This document discusses disseminated intravascular coagulopathy (DIC), an acquired syndrome characterized by widespread blood clotting. It can be acute or chronic. Acute DIC develops rapidly from sudden exposure to clotting factors, while chronic DIC reflects slower, continuous exposure. Signs include bleeding and organ dysfunction. Diagnosis is based on clinical evaluation and lab tests of clotting factors and platelets. Treatment focuses on the underlying cause, with replacement of platelets or clotting factors for severe bleeding.

1. DISSEMINATED
INTRAVASCULAR
COAGULOPATHY
Dr. ABIMBOLA B. O.

2. OUTLINE
• INTRODUCTION
• TYPES
• PATHOPHYSIOLOGY
• AETIOLOGY
• SIGNS AND SYMPTOMS
• DIFFERENTIAL DIAGNOSES
• DIAGNOSIS
• TREATMENT
• REFERRENCES

3. INTRODUCTION
•Disseminated Intravascular coagulopathy (DIC) is
an acquired clinicopathologic syndrome
characterized by widespread intravascular fibrin
formation in response to excessive blood
protease activity that overcomes the natural
anticoagulant mechanisms.

4. •Derangement of the fibrinolytic system further
contributes to intravascular clot formation, but
in some cases accelerated fibrinolysis may cause
severe bleeding. Hence, a patient with DIC can
present with a simultaneously occurring
thrombotic and bleeding problem
•DIC is estimated to be present in 1% of
hospitalized patients.

5. TYPES
•ACUTE DIC
•CHRONIC DIC

6. •ACUTE DIC develops when sudden exposure of blood
to procoagulants (e.g. Tissue factor, Tissue
thromboplastin) generates intravascular coagulation.
•Compensatory hemostatic mechanisms are
overwhelmed quickly resulting in a consumptive
coagulopathy leading to hemorrhage.
•Abnormalities of blood coagulation parameters are
readily identified and organ failure frequently results.

7. •Whereas, CHRONIC DIC reflects a compensated state
when blood is continuously or intermittently
exposed to small amounts of TF.
•Compensatory mechanisms in the liver and bone
marrow are not overwhelmed, and there may be
little obvious clinical or laboratory indication.
•It is more frequently observed in patients with solid
tumors and those with large aortic aneurysms.

8. PATHOPHYSIOLOGY
•Four simultaneously occurring mechanisms are
known to occur, to include:
•Increased Thrombin generation. Mediated
predominantly by tissue factor/factor VIIa
pathway.

9. • Impaired function of physiological anticoagulant
pathway.
a) Reduction of antithrombin levels, the result of a
combination of increased consumption, enzyme
degradation, impaired liver synthesis and vascular
leakage.
b) Depression of protein C system, the result of a
combination of increased consumption, impaired liver
synthesis, vascular leakage and down leakage of
thrombodulin.

10. c) Insufficient Tissue Factor Pathway Inhibitor (TFPI)
•Impaired fibrinolysis. Mediated by release of
plasminogen activators from endothelial cells
immediately followed by an increase in the plasma
levels of plasminogen inhibitor type 1 (PAI-1)

11. •Activation of inflammatory response. Mediated
by activated coagulation proteins and by
depression of the protein C system

13. AETIOLOGY
Occurs generally via one of the following pathways:
• A systemic inflammatory response leading to
activation of the cytokine network and subsequent
activation of coagulation (sepsis, major trauma).
• Release or exposure of pro coagulant material in the
bloodstream (cancer, obstetric cases)

14. TYPE CAUSE
INFECTIOUS Bacterial
Viral
Fungal
Parasitic
MALIGNANCY Hematologic
Metastatic
OBSTETRIC Amniotic fluid embolism
Abruptio placentae
PreEclampsia/Eclampsia/HELLP syndrome
Septic abortion/Retained stillbirth
TRAUMA Burns
RTA
Snake envenomation
TRANSFUSION Hemolytic reactions
OTHER Prosthetic devices
Shunts
Ventricular assist devices
**ACUTE

15. **CHRONIC
TYPE CAUSE
MALIGNANCIES Solid tumors
Leukemias
OBSTETRIC Retained dead fetus syndrome
Retained products of conception
HEMATOLOGIC Myeloproliferative syndromes
VASCULAR Rheumatoid arthritis
Reynaud's disease
CARDIOVASCULAR Myocardial infarction
INFLAMMATORY Ulcerative colitis
Chron disease
Sarcoidosis

16. SIGNS AND SYMPTOMS
•Symptoms are often those of the underlying
condition.
•In addition there is typically a history of blood
loss through bleeding in areas such as the
gingivae and GI system.

