Fig. 20.1
Example of ineffective esophageal motility, Swallow (Sw) 1–10: Hypotensive contraction (Swallow 1, 4, 6, 7, 8, 9); Failed peristalsis (Swallow 2, 3, 5, 10); Weak peristalsis with small (2–5 cm) and large (>5 cm) breaks in the isobaric contour of 20 mmHg (Swallow 7–9)
Fig. 20.2
Incomplete bolus transit due to a large break in the 20 mmHg isobaric contour in high-resolution impedance manometry. The pink shaded area indicates bolus presence in the esophageal pressure topography. The corresponding line tracing shows inadequate recovery (<50 %), which indicates incomplete clearance (dashed line)
Although not part of the current classification of ineffective or weak esophageal motility, the distal contractile integral (DCI) provides further assessment of global distal esophageal circular muscle strength. The DCI is calculated as the product of mean amplitude of the contraction (excluding pressure below 20 mmHg) from the transition of the striated to smooth esophageal muscles (proximal pressure trough) to the proximal border of the LES by duration and by length and gives an overall value of the circular muscle strength of the distal esophagus. To date, the DCI has largely been used to define hypercontractility, focusing on the upper limits of normal, differentiating hypercontractility from normal contractions, rather than the lower limits of esophageal motility. Figure 20.3 shows a normal esophageal body contraction in esophageal pressure topography and its corresponding line tracing in a patient with distal contraction amplitude and DCI within normal limits. A limitation of the automated DCI calculation provided by the analysis software is that repetitive pressure signals separated from the esophageal contractile complex such as vascular artifacts are included in this calculation. This may lead to artifactual overestimation of the circular contraction strength in patients with a hypocontractile esophagus [10]. The lower limit of the DCI, expressed by the 5th percentile of asymptomatic controls is 500 mmHg • cm • s.
Fig. 20.3
Normal contraction amplitude and distal contractile integral (DCI): Color plot (A) and corresponding line tracing (B). Black and red dots indicate begin and end of contraction. Peak of contraction (contraction amplitude) displayed by white square in A and as vertical red line in B. DCI is calculated by average pressure (in an isobaric contour of 20 mmHg) × time × length (doted white box). Contraction amplitude: 120 mmHg; DCI 1,800 mmHg • s • cm
The Tailored Approach in the Current Literature
The benefits of tailoring the degree of fundoplication, either by performing an alternative wrap or by altering the Nissen wrap in some way, based upon the patients esophageal motility remain unknown mostly due to insufficient and poor quality data to date. Nearly all published studies (Tables 20.1 and 20.2) suffer from one or more of the following problems.
Table 20.1
Dysphagia after Nissen fundoplication in patients with ineffective esophageal motility (IEM) vs. normal motility (N); CA: Contraction Amplitude
Definition of poor motility | IEM | N | OP | Use of Bougie | Hiatal closure | f/u | Postoperative dysphagia | |
---|---|---|---|---|---|---|---|---|
Biertho [20] | Mean CA < 30 mmHg | 38 | 533 | Nissen | No | n/r | Up to 5 years | No difference in dysphagia score |
Ravi [21] | CA < 30 mmHg or failed in ≥30 % | 38 | 60 | Nissen | No | Yes | Six months | Moderate/severe: 13 % (IEM) vs. 8 % (N) |
Munitiz [22] | CA < 30 mmHg in ≥50 % | 41 | 52 | Open Nissen | 48–50 Fr | Yes | Median 5–6.5 years | New onset: 7.3 % (IEM) vs. 3.9 % (N) |
Table 20.2
Postoperative dysphagia after total (Nissen) and partial (Toupet) fundoplication in a cohort of ineffective esophageal motility (IEM) and normal motility (N); CA: Contraction Amplitude
Definition of poor motility | IEM | N | OP | Use of Bougie | Hiatal closure | f/u | Postoperative dysphagia | |
---|---|---|---|---|---|---|---|---|
Strate [19] | CA < 40 mmHg and/or failed peristalsis >40 % | 50 | 50 | Nissen | 36 Fr | Yes | 2 years | IEM: 26 % (Nissen) vs. 10 % (Toupet) N: 12 % (Nissen) vs. 6 % (Toupet) |
50 | 50 | Toupet | ||||||
Booth [15] | CA < 30 mmHg and/or non-propagating ≥30 % | 26 | 38 | Nissen | 56 Fr | Yes | 1 year | No difference in prevalence of new onset of worsened dysphagia |
26 | 37 | Toupet | ||||||
Shaw [18] | CA < 40 mmHg and/or failed peristalsis >40 % | 14 | 36 | Nissen | 52 Fr | Yes | ~5 years | IEM: 14 % (Nissen) vs. 0 % (Toupet) |
11 | 39 | Toupet | ||||||
Patti [17] | mean CA ≤ 40 mmHg | 55 | 67 | Nissen | 56 Fr | Yes | Mean 70 months | IEM: 9 % (Nissen) vs. 8 % (Toupet) |
141 | – | Toupet | ||||||
Chrysos [16] | CA <35 mmHg | 14 | – | Nissen | No | Yes | 1 year | IEM: 14 % (Nissen) vs. 16 % (Toupet) |
19 | – | Toupet | ||||||
Wetscher [13] | CA <30 mmHg or simultaneous or interrupted >10 % | – | 17 | Nissen | 58–60 Fr | Yes | Median 15 months
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