Marc Maegele

Volume replacement during trauma resuscitation: a brief synopsis of current guidelines and recommendations

IntroductionIntravascular volume and fluid replacement are still cornerstones to correct fluid deficits during early trauma resuscitation, but optimum strategies remain under debate.MethodsA synopsis of best current knowledge with reference to the following guidelines and recommendations is presented: (1) The European Guideline on Management of Major Bleeding and Coagulopathy following Trauma (fourth edition), (2) S3 Guideline on Treatment of Patients with Severe and Multiple Injuries [English Version of the German Guideline S3 Leitlinie Polytrauma/Schwerverletzten-Behandlung/AWMF Register-Nr. 012/019 sponsored by the German Society for Trauma Surgery/Deutsche Gesellschaft für Unfallchirurgie (DGU)], and (3) S3 Guideline Intravascular Volume Treatment in the Adult [AWMF Register-Nr 001/020 sponsored by the German Society for Anesthesiology and Intensive Medicine/Deutsche Gesellschaft für Anästhesiologie und Intensivmedizin (DGAI)].Results and conclusionsVolume replacement at a reduced level in severely injured and bleeding trauma patients is advocated (permissive hypotension) until the bleeding is controlled. ATLS principles with Hb, BE, and/or lactate can assess perfusion, estimate/monitor the extent of bleeding/shock, and guide therapy. Isotonic crystalloid solutions are first-line and specific recommendations apply for patients with TBI.

In vitro effects of different sources of fibrinogen supplementation on clot initiation and stability in a model of dilutional coagulopathy

To analyse which fibrinogen source may improve coagulation using an in vitro 33% dilutional coagulopathy model.

Is the shock index based classification of hypovolemic shock applicable in multiple injured patients with severe traumatic brain injury?-an analysis of the TraumaRegister DGU(®).

BackgroundA new classification of hypovolemic shock based on the shock index (SI) was proposed in 2013. This classification contains four classes of shock and shows good correlation with acidosis, blood product need and mortality. Since their applicability was questioned, the aim of this study was to verify the validity of the new classification in multiple injured patients with traumatic brain injury.MethodsBetween 2002 and 2013, data from 40 888 patients from the TraumaRegister DGU® were analysed. Patients were classified according to their initial SI at hospital admission (Class I: SI < 0.6, class II: SI ≥0.6 to <1.0, class III SI ≥1.0 to <1.4, class IV: SI ≥1.4). Patients with an additional severe TBI (AIS ≥ 3) were compared to patients without severe TBI.Results16,760 multiple injured patients with TBI (AIShead ≥3) were compared to 24,128 patients without severe TBI. With worsening of SI class, mortality rate increased from 20 to 53% in TBI patients. Worsening SI classes were associated with decreased haemoglobin, platelet counts and Quick’s values. The number of blood units transfused correlated with worsening of SI. Massive transfusion rates increased from 3% in class I to 46% in class IV. The accuracy for predicting transfusion requirements did not differ between TBI and Non TBI patients.DiscussionThe use of the SI based classification enables a quick assessment of patients in hypovolemic shock based on universally available parameters. Although the pathophysiology in TBI and Non TBI patients and early treatment methods such as the use of vasopressors differ, both groups showed an identical probability of recieving blood products within the respective SI class.ConclusionRegardless of the presence of TBI, the classification of hypovolemic shock based on the SI enables a fast and reliable assessment of hypovolemic shock in the emergency department. Therefore, the presented study supports the SI as a feasible tool to assess patients at risk for blood product transfusions, even in the presence of severe TBI.

How do external factors contribute to the hypocoagulative state in trauma-induced coagulopathy? – In vitro analysis of the lethal triad in trauma

BackgroundExternal factors following trauma and iatrogenic intervention influence blood coagulation and particularly clot formation. In particular, three external factors (in detail dilution via uncritical volume replacement, acidosis and hypothermia), in combination, referred to as the “lethal triad”, substantially aggravate the hypocoagulative state after trauma. Contribution of these external factors to the resulting hypocoagulative state in trauma and especially their influence on primary haemostasis has still not been investigated systematically.This study aims to assess this contribution to the aggravating hypocoagulative state in trauma-induced coagulopathy (TIC) using an in vitro simulation assay. Emphasis is given to platelet contribution to clot formation and to the investigation of how platelet activation alters under the respective conditions.MethodsTo simulate the conditions of lethal triad in vitro, whole blood samples taken from five healthy volunteers were introduced to the respective conditions. Besides standard coagulation testing, thrombelastometric analysis and differentiated platelet mapping were performed.ResultsAll three simulated conditions induced significant impairments of clot formation (clot formation time, CFT; α -angle) and propagation (maximum clot firmness, MCF; Diameter A5-A25), with the highest impact under hypothermia and dilution. Consistently, lethal triad resulted in an additive effect of all conditions. None of the simulated conditions induced a statistically relevant change in coagulation initiation assessed by EXTEM and FIBTEM thrombelastometry.Platelet contribution to clot formation decreased gradually under the respective conditions, reaching statistical significance for simulated dilution, and attaining its greatest extent under the conditions of lethal triad (Δtrias/baseline 0.59; p = 0.01). Consistent, reduced CD62 expression levels were observed under experimental acidosis (Δacidosis/baseline 0.32; p = 0.006), dilution (Δdilution/baseline 0.34; p = 0.01) and lethal triad (Δlethal triad/baseline 0.24; p = 0.01).ConclusionThe respective external factors of lethal triad play a pivotal role in the development of coagulopathy, essentially influencing the kinetics of clot formation, and to a varying extent clot diameter, as measured by thrombelastometry. Moreover, impairment of platelet function under the conditions of lethal triad plays a key role in the pathophysiology of TIC, resulting in reduced responsiveness to stimulation with ADP that might also be present after trauma. Our data indicate that impairment of primary haemostasis contribute to the hypocoagulative state in TIC after trauma aggravated by external factors of lethal triad.