Summary
Unexplained intraoperative coagulopathies continue to be a diagnostic and therapeutic
dilemma. The pathophysiology behind unexplained intraoperative coagulopathies is of
great variety and complexity (preexisting coagulopathies, dilutional coagulopathy,
interactions of medications etc.). We have shown in prospective studies that patients
undergoing elective surgery who develop, unexplained“ intraoperative coagulopathies
have significantly less FXIII per unit thrombin available at any point in time (i.e.
already preoperatively) than patients without such coagulopathies. The consequence
is a significant loss of clot firmness associated with an increase in intraoperative
blood loss. Thus, these patients have less cross-linking capacity to begin with, which
explains their preoperatively increased fibrin monomer concentration. The association
of increased preoperative fibrin monomer and increased intraoperative blood loss was
prospectively evaluated and cofirmed in a separate clinical study. It is important
to note that the acquired or (compared to the amount of thrombin generated) relative
F. XIII deficiency in situations with surgical stress shows early clinical relevance
(even if only mild to moderate changes are present); this differs from the experiences
with patients with inborn FXIII deficiency, where a pronounced deficiency must be
present to have clinically significant spontaneous bleeding.
Patients undergoing elective surgery, without clinically obvious coagulopathy but
increased preoperative fibrin monomer concentration (as a marker of decreased crosslinking
capacity) are at risk for increased intraoperative blood loss. This new concept helps
to explain the pathophysiology behind unexplained intraoperative coagulopathies and
thus allows for corresponding treatment strategies. Further clinical studies for early
detection and interventions in patients with such coagulopathies are necessary.
Keywords
Thrombin - fibrin monomer - FXIII - clot firmness - intraoperative blood loss
