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Background Non-technical skills (NTS) failures have been implicated in a large proportion of surgical errors. The objective of this meta-analysis was to investigate whether NTS training of theatre staff improves patient outcomes. Methods In a systematic literature search all interventional studies evaluating the effects of NTS training of theatre staff were identified. Primary outcomes included mortality, morbidity, readmission rate and length of hospital stay. Secondary outcomes included staff NTS, checklist use and technical surgical performance. Pooled odds ratios (OR) were determined for event rates and weighted mean differences (WMD) for continuous data. An inverse variance method in a random effects model was used for meta-analysis. Results A total of 1381 records were identified and nine studies were included. Meta-analysis of mortality was not carried out because only two controlled studies with different study designs were identified. No statistically significant differences were seen in complication rate (5 studies, OR 0.91 [0.73, 1.14]; p = 0.43), readmission rate (3 studies, OR 0.90 [0.63, 1.28], p = 0.56) and length of hospital stay (3 studies, WMD −0.88 days [−2.06, 0.31], p = 0.31) after NTS training. Of the secondary outcomes, an improvement of whole team NOTECHS II scores was observed in the intervention group (3 studies, WMD 6.97 [3.88, 10.06], p Conclusions This meta-analysis failed to find a statistically significant improvement of patient outcomes. These conclusions are based on a small number of heterogeneous studies. Further appropriately powered studies are likely to improve our understanding of the effects of NTS training.

Chronic wounds are of high socio-economic importance. Accurate and efficient treatment includes the use of outcomes measures in clinical care and in research. To date, consented standards for documentation of chronic wounds, agreements on interpretation of wound outcomes and harmonisation about standardised goal setting in wound treatment are lacking. Objective (1) To establish a national German consensus group for the definition of standards in outcomes measurement of chronic wounds, (2) to agree on recommendations for practice and research based on a continuous decision process, including implementation of the standards. Methods The national consensus group includes delegates from the German scientific medical societies involved in health care for chronic wounds, the national boards on nursing, and the chairs of regional wound networks. Moreover, the roof organisations of the German health insurances, the German ministry of health and further single wound experts were invited. The consensus work is based on a structured decision process. Results The consensus group consists of 58 representatives and co-representatives of 26 societies and organisations. Since 2012, in the regular bi-annual meetings a Delphi-based workflow has been followed starting with standards for documentation and outcomes measurement in patients with leg ulcers. Additionally, web-based decision processes are conducted and the results are presented for finalisation in the face-to-face meetings. The following application areas of particular interests were defined: clinical routine, health services research, clinical research, and health economics. In the meantime, 245 single decisions have been approved. Conclusions Based on a national joint process involving medical societies, nursing groups, German sickness funds and health politics, a continuous decision process on standards for outcomes measurement and interpretation could be established. The Delphi based decision processes showed high levels of participations, thus providing a valid and robust set of standards. First results are in process of approval by the societies.

Summary The number of patients suffering from chronic wound healing disorders in Germany alone is estimated to be 2.5–4 million. Therapy related expenses reach 5–8 billion Euros annually. This number is partially caused by costly dressing changes due to non-standardized approaches and the application of non-evidence-based topical wound therapies. The purpose of this paper is to elucidate a straightforward principle for the management of chronic wounds, and to review the available evidence for the particular therapy options. The T.I.M.E.-principle (Tissue management, Inflammation and infection control, Moisture balance, Epithelial [edge] advancement) was chosen as a systematic strategy for wound bed preparation. Literature was retrieved from the PubMed and Cochrane Library databases and subjected to selective analysis. Topical wound management should be carried out according to a standardized principle and should further be synchronized to the phases of wound healing. Despite the broad implementation of these products in clinical practice, often no benefit exists in the rate of healing, when evaluated in meta-analyses or systematic reviews. This insufficient evidence is additionally limited by varying study designs. In case of non-superiority, the results suggest to prefer relatively inexpensive wound dressings over expensive alternatives. Arbitrary endpoints to prove the effectiveness of wound dressings, contribute to the random use of such therapies. Defining rational endpoints for future studies as well as the deployment of structured therapy strategies will be essential for the economical and evidence-based management of chronic wounds.

