Disseminated intravascular coagulation (DIC) is caused by simultaneous activation of coagulation and suppression of fibrinolysis, resulting in microvascular thrombosis and hemorrhage. It can be triggered by infection, trauma, malignancy or other medical conditions. Clinically, it presents as bleeding symptoms and organ dysfunction. Laboratory findings include low platelets, elevated D-dimer and markers of thrombin generation. Treatment involves managing the underlying cause, replacing blood products to control bleeding, and anticoagulants to inhibit thrombin formation. Prognosis depends on promptly treating both the DIC and precipitating condition.

1. DNB OBS AND GYN THEORY QUESTION
DEC 2007 -
DISSEMINATED INTRAVASCULAR
COAGULATION – DESCRIBE ITS CAUSES,
PATHOGENESIS AND MANAGEMENT
( 10 MARKS )
DNBCENTRAL.IN
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2. • DEFINITION
• ETIOLOGY
• PATHOPHYSIOLOGY
• CLINICAL MANIFESTATIONS
• LABORATORY FINDINGS
• DIFFERENTIAL DIAGNOSIS
• TREATMENT
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3. DEFINITION
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 & SHOCK.
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4. MECHANISMS
Occurs due to simultaneous action of the following 4
mechanisms
1) Increased thrombin generation
2) Suppressed physiological anticoagulant pathways
3) Activation & subsequent impairment of fibrinolysis
4) Activation of inflammatory pathways
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5. ETIOLOGY
 INFECTIOUS:
Meningococcemia- purpura fulminans
Bacterial sepsis- staphylococcal, streptococcal, E coli Rickettsia-
Rocky Mountain spotted fever
Viral- CMV, varicella, arboviruses
Malaria, Candida, Aspergillus
 TISSUE INJURY:
Multiple fractures with fat emboli, crush injury, head injury
 MALIGNANCY:
Acute promyelocytic leukemia, acute myeloid leukemia,
neuroblastoma
 VENOM OR TOXIN:
Snake bites, insect bitesWWW.DNBCENTRAL.IN 5

6. CONTD…
 MICROANGIOPATHIC DISORDERS:
TTP, HUS, Kasabach-Meritt syndrome
 GI DISORDERS:
Fulminant hepatitis, Inflammatory bowel disease, Pancreatitis
 HEREDITARY THROMBOTIC DISORDERS:
Antithrombin III deficiency, Homozygous protein C deficiency
 NEWBORN:
Maternal toxemia, Abruptio placentae, Necrotizing enterocolitis,
Erythroblastosis fetalis
 MISCELLANEOUS:
Acute graft rejection, Acute hemolytic transfusion reaction,
Collagen vascular disorders, Heparin induced thrombosis,
hyperpyrexiaWWW.DNBCENTRAL.IN 6

7. WWW.DNBCENTRAL.IN 7

8. PATHOPHYSIOLOGY
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9. CLINICAL MANIFESTATIONS
DIC
NON OVERT DIC OVERT DIC
ACUTE DIC CHRONIC DIC
CONTROLLED
UNCONTROLLEDWWW.DNBCENTRAL.IN 9

10. Non overt DIC:
Stressed & compensated hemostatic system. Lab tests-
abnormal but no clinical manifestations.
Overt DIC:
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.
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11. Acute DIC:
• Bleeding from vein puncture site, surgical wound.
• Grayish discoloration of tips of fingers, toes &
ears in a symmetrical distribution.
• Meningococcemia(PURPURA FULMINANS)-
bleeding from GI tract, gingival bleeding,
epistaxis, pulmonary hemorrhage, hematuria.
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12. PURPURA FULMINANSWWW.DNBCENTRAL.IN 12

13. Chronic DIC:
• Superficial and extensive ecchymosis of extremities
without petechiae which may be intermittent or can
persist.
• Recurrent episodes of epistaxis or internal mucosal
bleeding.
• Trousseau sign- Recurrent migratory
thrombophlebitis in association with cancer.
• Impairment of renal function, confusion, repeated
episodes of cerebral thrombosis.WWW.DNBCENTRAL.IN 13

