In emergency situations, care is directed at stopping blood loss, maintaining plasma volume, correcting disorders in coagulation induced by cirrhosis, and appropriate use of antibiotics such as quinolones or ceftriaxone. Blood volume resuscitation should be done promptly and with caution. The goal should be hemodynamic stability and hemoglobin of over 8 g/dl. Resuscitation of all lost blood leads to increase in portal pressure leading to more bleeding. Volume resuscitation can also worsen ascites and increase portal pressure. (AASLD guidelines)

Therapeutic endoscopy is considered the mainstay of urgent treatment. The two main therapeutic approaches are variceal ligation or banding and sclerotherapy.

In cases of refractory bleeding, balloon tamponade with a Sengstaken-Blakemore tube may be necessary, usually as a bridge to further endoscopy or treatment of the underlying cause of bleeding (usually portal hypertension). Esophageal devascularization operations such as the Sugiura procedure can also be used to stop complicated variceal bleeding. Methods of treating the portal hypertension include: transjugular intrahepatic portosystemic shunt, or a distal splenorenal shunt procedure or a liver transplantation.

Nutritional supplementation is not necessary if the patient is not eating for four days or less.

Terlipressin and octreotide for 1 to 5 days have also been used.

In ideal circumstances, patients with known varices should receive treatment to reduce their risk of bleeding. The non-selective β-blockers (e.g., propranolol, timolol or nadolol) and nitrates (e.g., isosorbide mononitrate (IMN) have been evaluated for secondary prophylaxis. Non-selective β-blockers (but not cardioselective β-blockers like atenolol) are preferred because they decrease both cardiac output by β blockade and splanchnic blood flow by blocking vasodilating β receptors at splanchnic vasculature. The effectiveness of this treatment has been shown by a number of different studies.

However, non-selective β-blockers do not prevent the "formation" of esophageal varices.

When medical contraindications to beta-blockers exist, such as significant reactive airway disease, then treatment with prophylactic endoscopic variceal ligation is often performed.

Both before and after treatment, achalasia patients may need to eat slowly, chew very well, drink plenty of water with meals, and avoid eating near bedtime. Raising the head off the bed or sleeping with a wedge pillow promotes emptying of the esophagus by gravity. After surgery or pneumatic dilatation, proton pump inhibitors are required to prevent reflux damage by inhibiting gastric acid secretion, and foods that can aggravate reflux, including ketchup, citrus, chocolate, alcohol, and caffeine, may need to be avoided.

Drugs that reduce LES pressure are useful. These include calcium channel blockers such as nifedipine and nitrates such as isosorbide dinitrate and nitroglycerin. However, many patients experience unpleasant side effects such as headache and swollen feet, and these drugs often stop helping after several months.

Botulinum toxin (Botox) may be injected into the lower esophageal sphincter to paralyze the muscles holding it shut. As in the case of cosmetic Botox, the effect is only temporary and lasts about 6 months. Botox injections cause scarring in the sphincter which may increase the difficulty of later Heller myotomy. This therapy is recommended only for patients who cannot risk surgery, such as elderly people in poor health. Pneumatic dilatation has a better long term effectiveness than botox.

In the great majority of cases, sufferers experience no life-altering discomfort, and no treatment is required. If there is pain or discomfort, 3 or 4 sips of room temperature water will usually relieve the pain. Symptomatic patients should elevate the head of their beds and avoid lying down directly after meals. If the condition has been brought on by stress, stress reduction techniques may be prescribed, or if overweight, weight loss may be indicated. Antisecretory drugs like proton pump inhibitors and H receptor blockers can be used to reduce acid secretion. Medications that reduce the lower esophageal sphincter (LES) pressure should be avoided.

