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Bolus entry at a specific level measured by impedance is considered to occur at the 50% point between 3 s before swallow impedance baseline and impedance nadir during bolus presence. Bolus exit is determined as return to this 50% point on the impedance recovery curve (see Figure 9.1). These relationships have been validated by simultaneous MII and videofluoroscopy with barium [1, 2]. Calculated impedance parameters are shown in Figure 9.6: total bolus transit time, bolus head advance time, bolus presence time, and segmental transit time [4].

Swallows are classified manometrically in standard fashion (see Chapter 8). Swallows are classified by MII as showing (i) complete bolus transit (Figure 9.7a), if bolus entry is seen at the most proximal site (20 cm above the LES) and bolus exit points are recorded at all three distal impedance measuring sites (i.e. 15, 10, and 5 cm above the LES); and (ii) incomplete bolus transit (Figure 9.7b) if bolus exit is not identified at any of the three distal impedance measuring sites.

Figure 9.5 Nine‐channel combined multichannel intraluminal impedance (MII) and manometry (EM) catheter. Circumferential solid‐state pressure sensors located in lower esophageal sphincter (LES) high‐pressure zone (P5) and 5 cm above it (P4); unidirectional solid‐state pressure sensors located 10 cm (P3), 15 cm (P2), and 20 cm (P1) above LES. Impedance measuring segments centered at 5 cm (Z4), 10 cm (Z3), 15 cm (Z2), and 20 cm (Z1) above LES.

Studies using MII–EM in patients with manometrically defined motility abnormalities have aimed to provide a better understanding of bolus transit in various categories of motility abnormalities. The effect of motility abnormalities on bolus transit (or lack thereof) has been clarified by MII–EM studies showing that more than half of patients with manometrically defined distal esophageal spasm (DES) or ineffective esophageal motility (IEM) have complete bolus transit measured by MII. Patients with nutcracker esophagus or isolated LES abnormalities (i.e. hypertensive or hypotensive LES, poorly relaxing LES) have complete bolus transit during swallowing, whereas patients with achalasia or scleroderma have incomplete bolus transit during swallowing (Figure 9.8) [6].

IEM was diagnosed in the past when more than 20% of the swallows were weak. MII‐EM was useful in clarifying the functional defect in patients with manometric IEM. Tutuian and Castell [36] raised the question of whether the manometric diagnosis of IEM should be based on a new criterion; i.e. ≥50% ineffective liquid swallows (“new” IEM) [12]. The authors observed that patients with ≥50% ineffective liquid swallows were more likely to have bolus transit abnormalities than those with <50% ineffective liquid swallows. This new criterion was adopted by the most recent Chicago classification of esophageal motility disorders v3.0 [37].

Furthermore, MII‐EM helped to subdivide IEM patients into those with normal bolus transit for both liquid and viscous swallows (mild IEM), abnormal bolus transit for either liquid or viscous swallows (moderate IEM), and abnormal bolus transit for both liquid and viscous swallows (severe IEM) [37].

In DES, combined MII‐EM provided additional information on the functional defect in patients with DES. A study of 71 patients with manometric diagnosis of DES found that patients with chest pain and DES (i.e. classic esophageal spasm) have higher‐amplitude contractions and normal bolus transit as compared to those presenting with dysphagia [38]. The study suggested that chest pain might be associated with increased contraction amplitudes, while dysphagia may be associated with impaired bolus transit. Further outcomes data are warranted to evaluate whether stratifying DES patients based on pressure and bolus transit information may improve the clinical approach.

Esophagogastric junction outflow obstruction (EGJOO) is a heterogeneous group of disorders with variable clinical significance defined by the Chicago classification 3.0 as impaired relaxation of the esophagogastric junction (EGJ) and elevated median integrated relaxation pressure (IRP) on HRM, but with preserved esophageal peristalsis such that a diagnosis of achalasia is not reached.

Zheng et al. [74] reported that 29% of EGJOO cases were associated with coexistent abnormal bolus transit. In addition, a study by Jain et al. [75] reported that bolus transit is impaired in EGJOO, but not as severely as in achalasia. These two studies clearly showed the association between abnormal bolus transit and EGJOO. In a study of 169 patients with manometric EGJOO, Song et al. [76] aimed to evaluate whether bolus transit was useful for discriminating clinically relevant EGJOO. This study defined clinically relevant EGJOO when subjects evolved to achalasia or had significant dysphagia and/or passage disturbance on barium esophagram. The study showed that a combination of delayed bolus transit, dysphagia, and compartmentalized pressurization had the highest predictive value for identifying clinically relevant EGJOO (sensitivity, 90%; specificity, 92.5%; negative predictive value, 99.3%). Thus, we can infer that bolus transit measured using an impedance test might be a significant variable for differentiating between clinically relevant EGJOO and non‐clinically relevant EGJOO [77].

Figure 9.6 Definitions of impedance parameters. (A) Total bolus transit time (TBTT) as time elapsed between bolus entry at 20 cm above lower esophageal sphincter (LES) and bolus exit at 5 cm above LES. (B) Bolus head advance time as time elapsed between bolus entry at 20 cm above LES and bolus entry at 15, 10, and 5 cm above LES. (C) Bolus presence time (BPT) as time elapsed between bolus entry and bolus exit at each impedance measuring site (5, 10, 15, and 20 cm above LES). (D) Segmental transit time (STT) as time elapsed between bolus entry at a given level above LES and bolus exit at the next lower level.