14. CHRONIC DICWWW.DNBCENTRAL.IN 14

15. WWW.DNBCENTRAL.IN 15

16. PURPURA FULMINANS OF A CHILD'S LEG
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17. Specific features of DIC in neonates and
infants
 CAUSES:
• 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 .
 PRECIPITATING FACTOR:
Asphyxia, septicemia, eclampsia
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18. CLINICAL FEATURES:
 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
 Mortality 40-70%
TREATMENT:
Heparin. Relapse common after cessation.
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19. BULLAE SEEN IN DIC
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20. LABORATORY FINDINGS
 COMPLETE BLOOD COUNT:
Severe thrombocytopenia(50000-100000/µl) with or without
anemia
 PERIPHERAL BLOOD SMEAR:
Schistocytes- Microangiopathic hemolysis
 PROTHROMBIN TIME & aPTT:
Prolonged in early cases but may be normal or short in chronic
cases
 FIBRINOGEN LEVEL:
LowWWW.DNBCENTRAL.IN 20

21. SCHISTOCYTES IN PERIPHERAL BLOOD SMEAR
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22.  D dimer, FIBRINOGEN / FIBRIN DEGRADATION
PRODUCTS:
Increased >25µg fibrinogen equivalents/ml
 PROTEIN C & S, ANTITHROMBIN:
decreased
 MARKERS OF ENDOGENOUS THROMBIN
GENERATION:
Prothrombin fragment 1.2 and
Thrombin-Antithrombin complexes(TATs) are elevatedWWW.DNBCENTRAL.IN 22

23. Overt DIC Scoring System
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24. DIFFERENTIAL DIAGNOSIS
 Primary fibrinogenolysis or Pathologic
fibrinolysis:
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
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25. TREATMENT
BLOOD COMPONENT THERAPY:
INDICATIONS:
Active bleeding
Invasive procedure
Risk of bleeding complication
GOALS: To maintain
Platelet count >50000/µl
Fibrinogen concentration >1g/L
Prothrombin values less than double the normal
rangeWWW.DNBCENTRAL.IN 25

26.  FRESH FROZEN PLASMA(FFP):
 Constituents:
0.7-1.0 U/ml of factors II,V, VII, VIII, X, XI, XII, XIII and
2.5mg/ml fibrinogen.
 Dosage:
15ml/kg
CRYOPRECIPITATE:
 Constituents;
fibrinogen 150mg/bag
factor VIII 80-120units/bag
factor XIII & vWB
 Dosage:
1 bag/5kg body wt.
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27. PLATELETS:
 Random donor platelets(RDP):
• Constituents:
5.5×10¹° platelets
• Dosage:
1 unit/ 10 kg
 Single donor platelets:
• Constituents:
3×10¹¹ platelets
FRESH BLOOD:
Indicated in severe trauma to replace acute massive blood loss.
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28. ANTICOAGULANT THERAPY:
Heparin and other anticoagulant therapy to inhibit thrombin.
Indicated in patients with clinically overt thromboembolism ,
chronic DIC and extensive fibrin deposition.
Dosage:
Weight < 30kg – 10U/kg/hr
Weight > 30kg – 4U/kg/hr
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29. REPLACEMENT OF NATURAL
ANTICOAGULANT PATHWAY
Recombinant human activated protein c 24µg/kg/hr.
Adverse effects include bleeding.
ANTI-THROMBIN INDEPENDENT INHIBITORS
desirudin
gabexate mesylate
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30. COMPLICATIONS
 Respiratory failure
Renal failure
Stroke
Cardiac tamponade
Hemothorax
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31. PROGNOSIS
• Since DIC is a result of an acute medical illness,
prognoses depends almost entirely upon the
speed of the intensivist in handing the bleeding
emergency, as well as the ability to treat the
underling disorder
• The underlying disease that causes the disorder
will usually predict the probable outcome.
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Thank you
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