Intraoperative endoscopic pneumatic testing for gastrojejunal anastomotic integrity during laparoscopic Roux-en-Y gastric bypass.

BACKGROUND: Gastrojejunal anastomotic leaks remain a major source of morbidity following laparoscopic gastric bypass. Intraoperative pneumatic testing has been offered as a method to reduce the incidence of this complication. This study's purpose was to assess the efficacy of intraoperative pneumatic testing during laparoscopic gastric bypass, to evaluate the types of air leaks detected, and to develop an algorithm for management that takes into account air leak categorization and drainage. METHODS: A retrospective analysis was performed on the initial 257 consecutive patients undergoing laparoscopic gastric bypass by a single surgeon over a 36-month period. The gastrojejunostomy was constructed using a linear stapler technique. All patients underwent intraoperative endoscopic pneumatic testing with a clamp applied to the Roux limb. All patients underwent water-soluble upper gastrointestinal radiography on the first postoperative day. RESULTS: Patients were divided based on the pneumatic testing results into groups for data analysis: persistent air leak (group 1), non-reproducible air leak (group 2), and no air leak (group 3). The overall age (41.7+/-9.3 years), body mass index (BMI) (47.3+/-6.4 kg/m2), conversion rate (2%), and length of stay (1.9+/-2.0 days) were not statistically different among groups (p>0.05). In group 1, the air leak site was repaired, and 11 (92%) were drained. In group 2, the air leak site could not be identified, and all 12 (4.7%) were treated by drainage alone. In group 3, drains were placed in 12 (5.2%) due to difficult construction of the gastrojejunostomy. Overall postoperative gastrointestinal leak rate was 0.78%. No postoperative clinical or radiological gastrointestinal leaks occurred within the region tested pneumatically. Intraoperative complications related to pneumatic testing occurred in 1 (0.39%) patient. CONCLUSIONS: Intraoperative pneumatic testing of the gastrojejunal anastomosis is a safe and rapid means of evaluating anastomotic integrity. Application of this technique permitted timely repair of flawed anastomoses, thereby averting potential postoperative leaks.

Laparoscopic transcystic sphincter of Oddi manometry is not affected by carbon dioxide pneumoperitoneum.

Sphincter of Oddi (SO) dysfunction as a potential cause of chronic acalculous cholecystitis (CAC) has not been studied in cases for which intraoperative SO manometry was used during laparoscopic cholecystectomy. In this study, we evaluated the effects of carbon dioxide pneumoperitoneum on laparoscopic transcystic SO manometry. In 27 patients with CAC, transcystic SO manometry had been attempted during laparoscopic cholecystectomy. The mean age of the patients was 46 years (range, 22-71). Complete manometric data sets were obtained in 18 patients. The mean SO pressure, phasic SO pressure, and phasic frequency were 35.4 +/- 29.1 mm/Hg versus 30.8 +/- 23.8 mm/Hg, 104.8 +/- 63.0 mm/Hg versus 73.6 +/- 34.6 mm/Hg, and 2.1 +/- 1.8 contractions/min versus 2.8 +/- 3.4 contractions/min with and without pneumoperitoneum, respectively. All differences were nonsignificant (P > 0.05). Two complications (7.4%) were observed: pancreatitis and jaundice. SO manometry is not affected by CO2 pneumoperitoneum. It may be used to study SO motility in patients with CAC.

Railway train versus motor vehicle collisions: a comparative study of injury severity and patterns.

OBJECTIVE: This study compares the demographics, injury severity, resource use, and injury patterns of patients involved in railway train-motor vehicle (RT-MV) to motor vehicle-motor vehicle (MV-MV) collisions. METHODS: Retrospective trauma registry review of 74 RT-MV and 1,931 MV-MV consecutive patients, age more than 14 years, presenting to two Level I trauma centers, January of 1991 to May of 1998. RESULTS: Compared with MV-MV, RT-MV had significantly more males (72% vs. 54%), higher mortality (15% vs. 7%), higher Injury Severity Score (median, 20 vs. 9), longer intensive care unit length of stay (1.7 vs. 0.04 days), and longer hospital length of stay (7.5 vs. 4 days). RT-MV patients had a higher percentage of scalp/facial lacerations; intracranial hemorrhage; hemothorax and pneumothorax; fractures of the rib/sternum, upper extremity, skull, and face; and lung, splenic, and renal injuries. After adjusting for the difference in Injury Severity Score between groups, the only remaining significant group difference was the odds of a scalp/facial laceration. CONCLUSION: RT-MV collisions are a marker for more severe injuries, but not a different pattern of injury, compared with MV-MV collisions.

