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

Barium esophagography and videofluoroscopy will help to detect esophageal webs. Esophagogastroduodenoscopy will enable visual confirmation of esophageal webs.

Currently, there is no direct treatment for AEN. Only treatment is for the underlying main diseases or conditions. Appropriate hydration is set. Antacids are also added for further recovery support. Common support drugs of antacids are either H receptor antagonists, and/or a proton pump inhibitor. Sucralfate was used as an option. Parenteral nutrition greatly increased chance of recovery. An esophagectomy can be issued if the disorder is severe enough.

complete blood cell (CBC) counts, peripheral blood smears, and iron studies (e.g., serum iron, total iron-binding capacity [TIBC], ferritin, saturation percentage) to confirm iron deficiency, with or without hypochromic microcytic anemia.

Esophageal webs and rings can be treated with endoscopic dilation.

Once a patient complains of dysphagia they should have an "upper endoscopy" (EGD). Commonly patients are found to have esophagitis and may have an esophageal stricture. Biopsies are usually done to look for evidence of esophagitis even if the EGD is normal. Usually no further testing is required if the diagnosis is established on EGD. Repeat endoscopy may be needed for follow up.

If there is a suspicion of a proximal lesion such as:

- history of surgery for laryngeal or esophageal cancer

- history of radiation or irritating injury

- achalasia

- Zenker's diverticulum

a "barium swallow" may be performed before endoscopy to help identify abnormalities that might increase the risk of perforation at the time of endoscopy.

If achalasia suspected an upper endoscopy is required to exclude a malignancy as a cause of the findings on barium swallow. Manometry is performed next to confirm. A normal endoscopy should be followed by manometry, and if manometry is also normal, the diagnosis is functional dysphagia.

The patient is generally sent for a GI, pulmonary, or ENT, depending on the suspected underlying cause. Consultations with a speech therapist and registered dietitian nutritionist (RDN) are also needed, as many patients may need dietary modifications such as thickened fluids.

The diagnosis of Boerhaave's syndrome is suggested on the plain chest radiography and confirmed by chest CT scan. The initial plain chest radiograph is almost always abnormal in patients with Boerhaave's syndrome and usually reveals mediastinal or free peritoneal air as the initial radiologic manifestation. With cervical esophageal perforations, plain films of the neck show air in the soft tissues of the prevertebral space.

Hours to days later, pleural effusion(s) with or without pneumothorax, widened mediastinum, and subcutaneous emphysema are typically seen. CT scan may show esophageal wall edema and thickening, extraesophageal air, periesophageal fluid with or without gas bubbles, mediastinal widening, and air and fluid in the pleural spaces, retroperitoneum or lesser sac.

The diagnosis of esophageal perforation could also be confirmed by water-soluble contrast esophagram (Gastrografin), which reveals the location and extent of extravasation of contrast material. Although barium is superior in demonstrating small perforations, the spillage of barium sulfate into the mediastinal and pleural cavities can cause an inflammatory response and subsequent fibrosis and is therefore not used as the primary diagnostic study. If, however, the water-soluble study is negative, a barium study should be performed for better definition.

Endoscopy has no role in the diagnosis of spontaneous esophageal perforation. Both the endoscope and insufflation of air can extend the perforation and introduce air into the mediastinum.

Patients may also have a pleural effusion high in amylase (from saliva), low pH, and may contain particles of food.

A gastroenterologist is a medical professional that can diagnose esophagitis. To diagnose esophagitis, the doctor will interview the patient regarding their signs and symptoms. If the doctor suspects esophagitis, tests can be ordered. Esophagitis can be diagnosed by an upper endoscopy, biopsy, upper GI series (or barium swallow), and laboratory tests.

An upper endoscopy is a procedure to look at the esophagus by using an endoscope. While looking at the esophagus, the doctor is able to take a small biopsy. The biopsy can be used to confirm inflammation of the esophagus.

