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.

Odynophagia may have environmental or behavioral causes, such as:

- Very hot or cold food and drinks

- Taking certain medications

- Using drugs, tobacco, or alcohol

- Trauma or injury to the mouth, throat, or tongue

The current first-line treatment is fluconazole, 200 mg. on the first day, followed by daily dosing of 100 mg. for at least 21 days total. Treatment should continue for 14 days after relief of symptoms.

Other therapy options include:

- nystatin is not an effective treatment for esophageal candidiasis. It can be used as (swish, do not swallow) treatment for oral candidiasis that occurs with the use of asthma pumps.

- other oral triazoles, such as itraconazole

- caspofungin, used in refractory or systemic cases

- amphotericin, used in refractory or systemic cases

Odynophagia (; from "-" "pain" and "" "to eat") is pain when swallowing. The pain may be felt in the mouth or throat and can occur with or without difficulty swallowing. The pain may be described as an ache, burning sensation, or occasionally a stabbing pain that radiates to the back. Odynophagia often results in inadvertent weight loss.

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.

Many people with Barrett's esophagus do not have dysplasia. Medical societies recommend that if a patient has Barrett's esophagus, and if the past two endoscopy and biopsy examinations have confirmed the absence of dysplasia, then the patient should not have another endoscopy within three years.

Endoscopic surveillance of people with Barrett's esophagus is often recommended, although little direct evidence supports this practice. Treatment options for high-grade dysplasia include surgical removal of the esophagus (esophagectomy) or endoscopic treatments such as endoscopic mucosal resection or ablation (destruction).

The risk of malignancy is highest in the U.S. in Caucasian men over fifty years of age with more than five years of symptoms. Current recommendations include routine endoscopy and biopsy (looking for dysplastic changes). Although in the past physicians have taken a watchful waiting approach, newly published research supports consideration of intervention for Barrett's esophagus. Balloon-based radiofrequency ablation, invented by Ganz, Stern, and Zelickson in 1999, is a new treatment modality for the treatment of Barrett's esophagus and dysplasia, and has been the subject of numerous published clinical trials. The findings demonstrate radiofrequency ablation has an efficacy of 90% or greater with respect to complete clearance of Barrett's esophagus and dysplasia with durability up to five years and a favorable safety profile.

Proton pump inhibitor drugs have not been proven to prevent esophageal cancer. Laser treatment is used in severe dysplasia, while overt malignancy may require surgery, radiation therapy, or systemic chemotherapy. Additionally, a recent five-year random-controlled trial has shown that photodynamic therapy using photofrin is statistically more effective in eliminating dysplastic growth areas than sole use of a proton pump inhibitor. There is presently no reliable way to determine which patients with Barrett esophagus will go on to develop esophageal cancer, although a recent study found the detection of three different genetic abnormalities was associated with as much as a 79% chance of developing cancer in six years.

Endoscopic mucosal resection has also been evaluated as a management technique. Additionally an operation known as a Nissen fundoplication can reduce the reflux of acid from the stomach into the esophagus.

In a variety of studies, nonsteroidal anti-inflammatory drugs (NSAIDS), like aspirin, have shown evidence of preventing esophageal cancer in people with Barrett's esophagus. However, none of these studies have been randomized, placebo-controlled trials, which are considered the gold standard for evaluating a medical intervention. In addition, the best dose of NSAIDs for cancer prevention is not yet known.

Treatment is by removing the pus, antibiotics, sufficient fluids, and pain medication. Steroids may also be useful. Admission to hospital is generally not needed.

The infection is frequently penicillin resistant. There are a number of antibiotics options including amoxicillin/clavulanate, clindamycin, or metronidazole in combination with benzylpenicillin (penicillin G) or penicillin V. Piperacillin/tazobactam may also be used.

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%.

Patients with esophageal candidiasis present with odynophagia, or painful swallowing. Longstanding esophageal candidiasis can result in weight loss. There is often concomittant thrush.

Some patients present with esophageal candidiasis as a first presentation of systemic candidiasis.

