Infection by fungi or bacteria can be primary or complicate a preexisting ulcer. Nonpathogenic oral bacteria frequently are found in ulcer beds, while pathogenic organisms, which account for about 10% of infectious esophagitis cases, may invade the lamina propria and cause necrosis of overlying mucosa. Candidiasis in its most advanced form is characterized by adherent, gray-white pseudomembranes composed of densely matted fungal hyphae and inflammatory cells covering the esophageal mucosa.
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Fig. 15.8 Traumaticandviralesophagitis.(A)Endoscopicviewofalongitudinally-orientedMallory-Weisstear.Thesesuperficiallacerationscanrangefrommillimeterstoseveralcentimetersinlength.(B)Postmortemspecimenwithmultipleherpeticulcersinthedistalesophagus.(C)Multinucleatesquamouscellscontainingherpesvirusnuclearinclusions.(D)Cytomegalovirus-infectedendothelialcellswithnuclearandcytoplasmicinclusions.(Endoscopic image courtesy of Dr. Ira Hanan,The University of Chicago, Chicago, Illinois.)
The endoscopic appearance often provides a clue to the identity of the infectious agent in viral esophagitis. Herpes-viruses typically cause punched-out ulcers (
Fig. 15.8B ), and histopathologic analysis demonstrates nuclear viral inclusions within a rim of degenerating epithelial cells at the ulcer edge (
Fig. 15.8C ). By contrast, CMV causes shallower ulcerations. Biopsy of these lesions show the characteristic nuclear and cytoplasmic inclusions within capillary endothelium and stromal cells (
Fig. 15.8D ). Immunohistochemical staining for viral antigens can be a useful ancillary diagnostic tool.
Reflux of gastric contents into the lower esophagus is the most frequent cause of esophagitis and the most http://ebooksmedicine.net common gastrointestinal ailment with which patients present in the out patient setting in the United States.
The associated clinical condition is termed gastroesophageal reflux disease (GERD). The stratified squamous epithelium of the esophagus is resistant to abrasion from foods but is sensitive to acid. The submucosal glands of the proximal and distal esophagus contribute to mucosal protection by secreting mucin and bicarbonate. More important, high lower esophageal sphincter tone protects against reflux of acidic gastric contents, which are under positive pressure.
Reflux of gastric juices is central to the development of mucosal injury in GERD. In severe cases, duodenal bile reflux may exacerbate the damage. Conditions that decrease lower esophageal sphincter tone or increase abdominal pressure contribute to GERD and include alcohol and tobacco use, obesity, central nervous system depressants, pregnancy, hiatal hernia (discussed later), delayed gastric emptying, and increased gastric volume. In many cases, no definitive cause is identified.
MORPHOLOGYSimplehyperemia,evidenttotheendoscopistasredness,maybetheonlyalteration.InmildGERDthemucosalhistologyisoftenunremarkable.Withmoresignificantdisease,eosinophilsarerecruitedintothesquamousmucosa,followedbyneutrophils,whichusuallyareassociatedwithmoresevereinjury(
Fig.15.9A ).Basalzonehyperplasiaexceeding20%ofthetotalepithelialthicknessandelongationoflaminapropriapapillae,suchthattheyextendintotheupperthirdoftheepithelium,alsomaybepresent.