Defektdeckung des beuge- und streckseitigen Hand- und Unterarmbereichs bis zu einer maximalen Defektgrose von 10 × 25 cm. Weichteildefekte des beuge- und streckseitigen Hand- und Unterarmbereichs bis zu einer maximalen Defektgrose von 10 × 25 cm. Polytraumatisierte Patienten mit lebensbedrohlichen Begleitverletzungen. In diesen Fallen sollte die definitive Weichteildeckung spatprimar oder sekundar nach Kreislaufstabilisierung erfolgen. Schlecht vaskularisiertes Empfangergebiet (z.B. nach Radiatio). Floride Infekte im Empfanger- und/oder Spendergebiet sowie Nekrosen. Voroperationen der Leistenregion mit Kompromittierung der Gefase. Nicht kooperativer Patient. Orientierungspunkte zur Lappenumschneidung sind der tastbare Puls der Arteria femoralis, das Leistenband, die Spina iliaca anterior superior und der Musculus sartorius. Einzeichnung des Lappenober- und -unterrandes parallel zum Leistenband, wobei die Langsachse des Lappens dem Verlauf der Arteria circumflexa ilium superficialis entspricht, die anteilig oberhalb des Leistenbandes verlauft. Ein Drittel des Lappens sollte oberhalb und zwei Drittel sollten unterhalb des Leistenbandes zu liegen kommen. Die Lappenpraparation beginnt im lateralen Abschnitt ohne Einschluss der Faszie. Um eine Verletzung des Gefasstiels zu vermeiden, erfolgt die vorsichtige Identifikation des lateralen Sartoriusrandes, dessen Faszie eingeschnitten und in den Lappen miteinbezogen wird. Ein langer Rundstiel erfordert unter Umstanden, die Praparation der A. circumflexa ilium superficialis bis zu ihrem Ursprung fortzusetzen. Nach Hebung des Lappens Einschwenken des Lappens in den Defektbereich und Einnaht mit Rundstielbildung. Der Rundstiel schutzt die Lappengefase und erleichtert die ischamische Konditionierung des Lappens in der postoperativen Phase. Je nach Lappengrose spannungsfreier Primarverschluss des Hebedefekts oder Spalthautdeckung. Die durchschnittliche Operationszeit in einer Ausbildungsklinik betragt 120 min (Daten aus dem eigenen Pa-tientengut). 3-wochige Stielung des Lappentransplantats und sofortige Mobilisierung des Patienten. Vermeidung von Abknickungen des Lappenstiels; hierzu ggf. Unterpolsterung des Arms und Lagerung in angepasster Schulterabduktion. Tagliche Verbandswechsel und Lappenmonitoring zur Vitalitatsprufung. Ab dem 10.–14. postoperativen Tag Lappentraining mit Abklemmen des Lappenstiels mit einer Darmklemme. Steigerung der Abklemmzeit um taglich 5–10 min von initial 3 × 5 min/d auf 3 × 1 h/d. Lappenstieldurchtrennung nach Erreichen der maximalen Abklemmzeit nach 3 Wochen unter Belassung eines ausreichend langen Lappenstiels im Empfangergebiet und Sekundarverschluss der Leiste. Nach Demarkierung des Lappenstielendes endgultige Einpassung des Leistenlappens. In einem 3-Jahres-Zeitraum wurde bei insgesamt 14 Patienten eine Defektdeckung mit dem gestielten Leistenlappen durchgefuhrt. Indikationen fur das Verfahren waren die Daumenrekonstruktion nach Avulsionsamputation zum Langenerhalt und zur Defektdeckung, die spatsekundare Wiederherstellung der Daumenlange durch eine Beckenkammspaninterposition, die Rekonstruktion der Daumenweichteile nach radikalem Debridement einer tiefen zweitgradigen Verbrennung, Hautweichteildefekte im Bereich des Handruckens nach traumatischer Kontusion und Infekt, ausgedehnte Hautweichteildefekte nach Kombinationsverletzung des distalen Unterarms, Handgelenks und der Hohlhand sowie ein plastisch-rekonstruktiver Langfingererhalt mit nachfolgender Phalangealisierung bzw. Syndaktylietrennung. Die Anwendung des Leistenlappens fuhrte in allen Fallen zur vollstandigen Defektdeckung. In keinem der Falle kam es zu einem Lappenverlust, und bei samtlichen Patienten konnte ein zufriedenstellendes funktionelles und asthetisches Ergebnis erzielt werden.

Antiseptika zur Behandlung chronischer und infizierter Wunden gehoren zur Standardtherapie. Erkenntnisse uber toxische Eigenschaften gegenuber dem Wund- und Hautgewebe sind jedoch kaum vorhanden. Diese Studie untersucht den Einfluss von Wundantiseptika auf die Vitalitat und Proliferation humaner kutaner Zellen. Die Antiseptika Lavasept (PHMB), Octenisept (Octenidin) und Betaisodona (PVP-Jod) wurden mittels MTT-Assay und BrDU-ELISA auf zytotoxische Effekte gegenuber der HaCaT-Zelllinie, primaren humanen Keratinozyten und Fibroblasten untersucht. Lavasept besas nur geringen Einfluss auf Vitalitat und Zellproliferation. Betaisodona und Octenisept induzierten eine signifikante Reduktion der Zellvitalitat (p

Background Topical inhibition of activated p38 MAPK within burn wounds attenuates the local and systemic inflammatory response. In this study, we investigated the effects of local activated p38 MAPK inhibition on burn-induced cardiac dysfunction. Methods Using a standardized rat model of scald burn injury, rats were given a 30% total body surface area partial thickness burn or sham injury, and the wounds were treated with an activated p38 MAPK inhibitor (SB) or vehicle. Systemic blood pressure measurements were recorded in vivo followed by in vitro assessment of sarcomere contraction in single-cell suspensions of isolated cardiomyocytes. Results Systolic blood pressure or maximum left ventricular pressures in vivo and peak cardiomyocyte sarcomere contractility in vitro were significantly reduced after burn injury. These functional deficits were abolished 24 h after burn injury following local p38 MAPK inhibition. In vitro incubation of normal cardiomyocytes with homogenate from burned skin or burn serum resulted in a similar pattern of impaired cardiomyocyte contractility. These effects were reversed in normal cardiomyocytes exposed to burn skin homogenates treated topically with a p38 MAPK inhibitor. A Western blot analysis showed that cardiac p38 MAPK activation was not affected by dermal blockade of activated p38 MAPK, arguing against systemic absorption of the inhibitor and indicating the involvement of systemic cytokine signaling. Conclusion Topical activated p38 MAPK inhibition within burned skin attenuates the release of proinflammatory mediators and prevents burn-induced cardiac dysfunction after thermal injury. These results support the inhibition of burn-wound inflammatory signaling as a new therapeutic approach to prevent potential postthermal injury multiorgan dysfunction syndrome.

