Disseminated intravascular coagulation (DIC) is a pathological condition associated with activation of both the coagulation system and fibrinolytic system. It is considered a secondary phenomenon caused by an underlying disease. DIC can be acute, beginning with clotting in small blood vessels leading to serious bleeding, or chronic, causing blood clotting but usually not bleeding. Common causes include sepsis, trauma, cancer, pregnancy complications, and transfusion. Diagnosis involves tests showing decreased platelets, elevated D-dimer and fibrin split products, prolonged clotting times, and low fibrinogen. Treatment focuses on treating the underlying cause, supportive care, and replacing clotting factors, platelets, and fibrinogen.

1. Disseminated Intravascular
Coagulation

3. Definition of DIC
A pathological condition associated with activation
of both:
• Coagulation system and
• Fibrinolytic one
It should be considered as a secondary phenomena of
an underlying disease as …………………………….

4. Hemostasis

5. Step 1: Vasoconstriction.

6. Step 2: Platelet plug formation

7. • Step 3: Coagulation
• Extrinsic coagulation cascade
• Intrinsic coagulation cascade
• Clot formation

8. Causes
• Sepsis (an infection in the bloodstream)
• Surgery and trauma
• Cancer
• Serious complications of pregnancy and
childbirth

9. Common Obstetric Conditions
• Inadequate replacement of blood loss
• Pre-eclampsia-Eclampsia….HELP syndrome
• Ante partum hge (abruptio placenta and P.P.)
• I U F D when prolonged more than 4 weeks
• Blood transfusion when massive or incompatible
• Septic abortion or massive tissue injury
• Amniotic fluid embolism

10. Two types of DIC :
Acute DIC begins with clotting in the small
blood vessels and quickly leads to serious
bleeding.
Chronic DIC causes blood clotting, but it
usually doesn't lead to bleeding. Cancer is
the most common cause of chronic DIC

11. Pathogenesis
• The most accepted theory is the Cascade
theory in which there is activation of both
Extrinsic and Intrinsic pathways leading to
activation of factor xa leading to formation
of thrombin from prothrombin to form
fibrin from fibrinogen
• With associated activation of fibrinolytic
system as a protective mechanism.

12. Path physiology, continued
Decrease in platelets count is a result of :
1. Consumption
2. Aggregation of platelets

13. Path physiology, continued
• So DIC is a state of increase thrombin
activity at first, followed by increased
fibrinolytic activity, leading to…
• consumption of coagulation factor (source
of old name consumptive coagulopathy) and
the formation of FDP impairing
homeostasis.

14. Path physiology, continued
• Deposition of fibrin in organs and tissues
may lead to ischemic tissue damage.
• The decreased number of platelets and
elevated FDP increase the problem of
homeostasis.

16. Symptoms of DIC
It is variable according to the cause, the
presentation of the primary cause with:
• Generalized or localized hemorrhage
• Peticheae
• Thromboembolc manifestation, organ failure as:
liver, lung, kidneys, brain and frank gangrene have
been described.
• Chronic DIC, (that occurs with IUFD) may be
asymptomatic.

17. Diagnosis
Although the definite diagnosis is only by
histological finding of fibrin deposits, there are
many indirect tests as:
• Bedside clot retraction test
• clotting time (fibrinogen)
• D. Dimer (90%)
• Platelets count (90%)
• FDP (90%)
• Thrombin time (80%)
• PTT and PT (60%)

19. Bedside Clot Retraction Tes(CT)
• It simply tests the clotting time - a test of
decreased fibrinogen
• 2 ml blood in test tube - no clot formed but
if occurs it is prolonged, soft and not
retracted after half an hour, leaving a clot
volume more than serum volume.
(the clot doesn't retract)

20. Skin Puncture Test (bleeding time)
• Prolonged skin puncture ooze is observed
when the platelets count is less than
100,000/ul
• Continuous bleeding at puncture site occurs
when pl count is less than 30,000 /ul

