1. Disseminated intravascular coagulation (DIC)
Dr. Mohamed Haseen Basha
Assistant professor ( Paediatrics)
Faculty of Medicine
Al Maarefa College of Science and Technology

2. Definition
Disseminated intravascular coagulation (DIC) is an acquired disorder, it occurs when the normal hemostatic balance is disturbed primarily by excessive thrombin formation. It is a dynamic process triggered by a variety of conditions causing activation of the clotting cascade and generation of excess thrombin within the vascular system, which in turn leads to deposition of fibrin in the micro circulation. This definition implies that microclot formation and consequent ischemic organ failure and/or a hemorrhagic diathesis may occur.

3. Types of DIC
Acute DIC This is the most common form of DIC seen in clinical practice. Bleeding manifestations predominate Presents with sudden bleeding from multiple sites

4. Chronic DIC
Develops over a period of months, maybe subclinical, eventually evolves into an acute DIC pattern
This occurs from a weak or intermittent activating stimulus.
The destruction and production of clotting factors and platelets is balanced, so that the DIC is considered to be compensated.
Patients may have recurrent episodes of ecchymosis or mild bleeding and thrombophlebitis at unusual sites.
Trousseau’s sign is a form of chronic DIC.

5. Diseases Causing Acute or Chronic DIC
Causes
Acute DIC
Chronic DIC
Medical
Septicemia / Infections
Fulminant Hepatic failure
Allergic reactions
Transplantation
Heat Stroke
Hypothermia
Leukemia
Homozygous protein C deficiency
Solid tumors
Liver cirrhosis
Vasculitis
Kasabach-Merritt syndrome
Adult respiratory distress syndrome
Surgical
Poly trauma
Major operations
Brain injury
Extracorporeal circulation
Thermal injury
Fat embolism
Cardiac Bypass surgery Peritoneovenous shunt
Organ transplantation
Aortic aneurysm
Vascular tumors

6. Causes
Acute DIC
Chronic DIC
Obstetrics and Gynaecology
Amniotic fluid embolism Abruptio placentae
Septic abortion
Acute fatty liver
Uterine rupture
Toxemia of pregnancy Septicemia
Late gestation
HELLP syndrome
Retained dead fetus
Transfusion Medicine
Acute haemolytic transfusion reaction Massive Transfusion Artificial surfaces

7. Pathophysiology of DIC
Activation of Blood Coagulation
Suppression of Physiologic Anticoagulant Pathways
Impaired Fibrinolysis
Cytokines

8. Activation of Blood Coagulation
Tissue factor/factor VIIa mediated thrombin generation via the extrinsic pathway
complex activates factor IX and X
Tissue Factor
endothelial cells
monocytes
Extravascular:
lung
kidney
epithelial cells

9. Suppression of Physiologic Anticoagulant Pathways
reduced antithrombin III levels
reduced activity of the protein C-protein S system
Insufficient regulation of tissue factor activity by tissue factor pathway inhibitor (TFPI)
inhibits TF/FVIIa/Fxa complex activity

10. IL-6, and IL-1 mediates coagulation activation in DIC TNF-
Impaired Fibrinolysis
Relatively suppressed at time of maximal activation of coagulation due to increased plasminogen activator inhibitor type 1.
Cytokines
IL-6, and IL-1 mediates coagulation activation in DIC
TNF-
mediates dysregulation of physiologic anticoagulant pathways and fibrinolysis
modulates IL-6 activity
IL-10 may modulate the activation of coagulation

12. Clinical features The diagnosis of DIC is mainly clinical.
Hemorrhage is the commonest presentation characterized by spontaneous bruising, muscle oozing, bleeding from venipuncture sites, and secondary hemorrhage into surgical wounds.
Bleeding is associated with varying degrees of shock, which is often out of proportion to the degree of blood loss.
Shock is probably due to activation of contact factor XII that leads to production of bradykinin, and interaction between cytokines like TNF and IL-1.

13. Evidence of major organ dysfunction is common, usually involving the pulmonary, renal, hepatic and central nervous systems. These features are due to a combination of factors, namely microvascular thrombi, shock and cytokine effects.
Anemia caused by hemolysis may develop rapidly, owing to microangiopathic hemolytic anemia.

14. Most common sign of DIC is bleeding - Manifested by ecchymosis, petechiae and purpura - Bleeding from multiple sites either oozing or frank bleeding - Cool and or mottled extremities may be noted - Dyspnea and chest pain if pleura and pericardium involvement - Hematuria

15. ORGAN
ISCHEMIC
HEMORRAGIC
Skin
Purpura Fulminans
Gangrene
Acral cyanosis
Petechiae
Echymosis
Oozing
CNS
Delirium/Coma
Infarcts
Intracranial bleeding
Renal
Oliguria/Azotemia
Cortical Necrosis
Hematuria
Cardiovascular
Myocardial Dysfunction
Pulmonary
Dyspnea/Hypoxia
Infarct
Hemorrhagic lung GI
Endocrine
Ulcers, Infarcts
Adrenal infarcts
Massive hemorrhage

17. Factors Accelerating DIC
Shock
Chronic renal insufficiency
Acidosis
Chronic hepatic insufficiency
Hypoxemia
Malnutrition
Stasis
Impaired anti-coagulation activity
Dehydration
Impaired fibrinolytic activity
Hyperthermia
Phagocytic dysfunction

18. Diagnosis
The blood film may show fragmented red blood cells (schistocytes).
Fibrin degradation products (FDP) - high
D-dimer – high
Prothrombin time (PT) - high
Partial thromboplastin time (PTT) - high
Platelet count - low
Serum fibrinogen - low
Low levels of coagulation inhibitors
AT III, protein C
Low levels of coagulation factors
Factors V,VIII,X,XIII

19. Treatment The most critical steps in the treatment of DIC are :
(a) Treat the trigger that caused DIC and
(b) Restore normal homeostasis by correcting the shock, acidosis, and hypoxia that usually complicate DIC.
If the underlying problem can be controlled and the patient stabilized, bleeding quickly ceases, and there is improvement of the abnormal laboratory findings.

20. Blood components are used for replacement therapy in patients with hemorrhage and may consist of
Platelet infusions (for thrombocytopenia),
Cryoprecipitate (for hypofibrinogenemia), and/or
Fresh-frozen plasma (for replacement of other coagulation factors and natural inhibitors).
The role of heparin
In DIC is limited to patients who have vascular thrombosis in association with DIC or who require prophylaxis because they are at high risk for venous thromboembolism.