Background Regardless of the underlying cause, both sunburn and superficial thermal injuries are classified as first-degree burns, since data on morphological differences are scarce. Reflectance-Mode-Confocal Microscopy (RMCM) enables high-resolution non-invasive investigation of the human skin. Objective We studied in vivo histomorphological alterations in both sunburn and superficial thermal injuries using RMCM. Methods Ten patients (6 female, 4 male; aged 28.4 +/- 10.6 years) with first-degree thermal-contact Injuries (TI group), and 9 sunburned patients (SB group; 7 female, 2 male; aged 30.2 +/- 16.4 years), to a maximum extent of 10% of the body surface were evaluated 24 h after burn injury using RMCM. The following parameters were obtained using RMCM: stratum corneum thickness, epidermal thickness, basal layer thickness, granular cell size. Results Compared to the controls (12.8 +/- 2.5 microm), stratum corneum thickness decreased significantly to 10.6 +/- 2.1 microm in the TI group, whereas it increased significantly to 16.4 +/- 3.1 microm in the SB group. The epidermal thickness did not differ significantly in the TI group (47.9 +/- 2.3 microm) and SB group (49.1 +/- 3.5 microm); however, both increased significantly compared to their respective controls (41.8 +/- 1.4 microm). The basal layer thickness increased more in the SB group compared to the TI group (17.9 +/- 1.4 microm vs. 15.6 +/- 1.1 microm). Both differed also significantly compared to their controls (13.8 +/- 0.9 microm). The granular cell size increased significantly in both groups compared to the controls (731 +/- 42 microm); however, a significantly higher increase was observed in the TI group (852 +/- 58 microm) compared to the SB group (784 +/- 61 microm). Conclusions Ultraviolet radiation seems to influence predominantly deeper epidermal layers, whereas heat-induced burns affect more superficial epidermal layers. The term 'First-degree burn' should not be used synonymously for sunburn and superficial thermal burn injuries. Conflicts of interest None declared.

The stage-adjusted therapy of thermal injuries is based on pathophysiologic mechanisms as well as functional and aesthetic requirements. Plastic reconstructive surgical approaches are highly important in the prevention of the frequent grave sequelae of thermal trauma and to achieve optimal functional rehabilitation and favourable outcome. In reconstructive surgery of burns operative goals are subdivided into acute, secondary reconstructive, functional and aesthetic indications. The achievement of early wound closure to preserve functional skin and soft tissue components is an essential part of acute reconstructive procedures. Functional reconstructive and aesthetic procedures supplement the conservative treatment modalities of the secondary phase of burn care with physical therapy, ergotherapy and psychological support.

There are various approaches to the treatment of superficial burns. No modality exists to date for determining treatment efficiency on morphological features. We review the first application of high-resolution in vivo confocal-laser-scanning microscopy (CLSM) to the evaluation of superficial burns on a histomorphological level. Sixteen patients (6 women, 10 men; 34.5 +/- 16.2 years) with first-degree thermal contact injuries to a maximum extent of 1% of the body surface were enrolled into the study. CLSM was performed with the Vivascope 1500 (Lucid Inc., Rochester, NY) 24 hours after injury. The following parameters were assessed: cell size of the granular layer, thickness of the basal layer, minimal thickness of the epidermis, and diameter of capillary loops. Compared with the control sites 24 hours postburn, the minimal thickness of the epidermis increased on average by approximately 11% (P = .01; t-test); the thickness of the basal layer increased about 7% (P = .008; t-test); the diameter of capillary loops increased approximately by 17% (P = 0.003; t-test); and the cell size of the granular layer increased about 8% (P = .009; Wilcoxon's test). In vivo CLSM allows characterizing and quantifying histomorphological alterations in superficial burns. CLSM could be helpful in assessing the effects of various treatment approaches for superficial burns on a histomorphological level.

We recently showed that acute oxidant-related lung injury (ALI) in rats after application of 2-chloroethyl ethyl sulfide (CEES) is attenuated by the airway instillation of antioxidants. We investigated whether intratracheal administration of antioxidant-containing liposomes immediately after instillation of CEES would attenuate short-term as well as long-term (fibrotic) effects of CEES-induced lung injury. In the acute injury model (4 h after injury), N-acetylcysteine (NAC)-containing liposomes were protective and reduced to baseline levels both the lung permeability index and the appearance of proinflammatory mediators in bronchoalveolar lavage fluids from CEES-exposed lungs. Similar results were obtained when rat alveolar macrophages were incubated in vitro with either CEES or lipopolysaccharide in the presence of NAC-liposomes. When lung fibrosis 3 weeks after CEES was quantitated by using hydroxyproline content, liposomes containing NAC or NAC + glutathione had no effects, but liposomes containing alpha/gamma-tocopherol alone or with NAC significantly suppressed the increase in lung hydroxyproline. The data demonstrate that delivery of antioxidants via liposomes to CEES-injured lungs is, depending on liposomal content, protective against ALI, prevents the appearance of proinflammatory mediators in bronchoalveolar fluids, and suppresses progressive fibrosis. Accordingly, the liposomal strategy may be therapeutically useful in CEES-induced lung injury in humans.

