DIC Flashcards
diagnostic value of schistocytes on peripheral smear for DIC diagnosis
this finding is neither sensitive nor specific for DIC
Indications for cryo in DIC
critical bleeding AND
fibrinogen level <50 mg/dL
Why d-dimer is commonly elevated in metastatic cancer
Systemic activation of hemostasis is common in metastatic cancer, even in the absence of thrombosis. Moreover, it has been implicated in tumor progression, angiogenesis and metastatic spread.
how is DIC diagnosed
- Clinical + laboratory diagnosis (labs + inciting factor)
How does normal hemostasis work?
Blood clot forms at the site of vessel injury –> clot is resolved to allow tissue repair.
WHy is thrombocytopenia associated with DIC?
Microthrombi include platelets
Cancers highly associated with DIC
1) acute promyelocytic leukemia (APML)
2) mucinous tumors (eg, pancreatic, gastric, ovarian)
3) brain tumors
Thrombotic vs. bleeding risk of DIC
- acute DIC is much more likely to present with bleeding (consumption of fibrinogen and other procoagulant factors and the disruption of normal fibrin formation and platelet function by the large amount of fibrin degradation products)
- chronic DIC (more likely to present with thromboembolic complications because production of procoagulant factors keeps pace with ongoing generation of thrombi).
complication of chronic DIC in cancer patients
non-bacterial thrombotic endocarditis (marantic endocarditis, Libman-Sacks endocarditis, verrucous endocarditis)
organ dysfunction that can result from DIC
Mostly from vascular damage and hypoperfusion.
(basically everything)
- Acute renal failure
- Hepatic dysfunction
- Acute lung injury (damage to vascular endothelium)
- Neurologic dysfunction
- Adrenal failure
what is purpura fulminans?
Rare, life-threatening condition characterized by DIC, with extensive tissue thrombosis and hemorrhagic skin necrosis.
Laboratory differences between acute and chronic DIC
- Prolonged PT and PTT and hypofibrinogenemia + thrombocytopenia more common in acute setting (clotting factor consumption)
Key principle in treatment of DIC
Treat underlying cause (eliminate the stimulus)
why you can’t give TXA to counteract fibrinolysis
It will increase risk of thrombosis
Risk of thrombosis with DIC generally speaking
Low, it’s still rare, more common if underlying trigger is infection
*more common in chronic
When to expect coagulation abnormalities to resolve after underlying issue is treated
There’s a LAG. DIC does not resolve immediately once the inciting factor is corrected. Resolution generally requires synthesis of coagulation factors, which are produced at different rates; clearance of anticoagulant factors and fibrin degradation products from the circulation, which depend on hepatic function; and production of new platelets from the bone marrow, which may take several days.
Rule of thumb for cryo dosing and response in fibrinogen level
Each 10 units will increase fibrinogen by roughly 100
pathophysiology of DIC
- abnormally and massively activation of hemostasis and fibrinolysis
when chronic DIC is typically seen
advanced malignancy (pancreatic, gastric, ovarian, brain tumors)
