In an emergency room setting, someone with food bolus obstruction may be observed for a period to see if the food bolus passes spontaneously. This may be encouraged by administering fizzy drinks that release gas, which may dislodge the food.

Glucagon relaxes the lower esophageal sphincter and may be used in those with esophageal food bolus obstruction. There is little evidence for glucagon's effectiveness in this condition, and glucagon may induce nausea and vomiting, but considering the safety of glucagon this is still considered an acceptable option as long it does not lead to delays in arranging other treatments. Other medications (hyoscine butylbromide, benzodiazepines and opioids) have been studied but the evidence is limited.

Historical treatment of food bolus obstruction included administration of proteolytic enzymes (such as meat tenderizers) with the purpose of degrading the meat that was blocked; however, it is possible that these methods may increase the risk of perforation of the esophagus. Other modalities rarely used now include removal of boluses using catheters, and the use of large-bore tubes inserted into the esophagus to forcefully lavage it.

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.

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 most confirmatory investigation is endoscopy of upper gastrointestinal tract.

Laboratory

- Individuals with gastric outlet obstruction are often hypochloremic, hypokalemic, and alkalotic due to loss of hydrogen chloride and potassium. High urea and creatinine levels may also be observed if the patient is dehydrated.

Abdominal X-ray

- A gastric fluid level may be seen which would support the diagnosis.

Barium meal and follow through

- May show an enlarged stomach and pyloroduodenal stenosis.

Gastroscopy

- May help with cause and can be used therapeutically.

The standard treatment of food bolus obstruction is the use of endoscopy or fibre-optic cameras inserted by mouth into the esophagus. Endoscopes can be used to diagnose the cause of the food bolus obstruction, as well as to remove the obstruction. Traditional endoscopic techniques involved the use of an overtube, a plastic tube inserted into the esophagus prior to the removal of the food bolus, in order to reduce the risk of aspiration into the lungs at the time of endoscopy. However, the "push technique", which involves insufflating air into the esophagus, and gently pushing the bolus toward the stomach instead, has emerged as a common and safe way of removing the obstruction.

Other tools may be used to remove food boluses. The Roth Net® is a mesh net that can be inserted through the endoscope, and opened and closed from the outside; it can be used to retrieve pieces of obstructed food. Snares, which are normally used to remove polyps can be used to macerate the food causing the obstruction. Dormia baskets, which are metal baskets used to remove stones from the common bile duct in a procedure known as endoscopic retrograde cholangiopancreatography, can be opened and closed from the outside in a similar manner to macerate food and facilitate removal. Forceps used for biopsies can also be employed in a similar manner.

The differential diagnosis of gastric outlet obstruction may include: early gastric carcinoma hiatal hernia, gastroesophageal reflux, adrenal insufficiency, and inborn errors of metabolism.

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 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.

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.

If a horse is suspected of choke, a veterinarian will often pass a stomach tube down the animal's esophagus to determine if there is a blockage. Failure to access the stomach with the tube indicates a complete obstruction; difficulty passing the tube may represent a stenosis, or narrowing; or a partial obstruction. Radiography and endoscopy are also used in refractory cases.

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.

The treatment for bile reflux is the same as the treatment for acidic reflux. In general, everything that can

reduce acidic reflux can reduce bile reflux. Examples include lifestyle modification, weight reduction, and the avoidance of eating immediately before sleep or being in the supine position immediately after meals. In addition, smoking has been found to be a factor in the development of acidic reflux. Thus, all of these factors should be applied to bile reflux as well.

Likewise, drugs that reduce the secretion of gastric acid (e.g., proton pump inhibitors)

or that reduce gastric contents or volume can be used to treat acidic bile reflux. Because prokinetic drugs increase the motility of the stomach and accelerate gastric emptying, they can also reduce bile reflux. Other drugs that reduce the relaxations of the lower esophageal sphincter, such as baclofen, have also proven to reduce bile reflux, particularly in patients who are refractory to (medically unresponsive to) proton pump inhibitor therapy.

Medications used in managing biliary reflux include bile acid sequestrants, particularly cholestyramine, which disrupt the circulation of bile in the digestive tract and sequester bile that would otherwise cause symptoms when refluxed; and prokinetic agents, to move material from the stomach to the small bowel more rapidly and prevent reflux.

Biliary reflux may also be treated surgically, if medications are ineffective or if precancerous tissue is present in the esophagus.

