Non-technical skills training in the operating theatre: A meta-analysis of patient outcomes.

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 < 0.0001). Technical performance and checklist use were unchanged. 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.

Evidence-based topical management of chronic wounds according to the T.I.M.E. principle.

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.

An essential role for complement C5a in the pathogenesis of septic cardiac dysfunction.

Defective cardiac function during sepsis has been referred to as "cardiomyopathy of sepsis." It is known that sepsis leads to intensive activation of the complement system. In the current study, cardiac function and cardiomyocyte contractility have been evaluated in rats after cecal ligation and puncture (CLP). Significant reductions in left ventricular pressures occurred in vivo and in cardiomyocyte contractility in vitro. These defects were prevented in CLP rats given blocking antibody to C5a. Both mRNA and protein for the C5a receptor (C5aR) were constitutively expressed on cardiomyocytes; both increased as a function of time after CLP. In vitro addition of recombinant rat C5a induced dramatic contractile dysfunction in both sham and CLP cardiomyocytes, but to a consistently greater degree in cells from CLP animals. These data suggest that CLP induces C5aR on cardiomyocytes and that in vivo generation of C5a causes C5a-C5aR interaction, causing dysfunction of cardiomyocytes, resulting in compromise of cardiac performance.

Evaluation of signal transduction pathways after transient cutaneous adenoviral gene delivery.

BACKGROUND: Adenoviral vectors have provided effective methods for in vivo gene delivery in therapeutic applications. However, these vectors can induce immune responses that may severely affect the ability of vector re-application. There is limited information about the mechanisms and signal transduction pathways involved in adenoviral recognition. For optimization of cutaneous gene therapy it is necessary to investigate molecular mechanisms of virus recognition in epidermal cells. The aim of this study was to investigate the signal transduction of the innate immunity after adenoviral DNA internalization in keratinocytes. METHODS: In vitro, keratinocytes were transfected with DNA, in the presence and absence of inhibitors for signalling molecules. In vivo, immunocompetent and athymic mice (n = 3 per group) were twice transduced with an Ad-vector. RESULTS: The results show an acute induction of type-I-interferon after in vitro transfection. Inhibition of PI3K, p38 MAPK, JNK and NFkappaB resulted in a decreased expression of type-I-interferon. In contrast to immunocompetent mice, athymic mice demonstrated a constant transgene expression and reduced inflammatory response in vivo. CONCLUSION: The results suggest an induction of the innate immunity triggered by cytoplasm localised DNA which is mediated by PI3K-, p38 MAPK-, JNK-, NFkappaB-, JAK/STAT- and ERK1/2-dependent pathways. A stable transgene expression and a reduced inflammatory response in immunodeficient mice have been observed. These results provide potential for an effective adenoviral gene delivery into immunosupressed skin.

Burn-induced heart failure: lipopolysaccharide binding protein improves burn and endotoxin-induced cardiac contractility deficits.

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.

Inhibition of complement C5a prevents breakdown of the blood-brain barrier and pituitary dysfunction in experimental sepsis.

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.

Ability of antioxidant liposomes to prevent acute and progressive pulmonary injury.

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.

Role of host defense peptides of the innate immune response in sepsis.

Innate immune response and its effector molecules have received growing attention in research. Host defense peptides are known to be antimicrobially active. Recently, the peptides have been recognized as potent signaling molecules for cellular effectors of both innate and adaptive immunity. Mammalian peptides in particular revealed immunomodulatory functions, including endotoxin-binding and -neutralizing capacity, chemotactic activities, induction of cytokines and chemokines, promotion of wound healing, and angiogenesis. In sepsis, they present a family of natural substances that can be used in combination with antibiotics to complete a broad-spectrum antimicrobial regimen with endotoxin-neutralizing properties. Although there are side effects, host defense peptides have the potential to be significant reinforcements to the currently available therapeutic options in the future. In this review, we analyze the role of host defense peptides in infection and immune response, and discuss recent efforts to establish host defense peptides as potent novel therapeutic agents for the treatment of sepsis.

Complement-related molecular events in sepsis leading to heart failure.

Despite intensive ongoing research efforts, the mortality of patients with sepsis remains unacceptably high. A significant number of clinical trials have failed to produce sufficient therapeutic strategies despite showing promising results in animal models. So far, many studies have focused on deterioration of the humoral and cellular components of the immune system, the main cause of death in septic patients being multi-organ failure. However, not much is known about the effects of the complement system on parenchymal cells of organs such as the heart. Recently, septic cardiomyopathy has been recognized as one of the major complications during sepsis, often determining the clinical outcome. In this review, we describe molecular events which are thought to be related to cardiac dysfunction during sepsis. A special emphasis will be placed on the complement system, which generates powerful anaphylatoxins (such as C5a) and which has recently been associated with septic cardiomyopathy. Together with the impact on cardiac function of various cytokines we will provide a synopsis of the current knowledge regarding the pathophysiology underlying cardiac failure during sepsis with a special emphasis on C5a and C5aR.