An upper GI series uses a barium contrast, fluoroscopy, and an X-ray. During a barium X-ray, a solution with barium or pill is taken before getting an X-ray. The barium makes the organs more visible and can detect if there is any narrowing, inflammation, or other abnormalities that can be causing the disease. The upper GI series can be used to find the cause of GI symptoms. An esophagram is if only the throat and esophagus are looked at.

Laboratory tests can be done on biopsies removed from the esophagus and can help determine the cause of the esophagitis. Laboratory tests can help diagnose a fungal, viral, or bacterial infection. Scanning for white blood cells can help diagnose eosinophil esophagitis.

Some lifestyle indicators for this disease include: stress, unhealthy eating, smoking, drinking, family history, allergies, and an immunodeficiency. It is important for the doctor to review the patient's medical history before diagnosing with esophagitis. Specific subtypes and other causes should be taken into account when making the final diagnosis.

Diagnosis of gastric varices is often made at the time of upper endoscopy.

The Sarin classification of gastric varices identifies four different anatomical types of gastric varices, which differ in terms of treatment modalities.

A Schatzki ring is usually diagnosed by esophagogastroduodenoscopy or barium swallow. Endoscopy usually shows a ring within the lumen of the esophagus which can be of variable size (see picture). The ring is usually located a few centimetres above the gastro-esophageal junction, where the esophagus joins the stomach. Schatzki rings can often resemble a related entity called an esophageal web. Esophageal webs also contain extra mucosal tissue, but do not completely encircle the esophagus.

Endoscopies and barium swallows done for other reasons often reveal unsuspected Schatzki rings, meaning that many Schatzki rings are asymptomatic.

Two varieties of Schatzki rings have been described. The original description by Schatzki and Gary was of a ring of fibrous tissue seen on autopsy; this is the less common type of Schatzki ring. More commonly, the ring consists of the same mucosal tissue that lines the entire esophagus. Although many hypotheses have been proffered, the cause of Schatzki rings remains uncertain; both congenital and acquired factors may be involved.

About 6 to 14 percent of patients who receive a routine barium swallow test of the esophagus are found to have a Schatzki ring.

Endoscopy, the looking down into the stomach with a fibre-optic scope, is not routinely needed if the case is typical and responds to treatment. It is recommended when people either do not respond well to treatment or have alarm symptoms, including dysphagia, anemia, blood in the stool (detected chemically), wheezing, weight loss, or voice changes. Some physicians advocate either once-in-a-lifetime or 5- to 10-yearly endoscopy for people with longstanding GERD, to evaluate the possible presence of dysplasia or Barrett's esophagus.

Biopsies performed during gastroscopy may show:

- Edema and basal hyperplasia (nonspecific inflammatory changes)

- Lymphocytic inflammation (nonspecific)

- Neutrophilic inflammation (usually due to reflux or "Helicobacter" gastritis)

- Eosinophilic inflammation (usually due to reflux): The presence of intraepithelial eosinophils may suggest a diagnosis of eosinophilic esophagitis (EE) if eosinophils are present in high enough numbers. Less than 20 eosinophils per high-power microscopic field in the distal esophagus, in the presence of other histologic features of GERD, is more consistent with GERD than EE.

- Goblet cell intestinal metaplasia or Barrett's esophagus

- Elongation of the papillae

- Thinning of the squamous cell layer

- Dysplasia

- Carcinoma

Reflux changes may not be erosive in nature, leading to "nonerosive reflux disease".

The diagnosis of GERD is usually made when typical symptoms are present. Reflux can be present in people without symptoms and the diagnosis requires both symptoms or complications and reflux of stomach content.

Other investigations may include esophagogastroduodenoscopy (EGD). Barium swallow X-rays should not be used for diagnosis. Esophageal manometry is not recommended for use in diagnosis, being recommended only prior to surgery. Ambulatory esophageal pH monitoring may be useful in those who do not improve after PPIs and is not needed in those in whom Barrett's esophagus is seen. Investigation for H. pylori is not usually needed.

