EP.FRI.543 A rare case of acute jejuno-jenual intussusception in a patient with Roux-en-Y bypass secondary to a benign polyp

Introduction Roux-en-Y Gastric bypass (REYGB) amounts for a third of surgical bariatric interventions. Small bowel obstruction (SBO) is a long-term complication in REYGB and can be caused by intussusception of bowel, in approximately 0.5% of procedures. Intussusception in REYBG is mostly attributed to dysmotility. This report demonstrates a rare case of intussusception in REYGB secondary to a benign polyp. Case description A 45 year old female, three years post REYGB, presented to A&E with acute, extreme upper abdominal pain, with three days absolute constipation. She was tender on examination with normal blood tests. CT scan demonstrated small bowel intussusception. Initial concerns were of intussusception of the jejuno-jejunostomy anastomosis causing SBO. She had an exploratory laparotomy, which confirmed intussusception, however this was 20cm distal to the jejuno-jejunostomy. Bowel was gently reduced, and deemed viable. On thorough run-through, a small segment at the transition point, was considered abnormal on palpation. This region was resected and a 1x1cm intraluminal polyp was identified as the causative lead point. The patient did well postoperatively. Discussion Small bowel intussusception in adults is typically attributed to pathological lead point, such as benign or malignant lesions. Intussusception in REYBG is a rare but well-documented cause of intestinal obstruction, usually attributed to dysmotility, secondary to ectopic pacemaker cells particularly around anastomoses. In this case, the intussusception was caused by an unusual pathology separate from the jejuno-jejunal anastomosis. We recommend thorough examination of all adjacent bowel to exclude lesions, in this case a polyp, which could result in recurrence.

Effects of pacing parameters on entrainment of gastric slow waves in patients with gastroparesis

The aim of this study was to investigate the effect of pacing parameters on the entrainment of gastric slow waves in patients with gastroparesis. Four pairs of cardiac pacing wires were placed on the serosal surface of the stomach in 13 patients with gastroparesis. After a baseline recording for 30 min, gastric pacing was performed in a number of sessions with different effective parameters, each lasting for 30 min. The following parameters were found to be effective for the entrainment of the gastric slow wave: a pacing frequency 10% higher than the intrinsic gastric slow wave frequency (IGF), 300 ms pulse width, and 4 mA pacing amplitude. A reduction of pacing amplitude from 4 to 2 mA and 1 mA reduced the percentage of entrainment of the gastric slow wave to 79 ± 10% and 50 ± 11%, respectively. Pacing with a pulse width of 30 or 3 ms was not able to entrain the gastric slow wave in any of the patients. An ectopic pacemaker of tachygastria found in three patients was reversed with gastric pacing. It was concluded that gastric pacing at a frequency up to 10% higher than the IGF and with an amplitude of 4 mA and a pulse width of 300 ms is able to completely entrain the gastric slow wave and normalize gastric dysrhythmias in patients with gastroparesis.

Vagal-mediated atrial premature beats: a computer model

A computer algorithm is described that used experimental data to model the arrhythmogenic interaction of phasic vagal stimuli and atrial ectopic pacemakers. The model consisted of a dominant sinus node and a single ectopic pacemaker center separated by conducting atrial tissue. Its primary operation was to predict the timing and incidence of atrial premature beats resulting from transient escape of ectopic automatic impulses when vagal-induced entrance block of the sinus impulse was simulated near the ectopic focus. These predictions were based on a series of experimentally derived phase-response and corrected recovery time curves, describing the modulation of ectopic pacemaker periodicity by vagal input and overdrive suppression, respectively. Depending on the combination of curves tested, the model predicted premature beats to develop only with critically timed vagal stimuli. The coupling intervals of vagal-induced premature beats were > 300 ms and varied as a function of vagal timing and sinus cycle length. The model suggests therefore that phasic vagal stimuli within the atrium may transiently protect ectopic pacemaker foci from conducted sinus impulses and mediate the genesis of atrial extrasystoles with long coupling intervals.

Atrial ectopic pacemaker escape mediated by phasic vagal nerve activity

Effects of vagal nerve activity on atrial ectopic pacemaker foci were studied in vitro in strips of rabbit tricuspid valve. Transmembrane potentials were recorded from pacemaker and working atrial fibers superfused with Tyrode solution containing propranolol. Tissues were paced from the atrial muscle end at cycle lengths of 90, 70, or 50% of the intrinsic pacemaker cycle, and postganglionic vagal nerve endings were stimulated with brief trains of pulses (200 Hz; 100-200 microseconds) through a second electrode near the pacemaker. Vagal trains scanning diastole hyperpolarized pacemaker and surrounding fibers to a maximum membrane potential of -74.7 +/- 1.8 mV (normal maximum diastolic potential = -75.5 +/- 1.6 mV) and elicited a period of inexcitability lasting 217.9 +/- 27.3 ms (drive cycle = 90% of pacemaker cycle). Inexcitability was evident at critical diastolic intervals where vagal input prevented atrial impulses from activating the pacemaker allowing spontaneous discharges to occur, i.e., escape, late in diastole. Besides inexcitability, incidence and timing of escape impulses were determined by cumulative effects of drive cycle length, vagal stimulus, and subthreshold electrotonic input on intrinsic pacemaker cycle. These data suggest that phasic vagal stimuli may transiently protect atrial ectopic pacemaker foci from conducted sinus impulses by rendering pacemaker and surrounding fibers inexcitable. In the setting of a long sinus (drive) cycle length, phasic vagal activity may result in spontaneous discharges manifest as late atrial premature beats.