The initial evaluation of the VFE begins with an assessment of transit through the pharyngoesophageal segment (PES) . The presence of PES narrowing from cricopharyngeus muscle dysfunction (bar), web, stricture, or neoplasm is noted (Chap. 10). The right anterior oblique (RAO) view afforded by the VFE provides a unique and unobstructed view of PES anatomy and barium flow. Subtle pathology, such as a small cricopharyngeal web missed on lateral fluoroscopic view can be identified on the RAO view of the VFE (Fig. 11.1). After the PES is evaluated, the VFE evaluation proceeds with an assessment of esophageal mucosal pathology .

The double contrast phase of the study highlights mucosal pathology that may otherwise be missed. The normal distended esophagus has a smooth homogenous contour (Fig. 11.2). Partially collapsed mucosal relief views may reveal mucosal changes signifying underlying pathology such as neoplasm or esophagitis (Figs. 11.3 and 11.4). The most common cause of esophagitis is gastroesophageal reflux (peptic esophagitis). Esophageal inflammation and edema can result in a nodular appearance on VFE (Fig. 11.4). The VFE is poorly sensitive to diagnose mild esophagitis. Infectious esophagitis is much less common than reflux esophagitis. The most common cause of infectious esophagitis is candida. Candida esophagitis results in a characteristic granular appearance on VFE (Figs. 11.5 and 11.6). Other much less common causes of infectious esophagitis include herpes and cytomegalovirus (CMV) (Figs. 11.7 and 11.8). Eosinophillic esophagitis (EoE) is a rapidly increasing atopic cause of solid food dysphagia . Although the diagnosis of EoE is made on endoscopic biopsy displaying > 20 eosinophils per high-power field, there is a characteristic appearance on VFE that is highly suggestive of EoE. The distinguishing finding is that of segmental esophageal strictures giving the appearance of a corrugated or ringed esophagus (Figs. 11.9 and 11.10). In the absence of a ringed esophagus, a small caliber esophagus also suggests the presence of fibrotic narrowing secondary to the eosinophilic infiltrate (Fig. 11.11) .

An evaluation of the mucosa concludes with an assessment of the esophageal mucosal folds. The longitudinal mucosal folds of the esophagus are normally thin, straight, and less than 2 mm in width. Prominent mucosal folds indicate esophageal inflammation and suggest the presence of esophagitis (Figs. 11.12 and 11.13). Esophageal varices produce an irregular, serpiginous, almost colonic appearance to the distal esophagus and mucosal folds (Fig. 11.14). After the evaluation of mucosal pathology, the systematic analysis of the VFE proceeds with an assessment of esophageal motility .

An evaluation of esophageal motility is an essential aspect of the comprehensive VFE. Motility abnormalities can generally be classified into IEM, esophageal spasm, scleroderma, or achalasia. IEM is the much more frequent diagnosis. IEM is further classified on VFE as mild or severe. Motility assessment begins with an evaluation of primary peristalsis. Primary peristalsis is evaluated by assessing the primary stripping wave and esophageal stasis. This is initially performed in the upright and then prone position (Chap. 3). It is essential that the patient be instructed to consume the barium bolus in one effortful swallow. Taking additional swallows will terminate the esophageal contraction wave and give the impression of dysmotility when peristalsis is normal (deglutitive inhibition). Primary peristalsis is visualized fluoroscopically as a stripping wave. A normal esophageal stripping wave transmits a bolus along the esophagus at approximately 2 cm/s. A bolus should clear a normal 25 cm esophagus in less than 15 s. The barium should proceed throughout its entire length in one smooth stripping motion. The presence of secondary peristalsis is also evaluated. Secondary peristalsis is a contraction that originates in the esophagus as a response to esophageal distention or chemical (acid) stimulation. Secondary peristalsis on VFE is assessed in response to barium stasis within the esophagus . Secondary peristalsis should strip and clear the esophagus of retained barium without the patient initiating a swallow in the pharynx. Barium stasis in the esophagus > 15 s or alterations in the primary or secondary stripping wave are indications of IEM. The degree of peristaltic abnormality is classified as mild, severe (profound), or absent. In patients with profound esophageal dysmotility, it is essential to recognize the presence of any stripping wave. A complete absence of a primary and secondary stripping wave suggests achalasia and a complete absence of a stripping wave in the smooth muscle esophagus only (distal 2/3) suggests scleroderma. The visualization of a single primary or secondary stripping wave suggests a diagnosis other than achalasia. The presence of tertiary peristalsis is then evaluated. Tertiary peristalsis is simultaneous, isolated, nonperistaltic esophageal contractions (Fig. 6.​8 and Fig. 11.15) that occur irrespective of coordinated peristalsis. They are nonpropulsive and are considered a sign of esophageal dysmotility. Profound tertiary contractions can be seen in esophageal spasm and give the appearance of a corkscrew esophagus (Figs. 11.16 and 11.17). Tertiary contractions and esophageal spasm may be associated with underlying gastroesophageal reflux .