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
•So it is a paradoxical
condition characterised by
both thrombosis &
• DIC is a red flag for a severe
• DIC is never a primary diagnosis
• It is always a secondary diagnosis
INTRINSIC PATHWAY EXTRINSIC PATHWAY
XII XIIa VIIa
Xa (COMMON PATHWAY)
Fibrinogen Fibrin D-dimer
Coagulation is always the initial
TRIGGER MECHANISMS OF DIC
• Large foetomaternal
• Incompatible blood
• Abruptio placentae
• Amniotic fluid
• Retained dead foetus
• Intrauterine sepsis
• H. mole
• Placenta accreta
• Abortion induced by
• 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
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
• An unstable or fragile clot indicates presence
of FDPs in blood.
Lab parameters usually
associated with DIC are
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
Can use PT and PTT to
• Classically use to diagnose and
• Most cases not very helpful.
• Sensitivity of a low fibrinogen level for
the diagnosis of DIC is only 28%
• 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
for thrombosis and
Haemostasis ( ISTH )
• > 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
• Crystalloids (Ringer lactate) / Haemaccel
• Colloids X
Whatever fluid is used, it only acts as a stop gap
until suitable blood component therapy is
Packed red blood cells
• Are most effective to improve oxygen carrying
• 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 %.
• Platelets should be given rapidly over 10 mins.
• One unit raises the count between 5000 –
• 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
Fresh Frozen Plasma (FFP)
• Provides both volume & coagulation factor
• One unit of FFP (250 ml) raises fibrinogen by
5 – 10 mgm /dl.
• Dose 10 – 15 ml/ kg or one bag / 10 kg
• 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
• Dose is 1 unit/ 5 kg.
• No. of bags required is =0.2 x body weight in kg.
The main therapeutic goal is
• 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
• 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
• 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
• Intensive antibiotic therapy followed by
evacuation of uterine contents.
• Prompt restoration and maintenance of
• Removal of septic focus
The only proven treatment of DIC
Stop the triggering
CAN MAKE A GREAT DIFFERENCE
ALERT MIND !
TIMELY INTERVENTION !
AGGRESSIVE MANAGEMENT !
Normal values of blood
• 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