Results of a prospective multicenter trial evaluating the ePTFE peritoneal onlay laparoscopic inguinal hernioplasty.

A 2.8-year prospective multicenter trial was conducted to evaluate the ePTFE peritoneal onlay laparoscopic inguinal hernioplasty. A total of 441 inguinal hernias were repaired in 351 patients (326 male; 25 female). Two hundred twenty-six of the hernias were direct, 185 indirect, 4 femoral, 26 pantaloon, 90 bilateral, and 92 recurrent. Standardized data collection forms were used and submitted for centralized data analysis. For the hernioplasty, Cooper's ligament was exposed and an 8 cm x 12 cm x 1 mm GORE-TEX Soft Tissue Patch was stapled circumferentially to Cooper's ligament and the endoabdominal fascia. Patients were followed at 1 week, 6 months, 1 year, and then annually. Three-month intervals were used as needed. There was a mean follow-up of 447 days, with 21% of the total repairs followed for more than 2 years and 56% for more than a year. The overall follow-up rate was 95.5%. The operative and postoperative complication rates were 0.45% and 8%, respectively. There were 17 recurrent hernias (3.8%). The range of experience among the investigators was 13 to 168 hernioplasties. With the completion of 25 cases per investigator, the recurrence rate fell to 0.39%. Postoperative analgesia averaged a 24-hr supply of medication; 12.2% of patients required no analgesia. Convalescence averaged 5.4 days, and return to work averaged 7.7 days. This multicenter trial demonstrates that the ePTFE laparoscopic peritoneal onlay inguinal hernioplasty is a safe and dependable repair, especially after the initial learning curve is surmounted.

Use of the umbilical vein to study the splanchnic and portal beds in shock and trauma: II. Metabolic studies.

Perumbilical portal vein catheters and arterial and central venous catheters were inserted in 16 patients recovering from trauma or other shock-producing events, and in 5 patients who later developed shock. This permitted serial measurement of blood gases, pH, and the levels of ammonia, lactate and certain other metabolites in all three circulatory systems simultaneously. Nine of the trauma patients were never in shock, had no liver disease or injury and consequently formed a baseline group for comparison with the shock patients. In the shock patients there was a significant degree of hypoxemia in the portal venous blood and an increase in the arterialportal oxygen saturation difference. Their portal venous blood showed a lower pH and a higher pCO(2) than did the portal blood of the patients who had never been in shock. In 3 of the 4 shock patients who died, the total blood lactate showed a greater increase in portal venous than in the arterial or central venous blood. In shock there was also an increase in portal venous blood ammonia which was later accompanied by increments in arterial and central venous blood ammonia. This suggests impairment of hepatic urea synthesis, allowing escape of ammonia through the liver. These phenomena, when added to the finding previously reported of an elevated portal venous pressure in some shock patients, lend support to the hypothesis that in certain cases of shock there is increased impedance to flow of portal blood through the liver with resultant stasis in the portal-splanchnic bed and ischemichypoxic hepatocellular injury.