Search

Background Gastroparesis is characterized by delayed gastric emptying without mechanical obstruction, but remains difficult to diagnose and distinguish from other gastrointestinal (GI) disorders. Gastroparesis affects the gastric slow wave, but non-invasive assessment has been limited to the electrogastrogram (EGG), which reliably characterizes temporal dynamics but does not provide spatial information. Methods We measured gastric slow wave parameters from the EGG and magnetogastrogram (MGG) in patients with gastroparesis and in healthy controls. In addition to dominant frequency (DF) and percentage power distribution (PPD), we measured the propagation velocity from MGG spatiotemporal patterns and the percentage of slow wave coupling (%SWC) from EGG. Key Results No significant difference in DF was found between patients and controls. Gastroparesis patients had lower percentages of normogastric frequencies (60 ± 6% vs 78 ± 4%, p < 0.05), and higher brady (9 ± 2% vs 2 ± 1%, p < 0.05) and tachygastric (31 ± 2% vs 19 ± 1%, p < 0.05) frequency content postprandial, indicative of uncoupling. Propagation patterns were substantially different in patients and longitudinal propagation velocity was retrograde at 4.3 ± 2.9 mm/s vs anterograde at 7.4 ± 1.0 mm/s for controls (p < 0.01). No difference was found in %SWC from EGG. Conclusions & Inferences Gastric slow wave parameters obtained from MGG recordings distinguish gastroparesis patients from controls. Assessment of slow wave propagation may prove critical to characterization of underlying disease processes. Future studies should determine pathologic indicators from MGG associated with other functional gastric disorders, and whether multichannel EGG with appropriate signal processing also reveals pathology.

Our objective was to execute a prospective cohort study to determine relationships between plasma mtDNA DAMP levels and the occurrence of systemic inflammatory response syndrome (SIRS), multiple organ dysfunction syndrome (MODS), and mortality.Mitochondrial DNA damage-associated molecular patterns (DAMPs) accumulate in the circulation after severe injury. Observations in animal models demonstrate that mtDNA DAMPs contribute to organ dysfunction; however, the link between plasma mtDNA DAMPs and outcome in severely injured human subjects has not been established.DNA was isolated from plasma samples taken from severely injured patients at hospital days 0, 1, and 2. Real-time PCR was used to quantify selected ≈200 base pair sequences of mtDNA within the COX1, ND1, and ND6 genes, as well as from the D-Loop transcriptional regulatory region. MODS was defined as a Denver Multiple Organ Failure score of 4 or greater.MtDNA DAMPs were quantified as PCR threshold cycle number. Lower threshold cycles indicate increased mtDNA DAMP content. Patients with SIRS had significantly increased mtDNA DAMP levels in all 4 sequences examined (32.14 ± 0.90 vs 29.00 ± 1.15 for COX1, 31.90 ± 0.47 vs 30.16 ± 1.42 for ND1, 32.40 ± 0.61 vs 28.94 ± 1.13 for ND6, and 33.12 ± 0.83 vs 28.30 ± 1.14 for D-Loop). Patients who developed MODS also had elevated mtDNA DAMP levels compared with those who did not (32.57 ± 0.74 vs 27.12 ± 0.66 for COX1, 32.45 ± 0.65 vs 28.20 ± 0.73 for ND1, 32.52 ± 0.56 vs 27.60 ± 0.79 for ND6, and 32.85 ± 0.75 vs 27.86 ± 1.27 for D-Loop). Patients with above-median mtDNA DAMP levels had a significantly elevated relative risk for mortality. Four patients died secondary to severe MODS.These findings comprise the first observational evidence that plasma mtDNA DAMPs is associated with the evolution of SIRS, MODS, and mortality in severely injured human subjects.

