Transfusion massive et coagulopathie: physiopathologie et implications cliniques

Abstract

P Pu ur rp po os se e: : To review the pathophysiology of coagulopathy in massively transfused, adult and previously hemostatically competent patients in both elective surgical and trauma settings, and to recommend the most appropriate treatment strategies.M Me et th ho od ds s: : Medline was searched for articles on "massive transfusion," "transfusion," "trauma," "surgery," "coagulopathy" and "hemostatic defects." A group of experts reviewed the findings.P Pr ri in nc ci ip pa al l f fi in nd di in ng gs s: : Coagulopathy will result from hemodilution, hypothermia, the use of fractionated blood products and disseminated intravascular coagulation. The clinical significance of the effects of hydroxyethyl starch solutions on hemostasis remains unclear. Maintaining a normal body temperature is a first-line, effective strategy to improve hemostasis during massive transfusion. Red cells play an important role in coagulation and hematocrits higher than 30% may be required to sustain hemostasis. In elective surgery patients, a decrease in fibrinogen concentration is observed initially while thrombocytopenia is a late occurrence. In trauma patients, tissue trauma, shock, tissue anoxia and hypothermia contribute to the development of disseminated intravascular coagulation and microvascular bleeding. The use of platelets and/or fresh frozen plasma should depend on clinical judgment as well as the results of coagulation testing and should be used mainly to treat a clinical coagulopathy.C Co on nc cl lu us si io on ns s: : Coagulopathy associated with massive transfusion remains an important clinical problem. It is an intricate, multifactorial and multicellular event. Treatment strategies include the maintenance of adequate tissue perfusion, the correction of hypothermia and anemia, and the use of hemostatic blood products to correct microvascular bleeding. Objectif

Clinical review: The critical care management of the burn patient

“…Red cells facilitate haemostasis through a rheological effect by pushing platelets to the periphery of the vessel lumen to better interface at the endothelium as well as through direct effects on platelet biochemistry. Haematocrit <30% can therefore lead to significant extra blood loss [29]. …”

Stress repair mechanism activity explains inflammation and apoptosis

“…Reptiles thus thrive in warm environments and their activity is sluggish at low temperatures. Mammals achieve superior exercise tolerance and dominate cold environments by maintaining their body temperature above the level of fat liquefaction, which enables their bi-concave red cells to simultaneously optimize hemodynamic efficiency and atherosclerosis resistance, but this necessitates substantially greater caloric intake [456,457,459,460].…”

“…The abnormal coagulation activity reduces circulating red cell mass, which exaggerates blood turbulence and further inhibits effective coagulation. These abnormalities and imbalances cause the generalized failure of hemostasis that characterizes DIC [401,460,684]. DIC often occurs in patients who undergo extensive surgical intervention in the immediate aftermath of major trauma and massive blood loss [11,200,568].…”

“…DIC often occurs in patients who undergo extensive surgical intervention in the immediate aftermath of major trauma and massive blood loss [11,200,568]. Trauma and surgery both release tissue factor into systemic circulation and increase Factor VII activity, causing SRM hyperactivity and positive feedback [116,184,194,286,460,542,660,[684][685][686]. In addition, trauma patients are typically subjected to starvation, sepsis, hypothermia, fear, pain, hypoxia, and iatrogenic hyperoxia, and these additional forms of stress exaggerate positive feedback and SRM hyperactivity.…”

Moderate plasma dilution using artificial plasma expanders shifts the haemostatic balance to hypercoagulation

“…None of the artificial PEs contain the components of the clotting system; therefore, large volumes of PE infusion inevitably lead to plasma dilution and to changes in the concentrations of coagulation components (haemodilution), thereby affecting the state of the coagulation system. Haemostatic disorder in trauma patients having received large-volume infusions of various blood products and/or PEs is a complex multifactorial process 2–4 . The result depends primarily on the type and volume of the transfused product as well as on some other factors related to trauma and haemodilution, such as the degree of reduction in the concentrations of the procoagulant factors 4 , counts of platelets 5, 6 and red blood cells 7–10 , possible hypothermia 11–13 , and significant activation of coagulation in trauma patients due to the appearance of the extensive wound surface 14, 15 , etc.…”