The Experts below are selected from a list of 20106 Experts worldwide ranked by ideXlab platform
Martin Pollock - One of the best experts on this subject based on the ideXlab platform.
-
Chapter 21 Nerve Thermal Injury
Progress in brain research, 1998Co-Authors: C.d.p. Lynch, Martin PollockAbstract:Publisher Summary This chapter reviews the clinical aspects of nerve Thermal Injury and discusses the experimental studies that illuminate these conditions. The clinical syndromes of nerve Thermal Injury have been described since the time of Hippocrates. The experience of nerve Thermal Injury in the peripheral nervous system is largely restricted to emergency and military physicians and to the practitioners residing in environments with extremes of ambient temperature. Peripheral nerve Injury is a rare complication of hyperthermic syndromes with cases of peripheral neuropathy falling into two groups-a Guillain–Barre syndrome and a multifocal sensorimotor polyradiculoneuropathy. Neuropathy in burn patients is more common but not frequently diagnosed even in burns units. Most burn patients exhibit a mononeuritis multiplex; however, mononeuropathy, radiculopathy, and generalized axonal polyneuropathy have been described. Peripheral nerve Injury in hypothermic disorders is far more common than nerve heat Injury. Cases of cold-induced neuropathy are not limited to military exercises but may be seen in civilian practise.
-
Experimental nerve Thermal Injury
Brain, 1994Co-Authors: Martin PollockAbstract:Thermal Injury to rat sciatic nerve was produced by local heating (47 and 58 degrees C) and studied physiologically and morphologically. Unmyelinated nerve fibres showed a greater direct vulnerability to hyperthermia; first manifest as a reversible conduction block of C fibre action potentials and at higher temperatures by immediate and selective axonal degeneration. By contrast, lower grade nerve Thermal Injury resulted in delayed, selective loss of myelinated fibres. Evidence from this study suggests that this is secondary to a heat-induced angiopathy, immediately and diffusely manifest in the vasa nervorum and giving rise to a progressive and ultimately severe reduction in nerve blood flow. The relative sparing of unmyelinated fibres is likely to be a result of their greater resistance to ischaemia. The pathological vulnerability of unmyelinated fibres to Thermal Injury, coupled with the susceptibility of large myelinated nerve fibres to secondary ischaemia, largely resolves previous contradictions in the literature.
Imad F. Btaiche - One of the best experts on this subject based on the ideXlab platform.
-
Oxandrolone treatment in adults with severe Thermal Injury.
Pharmacotherapy, 2009Co-Authors: James T. Miller, Imad F. BtaicheAbstract:Severe Thermal Injury is associated with hypermetabolism and hyper-catabolism, leading to skeletal muscle breakdown, lean body mass loss, weight loss, and negative nitrogen balance. Muscle protein catabolism in patients with severe Thermal Injury is the result of stress-induced increased release of cytokines and counterregulatory hormones. Coupled with decreased serum anabolic hormone concentrations such as testosterone and growth hormone along with the presence of insulin resistance, anabolism in patients with severe Thermal Injury is inefficient or impossible during the acute postburn period. This causes difficulty in restoring lean body mass and regaining lost body weight, as well as poor healing of the burn wound and delayed patient recovery. Oxandrolone, a synthetic derivative of testosterone, has been used in adult patients with severe Thermal Injury to enhance lean body mass accretion, restore body weight, and accelerate wound healing. In clinical studies, oxandrolone 10 mg orally twice/day improved wound healing, restored lean body mass, and accelerated body weight gain. During the rehabilitation period, oxandrolone therapy with adequate nutrition and exercise improved lean body mass, increased muscle strength, and restored body weight. However, most data on oxandrolone use in adult patients with severe Thermal Injury are derived from single-center studies, many of which enrolled a relatively small number of subjects and some of which had a poor design. Multicenter, prospective, randomized studies are needed to better define the optimal oxandrolone dosage and to confirm the efficacy and safety of this drug in adult patients with severe Thermal Injury.
Satoshi Sawada - One of the best experts on this subject based on the ideXlab platform.
-
radiofrequency ablation combined with co2 injection for treatment of retroperitoneal tumor protecting surrounding organs against Thermal Injury
American Journal of Roentgenology, 2005Co-Authors: Shuji Kariya, Tomokuni Shiraishi, Noboru Tanigawa, Atsushi Komemushi, Yuzo Shomura, Yasuhiro Ueno, Hiroyuki Kojima, Satoshi SawadaAbstract:OBJECTIVE. The objective of this study was to separate target tumors from adjacent structures by injecting carbon dioxide (CO2) around the tumor to avoid Thermal Injury and the heat-sink effect from the blood vessel during percutaneous radiofrequency ablation.CONCLUSION. We successfully achieved complete ablation of a retroperitoneal tumor without Thermal Injury. Imaging-guided percutaneous CO2 injection is useful for preventing Thermal Injury while achieving complete ablation of the tumor during radiofrequency ablation.