The magnetogastrogram records clinically relevant parameters of the electrical slow wave of the stomach noninvasively. Besides slow wave frequency, gastric slow wave propagation velocity is a potentially useful clinical indicator of the state of health of gastric tissue, but it is a difficult parameter to determine from noninvasive bioelectric or biomagnetic measurements. We present a method for computing the surface current density (SCD) from multichannel magnetogastrogram recordings that allows computation of the propagation velocity of the gastric slow wave. A moving dipole source model with hypothetical as well as realistic biomagnetometer parameters demonstrates that while a relatively sparse array of magnetometer sensors is sufficient to compute a single average propagation velocity, more detailed information about spatial variations in propagation velocity requires higher density magnetometer arrays. Finally, the method is validated with simultaneous MGG and serosal EMG measurements in a porcine subject.

Gastric slow waves propagate in the electrical syncytium of the healthy stomach, being generated at a rate of approximately three times per minute in a pacemaker region along the greater curvature of the antrum and propagating distally towards the pylorus. Disease states are known to alter the normal gastric slow wave. Recent studies have suggested the use of biomagnetic techniques for assessing parameters of the gastric slow wave that have potential diagnostic significance. We present a study in which the gastric syncytium was uncoupled by mechanical division as we recorded serosal electric potentials along with multichannel biomagnetic signals and cutaneous potentials. By computing the surface current density (SCD) from multichannel biomagnetic recordings, we were able to quantify gastric slow wave propagation as well as the frequency and amplitude of the slow wave and to show that these correlate well with similar parameters from serosal electrodes. We found the dominant slow wave frequency to be an unreliable indicator of gastric uncoupling as uncoupling results in the appearance of multiple slow wave sources at various frequencies in external recordings. The percentage of power distributed in specific frequency ranges exhibited significant postdivision changes. Propagation velocity determined from SCD maps was a weak indicator of uncoupling in this work; we believe that the relatively low spatial resolution of our 19-channel biomagnetometer confounds the characterization of spatial variations in slow wave propagation velocities. Nonetheless, the biomagnetic technique represents a non-invasive method for accurate determination of clinically significant parameters of the gastric slow wave.

The largest series in the literature dealing with redo fundoplication was presented and published in 1999 and included 100 patients. Herein we update this initial series of 100, with 207 additional patients who have undergone redo fundoplication (n = 307).Increasing numbers of patients are failing esophagogastric fundoplication and requiring redo procedures. Data regarding the nature of these failures have been scant.Data on all patients undergoing foregut surgery are collected prospectively. Between 1991 and 2004, 307 patients underwent redo fundoplication for the management of anatomic complications or recurrent GERD. Statistical analysis was performed with multiple chi2 and Mann-Whitney U analyses, as well as ANOVA.Between 1991 and 2004, 1892 patients underwent primary fundoplication for GERD (1734) or paraesophageal hernia (158). Of these, 54 required redo fundoplication (2.8%). The majority of failures (73%) were managed within 2 years of the initial operation (P = 0.0001). The mechanism of failure was transdiaphragmatic wrap herniation in 33 of 54 (61%). In the 231 patients who underwent fundoplication elsewhere, 109 had transdiaphragmatic herniation (47%, P = NS). In this group of 285 patients, 22 (8%) required another redo (P = NS). The majority of the procedures were initiated laparoscopically (240/307, 78%), with 20 converted (8%). Overall mortality was 0.3%.Failure of fundoplication is unusual in experienced hands. Most are managed within 2 years of the initial operation. Wrap herniation has now become the most common mechanism of failure requiring redo. Redo fundoplication was successful in 93% of patients, and most could be safely handled laparoscopically.

