Payer status is related to differences in access and outcomes of abdominal aortic aneurysm repair in the United States.

BACKGROUND: The hypothesis of this study was that differences exist among patients with private insurance compared with patients with Medicaid or no insurance, regarding access to the timely treatment of abdominal aortic aneurysms (AAAs) and the outcomes of AAA repair. METHODS: The study comprised 5363 patients aged less than 65 years (mean age, 59 years) with a diagnostic code for intact or ruptured AAA and a procedure code for AAA repair in the National Inpatient Sample for 1995 to 2000. Dependent variables included ruptured AAA, intact AAA, and in-hospital postoperative mortality rates. Independent variables included payer status, median income, race, gender, age, and comorbid disease. Risk-adjusted analyses were performed with the use of binary logistic regression. RESULTS: AAA rupture was most likely (P <.001) to affect patients with no insurance (36%) or Medicaid (18%), compared with patients with private insurance (13%). After an adjustment for case-mix had been made, data showed that patients without insurance had an increased risk of rupture compared with patients with private insurance (odds ratio, 2.3; 95% CI, 1.5-3.5; P <.001). Operative mortality rates after elective AAA repair were greater (P =.04) for patients with no insurance (2.6%) or Medicaid (2.7%), compared with patients with private insurance (1.2%). Similarly, operative mortality rates for AAA repair after rupture were greater (P =.001) in patients without insurance (45.3%) or Medicaid (31.3%), compared with patients with private insurance (26.2%). CONCLUSIONS: Uninsured patients more often seek treatment of ruptured AAAs compared with patients with private insurance. Operative mortality rates in uninsured patients are greater for elective and emergent AAA repair. These data support the tenet that payer status is associated with mortality rates after AAA repair.

Peripheral nerve transplantation: the role of chemical acellularization in eliminating allograft antigenicity.

This study tests the hypothesis that a chemically acellularized peripheral nerve allograft is as immunologically inactive as a peripheral nerve isograft. Cellular and acellular sciatic nerves were transplanted from BALB/c into C57BL/6 mice. C57BL/6 sciatic nerves were also transplanted into C57BL/6 recipients as isograft controls. Fourteen days post-transplantation, recipient splenocytes were isolated, stimulated with donor alloantigens, and IL-2, IL-4, IL-5, and gamma-IFN production was quantified using the ELISPOT technique. Cellular peripheral nerve allografts stimulated robust Th1 and Th2 systemic immune responses, whereas acellular peripheral nerve allografts elicited a response that is comparable to or lower than that quantified following peripheral nerve isograft transplantation. Chemical acellularization of peripheral nerve allografts dramatically reduces the cellular and humoral immunologic responses. These data indicate that chemically acellularized peripheral nerve constructs are relatively non-antigenic and may be a readily available source of nerve for peripheral nerve reconstruction.