Download Thrombosis and Hemostasis Societies of North America April 15

Thrombosis and Hemostasis Societies of North
America
April 15, 2016
Chicago, Illinois
CRAIG S. KITCHENS, MD, MACP
Professor Emeritus, University of Florida
Gainesville FL
DIC is now defined as a pattern of consequences due
to the circulation of non-bound, non-inhibited
THROMBIN and PLASMIN.
These are generated via physiologic mechanisms
(thrombin the end product of coagulation and plasmin
the end product of fibrinolytic pathway) yet in
pathologic quantities due to excessive amounts or
duration of stimulation of the coagulation and/or
fibrinolytic systems to the point that the natural
inhibitors of thrombin and plasmin are overwhelmed
so that they may circulate at large.
Tissue Damage
Infections
Neoplasia
Obstetric Conditions
Trauma
Crush injuries
CNS injuries
Heat Stroke
Burns
Hemolytic transfusion reaction
Acute transplant rejection
Cancers
Leukemias
Cancer chemotherapy
Tumor lysis syndrome
Miscellaneous
Shock
Cardiac arrest
Near drowning, especially in fresh
water
Fat embolism
Aortic aneurysm
Giant hemangiomas
Snake bites
Gram-positive bacteria
Gram-negative bacteria
Spirochetes
Rickettsiae
Protozoa
Fungi
Viruses
Abruptio placentae
Placenta previa
Retained dead fetus syndrome
Amniotic fluid embolism
Uterine atony
Therapeutic abortion
Toxemia of pregnancy
Patient bleeding, thrombosing, or both, typically with
progressive organ dysfunction.
An underlying illness or process that may cause tissue
damage, cell death, or production/release of tissue factor.
Usually some perturbation exists of simple, readily
available tests such as thrombin time (TT), prothrombin
time (PT), partial thromboplastin time (PTT), fibrin
degradation products (FDP)/D-dimer, or platelet count.
These values may markedly change as the clinical
situation changes.
Mant & King: Am J Med 1979; 67:557
There is always an underlying problem that presents its
own varied perturbations of many tests.
Tests represent static “snapshots” of a highly dynamic
situation.
Special tests frequently are esoteric and results arrive
long after the dynamic situation has changed.
Diagnostic test results rarely direct or redirect therapy
and may confuse the clinical picture.
Table 7
Role of Blood Products in Treatment of DIC
RBCs
Keep hemoglobin in range of 6-10gm/dL
Platelets
Depends on risks for bleeding, not just the platelet count. Risk for
bleeding high if less than 20,000-30,000/ L especially if due to
decreased production; less so if due to sequestration or shortened
platelet survival; nil if due to thrombotic causes (TTP or HIT). In
DIC, reasonable target range is 50,000/ L
FFP
Enormously overrated in treatment of DIC, especially since recent
evolution of our understanding and danger of TRALI. Some
indication to supplement RBC transfusions in “total body exchange”
situations
Cryoprecipitate
Probably best source of fibrinogen. Reasonable target is to keep
fibrinogen levels between 50-100mg/dL
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If you ask yourself “is this DIC?” it’s probably not
There is always a cause that’s typically obvious
What you see at the bedside depends on relative
predominance of clotting vs thrombosis
Keep lab tests simple and readily available
Without appropriate clinical situation, lab tests are
worthless
“One new test for DIC” is hopelessly naïve
Replace blood products judiciously
Never “correct the coagulopathy” prior to needed
procedure
Don’t expect one therapeutic agent to work in all DIC
Therapy depends on turning off the stimulus and correcting
for volume, perfusion, acidosis, and hypothermia