The Effects of Rapid Rewarming on Tissue Salvage in Severe Frostbite Injury.

Frostbite is a high morbidity injury caused by soft tissue freezing, which can lead to digit necrosis requiring amputation. Rapid rewarming is a first-line treatment method that involves placing affected digits into a warm water bath. This study aims to assess the clinical practices for frostbite at facilities outside of dedicated burn centers, and any impact these practices have on tissue salvage.

An Institutional Protocol for the Treatment of Severe Frostbite Injury-A 6-Year Retrospective Analysis.

The treatment of severe frostbite injury has undergone rapid development in the past 30 years with many different diagnostic and treatment options now available. However, there is currently no consensus on the best method for management of this disease process. At our institution, we have designed a protocol for severe frostbite injury that includes diagnosis, medical treatment, wound cares, therapy, and surgery.

Severe Hypothermia and Frostbite Requiring ECMO and Four Limb Amputations.

Severe hypothermia and frostbite can result in significant morbidity and mortality. We present a case of a patient with severe hypothermia and frostbite due to cold exposure after a snowmobile crash. He presented in cardiac arrest with a core temperature of 19°C requiring prolonged cardiopulmonary resuscitation, active internal rewarming, venoarterial extracorporeal membrane oxygenation, and subsequently amputations of all four extremities.

Microangiography: An Alternative Tool for Assessing Severe Frostbite Injury.

Assessment of frostbite injury typically relies on computed tomography, angiography, or nuclear medicine studies to detect perfusion deficits prior to thrombolytic therapy. The aim of this study was to evaluate the potential of a novel imaging method, microangiography, in the assessment of severe frostbite injury. Patients with severe frostbite were included if they received a post-thrombolytic Technetium 99 (Tc99) bone scan, a Tc99 bone scan without thrombolytic therapy, and/or post-thrombolytic microangiography (MA) study.

Defective signal joint recombination in fanconi anemia fibroblasts reveals a role for Rad50 in V(D)J recombination.

V(D)J recombination of immunoglobulin loci is dependent on the immune cell-specific Rag1 and Rag2 proteins as well as a number of ubiquitously expressed cellular DNA repair proteins that catalyze non-homologous end-joining of DNA double-strand breaks. The evolutionarily conserved Rad50/Mre11/Nibrin protein complex has a role in DNA double-strand break-repair, suggesting that these proteins, too, may participate in V(D)J recombination. Recent findings demonstrating that Rad50 function is defective in cells from patients afflicted with Fanconi anemia provide a possible mechanistic explanation for previous findings that lymphoblasts derived from these patients exhibit subtle defects in V(D)J recombination of extrachromosomal plasmid molecules.