1. DIC Disseminated intravascular coagulation
( Consumptive coagulopathy )
إعداد الدكتور عمار جبار ألخالدي

2. Definition
DIC is a clinicopathologic syndrome k.k by widespread intravascular fibrin formation in response to excessive blood protease activity that overcomes the natural anticoagulant mechanisms.

3. Pathophysiology
Regardless of cause, the entry into the circulation of procoagulant substances that trigger systemic activation of the coagulation system and platelets and subsequent disseminated deposition of fibrin-platelet thrombi.
In most cases the procoagulant stimulus is tissue factor. tissue factor gains access to blood by tissue injury, its elaboration by malignant cells, or its expression on the surface of monocytes and endothelial cells by inflammatory mediators.
Tissue factor triggers generation of the coagulation protease thrombin, which induces fibrin formation and platelet activation.

4. Procoagulants other than tissue factor : 1
Procoagulants other than tissue factor : 1.cysteine protease or mucin in certain malignancies.
2. proteases other than thrombin :
Trypsin in pancreatitis.
Exogenous proteins in envenomation.
All are provide the procoagulant stimulus .

6. Clinical feature
Bleeding ranging from oozing from venipuncture sites, petechiae, and ecchymoses to severe hemorrhage from the GIT or lung or into the CNS.
. The hypercoagulability of DIC manifests as the occlusion of vessels in the microcirculation and resulting organ failure.
Thrombosis of large vessels and cerebral embolism can also
occur.
Hemodynamic complications and shock are common among
patients with acute DIC.
The mortality ranges from 30 to >80% depending on the underlying disease, the severity of the DIC, and the age of the patient.

7. diagnosis
1. Prolongation of PT and/or aPTT;
2. Platelet counts ≤ 100,000/mm3, or a rapid decline in platelet numbers;
3. The presence of schistocytes (fragmented red cells) in the blood Smear.
4. Elevated levels of FDP is the most sensitive test for DIC .
*DIC is an unlikely diagnosis in the presence of normal levels of FDP.
5. The D-dimer test is more specific for detection of fibrin
(but not fibrinogen) degradation products and indicates that the
cross-linked fibrin has been digested by plasmin.
6. Because fibrinogen has a prolonged half-life, plasma levels diminish acutely only in severe cases of DIC.
7. High-grade DIC is also associated with levels of antithrombin
III or plasminogen activity <60% of normal.

8. causes Sepsis Immunologic disorders
Bacterial Acute hemolytic transfusion
Staphylococci, streptococci, reaction
pneumococci, meningococci,
gram-negative bacilli Organ or tissue transplant rejection
viral Graft-versus-host disease
Mycotic
Parasitic
Rickettsial
Trauma and tissue injury Drugs
Brain injury (gunshot) Fibrinolytic agents
Extensive burns Aprotinin
Fat embolism
rhabdomyolysis
Warfarin (neonates with protein c deffeciency)
amphetamines

9. Vascular disorders Giant hemangiomas (Kasabach- Merrit syndrome)
Large vessel aneurysms(e.g., aorta) Obstetric
Abruptio placentae
Amniotic fluid embolism
Dead fetus syndrome
Septic abortion

10. venom Liver disease
snake Fulminant hepatic failure
insects cirrhosis
Fatty liver of pregnancy
Cancer Miscellaneous
Adenocarcinoma (prostate, shock
pancreas, etc)
Respiratory distress syndrome Hematologic malignancies (acute
promyelocytic leukemia)
Massive transfusion

11. Chronic DIC Low-grade, compensated DIC.
occur in giant hemangioma, metastatic carcinoma, or the dead fetus syndrome.
Plasma levels of FDP or D-dimers are elevated.
aPTT, PT, and fibrinogen values are within the normal range or high.
Mild thrombocytopenia or normal platelet counts are also common findings.
Red cell fragmentation is often detected but at a lower degree than in acute DIC.

12. DDx
1.TTP
2.Sever liver disease

13. In pt with TTP Thrombocytopenia Red cell fragmentation
Multi organ failure
How can we differentiate?
*In pt with TTP there is no consumption of clotting factors or hyper fibrinolysis
SO:
PT,PTT,D.Dimer will be NORMAL

14. In pt with liver disease
Thrombocytopenia( due to platelet sequestration, portal HT, or hypersplenism).
Prolong PT,PTT(decrease syn. Of coagulation factors)
Increase level of FDP (reduced hepatic clearance).
How can we differentiate from DIC?
these laboratory parameters in liver disease do not change rapidly.
the presence of portal hypertension or other clinical or laboratory evidence of underlying liver disease.

15. Management of DIC
A.The morbidity and mortality associated with DIC are primarily related to the underlying disease rather than the complications of the DIC.
*Attempts to treat DIC without accompanying treatment of the causative disease are likely to fail.

16. B.Control of bleeding
Replacement with FFP is indicated (1 unit of FFP increases most coagulation factors by 3%.
Cryoprecipitate ( enriched for fibrinogen, FVIII, and vWF).
*Low levels of fibrinogen (<100 mg/dL) or brisk hyperfibrinolysis will require infusion of cryoprecipitate.
*The replacement of 10 U of cryoprecipitate for every 2–3 U of FFP is sufficient to correct the homeostasis.

17. 3.Platelet conc. at a dose of 1–2 U/10 kg body weight are sufficient for most DIC pt with severe thrombocytopenia.

18. Is there is any indication of heparin in DIC? Answer is YES
1. Low-grade DIC associated with solid tumor or APL.
2. During the surgical resection of giant hemangiomas.
3. During removal of a dead fetus.
4. Purpura fulminans.
*it given continuous i.v infusion in a dose of
(5-10 unit/kg/hr).

19. Purpura fulminans It is a severe form of DIC resulting from
thrombosis of extensive areas of the skin;
It affects predominantly young children following viral or bacterial infection, particularly those
with inherited or acquired hypercoagulability due to deficiencies of the components of the protein C pathway.
Neonates homozygous for protein C deficiency also present high risk for purpura fulminans,
with or without thrombosis of large vessels.

20. The use of antifibrinolytic drugs, or tranexamic acid
* prevent fibrin degradation by plasmin may reduce bleeding episodes in pt with DIC and confirmed hyperfibrinolysis.
*these drugs can increase the risk of thrombosis, and concomitant use of heparin is indicated.
*Patients withAPL or chronic DIC ass with giant hemangiomas are among the few patients who may benefit from this therapy.

21. Thank you