We are reporting a case of a 43-year-old woman, who developed a soft tissue defect of the knee region following complex lower limb trauma. The defect was covered with a microvascular latissimus dorsi (LD) flap. The patient required a total knee replacement and developed a defect at the anterior aspect of the knee. This defect was covered by a second free LD flap from the ipsilateral side with anastomosis to the superficial femoral artery. Thrombosis of the superficial femoral artery resulted in complete flap loss. The soft tissue defect was covered with a pedicled medial gastrocnemius flap. Further surgery was undertaken to reconstruct the extensor mechanism of the knee. The resulting soft tissue defect was covered with a free anterolateral thigh (ALT) flap, which failed. The resulting defect left the knee prosthesis exposed. We used the first free LD flap covering the medial aspect of the lower leg as a pedicled axial myocutaneous flap. The deep portion of the flap remained in situ, covering the original soft tissue defect of the lower leg, and the main bulk of the LD was rotated by 180 degrees to the anterior defect of the knee. The crane flap healed uneventfully with a good outcome.

Background Although the inflammatory response is a prerequisite for wound healing, excessive activation of the innate immune system can induce epithelial cell damage and apoptosis, which may further compromise dermal integrity. In a noninfectious burn wound model, we previously demonstrated that topical inhibition of p38 MAPK, an important inflammatory signaling pathway, attenuated epithelial cell damage and apoptosis. We now question whether attenuating local inflammation would weaken bacterial wound resistance and compromise host defense. Methods Rats received 30% total body surface area burn, and the wound was treated with topical application of a p38 MAPK inhibitor or vehicle. At 24 hours after injury, burn wounds were inoculated with Pseudomonas aeruginosa . At 48 hours postinjury, animals were sacrificed, and the burn wound was analyzed. Results Inoculating burn wounds induced significant bacterial growth. Dermal inflammatory changes were markedly accentuated in the inoculated animals. Topical p38 MAPK inhibition reduced the proinflammatory cytokine expression in the burn wounds and neutrophil sequestration with or without bacterial inoculation. Interestingly, the bacterial wound growth was significantly attenuated in animals treated with topical p38 MAPK inhibitor. Conclusions Topical p38 MAPK inhibition attenuated wound inflammation without interfering with bacterial host defense. Attenuation of excessive burn wound inflammatory signaling may prevent secondary damage of the dermal barrier and reduce the growth of opportunistic pathogens.

We previously reported that generation of the anaphylatoxin C5a is linked to the development of cardiac dysfunction in sepsis due to C5a interaction with its receptor (C5aR) on cardiomyocytes. Burn injury involves inflammatory mechanisms that can lead to C5a generation as well. In this study, we investigated the effects of C5a blockade on burn-induced cardiac dysfunction. Using a standardized rat model of full thickness scald injury, left ventricular pressures were recorded in vivo followed by in vitro assessment of sarcomere contraction of single cardiomyocytes. Left ventricular pressures in vivo and cardiomyocyte sarcomere contractility in vitro were significantly reduced following burn injury. In the presence of anti-C5a Ab, these defects were greatly attenuated 1, 6, and 12 h after burn injury and completely abolished 24 h after burn. In vitro incubation of cardiomyocytes with bacterial LPS accentuated the impaired contractility, which was partially prevented in cardiomyocytes from burned rats that had received an anti-C5a Ab. Based on Western blot analyses, real-time PCR, and immunostaining of left ventricular heart tissue, there was a significant increase in cardiomyocyte expression of C5aR after burn injury. In conclusion, an in vivo blockade of C5a attenuates burn-induced cardiac dysfunction. Further deterioration of contractility due to the exposure of cardiomyocytes to LPS was partially prevented by C5a-blockade. These results suggest a linkage between C5a and burn-induced cardiac dysfunction and a possible contribution of LPS to these events.

Die Erfolgsbilanz der modernen Verbrennungstherapie in Spezialzentren beruht neben einer spezialisierten Intensivtherapie vor allem auf einer fruhen Hautexzision mit autologem Hautersatz. Die Moglichkeiten der konservativen Wundtherapie haben sich vor allem durch den Einsatz innovativer Externa und des Hautersatzes durch bioartifizielle Hautanaloga betrachtlich erweitert. In diesem Beitrag sollen daher aktuelle und innovative Verfahren der konservativen Wundtherapie sowie des Hautersatzes bei Verbrennungen dargestellt werden.

Beta-adrenoreceptor blocker (beta-blocker) therapy may improve outcomes in surgical patients by decreasing cardiac oxygen consumption and hypermetabolism. Because beta-blockers can lower the systemic blood pressure and cerebral perfusion pressure, there is concern regarding their use in patients with head injury. However, beta-blockers may protect beta-receptor rich brain cells by attenuating cerebral oxygen consumption and metabolism. We hypothesized that beta-blockers are safe in trauma patients, even if they have suffered a significant head injury.Using pharmacy and trauma registry data of a Level I trauma center, we identified a cohort of trauma patients who received beta-blockers during their hospital stay (beta-cohort). Trauma admissions who did not receive beta-blockers were in the control cohort. beta-blocker status, in combination with other variables associated with mortality, were placed in a stepwise multivariate logistic regression to identify independent predictors of fatal outcome.In all, 303 (7%) of 4,117 trauma patients received beta-blockers. In the beta-cohort, 45% of patients were on beta-blockers preinjury. The most common reason to initiate beta-blocker therapy was blood pressure (60%) and heart rate (20%) control. The overall mortality rate was 5.6% and head injury was considered to be the major cause of death. After adjusting for age, Injury Severity Scale score, blood pressure, Glasgow Coma Scale score, respiratory status, and mechanism of injury, the odds ratio for fatal outcome was 0.3 (p0.001) for beta-cohort as compared with control. Decreased risk of fatal outcome was more pronounced in patients with a significant head injury.beta-blocker therapy is safe and may be beneficial in selected trauma patients with or without head injury. Further studies looking at beta-blocker therapy in trauma patients and their effect on cerebral metabolism are warranted.

