Esophageal disease - I : Esophagitis

< Esophagitis >

Infectious Esophagitis Viral esophagitis HSV VZV CMV : only in immunocompromised patients particularly in the distal esophagus Bacterial esophagitis Lactobacillus beta-hemolytic streptococci Fungalesophagitis Cryptosporidium Pneumocystis Mycobacterium tuberculosis Candida : Candida species are normal commensals in the throat Parasitic esophagitis Other Types of Esophagitis Eosinophilic Esophagitis Radiation esophagitis Corrosive esophagitis Pill-induced esophagitis - Causes : above the classification - Signs & Symptoms acute onset of chest pain, odynophagia, and dysphagia bleeding tracheoesophageal fistula and food impaction Systemic manifestations such as nausea, vomiting, fever, chills, and mild leukocytosis - Diagnostic tests Barium swallow : HSV :inadequate to detect early lesions and cannot reliably distinguish HSV infection from other types Candida :may be normal or show multiple nodular filling defects of various sizes Large nodular defects may resemble grape clusters Endoscopy HSV : vesicles and small, discrete, punched-out superficial ulcerations with or without a fibrinous exudate. -> ("volcano-like") VZV CMV : intranuclear and small intracytoplasmic inclusions in large fibroblasts and endothelial cells Candida mild disease : small, yellow-white raised plaques with surrounding erythema extensive disease :confluent linear and nodular plaques Culture HSV : positive within days and is helpful in diagnosis and to identify acyclovir-resistant strains. Candida : not useful Staining Candida : yeast or hyphal forms in plaque smears and exudate stained with PAS or Gomori silver stains PCR assays : more sensitive than viral cultures Biopsyor cytolotic smear(Mucosal cells sample taken at the edge of an ulcer) HSV : ballooning degeneration, ground-glass changes in the nuclei with eosinophilic intranuclear inclusions (Cowdry type A), and giant cell formation on routine stains. VZV :is difficult to distinguish from HSV, but the distinction can be made immunohistologically or by culture. CMV - Treatments Viral esophagitis HSV VZV CMV Bacterial esophagitis Lactobacillus beta-hemolytic streptococci Fungalesophagitis Cryptosporidium Pneumocystis Mycobacterium tuberculosis Candida Parasitic esophagitis Other Types of Esophagitis Eosinophilic Esophagitis Radiation esophagitis Corrosive esophagitis Pill-induced esophagitis

Other Types of Esophagitis Eosinophilic Esophagitis Eosinophilic esophagitis is characterized by eosinophilic inflammation and submucosal fibrosis. The eosinophil chemokine eotaxin-3 is involved in the pathogenesis of the disease. Clinically, eosinophilic esophagitis is more common in children and in males. Presenting symptoms vary with age. Younger children present with failure to thrive and refusal to swallow. Older children present with regurgitation, vomiting, and pain. Adolescents usually present with heartburn and dysphagia. Adults often present with intermittent dysphagia and food impaction. A history of allergic disease or mild peripheral eosinophilia is present in about half of patients. Barium esophagogram may show a small-caliber esophagus, isolated esophageal narrowing, or single or multiple esophageal rings. Esophagoscopy may reveal one or more longitudinal fissures, fixed or transient concentric rings, proximal strictures, and focal white specks (abscesses). Endoscopic ultrasound may show thickening of the esophageal wall. Differential diagnosis includes reflux esophagitis, eosinophilic gastroenteritis, and esophageal rings and strictures. Diagnosis is confirmed by esophageal mucosal biopsies that show increased eosinophils (>15) per high-power field or eosinophilic microabscesses. Treatment consists of a 12-week course of swallowed fluticasone propionate (440 micro-g bid) using a metered dose inhaler. Oral prednisone may also be used. Dietary management involves identification of the offending food and its elimination from the diet or a trial of elemental diet for 4 weeks. Food impaction requires endoscopic dislodging. Esophageal dilation should be performed with great care because of a high rate of esophageal perforation in these cases. Antibody to interleukin 5 is an effective therapy emerging from clinical trials. Radiation esophagitis is a common occurrence during radiation treatment for thoracic cancers. The frequency and severity of esophagitis increase with the amount of radiation delivered and may be enhanced by radiosensitizing drugs like doxorubicin, bleomycin, cyclophosphamide, and cisplatin. Dysphagia and odynophagia may last several weeks to several months after therapy. The esophageal mucosa becomes erythematous, edematous, and friable. Superficial erosions coalesce to form larger ulcers. Submucosal fibrosis and degenerative changes in the blood vessels, muscles, and myenteric neurons may occur, and esophageal stricture may develop. The treatment aims to relieve the pain with viscous lidocaine during the acute phase; indomethacin treatment may reduce radiation damage. Esophageal stricture may need to be dilated. Corrosive esophagitis is caused by the ingestion of caustic agents, such as strong alkali or acid. Severe corrosive injury may lead to esophageal perforation, bleeding, and death. Glucocorticoids are not useful in acute corrosive esophagitis. Healing is usually associated with stricture formation. Caustic strictures are usually long and rigid (Fig. 286-2, panel 5) and generally require dilatation with dilators passed over a guide wire through the stricture. Pill-induced esophagitis is associated with the ingestion of certain types of pills. Antibiotics such as doxycycline, tetracycline, oxytetracycline, minocycline, penicillin, and clindamycin account for more than half the cases. Nonsteroidal anti-inflammatory agents such as aspirin, indomethacin, and ibuprofen may cause injury. Other commonly prescribed pills that cause esophageal injury include potassium chloride, ferrous sulfate or succinate, quinidine, alprenolol, theophylline, ascorbic acid, and pinaverium bromide. Bisphosphonates, particularly alendronate and pamidronate, are more common offenders. Pill-induced esophagitis can be prevented by avoiding the offending agents or taking pills in the upright position with copious amount of fluid. Sclerotherapy for bleeding esophageal varices usually produces transient retrosternal chest pain and dysphagia; esophageal ulcer, stricture, hematoma, or perforation may occur. Variceal banding causes similar complications, but less frequently. Esophagitis associated with mucocutaneous and systemic diseases is usually associated with blister and bulla formation, epithelial desquamation, and thin, weblike, or dense esophageal strictures. Pemphigus vulgaris and bullous pemphigoid form intraepithelial and subepithelial bullae, respectively, and can be distinguished by specific immunohistology; both are characterized by sloughing of epithelium or the presence of esophageal casts. Glucocorticoid treatment is usually effective. Cicatricial pemphigoid, Stevens-Johnson syndrome, and toxic epidermolysis bullosa can produce esophageal bullous lesions and strictures requiring gentle dilatation. Graft-versus-host disease (GVHD) occurs in patients who have received allogeneic bone marrow or cord blood transplant. If it involves the esophagus, dysphagia and odynophagia are common symptoms. Radiologic findings include mid- and upper esophageal rings or webs and strictures. Esophageal ulcers may be seen. Behçet's syndrome and eosinophilic gastroenteritis may involve the esophagus and respond to glucocorticoid therapy. An erosive lichen planus can also involve the esophagus. Crohn's disease may cause inflammatory strictures, sinus tracts, filiform polyps, and fistulas in the esophagus.