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The primary objective is to identify and describe the complications associated with the use of intravenous lipid emulsion (ILE) therapy as an antidote for lipophilic drug toxicity. This study is a retrospective chart review of patients treated with ILE at two academic medical centers between 2005 and 2012. Based on previously reported complications, we hypothesized that pancreatitis, ARDS, and lipemiainduced laboratory interference might occur. Clinical definitions of these complications were defined a priori. Subjects treated with ILE who did not develop at least one complication were excluded. A total of nine patients were treated with ILE during the study period, six of whom experienced potential complications as a result of the ILE. Two patients developed pancreatitis, and four patients had lipemia-induced interference of interpretation of laboratory studies, despite ultracentrifugation. Laboratory interference precluded one patient from being an organ donor. Three patients developed ARDS; although temporally associated, a causal relationship between ILE and the development of ARDS cannot be clearly established. As ILE is increasingly used for less severe cases of drug toxicity, clinicians should be aware of potential complications associated with its use. A risk-benefit assessment for the use of ILE should be implemented on a case-by-case basis.

Non-healing wounds represent a significant cause of morbidity and mortality for a large portion of the adult population. Wounds that fail to heal are entrapped in a self-sustaining cycle of chronic inflammation leading to the destruction of the extracellular matrix. Among cancer patients, malnutrition, radiation, physical dehabilitation, chemotherapy, and the malignancy itself increase the likelihood of chronic wound formation, and these co-morbidity factors inhibit the normal wound healing process. Current wound treatments are aimed at some, but not all, of the underlying causes responsible for delayed healing of wounds. These impediments block the normal processes that allow normal progression through the specific stages of wound healing. This review summarizes the current information regarding the management and treatment of complex wounds that fail to heal normally and offers some insights into novel future therapies [1,2].

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Mechanistically, adjunctive therapy with ketamine may attenuate the demonstrated neuroexcitatory contribution of N-methyl-D-aspartate receptor stimulation in severe ethanol withdrawal, reduce the need for excessive gamma-aminobutyric acid agonist mediated-sedation, and limit associated morbidity. A ketamine infusion in patients with delirium tremens was associated with reduced gamma-aminobutyric acid agonist requirements, shorter ICU length of stay, lower likelihood of intubation, and a trend toward a shorter hospitalization.

The complex interactions that characterize acute wound healing have stymied the development of effective therapeutic modalities. The use of computational models holds the promise to improve our basic approach to understanding the process. By modifying an existing ordinary differential equation model of systemic inflammation to simulate local wound healing, we expect to improve the understanding of the underlying complexities of wound healing and thus allow for the development of novel, targeted therapeutic strategies. The modifications in this local acute wound healing model include: evolution from a systemic model to a local model, the incorporation of fibroblast activity, and the effects of tissue oxygenation. Using these modifications we are able to simulate impaired wound healing in hypoxic wounds with varying levels of contamination. Possible therapeutic targets, such as fibroblast death rate and rate of fibroblast recruitment, have been identified by computational analysis. This model is a step toward constructing an integrative systems biology model of human wound healing.A soft tissue injury elicits a well-prescribed wound healing response.1,2 The process of wound healing is designed to restore anatomic and functional characteristics of the tissue; however, little progress has been made in improving the wound healing response time or in preventing complications such as fibrosis, infections, and formation of nonhealing wounds.3 In this paper, we describe a computational model of acute wound healing designed to allow a system-level analysis of the wound healing response using ordinary differential equations (ODEs). As a first step to a more comprehensive model, we have explored the combined effects of bacterial infections, inflammation, and tissue hypoxia on the rate and success of wound healing since these processes are well-known as affecters of healing. As this model matures, it will provide the opportunity to test new mechanisms and novel therapeutics of wound healing strategies in silico.Despite burgeoning interest in the field of computational biology, work of limited scope has been published on modeling the acute wound. Most of these studies show the difficulties of adequately accounting for the myriad of potential interactions. 4 For example, in their respective works on epidermal wound healing, Stekel et al., 5 Walker et al., 6 and Morel et al. 7 do not attempt to simulate healing by fibroblasts and do not implement inflammatory changes in their models. Dallon et al. 8 constructed an ODE model of collagen deposition focusing on the fibroblasts and their relationship to the underlying extracellular matrix, but do not account for inflammation or repair of underlying tissue damage. Schugart et al. 9 recently published a model of wound angiogenesis as a function of tissue oxygen tension but the model does not specifically address the wound healing process.Reynolds et al. 10,11 created an ODE model designed to simulate inflammation and repair on a systemic level in the setting of a systemic ins...

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It is well recognized that stress of any nature will cause a delay in the wound healing response. This delayed healing response appears closely associated with immune regulators. In this study, CD-1 mice were injected with a long acting form of methyl prednisolone to cause a steroid-induced immune suppression. After 24 hours, two 6-mm full thickness wounds were placed on the animals' backs and one group of animals received the immune-regulating hormone, androstenediol. Wound contraction was quantified by planimetry for the subsequent 14 days. Animals that were stressed with methyl prednisolone but receiving androstenediol contracted their open wounds at faster rates compared with methyl prednisolone-stressed animals treated with the vehicle alone. These findings suggest that restoration of immune regulation by androstenediol can reverse the delayed open wound contraction secondary to steroid stress.