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Introduction: Partial-thickness scalds are the most common pediatric burn injury, and primary management consists of wound dressings to optimize the environment for reepithelialization. Operative intervention is reserved for burns that fail to heal using conservative methods. Worldwide, paraffin-based gauze (Jelonet) is the most common burn dressing; but literature suggests that it adheres to wounds and requires more frequent dressing change that may traumatize newly epithelialized surfaces. Hydrocolloid dressings (DuoDERM) provide an occlusive moist environment to optimize healing and are associated with less frequent dressing changes., Aim: The aim of the study was to retrospectively analyze pediatric burns in a single tertiary referral center over a 10-year period comparing the impact of Jelonet and DuoDERM dressings relative to operative intervention rates., Methods: All pediatric burns admitted between 1997 and 2007 were identified using the Hospital Inpatient Enquiry system. Demographics were collected from hospital records and theater logbooks. Acute, partial-thickness burns in patients younger than 15 years were analyzed according to dressing type applied (Jelonet or DuoDERM)., Results: Two hundred forty-eight pediatric burns were analyzed between 1997 and 2007. One hundred thirty-nine patients were treated with Jelonet dressings, and 109 were treated with DuoDERM. Debridement and grafting were required in 60 (43%) of the Jelonet patients compared with 10 (9%) of the DuoDERM patients (P < .05). The DuoDERM-managed patients maintained a significantly lower graft rate on subanalysis of scalds excluding early grafting within 5 days (P < .001)., Conclusion: Observational evidence suggests that DuoDERM leads to less operative intervention and should be preferentially used in pediatric burns.

The resuscitation of severe burn remains a controversial area within the burn care profession. There is ongoing debate as to what percentage burn is associated with a sufficient quality of life to support initial resuscitation efforts. We conducted a survey of delegates at the 39th Annual Meeting of the British Burns Association (2005), regarding attitudes towards resuscitation following major burns. Respondents were asked the maximum percentage total body surface area (TBSA) burn beyond which they would not wish to be resuscitated. They were also asked what maximum TBSA they perceived to be commensurate with an acceptable quality of life (QOL). One hundred and forty three of 300 delegates responded to the questionnaire. Thirty three percent of respondents would not wish to be resuscitated with 50-75% TBSA burns or greater. A further 35% would not wish to have life-sustaining intervention with 75-95% TBSA burns or greater. The remaining 32% indicated that they would not want resuscitation with TBSA burns>95%. Regardless of TBSA affected, 16% would not wish resuscitation if they had full thickness facial burns, a further 10% did not want resuscitation if both their hands and faces were affected. Our survey demonstrates the diversity of personal preference amongst burn care professionals. This would suggest that a unifying philosophy regarding the resuscitation of extensive burns will remain elusive.

Although it is established that post-injury immune dysfunction involves alterations in T-cell function, the effects of injury on T-cell function in vivo are poorly understood. This study uses a mouse injury model and an antigen immunization approach to investigate the influence of injury on antigen-specific T-helper cell function. We report here that injury triggered a significant reduction in antigen-specific T-helper-1 (Th1)-dependent IgG2a antibody formation, while IgM, IgG1, and IgE production was unchanged. In addition, injury caused a reduction in cytokine production (IL-2, IFNgamma and IL-10) by antigen-stimulated T-cells. We also demonstrate that interleukin 12 (IL-12), a cytokine that promotes Th1 cell differentiation, restored IgG2a antibody formation and corrected the injury-induced reduction in antigen-stimulated cytokine production. Taken together, these findings indicate that severe injury induces a dramatic reduction in Th1 cell function in vivo and suggest that therapies designed to restore Th1 cell function may be beneficial to the injured host.

Background: The mechanisms responsible for altered T-cell responses and cytokine production after injury are not well understood. We used T-cell receptor (TCR) transgenic mice to study burn injury effects on naive versus antigen-activated CD4+ T cells in vivo., Methods: One week after sham or burn injury, lymph node cells were prepared from TCR transgenic mice and stimulated with TCR transgene-specific antigens. T-cell proliferation was measured and culture supernatants were tested for interleukin-2 (IL-2), interferon-gamma (IFN-gamma), IL-4, and IL-10 by enzyme-linked immunosorbent assay (ELISA). Burn injury effects on antigen-activated T cells were studied by immunizing TCR transgenic or wild-type mice at the time of injury., Results: The antigen-stimulated proliferation of native CD4+ T cells was unaffected by burn injury and no increase in T-helper 2 (Th2)-type cytokine production was observed. Instead, burn injury augmented INF-gamma production by naive CD4+ transgenic T cells, and IL-2 production was marginally reduced. Thus, burn injury primed native T cells for an enhanced Th1-type response. In contrast, antigen-specific proliferation, IL-2, and IFN-gamma production by T cells harvested from immunized wild-type mice were suppressed. Unexpectedly, high mortality was observed when burn-injured TCR transgenic mice were immunized., Conclusion: Our results show that burn injury has differential effects on naive and antigen-activated CD4+ T cells and can prime naive CD4+ T cells.