The relationship between local inflammation and the subsequent systemic inflammatory response is poorly described. In a burn injury model, the dermal inflammatory response may act as an ongoing trigger for the systemic inflammatory response syndrome (SIRS) and subsequent systemic complications. We hypothesized that topical attenuation of burn wound inflammatory signaling will control the dermal inflammatory source, attenuate SIRS, and reduce acute lung injury. Mice received a 30% total body surface area burn. Subgroups were treated with specific p38 MAPK inhibitor or vehicle, which was topically applied to wounds. Topical p38 MAPK inhibition significantly reduced burn wound inflammatory signaling and subsequent systemic expression of proinflammatory cytokines and chemokines. In vitro macrophage functional assays demonstrated a significant attenuation in serum inflammatory mediators from animals receiving the topical inhibitor. Topical p38 MAPK inhibition resulted in significantly less pulmonary inflammatory response via reduction of pulmonary neutrophil sequestration, pulmonary cytokine expression, and a significant reduction in pulmonary microvascular injury and edema formation. Although dermal activating transcription factor-2, a downstream p38 MAPK target, was significantly reduced, there was no reduction in pulmonary activating transcription factor-2 expression, arguing against significant systemic absorption of the topical inhibitor. These experiments demonstrate a strong interaction between dermal inflammation and systemic inflammatory response. Attenuating local inflammatory signaling appears effective in reducing SIRS and subsequent systemic complications after burn injury.

Die moderne Verbrennungstherapie, basierend auf allgemein anerkannten Eckpfeilern der Therapie, hat seit der flachendeckenden Einrichtung von Zentren fur Schwerbrandverletzte die Uberlebensprognose der betroffenen Patienten deutlich verbessern konnen. Wesentliche Grundlagen einer erfolgreichen Therapie bilden eine adaquate Volumentherapie, eine fruhe enterale Ernahrung, Infektionskontrolle und die fruhe Hautexzision mit autologem Hautersatz. Zu dieser Akutbehandlung gehort zwingend eine fruhe Rehabilitation, fruhe Reintegration in das Berufs- und Privatleben, Kontrolle der Narbenreifungen, sowie stadiengerechte plastische Korrektur der funktionellen und asthetischen Folgeerscheinungen.

A component of multiorgan dysfunction in burned patients is heart failure. Burn trauma induces cytokine synthesis of interleukin (IL) 1beta, IL-6, and tumor necrosis factor alpha (TNF-alpha) which can negatively impact cardiac function. Infectious complications are common following severe burn injury. We hypothesized that burn injury and lipopolysaccharide (LPS) exposure independently influence peak cardiomyocyte contraction and cytokine secretion. Rats underwent a full-thickness 30% total body surface area scald or sham burn. At 1, 6, 12, and 24 h after burn, cardiomyocytes were isolated and incubated with increasing LPS doses. Peak sarcomere shortening and contractile velocity parameters were recorded using a variable-rate video camera with sarcomere length detection software. Supernatants were assayed for IL-1beta, IL-6, and TNF-alpha by ELISA. Peak sarcomere shortening was decreased in the burn group at 1, 6, 12, and 24 h after burn. IL-1beta, IL-6, and TNF-alpha levels were increased in cardiomyocytes isolated 1 h after burn compared with sham controls, but returned to sham levels at 6, 12, and 24 h after burn. LPS exposure caused dose-dependent decreases in sarcomere shortening in sham and burn animals. LPS exposure did not produce increased cardiomyocyte cytokine expression. Burn injury diminished peak sarcomere shortening. Whereas exposure to LPS did not have an effect on cardiomyocyte cytokine expression, LPS significantly inhibited sarcomere shortening in a dose-dependent fashion. Combined burn and LPS exposure inhibited sarcomere shortening more than each alone. These results demonstrate that LPS exposure and burn injury independently decrease peak cardiac shortening. These decreases did not directly correlate with the levels of cytokines released in response to each stressor.

Background. Severe burn trauma leads to an immediate and strong inflammatory response inciting cardiac dysfunction that is associated with high morbidity and mortality. The aim of this study was to determine whether transdermal application of nicotine could influence the burn-induced cardiac dysfunction via its known immunomodulatory effects.Material and Methods. A standardized rat burn model was used in 35 male Sprague Dawley rats. The experimental animals were divided into a control group, a burn trauma group, a burn trauma group with additional nicotine treatment, and a sham group with five experimental animals per group. The latter two groups received nicotine administration. Using microtip catheterization, functional parameters of the heart were assessed 12 or 24 hours after infliction of burn trauma.Results. Burn trauma led to significantly decreased blood pressure (BP) values whereas nicotine administration normalized BP. As expected, burn trauma also induced a significant deterioration of myocardial contractility and relaxation parameters. After application of nicotine these adverse effects were attenuated.Conclusion. The present study showed that transdermal nicotine administration has normalizing effects on burn-induced myocardial dysfunction parameters. Further research is warranted to gain insight in molecular mechanisms and pathways and to evaluate potential treatment options in humans.

