The vacuum pack is the temporary abdominal wound closure of choice in patients undergoing open abdominal management at our institution. Primary closure is achieved in the majority of patients with a low rate of complication. The technique is simple and easily mastered. Technical complications are rare and easily repaired.

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In severe traumatic injuries to the lower extremity, it is often a difficult decision to attempt heroic efforts aimed at limb salvage or to amputate primarily. To answer this question, the authors performed a 5-year review of 70 limbs in 67 patients. Patients were identified as presenting with major lower extremity trauma and an associated arterial injury. Nineteen (27%) of the 70 limbs were amputated. Limb salvage was not related to the presence or absence of shock and order of repair (orthopedic or vascular). No statistical difference was noted between the time of injury to operative repair in either the amputated or limb salvage group. Limb salvage was related to warm ischemia time and the quantitative degree of arterial, nerve, bone, muscle, skin, and venous injury. A limb salvage index (LSI) was formulated based on the degree of injury to these systems. All 51 patients with an LSI score of less than 6 had successful limb salvage (p less than 0.001). All 19 patients with an LSI score of 6 or greater had amputations (p less than 0.001). Although statistics cannot replace clinical judgment, this index can be a valuable objective tool in the evaluation of the patient with a severely traumatized extremity.

The data presented indicate that in experimental infections of the mouse cornea, toxin A of Pseudomonas aeruginosa contributes to the organism's pathogenicity, whereas active elastase may not be required. After traumatization, corneas were infected with wild-type parental toxin A-producing strains, two toxin A-deficient mutants (Tox-), or an elastase mutant. The infections produced by both Tox- mutants were less severe than infections produced by their parental strains. Furthermore, the Tox- mutants were not able to persist in the eyes as long as their parental strains. Addition of subdamaging doses of exogenous toxin A to eyes infected with the Tox- mutant PA103-29 significantly increased is virulence. The course of infection and the resulting corneal damage produced by the elastase mutant were indistinguishable from those of its parental strain.

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The human CD80 costimulatory molecule is an important signal between professional antigen-presenting cells and T helper cells. The immunobiology of CD80 expression by keratinocytes, especially during allergic and irritant contact dermatitis, however, is less well understood. CD80 cell surface expression and gene transcription by keratinocytes was increased when keratinocytes were exposed to certain allergens (chemicals that induce inflammation via hapten-specific T cells) and irritants (chemicals that are toxic to epidermal cells). Therefore, the human CD80 promoter was cloned and luciferase reporter constructs containing various promoter fragments were engineered. Promoter mapping of these CD80 constructs in transiently transfected keratinocytes showed that a construct containing the proximal 231 bp immediately upstream of the transcription start site of the CD80 promoter was most active in keratinocytes and was inducible to a level ranging from 2- to 10-fold higher in keratinocytes treated with certain allergens and irritants, compared with untreated keratinocytes. This pattern of promoter fragment activity in keratinocytes is identical to that found in professional antigen-presenting cells. This is the first demonstration that the CD80 promoter is active in keratinocytes and that this activity is further increased in keratinocytes treated with certain allergens and irritants. These data suggest that allergens and irritants may, in part, break peripheral tolerance by their direct effects on keratinocyte costimulatory molecule expression, thereby facilitating interactions with epidermotropic T helper cells via the CD80-CD28 or CTLA-4 pathways.