17. • Acutely presenting DIC often manifests as petechiae
and ecchymosis along with blood loss from IV Lines
and Catheters.
FEATURES AFFECTED PATIENTS
Bleeding 64% (bleeding from at least 3 unrelated sites is particularly
suggestive of DIC)
Renal dysfunction 25%
Hepatic dysfunction 19%
Respiratory dysfunction 16%
Shock 14%
CNS dysfunction 2%

18. •Physical findings in acute DIC are usually those of
underlying condition, however there could also be
petechiae on the soft palate and extremities
(thrombocytopenia). and ecchymosis at
venipuncture or traumatized sites.
•In chronic DIC, primary manifestation is
thrombosis, and the signs of venous
thromboembolism may be present.

19. DIFFERENTIAL DIAGNOSES
•Dysfibrinogenemia
•Hemolytic-Uremic syndrome
•Heparin-Induced Thrombocytopenia
•Thrombotic Thrombocytopenic Purpura

20. DIAGNOSIS
• Could be difficult especially in cases of chronic DIC
where clinical and laboratory abnormalities may be
subtle.
• No single routinely available test is sufficiently specific
or sensitive.
• Diagnosis is made by combining clinical impression
with any laboratory abnormalities noted.

21. Standard Tests
• Platelet count: Typically, moderate – severe
thrombocytopenia is present in DIC (as many as 98%
of patients), which can dip below 50 * 103/cmm in up
to 50% patients.
• Repeated counts are often necessary, as single
measurement can be within normal range whereas
trend values might show precipitous drop from
previous levels.

22. •Clotting times and coagulation factors: aPTT and PT
are typically prolonged, however an attenuated or
normal value cannot exclude DIC, again serial tests are
usually more helpful.
•It is important to note that PT not INR is to used for
DIC monitoring as INR is only recommended for
monitoring oral anticoagulant therapy.

23. •Protein C and antithrombin are two natural
anticoagulants that are frequently decreased.
•Test for fibrinogen, D-dimer, and FDPs

24. DIC SCORING SYSTEMS
•The International Society on Thrombosis and
Hemostasis (ISTH)
•Japanese Association for Acute Medicine (JAAM)

25. • **ISTH
• A score of 5 or higher
indicates overt DIC.
• A score less than 5 does
no rule out DIC but may
indicate that it is not
overt.
• Sensitivity of this scoring
system is 91-93%
• And the specificity is 97-
98%

26. **JAAM

27. Histologic findings
•Grossly, hemorrhage into all tissues can develop
in acute DIC
•Microscopically, presence of ischemia and
necrosis due to fibrin deposition in small and
medium sized vessels of various organs

28. TREATMENT AND MANAGEMENT
•Treatment should primarily focus on addressing
the underlying disorder.

29. Management of DIC itself has the following basic
features:
•Monitor vital signs
•Assess and document the extent of hemorrhage
and thrombosis
•Correct hypovolemia
•Administer basic hemostatic procedures when
indicated

30. •Platelet and coagulation factor replacement
should not be instituted on the basis of
laboratory results alone; such therapy is
indicated only in patients with active bleeding,
those requiring an invasive procedure or
otherwise at risk for bleeding complications.

31. Platelets
•Platelets transfusion may be considered in
patients with DIC and severe thrombocytopenia,
with active bleeding or the risk of bleeding.
•Most clinicians provide platelet replacement in
non bleeding patients if count drops below
20*103/cmm (1 or 2 U/kg/day)

32. Coagulation factors
• Specific deficiencies in coagulation factors e.g.
fibrinogen can be corrected by administration of
cryoprecipitate or purified fibrinogen concentrate
with FFP (the suggested starting dose is 15mg/kg).
• In case of a relative Vit. K deficiency in the face of
consumption, administration of Vitamin K may be
required.

33. Anticoagulation
• Effectiveness of heparin therapy will be limited
without concomitant replacement of antithrombin.
• However use of heparin in chronic DIC where there is
preponderance of coagulation without consumptive
coagulopathy is well established.
• (a dose of 4-5U/kg constant infusion is safe)

34. Tissue factor pathway inhibitor
•TFPI mechanism of coagulation has received
attention as potential therapy in sepsis
associated DIC.

35. Long-Term Monitoring
• May include anti-platelet agents for those with low-
grade DIC, antibiotics appropriate with the primary
diagnosis or both.
• Chronic DIC in patients with cancer can be managed
with subcutaneous heparin or LMWH.
• Refer to a hematologist on outpatient basis after
initial assessment and stabilization.

36. CONCLUSION
•DIC alongside other coagulopathies and even
infectious diseases like VHFs could be life
threatening, therefore a sound clinical acumen
and an in-depth theoretical knowledge might be
required to differentiate one from the other and
take measures early enough to reduce mortality.

37. REFERENCES
• Costello RA, Nehring SM. Disseminated Intravascular Coagulation
(DIC). 2018 Jan
• Papageorgiou C, Jourdi G, Adjambari E, Walborn A, Patel P, Fareed J,
et al. Disseminated Intravascular Coagulation: An Update on
Pathogenesis, Diagnosis and Therapeutic Strategies. Clin Appl Thromb
Hemost. 2018 Oct 8. 1076029618806424.