However, in some unusual instances, as when the hiatal hernia is unusually large, or is of the paraesophageal type, it may cause esophageal stricture or severe discomfort. About 5% of hiatus hernias are paraesophageal. If symptoms from such a hernia are severe for example if chronic acid reflux threatens to severely injure the esophagus or is causing Barrett's esophagus, surgery is sometimes recommended. However surgery has its own risks including death and disability, so that even for large or paraesophageal hernias, watchful waiting may on balance be safer and cause fewer problems than surgery. Complications from surgical procedures to correct a hiatus hernia may include gas bloat syndrome, dysphagia (trouble swallowing), dumping syndrome, excessive scarring, and rarely, achalasia. Surgical procedures sometimes fail over time, requiring a second surgery to make repairs.

One surgical procedure used is called Nissen fundoplication. In fundoplication, the gastric fundus (upper part) of the stomach is wrapped, or plicated, around the inferior part of the esophagus, preventing herniation of the stomach through the hiatus in the diaphragm and the reflux of gastric acid. The procedure is now commonly performed laparoscopically. With proper patient selection, laparoscopic fundoplication recent studies have indicated relatively low complication rates, quick recovery, and relatively good long term results.

Asymptomatic Schatzki rings seldom worsen over time, and need no treatment.

Symptomatic Schatzki rings may be treated with esophageal dilatation, using bougie or balloon dilators. These have been found to be equally effective. Bougie dilatation involves passage of long dilating tubes of increasing size down the esophagus to stretch the area of narrowing, either over a guidewire passed into the stomach by endoscopy (the "Savary-Gillard" system) or using mercury-weighted dilators (the "Maloney" system). This is usually done with intravenous sedation to reduce discomfort. Dilatation can produce some temporary irritation. A short course of proton pump inhibitor therapy may decrease aggravation by stomach acid reflux into the esophagus. The duration of the benefit of dilation varies, but may be from months to years. Dilation may be repeated if narrowing recurs.

If small and asymptomatic, no treatment is necessary. Larger, symptomatic cases of Zenker's diverticulum have been traditionally treated by neck surgery to resect the diverticulum and incise the cricopharyngeus muscle. However, in recent times non-surgical endoscopic techniques have gained more importance (as they allow for much faster recovery), and the currently preferred treatment is endoscopic stapling (i.e. diverticulotomy with staples ). This may be performed through a diverticuloscope. Other methods include fibreoptic diverticular repair.

Other non-surgical treatment modalities also exist, such as endoscopic laser, which recent evidence suggests is less effective than stapling.

In patients who have no response to medical or endoscopic therapy, surgery can be performed. A Heller myotomy involves an incision to disrupt the LES and the myenteric plexus that innervates it. The Heller myotomy is used as a final treatment option in patients who do not respond to other therapies.

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.

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%.

Nutcracker esophagus is a benign, nonprogressive condition, meaning it is not associated with significant complications. Patients are usually reassured by their physicians that the disease is unlikely to worsen. However, the symptoms of chest pain and dysphagia may be severe enough to require treatment with medications, and rarely, surgery.

The initial step of treatment focuses on reducing risk factors. While weight reduction may be useful in reducing symptoms, the role of acid suppression therapy to reduce esophageal reflux is still uncertain. Very cold and very hot beverages may trigger esophageal spasms.

Medical therapy for nutcracker esophagus includes the use of calcium-channel blockers, which relax the lower esophageal sphincter (LES) and palliate the dysphagia symptoms. Diltiazem, a calcium-channel blocker, has been used in randomized control studies with good effect. Nitrate medications, including isosorbide dinitrate, given before meals, may also help relax the LES and improve symptoms. The inexpensive generic combination of belladonna and phenobarbital (Donnatal and other brands) may be taken three times daily as a tablet to prevent attacks or, for patients with only occasional episodes, as an elixir at the onset of symptoms. Phosphodiesterase inhibitors, such as sildenafil, can be given to reduce symptoms, particularly pain, but small trials have not been able to demonstrate clinical improvement. Finally, trazodone, an antidepressant that reduces visceral sensitivity, has also been shown to reduce chest pain symptoms in patients with nutcracker esophagus.

Endoscopic therapy with botulinum toxin, known also as Botox, can also be used to improve dysphagia which stabilizes unintentional weight loss, but the effect has limited effect on other symptoms, including pain, while also being a temporary treatment lasting a few weeks. Finally, pneumatic dilatation of the esophagus, which is an endoscopic technique where a high-pressure balloon is used to stretch the muscles of the LES, can be performed to improve symptoms, but again no clinical improvement is seen in regards to motility.

