DIC is a pathologic process secondary to an underlying illness where widespread activation of coagulation leads to microvascular fibrin deposition and compromised blood supply. The main features are attributable to excessive thrombin generation. Clinical conditions associated with DIC include sepsis, trauma, organ destruction, malignancy, and vascular abnormalities. The pathogenesis involves tissue factor-dependent microvascular fibrin deposition via the extrinsic coagulation pathway. Treatment focuses on treating the underlying condition, and transfusions are only used if bleeding risk is present.
4. DIC
It is not a primary disease entity but rather
a pathologic process secondary to an
underlying illness.
Most features of DIC are attributable to the
generation of thrombin or a thromboplastic
substance and plasmin from a variety of
inciting events.
The levels of protein C and antithrombin III
are frequently low in DIC.
5. Definition of DIC
Widespread and ongoing activation of
coagulation.
Leading to possible vascular or micro
vascular fibrin deposition.
Compromising and inadequate blood
supply to various organs.
Decreasing levels of procoagulant
proteins.
6. Clinical Conditions Associated
Sepsis.
Trauma.
Organ Destruction (pancreatitis).
Malignancy.
Obstetrical.
Vascular abnormalities.
Severe hepatic failure.
7. Cont. Associated Conditions
Severe toxic or immunogical
reactions.
snake bites
recreational drugs
transfusion reactions
transplant rejection
14. Treatment
Treat the underlying disorder.
Plasma (FFP), Cryoprecipitate, and
Platelet transfusions only, if risk of
bleeding.
Invasive procedures.
Anticoagulants like: Inact FVIIa,
Recombinant T.F. path. Inh.
Recombinant NAPc2. are
investigational.
15. Another modalities of Tx of DIC
Heparin for prevention of
microthrombosis and organ damage
Antifibrinolytic (EACA) agents for
hemorrhage despite above measures
Antithrombin III and/or Protein C
concentrates when low levels found
(?)
16. Use of Heparin
It is controversial.
Used in combination with EACA for
special cases.
It’s used in Trousseau syndrome,
purpura fulminans, and certain
obstetric complications. Also in AML-
M3.
17. Systemic Hyperfibrinolysis
Spontaneous bleeding
From acute states such as heatstroke, hypoxia,
hypotension, thoracic surgery, administration of
thrombolytics, and neoplasms.
Also found in Extracorporeal bypass, congenital
alpha2-antiplasmin deficiency, and Liver
transplant.
Lab’s: decreased plasminogen and fibrinogen,
elevated D-Dimer
Tx: Antifibrinolytic therapy with e-aminocaproic
acid (EACA) or trans-p-aminomethyl-cyclohexane
carbolyxix acid (AMCA).
18. HELLP Syndrome
Pregnant women
Severe preeclampsia
Microangiopathic hemolytic anemia
Elevated liver enzymes
Low platelets (Thrombocytopenia)
Elevated D-Dimer
Tx: Delivering the fetus, FFP,
Plasmapheresis.
19. Thrombotic Thrombocytopenic
Purpura (TTP)
Appears abruptly in previously completely
normal healthy individuals.
Pentad: Thrombocytopenia,
Microangiopathic hemolytic anemia,
Neurologic abnormalities, Abnormal Renal
function, and Fever.
Most of cases are women, white race.
LDH is very high.
Mortality is high within days.
The 2 organs relatively spared by the
vascular thrombi are the lungs and liver.
20. Causes of TTP
Most of the cases: Unknown
Obstetric emergencies
Infectious diseases
Drugs and Toxins
Neoplastic diseases receiving cytotoxic
therapy
Auto-immune mediated diseases
21. Hemolytic Uremic Syndrome (HUS)
Most common in children
Associated with E. coli &
Campylobacter jejuni.
Similar to TTP, but we see more
kidney damage.
22. Tx of TTP / HUS
Corticosteroids
Plasmapheresis / exchange
Tx of the underlying disease
The goal is to achieve:
LDH < 500 u/dl
Normal Platelets
Normal Hgb / Hct
23. Outcome of TTP / HUS
Relapse is common within the first month after
the initial diagnosis (85%). At 2 months the
relapse is in 15%.
Relapse after 5 years is extremely rare.
If patients do not respond to 1st line
therapy, then use:
Vincristine
Immunoglobulin
Aspirin + Persantine
Splenectomy
