Edward E. Tredget

A matched-pair, randomized study evaluating the efficacy and safety of acticoat* silver-coated dressing for the treatment of burn wounds

A new silver-coating technology was developed to prevent wound adhesion, limit nosocomial infection, control bacterial growth, and facilitate burn wound care through a silver-coated dressing material. For the purposes of this article, Acticoat (Westaim Biomedical Inc, Fort Saskatchawan, Alberta, Canada) silver-coated dressing was used. After in vitro and in vivo studies, a randomized, prospective clinical study was performed to assess the efficacy and ease of use of Acticoat dressing as compared with the efficacy and ease of our institutions standard burn wound care. Thirty burn patients with symmetric wounds were randomized to be treated with either 0.5% silver nitrate solution or Acticoat silver-coated dressing. The dressing was evaluated on the basis of overall patient comfort, ease of use for the wound care provider, and level of antimicrobial effectiveness. Wound pain was rated by the patient using a visual analog scale during dressing removal, application, and 2 hours after application. Ease of use was rated by the nurse providing wound care. Antimicrobial effectiveness was evaluated by quantitative burn wound biopsies performed before and at the end of treatment. Patients found dressing removal less painful with Acticoat than with silver nitrate, but they found the pain to be comparable during application and 2 hours after application. According to the nurses, there was no statistically significant difference in the ease of use. The frequency of burn wound sepsis (> 10(5) organisms per gram of tissue) was less in Acticoat-treated wounds than in those treated with silver nitrate (5 vs 16). Secondary bacteremias arising from infected burn wounds were also less frequent with Acticoat than with silver nitrate-treated wounds (1 vs 5). Acticoat dressing offers a new form of dressing for the burn wound, but it requires further investigation with greater numbers of patients in a larger number of centers and in different phases of burn wound care.

Rating the Resolving Hypertrophic Scar: Comparison of the Vancouver Scar Scale and Scar Volume

The increased focus of research interests and clinical documentation on outcomes demands that evaluation tools provide reliable and valid data. The Vancouver Scar Scale (VSS) was developed to provide a more objective measurement of burn scars; however, the validity (a tests ability to measure the phenomenon for which it was designed) of the VSS has not been tested. To examine the construct validity of the VSS, we compared it with scar volume, which has established face validity. Burn scars were evaluated monthly for a minimum of 7 months. Three scar volume measurements were performed on each scar. In addition, 3 independent examiners completed the VSS for the same scar. The data generated by these 2 measurements were used to establish the following: (1) the interrater agreement estimated by interclass correlation coefficient, (2) convergence validity, (3) the sensitivity of the assessments to discriminate changes in the scar over time, and (4) the prevalence of related parameters that are not currently being captured by the VSS. In an attempt to address some of the deficiencies of the VSS, we propose several modifications. We anticipate that these changes will increase the reliability and validity of the VSS through an increase in the awareness that training in the use of this scale is required, through improvement in the quality of the subscales, and through the documentation of additional pertinent information.

The metabolic effects of thermal injury.

