antunes & Copelin, 2022).

Patients should also be questioned about a history of H. pylori infection, gastroesophageal reflux disease (GERD), gastric surgery, or radiation to help distinguish a diagnosis of PUD from other causes of an upper GI bleed (Lanas & Chan, 2017). In addition, chronic GERD and alcohol use can make a diagnosis of erosive esophagitis more likely. Recent history of infection, cirrhosis, or repeated radiographic exposure increases a patient's risk for erosive esophagitis (Antunes & Sharma, 2021).

A patient with frequent vomiting or coughing episodes, a seizure disorder, heavy alcohol consumption, or recent blunt trauma to the abdomen places a Mallory-Weiss tear high on the differential (Rawla & Devasahayam, 2021). Nearly 50%-70% of patients presenting with a Mallory-Weiss tear have a history of heavy alcohol ingestion, and many suffer from GERD. It should be noted that 25% of patients with a Mallory-Weiss tear have no risk factors (Rawla & Devasahayam, 2021).

Risk factors for Dieulafoy lesions include cardiovascular disease, chronic kidney disease, hypertension, diabetes mellitus, and PUD. Age is also a risk factor in the formation of a Dieulafoy lesion. They are found twice as often in men than in women (Malik & Anjum, 2021). Risk factors such as advanced age, ESRD, von Willebrand disease, or aortic stenosis also raise the clinical suspicion of angiodysplasias (Aghighi et al., 2021). Autoimmune diseases such as systemic sclerosis, conditions suggestive of metabolic syndrome, cirrhosis, and chronic renal failure may make the diagnosis of GAVE more likely (Hsu et al., 2018). Prior aortic surgeries, a known history of an abdominal aortic aneurysm (AAA), atherosclerosis, and older age increase the likelihood of an AEF. Males are more likely than females to develop an AEF given their increased prevalence of AAA (Chung, 2018).

Finally, a detailed family history may help diagnose a gastric malignancy, as 10% of gastric cancers have a familial component (Smyth et al., 2020). H. pylori infection is also strongly associated with gastric malignancy. Other risk factors include older age, an alcohol and smoking history, radiation exposure, and GERD (Smyth et al., 2020).

Medication and Drug History

Clinicians should also inquire about medication and drug history, as their use raises suspicion for several diseases responsible for upper GI bleeding. Patients who are on chronic NSAIDs, steroids, drink alcohol regularly, or are on therapeutic anticoagulation are all at high risk for Dieulafoy lesions (Malik & Anjum, 2021). Similarly, NSAID, aspirin, and tobacco are risk factors for both PUD and erosive gastropathy (Jensen & Feldman, 2020; Malik, Gnanapandithan, & Singh, 2021). In addition, medications associated with the development of erosive gastropathy include chemotherapy, oral sodium phosphate, iron, and cocaine (Jensen & Feldman, 2020).

Signs and Symptoms

There are a variety of specific signs and symptoms that can help differentiate the types of upper GI bleeds. Acute variceal bleeds present with massive hematemesis, melena, or hematochezia. As cirrhosis and portal hypertension are significant risk factors for varices, examination findings may include spider angiomas, ascites, and jaundice (Antunes & Copelin, 2022). Symptoms of erosive esophagitis include retrosternal chest pain, dysphagia, and odynophagia (Antunes & Sharma, 2021). Acute erosive gastropathy may present with abdominal pain, heartburn, nausea, vomiting, and hematemesis (Jensen & Feldman, 2020). Patients with PUD commonly present with epigastric pain or dyspepsia, nausea, or abdominal bloating (Kavitt, Lipowska, Anyane-Yeboa, & Gralnek, 2019). The timing of epigastric pain can aid in distinguishing between a gastric or duodenal ulcer. Pain immediately following a meal may indicate a gastric ulcer, whereas pain 2-3 hours postprandial may be a sign of a duodenal ulcer (Malik et al., 2021).

Iron-deficiency anemia with associated symptoms such as fatigue and weakness can also be indicative of an upper GI bleed (Cappellini, Musallam, & Taher, 2020). Dieulafoy lesions, angiodysplasias, erosive esophagitis, and GAVE can present with occult bleeding leading to severe, symptomatic iron-deficiency anemia (Malik & Anjum 2021).

Signs of an AEF include bleeding, abdominal pain, and a palpable abdominal mass, although this is only present in 6%-12% of patients (Dorosh & Lin, 2022). Hematemesis, or back or epigastric pain places a Mallory-Weiss tear high on the differential (Rawla & Devasahayam, 2021). Symptoms such as early satiety, weight loss, abdominal pain, bleeding, or dysphagia raise the suspicion for malignancy. These symptoms typically arise when the cancer is advanced (Smyth et al., 2020).

