De Waele JJ, Vermassen FE. Coagulopathy, hypothermia and acidosis in trauma patients: the rationale for damage control surgery

Intensive Care Unit, Ghent University Hospital, 9000 Ghent, Belgium.
Acta chirurgica Belgica (Impact Factor: 0.44). 11/2002; 102(5):313-6.
Source: PubMed

ABSTRACT Severe trauma to the torso or extremities often results in significant hemorrhage, which contributes to morbidity and mortality. The pathophysiological mechanisms contributing to this traumatic blood loss are complex. We review its major components: coagulopathy, acidosis and hypothermia, which have led to the concept of damage control surgery.

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    ABSTRACT: SIMEONOVA, G. P., D. N. DINEV, I. I. TODOROVA: Influence of hypothermia and acidosis upon some indices of blood coagulation in three schemes of anaesthesia in dogs. Vet. arhiv 75, 233-242, 2005. ABSTRACT The aim of the present study was to investigate the influence of hypothermia and acidosis on blood coagulation in different anaesthesia protocols. Our experiment was performed with 28 dogs, divided into four groups: three experimental submitted to inhalation, balanced, and epidural anaesthesia and one control. In all animals blood pH, core body temperature and some principal parameters of blood coagulation (platelet count, activated partial prothrombine time-APPT, prothrombine time-PT and plasma fibrinogen concentrations) were investigated. The dynamics included five periods; prior to anaesthesia (0 th minute), at the time of pre-medication (30 th minute), during deep anaesthesia (120 th minute), after recovery (about 140 th minute), and on the next day (24 th hour). The results indicated that the most significant were changes in balanced anaesthesia. APPT was shortened after recovery from balanced anaesthesia (14.1 ± 0.9 seconds, P<0.05) and on the next day (14.5 ± 0.7, P<0.05) compared to the initial value (16.1 ± 0.5). The most pronounced acidosis in this group was recorded during deep anaesthesia (7.126 ± 0.041, P<0.001) and after recovery (7.241 ± 0.028, P<0.05) by comparison with the baseline (7.312 ± 0.008). Parameters of blood coagulation in inhalation anaesthesia group were unchanged. Statistically significant alterations in blood pH were observed only during the deep anaesthesia stage (7.199 ± 0.049, P<0.01) compared to the beginning (7.316 ± 0.006). Epidural anaesthesia did not result in blood pH and coagulation changes. In this group an increase in fibrinogen concentrations at 24 th hour (3.7 ± 0.2, P<0.05) were found, compared to the baseline (3.1 ± 0.2), which was probably due to the intervention. In the three groups the core body temperature was decreased at the 120 th minute and 140 th minute. In conclusion, balanced anaesthesia activated blood coagulation at the 140 th minute and 24 th hour, which was manifested by a shortening in APPT at these periods. Hypothermia and acidosis accompanying balanced and inhalation anaesthesia groups, as well as hypothermia in epidural anaesthesia had no influence upon blood coagulation parameters.
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