Major thermal injury is associated with extreme hypermetabolism and catabolism as the principal metabolic manifestations encountered following successful resuscitation from the shock phase of the burn injury. Substrate and hormonal measurements, indirect calorimetry, and nitrogen balance are biochemical metabolic parameters which are useful and more readily available biochemical parameters worthy of serial assessment for the metabolic management of burn patients. However, the application of stable isotopes with gas chromatography/mass spectroscopy and more recently, new immunoassays for growth factors and cytokines has increased our understanding of the metabolic manifestations of severe trauma.The metabolic response to injury in burn patients is biphasic wherein the initialebb phase is followed by a hypermetabolic and catabolicflow phase of injury. The increased oxygen consumption/metabolic rate is in part fuelled by evaporative heat loss from wounds of trauma victims, but likely also by a direct central effect of inflammation upon the hypothalamus. Although carbohydrates in the form of glucose appear to be an important fuel source following injury, a maximum of 5–6 mg/kg/min only is beneficial. Burn patients have accelerated gluconeogenesis, glucose oxidation, and plasma clearance of glucose. Additionally, considerable futile cycling of carbohydrate intermediates occurs which includes anaerobic lactate metabolism and Cori cycle activity arising from wound metabolism of glucose and other substrates. Similarly, accelerated lipolysis and futile fatty acid cycling occurs following burn injury. However, recent evidence suggests that lipids in the diet of burned and other injured patients serve not only as an energy source, but also as an important immunomodulator of prostaglandin metabolism and other immune responses.Amino acid metabolism in burn patients is characterized by increased oxidation, urea synthesis, and protein breakdown which is prolonged and difficult to reduce with current nutritional therapy. However, the current goal of nutritional support is to optimize protein synthesis. Specific unique requirements may exist for supplemental glutamine and arginine following burn injury but further research is needed before enhanced branched chain amino acids supplements can be recommended for burn patients. Recent research investigations have revealed the importance of enteral feeding to enhance mucosal defense against gut bacteria and endotoxin. Similarly, research has demonstrated that many of the metabolic perturbations of burns and sepsis may be due, at least in part, to inflammatory cytokines. Investigation of their pathogenesis and mechanism of action both at a tissue and a cellular level offer important prospects for improved understanding and therapeutic control of the metabolic disorders of burn patients.RésuméAprès récupération de la première phase de choc survient un hypercatabolisme majeur. Des paramètres de surveillance de lévolution et dévaluation de lefficacité du traitement sont facilement disponibles: dosages hormonaux et de différents subtats, calorimétrie indirecte et bilan azoté devraient être dosés de façon régulière chez les brûlés. Notre compréhension des perturbations métaboliques chez le blessé et chez la grand brûlé sest améliorée ces dernières années en raison de lapplication de techniques isotopiques avec des dosages par la chromatographie gazeuse et la spectrophotométrie de masse et plus récemment encore les dosages immunologiques des facteurs de croissance et des cytokines. La réponse métabolique à lagression chez le brûlé est biphasique. La phase initiale est descendante, suivie dune phase ascendante dhypercatabolisme. Laugmentation de la consommation en oxygène et du métabolisme est en partie provoquée par la perte en chaleur au niveau des plaies, mais aussi, par un effet direct central, liée à linflammation qui agit sur lhypothalamus. Bien que des hydrates de carbone, sous forme de glucose, semblent être une source importante dénergie après un traumatisme, lapport de seulement 5–6 mg/kg/min est suffisant. La néoglucogénèse, loxydation du glucose et la clairance plasmatique du glucose du brûlé sont accélérées. Les cycles métaboliques des hydrates de carbone, y compris le métabolisme anaérobie des lactates et le cycle de Cori sont inefficaces. De même, la lipolyse est accélérée et le cycle des acides gras est inefficace. Cependant, il est évident que les lipides chez le brûlé et dautres patients victimes du traumatisme ne sont pas seulement une source dénergie mais aussi un immunomodulateur du métabolisme des prostaglandines et dautres voies de réponse immune. Le métabolisme des acides aminés chez le brûlé est caractérisé par une oxydation, une synthèse durée et un catabolisme protéique accrus, phénomènes prolongés et difficiles à réduire avec les moyens actuels de nutrition artificielle. Le but du soutien nutritionnel est cependant doptimiser la synthèse protéique. Des besoins spécifiques peuvent nécessiter une supplémentation en glutamine et arginine après brûlures mais dautres recherches sont nécessaires avant de pouvoir dire quune supplémentation en acides aminés branchés peut être utile. La recherche moderne a démontré limportance de lalimentation entérale qui empêche la traversée de la barrière muqueuse par les germes et les endotoxines. De même, il a été démontré que beaucoup des perturbations métaboliques dans les suites de brûlures et dans les états septiques sont dues, du moins en partie, aux cytokines inflammatoires. Lanalyse de leur pathogénèse et leur mécanisme daction à la fois au niveau tissulaire et cellulaire offrent dimportantes perspectives pour améliorer la compréhension et le contrôle thérapeutique des désordres métaboliques du brûlé.ResumenLa lesión térmica mayor está relacionada con grados extremos de hipermetabolismo y catabolismo como las manifestaciones metabólicas principales que ocurren una vez cumplida exitosamente la resucitación de la fase de shock. Las