Conservative observational management with selective delayed repair for large abdominal aortic aneurysms in high risk patients.

AIM: Abdominal aortic aneurysms (AAAs) larger than 5.5 cm should generally undergo elective repair. However, some of these patients have serious comorbid conditions, which greatly increase operative risk. This study evaluated the outcomes of nonoperative, observational management and selective delayed AAA repair in high-risk patients with large infrarenal and pararenal AAAs. METHODS: Among 226 patients with AAAs >5.5 cm, we selected 72 with AAAs 5.6-12.0 cm (mean 7.0 cm) for periods of nonoperative management because of their prohibitive surgical risks. Comorbid factors included a low ejection fraction of 15-34% (mean 22%) in 18 patients; FEV1 <50% (mean 38%) in 25; prior laparotomy in 10; and morbid obesity in 22. Follow-up was complete in the 72 patients for the 6-76 months (mean 23 months) that they were treated nonoperatively. Fifty-three patients ultimately underwent repair because of AAA enlargement or onset of symptoms after 6-72 months (mean 19 months) of observational treatment. RESULTS: Of the 72 selected patients, 54 (75%) are living and 18 (25%) are dead. Seven patients undergoing only nonoperative treatment presently survive after 28-76 months (mean 48 months). Of the 18 deaths, AAA rupture occurred in only 3 patients (4%) who had been observed for 12, 31, and 72 months before rupture. Nine other deaths (13%) occurred after 6-72 months from comorbidities unrelated to the patient's AAA. Six of the 53 patients undergoing delayed AAA repair died within 30 days of operation (11% mortality). The mortality for the 154 good risk AAA patients, who underwent prompt open or endovascular repair, was 2.2%. CONCLUSION: These data indicate that some patients with large AAAs and serious comorbidities are acceptably managed for long periods (6-76 months) by nonoperative means. Substantial delays of 12 to 76 months resulted in an AAA rupture rate of only 4%, while 13% of these patients (9 of 72) died of their comorbidities unrelated to AAA rupture or surgery and mortality in this group of patients, when operated on, was 11% (6 of 53). These findings support the selective use of nonoperative observational management in some patients with large AAAs and serious comorbidities.

Hemorrhage exacerbates bacterial translocation at low levels of intra-abdominal pressure.

BACKGROUND: It has been shown previously that the adverse cardiopulmonary sequelae of increased intra-abdominal pressure (IAP) are worsened by hemorrhage and resuscitation. Bacterial translocation (BT) to the mesenteric lymph nodes (MLNs), liver, and spleen has also been shown to occur with increased IAP. OBJECTIVE: To investigate the hypothesis that BT associated with elevated IAP would be significantly increased after hemorrhage and resuscitation. MATERIALS AND METHODS: Anesthetized adult male rats had femoral artery and vein catheters placed, and an intra-abdominal catheter placed to measure IAP. Group 1 underwent surgery only and served as controls. Group 2 had IAP raised to 10 mm Hg by infused lactated Ringer's solution for 40 minutes. Group 3 had a 25% hemorrhage, followed by resuscitation by infused lactated Ringer's solution and shed blood. Group 4 first had a 25% hemorrhage, resuscitated using infused lactated Ringer's solution and shed blood, and then had IAP raised to 10 mm Hg by infused lactated Ringer's solution for 40 minutes. All groups were killed after 2 hours, and had MLNs, liver, and spleen harvested for quantitative cultures. RESULTS: Hemorrhage and resuscitation alone did not increase BT to the MLNs, liver, or spleen. An increase in IAP to 10 mm Hg resulted in a significant level of BT to the MLNs and liver on MacConkey II agar (P<.05), and a significant increase in the level of BT only to the liver on trypticase soy agar with 5% sheep's blood (P<.05). Hemorrhage and resuscitation did increase the level of BT to the liver and spleen when IAP was increased to 10 mm Hg (P<.05). CONCLUSIONS: In this model, hemorrhage and resuscitation alone did not increase BT to the MLNs, liver, or spleen. However, hemorrhage and resuscitation increased BT to the liver and spleen when IAP was increased to 10 mm Hg. This supports the concept that prior hemorrhage and resuscitation exacerbates the effects of increased IAP.