The Esophagus. Группа авторов

Figure 6.6 Representative frames from the pharyngeal phase of swallowing. (A) The bolus (b) has just entered the oropharynx. The soft palate (s) is rising to appose the posterior pharyngeal wall, but the velopharyngeal portal (arrow) is still open. The epiglottic tip is just beginning to tilt posteriorly. The laryngeal vestibule (l) is still open. (B) The bolus has just entered the hypopharynx. The soft palate (s) now apposes the posterior pharyngeal wall. The epiglottis (arrowhead) is partly obscured by the barium but is tilting. The pharyngoesophageal segment (arrow) remains closed. (C) The bolus is passing into the esophagus. Pharyngeal and laryngeal elevation is manifested by elevation of the hyoid bone (b) up underneath the mandible. The laryngeal vestibule is completely compressed and is no longer seen as an air‐filled space. The epiglottis (arrowhead) has tilted to appose the anterior wall of the hypopharynx. The posterior pharyngeal contraction wave (long arrow) is in the thyropharyngeal muscle. The pharyngoesophageal segment (short arrow, identified by redundant post‐cricoid mucosa on the opposite wall) is open. The C5 vertebral body is labeled 5 to allow a direct comparison to D. (D) The bolus has just passed through the pharynx. The pharynx and larynx have returned to their “resting” position. Compare the levels of the hyoid bone (b) and the pharyngoesophageal segment (thick arrow) on image C during swallowing and image D after swallowing. The epiglottic tip (arrowhead) has returned to its upright position. The soft palate now apposes the tongue, and the laryngeal vestibule is open. A small Killian–Jamieson diverticulum (thin arrow) is present. The C5 vertebral body is labeled 5.

Figure 6.7 Laryngeal penetration. (A) During drinking, barium enters the laryngeal vestibule (thick arrow). The anterior commissure (thin arrow) and true vocal cords (t) are identified. (B) Spot radiograph during phonation shows a huge epiglottic mass (arrows) with nodular mucosa (open arrow) as the cause of the laryngeal penetration.

      Source: Reproduced from Rubesin [10], with permission.

      Unilateral pharyngeal paresis should suggest vagal injury from the level of the pons to the recurrent laryngeal nerve, whereas abnormal epiglottic tilt as an isolated finding should suggest recurrent laryngeal nerve damage or intralaryngeal muscle problems. In general, however, the degree and types of swallowing dysfunction on barium swallows do not enable the radiologist to predict the underlying neuromuscular diseases causing this dysfunction.

      Pouches and diverticula

      Zenker’s diverticula

Zenker’s diverticulum is an acquired mucosal herniation through an area of congenital muscle weakness in the cricopharyngeal muscle, known as Killian’s dehiscence. This opening is found in about one‐third of people at autopsy and has been described as occurring between the thyropharyngeus and cricopharyngeus or between the oblique and horizontal fibers of the cricopharyngeus itself [25, 26]. The pathogenesis of Zenker’s diverticulum is unknown. Manometric studies have produced conflicting findings [27, 28]. Some of these studies have shown a normal tonic pressure in the upper esophageal sphincter (UES) and normal coordination between pharyngeal contraction and relaxation of the UES, whereas others have shown elevated UES pressure or abnormal relaxation of the UES. It is also unknown whether chronic gastroesophageal reflux predisposes patients with Killian’s dehiscence to the development of a Zenker’s diverticulum. Nevertheless, most patients with Zenker’s diverticulum have a hiatal hernia and gastroesophageal reflex [29, 30].

Figure 6.8 Asymmetric epiglottic tilt. There is diminished epiglottic tilt on the left side (arrow).

When detected on barium studies, Zenker’s diverticulum appears on frontal views as a persistent, barium‐filled sac in the midline below the tips of the piriform sinuses (Figure 6.10). On lateral views during swallowing, the opening of the Zenker’s diverticulum above the incompletely opened pharyngoesophageal segment is often surprisingly broad [10, 31]. The sac then courses behind the pharyngoesophageal segment and proximal cervical esophagus. Barium within the diverticulum can be regurgitated back into the lower hypopharynx during breathing or additional swallowing (Figure 6.11), but overflow aspiration is uncommon. Contour deformities in a Zenker’s diverticulum may be caused by adherent debris, inflammation, or, rarely, carcinoma [32, 33].

Figure 6.9 Overflow aspiration. This man had global pharyngeal weakness due to polymyositis and poor clearance of barium from the pharynx during swallowing with resultant stasis of barium in the piriform sinuses. Note that the barium level lies above the interarytenoid notch (straight arrow). After the swallow has passed, barium pours over and down into the larynx (curved arrow), outlining the false vocal cords (right cord – f) and laryngeal ventricle.

Figure 6.10 Zenker’s diverticulum. (A) Frontal view of the pharynx demonstrates a 3 × 2 cm sac (S) with an air–barium level. The sac lies in the midline below the tips of the piriform sinuses (right piriform sinus tip identified by arrow). (B) Lateral view of the pharynx during drinking. The sac has a broad opening (double arrow). The sac (S) lies posterior to the pharyngoesophageal segment and proximal cervical esophagus (small arrows). (Laryngeal penetration resulted from abnormal timing between the oral and pharyngeal phases.

      Source: Reproduced from Rubesin [10], with permission.

Figure 6.11 Pharyngeal regurgitation from Zenker’s diverticulum. (A) Frontal view of the pharynx shows a 2 cm sac (S) in the midline below the tips of the piriform sinuses. (B) Frontal view of the pharynx as the patient begins a second swallow. Barium (arrows) has been regurgitated from the Zenker’s diverticulum back into the lower hypopharynx.