determinaciones de sustratos y niveles hormonales, la calorimetría indirecta y el balance de nitrógeno son parámetros metabólicos de carácter bioquímico que son útiles y fácilmente disponibles, los cuales merecen estudios seriados para el manejo metabólico de los pacientes quemados. Sin embargo, la aplicación de isótopos estables con cromatografía de gas/espectrometría de masa y, más recientemente, nuevas inmunodeterminaciones para factores de crecimiento y citocinas, ha incrementado nuestro conocimiento y comprensión de las manifestaciones metabólicas del trauma severo.La respuesta metabólica en los pacientes quemados es bifásica, en tanto que lafase ebb inicial es seguida de unafase flow hipermetabólica y catabólica. El aumento en el consumo de oxígeno/tasa metabólica se debe en parte a la pérdida evaporativa de calor a partir de las heridas de las víctimas de trauma, pero posiblemente también a un efecto central de la inflamación sobre el hipotálamo. Aunque los carbohidratos en forma de glucosa parecen ser una fuente energética importante, sólo hasta un máximo de 5–6 mg/kg/min son de beneficio. Los pacientes quemados exhiben aceleradas ratas de gluconeogénesis, oxidación de glucosa y depuración plasmática de glucosa. Además, se presenta considerable ciclaje futil de intermediarios de carbohidratos, lo cual incluye metabolismo anaeróbico de lactato y actividad del ciclo de Cori originados en el metabolismo de la glucosa y de otros sustratos a nivel de la herida. También se presenta lipolisis acelerada y ciclaje futil de ácidos grasos. Sin embargo, evidencias recientes sugieren que los lípidos en la dieta de los pacientes con quemaduras y otras formas de trauma sirven no sólo como fuentes energéticas, sino también como un factor importante de modulación del metabolismo de las prostaglandinas y de otras respuestas inmunitarias.El metabolismo de aminoácidos en el paciente quemado se caracteriza por una oxidación incrementada, síntesis de urea y degradación proteica prolongada y difícil de controlar mediante la terapia nutricional actual. Sin embargo, el propósito actual del soporte nutricional es optimizar la síntesis proteica. Pueden existir requerimientos específicos de glutamina arginina suplementarias en las quemaduras, pero se requieren investigaciones adicionales antes de poder recomendar suplementos enriquecidos con aminoácidos racémicos en los pacientes quemados. Recientes investigaciones han revelado la importancia de la alimentación enteral para estimular las defensas de la mucosa intestinal contra bacterias y endotoxinas. También hay investigaciones que han demostrado que muchas de las alteraciones metabólicas de las quemaduras y las sepsis pueden ser debidas, por lo menos en parte, a las citocinas inflamatorias. La investigación de su patogénesis y mecanismo de acción, tanto al nivel tisular como celular, ofrece perspectivas importantes de una mejor comprensión y de superior control terapéutico de las alteraciones metabólicas de los pacientes quemados.Major thermal injury is associated with extreme hypermetabolism and catabolism as the principal metabolic manifestations encountered following successful resuscitation from the shock phase of the burn injury. Substrate and hormonal measurements, indirect calorimetry, and nitrogen balance are biochemical metabolic parameters which are useful and more readily available biochemical parameters worthy of serial assessment for the metabolic management of burn patients. However, the application of stable isotopes with gas chromatography/mass spectroscopy and more recently, new immunoassays for growth factors and cytokines has increased our understanding of the metabolic manifestations of severe trauma. The metabolic response to injury in burn patients is biphasic wherein the initialebb phase is followed by a hypermetabolic and catabolicflow phase of injury. The increased oxygen consumption/metabolic rate is in part fuelled by evaporative heat loss from wounds of trauma victims, but likely also by a direct central effect of inflammation upon the hypothalamus. Although carbohydrates in the form of glucose appear to be an important fuel source following injury, a maximum of 5–6 mg/kg/min only is beneficial. Burn patients have accelerated gluconeogenesis, glucose oxidation, and plasma clearance of glucose. Additionally, considerable futile cycling of carbohydrate intermediates occurs which includes anaerobic lactate metabolism and Cori cycle activity arising from wound metabolism of glucose and other substrates. Similarly, accelerated lipolysis and futile fatty acid cycling occurs following burn injury. However, recent evidence suggests that lipids in the diet of burned and other injured patients serve not only as an energy source, but also as an important immunomodulator of prostaglandin metabolism and other immune responses. Amino acid metabolism in burn patients is characterized by increased oxidation, urea synthesis, and protein breakdown which is prolonged and difficult to reduce with current nutritional therapy. However, the current goal of nutritional support is to optimize protein synthesis. Specific unique requirements may exist for supplemental glutamine and arginine following burn injury but further research is needed before enhanced branched chain amino acids supplements can be recommended for burn patients. Recent research investigations have revealed the importance of enteral feeding to enhance mucosal defense against gut bacteria and endotoxin. Similarly, research has demonstrated that many of the metabolic perturbations of burns and sepsis may be due, at least in part, to inflammatory cytokines. Investigation of their pathogenesis and mechanism of action both at a tissue and a cellular level offer important prospects for improved understanding and therapeutic control of the metabolic disorders of burn patients. Après récupération de la première phase de choc survient un hypercatabolisme majeur. Des paramètres de surveillance de lévolution et dévaluation