Barrett's esophagus refers to an abnormal change (metaplasia) in the cells of the lower portion of the esophagus. It is characterized by the replacement of the normal stratified squamous epithelium lining of the esophagus by simple columnar epithelium with goblet cells (which are usually found lower in the gastrointestinal tract). The medical significance of Barrett's esophagus is its strong association (0.1 per 1 cm Prague C>M> total segment length per patient-year) with esophageal adenocarcinoma, a very often deadly cancer, because of which it is considered to be a premalignant condition.

The main cause of Barrett's esophagus is thought to be an adaptation to chronic acid exposure from reflux esophagitis. The incidence of esophageal adenocarcinoma has increased substantially in the Western world in recent years. The condition is found in 5–15% of patients who seek medical care for heartburn (gastroesophageal reflux disease), although a large subgroup of patients with Barrett's esophagus do not have symptoms. Diagnosis requires endoscopy (more specifically, esophagogastroduodenoscopy, a procedure in which a fibreoptic cable is inserted through the mouth to examine the esophagus, stomach, and duodenum) and biopsy. The cells of Barrett's esophagus, after biopsy, are classified into four general categories: nondysplastic, low-grade dysplasia, high-grade dysplasia, and frank carcinoma. High-grade dysplasia and early stages of adenocarcinoma can be treated by endoscopic resection and new endoscopic therapies such as radiofrequency ablation, whereas advanced stages (submucosal) are generally advised to undergo surgical treatment. Nondysplastic and low-grade patients are generally advised to undergo annual observation with endoscopy, with radiofrequency ablation as a therapeutic option. In high-grade dysplasia, the risk of developing cancer might be at 10% per patient-year or greater.

The condition is named after the Australian-born British thoracic surgeon Norman Barrett (1903–1979), who described it in 1950.

Those with the eating disorder bulimia are more likely to develop Barrett’s esophagus because bulimia can cause severe acid reflux, and because purging also floods the esophagus with acid.

Esophageal rupture in Boerhaave syndrome is thought to be the result of a sudden rise in internal esophageal pressure produced during vomiting, as a result of neuromuscular incoordination causing failure of the cricopharyngeus muscle (a sphincter within the esophagus) to relax. As the intra-oesophageal pressure increases, the bolus within the oesophagus has nowhere to go superiorly (as the cricopharyngeus fails to relax) which causes the oesophagus to rupture. (this makes little sense and should be justified if true: the lesion is down, the cricopharyngeus is up). The syndrome is commonly associated with the consumption of excessive food and/or alcohol as well as eating disorders such as bulimia.

The most common anatomical location of the tear in Boerhaave syndrome is at left posterolateral wall of the lower third of the esophagus, 2–3 cm before the stomach.

Currently, the most common cause of esophageal perforation is iatrogenic. However, iatrogenic perforations, while still constituting a serious medical condition, are easier to treat and less prone to complications, particularly mediastinitis and sepsis. This is because they usually do not involve contamination of the mediastinum with gastric contents.

Infection can occur from:

- Pharynx: acute and chronic infection of tonsil and adenoids

- Teeth: dental infection occurs from lower last molar tooth

- Ear: bezold abscess and petrositis

- Other space: infection of parotid retropharyngeal space

- External trauma: penetrating injuries of neck, injection of local anaesthetic

Fever, sore throat, odynophagia (painful swallowing), swelling in neck.

Treatment options vary from very conservative to aggressive. Conservative options include rest, observation, pain control, diet changes, use of a nasopharyngeal tube or oropharyngeal tube, and antibiotic therapy. More aggressive options include surgical repair of the hyoid bone and/or tracheotomy. Surgical treatment was used in 10.9% of cases in a 2012 meta-analysis.

The hyoid bone fracture is a very rare fracture of the hyoid bone, accounting for 0.002% of all fractures in humans. It is commonly associated with strangulation and rarely occurs in isolation. The fracture may be associated with gunshot injury, car accidents or induced vomiting. In 50% of strangulations and 27% of hangings, hyoid fractures occur.