Diagnostic Process

Figure 2 provides step-by-step guidance on the initial triaging of patients who present with hematemesis, coffee-ground emesis, or melena to determine the most appropriate setting for workup and treatment. All patients who are considered hemodynamically unstable should be admitted for further workup. Those who are hemodynamically stable can be risk stratified using the Glasgow-Blatchford Bleeding Score (GBS) (Blatchford, Murray, & Blatchford, 2000). This scoring system utilizes a patient's vital signs, medical history, hemoglobin levels, and blood urea nitrogen (BUN) to calculate the likelihood that a patient will require urgent intervention and hospital admission. A score of 0 indicates that it is safe for a patient to be discharged to home without endoscopy from the emergency department and to follow up as an outpatient if symptomology persists. A GBS of 1 or greater warrants further workup and medical intervention (Kim et al., 2014). Table 2 can be utilized to calculate the GBS.

FIGURE 2. Triaging a patient with an upper gastrointestinal bleed.

TABLE 2. Glasgow-Blatchford Scoring System

For patients requiring further workup, Supplemental Digital Content Figure 3 (available at: http://links.lww.com/GNJ/A100) can be utilized to help identify the most likely cause of an upper GI bleed so that prompt diagnostic intervention can be performed. Common etiologies are included by category to increase usability of the framework. It is a systematic approach that stratifies patients based upon validated risk criteria for hospitalization and hemodynamic stability to determine the most prudent intervention. A hemodynamically unstable patient should be immediately stabilized and undergo initial diagnostics to expedite treatment. In a patient who is hemodynamically stable, the presenting signs, symptoms, and associated risk factors help to differentiate between diagnoses. Finally, initial diagnostic workup is included to formally identify the etiology of the upper GI bleed.

Assessment of Hemodynamic Stability and Risk

Patients presenting with hematemesis, coffee-ground emesis, or melena should be assessed for an upper GI bleed, as they can rapidly become hemodynamically unstable.

Hemodynamically Unstable

Those who present with the above symptoms and have a mean arterial pressure of less than 65 mmHg, tachycardia, decreased urine output, altered mental status, and hemoglobin (Hgb) of less than 7 g/dl or a decrease in Hgb of more than 2 g/dl from their baseline are considered hemodynamically unstable (Kamboj, Hoversten, & Leggett 2019). These patients warrant immediate admission to the hospital for further workup and intervention. Hypotension, including orthostatic hypotension, and tachycardia are also signs of hypovolemia that require aggressive resuscitation with intravenous fluids and blood products to achieve a target Hgb of 7 g/dl. Patients with gross hematemesis may need elective intubation for airway protection to prevent aspiration (Kovacs & Jensen, 2019).

Once hemodynamic stability is achieved, these patients require an emergent EGD within 12 hours to diagnose and potentially treat the bleeding (Kamboj et al., 2019). If unable to achieve hemodynamic stability, transcatheter arteriography is indicated to diagnose and control the source of bleeding. If there is a high clinical suspicion for AEF in a hemodynamically unstable patient, the patient must proceed to surgery and forgo any other diagnostic studies due to high mortality. If there is no history of an aortic aneurysm or prior aortic surgery, an abdominal ultrasound may be useful in identifying an aneurysm during the immediate resuscitative period, making an AEF more likely (Dorosh & Lin, 2022).

Hemodynamically Stable

On the other hand, patients who are hemodynamically stable can be managed in a myriad of ways. Supplemental Digital Content Figure 3 (available at: http://links.lww.com/GNJ/A100) can be used to help guide practitioners to diagnosis once it is determined that a patient needs to be admitted for further workup. For hemodynamically stable patients, it is crucial to obtain a thorough medical history, perform a physical examination, and obtain vital signs and laboratory tests to begin the workup leading to the differential.

Differential Diagnosis Determination

Variceal Etiologies and Management

Once it is clear a patient will need admission or further workup for a GI bleed, it is important to utilize patient history to narrow down the possible differential diagnoses. A history of varices, portal hypertension, cirrhosis, viral hepatitis, or alcohol use assists in distinguishing a potential variceal bleed from a nonvariceal bleed. Patients with a history that places a variceal bleed high on the differential should be initiated on a continuous octreotide infusion, have complete blood count (CBC) monitoring, and receive blood transfusions as needed to keep the Hgb level above 7 g/dl, and receive a diagnostic EGD within 24 hours of presentation (Alqahtani & Jang, 2021). Unlike other diagnoses, patients with variceal bleeds are started on prophylactic antibiotics to prevent bacterial infections (Alqahtani & Jang, 2021).

