Oesophagitis

Oesophagitis is inflammation of the oesophagus.

There are two main types: corrosive oesophagitis, caused by accidental or intentional swallowing of caustic chemicals, and reflux oesophagitis, caused by regurgitation of the stomach’s contents.

Corrosive oesophagitis

Chemicals that are likely to cause severe corrosive oesophagitis include many cleaning and disinfecting products. The oesophagus may rupture, with fatal consequences; alternatively it may heal but may result in an oesophageal stricture (narrowing of the oesophagus).

Reflux oesophagitis

Reflux oesophagitis is due to poor function of the muscles in the lower oesophagus, which permits the stomach’s acidic contents to rise back into the oesophagus (see acid reflux). The main symptom, heartburn, may be worsened by alcohol, smoking, and obesity. Poor function of the lower oesophagus may be linked with a hiatus hernia, in which the top part of the stomach slides back and forth through the muscular diaphragm between the chest and the abdomen. Complications Barrett’s oesophagus a complication of reflux oesophagitis in which cells that normally line the stomach extend up into the oesophagus. It may lead to cancer. Severe, chronic oesophagitis can cause an oesophageal stricture. For more information about reflux oesophagitis please visit:

Treatment

The treatment for most cases of persistent reflux oesophagitis is a change of diet and lifestyle: weight loss, avoiding heavy meals, limiting alcohol intake, and stopping smoking. Antacid drugs help to reduce acidity. Surgical treatment (such as minimally invasive surgery) may be necessary for a hiatus hernia.

Go here for Gastro-oesophageal disease in detail - technical

Nonreflux causes of oesophagitis - in detail - technical

Infective oesophagitis

Infective oesophagitis has become more prevalent with the increasing number of people who are immunosuppressed through HIV infection or chemotherapy. The more important causes of infective oesophagitis are summarized in Table 1 below. Immune status is a major determinant of the pattern of infection and simultaneous infection with two or more infective agents is not unusual (Table 1). Helicobacter pylori does not appear to be of any primary significance in the pathogenesis of oesophageal mucosal disease.

Table 1  Major causes of infective oesophagitis
Pathogen Management Remarks
Immunocompetent patients
Candida albicans Topical/oral antifungals By far the most common
Herpes simplex Aciclovir if severe Unusual, may denude mucosa
Varicella zoster Aciclovir if severe In association with chickenpox/herpes zoster
Bacteria   Rare in well individuals
Immunocompromised patients
Candida albicans Systemic antifungals Most common; oral disease almost diagnostic
Cytomegalovirus Prophylaxis and treatment with  ganciclovir or foscarnet Serpiginous to giant ulcers in distal half
Herpes simplex Prophylaxis and treatment with aciclovir or foscarnet Circumscribed ulcers, raised edges to coalescence. Oral lesions
Tuberculosis Conventional From miliary and local spread
Gram-positive cocci, Gram-negative bacilli Intravenous antibiotics Often with systemic infection
Syphilis Conventional Associated with tertiary syphilis elsewhere. Inflammatory stricture

Patients may present with pain or dysphagia. Viral oesophagitis can sometimes cause major haemorrhage. The dysphagia is generally secondary to superficial mucosal damage and inflammation, but some disorders damage the full thickness of the oesophageal wall and so lead to stricturing.

A full history to determine the setting in which the oesophageal problem occurs is often very helpful. Cutaneous or oral disease can inform the oesophageal diagnosis. Endoscopy is the investigation of choice since the mucosal appearance and the distribution of oesophageal lesions can be virtually diagnostic. In addition, biopsies and brushings allow for histological diagnosis and identification of fungal elements, viral inclusions, or rarely, pathogenic bacteria.

Although infective oesophagitis may be severe in immunocompetent patients it is characteristically self-limiting and topical therapy is normally all that is needed. Immunocompromised patients usually need aggressive, systemic therapy to resolve the infection (Table 2). Some infections tend to recur, which can cause major disability.