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.

Esophageal webs and rings can be treated with endoscopic dilation.

The primary medications used for GERD are proton-pump inhibitors, H receptor blockers and antacids with or without alginic acid.

Proton-pump inhibitors (PPIs), such as omeprazole, are the most effective, followed by H receptor blockers, such as ranitidine. If a once daily PPI is only partially effective they may be used twice a day. They should be taken one half to one hour before a meal. There is no significant difference between agents in this class. When these medications are used long term, the lowest effective dose should be taken. They may also be taken only when symptoms occur in those with frequent problems. H receptor blockers lead to roughly a 40% improvement.

The evidence for antacids is weaker with a benefit of about 10% (NNT=13) while a combination of an antacid and alginic acid (such as Gaviscon) may improve symptoms 60% (NNT=4). Metoclopramide (a prokinetic) is not recommended either alone or in combination with other treatments due to concerns around adverse effects. The benefit of the prokinetic mosapride is modest.

Sucralfate has a similar effectiveness to H receptor blockers; however, sucralfate needs to be taken multiple times a day, thus limiting its use. Baclofen, an agonist of the GABA receptor, while effective, has similar issues of needing frequent dosing in addition to greater adverse effects compared to other medications.

In pregnancy, dietary modifications and lifestyle changes may be attempted, but often have little effect. Calcium-based antacids are recommended if these changes are not effective. Aluminum- and magnesium-based antacids are also safe, as is ranitidine and PPIs.

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.

Surgical intervention is nearly always required in form of exploratory laparotomy and closure of perforation with peritoneal wash. Occasionally they may be managed laparoscopically.

Conservative treatment including intravenous fluids, antibiotics, nasogastric aspiration and bowel rest is indicated only if the person is nontoxic and clinically stable.

Treatments for the condition vary depending on its severity. The most immediate and effective treatment in the majority of cases is a surgical repair to close the fistula/s and reconnect the two ends of the esophagus to each other. Although this is usually done through an incision between the ribs on right side of the baby, a technique using three small incisions (thoracoscopy) is being used at some centers. In a minority of cases, the gap between upper and lower esophageal segments may be too long to bridge. In some of these so-called long gap cases, though, an advanced surgical treatment developed by John Foker, MD, may be utilized to elongate and then join together the short esophageal segments. Using the Foker technique, surgeons place traction sutures in the tiny esophageal ends and increase the tension on these sutures daily until the ends are close enough to be sewn together. The result is a normally functioning esophagus, virtually indistinguishable from one congenitally well formed. Unfortunately, the results have been somewhat difficult to replicate by other surgeons and the need for multiple operations has tempered enthusiasm for this approach.

The optimal treatment in cases of long gap esophageal atresia remains controversial. Traditional surgical approaches include gastrostomy followed by gastric pull-up, colonic transposition and jejunum transposition. Gastric pull-up has been the preferred approach at many specialized centers, including Great Ormond Street (London) and Mott Children's Hospital (Ann Arbor). Gastrostomy, or G-tube, allows for tube feedings into the stomach through the abdominal wall. Often a cervical esophagostomy will also be done, to allow the saliva which is swallowed to drain out a hole in the neck. Months or years later, the esophagus may be repaired, sometimes by using a segment of bowel brought up into the chest, interposing between the upper and lower segments of esophagus.

Post operative complications sometimes arise, including a leak at the site of closure of the esophagus. Sometimes a stricture, or tight spot, will develop in the esophagus, making it difficult to swallow. This can usually be dilated using medical instruments. In later life, most children with this disorder will have some trouble with either swallowing or heartburn or both. Esophageal dismotility occurs in 75-100% of patients.

Tracheomalacia—a softening of the trachea, usually above the carina (carina of trachea), but sometimes extensive in the lower bronchial tree as well—is another possible serious complication. Even after esophageal repair (anastomosis) the relative flaccidity of former proximal pouch (blind pouch, above) along with esophageal dysmotility can cause fluid buildup during feeding. Owing to proximity, pouch ballooning can cause tracheal occlusion. Severe hypoxia ("dying spells") follows and medical intervention can often be required.

