Perfusion Policies 101: DIC

dic

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FA 2016

Editor’s Note:

PERFUSION POLICIES 101

Welcome to PERFUSION POLICIES 101.  This will be a continuing series provided to assist your programs with that one puzzle piece we all run into now and then- that one time that an unexpected patient condition may give you pause…

The intention here is to disseminate some basic recipes that have probably been implemented at countless institutions, for God knows how long.  The usual disclaimers obviously apply:

Due Diligence is the Responsibility of the Reader!

Use the information as you feel fit, recognizing that this is information gleaned from multiple sources, it is recruited from the public domain of the internet, with no implied assurance of accuracy- but is cogent, and based on logical and reasonable clinical rationale.

Frank Aprile ?

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DIC

Definition

Disseminated intravascular coagulation is a condition in which coagulation factors normally present in the blood are depleted or inactivated, resulting in the inability oif the patient to form clots and maintain homeostasis.  Simultaneous clotting followed by lysis occurs in a DIC can be caused by the following factors:

*Inadequate heparinizaion

*Uncontrolled prolonged hemorrhage

*Total body washout   with replacement of volume with  banked blood products containing temporarily inactivated clotting factors

*Infection, sepsis, viremia

*Obstetrical compilations

*Burns, crush injuries, trauma

*Liver disease

When vascular integrity is list, large amounts of phospholipids are released, resulting in activation of platelets and the coagulation cascade, followed by consumption of these factors.  Phospholipids cause widespreaqd formation of fibrin, leading to consumption of factors, with a decrease of labile factors 5, 8, and fibrinogen.  These factors are used once in the coagulation process, and must be replenished.  When clots are broken down, large amounts of fibrin split products (FSPs) are released into the circulation.  Whit and increase in FSPs present, normal clot formation is inhibited, and platelets become dysfunctional.

A first clue of DIC can be detected by observing a handheld activated clotting time (ACT) sample for formation of clot, followed shortly by lysis of the clot.

*If DIC is suspected, send sample to lab for STAT complete coagulation profile.  A positive result is indicated by prolonged PTT and TT, thrombocytopenia, hypofibrinogenemia, and increased FSPs.

*Maintain or initiate complete heparinization with ACTs>480s.

*Replace coagulation factors by administering FFP, RBCs, platelets, and cryoprecipitate if necessary.  Continue factor replacement and platelet therapy post-operative for 24-48 hour, as indicated.

*May be necessary to maintain cardiopulmonary bypass to assist in homeostasis, until coagulation factors are reactive (approximately 4h).

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