Fibrinogen concentrate and cryoprecipitate
As a precursor of clot formation, fibrinogen plays a major
role in coagulation function. Fibrinogen deficiency is linked
to uncontrolled bleeding and compromised survival. Hypo-
fibrinogenemia is an important part of trauma associated
coagulopathy. The use of fibrinogen concentrate and cryoprecipitate
is recommended when the plasma fibrinogen
level falls below1.5e2.0 g/l or when there is a thromboelastometric
evidence of functional fibrinogen deficiency
(Grade 1C).16 An initial fibrinogen concentrate dose of 3e4 g
or 50 mg/kg of cryoprecipitate, which is approximately
equivalent to 15e20 units in a 70 kg adult and further doses
based on thromboelastometric analysis is recommended
(Grade 2C).16
Antifibrinolytics
Hyperfibrinolysis is an important contributor to trauma
induced coagulopathy. Fibrinolysis greater than 3% as
measured by thromboelastometry is the critical value for
initiation of antifibrinolytic therapy.26 Tranexamic acid has
been found to reduce the transfusion requirements and
improve mortality in trauma patients.16,27.
The use of tranexamic
acid with a loading dose of 1 g over 10 min followed
by 1 g over 8 h is recommended (Grade 1A). The use of drug in
the early period within 3 h of trauma has been found to be
beneficial and no improvement in outcome has been found
when used after 3 h27
Role of recombinant factor VIIa (rFVIIa)
Recombinant factor VIIa is not the first line treatment in
bleeding trauma patients. Since FVIIa acts on patient’s own
coagulation system, there must be adequate number of
platelets and fibrinogen levels available for it to cause
thrombin burst.28 The efficacy of rFVIIa as a pro-hemostatic
agent and to stop bleeding also varies widely with the physiological
state of the body like core body temperature and
acidosis. Decrease in body temperature up to 33 C has been
found to have very little impact on the effectiveness of rFVIIa,
but with further fall in body temperature there is a linear
reduction in the activity of FVIIa. At temperatures of 28 C and
below, its activity falls by more than 50%. In severe metabolic
acidosis as seen in bleeding trauma patients the activity of
rFVIIa is highly affected. At a pH of 7.0, the activity is reduced
medical journal armed forces india 70 (2014) 163 e169 167
by 90%. Therefore rFVIIa should be considered only after
adequate resuscitation, normalization of platelet and clotting
factor concentration, and in the absence of hypothermia and
acidosis (Grade 2C).16
Correction of hypothermia
Steps to prevent hypothermia and the risk of hypothermiainduced
coagulopathy include removing wet clothing,
covering the patient to avoid additional heat loss, increasing
the ambient temperature, forced air warming, warm fluid
therapy and, in extreme cases, extracorporeal re-warming
devices.29
Anti-inflammatory agents
Severe tissue injury is characterized by an intense inflammatory
response leading to a systemic inflammatory
response. Various drugs that decrease inflammation like recombinant
human activated protein C (APC), IL-1 receptor
antagonist, anti-TNF and anti-LPS agents are not found to be
effective in bleeding trauma patients. Albeit steroids have
been found to reduce the incidence of pneumonia and the
number of ventilator free days, however recent studies have
shown that there is no clear benefit in terms of mortality in
these patients and may even be harmful in patients with
traumatic brain injuries.30
Conclusion
Management of trauma patients with haemorrhagic shock
and acute traumatic coagulopathy is complex and difficult
and remains a challenge. In spite of better understanding of
pathophysiology of the events leading to acute traumatic
coagulopathy, the mortality associated with it remains high.
The role of the treating physician is, to identify the source of
bleeding and achieve rapid control of bleeding by various
measures. The main objective then would be to follow damage
control resuscitation guidelines by maintaining tissue
oxygenation, proper and judicious use of volume expanders.
Early use of blood and blood products is to be encouraged in
order to prevent development of acute traumatic coagulopathy.
The key would remain prevention, detection and early
management of acute traumatic coagulopathy