Table 2 Classification of oesophageal motor abnormalities for high-resolution manometry (adapted: original courtesy of John Pandolfino, Sudip Ghosh and Peter Kahrilas)
Diagnostic criteria for oesophageal motility
Normal

  • Normal OGJ pressure (10–35 mm Hg) and relaxation (see below)

  • Peristaltic velocity <8 cm/s in >90% of swallows*

  • Normal elevation of intra-bolus pressure at <8 cm/s to <30 mm Hg in >90% of swallows*

  • Mean distal contractile index (DCI) <5000 mm Hg·s·cm**

Peristaltic dysfunction

    • Mild: 3–6 swallows with failed peristalsis or a >2 cm defect in the 30 mm Hg isobaric contour of the distal oesophageal peristalsis (15 mm Hg in proximal–mid oesophagus)

    • Severe: ⩾7 swallows with either failed peristalsis or a >2 cm defect in the 30 mm Hg isobaric contour of distal oesophageal peristalsis (15 mm Hg in proximal–mid oesophagus)

    • Aperistalsis: Contractile pressure <30 mm Hg throughout mid-distal oesophagus in all swallows (Scleroderma pattern: aperistalsis with LOS pressure <10 mm Hg)

Hypertensive peristalsis

  • Peristaltic velocity <8 cm/s in >80% of swallows

  • Mean distal contractile index (DCI) >5000 mm Hg·s·cm**

    • Hypertensive peristalsis: mean DCI >5000–8000 mm Hg·s·cm

    • Segmental hypertensive peristalsis: hypertensive contraction restricted to mid- or distal oesophagus or LOS after-contraction: mean DCI 5000–8000 mm Hg·s·cm

    • Hypertensive peristalsis ± repetitive or prolonged contraction: DCI >8000 mm Hg·s·cm

Oesophageal spasm (rapidly propagated contractile wavefront)

  • Peristaltic velocity >8 cm/s in ⩾20% of swallows ± raised DCI

    • Diffuse oesophageal spasm: rapid contractile wavefront throughout distal oesophagus

    • Segmental oesophageal spasm: rapid contractile wavefront limited to mid or distal oesophageal segment

Rapid elevation of intra-bolus pressure (increased resistance to flow due to functional or structural obstruction in the oesophagus or at the oesophago-gastric junction (e.g. stricture, post-fundoplication, eosinophilic oesophagitis, poorly coordinated contractions)

  • Rapid elevation of intra-bolus pressure to >15 mm Hg in >8 cm/s in ⩾20% of swallows

    • Mild: Intra-oesophageal bolus pressure (15 to 30 mm Hg) with ⩾80% preserved peristalsis

    • Severe: Intra-oesophageal bolus pressure (>30 mm Hg) with ⩾20% failed peristalsis

Achalasia

  • Impaired deglutative OGJ relaxation and/or opening

  • Elevation of intra-oesophageal bolus pressure due to resistance to flow at OGJ

    • Classic: aperistalsis with no identifiable contractile activity

    • Vigorous: with persistent contractile activity (spasm) or gross elevation of intra-oesophageal bolus pressure with or without oesophageal shortening

    • Variant: with preserved peristalsis in the distal oesophagus in ⩾20% swallows

Abnormal LOS tone

  • Hypotensive: 10 s mean <10 mm Hg with normal peristaltic function

  • Hypertensive: 10 s mean >35 mm Hg with normal peristaltic function and OGJ relaxation

  • *In the original, the pressurisation front velocity (PFV) incorporated both rapidly propagated contractile wavefront (i.e. spasm) and also rapidly rising intra-bolus pressure (indicating increased resistance to flow).

  • **Distal contractile integral (or “contractile volume”) is pressure ×duration×length of contraction in the smooth muscle oesophagus. With SSI equipment, the distal contractile integral is calculated by the Smart Mouse tool in ManoView™ by outlining a space–time box that encompasses the distal peristaltic wave, from the transition zone to the proximal EGJ at the end of peristalsis or at 15 s if no peristaltic wave is noted. The distal contractile integral can then be calculated by multiplying the mean pressure in the space–time box by the length and duration of the space–time box. If this is not available then a peak contractile pressure of 180 mm Hg and 260 mm Hg (± repetitive contractions) should be taken for DCI 5000 and 8000 mm Hg·s·cm respectively.