Herpetic esophagitis

Herpetic esophagitis Herpetic esophagitis is a viral infection that involves inflammation and ulceration of the esophagus. After candidiasis, herpes simplex type I infection is the most common cause of esophagitis in immunocompromised patients encountered by HIV / AIDS, neoplasms, debilitating disease or those who have undergone radiation therapy, corticosteroid therapy or chemotherapy. Oesophageal acute self-limited disease progresses as patients without depression to immune system disorders.
Pathogenesis
Originally herpetic esophagitis develops through the appearance of small vesicles that rupture and cause superficial mucosal ulcers. Epithelial cells on the edges of ulcers are characterized by multinucleated, nuclei and eosinophilia-like grains of sand impaction with the body of Cowdry type A
In immunocompetent patients the host immune response initiates the healing process of injuries. In the immunocompromised infection can progress from areas of ulceration until the formation of diffuse bleeding. Nerotice herpetic ulcers may be colonized by Candida.
Signs and symptoms
Patients with herpetic esophagitis shows typical acute severe odynophagia. Other manifestations include dysphagia, chest pain and upper digestive hemorrhage. The labial and oropharyngeal lesions suggest the diagnosis, some patients still present and these injuries.
Some patients may also candida esophagitis. In immunocompetent herpetic oesophagitis resolves spontaneously in 1-2 weeks with conservative treatment: analgesics and sedation. Rare complication of herpes esophagitis include: perforation, tracheo-esophageal fistula and dissemination to other organs.
Diagnosis
Imaging Studies
Rediologic double contrast examination reveals small ulcers, or deep superficilae extended to middle and distal esophagus.
Esophagoscopy with small ulcers endobiopsie highlights prominent yellow edges that may conflict. Ulcers can be dotted, linear, or stellate-like volcanoes, surrounded by edema.
Histological examination showed edema and cellular degeneration. Nuclei of infected cells can enter the giant cell division forming amitotica multinuleate. Shows cell nuclei and eosinophilic intranuclear inclusions marginatia nuclear chromatin. As local inflammation progresses to form vesicles that rupture and cause ulcers.
Treatment
The people who have normal immunity may recommend acyclovir be taken orally. In patients with poor immunity recommend intravenous acyclovir, 15mg/kgcorp/zi to 8 hours for 7-10 days. In cases with resistance to acyclovir is recommended in slow infusion intravenous foscarnet 60mg/kgcorp to 8 hours, 14 to 21 days.