Since the first report of laparoscopic Heller myotomy in 1991 by Shimi et al1 and thoracoscopic Heller myotomy by Pellegrini et al2 in 1992, minimally invasive techniques have been increasingly used for the treatment of achalasia. Many surgeons have noticed a distinct change in the referral patterns for treatment of achalasia now that minimally invasive techniques are available. Patti and colleagues3 in 2002 reported that during the past decade, their center at the University of California, San Francisco, saw a marked increase in the number of patients who were referred for laparoscopic Heller myotomy with a corresponding decrease in use of pneumatic balloon dilation or botulinum toxin injection. Laparoscopic Heller myotomy is the preferred treatment at Vanderbilt, and we have previously reported our results and technique.4 A great deal of controversy exists over the appropriate use of antireflux procedures to prevent reflux after myotomy. The arguments for using a partial antireflux procedure with laparoscopic Heller myotomy have been summarized nicely by Peters,5 and the arguments against the routine use of an antireflux procedure were presented by our group during a Society for Surgery of the Alimentary Tract symposium in 2000.6 A recent meta-analysis of laparoscopic Heller myotomy with or without antireflux procedure from 1991 to 2001 was performed by Lyass et al.7 Pathologic acid exposure was identified by 24-hour pH studies in 7.9% of 489 patients who underwent Heller with partial fundoplication. Forty-seven patients who had previously undergone Heller without antireflux procedure were studied with 24-hour pH monitoring and only 4, or 10%, of the 40 patients had pathologic acid exposure. This meta-analysis concluded “based on the reported data in human subjects that no recommendations could be made regarding the efficacy of partial antireflux procedures in protecting against pathologic gastroesophageal reflux (GER) after esophageal Heller myotomy.” We have completed a study that randomized 43 patients with achalasia to Heller myotomy alone or to Heller myotomy plus Dor fundoplication. The study was designed as a double-blind, parallel-group randomized trial to test the null hypothesis that the addition of Dor fundoplication will not alter the incidence of pathologic GER in these patients.

The basic electrical rhythm (BER) of the intestine is known to decrease during mesenteric ischaemia. Some studies have reported the relationship between the BER and the pathologic changes that occur in the bowel during vascular injury. However, these changes have not been completely elucidated. This study describes the histopathologic pattern when the rabbit small intestine was subjected to ischaemia of varying time lengths (30 – 150 minutes) and subsequent reperfusion for six hours. Intestinal biopsies were taken at baseline, at the end of ischaemia, and at hourly intervals during reperfusion. Microscopic examination of the biopsies revealed evidence of progressive infarction of the mucosa during ischaemia. There was an acute worsening of the pathology during reperfusion, the severity being greater when reperfusion was preceded by longer periods of ischaemia. These changes were statistically significant. The observed pattern in this study shows clearly that reperfusion injury is reflected in the histopathologic response and that this is worse in severity than the response to ischaemia. Studies of longer duration should further clarify the picture during recovery in ischaemia/reperfusion injuries of the bowel. Keywords: Mesenteric, Ischaemia, Reperfusion, Pathology. Resume Le rythme electrique normal (Basic Electrical Rhythm, BER) de l'intestin diminue pendant la deficience de sang. Quelques etudes ont releve une relation entre le rythme electrique normal (BER) et les changements pathologiques qui se produisent dans la cavite intestinale lors de l'injurie vasculaire. Neanmoins ces changements n'ont pas ete completement elucides. Cette etude decrit le type histopathologique quand l'intestin grele du cobaye etait soumis a la deficience pendant un temps varie (30 – 150mn) et la reperfusion subsequent de six heures. Les biopsies intestinales etaient portees a la baseline a la baseline a la fin de la deficience et a intervals d'une heure durant la reperfusion. L'examen microscopique des biopsies revele l'evidence d'infarction progressive de muchose durant la deficience. Il y avait une detoriation accrue de la pathologie durant la reperfusion la severite etait plus grande que quand la reperfusion etait precedee par une plus longue periode de deficience. Ces changement etaient significants statistiquement. Le model observe dans cette montre clairement que l'injurie de reperfusion est reflectee dans la reponse histopathologique et que ca s'empire en severite que dans la reponse a la deficience. Les etudes d'une duree plus longue peuvent clarifier l'image durant le retablissement de l'injurie de la deficience reperfusion de la cavite intestinale. West African Journal of Medicine Vol.22(1) 2003: 59-62