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.

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.

Attempts must be made to determine whether there is a secondary cause amenable to treatment.

Primary (idiopathic) intestinal pseudo-obstruction is diagnosed based on motility studies, x-rays and gastric emptying studies.

The patient swallows a barium solution, with continuous fluoroscopy (X-ray recording) to observe the flow of the fluid through the esophagus. Normal peristaltic movement of the esophagus is not seen. There is acute tapering at the lower esophageal sphincter and narrowing at the gastro-esophageal junction, producing a "bird's beak" or "rat's tail" appearance. The esophagus above the narrowing is often dilated (enlarged) to varying degrees as the esophagus is gradually stretched over time. An air-fluid margin is often seen over the barium column due to the lack of peristalsis. A five-minutes timed barium swallow can provide a useful benchmark to measure the effectiveness of treatment.

Because of its sensitivity, manometry (esophageal motility study) is considered the key test for establishing the diagnosis. A catheter (thin tube) is inserted through the nose, and the patient is instructed to swallow several times. The probe measures muscle contractions in different parts of the esophagus during the act of swallowing. Manometry reveals failure of the LES to relax with swallowing and lack of functional peristalsis in the smooth muscle esophagus.

Characteristic manometric findings are:

- Lower esophageal sphincter (LES) fails to relax upon wet swallow (<75% relaxation)

- Pressure of LES 100 is considered achalasia, > 200 is nutcracker achalasia.

- Aperistalsis in esophageal body

- Relative increase in intra-esophageal pressure as compared with intra-gastric pressure

Choking horses should be deprived of food and drink pending veterinary attention, so as not to increase the obstructive load within the esophagus. The veterinarian will often sedate the horse and administer spasmolytics, such as butylscopolamine, to help the esophagus to relax. Once the muscles of the esophagus no longer force the food down the throat (active peristalsis), it may slip down on its own accord. If spasmolytics do not solve the problem, the veterinarian will usually pass a stomach tube through one of the nostrils and direct it into the esophagus until the material is reached, at which point "gentle" pressure is applied to manually push the material down. Gentle warm water lavage (water sent through the stomach tube, to soften the food material) may be required to help the obstructing matter pass more easily, but caution should be exercised to prevent further aspiration of fluid into the trachea.

Refractory cases are sometimes anesthetised, with an orotracheal tube placed to prevent further aspiration and to allow for more vigorous lavage. Disruption of the impacted material can sometimes be achieved via endoscopy. If these methods still do not lead to results, the horse may require surgery to remove the material.

Some workers have advocated the use of oxytocin in choke, on the grounds that it decreases the esophageal muscular tone. However, this technique is not suitable in pregnant mares, as it may lead to abortion.

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.

Treatments for esophagitis include medications to block acid production, to manage pain, and to reduce inflammation. Other treatments include antibiotics and intravenous nutrition.

To treat reflux esophagitis, over the counter antacids, medications that reduce acid production (H-2 receptor blockers), and proton pump inhibitors are recommended to help block acid production and to let the esophagus heal. Some prescription medications to treat reflux esophagitis include higher dose H-2 receptor blockers, proton pump inhibitors, and prokinetics, which help with the emptying of the stomach.

To treat eosinophilic esophagitis, avoiding any allergens that may be stimulating the eosinophils is recommended. As for medications, proton pump inhibitors and steroids can be prescribed. Steroids that are used to treat asthma can be swallowed to treat eosinophil esophagitis due to nonfood allergens. The removal of food allergens from the diet is included to help treat eosinophilic esophagitis.

For infectious esophagitis, a medicine is prescribed based on what type of infection is causing the esophagitis. These medicines are prescribed to treat bacterial, fungal, viral, and/or parasitic infections.

An endoscopy can be used to remove ill fragments. Surgery can be done to remove the damaged part of the esophagus. For reflux esophagitis, a fundooplication can be done to help strengthen the lower esophageal sphincter from allowing backflow of the stomach into the esophagus. As for patients that have a narrowing esophagus, a gastroenterologist can perform a procedure to dilate the esophagus.

Some home remedies and lifestyle changes to help with esophagitis include losing weight, stop smoking, lowering stress, avoid sleeping/lying down after eating, raise your head while laying down, taking medicines correctly, avoiding certain medications, and avoiding foods that cause the reflux that might be causing the esophagitis.

