Barrett’s esophagus is the precursor lesion for esophageal adenocarcinoma. Screening and surveillance of Barrett’s esophagus are undertaken with the goal of earlier detection and lowering the mortality from esophageal adenocarcinoma. The widely used technique is standard esophagogastroduodenoscopy with biopsies per the Seattle protocol for screening and surveillance of Barrett’s esophagus. Surveillance intervals vary depending on the degree of dysplasia with endoscopic eradication therapy confined to patients with Barrett’s esophagus and confirmed dysplasia. In this review, we present various novel techniques for screening of Barrett’s esophagus such as unsedated transnasal endoscopy, cytosponge with trefoil factor-3, balloon cytology, esophageal capsule endoscopy, liquid biopsy, electronic nose, and oral microbiome. In addition, advanced imaging techniques such as narrow band imaging, dye-based chromoendoscopy, confocal laser endomicroscopy, volumetric laser endomicroscopy, and wide-area transepithelial sampling with computer-assisted three-dimensional analysis developed for better detection of dysplasia are also reviewed.

Current management of Barrett esophagus and esophageal adenocarcinomaA ll cases of esophageal adenocarcinoma are thought to arise from Barrett esophagus. 1 But most cases of Barrett esophagus go undiagnosed. And Barrett esophagus is seen in 5% to 15% of patients with gastroesophageal refl ux disease. 2 These facts clearly emphasize the need for screening. Here, we review the rationale and recommendations for screening and surveillance, as well as the range of treatment options. ■ SCOPE OF THE PROBLEMThe American Cancer Society estimated there were 17,290 new cases of esophageal cancer and 15,850 deaths from it in the United States in 2018. 3 Of the 2 main histologic types of esophageal cancer, adenocarcinoma and squamous cell cancer, adenocarcinoma is more common in the United States.The precursor lesion is Barrett esophagus, defi ned as an extension of salmon-colored mucosa at least 1 cm into the tubular esophagus proximal to the gastroesophageal junction, with biopsy confi rmation of intestinal metaplasia. 4 The natural course of progression to dysplasia and cancer in Barrett esophagus is unknown but is thought to be stepwise, from no dysplasia to low-grade dysplasia to high-grade dysplasia and cancer, and the cancer risk depends on the degree of dysplasia: the annual risk is 0.33% if there is no dysplasia, 0.54% with low-grade dysplasia, and 7% with highgrade dysplasia. 4 Although all cases of esophageal adenocarcinoma are thought to arise from Barrett REVIEW

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Hypernatremia is a frequent cause of intensive care unit admission. The patient presented in this article had hypernatremia refractory to D5W (dextrose 5% water) therapy, which led to a complex investigation. Workup revealed central diabetes insipidus most likely secondary to flare up of neurosarcoidosis. The challenge in terms of diagnosis was a presentation with low urine output in the setting of hypernatremia resistant to treatment with desmopressin. This case unfolded the role of hypothyroidism causing secondary renal dysfunction and hence needed continued treatment with thyroxine in addition to treatment for hypernatremia.