AEN has never been recorded as a one symptom disorder, but instead present by multiple symptoms. The symptoms vary from the severity of the disorder. The most classic sign of AEN is the dark pigmentation of esophageal mucosa in an upper endoscopy, usually viewed as an ulcer or as an infectious disease. Necrosis can be found mostly between the three distals of the esophagus, but stops abruptly at the gastroesophageal junction. The basic and most common symptoms reported are blood in stool and blood in vomiting. Upper gastrointestinal bleeding then is reported, and is very commonly represented in elderly patients. Black or bloody stools and hematemesis account for over three quarters of the case presentations. Abdominal pain, nausea, vomiting, and unstable vital signs are common. A cardiovascular event (such as a heart attack) was reported in ten percent of the total known cases.

Acute esophageal necrosis can only be diagnosed by an upper gastrointestinal endoscopy.

PVS sufferers often complain of a burning sensation with the tongue and oral mucosa, and atrophy of lingual papillae produces a smooth, shiny, red, dorsum of the tongue. Symptoms include:

Serial contrasted gastrointestinal radiography or upper gastrointestinal endoscopy may reveal the web in the esophagus. Blood tests show a hypochromic microcytic anemia that is consistent with an iron-deficiency anemia. Biopsy of involved mucosa typically reveals epithelial atrophy (shrinking) and varying amounts of submucosal chronic inflammation. Epithelial atypia or dysplasia may be present.It may also present as a post-cricoid malignancy which can be detected by loss of laryngeal crepitus. Laryngeal crepitus is found normally and is produced because the cricoid cartilage rubs against the vertebrae.

Following clinical presentations may be used in the diagnosis of this condition.

1. Dizziness

2. Pallor of the conjuctiva and face

3. Erythematous oral mucosa with burning sensation

4. Breathelessness

5. Atropic and smooth tongue

6. Peripheral rhaggades around the oral cavity

The following tests are helpful in the diagnosis of Plummer–Vinson syndrome.

Its main symptoms are pain and difficulty in swallowing (dysphagia).

Esophageal webs are thin (2-3mm) membranes of normal esophageal tissue consisting of mucosa and submucosa that can partially protrude/obstruct the esophagus. They can be congenital or acquired. Congenital webs commonly appear in the middle and inferior third of the esophagus, and they are more likely to be circumferential with a central or eccentric orifice. Acquired webs are much more common than congenital webs and typically appear in the cervical area (postcricoid).

Clinical symptoms of this condition are selective (solid more than liquids) dysphagia, thoracic pain, nasopharyngeal reflux, aspiration, perforation and food impaction (the last two are very rare).

They are mainly observed in the Plummer–Vinson syndrome, which is associated with chronic iron deficiency anemia. One in 10 patients with Plummer-Vinson syndrome will eventually develop squamous cell carcinoma of the esophagus, but it is unclear if esophageal webs in and of themselves are a risk factor.

Esophageal webs are associated with bullous diseases (such as epidermolysis bullosa, pemphigus, and bullous pemphigoid), with graft versus host disease involving the esophagus, and with celiac disease.

Esophageal webs are more common in white individuals and in women (with a ratio 2:1). The literature describes relations between these webs and Plummer-Vinson Syndrome, bullous dermatologic disorders, inlet patch, graft-versus-host disease and celiac disease. The postulated mechanisms are sideropenic anemia (mechanism unknown) or some interference of the immune system.

Esophageal webs can be ruptured during upper endoscopy.

Curling's ulcer (stress ulcer) or a Curling ulcer is an acute gastric erosion resulting as a complication from severe burns when reduced plasma volume leads to ischemia and cell necrosis (sloughing) of the gastric mucosa. The condition was first described in 1823 and named for a doctor, Thomas Blizard Curling, who observed ten such patients in 1842.

These stress ulcers (actually shallow multiple erosions) were once a common complication of serious burns, presenting in over 10% of cases, and especially common in child burn victims. They result in perforation and hemorrhage more often than other forms of intestinal ulceration and had correspondingly high mortality rates (at least 80%).

A similar condition involving elevated intracranial pressure is known as Cushing's ulcer.