If the disease remains untreated, it can cause scarring and discomfort in the esophagus. If the irritation is not allowed to heal, esophagitis can result in esophageal ulcers. Esophagitis can develop into Barrett's esophagus and can increase the risk of esophageal cancer.

The prognosis for a person with esophagitis depends on the underlying causes and conditions. If a patient has a more serious underlying cause such as a digestive system or immune system issue, it may be more difficult to treat. Normally, the prognosis would be good with no serious illnesses. If there are more causes than one, the prognosis could move to fair.

Diagnosis is achieved mainly by plain and contrasted radiographical and ultrasound imaging. Colonic marker transit studies are useful to distinguish colonic inertia from functional outlet obstruction causes. In this test, the patient swallows a water-soluble bolus of radio-opaque contrast and films are obtained 1, 3 and 5 days later. Patients with colonic inertia show the marker spread throughout the large intestines, while patients with outlet obstruction exhibit slow accumulations of markers in some places. A colonoscopy can also be used to rule out mechanical obstructive causes. Anorectal manometry may help to differentiate acquired from congenital forms. Rectal biopsy is recommended to make a final diagnosis of Hirschsprung disease.

The simple barium swallow will normally reveal the diverticulum. It may also be found with upper GI endoscopy, or CT with oral contrast.

LPR presents with non-specific symptoms and signs that make differential diagnosis difficult to achieve. Furthermore, symptoms of the disorder overlap greatly with symptoms of other disorders. Therefore, LPR is under-diagnosed and under-treated. As there are multiple potential etiologies for the respiratory and laryngeal symptoms of LPR, diagnosing LPR based on symptoms alone is unreliable. Laryngoscopic findings such as erythema, edema, laryngeal granulomas, and interarytenoid hypertrophy have been used to establish the diagnosis; however, these findings are nonspecific and have been described in the majority of asymptomatic subjects undergoing laryngoscopy. Response to acid-suppression therapy has been suggested as a diagnostic tool for confirming diagnosis of LPR, but studies have shown that the response to empirical trials of such therapy (as with proton-pump inhibitors) in these patients is often disappointing. Several studies have emphasized the importance of measuring proximal esophageal, or ideally pharyngeal acid exposure, in patients with clinical symptoms of LPR to document reflux as the cause of the symptoms.

Additionally, several potential biomarkers of LPR have been investigated. These include inflammatory cytokines, carbonic anyhydrase, E-cadherin and mucins; however, their direct implications in LPR are still being established. The presence of pepsin, an enzyme produced in the stomach, in the hypopharynx has also become an increasingly researched biomarker for LPR. Research suggests that the stomach enzyme pepsin plays a crucial role in the complex mechanism behind LPR.

Before a diagnosis can be made, a physician will need to record the patient’s medical history and ask for details about the presenting symptoms. Questionnaires such as the Reflux Symptom Index (RSI), Quality-of-Life Index (QLI) for LPR, Glottal Closure/Function Index (GCI) and Voice Handicap Index (VHI) can be administered to gain information about the patient's medical history as well as their symptomatology. A physical examination will then need to be performed with particular concentration around the head and neck. A scope with a specialized camera lens made of fiber optic strands is gently fed down the throat and feeds back images to a monitor. This provides a clear view of the throat and larynx. Signs of LPR include redness, swelling, and obvious irritation. Other, more invasive tests, such as fibre-optic transnasal laryngoscopy, 24-hour ambulatory dual probe pHmetry, pharyngeal pHmetry, transnasal esophagoscopy (TNE) and biopsy may be used. A noninvasive test for diagnosis of LPR is the collection of refluxate where the refluxed material is collected and analyzed. Another noninvasive diagnostic test that can be used is an empirical trial of proton-pump inhibitor therapy; however, this test is mostly successful in diagnosing GERD.

There is no agreed-upon assessment technique to identify LPR in children. Of the debated diagnostic tools, multichannel intraluminal impedance with pH monitoring (MII-pH) is used as it recognizes both acid and non-acid reflux. A more common technique that is used is 24-hour dual probe pH monitoring. Both of these tools are expensive and are therefore not widely used.

Most damage to the pyloric valve occurs as a complication of gastric surgery. Other causes of biliary reflux may be:

- Peptic ulcer

- Gallbladder surgery (cholecystectomy)

A significant fraction of cases are idiopathic, with no identified specific etiology.

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.