The current gold standard for diagnosis of GERD is esophageal pH monitoring. It is the most objective test to diagnose the reflux disease and allows monitoring GERD patients in their response to medical or surgical treatment. One practice for diagnosis of GERD is a short-term treatment with proton-pump inhibitors, with improvement in symptoms suggesting a positive diagnosis. Short-term treatment with proton-pump inhibitors may help predict abnormal 24-hr pH monitoring results among patients with symptoms suggestive of GERD.

With the exception of a few case reports describing survival without surgery, the mortality of untreated Boerhaave syndrome is nearly 100%. Its treatment includes immediate antibiotic therapy to prevent mediastinitis and sepsis, surgical repair of the perforation, and if there is significant fluid loss it should be replaced with IV fluid therapy since oral rehydration is not possible. Even with early surgical intervention (within 24 hours) the risk of death is 25%.

After the initial diagnosis of Barrett's esophagus is rendered, affected persons undergo annual surveillance to detect changes that indicate higher risk to progression to cancer: development of epithelial dysplasia (or "intraepithelial neoplasia").

Considerable variability is seen in assessment for dysplasia among pathologists. Recently, gastroenterology and GI pathology societies have recommended that any diagnosis of high-grade dysplasia in Barrett be confirmed by at least two fellowship-trained GI pathologists prior to definitive treatment for patients. For more accuracy and reproductibility, it is also recommended to follow international classification system as the "Vienna classification" of gastrointestinal epithelial neoplasia (2000).

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.

The presence of goblet cells, called intestinal metaplasia, is necessary to make a diagnosis of Barrett's esophagus. This frequently occurs in the presence of other metaplastic columnar cells, but only the presence of goblet cells is diagnostic. The metaplasia is grossly visible through a gastroscope, but biopsy specimens must be examined under a microscope to determine whether cells are gastric or colonic in nature. Colonic metaplasia is usually identified by finding goblet cells in the epithelium and is necessary for the true diagnosis.

Many histologic mimics of Barrett's esophagus are known (i.e. goblet cells occurring in the transitional epithelium of normal esophageal submucosal gland ducts, "pseudogoblet cells" in which abundant foveolar [gastric] type mucin simulates the acid mucin true goblet cells). Assessment of relationship to submucosal glands and transitional-type epithelium with examination of multiple levels through the tissue may allow the pathologist to reliably distinguish between goblet cells of submucosal gland ducts and true Barrett's esophagus (specialized columnar metaplasia). Use of the histochemical stain Alcian blue pH 2.5 is also frequently used to distinguish true intestinal-type mucins from their histologic mimics. Recently, immunohistochemical analysis with antibodies to CDX-2 (specific for mid and hindgut intestinal derivation) has also been used to identify true intestinal-type metaplastic cells. The protein AGR2 is elevated in Barrett's esophagus and can be used as a biomarker for distinguishing Barrett epithelium from normal esophageal epithelium.

The presence of intestinal metaplasia in Barrett's esophagus represents a marker for the progression of metaplasia towards dysplasia and eventually adenocarcinoma. This factor combined with two different immunohistochemical expression of p53, Her2 and p16 leads to two different genetic pathways that likely progress to dysplasia in Barrett's esophagus.

It can be diagnosed with an X-ray while the patient swallows barium (called a barium study of the esophagus), by a computerized tomography scan, a biopsy, or by an endoscopy.

Predicts mortality risk in pancreatitis with fewer variables than Ranson's criteria. Data should be taken from the first 24 hours of the patient's evaluation.

- BUN >25 mg/dL (8.9 mmol/L)

- Abnormal mental status with a Glasgow coma score <15

- Evidence of SIRS (systemic inflammatory response syndrome)

- Patient age >60 years old

- Imaging study reveals pleural effusion

Patients with a score of zero had a mortality of less than one percent, whereas patients with a score of five had a mortality rate of 22 percent. In the validation cohort, the BISAP score had similar test performance characteristics for predicting mortality as the APACHE II score. As is a problem with many of the other scoring systems, the BISAP has not been validated for predicting outcomes such as length of hospital stay, need for ICU care, or need for intervention.

