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Hemostasis Problems in CriticalHemostasis Problems in CriticalIllnessIllness
Per Thorborg, MD, PhD, FCCMPer Thorborg, MD, PhD, FCCM
Director, Critical Care MedicineDept.of Anesthesiology and Perioperative Medicine,Oregon Health & Science University, Portland, OR
 
 
IntroductionIntroduction
While coagulation-associated problems in critical care medicine include both hyper-and hypocoagulable states, venous thromboembolism (VTE) is addressed in another module.In the ICU,
acquired
hypocoagulable states are much more common than
congenital
states (such as vWD [types I, II, III]; Hemophilia A, B, C; Bernard-Soulier’s, and Glanzmann’s thrombasthenias; inborn platelet abnormalities; isolatedcoagulation factor deficiencies; dysfibrinogenemias; alpha2-antiplasmin deficiency,other rare disorders). Of these disorders, vWD is by far the most common (1%).In the following teaching module, due to space restrictions only some of the mostcommon acquired coagulation problems seen in the ICU patient are addressed. It isrecommended to involve hematology and blood bank early in the managementcourse of a severely bleeding patient.The order in which they will be presented is: 1. an updated view of the coagulationcascade, 2.critical illness coagulopathies and treatment, 3.uncontrolled bleeding andmassive transfusion, 4. anticoagulation-associated problems, 5.case scenarios, 6.references.
 
 
In the
primary
hemostasis a platelet plug is formed within 5 minutesto seal the site of injury.In the
secondary
hemostasis fibrin is formed (coagulation) and afibrin mesh reinforces the frail platelet plug (timescale hours).The third part is (secondary)
fibrinolysis
which dissolves the clotbut takes place first after tissue repair (timescale days).The coagulation cascade for fibrin formation described in the early1960s by Davie, Ratnoff, and MacFarlane was based on vitro data.While its extrinsic and intrinsic pathways setup explained many PTand APTT abnormalities, it failed to explain other clinicalobservations.Newer data from the 1990s have replaced this older model with acell-based model where interactions between endothelial cells,platelets, and thrombin have taken center stage.
The Three Stages of HemostasisThe Three Stages of Hemostasis
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