Nonvariceal Etiologies and Stabilization

The varying etiologies of a nonvariceal upper GI bleed are best distinguished based on the presence of risk factors as well as signs and symptoms. Patients who present with back or epigastric pain and have a history of repeated vomiting or coughing, abdominal trauma, alcohol, or NSAID and aspirin use may have a Mallory-Weiss tear. Similarly, NSAID use and heavy alcohol use, in addition to anticoagulant use, are all risk factors for bleeding Dieulafoy lesions. The difficulty is that these patients often experience occult bleeds (Malik & Anjum, 2021).

Patients with erosive esophagitis often have a history of GERD and heavy alcohol use. In addition, agents that can irritate the esophageal lining, such as NSAIDs and aspirin, are common among these patients. The presentation and time course vary as esophagitis can be caused by infection, reflux, medications, eosinophilia, and radiographic exposure. Despite the various causes, retrosternal chest pain, heartburn, dysphagia, and odynophagia are the hallmark signs and symptoms associated with this disease process (Antunes & Sharma, 2021). Patients with erosive gastropathy typically experience abdominal pain, heartburn, and nausea. Those with a history of alcohol use, NSAID or aspirin use, trauma, oral sodium phosphate or iron use, certain chemotherapies, ischemia, or stress are most at risk.

Patients who present without any overt abdominal symptoms with bleeding; have a history of recurrent bleeding and chronic anemia; are older; or have a history of ESRD, aortic stenosis, or von Willebrand disease may have a bleeding angiodysplasia (Aghighi et al., 2021). Furthermore, characteristics that should alert the clinician to a vascular etiology of upper GI bleeding include a history of hyperlipidemia, obesity, diabetes, cirrhosis, autoimmune disease, or chronic kidney disease. These, coupled with iron-deficiency anemia, should raise suspicion for GAVE. Furthermore, patients presenting with abdominal pain, an abdominal mass, and hemorrhagic shock with a known history of an AAA or prior aortic surgery are highly indicative of an AEF.

All patients who meet the criteria for admission based upon the GBS score are started on an intravenous proton pump inhibitor, have CBCs checked at regular intervals, receive blood products to maintain a Hgb above 7 g/dl, platelets above 50,000 mcL, and are kept nothing by mouth in preparation for a diagnostic, and potentially therapeutic, EGD (Kamboj et al., 2019). If the provider completing the scope suspects PUD or gastric cancer, an EGD with biopsy is typically performed (Kavitt et al., 2019).

Diagnostic Tests

Esophagogastroduodenoscopy

The standard of care for a patient presenting with an acute upper GI bleed is to undergo an EGD to diagnose and potentially treat the cause. Esophagogastroduodenoscopy is a highly specific and sensitive test in determining the etiology of an upper GI bleed (Saltzman, 2022). However, in hemodynamically stable patients presenting with an AEF, EGD is a poor diagnostic test with only a 50% sensitivity (Dorosh & Lin, 2022). An EGD should be performed within 24 hours of presentation to reduce the risk of rebleeding and assess the need for surgical intervention. Patients who receive an EGD within this timeframe have a reduced hospital length of stay (Samuel et al., 2018). On the other hand, a patient with a suspected variceal hemorrhage should have an EGD within 12 hours of presentation (Kamboj et al., 2019). Prior to undergoing endoscopy, all patients with an upper GI bleed should be adequately resuscitated and hemodynamically stable to prevent iatrogenic complications.

Computed Tomography With Angiography

In some cases, an EGD can be nondiagnostic. In an acute nonvariceal bleed, it may be difficult to visualize the bleeding lesion because of the presence of blood and clots. In this situation, a CT with angiography (CTA) can help diagnose the source of the bleed. A CTA should be immediately pursued if an AEF is suspected and the patient is stable. A CTA is a highly sensitive (50%-86%) and specific (92%-95%) scan in determining the location and etiology of the bleed. Furthermore, the information gained with a CTA can help guide therapeutic endovascular intervention if an upper endoscopy is unsuccessful (Ramaswamy et al., 2014).

Most patients presenting with bleeding from gastric cancer are in the more advanced stages of the disease (Mansfield, 2021). Therefore, a presenting patient with an upper gastrointestinal bleed with a history and symptoms highly suspicious for malignancy should, in addition to an EGD, undergo CT of the abdomen and pelvis or positron emission tomography (PET) scan for staging.