Impairment of blood volume restitution after large hemorrhage: a mathematical model.

A mathematical model tests possible mechanisms for the progressive failure of blood volume restitution seen after larger hemorrhages ( > 26%) with increasing changes in plasma osmolality. After 10% hemorrhage, the model requires a decrease in net hydrostatic capillary pressure, the release of solute into the extracellular space, and the release of Na+ and K+ from a bound pool in equilibrium with the interstitium to match the experimental data. The solute and released cations expand the interstitium to drive the restitution of volume and protein from 3 to 24 h. After 30% hemorrhage, the best prediction of the average experimental responses occurs when the Na(+)-K(+)-adenosinetriphosphatase (ATPase) in the cell membrane is inhibited by 38.7% from 0.8 to 3 h, and the proportionality between capillary pressure and blood volume is reduced by 68% from its value for 10% hemorrhage. When the change in plasma osmolality is doubled after 30% hemorrhage, an increase in the inhibition of the ATPase to 85% and extension of its duration to 24 h are necessary to match experimental findings. The associated defect in sodium transport may occur after large hemorrhage so that sodium and water move into cells. This response may oppose osmotically driven expansion of the interstitium and thus account for the failure of restitution.

Hemodynamic and respiratory responses to carotid sinus pressure alteration in experimental hypertension.

The purpose of this study was to determine whether baroreflex control of respiratory responses is diminished in hypertension. Ten dogs were made chronically hypertensive with use of a bilateral renal wrap technique. Eight sham-operated dogs served as normotensive controls. After the development of experimental hypertension, carotid baroreflex control of arterial pressure, heart rate, respiratory frequency, tidal volume, and ventilation was acutely assessed. Under pentobarbital anesthesia and with bilateral vagotomy, the carotid sinuses were isolated and perfused at controlled pressures. Before the carotid sinus region was manipulated, the mean arterial pressure was significantly higher (P < 0.005) in the hypertensive group (146.4 +/- 2.3 mmHg) than in the normotensive group (124.7 +/- 2.6 mmHg). The mean arterial pressures and heart rates measured at every level of carotid sinus pressure were significantly higher in the hypertensive group. Reflex gain of heart rate, but not mean arterial pressure, was significantly reduced in the hypertensive group. Respiratory frequency, tidal volume, and ventilatory responses to changes in carotid sinus pressure were significant and resulted in an approximately 40% reflex change in ventilation. These responses were not diminished in the hypertensive group. We conclude that respiratory baroreflex responses are preserved in experimental hypertension.

Rapid resetting of baroreflexes in hypertensive dogs.

The hypothesis tested was that the rapid resetting of the arterial baroreflex control of arterial pressure in normotension could be demonstrated in experimental hypertension. After the development of experimental hypertension (using a bilateral renal wrap technique), rapid resetting of arterial pressure and heart rate (HR) was acutely assessed under pentobarbital sodium anesthesia in hypertensive and normotensive vagotomized dogs. The carotid sinus area was isolated and perfused at controlled carotid sinus pressures (CSPs). Baroreflex response [mean arterial pressure (MAP) and HR] curves were measured after three carotid sinus conditioning pressures (50, 125, and 200 mmHg) were applied. For the MAP response, the CSPo (CSP at point of maximum reflex gain) increased significantly to the same extent in both groups with increasing conditioning pressures (with 22.2 and 16.7% resetting in the normotensive group, and 20.3 and 14.2% resetting in the hypertensive group). We conclude that short-term adjustments to changes in prevailing pressure (rapid resetting) occur in the arterial pressure response in experimental hypertension to the same extent seen in normotension.