Background: Studies have shown that susceptibility to sepsis after severe injury correlated with reduced production of T-helper 1 (Th1) cytokines (interleukin-2 [IL-2] and interferon-gamma [IFN-gamma]) and a persistence of T-helper 2 (Th2) cytokines (IL-4 and IL-10). The mechanisms responsible for this effect are not clear. We used a T-dependent antigen to study both the effect of burn injury on antigen-specific Th functions in vivo and the effect of anti-IL-10 antibody on these functions., Methods: Male A/J mice were anesthetized and given a 25% scald burn or a sham burn. On day 0 all mice were immunized with 100 micrograms trinitrobenzene sulfonic acid (TNP) haptenated ovalbumin (TNP-OVA) in complete Freund's adjuvant. Mice (10 per group) were given 250 micrograms monoclonal rat antimurine IL-10 antibody (anti-IL-10 MAB) or control rat immunoglobin G (IgG) on day 0 and 100 micrograms anti-IL-10 MAB or IgG on day 2. On day 10 the mice were killed to obtain serum and spleen cells. TNP-specific serum antibody isotype titers were determined by enzyme-linked immunosorbent assay (ELISA). Splenocyte proliferation and cytokine-production in response to TNP-OVA or to anti-CD3 MAB were determined by tritiated thymidine incorporation and by ELISA, respectively., Results: Burn injury resulted in depressed levels of the TNP-specific IgG2a antibody isotype (Th1 dependent), whereas TNP-specific IgG1 and IgE (Th2 dependent) levels were not decreased in burn versus sham burn mice. Anti-IL-10 MAB but not IgG restored the IgG2a response. Burn injury also resulted in reduced TNP-OVA-specific proliferation of splenocytes, whereas anti-CD3 proliferation was equivalent in burn and sham mice. TNP-OVA-specific IL-2 and IFN-gamma production were significantly reduced by burn injury. Anti-IL-10 MAB restored TNP-OVA-specific proliferation and antigen-specific IL-2 and interferon-gamma production by splenocytes from burn mice., Conclusions: Burn injury induces the loss of antigen-specific Th1 cell function, and IL-10 acts as a trigger to down-regulate Th1 activity after injury.

Background: Preliminary studies in this laboratory have shown that treatment with interleukin-12 (IL-12), a cytokine that induces expression of the T-helper-1 lymphocyte phenotype, in an animal model of burn injury increased survival after a septic challenge. The purpose of this study was to define the efficacy of IL-12 therapy and to explore its mechanism of action., Methods: Adult male A/J mice were subjected to 25% full-thickness scald or sham burn. Starting on day 3 after burn, groups of mice received five daily injections of IL-12, interferon-gamma (IFN-gamma), or saline solution. Some animals received anti-IFN-gamma monoclonal antibody. At day 10 most animals underwent cecal ligation and puncture (CLP) and were observed for survival. Some animals were killed at day 10, and CD4-enriched splenocytes were stimulated with anti-CD3 antibody or concanavalin A and were studied for cytokine production and mRNA expression., Results: IL-12 treatment, 25 ng daily for 5 days, increased survival of the burn group after CLP to that of the sham burn control group. Anti-IFN-gamma antibody, 500 micrograms, administered 1 day before IL-12 treatment, reduced the efficacy of IL-12. IFN-gamma treatment, 7000 units, moderately increased survival. IL-12 had no effect on survival of the sham burn group. At the time of CLP IL-12 therapy had induced a marked decrease in CD4+ lymphocyte IL-4 and a moderate increase in IFN-gamma production and mRNA expression without affecting IL-2., Conclusions: IL-12 is the most effective therapy so far tested in this burn plus CLP model. It acts at least in part through IFN-gamma. However, IFN-gamma therapy was not as effective as IL-12.