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D - DEATH
I - IS
C - COMING
DIC is an important contributor to
maternal mortality and morbidity
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.
• DIC is a red flag for a severe
underlying disease
• DIC is never a primary diagnosis
• It is always a secondary diagnosis
INTRINSIC PATHWAY EXTRINSIC PATHWAY
XII XIIa VIIa
XIa
IXa
Ca
VIIIa
Xa (COMMON PATHWAY)
Prothrombin Thrombin
Plasmin
Fibrinogen Fibrin D-dimer
Plasmin
FDPs
Coagulation is always the initial
event
A delicate
balance exists
between
coagulation
mechanism &
fibrinolytic
system.
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.
CLINICAL MANIFESTATIONS
• Bleeding from multiple sites ( most common )
( either oozing or frank bleeding)
• Renal dysfunction
• Hepatic dysfunction
• Respiratory dysfunction
• Shock and death
Diagonosis of DIC
• No single test diagnoses DIC
• Clinical picture leads to diagnosis of
DIC
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.
Lab parameters usually
associated with DIC are
Thrombocytopenia
Develops due to activation of clotting
system and consumption by clot formation
Sensitive but not specific
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
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
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%
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
Schistocytes (Fragmented RBCs)
•Fragmented red blood cells rarely constitute
>10% of the red cells.
•Neither sensitive nor specific to DIC.
Antithrombin & Protein C
• Antithrombin and protein C are often
reduced in DIC.
• Have shown to have both diagnostic and
prognostic significance .
DIC Scoring System
International Society
for thrombosis and
Haemostasis ( ISTH )
5 step diagnostic algorithm
Sensitivity 91%
Specificity 97%
ISTH Scoring System
Prerequisite
Does the patient have an
underlying disorder known to
be associated with overt DIC ?
NO
Do NOT use
this algorithm.
YES
Coagulation Tests
• Prothrombin time
• Platelet count
• Fibrinogen levels
• Fibrin related marker (FDPs, D-dimer)
Score Test Results
Prothrombin Time
<3 sec = 0
>3 but <6 sec = 1
>6 sec = 2
Platelet Count
> 100,000 /cumm = 0
50-100,000 /cumm = 1
< 50,000 /cumm = 2
Fibrinogen Level
•> 1 g / l = 0
•< 1 g / l = 1
Fibrin Marker (e.g. D-dimer, FDPs)
• No increase = 0
• Moderate increase = 2
• Strong increase = 3
Calculate score
• > or = to 5 compatible with overt DIC
• < 5 suggestive for non - overt DIC
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
• 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
Blood component therapy
• Fresh frozen plasma
• Cryoprecipitate
• Platelets
• Packed red blood cells
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 %.
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.
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
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.
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
Treatment of the
underlying condition
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
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
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 )
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
SEPSIS
• Intensive antibiotic therapy followed by
evacuation of uterine contents.
• Prompt restoration and maintenance of
circulation.
• Removal of septic focus
To conclude
The only proven treatment of DIC
Stop the triggering
process .
CRITICAL CARE
CAN MAKE A GREAT DIFFERENCE
ALERT MIND !
TIMELY INTERVENTION !
AGGRESSIVE MANAGEMENT !
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

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Abc critical care of dic dr. jyoti agarwal

  • 1.
  • 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
  • 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.
  • 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