While emergency surgery was once the only treatment, combination therapies including enteral feeding with powerful antacids such as H-receptor antagonists or, more recently, proton pump inhibitors such as omeprazole have made Curling's ulcer a rare complication.

Esophageal stricture, or narrowing of the esophagus, is usually a complication of acid reflux, most commonly due to gastroesophageal reflux (GERD). These patients are usually older and have had GERD for a long time. Esophageal stricture can also be due to other causes, such as acid reflux from Zollinger-Ellison syndrome, trauma from a nasogastric tube placement, and chronic acid exposure in patients with poor esophageal motility from scleroderma. Other non-acid related causes of peptic strictures include infectious esophagitis, ingestion of chemical irritant, pill irritation, and radiation. Peptic stricture is a progressive mechanical dysphagia, meaning patients will complain of initial intolerance to solids followed by inability to tolerate liquids. When the diameter of the stricture is less than 12 mm the patient will always have dysphagia, while dysphagia is not seen when the diameter of the stricture is above 30 mm. Symptoms relating to the underlying cause of the stricture usually will also be present.

Esophageal cancer also presents with progressive mechanical dysphagia. Patients usually come with

rapidly progressive dysphagia first with solids then with liquids, weight loss (> 10 kg), and anorexia (loss of appetite). Esophageal cancer usually affects the elderly. Esophageal cancers can be either squamous cell carcinoma or adenocarcinoma. Adenocarcinoma is the most prevalent in the US and is associated with patients with chronic GERD who have developed Barrett's esophagus (intestinal metaplasia of esophageal mucosa). Squamous cell carcinoma is more prevalent in Asia and is associated with tobacco smoking and alcohol use.

Esophageal rings and webs, are actual rings and webs of tissue that may occlude the esophageal lumen.

- "Rings" --- Also known as Schatzki rings from the discoverer, these rings are usually mucosal rings rather than muscular rings, and are located near the gastroesophageal junction at the squamo-columnar junction. Presence of multiple rings may suggest eosinophilic esophagitis. Rings cause intermittent mechanical dysphagia, meaning patients will usually present with transient discomfort and regurgitation while swallowing solids and then liquids, depending on the constriction of the ring.

- "Webs" --- Usually squamous mucosal protrusion into the esophageal lumen, especially anterior cervical esophagus behind the cricoid area. Patients are usually asymptomatic or have intermittent dysphagia. An important association of esophageal webs is to the Plummer-Vinson syndrome in iron deficiency, in which case patients will also have anemia, koilonychia, fatigue, and other symptoms of anemia.

Achalasia is an idiopathic motility disorder characterized by failure of lower esophageal sphincter (LES) relaxation as well as loss of peristalsis in the distal esophagus, which is mostly smooth muscle. Both of these features impair the ability of the esophagus to empty contents into the stomach. Patients usually complain of dysphagia to both solids and liquids. Dysphagia to liquids, in particular, is a characteristic of achalasia. Other symptoms of achalasia include regurgitation, night coughing, chest pain, weight loss, and heartburn. The combination of achalasia, adrenal insufficiency, and alacrima (lack of tear production) in children is known as the triple A (Allgrove) syndrome. In most cases the cause is unknown (idiopathic), but in some regions of the world, achalasia can also be caused by Chagas disease due to infection by "Trypanosoma cruzi".

Scleroderma is a disease characterized by atrophy and sclerosis of the gut wall, most commonly of the distal esophagus (~90%). Consequently, the lower esophageal sphincter cannot close and this can lead to severe gastroesophageal reflux disease (GERD). Patients typically present with progressive dysphagia to both solids and liquids secondary to motility problems or peptic stricture from acid reflux.

Spastic motility disorders include diffuse esophageal spasm (DES), nutcracker esophagus, hypertensive lower esophageal sphincter, and nonspecific spastic esophageal motility disorders (NEMD).

- "DES" can be caused by many factors that affect muscular or neural functions, including acid reflux, stress, hot or cold food, or carbonated drinks. Patients present with intermittent dysphagia, chest pain, or heartburn.

