Guidelines. Blood transfusion and the anaesthetist: management of massive haemorrhage.

Thomas D, Wee M, Clyburn P, Walker I, Brohi K, Collins P, Doughty H, Isaac J, Mahoney PM, Shewry L.

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1. Hospitals must have a major haemorrhage protocol in
place and this should include clinical, laboratory and
logistic responses.
2. Immediate control of obvious bleeding is of paramount
importance (pressure, tourniquet, haemostatic
3. The major haemorrhage protocol must be mobilised
immediately when a massive haemorrhage situation is
4. A fibrinogen < 1 g.l)1 or a prothrombin time (PT) and activated partial thromboplastin time (aPTT) of > 1.5 times normal represents established haemostatic
failure and is predictive of microvascular bleeding.
Early infusion of fresh frozen plasma (FFP;
15 should be used to prevent this occurring
if a senior clinician anticipates a massive haemorrhage.
5. Established coagulopathy will require more than
15 of FFP to correct. The most effective way
to achieve fibrinogen replacement rapidly is by giving
fibrinogen concentrate or cryoprecipitate if fibrinogen
is unavailable.
6. 1:1:1 red cell:FFP:platelet regimens, as used by the
military, are reserved for the most severely traumatised
7. A minimum target platelet count of 75 · 109.l)1 is
appropriate in this clinical situation.
8. Group-specific blood can be issued without performing
an antibody screen because patients will have
minimal circulating antibodies. O negative blood
should only be used if blood is needed immediately.
9. In hospitals where the need to treat massive
haemorrhage is frequent, the use of locally developed
shock packs may be helpful.
10. Standard venous thromboprophylaxis should be
commenced as soon as possible after haemostasis has
been secured as patients develop a prothrombotic
state following massive haemorrhage.

Pathophysiology and Treatment of Coagulopathy in Massive Hemorrhage and Hemodilution

Daniel Bolliger, M.D.,* Klaus Go¨ rlinger, M.D.,† Kenichi A. Tanaka, M.D., M.Sc.‡
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Fluid resuscitation after massive hemorrhage in major surgery and trauma may result in extensive hemodilution and
coagulopathy, which is of a multifactorial nature. Although
coagulopathy is often perceived as hemorrhagic, extensive
hemodilution affects procoagulants as well as anticoagulant, profibrinolytic, and antifibrinolytic elements, leading to a complex coagulation disorder. Reduced thrombin activation is partially compensated by lower inhibitory activities of antithrombin and other protease inhibitors, whereas plasma fibrinogen is rapidly decreased proportional to the extent of hemodilution. Adequate fibrinogen levels are essential in managing dilutional coagulopathy. After extensive hemodilution,
fibrin clots are more prone to fibrinolysis because
major antifibrinolytic proteins are decreased.
Fresh frozen plasma, platelet concentrate, and cryoprecipitate are considered the mainstay hemostatic therapies. Purified factor concentrates of plasma origin and from recombinantsynthesis are increasingly used for a rapid restoration of targeted factors. Future clinical studies are necessary to establish the specific indication, dosing, and safety of novel hemostatic interventions.
IN patients with trauma and those who undergo major
surgery, multiple breaches of vascular integrity result in
bleeding, and in some cases, exsanguination. Fluid (volume)
replacement with crystalloids or colloids is usually the initial measure to stabilize systemic circulation by compensating for hypovolemia. When the blood loss is considered major (hemoglobin concentration below 6–10 g/dl),1 erythrocyte(RBC) concentrates are transfused to sustain hemoglobin levels (i.e., oxygen-carrying capacity). The transfusion of ten or more erythrocyte units (i.e., replacement of one blood volume) within 24 h is generally considered as massive transfusion in adults.2 Other arbitrary definitions include six or more erythrocyte units within 12 h and over 50 units of
blood product use within 24 h, including erythrocytes, platelet concentrates, and fresh frozen plasma (FFP).3,4 There are differences in the initial pathophysiology of coagulopathy between trauma and major surgery, which can be attributed in part to the mechanism of vascular injury, extent of hemorrhage, type of fluid resuscitation, and prophylactic use of antifibrinolytic therapy.5–8 However, hemostatic defects based on conventional laboratory data are often indistinguishable between trauma and major surgery after massive transfusion. Unlike congenital bleeding disorders that are due mostly to a single factor deficiency (e.g., hemophilia, afibrinogenemia), coagulopathy encountered in trauma and major surgery is of a multifactorial nature. All elements incoagulation, including procoagulant, anticoagulant, fibrinolytic,
and antifibrinolytic proteins, exhibit various degrees of
deficiency. Although this topic has been reviewed recently by others,5,8,9 the mechanism of coagulopathy related to massive transfusion and hemodilution is not fully understood. In this review, we focus on the effects of hemodilution on thrombin generation, fibrin polymerization, and fibrinolysis, using experimental results as well as existing clinical data to shed light on the mechanisms of dilutional coagulopathy. In
addition, we discuss various therapeutic approaches and their clinical implications.

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