de lefficacité du traitement sont facilement disponibles: dosages hormonaux et de différents subtats, calorimétrie indirecte et bilan azoté devraient être dosés de façon régulière chez les brûlés. Notre compréhension des perturbations métaboliques chez le blessé et chez la grand brûlé sest améliorée ces dernières années en raison de lapplication de techniques isotopiques avec des dosages par la chromatographie gazeuse et la spectrophotométrie de masse et plus récemment encore les dosages immunologiques des facteurs de croissance et des cytokines. La réponse métabolique à lagression chez le brûlé est biphasique. La phase initiale est descendante, suivie dune phase ascendante dhypercatabolisme. Laugmentation de la consommation en oxygène et du métabolisme est en partie provoquée par la perte en chaleur au niveau des plaies, mais aussi, par un effet direct central, liée à linflammation qui agit sur lhypothalamus. Bien que des hydrates de carbone, sous forme de glucose, semblent être une source importante dénergie après un traumatisme, lapport de seulement 5–6 mg/kg/min est suffisant. La néoglucogénèse, loxydation du glucose et la clairance plasmatique du glucose du brûlé sont accélérées. Les cycles métaboliques des hydrates de carbone, y compris le métabolisme anaérobie des lactates et le cycle de Cori sont inefficaces. De même, la lipolyse est accélérée et le cycle des acides gras est inefficace. Cependant, il est évident que les lipides chez le brûlé et dautres patients victimes du traumatisme ne sont pas seulement une source dénergie mais aussi un immunomodulateur du métabolisme des prostaglandines et dautres voies de réponse immune. Le métabolisme des acides aminés chez le brûlé est caractérisé par une oxydation, une synthèse durée et un catabolisme protéique accrus, phénomènes prolongés et difficiles à réduire avec les moyens actuels de nutrition artificielle. Le but du soutien nutritionnel est cependant doptimiser la synthèse protéique. Des besoins spécifiques peuvent nécessiter une supplémentation en glutamine et arginine après brûlures mais dautres recherches sont nécessaires avant de pouvoir dire quune supplémentation en acides aminés branchés peut être utile. La recherche moderne a démontré limportance de lalimentation entérale qui empêche la traversée de la barrière muqueuse par les germes et les endotoxines. De même, il a été démontré que beaucoup des perturbations métaboliques dans les suites de brûlures et dans les états septiques sont dues, du moins en partie, aux cytokines inflammatoires. Lanalyse de leur pathogénèse et leur mécanisme daction à la fois au niveau tissulaire et cellulaire offrent dimportantes perspectives pour améliorer la compréhension et le contrôle thérapeutique des désordres métaboliques du brûlé. La lesión térmica mayor está relacionada con grados extremos de hipermetabolismo y catabolismo como las manifestaciones metabólicas principales que ocurren una vez cumplida exitosamente la resucitación de la fase de shock. Las determinaciones de sustratos y niveles hormonales, la calorimetría indirecta y el balance de nitrógeno son parámetros metabólicos de carácter bioquímico que son útiles y fácilmente disponibles, los cuales merecen estudios seriados para el manejo metabólico de los pacientes quemados. Sin embargo, la aplicación de isótopos estables con cromatografía de gas/espectrometría de masa y, más recientemente, nuevas inmunodeterminaciones para factores de crecimiento y citocinas, ha incrementado nuestro conocimiento y comprensión de las manifestaciones metabólicas del trauma severo. La respuesta metabólica en los pacientes quemados es bifásica, en tanto que lafase ebb inicial es seguida de unafase flow hipermetabólica y catabólica. El aumento en el consumo de oxígeno/tasa metabólica se debe en parte a la pérdida evaporativa de calor a partir de las heridas de las víctimas de trauma, pero posiblemente también a un efecto central de la inflamación sobre el hipotálamo. Aunque los carbohidratos en forma de glucosa parecen ser una fuente energética importante, sólo hasta un máximo de 5–6 mg/kg/min son de beneficio. Los pacientes quemados exhiben aceleradas ratas de gluconeogénesis, oxidación de glucosa y depuración plasmática de glucosa. Además, se presenta considerable ciclaje futil de intermediarios de carbohidratos, lo cual incluye metabolismo anaeróbico de lactato y actividad del ciclo de Cori originados en el metabolismo de la glucosa y de otros sustratos a nivel de la herida. También se presenta lipolisis acelerada y ciclaje futil de ácidos grasos. Sin embargo, evidencias recientes sugieren que los lípidos en la dieta de los pacientes con quemaduras y otras formas de trauma sirven no sólo como fuentes energéticas, sino también como un factor importante de modulación del metabolismo de las prostaglandinas y de otras respuestas inmunitarias. El metabolismo de aminoácidos en el paciente quemado se caracteriza por una oxidación incrementada, síntesis de urea y degradación proteica prolongada y difícil de controlar mediante la terapia nutricional actual. Sin embargo, el propósito actual del soporte nutricional es optimizar la síntesis proteica. Pueden existir requerimientos específicos de glutamina arginina suplementarias en las quemaduras, pero se requieren investigaciones adicionales antes de poder recomendar suplementos enriquecidos con aminoácidos racémicos en los pacientes quemados. Recientes investigaciones han revelado la importancia de la alimentación enteral para estimular las defensas de la mucosa intestinal contra bacterias y endotoxinas. También hay investigaciones que han demostrado que muchas de las alteraciones metabólicas de las quemaduras y las sepsis pueden ser debidas, por lo menos en parte, a las citocinas inflamatorias. La investigación de su patogénesis y mecanismo de acción, tanto al nivel tisular como celular, ofrece perspectivas importantes de una mejor comprensión y de superior control terapéutico de las alteraciones metabólicas de los pacientes quemados.