Rare causes of esophageal dysphagia not mentioned above

- Diverticulum

- Aberrant subclavian artery, or (dysphagia lusoria)

- Cervical osteophytes

- Enlarged aorta

- Enlarged left atrium

- Mediastinal tumor

The classic history of esophageal rupture is one of severe retching and vomiting followed by excruciating retrosternal chest and upper abdominal pain. Odynophagia, tachypnea, dyspnea, cyanosis, fever, and shock develop rapidly thereafter.

Physical examination is usually not helpful, particularly early in the course. Subcutaneous emphysema (crepitation) is an important diagnostic finding but is not very sensitive, being present in only 9 of 34 patients (27 percent) in one series. A pleural effusion may be detected.

Mackler's triad includes chest pain, vomiting, and subcutaneous emphysema, and while it is a classical presentation, it is only present in 14% of people.

Pain can occasionally radiate to the left shoulder, causing physicians to confuse an esophageal perforation with a myocardial infarction.

It may also be audibly recognized as Hamman's sign.

Gastric varices are dilated submucosal veins in the stomach, which can be a life-threatening cause of bleeding in the upper gastrointestinal tract. They are most commonly found in patients with portal hypertension, or elevated pressure in the portal vein system, which may be a complication of cirrhosis. Gastric varices may also be found in patients with thrombosis of the splenic vein, into which the short gastric veins which drain the fundus of the stomach flow. The latter may be a complication of acute pancreatitis, pancreatic cancer, or other abdominal tumours, as well as hepatitis C. Gastric varices and associated bleeding are a potential complication of schistosomiasis resulting from portal hypertension.

Patients with bleeding gastric varices can present with bloody vomiting (hematemesis), dark, tarry stools (melena), or rectal bleeding. The bleeding may be brisk, and patients may soon develop shock. Treatment of gastric varices can include injection of the varices with cyanoacrylate glue, or a radiological procedure to decrease the pressure in the portal vein, termed transjugular intrahepatic portosystemic shunt or TIPS. Treatment with intravenous octreotide is also useful to shunt blood flow away from the stomach's circulation. More aggressive treatment including splenectomy (or surgical removal of the spleen) or liver transplantation may be required in some cases.

Patients usually complain of dysphagia (the feeling of food getting stuck "several seconds" after swallowing), and will point to the suprasternal notch or behind the sternum as the site of obstruction.

Esophageal diseases can derive from congenital conditions, or they can be acquired later in life.

Many people experience a burning sensation in their chest occasionally, caused by stomach acids refluxing into the esophagus, normally called heartburn. Extended exposure to heartburn may erode the lining of the esophagus, leading potentially to Barrett's esophagus which is associated with an increased risk of adenocarcinoma most commonly found in the distal one-third of the esophagus.

Some people also experience a sensation known as globus esophagus, where it feels as if a ball is lodged in the lower part of the esophagus.

The following are additional diseases and conditions that affect the esophagus:

- Achalasia

- Acute esophageal necrosis

- Barrett's esophagus

- Boerhaave syndrome

- Caustic injury to the esophagus

- Chagas disease

- Diffuse esophageal spasm

- Esophageal atresia and Tracheoesophageal fistula

- Esophageal cancer

- Esophageal dysphagia

- Esophageal varices

- Esophageal web

- Esophagitis

- GERD

- Hiatus hernia

- Jackhammer esophagus (hypercontractile peristalsis)

- Killian–Jamieson diverticulum

- Mallory-Weiss syndrome

- Neurogenic dysphagia

- Nutcracker esophagus

- Schatzki's ring

- Zenker's Diverticulum

The signs and symptoms for esophagitis include:

- Heartburn feels like the inside of your chest is burning. It is a symptom of acid reflux or GERD.

- Nausea is the feeling of being sick, specifically with the urge to vomit.

- Swallowing is painful and difficult to pass food through your throat into your esophagus.

- Vomiting, also known as emesis, is the release of the contents of the stomach through the mouth or nose.

- Abdominal pain is when pain is felt in the abdomen.

- Food bolus impaction is an obstruction of the esophagus by swallowed food.

- Acid regurgitation is the backflow of acid from the stomach to the mouth.

- Chest pain is pain felt between the neck and upper abdomen. There are many causes and the pain can range.