In predicting the prognosis, there are several scoring indices that have been used as predictors of survival. Two such scoring systems are the Ranson criteria and APACHE II (Acute Physiology and Chronic Health Evaluation) indices. Most, but not all studies report that the Apache score may be more accurate. In the negative study of the APACHE-II, the APACHE-II 24-hour score was used rather than the 48-hour score. In addition, all patients in the study received an ultrasound twice which may have influenced allocation of co-interventions. Regardless, only the APACHE-II can be fully calculated upon admission. As the APACHE-II is more cumbersome to calculate, presumably patients whose only laboratory abnormality is an elevated lipase or amylase do not need assessment with the APACHE-II; however, this approach is not studied. The APACHE-II score can be calculated at www.sfar.org.

Practice guidelines state:

Several radiographic findings are suggestive of DES, such as a "rosary bead esophagus" or "corkscrew" appearance on barium swallow x-ray, although these findings are not unique to DES.

The diagnosis of nutcracker esophagus is typically made with an esophageal motility study, which shows characteristic features of the disorder. Esophageal motility studies involve pressure measurements of the esophagus after a patient takes a wet (fluid-containing) or dry (solid-containing) swallow. Measurements are usually taken at various points in the esophagus.

Nutcracker esophagus is characterized by a number of criteria described in the literature. The most commonly used criteria are the Castell criteria, named after American gastroenterologist D.O. Castell. The Castell criteria include one major criterion: a mean peristaltic amplitude in the distal esophagus of more than 180 mm Hg. The minor criterion is the presence of repetitive contractions (meaning two or more) that are greater than six seconds in duration. Castell also noted that the lower esophageal sphincter relaxes normally in nutcracker esophagus, but has an elevated pressure of greater than 40 mm Hg at baseline.

Three other criteria for definition of the nutcracker esophagus have been defined. The Gothenburg criterion consists of the presence of peristaltic contractions, with an amplitude of 180 mm Hg at any place in the esophagus. The Richter criterion involves the presence of peristaltic contractions with an amplitude of greater than 180 mmHg from an average of measurements taken 3 and 8 cm above the lower esophageal sphincter. It has been incorporated into a number of clinical guidelines for the evaluation of dysphagia. The Achem criteria are more stringent, and are an extension of the study of 93 patients used by Richter and Castell in the development of their criteria, and require amplitudes of greater than 199 mm Hg at 3 cm above the lower esophageal sphincter (LES), greater than 172 mm Hg at 8 cm above the LES, or greater than 102 mm Hg at 13 cm above the LES.

In patients who have dysphagia, testing may first be done to exclude an anatomical cause of dysphagia, such as distortion of the anatomy of the esophagus. This usually includes visualization of the esophagus with an endoscope, and can also include barium swallow X-rays of the esophagus. Endoscopy is typically normal in patients with nutcracker esophagus; however, abnormalities associated with gastroesophageal reflux disease, or GERD, which associates with nutcracker esophagus, may be seen. Barium swallow in nutcracker esophagus is also typically normal, but may provide a definitive diagnosis if contrast is given in tablet or granule form. Studies on endoscopic ultrasound show slight trends toward thickening of the muscularis propria of the esophagus in nutcracker esophagus, but this is not useful in making the diagnosis.

If it is caused by esophagitis, in turn caused by an underlying infection, it is commonly treated by treating the infection (typically with antibiotics). In order to open the stricture, a surgeon can insert a bougie – a weighted tube used to dilate the constricted areas in the esophagus. It can sometimes be treated with other medications. For example, an H2 antagonist (e.g. ranitidine) or a proton-pump inhibitor (e.g. omeprazole) can treat underlying acid reflux disease.