2. D - DEATH I - IS C - COMING DIC is an important contributor to maternal mortality and morbidity

3. What is DIC ? DIC is a massive activation of the coagulation system leading to multiple clot formation throughout the body. As a result there is rapid consumption of clotting factors which leads to bleeding. So it is a paradoxical condition characterised by both thrombosis & haemorrhage.

4. DIC is a red flag for a severe underlying disease DIC is never a primary diagnosis It is always a secondary diagnosis

5. INTRINSIC PATHWAY EXTRINSIC PATHWAY XII XIIa VIIa XIa IXa Ca VIIIa Xa (COMMON PATHWAY) Prothrombin Thrombin Plasmin Fibrinogen Fibrin D-dimer Plasmin FDPs

6. Coagulation is always the initial event A delicate balance exists between coagulation mechanism & fibrinolytic system.

7. TRIGGER MECHANISMS OF DIC DURING PREGNANCY Pre- eclampsia Hypovolaemia Septicaemia Large foetomaternal bleed Incompatible blood transfusion Abruptio placentae Amniotic fluid embolism Retained dead foetus Intrauterine sepsis H. mole Placenta accreta Abortion induced by hypertonic fluids.

8. CLINICAL MANIFESTATIONS Bleeding from multiple sites ( most common ) ( either oozing or frank bleeding) Renal dysfunction Hepatic dysfunction Respiratory dysfunction Shock and death

9. Diagonosis of DIC No single test diagnoses DIC Clinical picture leads to diagnosis of DIC

10. Bed side Tests Clot Observation Test (CT)- if a firm clot forms within 10 mins it is unlikely that pt has DIC and that fibrinogen levels are normal. Clot Retraction Time-if the clot retracts well by end of one hour it means the platelets are adequate An unstable or fragile clot indicates presence of FDPs in blood.

11. Lab parameters usually associated with DIC are Thrombocytopenia Develops due to activation of clotting system and consumption by clot formation Sensitive but not specific

12. Fibrinogen degradation products and D- Dimer It is the most sensitive test for DIC. (85-100%) It is unlikely to be DIC if FDP’s levels are normal. FDPs are metabolized in liver and kidney. Hepatic or renal dysfunction may lead to falsely elevated levels of FDPs

13. PT & PTT PTT measures intrinsic pathway PT measures extrinsic pathway PT and PTT prolonged in 50-60% of DIC cases Can use PT and PTT to monitor DIC

14. Fibrinogen Classically use to diagnose and monitor DIC. Most cases not very helpful. Sensitivity of a low fibrinogen level for the diagnosis of DIC is only 28%

15. Fibrinogen Fibrinogen is an acute-phase reactant so may be falsely normal in DIC. Hypofibrinogenemia is detected only in very severe cases of DIC. The blood fibrinogen level of 100mgm/100ml is considered to be the critical level

16. Schistocytes (Fragmented RBCs) Fragmented red blood cells rarely constitute >10% of the red cells. Neither sensitive nor specific to DIC.

17. Antithrombin & Protein C Antithrombin and protein C are often reduced in DIC. Have shown to have both diagnostic and prognostic significance.

18. DIC Scoring System International Society for thrombosis and Haemostasis ( ISTH )

19. 5 step diagnostic algorithm Sensitivity 91% Specificity 97%

20. ISTH Scoring System Prerequisite Does the patient have an underlying disorder known to be associated with overt DIC ?

21. NO

22. Do NOT use this algorithm.

23. YES

24. Coagulation Tests Prothrombin time Platelet count Fibrinogen levels Fibrin related marker (FDPs, D-dimer)

25. Score Test Results

26. Prothrombin Time <3 sec = 0 >3 but <6 sec = 1 >6 sec = 2

27. Platelet Count > 100,000 / cumm = 0 50-100,000 / cumm = 1 < 50,000 / cumm = 2

28. Fibrinogen Level > 1 g / l = 0 < 1 g / l = 1

29. Fibrin Marker (e.g. D-dimer, FDPs) No increase = 0 Moderate increase = 2 Strong increase = 3

30. Calculate score > or = to 5 compatible with overt DIC < 5 suggestive for non - overt DIC

31. PROTOCOL OF MANAGEMENT Maintenance of blood pressure and oxygenation Maintenance of blood volume (crystalloids, albumin, plasma expanders). Blood Component therapy Treatment of underlying etiology of DIC

32. Management of blood volume includes prompt & adequate fluid replacement to prevent renal shutdown. Crystalloids (Ringer lactate) / Haemaccel Colloids X Whatever fluid is used, it only acts as a stop gap until suitable blood component therapy is available

33. Blood component therapy Fresh frozen plasma Cryoprecipitate Platelets Packed red blood cells

34. Are most effective to improve oxygen carrying capacity Each unit contains about 300 ml ( 250 ml RBC & 50 ml plasma) One unit of PRBC raises the Hb by 1 gm/dl and PCV by 3 %.

35. Platelet concentrates Platelets should be given rapidly over 10 mins. One unit raises the count between 5000 – 10,000/ ml. Dose is = one unit / 10 kg. single donor concentrates are preferred as the antigenic risk is low. Platelets count can be assessed 10 – 60 mins after transfusion.

36. Fresh Frozen Plasma (FFP) Provides both volume & coagulation factor replacement. One unit of FFP (250 ml) raises fibrinogen by 5 – 10 mgm /dl. Dose 10 – 15 ml/ kg or one bag / 10 kg

37. Cryoprecipitate It is rich in fibrinogen so its use is indicated if blood fibrinogen levels are < 1 gm / L. One unit increases the fibrinogen level by 5- 10 mg/dl. Dose is 1 unit/ 5 kg. No. of bags required is =0.2 x body weight in kg.

38. The main therapeutic goal is to maintain Hb > 8 gm / L Platelet count > 75,000 / cumm Prothrombin time < 1.5 times the normal Activated prothrombin time < 1.5 Fibrinogen > 1.0 gm / L

39. Treatment of the underlying condition

40. PLACENTAL ABRUPTION-- The severity of DIC is directly related to time interval between the placental separation and delivery Management thus includes emptying the uterus as soon as possible

41. PRE ECLAMPSIA- ECCLAMPSIA SYNDROME Majority of women with pre-ecclampsia have sub-clinical consumptive coagulopathy. Frank DIC is seen when there is associated placental abruption or HELLP syndrome. Immediate delivery is recommended

42. AMNIOTIC FLUID EMBOLISM Carries high maternal mortality (80%) Treatment is mainly supportive as there is no proven effective therapy. Heparin may be considered (80-100 units /kg s/c 4-6 hly )

43. INTRAUTERINE FETAL DEMISE Goal: to raise fibrinogen level to 200-300 mg/dL before termination of pregnancy. Heparin may be considered for chronic DIC associated with IUD

44. SEPSIS Intensive antibiotic therapy followed by evacuation of uterine contents. Prompt restoration and maintenance of circulation. Removal of septic focus

45. To conclude The only proven treatment of DIC Stop the triggering process.

46. CRITICAL CARE CAN MAKE A GREAT DIFFERENCE ALERT MIND ! TIMELY INTERVENTION ! AGGRESSIVE MANAGEMENT !

47. THANK YOU

48. Normal values of blood coagulation profile Prothrombin time(11-16s)-Extr.pathway PTT-(30-45s) –Intrinsic pathway Thrombin time (TT) 10-15s S. Fibrinogen- (300-600mg%) Platelets (1.5-3.0L) D-dimer (<0.5mg/L) 0-200mgm/ml Fibrin degradation products (10µ/dl) 0-5 microgm/ml