Early Predictive Factors of Hypofibrinogenemia in Acute Trauma Patients.

It is a well-known fact that the seriously injured have a six times higher risk of fatality in developing countries due to the lack of mature trauma systems. Nearly, 25%–40% of early trauma deaths is due to bleeding which is potentially preventable and hence can be targeted to reduce mortality. Necessary infrastructure for prompt surgical control is of prime importance, and most of the major hospitals in developing countries do have the expertise. However, trauma-induced coagulopathy (TIC) is a well-recognized entity and leads to bad outcomes in spite of prompt surgical control.[1]

TIC results from a combination of bleeding-induced shock, tissue injury-related thrombin-thrombomodulin-complex generation, and the activation of anticoagulant and fibrinolytic pathways.[2]

Hypofibrinogenemia and increased fibrinogen breakdown are key elements of TIC.[1] Hence, immediate correction of the acquired coagulation disorder should be the primary goal of the treatment protocols for bleeding.[2] TIC has already set in by the time patient reaches the hospital, more so in immature trauma systems, which the authors have rightly highlighted.

TIC is multifactorial no doubt but fibrinogen is the first coagulation factor to reach a critically low concentration during activation of coagulation in bleeding, and its reduction is associated with a worse outcome in injured patients.[3]

Thus, an attempt at early detection of derangements with available resources is prudent. Among the various hemostatic treatments available, supplementation of fibrinogen has received growing attention in the last decade.[4]

Fibrinogen can be given as fresh frozen plasma (FFP), cryoprecipitate, or fibrin concentrate. Each of these components has specific limits to the level and timing that fibrin can be replenished. The role of fibrinogen concentrate in trauma-induced coagulopathy has been the object of intense research in the past 10 years.

Developing countries do have stand alone trauma centers with state of the art blood bank services and point of care assessment to detect the specific deranged component in TIC. However, most of the seriously injured are cared for in high volume general hospitals where resource allocation will depend on the priorities essential for that particular health-care system. Resource allocation in trauma itself may be fragmented. Fibrin is available in their facility, but point of care measurements of coagulopathy like Rotem is not available. The authors have attempted to pin point clinical parameters to predict hypofibrinogenemia. A prospective study by Meyer et al. involving 182 seriously injured patients to a level 1 trauma center, sought to delineate the level of fibrinogen by Clauss method as that ascertained by the gold standard of thromboelastography. The viscoelastic hemostatic assays for determining fibrinogen levels correlated with the Clauss fibrinogen level, and there are no differences in the strength of these correlations.[5]

Indeed, although a number of randomized controlled trials investigating the use of fibrinogen concentrate in severe traumatic hemorrhage are currently underway, their results have not yet been published in full.[2]

Recently, published trauma guidelines suggest that fibrinogen supplementation should occur in the presence of plasma fibrinogen levels <1.5–2 g/L or thromboelastometric signs of fibrinogen deficiency.[6] The results of a meta-analysis do not support a benefit in terms of survival from the use of fibrinogen concentrate in the setting of severe trauma.[7] However, the ideal massive transfusion protocol in trauma remains elusive, with considerable geographical and institutional variation.[8] The authors have attempted to find out what could work best for them in their set up. This first step, in the right direction would augur well if they can take this forward, by a prospectively designed study where hypothermia (an easily available clinical parameter) is also factored in.