- Cough is a reflex to clear the throat of irritants or mucus.

A doctor should be consulted if the signs and/or symptoms do not subside after a few days, are accompanied with flu-like symptoms, do not lessen after treating with over-the counter antacids, and/or make eating food difficult.

Gastric varices can present in two major ways. First, patients with cirrhosis may be enrolled in screening gastroscopy programs to detect esophageal varices. These evaluations may detect gastric varices that are asymptomatic. When gastric varices are symptomatic, however, they usually present acutely and dramatically with upper gastrointestinal bleeding. The symptoms can include vomiting blood, melena (passing black, tarry stools); or passing maroon stools or frank blood in the stools. Many people with bleeding gastric varices present in shock due to the profound loss of blood.

Secondly, patients with acute pancreatitis may present with gastric varices as a complication of a blood clot in the splenic vein. The splenic vein sits over the pancreas anatomically and inflammation or cancers of the pancreas may result in a blot clot forming in the splenic vein. As the short gastric veins of the fundus of the stomach drain into the splenic vein, thrombosis of the splenic vein will result in increased pressure and engorgement of the short veins, leading to varices in the fundus of the stomach.

Laboratory testing usually shows low red blood cell count and often a low platelet count. If cirrhosis is present, there may be coagulopathy manifested by a prolonged INR; both of these may worsen the bleeding from gastric varices.

In very rare cases, gastric varices are caused by splenic vein occlusion as a result of the mass effect of slow-growing pancreatic neuroendocrine tumors.

The most common symptoms of GERD in adults are an acidic taste in the mouth, regurgitation, and heartburn. Less common symptoms include pain with swallowing/sore throat, increased salivation (also known as water brash), nausea, chest pain, and coughing.

GERD sometimes causes injury of the esophagus. These injuries may include one or more of the following:

- Reflux esophagitis – inflammation of esophageal epithelium which can cause ulcers near the junction of the stomach and esophagus

- Esophageal strictures – the persistent narrowing of the esophagus caused by reflux-induced inflammation

- Barrett's esophagus – intestinal metaplasia (changes of the epithelial cells from squamous to intestinal columnar epithelium) of the distal esophagus

- Esophageal adenocarcinoma – a form of cancer

Some researchers have proposed that recurrent ear infections, and idiopathic pulmonary fibrosis might be tied, in some cases, to GERD; however, a causative role has not been established. GERD does not appear to be linked to chronic sinusitis.

Not all patients with Schatzki rings have symptoms; barium swallow tests of the esophagus sometimes show Schatzki rings in patients with no swallowing difficulties.

When Schatzki rings cause symptoms, they usually result in episodic difficulties with swallowing (dysphagia) solid foods, or a sensation that the food "sticks" while swallowing, especially if the food is not chewed thoroughly. Patients usually are able to regurgitate or force through the food material and resume eating. However, complete obstruction of the esophagus by a bolus of food (often called steakhouse syndrome) can occur. This can cause crushing chest pain and may need immediate treatment with endoscopy, which is the use of a specialized fibre-optic camera in order to remove the lodged food. After the obstruction is located, snares or forceps are inserted to pull the food out of the esophagus or to push it into the stomach. The latter is done with caution, usually when the anatomy of the structures around the obstruction is already known.

DES manifests as intermittent difficulty swallowing (dysphagia) for solid foods and liquids, and atypical chest pain. The chest pain may appear similar to cardiac chest pain (angina pectoris), so investigating the possible existence of heart disease is often indicated.

A Schatzki ring or Schatzki–Gary ring is a narrowing of the lower esophagus that can cause difficulty swallowing (dysphagia). The narrowing is caused by a ring of mucosal tissue (which lines the esophagus) or muscular tissue. A Schatzki ring is a specific type of "esophageal ring", and Schatzki rings are further subdivided into those above the esophagus/stomach junction (A rings), and those found at the squamocolumnar junction in the lower esophagus (B rings).

Patients with Schatzki rings can develop intermittent difficulty swallowing or, more seriously, a completely blocked esophagus. The ring is named after the German-American physician Richard Schatzki.

