Rapid Responses to:

CLINICAL REVIEW: Cheng Hock Toh and Michael Dennis Disseminated intravascular coagulation: old disease, new hope BMJ 2003; 327: 974-977 [Full text]

Rapid Responses: Submit a response to this article

Rapid Responses published:

Lethal Triad: Coagulopathy inTrauma

Ian Pallister   (8 December 2003)

Lethal Triad: Coagulopathy inTrauma 8 December 2003
Ian Pallister, Senior Lecturer Trauma & Orthopaedics Morriston Hospital, Swansea, SA6 6NL Send response to journal: Re: Lethal Triad: Coagulopathy inTrauma	Editor I read Dr Toh and Dr Dennis’ Clinical Review of DIC with interest 1. The coagulopathy associated with haemorrhagic shock, which complicates major trauma, is a common scenario and a difficult challenge. Rather than resulting from tissue trauma, or traumatic brain injury alone, this is invariably a consequence of uncontrolled haemorrhage, and attempts to restore the circulating volume. Strictly speaking, this is not DIC, as characteristic microthrombi are absent 2. However, the concept of non- overt diagnosis proposed in Dr Toh’s clinical review is particularly relevant. Hypovolaemic shock, if present, is usually obvious at the time of a major trauma patients’ arrival in the resuscitation room. The source of haemorrhage is sought at the same time as the initial fluid bolus is given, and the response assessed. If the patient shows only a transient response, or no response at all, the need for surgical control of bleeding is assumed, and along with this, massive transfusion volumes can be anticipated. At this point, incipient “shock trauma” coagulopathy should be recognised 3. A synergy of pathological problems beset the patient’s own efforts to achieve haemostasis 4. Coagulopathy results directly from the consumption of circulating clotting factors and platelets, with further dilution of the remaining factors because of volume resuscitation. Hypothermia, a constant threat to the trauma patient, results in further slowing of the coagulation cascade and impairment of platelet function. Excessive fibrinolysis may exacerbate matters further, as tissue plasminogen activator is released from injured tissues. All of this occurs in the presence of continued haemorrhage and worsening metabolic acidosis. Once this lethal triad of hypothermia, acidosis and coagulopathy is manifest, the DIC synonym “death is coming” is likely to prove apt. Current strategies for resuscitation from severe hypovolaemic shock in major trauma recognise the need for the treatment of coagulopathy before it is manifest in laboratory coagulation screening tests 5-7. Close liaison between the clinicians with the patient, and their haematology colleagues is essential. Early coagulation studies are likely to be close to or even completely normal, as the test is carried out at 37oC, rather than 34o-35oC, which is often the patients core temperature. In spite of surgical control of major bleeding, rational use of blood products and aggressive re-warming of the trauma patient, sometimes this “shock trauma” coagulopathy is refractory. An increasing number of case reports indicate promising results from the administration of recombinant activated factor VII (rFVIIa) 2 8. The case for this intervention has not yet been proven, but it’s effects can be striking. Management of coagulopathy is without doubt a multidisciplinary endeavour, and each speciality involved has its own perspective. The successful management of major trauma hinges upon teamwork, and this is no where more apparent than in the management of “shock trauma” coagulopathy, in the presence of on-going surgical and “medical” haemorrhage. Ian Pallister FRCS (Tr & Orth) Senior Lecturer/Consultant Trauma & Orthopaedic Surgery References: 1. Toh CHD, M. Disseminated intravascular coagulation: old disease, new hope. BMJ 2003;327(7421)(Oct 25):974-7. 2. Martinowitz UK, G. Segal, E. Luboshitz, J. Lubetsky, A. Ingerslev, J. Lynn, M. Recombinant activated factor VII for adjunctive hemorrhage control in trauma. J Trauma 2001;51(3)(Sep):431-8. 3. MacLeod JBL, M. McKenney, M.G. Cohn, S.M. Murtha, M. Early coagulopathy predicts mortality in trauma. J Trauma 2003;55(1)(Jul):39-44. 4. Cosgriff NM, E.E. Sauaia, A. Kenny-Moynihan, M. Burch, J.M. Galloway, B. Predicting life-threatening coagulopathy in the massively transfused trauma patient: hypothermia and acidoses revisited. J Trauma 1997;42(5)(May):857-61. 5. Cinat MEW, W.C. Nastanski, F. West, J. Sloan, S. Ocariz, J. Wilson, S.E. Improved survival following massive transfusion in patients who have undergone trauma. Arch Surg 1999;134(9)(Sep):964-8. 6. Denton JRM, E.E. Coldwell, D.M. Multimodality treatment for grade V hepatic injuries: perihepatic packing, arterial embolization, and venous stenting. J Trauma 1997;42(5)(May):964-7. 7. Vaslef SNK, N.W. Neligan, P.J. Sebastian, M.W. Massive transfusion exceeding 50 units of blood products in trauma patients. J Trauma 2002;53(2)(Aug):291-5. 8. Dutton RPH, J.R. Scalea, .TM. Recombinant factor VIIa for control of hemorrhage: early experience in critically ill trauma patients. J Clin Anesth 2003;15(3)(May):184-8. Competing interests: None declared