The recliner position: a new operating position for burn surgery.
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Biomedical subjects
Publications and source records attributed to Stephen M Milner.
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Severe burn causes immunosuppression, and the eschar remains a perfect culture medium for microbial growth. The resulting sepsis is a common complication of burns with a high mortality. The skin produces a number of molecules including antimicrobial peptides (AMPs) that act in the first line of host defense. Previous studies from our laboratory suggested decreased expression of human beta-defensin-2 (HBD-2) in burned wounds. Here, we have expanded our work by identifying HBD-1, HBD-2, HBD-3 and human neutrophil peptide (HNP) in normal and burn skin samples using fluorescence deconvolution microscopy. In normal skin, HBD-1 was localized to the perinuclear region of keratinocytes, while HBD-2 was seen primarily in the stratum basale of the epidermis. HBD-3 was found in dendritic cells of the stratum spinosum. HNP was distributed in a somewhat random pattern in the papillary dermis. In burned skin, in which the epidermis had been destroyed or disrupted, the presence of HBD-1 was localized to dermal glandular structures and hair shafts. HBD-2 was found in both the upper portions of the remaining keratin layers, and localized to lower, f-actin containing, acini-like structures, a pattern also evident with HBD-3. We conclude that although the upper layers of skin are destroyed and disrupted by burn, cells in the lower portions of the skin demonstrate an ability to synthesize most of the AMPs, thereby maintaining some barrier against infection. The results of these studies further contribute to an understanding of the role of AMPs in the pathophysiology of cutaneous burn and the possibility of using these sites for upregulation of AMP synthesis in the prevention of burn sepsis.
It is important to have an accurate understanding of mortality risk in children to make sound treatment decisions and to advise parents and families. Several studies have found that children younger than 4 years are at greater risk for mortality from burn injury than older children, although other studies have found no difference. All of these studies, however, have been limited by small sample sizes from single burn centers. The objective of this study was to assess age-related mortality risk in a sample of more than 12,000 children from a national burn registry who were admitted to 43 burn centers in the United States from 1992 to 2002. The study showed that, compared with older children, children younger than 4 years were significantly more likely to be admitted with scalds rather than flame burns, had smaller burn injuries, and were less likely to have an inhalation injury. Logistic regression analysis was used to assess age-related mortality risk. After adjusting for sex, burn size, inhalation injury, and type of burn (flame versus scald), the risk of mortality was substantially higher for children aged 0 to 1.9 years (odds ratio, 2.70; P<0.001) and for children aged 2.0 to 3.9 years (odds ratio, 2.00; P<0.01) as compared with children aged 4 years or older. This study provides strong evidence that when comparing children based on burn injuries of similar size and etiology, children younger than 4 years are at substantial risk for death as compared with older children.
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Orthogonal polarization spectral imaging (OPS) utilizes the illumination of the tissue with polarized light within the haemoglobin spectrum. We report here on OPS for the assessment of the skin microcirculation non-invasively through the surface of the human burn wound. This allows inspection of individual capillaries of the cutaneous microcirculation and flow through these vessels in real time. Two distinct microcirculatory patterns were seen. Superficial burns had small visible dermal capillaries studied throughout the field of view. The flow of individual erythrocytes through these capillaries was clearly visible in real-time. Conversely, deep burns showed large thrombosed vessel coursing in a criss-cross fashion. There was marked difference between the mean optical densities for normal skin and superficial burns (65.8+/-15.6 and 64+/-14.6, respectively) and deep burns (131.2+/-31.1). These findings indicate that OPS may have utility in the assessment of cutaneous microcirculation in burns.