Nutcracker esophagus is characterized as a motility disorder of the esophagus, meaning that it is caused by abnormal movement, or peristalsis of the esophagus. Patients with motility disorders present with two key symptoms: either with chest pain (typically reported as non-cardiac chest pain as it is esophageal in origin), which is usually found in disorders of spasm, or with dysphagia (difficulty with swallowing). Nutcracker esophagus can present with either of these, but chest pain is the more common presentation. The chest pain is very severe and intense, and mimics cardiac chest pain. It may spread into the arm and back. The symptoms of nutcracker esophagus are intermittent, and may occur with or without food. Rarely, patients can present with a sudden obstruction of the esophagus after eating food (termed a food bolus obstruction, or the 'steakhouse syndrome') requiring urgent treatment. The disorder does not progress to produce worsening symptoms or complications, unlike other motility disorders (such as achalasia) or anatomical abnormalities of the esophagus (such as peptic strictures or esophageal cancer). Many patients with nutcracker esophagus do not have any symptoms at all, as esophageal manometry studies done on patients without symptoms may show the same motility findings as nutcracker esophagus. Nutcracker esophagus may also be associated with metabolic syndrome. The incidence of nutcracker esophagus in all patients is uncertain.

The acute syndrome presents with rapidly progressive severe upper abdominal pain, yellow discoloration of the skin and whites of the eyes, liver enlargement, enlargement of the spleen, fluid accumulation within the peritoneal cavity, elevated liver enzymes, and eventually encephalopathy. The fulminant syndrome presents early with encephalopathy and ascites. Liver cell death and severe lactic acidosis may be present as well. Caudate lobe enlargement is often present. The majority of patients have a slower-onset form of Budd–Chiari syndrome. This can be painless. A system of venous collaterals may form around the occlusion which may be seen on imaging as a "spider's web". Patients may progress to cirrhosis and show the signs of liver failure.

On the other hand, incidental finding of a silent, asymptomatic form may not be a cause for concern.

Most patients with portal hypertensive gastropathy have either a stable or improving course in the appearance of the gastropathy on endoscopy. However, according to retrospective data, roughly one in seven patients with portal hypertensive gastropathy will develop bleeding (either acute or chronic) attributable to the gastropathy. Patients with chronic bleeding will usually come to the attention of the medical system because of anemia.

The diagnosis of portal hypertensive gastropathy is usually made on endoscopy. The usual appearance of portal hypertensive gastropathy on endoscopy is a mosaic-like or reticular pattern in the mucosa. Red spots may or may not be present. The pattern is usually seen throughout the stomach. A similar pattern can be seen with a related condition called gastric antral vascular ectasia (GAVE), or watermelon stomach. However, in GAVE, the ectatic blood vessels are more commonly found in the antrum or lower part of the stomach.

Cricopharyngeal spasms occur in the cricopharyngeus muscle of the pharynx. These spasms are frequently misunderstood by the patient to be cancer due to the 'lump in the throat' feeling (Globus pharyngis) that is symptomatic of this syndrome. In practice, real lumps in the throat, such as a thyroid cancer, are generally not felt until they impede ingestion of food. This is one of the reasons that a cancer can get so big before it is discovered. In contrast, a cricopharyngeal spasm is an uncomfortable but harmless and temporary disorder.

Common misdiagnoses include myocardial infarction, pancreatitis, lung abscess, pericarditis, and spontaneous pneumothorax. If esophageal perforation is suspected, even in the absence of physical findings,chest xray, water soluble contrast radiographic studies of the esophagus and a CT scan should be promptly obtained. In most cases, non-operative management is administered based on radiological evidence contained in mediastinal collection.

The change from normal to premalignant cells that indicate Barrett's esophagus does not cause any particular symptoms. Barrett's esophagus, however, is associated with these symptoms:

- frequent and longstanding heartburn

- trouble swallowing (dysphagia)

- vomiting blood (hematemesis)

- pain under the sternum where the esophagus meets the stomach

- unintentional weight loss because eating is painful (odynophagia)

The risk of developing Barrett's esophagus is increased by central obesity (vs. peripheral obesity). The exact mechanism is unclear. The difference in distribution of fat among men (more central) and women (more peripheral) may explain the increased risk in males.