1. DISSEMINATED
INTRAVASCULAR
COAGULATION (DIC)

2.  DEFINITION
 ETIOLOGY
 PATHOPHYSIOLOGY
 CLINICAL MANIFESTATIONS
 LABORATORY FINDINGS
 DIFFERENTIAL DIAGNOSIS
 TREATMENT

3. 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.

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

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 bites

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,
hyperpyrexia

8. PATHOPHYSIOLOGY

9. CLINICAL
MANIFESTATIONS
DIC
NON OVERT DIC OVERT DIC ACUTE DIC CHRONIC DIC
CONTROLLED
UNCONTROLLED

10. Non overt DIC:
Stressed & compensated hemostatic system. Lab testsabnormal 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.

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.

12. PURPURA FULMINANS

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.

14. CHRONIC DIC

15. 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

16.  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.

17. BULLAE SEEN IN DIC

18. 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:
Low

19. SCHISTOCYTES IN PERIPHERAL BLOOD
SMEAR

20.  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
elevated

21. Overt DIC Scoring System

22. 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

23. 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
range

24.  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.

25. 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.

26. 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

27. REPLACEMENT OF NATURAL
ANTICOAGULANT PATHWAY
Recombinant human activated protein c 24µg/kg/hr.
Adverse effects include bleeding.
ANTI-THROMBIN INDEPENDENT
INHIBITORS
desirudin
gabexate mesylate

28. COMPLICATIONS
 Respiratory failure
Renal failure
Stroke
Cardiac tamponade
Hemothorax