Sulfur mustard is an alkylating chemical warfare agent that primarily affects the eyes, skin, and airways. Sulfur mustard injuries can take several months to heal, necessitate lengthy hospitalizations, and result in significant cosmetic and/or functional deficits. Historically, blister aspiration and/or deroofing (epidermal removal), physical debridement, irrigation, topical antibiotics, and sterile dressings have been the main courses of action in the medical management of cutaneous sulfur mustard injuries. Current treatment strategy consists of symptomatic management and is designed to relieve symptoms, prevent infections, and promote healing. There are currently no standardized or optimized methods of casualty management that prevent or minimize deficits and provide for speedy wound healing. Several laboratories are actively searching for improved therapies for cutaneous vesicant injury, with the aim of returning damaged skin to optimal appearance and normal function in the shortest time. Improved treatment will result in a better cosmetic and functional outcome for the patient, and will enable the casualty to return to normal activities sooner. This editorial gives brief overviews of sulfur mustard use, its toxicity, concepts for medical countermeasures, current treatments, and strategies for the development of improved therapies.
Burns have been associated with high levels of circulating pro-inflammatory cytokines which promote systemic inflammatory response syndrome (SIRS), immunosuppression and sepsis for which no effective treatment is currently available. Defensins, a family of cationic naturally occurring antimicrobial peptides, are considered important components of the innate immune system and enhance adaptive immunity. This study examines the effects of pro-inflammatory cytokines, interleukin-1beta (IL-1beta), gamma-interferon (IFNgamma) and tumor necrosis factor-alpha (TNFalpha) on human beta-defensin-2 (HBD-2) levels in cultured keratinocytes. We also examined the effects of heat shock at 42 degrees C. The results demonstrate that only TNFalpha shows significant induction of HBD-2 but this induction was not sustained in the long-term. In addition, endogenous levels of defensin were significantly reduced by exposure to heat shock. The keratinocytes also responded to IL-1beta by becoming hypertrophic. These results indicate that stress-related, pro-inflammatory cytokines can induce keratinocytes to synthesize HBD-2, while heat shock appears to reduce its production. These experiments give us further insight into the role of natural antimicrobial peptides under conditions of stress.
Sepsis is a common and serious complication of major burn injury and accounts for over 54% of deaths in burn patients. Burns are associated with high levels of circulating pro-inflammatory cytokines and immunosuppression, promoting systemic inflammatory response syndrome (SIRS) and sepsis, for which no effective treatment is currently available. Defensins, a family of cationic, naturally occurring, antimicrobial peptides are important components of the innate immune system, playing a major role in the body's defence by inhibiting activities of bacteria, fungi and enveloped viruses. These natural antimicrobials also chemoattract immature dendritic cells, some types of T and B-lymphocytes, neutrophils and macrophages, and act as an adjuvant, enhancing adaptive immunity. Our prior studies suggested a decreased expression of human beta defensin 2 (HBD2) in burn wounds. Here we have identified HBD2 protein in skin samples of partial and full thickness burns and in normal skin using fluorescence deconvolution microscopy. Images showed that in normal skin the majority of HBD2 is located in the Malpighian layer and, in smaller amounts, in the more superficial layers, a pattern that is absent in burned skin in which the epidermis is destroyed or damaged. However, surviving dermal and subcutaneous layers revealed the presence of HBD2 in a number of other cell types and structures, such as hair follicles and sweat gland acini, but not in vascular endothelium and fat cells. The results of these studies further contribute to an understanding of the role of antimicrobial peptides in the pathophysiology of burn injury, associated immunosuppression and sepsis and the possibility of using these other sites of HBD2 deposition for upregulation of antimicrobial synthesis in the treatment of burns.