Tissue damage due to direct contact of liquid propane with the integument is extremely rare. Only five such cases have been described in the literature. We report the case of a girl who sustained a full-thickness skin necrosis of 14.5 % of her body surface area. There is little agreement about the optimal treatment of these injuries in previous reports. The pathophysiological mechanism suggests a freezing injury. The treatment, however, should be analogous to that of third-degree burns.

INTRODUCTION: For the survival of a microvascular tissue transfer, early detection of vascular complications is crucial. In vivo confocal laser scanning microscopy allows real-time, non-invasive evaluation of tissue microcirculation with a high cellular resolution. The aim of this study was to evaluate confocal laser scanning microscopy for early recognition of flap failure. METHODS: Fourteen patients (ages: 40.2+/-12.4 years) were monitored postoperatively for a period of 24h following free microvascular M. latissimus dorsi transfer to the lower extremity using confocal laser scanning microscopy (Vivascope1500; Rochester; New York; USA). The following parameters were evaluated: quantitative blood-cell flow, diameter of capillary loops and minimal thickness of the epidermis. RESULTS: Venous congestion was characterised by a decrease in blood-cell flow of up to 41%, accompanied by an increase of the diameter of capillary loops of up to 22% and the minimal thickness of the epidermis up to 32%. By contrast, arterial occlusion was clearly verified by a decrease in blood flow of up to 90%, accompanied by an insignificant change of both capillary loop size and epidermal thickness. CONCLUSION: Confocal laser scanning microscopy appears to be a useful non-invasive tool for early recognition of flap failure during the monitoring of microsurgical tissue transfer prior to its clinical manifestation.

Purpose Microcirculatory disturbances are well known during shock; however, the accompanied histomorphological alterations are widely unknown. We used high resolution confocal-laser-scanning microscopy for the evaluation of microcirculation and histomorphology during Burn Shock treatment. Methods Confocal-laser-scanning microscopy was performed in 10 burn shock patients (4 women, 6 men; aged 40.6 ± 11.4 years, burn extent >20% body surface area) initially and 24 hours after shock resuscitation. Ten matched hemodynamic stable burn intensive care unit patients served as controls. The following parameters were evaluated: quantitative blood cell flow, cell size of the granular layer, basal layer thickness, and epidermal thickness. Results Quantitative blood cell flow in controls was 62.45 ± 3.39 cells per minute. Burn shock significantly reduced blood cell flow to 37.27 ± 3.64 cells per minute; fluid resuscitation effectively restored baseline blood flow (65.18 ± 3.76 cells per minute) after 24 hours. Granular cell size was 793.61 ± 41.58 μ m 2 in controls vs 644.27 ± 42.96 μ m 2 during burn shock. Post resuscitation granular cell size measured 932.74 ± 38.83 μ m 2 . Basal layer thickness was 14.84 ± 0.59 μ m in controls, 13.26 ± 0.54 μ m in burn patients at admission and before resuscitation, and 17.50 ± 0.46 μ m after resuscitation. Epidermal thickness in control patients was 49.60 ± 2.36 μ m, 37.83 ± 2.47 μ m in burn patients at admission and 69.50 ± 3.18 μ m after resuscitation. Conclusions Confocal-laser-scanning microscopy provides a noninvasive tool for simultaneous evaluation of microcirculation and tissue histomorphology. It may help to assess the adequacy of and response to resuscitation of burn patients early after trauma.

Background Burn injury is frequently complicated by bacterial infection. Following burn injury, exposure to endotoxin produces a measurable decrease in cardiomyocyte sarcomere contractile function. Lipopolysaccharide-binding protein (LBP) is an acute phase protein that potentiates the recognition of lipopolysaccharide (LPS) by binding to the lipid A moiety of LPS. In this study, we sought to determine the effect of recombinant rat LBP (rLBP) on cardiomyocyte sarcomere function after burn or sham injury in the presence or absence of bacterial endotoxin. Methods Rats underwent a full-thickness 30% total body surface area scald or sham burn. At 24 h post-injury, cardiomyocytes were isolated, plated at 50,000 cells/well, and incubated with 50 μg/mL LPS and rLBP or chloramphenicol acetyltransferase (BVCat, an irrelevant control protein produced using the same expression system as rLBP) at concentrations by volume of 1%, 5%, 10%, and 30%. Subsets of cardiomyocytes were incubated with 5% rat serum or 30% rLBP and blocking experiments were conducted using an LBP-like synthetic peptide (LBPK95A). In vitro sarcomere function was measured using a variable rate video camera system with length detection software. Results Co-culture of burn and sham injury derived cardiomyocytes with high-dose rLBP in the presence of LPS resulted in a significant reduction to the functional impairment observed in peak sarcomere shortening following exposure to LPS alone. LBP-like peptide LBPK95A at a concentration of 20 μg/mL, in the presence of LPS, abolished the ability of 30% rLBP and 5% rat serum to restore peak sarcomere shortening of cardiomyocytes isolated following burn injury to levels of function exhibited in the absence of endotoxin exposure. Conclusions In the setting of LPS challenge following burn injury, rLBP at high concentrations restores cardiomyocyte sarcomere contractile function in vitro . Rather than potentiating the recognition of LPS by the cellular LPS receptor complex, rLBP at high concentrations likely results in an inhibitory binding effect that minimizes the impact of endotoxin exposure on cardiomyocyte function following thermal injury.

