Disseminated Intravascular

Coagulation
Introduction
• Disseminated intravascular coagulation (DIC) is a serious, acquired clinical
condition that is characterised by systemic activation of the haemostatic system
resulting in excess thrombin deposition leading to microvascular thrombi.

• Can be disseminate to the different organs and cause a spectrum of clinical effects

• “an acquired syndrome characterized by intravascular activation of coagulation

with loss of localization arising from different causes. It disrupts the microvascular
endothelium and leads to multi-organ dysfunction syndrome (MODS) if the
process is sufficiently severe”  International Society of Thrombosis and
Haemostasis
Aetiology
• DIC is a secondary effect
caused by various underlying
clinical conditions.

• Any life-threatening severe systemic

disease associated with hypoxia,
acidosis, tissue necrosis, shock, or
endothelial damage may trigger DIC
Aetiology
Neonates
• Neonates are more vulnerable to DIC
than older infants and children
• Platelets are found to be
hyporeactive and aggregation is
impaired due to deficiency of a-
adrenergic receptors on platelet
membrane, especially in preterm
infants <30 weeks of gestation, but
this dysfunction is balanced by
elevated von Willebrand factor levels.
Older infants and children
• Sepsis is the most common cause of DIC in
older infants and children
• Sepsis (95%) was the most common
aetiologic factor followed by major trauma
(5%).
• Acquired inhibitors of coagulation factors
such as prothrombin inhibitors in transient
lupus anticoagulant following infection,
factor VIII inhibitors in autoimmune disease
and other inhibitors post major surgery are
other miscellaneous factors in paediatric DIC
Pathophysiology
• Sepsis, trauma, major surgery or severe hypoxia leads to release of tissue factor (TF) from
endothelial cells and mononuclear cells, which activates extrinsic pathway involving factor
VIIa (FVIIa).
• Activation and release of cytokines and chemokines alter endothelial function to a more
prothrombotic state, enhancing the formation of microvascular thromboses, with resultant
consumption of pro- and anticoagulant proteins
• Neutrophil extracellular traps in patients with sepsis promote the apoptosis of endothelial
cells, platelet aggregation and decompose tissue factor pathway inhibitor (TFPI) in order to
augment thrombogenesis
• the consumption of the endogenous anticoagulants AT, PC, PS and downregulation of
thrombomodulin and TFPI activity to promote thrombosis
• The inflammatory process that activates the coagulation system also plays a crucial role in
the organ damage of DIC
Clininical manifestation
• DIC is classically described as a thrombo-haemorrhagic disorder
• the possibility of DIC only when there is extensive and uncontrollable bleeding from
multiple sites. Bleeding frequently first occurs from sites of venipuncture or surgical
incision. The skin may show petechiae and ecchymoses.
• Tissue necrosis may involve many organs and can be most spectacularly seen as
infarction of large areas of skin, subcutaneous tissue, or kidneys.
• Consumptive coagulopathy with massive bleeding is observed
• The haemostatic derangement in children with DIC results from cumulative effects of
hypercoagulation and hyperfibrinolysis
• When hypercoagulation is dominant, organ failure is the main clinical manifestation and
this is frequently seen in infection and trauma.
• when both hypercoagulation and hyperfibrinolysis are simultaneously activated
Diagnosis
• DIC is a clinico-laboratory diagnosis
• The laboratory tests commonly used are platelet count, coagulation
screen, serum fibrinogen and D-dimer or fibrin degradation products
(FDP)
• A reduction in platelet count, prolongation of the clotting screen,
decrease in fibrinogen level and an increase in the D-dimer values all
point towards extreme coagulation activation and uncontrolled
thrombin generation
• Additional investigations such as
haemoglobin level, white blood cell
count, blood film (looking for red
cell fragmentation or schistocytes),
liver and renal function tests, lactic
dehydrogenase level, arterial blood
gas, blood culture and appropriate
imaging (eg, chest X-ray, brain MRI)
may provide clues on precipitating
factors and extent of organ
involvement
• The ISTH criteria recommended five-step diagnostic algorithm to
calculate the DIC score by using four laboratory tests. The criteria
have 91% sensitivity with 97% specificity among adults and
demonstrated strong correlation between DIC score with incidence of
mortality
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