Pathophysiology and treatment of fibroproliferative disorders following thermal injury.

Keloids and hypertrophic scars (HSc) are unique human dermal fibroproliferative disorders (FPD) that occur following trauma, inflammation, surgery, and burns, or possibly spontaneously.1 Keloids occur in individuals with a familial predisposition, enlarge and extend beyond the margins of the original wounds, and rarely regress. HSc are raised, erythematous, pruritic, fibrous lesions that typically remain within the confines of the original wound, usually undergo at least partial spontaneous resolution over widely varying time courses, and are often associated with contractures of the healing tissues. The development of contractures is by definition the pathologic shortening of scar tissue resulting in deformities, as opposed to wound contraction which occurs in an open wound, with the positive outcome of reducing the wound surface area. These disorders represent aberrations in the fundamental processes of wound healing, which include cell migration and proliferation, inflammation, increased synthesis and secretion of cytokines and extracellular matrix (ECM) proteins, and finally remodeling of the newly synthesized matrix. Conceptually, it is the goal of individuals caring for wounds to facilitate regeneration of the injured skin and associated structures (FIGURE 1); however, at present, adult mammalian healing occurs by the formation of scar, characterized by a disordered architecture, which in the case of HSc and keloids is also associated with excessive deposition of ECM proteins.

Electrical Injuries in Canadian Burn Care: Identification of Unsolved Problems

ABSTRACT: Over the past decade, the Firefighters Burn Treatment Unit of the University of Alberta Hospital in Edmonton, Alberta, Canada, has treated 1399 in‐patients suffering from thermal injury. Regional burn care is provided in a 10‐bed intensive care unit with 18 plastic surgery reconstructive beds for a large referral region of central and northern Alberta, portions of the Northwest Territories, and neighboring provinces of British Columbia and Saskatchewan.

Hydrofiber dressing with silver for the management of split-thickness donor sites: a randomized evaluation of two protocols of care.

BACKGROUNDnThis randomized, open-label study evaluated Aquacel Ag Hydrofiber dressing with silver (HDS; ConvaTec, Skillman, NJ, USA) with an adherent or gelled protocol in the management of split-thickness donor sites.nnnMETHODSnHDS was the primary dressing in the adherent group (gauze as secondary covering) and gelled group (transparent film as secondary covering). Dressings were changed on study day 1 or 2 and study days 5 (optional), 10 (optional), and 14. The primary outcome was healing (>or=90% re-epithelialization) at study day 14.nnnRESULTSnSeventy subjects were treated (36 adherent, 34 gelled). By study day 14, 77% of donor sites had healed (67% adherent, 88% gelled). Pain scores decreased over time in both treatment groups. Investigators were very satisfied or satisfied with (adherent, gelled) time required to manage dressing change (89%, 79% of subjects), minimization of donor-site pain (64%, 82%), ease of application (97%, 94%), management of drainage (92%, 82%), ease of removal (77%, 85%), and ability of dressing to remain in place (69%, 76%). Thirty-nine (56%) subjects had adverse events, most commonly non-donor-site infection (11%) and gastrointestinal events (11%).nnnCONCLUSIONnIn this randomized, open-label study, HDS was well-tolerated, versatile, and effective in the management of split-thickness donor sites.