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Background: Damage control surgery (DCS) and treatment of abdominal compartment syndrome have had major impacts on care of the severely injured. The objective of this study was to see whether advances in critical care, DCS, and recognition of abdominal compartment syndrome have improved survival from penetrating abdominal injury (PAI)., Methods: The care of 250 consecutive patients requiring laparotomy for PAI (1997-2000) was reviewed retrospectively. Organ injury patterns, survival, and use of DCS and its impact on outcome were compared with a similar experience reported in 1988., Results: Two hundred fifty patients had a positive laparotomy for PAI. Twenty-seven (10.8%) required abdominal packing and 45 (17.9%) did not have fascial closure. Seven (2.8%) required emergency department thoracotomy and 21 (8.4%) required operating room thoracotomy. Two hundred seventeen (86.8%) survived overall. Small bowel (47.2%), colon (36.4%), and liver (34.4%) were most often injured. Mortality was associated with the number of organs injured (odds ratio, 1.98; 95% confidence interval, 1.65-2.37; p < 0.001). Vascular injury was a risk factor for mortality (p < 0.001), as was need for DCS (p < 0.001), emergency department thoracotomy (p < 0.001), and operating room thoracotomy (p < 0.001). Seventy-nine percent of deaths occurred within 24 hours from refractory hemorrhagic shock. DCS was used in 17.9% (n = 45) versus 7.0% (n = 21) in 1988, with a higher survival rate (73.3% vs. 23.8%, p < 0.001). DCS was associated with significant morbidity including sepsis (42.4%, p < 0.001), intra-abdominal abscess (18.2%, p = 0.009), and gastrointestinal fistula (18.2%, p < 0.001)., Conclusion: Penetrating abdominal organ injury patterns and survival from PAI have remained similar over the past decade. Death from refractory hemorrhagic shock in the first 24 hours remains the most common cause of mortality. DCS and the open abdomen are being used more frequently with improved survival but result in significant morbidity.

While gamma/delta T cells are involved in host defense and immunopathology in a variety of infectious diseases, their precise role is not yet clearly defined. In the absence of gamma/delta T cells, mice die after infection with a dose of Listeria monocytogenes that is not lethal in immunologically intact animals. Morbidity might result from insufficient levels of cytokines normally produced by gamma/delta T cells or conversely from an excess of cytokines due to a lack of down-regulation of the inflammatory response in the absence of gamma/delta T cells. Consistent with a regulatory role, we found that systemic levels of proinflammatory cytokines (interleukin-6 [IL-6], IL-12, and gamma interferon [IFN-gamma]) were significantly higher in the absence of gamma/delta T cells during the innate phase of the response. Using combinations of genetically altered and immunodepleted mice, we found evidence for gamma/delta T-cell-mediated regulation of IFN-gamma production by multiple cell types of both lymphoid and myeloid lineages. The antigen-specific alpha/beta T-cell response that followed the exaggerated innate response was also increased in gamma/delta T-cell-deficient mice. These findings are consistent with an emerging picture from a variety of immune response models of a critical role for gamma/delta T cells in down-modulation of the immune response.