Faculty Bibliography

Of the patients with penetrating neck wounds treated between 1979 and 1986, 61 patients with 65 injuries had arteriography during their evaluation. Twenty-seven patients had stab wounds and 34 had gunshot wounds, with a relatively equal distribution between the zones of injury. Fifty-seven arteriograms were normal and six were abnormal. Of the six arteriographic defects, three were thought to be spurious on subsequent review, two were clinically insignificant, and one required surgery. No significant arterial injuries were identified by arteriography in the absence of suggestive physical findings. No major arterial injuries were discovered during neck surgery that were missed preoperatively. Neither abnormal nor normal angiograms significantly altered the course of management, including the approach to neck exploration. These data suggest that arteriography for penetrating neck trauma is usually unnecessary for observation of patients in stable condition without suggestive physical findings. Thorough neck exploration with dissection of the carotid sheath in patients with physical diagnostic criteria for surgery eliminates the need for angiography in most cases and avoids the consequences of a possible false-negative study

During the past 15 years, we have employed a modified classification and management plan to treat infections involving nonaortic peripheral arterial prosthetic grafts (PAPGs) without graft removal whenever possible. Sixty-eight infected wounds potentially involving PAPGs were initially treated by excision of necrotic and infected wound tissue in the operating room (wound excision). This was sufficient for all 34 minor infections that did not directly involve the graft. In the 34 remaining infected wounds with graft involvement (major infections), partial removal of a PAPG in 13 cases allowed preservation for up to 15 years of a functioning arterial segment and its collaterals. Ten other grafts were entirely saved. Only 11 of 34 major graft infections ultimately required total graft removal. This approach to infection complicating PAPGs resulted in only two deaths (6%) and directly led to limb loss or amputation at a higher level in eight patients (24%). Total removal of an infected PAPG is often unnecessary and may increase mortality and morbidity

Cost factors are an increasingly important aspect of medical care. In the United States, more than 150,000 patients per year have limb-threatening ischaemia due to infrainguinal atherosclerosis. We studied the economic impact of this disease process and its treatment in 313 consecutive patients seen at our hospital between 1979 and 1981. Minimum follow-up was 3 years. Seventy-nine percent of our patients undergoing revascularisation attempts had limb salvage with full function at 1 year and 60% had full function at 3 years. Of the patients who died, 85% died with their limbs intact. The mean patient cost for all 289 arterial reconstructions was $26,194 +/- $876 S.E. ($23,026 +/- $1117 for 166 femoropopliteal bypasses; $30,380 +/- $1349 for 123 distal bypasses). The mean length of stay (LOS) for the reconstruction group was 50 days. In this patient population, the following adverse risk factors were present: Gangrene or necrosis in the foot (72%), age more than 70 (56%), and previous vascular surgery (21%). A significantly higher cost was associated with each of these factors (gangrene, $32,653 +/- $1534; age greater than 70, $28,089 +/- $1235; previous bypass, $29,666 +/- $1962). During the same time period, initial patient costs for 24 patients undergoing primary below-knee amputation and rehabilitation were $27,225 +/- $2896 S.E. Twenty-nine percent of the patients with below-knee amputations never walked again. The nonambulatory patients had a significant continuing expenditure for institutionalisation ($100/day) or home care ($270/week). These facts document the high cost of limb-threatening arteriosclerosis and its treatment by vascular reconstruction or primary below-knee amputation.(ABSTRACT TRUNCATED AT 250 WORDS)

Immunologic, morphologic, and functional evaluations were performed in beagle dogs with single lung allografts surviving 3-13 years after transplantation. Immunosuppressive treatment included lethal total-body irradiation, autologous bone marrow reconstitution, and three doses of methotrexate. Three beagle recipients with full DLA-haplotype-matched grafts and five recipients with one-haplotype-mismatched grafts were studied. Evidence of rejection--i.e., infiltrates on chest roentgenograms, hypoperfusion on radionuclide lung scans, and histopathologic changes--were absent in the matched recipients and in three of the five mismatched recipients. Two of the mismatched recipients had decreased perfusion to their allografted lungs, and open-lung biopsy specimens revealed diffuse fibrotic blood vessels with narrowed lumina but no other abnormalities. Decreased fractional blood flow to the lung allograft of the five one-haplotype-mismatched recipients was correlated (r = -0.92) with the level of donor-specific cytolytic lymphocyte activity generated in mixed lymphocyte cultures (MLC). In contrast, the level of proliferative activity in donor-specific MLC did not correlate well with graft function. These findings suggest that the mechanism of tolerance to these lung allografts (with particular regard to vascular integrity) involves attenuation of the response against major histocompatibility complex (MHC) class I alloantigen since the induction of cytolytic T lymphocytes in MLC is directed primarily against these molecules. Though all of the mismatched recipients had the ability to react against MHC class II alloantigens in vitro (as demonstrated by proliferative responses in MLC), in vivo responses to class II gene products may not occur because of the lack of expression of these molecules on long-term surviving grafts

Alloreactivity of intragraft and peripheral blood lymphocytes from tolerant canine lung allograft recipients was examined. Tolerance was induced by variable periods of treatment with cyclosporine. Analysis of effector cells from lung allografts (obtained by bronchoalveolar lavage) revealed the absence of specific cytolytic T lymphocyte (CTL) activity and the presence of a low level of cytolytic activity detected in a lectin-dependent cell-mediated cytotoxicity assay. In contrast, high levels of specific CTL activity and lectin-dependent activity were detected in cell preparations from lung allografts undergoing rejection. Tolerant recipients retained normal ability to generate specific CTL activity to third party alloantigens in mixed lymphocyte cultures (MLC) but had diminished ability to generate CTL to donor alloantigens in recipient X donor MLC. Addition of exogenous interleukin 2 to these MLC was unable to restore donor-specific CTL activity. Lymphocytes from tolerant recipients were, however, capable of generating proliferative responses and lectin-dependent cytotoxicity on exposure to donor alloantigens in MLC. Evidence presented in this report suggests that the lectin-dependent cytolytic activity generated in these MLC is mediated by lymphokine-activated killer cells. Such cells are likely to be activated by interleukin 2 released in the proliferative response. The results support the proposal that the cyclosporine-induced tolerant state is characterized by the relative inability to respond against major histocompatibility complex class I antigens in contrast to class II antigens and/or minor histocompatibility antigens since MLC-induced CTL are directed, for the most part, against class I molecules