A variety of treatments for tracheomalacia associated with esophageal atresia are available. If not severe, the condition can be managed expectantly since the trachea will usually stiffen as the infant matures into the first year of life. When only the trachea above the carina is compromised, one of the "simplest" interventions is aortopexy wherein the aortic loop is attached to the rear of the sternum, thereby mechanically relieving pressure from the softened trachea. An even simpler intervention is stenting. However, epithelial cell proliferation and potential incorporation of the stent into the trachea can make subsequent removal dangerous.

Several drugs are used to treat DES, including nitroglycerin, hyoscine butylbromide, calcium channel blockers, hydralazine, and anti-anxiety medications. Acid suppression therapy, such as proton pump inhibitors, are often the first line therapy. Botulinum toxin, which inhibits acetylcholine release from nerve endings, injected above the lower esophageal sphincter may also be used in the treatment of DES. Small studies have suggested benefit from endoscopic balloon dilation in certain patients, but all of the above have a low percentage of success in treating the condition; whilst the treatments work in some sufferers, it does not work for everyone. In extremely rare cases, surgery may be considered.

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.

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.

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.

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

Esophageal rupture is a rupture of the esophageal wall. Iatrogenic causes account for approximately 56% of esophageal perforations, usually due to medical instrumentation such as an endoscopy or paraesophageal surgery. In contrast, the term Boerhaave syndrome is reserved for the 10% of esophageal perforations which occur due to vomiting.

Spontaneous perforation of the esophagus most commonly results from a full-thickness tear in the esophageal wall due to a sudden increase in intraesophageal pressure combined with relatively negative intrathoracic pressure caused by straining or vomiting (effort rupture of the esophagus or Boerhaave's syndrome). Other causes of spontaneous perforation include caustic ingestion, pill esophagitis, Barrett's esophagus, infectious ulcers in patients with AIDS, and following dilation of esophageal strictures.

In most cases of Boerhaave's syndrome, the tear occurs at the left postero-lateral aspect of the distal esophagus and extends for several centimeters. The condition is associated with high morbidity and mortality and is fatal without treatment. The occasionally nonspecific nature of the symptoms may contribute to a delay in diagnosis and a poor outcome. Spontaneous effort rupture of the cervical esophagus, leading to localized cervical perforation, may be more common than previously recognized and has a generally benign course. Preexisting esophageal disease is not a prerequisite for esophageal perforation but it contributes to increased mortality.

This condition was first documented by the 18th-century physician Herman Boerhaave, after whom it is named. A related condition is Mallory-Weiss syndrome which is only a mucosal tear.

In case of iatrogenic perforation common site is cervical esophagus just above the upper sphincter whereas spontaneous rupture as seen in Boerhaave's syndrome perforation commonly occurs in the lower (1/3)rd of esophagus.

A method for repairing long-gap esophageal atresia using magnets has been developed, that does not require replacing the missing section with grafts of the intestine or other body parts. Using electromagnetic force to attract the upper and lower ends of the esophagus together was first tried in the 1970s by using steel pellets attracted to each other by applying external electromagnets to the patient. In the 2000s a further refinement was developed by Mario Zaritzky's group and others. The newer method uses permanent magnets and a balloon.

1. The magnets are inserted into the upper pouch via the baby's mouth or nose, and the lower via the gastrotomy feeding tube hole (which would have had to be made anyway to feed the baby, therefore not requiring any additional surgery).

2. The distance between the magnets is controlled by a balloon in the upper pouch, between the end of the pouch and the magnet. This also controls the force between the magnets so it is not strong enough to cause damage.

3. After the ends of the esophagus have stretched enough to touch, the upper magnet is replaced by one without a balloon and the stronger magnetic attraction causes the ends to fuse (anastomosis).

In April 2015 Annalise Dapo became the first patient in the United States to have their esophageal atresia corrected using magnets.