TY - JOUR
AU - Dubick,, M
AB - Abstract Introduction Traumatic injury remains one of the leading causes of death, with coagulation dysfunction as an important contributor for the mortality. Of these, burns can result in profound metabolic deteriorations with subsequent severe loss of lean body mass. However, a comprehensive understanding of the dynamic and related changes of coagulation and metabolism after burn is lacking. This study investigated metabolic responses of plasma fibrinogen and changes of coagulation in severely burned adults. Methods Ten patients (27±4 years; 91±6kg) with 51±3% total body surface area burn were consented and enrolled into an institutional review board approved prospective study at the Burn Intensive Care Unit. On the study day (18±4 days after burn), a primed (12 µmol/kg) constant infusion of stable isotope 1-13C-phenylalanine (phe, 0.2 µmol/kg/min, 8 hours) and d5-phe (0.2 µmol/kg/min, 4 hours) was performed. During the infusion, vital signs were recorded and arterial blood samples were drawn every hour. The isotopic enrichments in blood samples were used to quantify fibrinogen synthesis rate (from 1-13C-phe infusion), fibrinogen breakdown rate and whole body protein breakdown rate (from d5-phe infusion), using gas chromatography and mass spectrometry analysis. Coagulation changes from the blood samples were measured by clinical coagulation analysis and using Thromboelastography (TEG). Ten normal healthy volunteers (37±7years; 74±5kg) were included with the same isotope infusion and blood samplings as the control group. Results Physiological steady state was observed during the infusion in both groups. Burned adults had elevated heart rates (120±2 vs. 73±5 (control) beats/min), respiration rates (23±2 vs. 15±1 (control) breaths/min), plasma glucose (127±10 vs 89±2 (control) mg/dL) and fibrinogen (613±35 vs 239±17 (control) mg/dL); and reduced plasma albumin (1.3±0.2 vs. 3.7±0.1 (control) g/dL) and total protein (4.4±0.2 vs. 6.8±0.1 (control) g/dL,all p<0.05). In the burn group, the whole body protein breakdown was increased (1.8±1.1 vs. 0.6±0.0 (control) µmol/kg/min); fibrinogen breakdown was elevated (2.3±0.4 vs. 1.0±0.3 (control) µmol/kg/min); and fibrinogen synthesis rate was even more enhanced (4.4±0.7 vs. 0.7±0.2 (control) µmol/kg/min, all p<0.05). Clotting speed (TEG-alpha) and clot strength (TEG-MA) were also increased in the burn group (62±4 vs. 50±4 (control) degrees, and 76±2 vs. 56±2 (control) mm, respectively, both p<0.05). Conclusions The hypercoagulable state postburn is in part a result of increased fibrinogen synthesis, over and above increased fibrinogen breakdown. Applicability of Research to Practice Many burn patients may present with increased risk of complications related to thrombosis, reflecting in part the observed changes in fibrinogen metabolism. This content is only available as a PDF. © American Burn Association 2019. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com This article is published and distributed under the terms of the Oxford University Press, Standard Journals Publication Model (https://academic.oup.com/journals/pages/open_access/funder_policies/chorus/standard_publication_model)
TI - 114 Hypercoagulation and Hypermetabolism of Fibrinogen in Severely Burned Adults
JO - Journal of Burn Care & Research
DO - 10.1093/jbcr/irz013.115
DA - 2019-03-09
UR - https://www.deepdyve.com/lp/oxford-university-press/114-hypercoagulation-and-hypermetabolism-of-fibrinogen-in-severely-FrhZb7vRyD
SP - S73
VL - 40
IS - Supplement_1
DP - DeepDyve
ER -