21. Other laboratory tests
• Platelets count decreases in 90% of cases
(count less than 100,000/dl)
• PT, which measures the time required by
extrinsic pathway, elevated in 80% of DIC
• PPT which measure the time required by
intrinsic pathway - not helpful.
• Thrombin time elevated in 80% of cases

22. Other laboratory tests
• Fibrinogen level/ less than150mg. This is
present in 70% of cases.
• Fibrin split product >40ug/dl, 90% of cases
• D-Diamer - an antigen formed as a result of
plasmin digestion, elevated in 90%of cases.

23. Treatment of DIC
• Essentially treat the underlying cause. In most
cases prompt termination of pregnancy is
required.
• Supportive therapy should be directed to the
correction of shock, acidosis and tissue ischemia.
• Cardiopulmonary support including inotropic
therapy, blood transfusion and assisted ventilation

24. Treatment
• Careful monitoring of fluid balance
• Serial evaluation of coagulation parameters
• If sepsis is suspected, antibiotic is indicated
with evacuation of the septic focus

25. Obtain and send 2 blood samples:
1) To blood bank for grouping and cross
matching
2) To lab to obtain baseline for Hb, Htc,
PT, PTT, platelet count and fibrinogen
levels

26. DIC Treatment
• Treatment of hypovolemia should be
applied according to the guideline of
National Institute of Health.
• Crystalloid first
• Plenty blood transfusion
• Treat hypothermia
• Red cell transfusion, if bleeding.
(anticipated)
Wies et al2007

27. Treatment of Coagulopathy
• FFP for a prolonged PT - The idea is to keep it 2 to 3
seconds from control, (it contains coagulation factors),
each unit volume is 250ml
2-Cryoprecipitate
• For a fibrinogen level less than 100 mg/dL. it is a fresh
frozen plasma concentrate, (each bag volume is 10ml),
contains 100mg fibrinogen raising f by 10mg/dl.
1-Fresh Frozen PASMA

28. Platelet Transfusion
• Transfuse platelets for platelet counts less
than 20,000/mm3in active bleeding or less
than 50,000 if c s is planned.
• The rate of pl transfusion is one unit to
every 10 kg/body w.

29. Treat Coagulopathy
• Parental vitamin k and folic acid as pt of
DICare deficient in these vitamins
• There is much data not in favor of use of the
antifibrinolytic drugs
• In DIC 10 UNITES OF CRYOPPT, FOE
2/3 UNITE OF FF PLASMA SHOUID BE
READY

30. Role of Heparin in low dose
• Although there is a controversy in regards to
giving a low dose of LMWH, its idea is to stop the
consumption of coagulation factors, however its
role is established in case of chronic DIC, (as in
case IUFD of single twin for example or any case
of IUFD before termination with follow up with
fibrinogen level)
• Full dose if thrombosis is definitely diagnosed

31. Prognosis
• Most cases of obstetric DIC will improve
with delivery of the fetus or evacuation of
the uterus
• This improved prognosis seems to be
related to the recent advance in critical care

32. Conclusion
• DIC is a secondary phenomena, therefore it
is mostly predictable
• It occurs in an acute or chronic form,
therefore it can be anticipated in the later
form.
• The commonest cause is inadequate
resuscitation, therefore it is preventable by
early intervention.

33. Take Home Message
DIC can be predicted and
even prevented in most of
the cases.

40. Procedures

41. Platelets transfusion Triggers

42. TTP

44. Pathophysiology

48. Mangement
• Plama infusion : 30cc/Kg/day
• Plama Exchange : daily PV/3-6days
• Steroids :1mg/kg prednisolone
• Immunosupressive ; Rituximab or Cyclosporin
• Twice daily PE with Rituximab
• Anticoaulations : Plt >50.000

49. Plasma therapy

50. Plama Exchange

51. Steroids and Immunosupressive

53. HIT

68. Thank you