Introduction Septic encephalopathy secondary to a breakdown of the blood-brain barrier (BBB) is a known complication of sepsis. However, its pathophysiology remains unclear. The present study investigated the effect of complement C5a blockade in preventing BBB damage and pituitary dysfunction during experimental sepsis. Methods Using the standardised caecal ligation and puncture (CLP) model, Sprague-Dawley rats were treated with either neutralising anti-C5a antibody or pre-immune immunoglobulin (Ig) G as a placebo. Sham-operated animals served as internal controls. Results Placebo-treated septic rats showed severe BBB dysfunction within 24 hours, accompanied by a significant upregulation of pituitary C5a receptor and pro-inflammatory cytokine expression, although gene levels of growth hormone were significantly attenuated. The pathophysiological changes in placebo-treated septic rats were restored by administration of neutralising anti-C5a antibody to the normal levels of BBB and pituitary function seen in the sham-operated group. Conclusions Collectively, the neutralisation of C5a greatly ameliorated pathophysiological changes associated with septic encephalopathy, implying a further rationale for the concept of pharmacological C5a inhibition in sepsis.

Introduction The interaction of the CNS and the immune system is well known. A parasympathetic anti-inflammatory pathway has recently been described. Both electrical and pharmacological parasympathetic stimulation attenuate proinflammatory mediator generation. Burn induces abacterial cytokine generation and we sought to evaluate whether parasympathetic stimulation after experimental burn decreases cardiodepressive mediator generation. Material and methods A 30% TBSA full-thickness rat burn model was used. After microsurgical preparation of the cervical portion of the vagus nerve, we performed electric vagus nerve stimulation. Serum was harvested and organ samples of heart and liver were homogenized. Samples were subjected to sandwich-ELISA specific for TNF-α, IL-1β and IL-6. Heart rate measurements were done using left ventricular microcatheterization. Statistical analysis was done using Student's t-tests and analysis of variance (ANOVA). Results Burn induced a significant rise of TNF-α, IL-1β and IL-6 in organ homogenates and serum. After cervical vagal electrostimulation, serum and organ homogenate levels of proinflammatory cytokines were markedly reduced compared to burn controls. Left ventricular microcatheter assessment demonstrated no cardiodepressive effect of the vagal stimulation itself. Conclusion Our results encourage further research regarding the neuroimmunologic background of burn, possibly leading to the development of a novel therapeutic approach to burn-induced organ dysfunction and immunodysregulation.

Erb's palsy is well known to physicians across medical specialties, and its clinical manifestations present a formidable challenge to reconstructive surgeons. Although the condition is well established, knowledge pertaining to its namesake, Wilhelm Heinrich Erb, is rather obscure in the existing scientific literature. Erb was influential not only through his description of classic brachial plexus palsy involving the superior (or upper) roots, but also by his indelible contributions to our understanding of peripheral nerve physiology, deep tendon reflexes, and the muscular dystrophies. Erb's contributions to medicine transcend specialty boundaries. In this article, the authors seek to convey his scientific achievements and the character of the man through translation of his German manuscripts. These texts, complemented by the existing English literature, provide a unique perspective on Wilhelm Heinrich Erb's contribution to medicine. The authors will also emphasize his role in describing and clarifying the nature of Erb's palsy.

The success of a free microvascular tissue transfer is based on a sufficient microanastomosis which meets the following requirements: a pedicle placed without kinking or twisting, good drainage, a well-defined recipient vessel, integrity of the endothelium, and duration of ischemia. The extent of skin and muscle necrosis increases significantly with increases in ischemia time. Reperfusion of ischemic tissue results in local and systemic damage associated with the release of oxygen free radicals, polymorphonuclear leucocytes, and such endothelial hormones as endothelin-1, EDRF (endothelial-derived relaxing factor), thromboxane, complement, and cytokines. Ischemia-reperfusion disrupts the delicate balance that maintains homeostasis in the microcirculation. This review discusses the clinical and therapeutic aspects of such injury, concentrating on perioperative management in free flap transfer. It points out the possible influence of endothelin-1 on vasospasm at the site of anastomosis, and emphasizes the importance of the endothelium as a highly dynamic network. Finally, future diagnostic and therapeutical aspects are discussed.

Thermal injury induces dermal inflammatory and proapoptotic signaling. These phenomena extend burn wound size and trigger a systemic inflammatory response, factors known to adversely affect outcomes. p38MAPK is known to trigger inflammatory responses and induce epithelial proapoptotic genes. We hypothesize that topical p38MAPK inhibition will attenuate excessive inflammatory and apoptotic signaling and reduce dermal tissue loss. Rats were given a 30% total body surface area partial thickness burn or sham injury. Some of the animals were treated with a p38MAPK inhibitor or vehicle, which was applied directly to the wound. Dermal inflammation was investigated with enzyme-linked immunosorbent assay, reverse transcriptase polymerase chain reaction, myeloperoxidase assay, and Evans blue extravasation. Apoptotic changes were detected using terminal deoxynucleotidyl transferase dUTP nick-end labeling assay and Caspase-3 in situ staining. Burn injury activated dermal p38MAPK and induced a significant rise in dermal IL-6, TNF-alpha, and IL-1beta expression. Neutrophil sequestration, microvascular damage, and hair follicle apoptosis were significantly elevated after injury. Topical p38MAPK inhibition significantly attenuated downstream dermal p38MAPK targets, proinflammatory cytokine expression, neutrophil sequestration, and microvascular injury. A significant reduction in hair follicle apoptosis was seen. This study demonstrates the attenuation of burn-induced cellular stress by topical application of p38MAPK inhibitors. Blunting early excessive inflammatory signaling may be an efficient strategy to improve patient outcomes after burn injury.

