This study shows several pathologic abnormalities in the gastric tissue in some patients with refractory gastroparesis. An inflammatory infiltrate was present in nearly half of the patients with diabetic gastroparesis. There was a reduction in nerve cell bodies in both idiopathic and diabetic gastroparesis. A reduced number of ICCs were found in the myenteric plexus. Thus, histologic abnormalities in gastroparesis are heterogeneous and include myenteric inflammation, decreased innervation, and reduction of ICCs.

Our hypothesis states that variceal pressure and wall tension increase dramatically during esophageal peristaltic contractions. This increase in pressure and wall tension is a natural consequence of the anatomy and physiology of the esophagus and of the esophageal venous plexus. The purpose of this study was to evaluate variceal hemodynamics during peristaltic contraction. A simultaneous ultrasound probe and manometry catheter was placed in the distal esophagus in nine patients with esophageal varices. Simultaneous esophageal luminal pressure and ultrasound images of varices were recorded during peristaltic contraction. Maximum variceal cross-sectional area and esophageal luminal pressures at which the varix flattened, closed, and opened were measured. The esophageal lumen pressure equals the intravariceal pressure at variceal flattening due to force balance laws. The mean flattening pressures (40.11 Ϯ 16.77 mmHg) were significantly higher than the mean opening pressures (11.56 Ϯ 25.56 mmHg) (P Յ 0.0001). Flattening pressures Ͼ80 mmHg were generated during peristaltic contractions in 15.5% of the swallows. Variceal cross-sectional area increased a mean of 41% above baseline (range 7-89%, P Ͻ 0.0001) during swallowing. The peak closing pressures in patients that experience future variceal bleeding were significantly higher than the peak closing pressures in patients that did not experience variceal bleeding (P Ͻ 0.04). Patients with a mean peak closing pressure Ͼ61 mmHg were more likely to bleed. In this study, accuracy of predicting future variceal bleeding, based on these criteria, was 100%. Variceal models were developed, and it was demonstrated that during peristaltic contraction there was a significant increase in intravariceal pressure over baseline intravariceal pressure and that the peak intravariceal pressures were directly proportional to the resistance at the gastroesophageal junction. In conclusion, esophageal peristalsis in combination with high resistance to blood flow through the gastroesophageal junction leads to distension of the esophageal varices and an increase in intravariceal pressure and wall tension. esophageal varices; simultaneous ultrasound and manometry; variceal bleeding ESOPHAGEAL VARICEAL BLEEDING occurs when an expanding force within the varix exceeds the maximum wall tension. Wall tension is an inwardly directed force opposing an outwardly directed expanding force. Wall tension can be calculated by the Laplace equation. The Laplace equation (WT ϭ p v Ϫ p e ϫ r/w) states that the wall tension (WT) is equal to the transmural pressure difference (p v Ϫ p e ) (where p v is the intravariceal pressure and p e is the esophageal lumen pressure) times the radius of the varix (r) divided by the wall thickness (w). Thus this force is directly proportional to the transmural pressure difference and the radius of the varix and inversely proportional to the wall thickness of the varix.No methods are presently available that can measure variceal pressures during a peristaltic contraction of the e...

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