Treatment

Endoscopic Intervention

Often, an EGD can provide therapeutic interventions if a bleeding source is identified. If bleeding esophageal or gastric varices are found, band ligation is the preferred treatment. If the EGD is diagnostic for a bleeding ulcer from PUD, then clipping, an injection of epinephrine and thermal coagulation, or application of a hemostasis powder is indicated (Saltzman, 2022). If an actively bleeding Mallory-Weiss tear is found, treatment consists of thermal coagulation, ligation or hemoclips, or an injection of epinephrine. However, monotherapy with epinephrine carries a higher risk of recurrent bleeding (Guelrud, 2020).

Erosive Gastropathy

An EGD will reveal multiple petechial hemorrhages and/or small red or black erosions in a patient with a bleed from acute erosive gastropathy. Stress-related erosions are found near the fundus, whereas alcohol and NSAID-related erosions usually involve the entire stomach and are more prominent in the antrum. If the bleeding is severe, plasma coagulation during EGD is indicated, whereas a more stable patient may be treated with a proton pump inhibitor and cessation of the offending substance (Jensen & Feldman, 2020).

Dieulafoy Lesion

Mechanical banding and hemoclips have a 95% rate of success when controlling bleeding from a Dieulafoy lesion. Injection of epinephrine, norepinephrine, and sclerotherapy may also be utilized to control these fast-bleeding vessels in an attempt to achieve hemostasis (Malik & Anjum, 2021).

Angiodysplasias

In patients with angiodysplasias, controlling acute bleeding is typically achieved with endoscopic interventions such as cautery, although location and access to the lesions are factors to be considered. If rebleeding episodes occur, mechanical hemostasis through endoscopic clips may be considered to avoid cautery-associated vessel injury (Saltzman, 2022). If nonbleeding angiodysplasias are found at endoscopy, and the patient has known iron-deficiency anemia or evidence of either overt or occult GI bleeding, endoscopic treatment is recommended (Aghighi et al., 2021). If there is persistent anemia or signs of GI bleeding after these initial measures are taken, then further workup with capsule endoscopy, radiographic imaging such as CTA or MRI, or enteroscopy should be pursued (Saltzman, 2022).

GAVE

Endoscopic intervention is the mainstay treatment of upper GI bleeding due to GAVE. Neodymium: yttrium-aluminum-garnet (Nd:YAG) laser is a thermal device used to induce coagulation of superficial and submucosal vessels (Hsu et al., 2018). Argon plasma coagulation is another thermal method utilized to control bleeding by utilizing ionized argon gas to produce high-frequency electrical flows to cauterize and eliminate dilated vessels in the antrum (Hsu et al., 2018). Endoscopic band ligation, used to control or prevent variceal bleeding, is also utilized in GAVE to achieve hemostasis. Finally, radiofrequency ablation is another endoscopic thermal modality that destroys vascular ectasia. In circumstances where endoscopic therapies fail, surgical intervention is pursued. Most patients undergo an antrectomy, or removal of the distal region of the stomach. There are case reports, however, using a partial gastrectomy, gastrectomy, or an esophagogastrectomy to treat GAVE (Hsu et al., 2018).

Aortoenteric Fistula

As most patients presenting with an AEF are hemodynamically unstable, immediate surgery for aortic repair is indicated. As AEF development is commonly associated with infection, broad-spectrum antibiotics should also be initiated prior to surgical repair with gram-positive, gram-negative, anaerobic, and antifungal coverage (Chung, 2018).

Gastric Malignancy

In an ulcerated malignant gastric lesion, hemostasis can be achieved through endoscopic intervention. These include hemoclips, epinephrine injection, laser photocoagulation, or argon plasma coagulation. If the patient continues to bleed, palliative gastrectomy or radiation therapy may be pursued. Despite the reported 69%-91% response rate in controlling bleeding with radiotherapy, its effects, are not immediate and take time (Harada, Zhao, Shanbhag, Baba, & Ajani, 2020). In an emergent situation, EGD with intervention or transcatheter arterial embolization (TAE) should be first-line therapies.

Transcatheter Arterial Embolization

Angiography with endovascular intervention should be pursued in an unstable patient with a bleed that cannot be identified by endoscopy or imaging. It can also be useful in a patient who continues to bleed despite endoscopic intervention and aggressive medical management (Orron, Bloom, & Neeman, 2018). The goal of TAE is to achieve thrombosis of the bleeding vessel. A catheter is placed into the identified bleeding artery, allowing for the administration of a temporary or permanent occlusive agent. Temporary agents include gelfoam, microfibrillar bovine collagen, an autologous blood clot, or thrombin. Some examples of permanent agents include coils, vascular plugs, or glues such as N-butyl cyanoacrylate (Orron et al., 2018).