Topical p38 MAPK inhibition reduces bacterial growth in an in vivo burn wound model.

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.

Topical p38MAPK inhibition reduces dermal inflammation and epithelial apoptosis in burn wounds.

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.

Cardiomyocyte function after burn injury and lipopolysaccharide exposure: single-cell contraction analysis and cytokine secretion profile.

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.

Altered Kupffer cell function in biliary obstruction.

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.

Transdermal Nicotine Application Attenuates Cardiac Dysfunction after Severe Thermal Injury.

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.

Lipoteichoic acid from Staphylococcus aureus directly affects cardiomyocyte contractility and calcium transients.

Lipoteichoic acid (LTA) is the key pathogenic factor of gram-positive bacteria and contributes significantly to organ dysfunction in sepsis, a frequent complication in critical care patients. We hypothesized that LTA directly affects cardiomyocyte function, thus contributing to cardiac failure in sepsis. This study was designed to evaluate the effects of LTA on contractile properties and calcium-transients of isolated adult rat cardiomyocytes. When myocytes were exposed to LTA for 1h prior to analysis, the amplitudes of calcium-transients as well as sarcomere shortening increased to 130% and 142% at 1 Hz stimulation frequency. Relengthening of sarcomeres as well as decay of calcium-transients was accelerated after LTA incubation. Exposure to LTA for 24 h resulted in significant depression of calcium-transients as well as of sarcomere shortening compared to controls. One of the major findings of our experiments is that LTA most likely affects calcium-handling of the cardiomyocytes. The effect is exacerbated by reduced extracellular calcium, which resembles the clinical situation in septic patients. Functionally, an early stimulating effect of LTA with increased contractility of the cardiomyocytes may be an in vitro reflection of early hyperdynamic phases in clinical sepsis. Septic disorders have been shown to induce late hypodynamic states of the contractile myocardium, which is also supported at the single-cell level in vitro by results of our 24h-exposure to LTA.

Anticoagulative strategies in reconstructive surgery--clinical significance and applicability.

Advanced strategies in reconstructive microsurgery and especially free tissue transfer with advanced microvascular techniques have been routinely applied and continuously refined for more than three decades in day-to-day clinical work. Bearing in mind the success rates of more than 95%, the value of these techniques in patient care and comfort (one-step reconstruction of even the most complex tissue defects) cannot be underestimated. However, anticoagulative protocols and practices are far from general acceptance and - most importantly - lack the benchmark of evidence basis while the reconstructive and microsurgical methods are mostly standardized. Therefore, the aim of our work was to review the actual literature and synoptically lay out the mechanisms of action of the plethora of anticoagulative substances. The pharmacologic prevention and the surgical intervention of thrombembolic events represent an established and essential part of microsurgery. The high success rates of microvascular free tissue transfer as of today are due to treatment of patients in reconstructive centers where proper patient selection, excellent microsurgical technique, tissue transfer to adequate recipient vessels, and early anastomotic revision in case of thrombosis is provided. Whether the choice of antithrombotic agents is a factor of success remains still unclear. Undoubtedly however the lack of microsurgical experience and bad technique can never be compensated by any regimen of antithrombotic therapy. All the more, the development of consistent standards and algorithms in reconstructive microsurgery is absolutely essential to optimize clinical outcomes and increase multicentric and international comparability of postoperative results and complications.

[The pedicled groin flap for defect closure of the hand]. / Der gestielte Leistenlappen zur Defektdeckung an der Hand.

