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COMBATING COAGULOPATHY
Author(s) -
Gunn K. N.
Publication year - 2007
Publication title -
anz journal of surgery
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.426
H-Index - 70
eISSN - 1445-2197
pISSN - 1445-1433
DOI - 10.1111/j.1445-2197.2007.04133_12.x
Subject(s) - medicine , coagulopathy , intensive care medicine , fibrinolysis , shock (circulatory) , coagulation , thromboelastography , coagulation testing , partial thromboplastin time , anesthesia , surgery
The clinical trigger to consider the presence of a coagulopathy is the onset of non‐surgically controllable bleeding. While earlier consensus documents considered this event predictable by modelling blood loss, and factor level decline, we now recognize confounding variables such as shock, hypothermia, metabolic disturbances and fibrinolysis confuse the picture to such an extent traditional treatment algorithms are irrelevant. The monitoring of coagulopathy by traditional coagulation screens also lacks validation, and is usually so delayed in response time to become irrelevant to appropriate management. Attaining euvolaemia is possible with large volume dedicated infusion systems but in a patient with massive mediator release and comorbidities may not achieve adequate tissue oxygen delivery. Evidence based transfusion triggers are still lacking. Management of coagulopathy is by component replacement early. Delays occur because of slow coagulation test turnaround times, and the place of newer point of care monitors and thrombelastography needs evaluation. Delay in delivery of blood components due to processing time may worsen the outcome. Factor VIIa probably has a unique place in the management of coagulopathy in these patients, but studies are needed to define dosage and time of dose (2). The management of acidosis and hyperlactaemia are fundamentally improved by better perfusion, but short term correction may be indicated to reinforce coagulation factor function.