Perdarahan: DR - Suhaemi, SPPD, Finasim

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perdarahan

Dr.suhaemi, SpPD, Finasim


6.Disseminated Intravascular
Coagulation (DIC)
• DIC is characterized by
– the systemic activation of the coagulation system
followed by activation of fibrinolytic system
– high thrombin and plasmin generation

• DIC is not a disease itself, but is a


manifestation of a serious underlying disorder.

2
Disseminated intravascular
coagulation (DIC)
 secondary complication
of some serious condition
 consumption coagulopathy

 thrombohemorrhagic diathesis

 acute, subacute, chronic


Disseminated intravascular
coagulation (DIC)

activation of coagulation sequence

microthrombi
- consumption of platelets and clotting factors

secondary
activation of fibrinolysis
DIC
Thrombotic and hemorrhagic diathesis
Consequences
Microthrombi infarctions

depletion of platelets and clotting factors

+ secondary activation of fibrinolysis

hemorrhages
Causes of DIC

• Infection - bacterial sepsis, viral


infections

• Neoplasm - AML, adenocarcinoma

• Obstetrical disorders - retained dead


fetus, abruption, etc

• Trauma/surgery - brain injury, crush, burns,


etc.

• Others - acute hemolytic


transfusion reaction, etc.

6
Hemostatic Balance

PAI-1 Prot. S

Antiplasmin Prot. C

Tissue factor* TFPI


Fibrinolytic System
Clotting Factors
ATIII

Procoagulant Anticoagulant

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DIC
SYSTEMIC
• An acquired syndrome ACTIVATION OF
COAGULATION
characterized by
systemic intravascular
coagulation
Intravascular Depletion of
• Coagulation is always deposition of platelets and
the initial event fibrin coagulation
factors

Thrombosis of
small and Bleeding
midsize vessels

8 Organ failure DEATH


Pathophysiology of DIC
• Activation of Blood Coagulation
– Tissue factor/factor VIIa mediated thrombin
generation via the extrinsic pathway
• complex activates factor IX and X
– TF
• endothelial cells
• monocytes
• Extravascular:
– lung
– kidney
– epithelial cells

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PATHOPHYSIOLOGIC
Pathophysiology of DIC
LABORATORY CLINICAL
EVENTS MANIFESTATIONS MANIFESTATIONS

underlying disorder

depletion of clotting factors


prolonged PT, PTT
tissue factor release

thromboctyopenia (consumption)
activation of intrinsic hemorrhage
pathway of coagulation
(systemic thrombin
depletion of physiologic anticoagulants
generation)

decreased fibrinogen

generalized intravascular
fibrin deposition microangiopathic hemolytic anemia

thrombosis/infarction
activation of
fibrinolytic system
(systemic plasmin increased FDP and D-dimer
generation)

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Laboratory Tests Used in DIC
• D-dimer* • Thrombin time
• Antithrombin III* • Fibrinogen
• F. 1+2* • Prothrombin time
• Fibrinopeptide A* • Activated PTT
• Platelet factor 4* • Protamine test
• Fibrin Degradation • Reptilase time
Prod • Coagulation factor
• Platelet count levels
• Protamine test
*Most reliable test

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The main bleeding sickness types
• Hematomic (massive, deep, painful; bleeding may occur anywhere.
The most common sites of bleeding are into joints (knees, ankles, elbows),
into muscles, from the gastrointestinal tract, cause of the bleeding can be
intramuscular injection; characterized by early postoperative &
posttraumatic bleeding)
• hematoma
• petechia-spotted
(macula)
macula-hematoma
vasculitic purpura
angioma
Hemophilia
Diagnostic
criteria
Hematomic
bleeding sickness
Arhtropathy
types
Thrombocytopenia

Diagnostic
criteria

Petechial-
ecchymosic 1. Deacrease
of
platelets
Queen Victoria

Carrier for Hemophilia


Hemophilia is carried on the X chromosome

Females X H X H normal
X H X h carrier
X h X h hemophiliac

Males X H Y normal
X h Y hemophiliac
Hemophilic arthropathy

“Target joint” = irreversibly damaged joint


with vicious cycle of injury and repeated
bleeding

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