James T. Miller - One of the best experts on this subject based on the ideXlab platform.
-
Oxandrolone treatment in adults with severe Thermal Injury.
Pharmacotherapy, 2009Co-Authors: James T. Miller, Imad F. BtaicheAbstract:Severe Thermal Injury is associated with hypermetabolism and hyper-catabolism, leading to skeletal muscle breakdown, lean body mass loss, weight loss, and negative nitrogen balance. Muscle protein catabolism in patients with severe Thermal Injury is the result of stress-induced increased release of cytokines and counterregulatory hormones. Coupled with decreased serum anabolic hormone concentrations such as testosterone and growth hormone along with the presence of insulin resistance, anabolism in patients with severe Thermal Injury is inefficient or impossible during the acute postburn period. This causes difficulty in restoring lean body mass and regaining lost body weight, as well as poor healing of the burn wound and delayed patient recovery. Oxandrolone, a synthetic derivative of testosterone, has been used in adult patients with severe Thermal Injury to enhance lean body mass accretion, restore body weight, and accelerate wound healing. In clinical studies, oxandrolone 10 mg orally twice/day improved wound healing, restored lean body mass, and accelerated body weight gain. During the rehabilitation period, oxandrolone therapy with adequate nutrition and exercise improved lean body mass, increased muscle strength, and restored body weight. However, most data on oxandrolone use in adult patients with severe Thermal Injury are derived from single-center studies, many of which enrolled a relatively small number of subjects and some of which had a poor design. Multicenter, prospective, randomized studies are needed to better define the optimal oxandrolone dosage and to confirm the efficacy and safety of this drug in adult patients with severe Thermal Injury.
S T Zeigler - One of the best experts on this subject based on the ideXlab platform.
-
Bacterial translocation after Thermal Injury
Critical Care Medicine, 1993Co-Authors: David N Herndon, S T ZeiglerAbstract:ObjectivesTo review the mechanisms responsible for bacterial translocation after Thermal Injury. Areas investigated were the rate of bacterial translocation, blood flow to the gastrointestinal tract, potential of reversibility of mesenteric vasoconstriction, specific vasomediators responsible for po
-
Bacterial translocation after Thermal Injury.
Critical care medicine, 1993Co-Authors: D N Herndon, S T ZeiglerAbstract:To review the mechanisms responsible for bacterial translocation after Thermal Injury. Areas investigated were the rate of bacterial translocation, blood flow to the gastrointestinal tract, potential of reversibility of mesenteric vasoconstriction, specific vasomediators responsible for postburn mesenteric vasoconstriction, potential reversal of gut mucosal atrophy with decreased translocation, and evidence of gut mucosal damage after Thermal Injury. Using three different animal models consisting of rats, sheep, and minipigs, the objectives were defined. Using the sheep model, the relationship of decreased mesenteric blood flow after Thermal Injury was defined along with rates of translocation, and the potential reversibility of the postburn mesenteric vasoconstriction and its effect on translocation. The effect of smoke inhalation and the combination of Thermal Injury and inhalation Injury on rates of translocation are explained. Using minipigs, the role that thromboxane A2 plays on the postburn mesenteric vasoconstriction was defined by blocking thromboxane A2 synthesis with OKY046, a specific thromboxane synthetase inhibitor. Evidence of gut mucosal Injury was determined using ornithine decarboxylase as an indicator of gut mucosal damage and subsequent repair in the minipig model. The rat model was used to demonstrate gut mucosal atrophy after Thermal Injury and the potential for reversal of atrophy with the use of bombesin, a specific gut mucosal growth stimulator. After Thermal Injury, there were significant decreases in mesenteric blood flow. There was also an increase in bacterial translocation. Selective infusion of nitroprusside into the cephalic mesenteric artery prevented the post-burn mesenteric vasoconstriction and attenuated bacterial translocation. Smoke inhalation and smoke inhalation with Thermal Injury resulted in mesenteric vasoconstriction and increased rates of bacterial translocation. OKY046 infusion prevented the postburn increase in mesenteric vascular resistance. There were increased concentrations of ornithine decarboxylase within the colonic mucosa, indicating a previous Injury and the presence of ongoing repair. Likewise, there was gut mucosal atrophy after Thermal Injury with bacterial translocation. Treating with bombesin attenuates the postburn mucosal atrophy and prevents bacterial translocation. Thermal Injury is associated with mesenteric vasoconstriction. This postburn mesenteric vasoconstriction results in damage to gut mucosa and allows for increases in bacterial translocation. The postburn mesenteric ischemia can be ameliorated with nitroprusside infusion, thus preventing translocation. Thromboxane A2 appears to be a major mediator of the postburn decrease in mesenteric blood flow. Likewise, prevention of postburn gut mucosal atrophy with bombesin attenuates bacterial translocation.