Transarterial embolization controls 80%-98% of bleeding in those with a nonvariceal upper GI bleed. However, rebleeding is still a risk and can occur in up to 47% of patients (Orron et al., 2018). If TAE fails, surgery should be considered.

Specimen Collection

In a patient with confirmed PUD via endoscopy, biopsies should be collected to diagnose H. pylori. Biopsies are not recommended if a Dieulafoy lesion is present as doing so may promote further bleeding. However, if obtained, histopathology of these lesions reveals a normal artery with occasional amyloid deposition and impingement of the elastic lamina into the muscularis mucosa (Malik & Anjum, 2021).

In GAVE, an EGD will reveal the classic sign of a "watermelon stomach," or diffuse angiodysplasias in a honeycomb pattern distribution or nodules. Histological features of GAVE include dilated mucosal vessels, fibrin thrombi, spindle cell proliferation, and fibromuscular hyperplasia (Smith et al., 2018).

If malignancy is suspected, an EGD with tumor biopsies is indicated. H. pylori testing should also occur as infection with this bacterium is a strong risk factor in the development of gastric cancer.

Risks and Complications

Upper endoscopy is a very safe procedure with an adverse event rate of 0.13% and a mortality rate of 0.004% (Levy & Gralnek, 2016). Sixty percent of all adverse effects are cardiopulmonary due to either hypoxia or respiratory depression from sedatives or aspiration of gastric contents during endoscopy. Stabilizing a patient before undergoing endoscopy is paramount to mitigate these risks. Other complications include esophageal or intra-abdominal perforation, bleeding, and infection. Bleeding and infection are very rare complications of an upper endoscopy (Levy & Gralnek, 2016).

Transarterial embolization also carries risks. Contrast administration to identify the offending vessel during TAE may lead to contrast-induced nephropathy. Vascular damage may also occur at the puncture site or when accessing the vessel to achieve hemostasis. Bowel ischemia is also of concern post-arterial embolization. However, due to the abundant collateral supply to the stomach and duodenum, TAE is still considered a safe procedure. Treatment failure is also of concern especially in patients with coagulopathy (Foltz & Khaddash, 2019).

Implications for Practice

Patients in both inpatient and outpatient clinical areas with differing primary diagnoses and comorbidities may present with an upper GI bleed. Ensuring hemodynamic stability and airway protection, breathing, and circulation should be prioritized in the immediate setting. In most clinical settings, nurses will be the first to triage a patient with an upper GI bleed. It is paramount that nurses recognize, assess, and immediately respond to any change in patient stability, as this GI emergency can be life-threatening. Through evaluation of vital signs, mental status assessment, laboratory monitoring, and timely medication administration, nurses play an integral role in the management of a patient with an upper GI bleed. Nurses must be familiar with the current treatment modalities to prepare for subsequent interventions. They serve as an invaluable resource in educating patients and their caregivers about the next steps in their care.

Furthermore, maintaining a broad list of differential diagnoses will ensure the clinician considers all etiologies of an upper GI bleed. Through the collection of a complete and thorough medical, surgical, and family history coupled with presenting patient characteristics, unlikely diagnoses can be ruled out, and appropriate diagnostic tests prescribed. If there is any sign of respiratory compromise or question of stability, admission to the hospital or referral to the emergency department is prudent. Maintaining close monitoring of CBCs, vital signs, and quantifying blood loss from hematemesis, melena, and coffee-ground emesis can help guide transfusion needs and better risk stratify the severity of the upper GI Bleed.

Conclusion

An upper GI bleed is a life-threatening emergency that requires prompt diagnostic and therapeutic intervention. Any patient presenting with hematemesis, coffee-ground emesis, or melena should raise the concern for acute upper GI bleed. Obtaining a thorough patient history and physical is a crucial step in determining the etiology of the bleed, and patient stabilization is paramount before proceeding with any diagnostic tests. Upper endoscopy remains the gold standard and first-line procedure for diagnosing and treating an upper GI bleed.

The algorithm presented is an innovative tool that can be used by nurses and advanced practice nurses to quickly identify potential causes of an upper GI bleed. The algorithm clearly identifies the parameters and immediate interventions for unstable patients with an upper GI bleed. These lifesaving measures can often be initiated by a nurse before an advanced practice nurse or other provider is able to assess the patient.

Nurses as well as advanced practice registered nurses can benefit from this novel diagnostic approach. The algorithm provides a concise, compact visual aid to assess a patient with an upper GI bleed and form a prompt differential diagnosis to help guide treatment.

REFERENCES