Eosiniphilic oesophagitis

Eosinophilic oeosphagitis (sometimes referred to as allergic oesophagitis) affects children and adults worldwide, with a male preponderance. The incidence appears to be increasing in line with other associated allergic conditions such as asthma, hay fever, allergic rhinitis, and atopic dermatitis. Although the exact aetiology is not understood there does seem to be an aberrant immune-mediated response and activated eosinophils may cause activation of acetyl choline via histamine. Food impaction and dysphagia are the common presenting symptoms. Heartburn is often present but refractory to standard treatments for gastro-oesophageal reflux disease. Approximately 50% of patients will have other allergic symptoms. Endoscopy is the investigation of choice and the findings range from grossly abnormal to normal. Findings include a small-calibre oesophagus, proximal strictures, white exduates, oeosphageal rings, and fragile mucosa. The diagnosis is made on oesophageal biopsy in which there is a dense eosiniphilic infiltration within the epithelium. If the eosinophilic infiltration is more generalized this suggests eosinophilic gastroenteritis. There is a lack of randomized controlled trial evidence to guide treatment. Strategies include dietary elimination in consultation with an allergy assessment and steroids given topically or systemically in severe cases. Endoscopic food disimpaction and dilatation may be necessary. There is some data on leukotriene inhibitors and anti-interleukin-5 antibody therapy. There is limited data on the long-term outcome for these patients.

Medication-induced oesophagitis

This entity was only recognized in 1970. The chemical properties of medications pose hazards to the oesophageal mucosa because of its relative susceptibility to injury through pH-dependent mechanisms. This susceptibility arises in part from the high local concentrations of medications that occur in the oesophageal lumen, since pills move surprisingly slowly through the normal oesophagus especially at the level of the aortic arch. Defective oesophageal transport, poor pill design, increased mucosal susceptibility to injury, and poor pill-taking technique contribute to the problem. Medications known to have an especially high risk for oesophageal damage are listed in Table 2 below.

Table 2  Common causes of medication-induced oesophagitis
Severe injury—high risk Slow-release potassium chloride
Aspirin and nonsteroidal anti-inflammatory drugs
Doxycycline/tetracycline
Quinidine
Alendronate
Potassium chloride
Less severe injury—high risk Many antibiotics
Iron supplements
Occasional injury Ascorbic acid
Mexiletine
Slow-release theophylline
Captopril
Phenytoin
Zidovudin
Corticosteroids

Symptoms are those for any form of stricture associated oesophagitis, and much pill-induced injury probably goes unrecognized. Injury at the distal oesophagus, the other common site of hold-up, may be commonly misdiagnosed as being due to reflux disease.

Medications and formulations with a high risk of injury should be identified and avoided if possible, especially in older patients with reflux disease or abnormal oesophageal transit. Pill transit is facilitated if medications are taken in the erect position with plenty of water. Pharmaceutical companies need to pay more attention to the use of shapes, sizes, and coatings that can assist transit of pills through the oesophagus. Stricturing may occasionally require surgery.

Caustic injury and caustic ingestion

Definition and aetiology

Strong acids and alkalis are both very damaging to the oesophagus and are found in high concentrations in many agents commonly used in the household for cleaning and maintenance. Laryngeal and gastric injuries may overshadow oesophageal injury. Because of their relative lack of taste, alkaline solutions are more likely to be swallowed accidentally in large amounts. Alkaline injury is especially deep; acid tends to form a superficial coagulant, which limits penetration.

Symptoms

The severity and extent of injury are immensely variable and cannot be predicted accurately from estimates of the volume ingested. Around one-half of patients with a history of caustic ingestion have no significant injury. Oropharyngeal and laryngeal injury confirm caustic ingestion and can be a major threat to the airway, but do not predict the existence and severity of oesophageal injury which causes odynophagia, dysphagia, or haematemesis. Prompt fibreoptic panendoscopy appears to be safe. This may be normal or show only patchy mucosal oedema, erythema, and small haemorrhagic ulcers, indicative of superficial damage with a good prognosis. Extensive and circumferential ulceration, and grey or brown/black ulceration suggest transmural injury.

Treatment

Patients with severe injury must be observed closely for signs of perforation. Nasogastric suction should be used with the administration of broad-spectrum antibiotics as these appear to reduce the severity of infective complications. The use of steroids is controversial, the balance of evidence tending to oppose their use. Oesophageal stricture is to be expected with severe injury and appears not to be prevented by routine dilatation in the first 2 weeks after injury. A barium study should be done at 2 to 3 weeks to screen for stricturing, and then subsequently at about 3-monthly intervals thereafter for a year, so that the development of stricturing is recognized at a stage when dilatation may have some impact.

Prognosis

The main short- to medium-term risk is the development of stricture. Caustic strictures are difficult and hazardous to treat by peroral dilatation so that about half of patients require oesophageal resection. In the long term (average onset 40 years after injury) carcinoma of the oesophagus is a major hazard, the risk being 1000 to 3000 times the expected risk.