Disseminated intravascular coagulation (DIC) is an acquired condition that disturbs the normal coagulation physiology, leading to widespread blood clotting throughout small blood vessels. This causes organ dysfunction due to leakage from blood vessels and shock. DIC can be caused by infections, tissue injuries, cancers, and other medical conditions. Clinically, DIC may present as bleeding, organ failure, and microvascular thrombosis. Laboratory findings include low platelet count and signs of intravascular hemolysis. Treatment focuses on treating the underlying cause, replacing clotting factors, and using anticoagulants to prevent further thrombosis. The prognosis depends on promptly diagnosing and managing DIC while also treating the triggering disease.

2. DISSEMINATED
INTRAVASCULAR
COAGULATION (DIC)
Dr. Sahar Mirza
Post Graduate Resident
Paediatric Department

3. CONTENTS
 DEFINITION
 ETIOLOGY
 PATHOPHYSIOLOGY
 CLINICAL MANIFESTATIONS
 LABORATORY FINDINGS
 DIFFERENTIAL DIAGNOSIS
 TREATMENT

4. 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.

5. MECHANISMS
Occurs due to simultaneous actionof the following 4
mechanisms
• Increased thrombin generation
• Suppressed physiological anticoagulant pathways
• Activation & subsequent impairmentof fibrinolysis
• Activation of inflammatory pathways

6. ETIOLOGY
INFECTIOUS:
Meningococcemia- purpura fulminans
Bacterial sepsis- staphylococcal, streptococcal, Ecoli
Rickettsia- Rocky Mountain spotted fever
Viral- CMV,varicella, arboviruses
Malaria, Candida, Aspergillus
TISSUE INJURY:
Multiple fractures with fat emboli, crush injury, headinjury
MALIGNANCY:
Acute promyelocytic leukemia, acute myeloidleukemia,
neuroblastoma
VENOM OR TOXIN:
Snake bites, insect bites

7. Contd…
MICROANGIOPATHIC DISORDERS:
TTP, HUS, Kasabach-Meritt syndrome
GI DISORDERS:
Fulminant hepatitis, Inflammatory boweldisease,
Pancreatitis
HEREDITARY THROMBOTIC DISORDERS:
Antithrombin III deficiency, Homozygous proteinC deficiency
NEWBORN:
Maternal toxemia, Abruptio placentae, Necrotizing
enterocolitis, Erythroblastosis fetalis
MISCELLANEOUS:
Acutegraft rejection, Acute hemolytic transfusion reaction, Collagen
vascular disorders, Heparin induced thrombosis, hyperpyrexia

8. PATHOPHYSIOLOGY

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

10. Non overtDIC:
• Stressed & compensated hemostatic system. Labtests-
abnormal but no clinicalmanifestations.
Overt DIC:
• Stressed and decompensated hemostatic system.Lab
tests- abnormal with clinical bleeding or micro vascular
thrombosisand organ dysfunction.Further divided into
controlledand uncontrolled based on whether the
process will resolve when the underlying condition is
removed.

11. Acute DIC:
• Bleeding from vein puncturesite, 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 FILMINANS

13. Chronic DIC:
• Superficial and extensive ecchymosis of extremities without
petechiaewhich may be intermittent or can persist.
• Recurrentepisodes of epistaxis or internal mucosal bleeding.
• Trousseau sign- Recurrent migratory
thrombophlebitis in association withcancer.
• Impairment of renal function, confusion,repeated episodes
of cerebralthrombosis.

14. CHRONIC DIC

15. Specific features of DIC in
neonates and infants
CAUSES:
• Transplacental passage of thromboplastin or other
procoagulant substances in neonates born ofmothers
affected with DIC owing to abruptio placenta, eclampsia or
septicemia.
• Development of DIC in a twin fetus may be due to feto-
fetal passage ofthromboplastin.
• DIC secondary to hemangioma.
• PRECIPITATING FACTOR:
Asphyxia, septicemia,eclampsia

16. CLINICAL FEATURES
• Symmetricecchymosis of lowerextremities and
buttocks. Later these lesions become necrotic
ultimately forming blood filled bullae.
• Sharplycircumscribed infarcts of skin and genitalia
• Gangrene of extremities involves digitssymmetrically.
• Fever andprostration
• Mortality 40-70%

17. TREATMENT
• Heparin. Relapse common aftercessation.

18. BULLAE SEEN IN DIC

19. LABORATORY FINDINGS
COMPLETE BLOOD COUNT:
• Severe thrombocytopenia(50000-100000/µl) withor
withoutanemia
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

20. SCHISTOCYTES IN PAREPHERAL
BLOOD SMEAR

22. DIFFERENTIAL DIAGNOSIS
Primary fibrinogenolysis orPathologic fibrinolysis:
• Platelet count isnormal
• D dimer may be normal or minimally increased
• No hypoprothombinemia & No deficiency of coagulation
factors (VII, IX, X,XI)
Severe liverdisease:
• D dimer test isnormal

23. TREATMENT
BLOOD COMPONENT THERAPY:
INDICATIONS:
Active bleeding
Invasiveprocedure
Risk of bleeding complication
GOALS:
Tomaintain Platelet count
>50000/µl
Fibrinogen concentration>1g/L
Prothrombin values less than double thenormal range

24. FRESH FROZEN PLASMA (FFP)
Constituents:
• 0.7-1.0 U/ml of factors II,V, VII, VIII, X, XI, XII, XIIIand 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 donorplatelets(RDP):
Constituents:
5.5×10¹° platelets
Dosage:
1 unit/ 10 kg
Single donorplatelets:
Constituents: 3×10¹¹
platelets
FRESH BLOOD:
Indicated in severe trauma to replaceacute massive blood
loss.

26. ANTICOAGULANT THERAPY
Heparin and other anticoagulant therapy to inhibit thrombin.
Indicated in patients with clinically overt thromboembolism ,
chronic DICand extensive fibrin deposition.
• Dosage:
Weight < 30kg – 10U/kg/hr
Weight > 30kg – 4U/kg/hr

27. REPLACEMENT OF NATURAL
ANTICOAGULANT PATHWAY:
Recombinant human activated protein c24µg/kg/hr.
Adverse effects includebleeding.
ANTI-THROMBIN INDEPENDENT INHIBITORS:
Desirudin gabexate
Mesylate

28. COMPLICATIONS
• Respiratory failure
• Renal failure
• Stroke
• Cardiactamponade
• Hemothorax

29. PROGNOSIS
• Since DIC is a result of an acute medical illness, prognosis
depends almost entirely upon the speed of the staff 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.
• An awareness of the clinical settings in which DIC can occur
and the diagnostic features that warn of its presence should
enable the physician to diagnose and treat DIC appropriately.

30. CONTINUED….
• DIC may occur in 30-50% of patients with sepsis, andit
develops in an estimated 1% of all hospitalized patients
• DIC occurs at all ages and in all races, and no particular sex
predisposition has been noted.

31. THANK YOU !