OBJECTIVE: Soft-tissue defect closure of the volar and dorsal aspect of the hand and lower arm with a maximum defect size of 10 × 25 cm. INDICATIONS: Soft-tissue defects of the entire palm and dorsum of the hand and lower arm with a maximum defect size of 10 × 25 cm. CONTRAINDICATIONS: Polytraumatized patients presenting with concomitant life-threatening injuries. In these cases one should perform the definite defect closure secondary after cardiovascular stabilization. Scars and vascular injury at the donor site. Lack of vascularity and necrosis of implantation site. Poorly vascularized recipient site (e.g. after radiation) Infection and necrosis at the donor and/or recipient site. Prior operations of the groin with impairment of the vasculature. Noncompliant patient. SURGICAL TECHNIQUE: Landmarks are the femoral artery, inguinal ligament, anterior superior iliac spine, and sartorius muscle. The superior and inferior border of the flap should be orientated parallel to the inguinal ligament. The longitudinal axis of the flap is parallel to the superficial circumflex iliac artery, which is partially located superior to the inguinal ligament. One third of the flap is located superior, and two thirds inferior, to the inguinal ligament. Flap dissection starts at the lateral border without including the fascia. Identification of the lateral border of the sartorius muscle, incision of its fascia and inclusion of the fascia into flap dissection in order to preserve the vessel. If a long flap pedicle is favored, flap dissection is continued to the source of the superficial circumflex iliac artery. Primary closure of the donor site and, finally, inset of the flap. A tubed pedicle protects the vessels and simplifies the ischemic preconditioning during the postoperative phase. According to the flap size, the donor site closure is either primary or split-thickness skin grafting is necessary at the lateral aspect of the donor site. The mean duration of the procedure is 120 min in a teaching hospital (own data). POSTOPERATIVE MANAGEMENT: The patient should be mobilized as early as possible. Dressings and flap monitoring should be performed daily. Ischemic preconditioning by applying a tourniquet starts after 10-14 days. The ischemic period is increased continuously from 3 × 5 min/d in the beginning to 3 × 1 h/d before flap dissection. Flap dissection of the pedicle is performed after 3 weeks. The residual donor site is closed, while the distal pedicle is left untrimmed and closed secondarily a few days later to allow for sufficient venous drainage. Finally, defect closure can be completed after demarcation of the pedicle. RESULTS: In a 3-year period, defect closure with a pedicled groin flap was performed in 14 patients. Indications for this procedure were the following: thumb reconstruction for lengthening and defect closure after amputation and burn injury, soft-tissue reconstruction of the dorsum of the hand after decollement and infection, soft-tissue reconstruction of the distal part of the lower arm, wrist and palm after complex and combined trauma, and plastic reconstructive preservation of multiple fingers with subsequent phalangealization and syndactyly release, respectively. In all patients, complete soft-tissue coverage and flap survival could be achieved. The functional and aesthetic result was satisfactory in all cases.

Insight in microcirculation and histomorphology during burn shock treatment using in vivo confocal-laser-scanning microscopy.

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 microm(2) in controls vs 644.27 +/- 42.96 microm(2) during burn shock. Post resuscitation granular cell size measured 932.74 +/- 38.83 microm(2). Basal layer thickness was 14.84 +/- 0.59 microm in controls, 13.26 +/- 0.54 microm in burn patients at admission and before resuscitation, and 17.50 +/- 0.46 microm after resuscitation. Epidermal thickness in control patients was 49.60 +/- 2.36 microm, 37.83 +/- 2.47 microm in burn patients at admission and 69.50 +/- 3.18 microm 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.

Burn-induced organ dysfunction: vagus nerve stimulation improves cardiac function.

INTRODUCTION: Many studies have demonstrated the existence of an anti-inflammatory, parasympathetic pathway, termed as the inflammatory reflex. Burn-induced heart failure has been investigated in many previous studies. Proinflammatory cytokines, such as TNF-alpha, IL-1beta, and IL-6, have been shown to play a key pathogenetic role and vagus nerve stimulation attenuates proinflammatory cytokine production. This study was designed to evaluate postburn alterations of cardiac functional parameters after vagal electrostimulation. MATERIAL AND METHODS: A 30% total body surface area standardized, full-thickness rat burn model was used. Electric stimulation of the vagus nerve was performed. The following functional cardiac parameters were measured by ventricular microcatheterization: Maximal and minimal left ventricular pressure, mean left ventricular pressure, end-diastolic pressure (EDP), positive and negative pressure rise and fall (+/-dP/dt), cardiac contractility index, and assessment of the heart rate. RESULTS: Vagus nerve stimulation improved maximal and minimal left ventricular pressure values compared with burn-only animals. End-diastolic pressure was elevated significantly in stimulated animals; however, EDP values were comparable with those in sham-injured animals. Analyzing positive and negative pressure development, +/-dP/dt was restored to levels measured in sham-injured animals but not to control animal levels. No variations in heart rate were found. CONCLUSION: We as well as others have shown that inflammation after burn injury is a key pathogenetic element, and this study provides new evidence that cardiac function is also improved by vagus nerve stimulation. These results lead us to consider novel therapeutic options for the treatment of postburn cardiac dysfunction.