Relationship between tissue perfusion and coagulopathy in traumatic brain injury.
Traumatic brain injury (TBI)-related coagulopathy appears to be most prevalent in patients with tissue hypoperfusion, but evidence for this association is scarce. This study investigated the relationship between tissue perfusion and hemostatic derangements in TBI patients.



Coagulation parameters were measured on emergency department admission in patients with TBI (head abbreviated injury scale ≥ 3). The level of hypoperfusion was simultaneously assessed by near-infrared spectroscopy (NIRS) at the forehead and arm, and by base excess and lactate. Coagulopathy was defined as an international normalized ratio > 1.2 and/or activated partial thromboplastin time > 40 s and/or thrombocytopenia (<120 × 10(9)/L).



TBI patients with coagulopathy (42%) had more signs of tissue hypoperfusion as indicated by increased lactate levels (2.1 [1.1-3.2] mmol/L versus 1.2 [1.0-1.7] mmol/L; P = 0.017) and a larger base deficit (-3.0 [-4.6 to -2.0] mmol/L versus -0.1 [-2.5 to 1.8] mmol/L; P < 0.001). There was no difference in the cerebral or somatic tissue oxygenation index. However, there was a distinct trend toward a moderate inverse association between the cerebral tissue oxygenation index and D-dimer levels (r=-0.40; P = 0.051) as marker of fibrinolysis. The presence of coagulopathy was associated with an increased inhospital mortality rate (45.5% versus 6.7%; P = 0.002).



This is the first study to investigate the relationship between hemostatic derangements and tissue oxygenation using NIRS in TBI patients. This study showed that TBI-related coagulopathy is more profound in patients with metabolic acidosis and increased lactate levels. Although there was no direct relationship between tissue oxygenation and coagulopathy, we observed an inverse relationship between NIRS tissue oxygenation levels and fibrinolysis.
Department of Anesthesiology, VU University Medical Center, Amsterdam, The Netherlands. Electronic address: s.dekker@vumc.nl.
Simone E
SE
Dekker
Department of Anesthesiology, VU University Medical Center, Amsterdam, The Netherlands.
Anne
A
Duvekot
Department of Anesthesiology, VU University Medical Center, Amsterdam, The Netherlands.
Hielke-Martijn
HM
de Vries
Department of Surgery, VU University Medical Center, Amsterdam, The Netherlands.
Leo M G
LM
Geeraedts
Department of Neurosurgery, VU University Medical Center, Amsterdam, The Netherlands.
Saskia M
SM
Peerdeman
Department of Intensive Care, VU University Medical Center, Amsterdam, The Netherlands.
Monique C
MC
de Waard
Department of Anesthesiology, VU University Medical Center, Amsterdam, The Netherlands.
Christa
C
Boer
Department of Anesthesiology, VU University Medical Center, Amsterdam, The Netherlands.
Patrick
P
Schober
D000328:Adult; D000368:Aged; D001778:Blood Coagulation Disorders / Q000097:blood / Q000209:etiology*; D000070642:Brain Injuries, Traumatic / Q000097:blood / Q000150:complications*; D002560:Cerebrovascular Circulation; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D010100:Oxygen / Q000097:blood*; D012189:Retrospective Studies
D010100:Oxygen
Bleeding; Coagulopathy; Oxygenation; Perfusion; Trauma; Traumatic brain injury