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Literature reports dating as far back as 1927 have lured clinicians into the belief that alkaline skin burns are best treated by water dilution and that neutralization attempts should be avoided. Although this belief has never been substantiated, neutralization of an alkaline burn of the skin with acid was thought to increase tissue damage secondary to the exothermic nature of acid-base reactions. The authors proposed that topical treatment of alkaline burns with a weak acid such as 5% acetic acid (i.e., household vinegar) would result in rapid tissue neutralization and reduction of injury in comparison to water irrigation alone. In a rat skin burn model, animals were exposed to an alkaline injury when filter paper (2 cm in diameter) saturated with 2N sodium hydroxide was placed over the volar aspect of the animal for a period of 1 minute. Treatment was initiated 1 minute after injury and included either neutralization with a 5% acetic acid solution (n = 8) or irrigation (n = 8) with water. Skin temperature and pH were monitored using subdermal needle probes until the pH of the skin returned to physiologic values. Punch-biopsy specimens were obtained from the wound edges 24 hours after injury to assess burn depth and leukocyte infiltration, and biopsies were repeated 10 days later to assess wound healing. The authors proposed that neutralization of an alkaline substance with household vinegar (i.e., 5% acetic acid solution) would result in rapid neutralization and thus reduce extent of tissue injury. Animals treated with acetic acid demonstrated a more rapid return to physiologic pH (14.69 +/- 4.06 minutes versus 31.62 +/- 2.83 minutes; p < 0.001), increased depth of dermal retention (0.412 +/- 0.136 mm versus 0.214 +/- 0.044 mm; p = 0.015), decreased leukocyte infiltrate (31.0 +/- 5.1 cells/high-power field versus 51.8 +/- 6.8 cells/high-power field; p < 0.001), and improved epithelial regeneration (4.0 +/- 0.6 cell layers versus 1.7 +/- 0.5 cell layers; p < 0.001) when compared with animals treated with water irrigation. No difference was detected in peak pH (10.35 +/- 0.28 pH versus 10.36 +/- 0.25 pH; p = 0.47) nor in rise of skin temperature (maximum temperature, 32.8 degrees C versus 32.9 degrees C; p = 0.33) between acetic acid-neutralized and water-irrigated burn wounds. The observed benefits of treating alkaline burns with 5% acetic acid in the rat model are significant and require clinical testing.
Coverage of large burns may be difficult when skin graft donor sites are limited. This study explored the use of the split-thickness dermal graft (STDG), as an alternative to the standard split-thickness skin graft (STSG). STSGs and STDGs were compared experimentally by their ability to resurface full thickness skin defects in a pig model. Both types of grafts were harvested from the backs of six pigs and placed on full thickness wounds. From the same donor site a 0.012in. thick STSG and another two 0.012in. thick STDGs were harvested. Thus the deep surface of grafts measured 0.012, 0.024 and 0.036in. from the skin surface, respectively. All grafts were placed on 6cmx6cm full thickness wounds. The donor areas healed at 1 week. Epithelialization of the STDGs, was assessed by computerized planimetry, and was 100% at 4 weeks. Graft biopsies revealed that STSGs were significant thinner than STDGs at 1 week (P=0.0422, 0.0135), 2 weeks (P=0.0240) and 4 weeks (P=0.0516, 0.0425). We conclude that STDGs my provide definitive coverage of full thickness skin deficits in a pig wound model.
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Postburn contractures of the hand and wrist can range from a minor cosmetic problem to a crippling condition. The contractures, initially limited to the skin, extend to all the soft-tissue structures over time, often necessitating capsulotomies and tendon lengthening, although they still may not be amenable to total correction. The Joshi External Stabilizing System (JESS) is a versatile, lightweight external fixator consisting of K wires, distractors, and connecting rods (both hinged and nonhinged) along with various link joints. JESS is a dynamic system that allows the lengthening of the contracted tissues via slow distraction, causing minimal surgical insult. This is a retrospective review of 218 cases of postburn contractures of the hand treated with JESS during the last 20 years. Deformities varied from finger contractures to metacarpophalangeal joint and wrist contractures. All cases were of long duration at the time of presentation with the original injury being 4 months to 20 years old. All were assessed for the degree of function and deformity. The patients' activities of daily living were recorded and x-rays taken to evaluate joint configuration. The patients underwent a conservative surgical release followed by application of the appropriate JESS frame for the correction of the residual deformity. After 6 weeks, the frame was removed and hand therapy continued. An analysis is provided of the outcome. The technique produces functional hands with minimal surgical insult.