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Disseminated Intravascular Coagulation (Dic)

Disseminated Intravascular Coagulation (DIC) is a serious condition characterized by widespread clotting that can lead to multiple organ dysfunction. It is often associated with life-threatening illnesses and requires treatment of the underlying cause. Risk factors include blood transfusion reactions, infections, and severe tissue injuries, with clinical features such as bleeding, organ damage, and laboratory findings indicating low platelet counts and prolonged coagulation times.

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0% found this document useful (0 votes)
17 views13 pages

Disseminated Intravascular Coagulation (Dic)

Disseminated Intravascular Coagulation (DIC) is a serious condition characterized by widespread clotting that can lead to multiple organ dysfunction. It is often associated with life-threatening illnesses and requires treatment of the underlying cause. Risk factors include blood transfusion reactions, infections, and severe tissue injuries, with clinical features such as bleeding, organ damage, and laboratory findings indicating low platelet counts and prolonged coagulation times.

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sdmlovesjithu
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DISSEMINATED INTRAVASCULAR COAGULATION (DIC)

Widespread hypercoagulable state that can lead to both microvascular and macrovascular clotting

and compromised blood flow, ultimately resulting in multiple organ dysfunction syndrome
• Commonly, life-threatening illnesses accompany disseminated intravascular coagulation.

• Treatment centers on identifying and treating the underlying cause.

• Also termed defibrination syndrome or consumption coagulopathy.


Risk factors for DIC include:

• Blood transfusion reaction

• Cancer, especially certain types of leukemia

• Inflammation of the pancreas (pancreatitis)

• Infection in the blood, especially by bacteria or fungus

• Liver disease

• Pregnancy complications (such as placenta that is left behind after delivery)

• Recent surgery or anesthesia

• Severe tissue injury (as in burns and head injury)

• Large hemangioma (a blood vessel that is not formed properly)


ETIOLOGY

1. Massive tissue injury:

Obstetrical syndromes (e.g. abruptio placentae, amniotic fluid embolism, retained dead foetus),

massive trauma, metastatic malignancies, surgery.

2. Infections:

Endotoxaemia, gram-negative and meningococcal septicaemia, certain viral infections, malaria,

aspergillosis.
3. Widespread endothelial damage:

Aortic aneurysm, haemolytic-uraemic syndrome, severe burns, acute glomerulonephritis.

4. Miscellaneous:

Snake bite, shock, acute intravascular haemolysis, heat stroke.


PATHOGENESIS

1. Activation of coagulation.

Etiologic factors initiate widespread activation of coagulation pathway by release of tissue factor.

2. Thrombotic phase.

Endothelial damage from the various thrombogenic stimuli causes generalised platelet
aggregation and adhesion with resultant deposition of small thrombi and emboli throughout the
microvasculature.
3. Consumption phase.

The early thrombotic phase is followed by a phase of consumption of coagulation factors and
platelets.

4. Secondary fibrinolysis.

Fibrinolytic system is secondarily activated at the site of intravascular coagulation. Secondary


fibrinolysis causes breakdown of fibrin resulting in formation of FDPs in the circulation.
CLINICAL FEATURES

• Bleeding most common

• Organ damage due to ischaemia


• Microangiopathic haemolytic anaemia

• Thrombosis in larger arteries and veins.


• Bleeding at wound sites or from the nose, gums, or mouth.

• Blood in the stool or urine.

• Bruising in small dots or larger patches on the body.

• Chest pain.

• Pain, redness, warmth, and swelling of the leg.


LABORATORY FINDINGS

• Platelet count is low.

• Blood film shows microangiopathic haemolytic anaemia.

• Presence of schistocytes and fragmented red cells.

• Prothrombin time, thrombin time and activated partial thromboplastin time, are all prolonged.

• Plasma fibrinogen levels are reduced.

• Fibrin degradation products (FDPs) are raised due to secondary fibrinolysis.

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