Abc critical care of dic dr. jyoti agarwal
- 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)
- 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. Packed red blood cells • 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 !
- 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