Preconditions of hemostasis in trauma: a review. The influence of acidosis, hypocalcemia, anemia, and hypothermia on functional hemostasis in trauma

Abstract

Background: Beside the often discussed topics of consumption and dilution coagulopathy, additional perioperative impairments of coagulation are caused by acidosis, hypocalcemia, anemia, hypothermia, and combinations.

Methods: Reviewing current literature, cutoff values of these parameters become obvious at which therapy should commence.

Results: A notable impairment of hemostasis arises at a pH < or = 7.1. Similar effects are caused by a BE of -12.5 or less. Thus, in case of severe bleeding, buffering toward physiologic pH values is recommended, especially with massive transfusions of older RBCCs displaying exhausted red blood cell buffer systems. It completes the optimization of the volume homeostasis to ensure an adequate tissue perfusion. Combining beneficial cardiovascular and coagulation effects, the level for ionized calcium concentration should be held > or = 0.9 mmol/L. From the hemostatic point of view, the optimal Hct is higher than the one required for oxygenation. Even without a "classical" transfusion trigger, the therapy of acute, persistent bleeding should aim at reaching an Hct > or = 30%. A core temperature of < or = 34 degrees C causes a decisive impairment of hemostasis. A controlled hypotensive fluid resuscitation should aim at reaching a mean arterial pressure of > or = 65 mm Hg (possibly higher for cerebral trauma). Prevention and later aggressive therapy of hypothermia by exclusive infusion of warmed fluids and the use of warming devices are prerequisites for the cure of traumatic coagulopathy. Combined appearance of single preconditions cause additive impairments of the coagulation system.

Conclusions: The prevention and timely correction, especially of the combination acidosis plus hypothermia, is crucial for the treatment of hemorrhagic coagulopathy.