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Disseminated Intravascular Coagulation

(DIC)
Pembimbing :
Dr. Hasanul Arifin
DEFINISI
Hemostasis
Hemostasis Component
Blood Vessel
Trombosit
Coagulation cascade
Inhibitor coagulation
Fibrinolysis

Komponen Hemostasis
PRIMARY HAEMOSTATIC PLUG
Pembentukan agregasi trombosit
SECONDARY PRIMARY PLUG
Pembentukan fibrin
Blood Vessel
The Endotheliums contains :
1. Nitric Oxide
2. Endotelin
3. Weibel-Palade :
- Faktor von Willebrand (vW)
- Antigen Vw
- P-selektin
4. Integrin
5. Trombomodulin





TROMBOSIT
Bila endotel rusak endotelin akan menarik trombosit untuk adesi
pada kolagen pembuluh darah
Trombosit diaktifkan akan membentuk pseudopodia sehingga :
- Melepas substasi ADP, serotonin, dll
- Mudah melekat ke kolagen endotel
- Mudah melekat ke trombosit lain
(agregasi trombosit)
Trombin menghambat sintesaAMP siklik -> peningkatan ion
kalsium-> hiperagregasi trombosit
Pada sikresi ADP yang berlebih akan mengaktifkan membran
fosfolipid (faktor trombosit 3) sehingga terjadi aktifasi sistim
koagulasi

Pathophysiology of DIC

Thrombosis-brief period of
hypercoagulability
1) Coagulation cascade is
initiated, causing
widespread fibrin formation
2) Microthrombi are deposited
throughout he
microcirculatory
3) Fibrin deposits result in
tissue ischemia, hypoxia,
necrosis
4) Leads to multi organ
dysfunction



Fibrinolysis-period of
hypocoagulability (the
hemorrhagic phase)
1) Activates the complement
system
2) Byproducts of fibrinolysis
(fibrin/fibrin degradation
products(FDP)) further
enhance bleeding by
interfering with platelet
aggregation, fibrin
polymerization, & thrombin
activity
3) Leads to Hemorrhage


Pathophysiology






(Porth, 2004)
Risk Factors and Etiology
Almost always a secondary event from
activation of one of the coagulation pathways
Underlying pathology creates a triggering
event: Either-
endothelial tissue injury (Extrinsic)
blood vessel injury (Intrinsic)


Pathologic Pathways
Extrinsic (endothelial)
Shock or trauma
Infections ( gram positive and
gram negative sepsis,
aspergillosis)
Obstetric complications
(eclampsia, placenta
abruptio, fetal death
syndrome)
Malignancies: APML, AML,
cancers of the lung, colon,
breast, prostate)

Intrinsic (blood vessel)
Infectious vasculitis (certain
viral infections, rocky
mountain spotted fever)
Vascular disorders
Intravascular hemolysis
(hemolytic transfusion
reactions)
Miscellaneous: snakebite,
pancreatitis, liver disease

Clinical Features
Onset maybe Acute or Chronic
Acute DIC
Develops rapidly over a period of hours
Presents with sudden bleeding from multiple sites
Treated as a medical emergency
Chronic DIC
Develops over a period of months
Maybe subclinical
Eventually evolves into an acute DIC pattern


Signs and Symptoms
Most common sign of DIC is bleeding
-manifested by ecchymosis, petechiae,and purpura
-bleeding from multiple sites either oozing or frank
bleeding
-cool and or mottled extremities may be noted
-dyspnea and chest pain if pleura and pericardium
involvement
-hematuria

Inflammation and DIC
Sepsis is usually underlying process for development
Endotoxins associated with sepsis activate factors
and initiate coagulation.
Bacteria, virus also trigger the clotting cascade.
Sepsis activates complement cascade
Diagnosis/Lab Findings
Test
Platelet count
Fibrin degradation product
(FDP)
Factor assay
Prothrombin time (PT)
Activated PTT
Throbimn time
Fibrinogen
D-dimer
Antithrombin


Abnormality
Decreased
Increased

Decreased
Prolonged
Prolonged
Prolonged
Decreased
Increased
Decreased (Otto,2001)
Treatment Modalities
Treat the underlying cause
Provide supportive management of complications
Support organ function
Stop abnormal coagulation and control bleeding by
replacement of depleted blood and clotting
components (FFP,Platelets,PRBC)
Medications can be used and choice depends on the
patients condition (Heparin, Antithrombin III (ATIII),
Fibrinolytic inhibitors)