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It is an acquired condition in which normal
physiology of coagulation is disturbed leading to
widespread intravascular coagulation process
associated with injury to microvasculature which
results in organ dysfunction, capillary leak &
Occurs due to simultaneous action of the
following 4 mechanisms
1) Increased thrombin generation
2) Suppressed physiological anticoagulant
3) Activation & subsequent impairment of
4) Activation of inflammatory pathways
Non overt DIC:
Stressed & compensated hemostatic system. Lab testsabnormal but no clinical manifestations.
Stressed and decompensated hemostatic system. Lab
tests- abnormal with clinical bleeding or micro
vascular thrombosis and organ dysfunction.
Further divided into controlled and uncontrolled
based on whether the process will resolve when the
underlying condition is removed.
Bleeding from vein puncture site, surgical wound.
Grayish discoloration of tips of fingers, toes & ears in a
Meningococcemia(PURPURA FULMINANS)- bleeding
from GI tract, gingival bleeding, epistaxis, pulmonary
Superficial and extensive ecchymosis of extremities
without petechiae which may be intermittent or can
Recurrent episodes of epistaxis or internal mucosal
Trousseau sign- Recurrent migratory
thrombophlebitis in association with cancer.
Impairment of renal function, confusion, repeated
episodes of cerebral thrombosis.
Specific features of DIC in neonates
Transplacental passage of thromboplastin or other
procoagulant substances in neonates born of mothers
affected with DIC owing to abruptio placenta,
eclampsia or septicemia
Development of DIC in a twin fetus may be due to
feto-fetal passage of thromboplastin.
DIC secondary to hemangioma .
Asphyxia, septicemia, eclampsia
Symmetric ecchymosis of lower extremities and
buttocks. Later these lesions become necrotic
ultimately forming blood filled bullae.
Sharply circumscribed infarcts of skin and genitalia
Gangrene of extremities involves digits symmetrically.
Fever and prostration
Heparin. Relapse common after cessation.
COMPLETE BLOOD COUNT:
Severe thrombocytopenia(50000-100000/µl) with or
PERIPHERAL BLOOD SMEAR:
Schistocytes- Microangiopathic hemolysis
PROTHROMBIN TIME & aPTT:
Prolonged in early cases but may be normal or short in
D dimer, FIBRINOGEN / FIBRIN
Increased >25µg fibrinogen equivalents/ml
PROTEIN C & S, ANTITHROMBIN:
MARKERS OF ENDOGENOUS THROMBIN
Prothrombin fragment 1.2 and
Thrombin-Antithrombin complexes(TATs) are
Primary fibrinogenolysis or Pathologic
Platelet count is normal
D dimer may be normal or minimally increased
No hypoprothombinemia & No deficiency of
coagulation factors (VII, IX, X, XI)
Severe liver disease:
D dimer test is normal
BLOOD COMPONENT THERAPY:
Risk of bleeding complication
GOALS: To maintain
Platelet count >50000/µl
Fibrinogen concentration >1g/L
Prothrombin values less than double the normal
FRESH FROZEN PLASMA(FFP):
0.7-1.0 U/ml of factors II,V, VII, VIII, X, XI, XII, XIII and
factor VIII 80-120units/bag
factor XIII & vWB
1 bag/5kg body wt.
Random donor platelets(RDP):
1 unit/ 10 kg
Single donor platelets:
Indicated in severe trauma to replace acute massive
Heparin and other anticoagulant therapy to inhibit
Indicated in patients with clinically overt
thromboembolism , chronic DIC and extensive fibrin
Weight < 30kg – 10U/kg/hr
Weight > 30kg – 4U/kg/hr
REPLACEMENT OF NATURAL
Recombinant human activated protein c 24µg/kg/hr.
Adverse effects include bleeding.