DIC

Content:
Disseminated Intravascular Coagulation

Definition & synonyms

Aetiology
Pathogenesis
Pathophysiology/ consequences
Morphology & clinical features
Laboratory finding

Learning outcomes
Define disseminated intravascular
coagulation ,List its common causes.
Describe the pathogenesis &
pathophysiology of DIC.
Outline the clinical features of DIC.
Outline the laboratory findings in DIC.

Disseminated intravascular coagulation

Definition
Widespread inappropriate intravascular deposition of fibrin with
consumption of coagulation factors and platelets occurs as a
consequence of many disorders that release procoagulant material into
the circulation or cause widespread endothelial damage or platelet
aggregation.
Endothelial damage and
platelet aggregation area.

DIC is also terms : Consumption coagulopathy

Defibrination syndrome

Microthrombi in the
circulation

Causes of Disseminated intravascular coagulation

Acute

Obstetrical accidents
abruption placentae
aminiotic fluid embolism
abortion
Surgery,especially the heart and lung
Haemolytic transfusion reaction
Septicemia, especially Gram-negative and Meningococcal
Pulmonary embolism
Snake bite
Hypersensitivity reactions
Heat stroke
Subacute or chronic
Disseminated or localized carcinoma
Septicemia
Acute promyelocytic leukaemia
Fetal death in utero, Purpura fulminans, Giant haemangioma

Pathogenesis of DIC
Two main triggering mechanisms
Two major mechanisms trigger DIC:
1. Release of tissue factor or other thromboplastic substances into the
circulation, and
2. Widespread injury to the endothelial cells.
Thromboplastic substances, derived from a variety of sources, can directly
activate factor X such as ,the placenta in obstetric complication
;cytoplasmic granules of acute promyelocytic leukaemia cells;
Mucus released from certain adenocarcinoma are triggering factors.

Pathogenesis of DIC
Sequence of events- In general , can be summarized as 4 phases:
Activation of coagulation initiate widespread activation of coagulation
cascade by release of tissue factor.
Thrombotic phase endothelial damage from various thrombotic
stimuli causes generalized platelet aggregation and adhesion with
resultant formation and deposition of small microthrombi and
microemboli throughout the microvascular.
Comsumption phase the early thrombotic phase is followed by a
phase of consumption of coagulation factors & platelets.
Secondary fibrinolysis- as a protective mechanism, the fibrinolytic
system is activated secondarily at site of intravascular coagulation
.Secondary fibrinolysis causes breakdown of fibrin, resulting in the
formation of fibrin degradation products ( FDPs) in the circulation.

DIC can be initiated by either the extrinsic pathway or intrinsic

pathway
The extrinsic pathway, triggered by the release of tissue factors
(tissue thromboplastin )
Or the intrinsic pathway , which involves the activation of factor XII
by surface contact, collagen, or other negatively charge substances.
Both pathway lead to the generation of thrombin.
Clotting normally is limited by rapid clearance endogenous
anticoagulant (e.g, protein C)
and concomitant activation of fibrinolysis.

Clinical feature of DIC

Onset
Acute & fulminant in endotoxic shock or amniotic fluid embolism.
Insidious and chronic - in case of carcinomatosis or retention of a
death fetus.

Most common primary diseases

Overall, about 50% of the affected are obstetric patients having
complications of pregnancy .
The disorder tends to be reversible after delivery of the foetus.
About 33% of the affected patients have carcinomatosis .
The remaining cases are associated with the various entities previously
listed.

Clinical feature of DIC

Two main features

There are 2 main features:
1. Bleeding , as the most common manifestation , and
2. Organ damage, due to severe ischemia due to the effect of
widespread thrombosis, such as the brain, kidneys &lungs.
Less common manifestations
Microangiopathic haemolytic anaemia, and
Thrombosis in large arteries and veins.

Morphology & clinical features of DIC

Thrombi - most often found in the brain, heart, lungs kidneys,
Adrenals, spleen and liver in decreasing order of frequency,
but any tissue can be affected.
CNS manifestations
Fibrin thrombi - microinfarcts , ossasionally complicated by
simultaneous hemorrhage, which can sometimes lead to variable
neurologic signs and symptoms, such as convulsions and coma.
Renal manifestations
Small thrombi - glomeruli may evoke only reactive swelling of
endothelial cells or in severe cases , microinfarcts or even bilateral
renal cortical necrosis and acute renal failure.
Lungs
Numerous fibrin thrombi - in alveolar capillaries, sometimes associated
with pulmonary oedema and fibrin exudation causes acute respiratory

Morphology & clinical feature of DIC

In meningococcemia infection - fibrin thrombi in the microcirculation of

adrenal cortex causes the massive adrenal hemorrhage (WaterhouseFriderichsen syndrome),i.e., Acute adrenal failure.
Complication of labour and delivery -ischemic pituitary necrosis .Sheehan
syndrome
Pre-Eclampsia
The placenta exhibits widespread microthrombi, leading to premature
atrophy of the cytotrophoblast and syncytiotrophoblast that is encountered
in this condition, & may contribute to intrauterine foetal death.

Microinfarct in brain

, Glomeruli show microthrombi,Microinfarct in both cortex of kidneys

Haemorrhage infarct in lungs of DIC patient

Laboratory finding in DIC

Platelet count
Low
Bleeding time and clotting time prolong
Peripherial blood film
Microangiopathic haemolytic anaemia- schistocytes ( fragment red
cells) due to damage caused by trapping and passage through fibrin
thrombi in the microcirculation
Prothrombin Time (PT) , Thrombin Time (TT) & Activated Partial
Thromboplastin Time ( APTT)- All prolonged
Plasma fibrinogen levels
Reduced due to consumption in microvascular coagulation.
Fibrin Degradation Products ( FDPs)
Raised due to secondary fibrinolysis.

Skin
ecchymosis
in DIC
patient

Ecchymosis in both legs

Bleeding manifestation in DIC patient.