Background An altered Kupffer cell (KC) response is thought to be responsible for the characteristic phenotype observed after biliary obstruction: a phenotype marked by a defect in the hepatic reticuloendothelial system and a hypersensitivity to endotoxin. Few studies, however, have directly examined KC function. We have sought to define the specific alterations in function and phenotype that occur in the KC after biliary obstruction. Methods KCs were isolated from female C57BL/6 mice 4 days after a sham or common bile duct ligation (CBDL) operation. Phagocytosis, oxidative burst potential, and intracellular bacterial killing were measured as markers of reticuloendothelial system function. The KC response to endotoxin was assessed by measuring tumor necrosis factor alpha and interleukin 6 levels in the media after stimulation with lipopolysaccharide (LPS) or with LPS plus LPS-binding protein (LBP). Results CBDL KCs demonstrated a significant increase in phagocytic ability and significantly decreased baseline oxidative stress, compared with Shams. The oxidative burst potential, however, was equivalent or higher for CBDL KCs. CBDL KCs also demonstrated increased numbers of viable intracellular bacteria after infection; however, it is unclear if this finding represents impaired intracellular bacterial killing or increased phagocytosis of bacteria. With respect to the KC response to endotoxin, CBDL KCs were found to be less sensitive to the stimulatory effects of LPS alone but were exquisitely sensitive to the effects of LBP. LBP levels were found to be significantly elevated in CBDL animals, and CBDL KCs demonstrated a dose-dependent, exaggerated tumor necrosis factor alpha and interleukin 6 response to LPS administered with LBP. Conclusions KC function is clearly altered after biliary obstruction. Phagocytic ability is actually increased, although the ability of CBDL KCs to kill bacteria within the phagosome remains ill defined. CBDL KCs are exquisitely sensitive to the effects of LBP, and LBP levels are elevated after biliary obstruction. LBP may be responsible for the increased proinflammatory response observed after endotoxin challenge in animals with biliary obstruction.

Multimodal therapy including intraarterial chemotherapy is recognized as state-of-the art therapy for soft-tissue cancer. Multimodal therapy often involves regional limb perfusion followed by sarcoma surgery with reconstruction of the resulting defect. This study was performed in an effort to evaluate the potential of free flap reconstruction after intraarterial therapy. A retrospective chart review of 52 patients who had undergone limb perfusion between 1988 and 1998 at the University of Texas M. D. Anderson Cancer Center and the Division of Plastic Surgery, University of Bochum, Germany, identified 16 patients who had undergone intraarterial limb perfusion that was then followed by surgical resection and free flap reconstruction. There were seven women and nine men, with an average age of 37.9 years. All sixteen patients had received preoperative adjuvant systemic chemotherapy. Reconstruction of the lower extremity was performed most commonly with rectus abdominis and latissimus dorsi free flaps. All vessels used for donor recipient anastomosis had been previously perfused. A vein graft was used in one case. Split-thickness skin grafting over the free flaps was used in four cases. The average length of hospitalization was 21.75 days, with an average follow-up of 20 months. No flap loss or infection was observed. Two flaps demonstrated partial edge necrosis. Three patients developed partial split-thickness skin graft loss and one developed a seroma that required no treatment. A draining sinus tract required resection in one patient. The overall flap success rate was 100 percent, with no flap failures. The overall surgical outcome was considered to be good in 12 patients on the basis of improved function and ambulation, and fair in four who had limitations in function and/or ambulation on the basis of both the patient self-evaluation and the physical therapy evaluation. Seven patients had recurrence of their disease. The overall mean survival time after surgery was 20.6 months. Currently, 10 patients are alive and six have died from their disease. The results of this study indicate that preoperative intraarterial chemotherapy does not significantly increase the risk of immediate free flap complications. Although our numbers are small, we believe that there is no clinical evidence justifying hesitation or refusal of free flap reconstruction after limb perfusion and intraarterial chemotherapy. Routine care in vessel selection and microsurgical technique should be performed to maximize favorable outcomes. Vessels should be inspected for their suitability before undertaking any free flap reconstruction.

Background Complications arising from accidental intraarterial drug injections have been described in the past. However, given the multitude of injected substances and complex pathophysiology, guidelines regarding diagnosis and management of patients with intraarterial injections remain vague. As such it remains unclear, when to expect limb ischemia and whether and for how long to monitor patients after intraarterial injections. Case report We present the case of a "near miss event" in an i.v. drug abuser presenting to the emergency department 3 hours after injection of water dissolved zolpidem (Ambien™) tablets into the right ulnar artery. Chief complaint was forearm pain. Clinical examination at the time revealed no concern for limb ischemia and patient was discharged. The patient returned unplanned 18 hours after injection with an ischemic right hand. Angiography revealed no flow in the distal ulnar artery and minimal flow in the palmar arch. Emergent intraarterial thrombolysis with Urokinase was performed and restored hand perfusion. Clinical follow-up 3 months after injury showed full recovery with regular recapillarisation and normal Allen test. Conclusion This case report highlights the need to rigorously monitor patients with suspected intraarterial injections for potential delayed onset of limb ischemia. This is to our knowledge the first described case report of a successful revascularization after prolonged ischemia with delayed onset after zolpidem injection. We recommend close monitoring of these patients for at least 24 hours in addition to starting prophylactic anticoagulation.