Articles: trauma.
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J Vet Emerg Crit Care (San Antonio) · Jan 2014
ReviewTraumatic coagulopathy--part 1: Pathophysiology and diagnosis.
To review the current literature in reference to the pathophysiology and diagnostic modalities available for acute traumatic coagulopathy (ATC) in relationship to traumatic hemorrhagic shock. ⋯ Massive hemorrhage accounts for 30-56% of prehospital posttraumatic deaths in people, with coagulopathic hemorrhage remaining one of the major causes of preventable deaths within the first 24 hours posttrauma. Ten to twenty-five percent of human trauma patients experience ATC, which has been shown to prolong hemorrhage, deter resuscitative efforts, promote sepsis, and increase mortality by at least 4-fold. Prognosis in veterinary patients is not currently known.
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Critical care clinics · Jan 2014
Review Case ReportsThe FAST and E-FAST in 2013: Trauma Ultrasonography: Overview, Practical Techniques, Controversies, and New Frontiers.
This article reviews important literature on the FAST and E-FAST examinations in adults. It also reviews key pitfalls, limitations, and controversies. A practical "how-to" guide is presented. Lastly, new frontiers are explored.
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Frontiers in neuroscience · Jan 2014
ReviewCerebral metabolism following traumatic brain injury: new discoveries with implications for treatment.
Because it is the product of glycolysis and main substrate for mitochondrial respiration, lactate is the central metabolic intermediate in cerebral energy substrate delivery. Our recent studies on healthy controls and patients following traumatic brain injury (TBI) using [6,6-(2)H2]glucose and [3-(13)C]lactate, along with cerebral blood flow (CBF) and arterial-venous (jugular bulb) difference measurements for oxygen, metabolite levels, isotopic enrichments and (13)CO2 show a massive and previously unrecognized mobilization of lactate from corporeal (muscle, skin, and other) glycogen reserves in TBI patients who were studied 5.7 ± 2.2 days after injury at which time brain oxygen consumption and glucose uptake (CMRO2 and CMRgluc, respectively) were depressed. By tracking the incorporation of the (13)C from lactate tracer we found that gluconeogenesis (GNG) from lactate accounted for 67.1 ± 6.9%, of whole-body glucose appearance rate (Ra) in TBI, which was compared to 15.2 ± 2.8% (mean ± SD, respectively) in healthy, well-nourished controls. ⋯ Use of a diagnostic to monitor BES to provide health care professionals with actionable data in providing nutritive formulations to fuel the body and brain and achieve exquisite glycemic control are discussed. In particular, the advantages of using inorganic and organic lactate salts, esters and other compounds are examined. To date, several investigations on brain-injured patients with intact hepatic and renal functions show that compared to dextrose + insulin treatment, exogenous lactate infusion results in normal glycemia.
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J Emerg Trauma Shock · Jan 2014
ReviewCurrent concepts, which effect outcome following major hemorrhage.
There are a multitude of factors, which effect outcome following major trauma. The recent conflict in the middle-east has advanced our knowledge and developed clinical practice, here within the UK. This article reviews the current and emerging concepts, which effect the outcome of patients sustaining major hemorrage in trauma.
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Cumulating evidence indicated that nerve injury-associated cellular and molecular changes play an essential role in contributing to the development of pathological pain, and more recent findings implicated the critical role of epigenetic mechanisms in pain-related sensitization in the DRG subsequent to nerve injury. In this part of the dyad review (Part II), we reviewed and paid special attention on the etiological contribution of DGR gene expression modulated by epigenetic mechanisms of CRPS. As essential effectors to different molecular activation, we first discussed the activation of various signaling pathways that subsequently from nerve injury, and in further illustrated the fundamental and functional underpinnings of nerve injury-induced pain, in which we argued for the potential epigenetic mechanisms in response to sensitizing stimuli or injury. Therefore, understanding the specific mediating factors that influence individual epigenetic differences contributing to pain sensitivity and responsiveness to analgesics possesses crucial clinical implications.