Postoperative Digit and Hand Replantation Protocols: A Review of the Literature.

Successful replantation and revascularization of the hand and digit require a skilled team with urgent access to an operating room with microsurgical capabilities. Although careful indications and surgical techniques contribute to success, postoperative management also plays a vital role in the survival of a replanted digit. Previous research has assessed surgical efficiency and techniques to conduct these procedures, but few studies evaluate postoperative protocols to care for patients undergoing these procedures. Because of the lack of high-level evidence specific to replantation, many common postoperative practices related to monitoring, anticoagulation, and diet have been inferred from elective microsurgical procedures, despite notable differences in operating conditions. The highest level of evidence pertaining to digital replantation was found with the use of peripheral nerve blockade, leeching/bleeding, and nicotine use. This review provides an in-depth evaluation of the literature and insight into the rationale and level of evidence that support each postoperative intervention. It highlights institutional variability and a paucity of high-level evidence pertaining to this topic while identifying the areas of future research.

Updates on and Controversies Related to Management of Radial Nerve Injuries.

Radial nerve injuries are among the most common major traumatic peripheral nerve injuries. Recent literature has updated our knowledge of aspects ranging from radial nerve anatomy to treatment options. Observation and tendon transfers were, and still are, the mainstays of management. However, the improved outcomes of nerve repair even 5 months after injury have changed the treatment algorithm. Nerve repair techniques using conduits, wraps, autograft, and allograft allow tension-free coaptations to improve success. Nerve transfers have evolved to allow a more anatomic recovery of function if used in a timely manner. This review offers an update on radial nerve injuries that reflects recent advances.

Bench-to-bedside review: Burn-induced cerebral inflammation--a neglected entity?

Severe burn injury remains a major burden on patients and healthcare systems. Following severe burns, the injured tissues mount a local inflammatory response aiming to restore homeostasis. With excessive burn load, the immune response becomes disproportionate and patients may develop an overshooting systemic inflammatory response, compromising multiple physiological barriers in the lung, kidney, liver, and brain. If the blood-brain barrier is breached, systemic inflammatory molecules and phagocytes readily enter the brain and activate sessile cells of the central nervous system. Copious amounts of reactive oxygen species, reactive nitrogen species, proteases, cytokines/chemokines, and complement proteins are being released by these inflammatory cells, resulting in additional neuronal damage and life-threatening cerebral edema. Despite the correlation between cerebral complications in severe burn victims with mortality, burn-induced neuroinflammation continues to fly under the radar as an underestimated entity in the critically ill burn patient. In this paper, we illustrate the molecular events leading to blood-brain barrier breakdown, with a focus on the subsequent neuroinflammatory changes leading to cerebral edema in patients with severe burns.

Burn-induced organ dysfunction: vagus nerve stimulation attenuates organ and serum cytokine levels.

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-alpha, IL-1beta 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-alpha, IL-1beta 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.

New multifactorial burn resuscitation formula offers superior predictive reliability in comparison to established algorithms.

UNLABELLED: The Parkland-Baxter formula is a widely utilized resuscitation guideline for the initial management of fluid deficits in burn victims. Implementation of resuscitation formulas has helped to reduce the incidence of shock and hypovolemic organ failure such as acute renal failure in the setting of burn trauma. However, it has been shown that indiscriminate implementation of these formulas may inappropriately suit individual patient's requirements. In our experience resuscitation by the Parkland formula often forced corrections in order to reach predefined resuscitation goals. OBJECTIVE: Given these findings we felt the need to refine formula based resuscitation strategies. PATIENTS AND MEASUREMENTS: Reviewing a subset of 81 burn admissions we screened for predictive parameters in addition to total body surface area burned (TBSA burned) and body weight influencing resuscitation volume requirements. DESIGN: Using multivariate linear regression analysis (MRA) various parameters were integrated in a stepwise forward mathematical selection procedure resulting in a modified resuscitation formula. MAIN RESULTS: A new formula including body weight, TBSA burned, inhalation injury (IHI), high blood alcohol level (BAL) and a compensating factor for advanced age was set up. The new formula was compared to the original Parkland formula. Both were assessed for predictive reliability (PR(+/-20%)). Using this strategy we were able to improve PR(+/-20%) from 28.4% to 51.9%. CONCLUSIONS: Optimal fluid resuscitation of severe burn victims is a complex clinical challenge. Rigid-formula based resuscitation schemes often fail to match all subtleties of current clinical practice but need to provide a reliable starting point for fluid resuscitation. We demonstrate a new multifactorial formula resulting in a better guide to initial fluid resuscitation.

C5a-blockade improves burn-induced cardiac dysfunction.

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.

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.

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.