Disseminated intravascular coagulation (DIC) Flashcards

1
Q

Define DIC.

A

An acquired syndrome characterised by activation of coagulation pathways, causing widespread clotting and resultant bleeding.

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2
Q

How common is DIC?

A

Difficult to determine as many conditions cause it

Common in major trauma and sepsis

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3
Q

What are the risk factors/causes of DIC?

A
  • Sepsis
  • Major trauma and burns
  • Malignancies (AML and metastatic adenocarcinoma)
  • Obstetric disorders
  • Severe organ failure or destruction (e.g. severe pancreatitis, acute hepatic failure)
  • Vascular disorders (e.g. large aortic aneurysm)
  • Severe toxic or immunological reaction (e.g. transfusion, organ transplant, snake bite)
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4
Q

What are the two froms of DIC?

A
  1. Acute overt form where there is bleeding and depletion of platelets and clotting factors e.g. in major trauma, sepsis/severe infection
  2. Chronic non-overt form where thromboembolism is accompanied by generalised activation of the coagulation system e.g. malignancies, Raynaud’s disease.
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5
Q

What protein is a critical mediator of DIC?

A

Tissue factor - present on many cell types e.g. endothelial, macrophages, monocytes

Upon activation, TF binds with coagulation factors that then triggers the extrinsic pathway (via Factor VII) which subsequently triggers the intrinsic pathway (XII to XI to IX) of coagulation.

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6
Q

What is the pathophysiology of acute DIC?

A

Two hallmarks of DIC:

  • Generation of intravascular FIBRIN due to endothelial damage
  • CONSUMPTION/depletion of clotting factors, procoagulants and platelets due to thrombin generation

This manifests as:

  • This causes BLEEDING in the subcutaneous tissues, skin and mucous membranes.
  • OCCLUSION of blood vessels by fibrin in microcirculation results in MAHA and ischaemic organ damage.
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7
Q

How is DIC diagnosed?

A

Diagnosis is based on presence of

  • Presence of condition causing DIC
  • Abnormal coagulation

Investigations to order:

FBC:

  • low platelet count,
  • schistocytes due to MAHA on blood film

Clotting/D-dimer:

  • prolonged PT and aPTT,
  • low fibrinogen level.
  • high f_ibrin-related_ marker (D-dimer/fibrin degradation products),

CT/MRI - e.g. for pancreatitis alongside amylase and lipase

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8
Q

What are the clinical features of DIC?

A
  • oliguria, hypotension, tachycardia - circulatory collapse
  • petechiae, ecchymosis, GI bleeding
  • purpura fulminans, gangrene, acral cyanosis - vascular thrombosis
  • dyspnoea, cough
  • fever
  • delirium or coma
  • hypoxia
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9
Q

What is the difference in clotting findings in warfarin vs aspirin vs heparin administartion?

A

Warfarin causes prolonged PT Aspirin causes prolonged bleeding time Heparin causes prolonged APTT

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10
Q

What is the management of DIC?

A

Active treatment of the underlying cause

Supportive measures

  • Heparin - inhibits coagulation cascade
  • Replacement therapy e.g. FFP or platelet concentrates - only if active bleeding, invasive procedure needed, at risk of complications and known deficiencies
  • Antifibrinolytic agents e.g. aminocaproic acid and tranexamic acid but with extreme caution
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11
Q

What are the complications of DIC?

A
  • Acute renal failure
  • Life-threatening haemorrhage
  • Cardiac tamponade, haemothorax, intracerebral haematoma
  • Gangrene and loss of digits
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12
Q

What is the prognosis with DIC?

A

Mortality can be as high as 60%

But condition may resolve soon after resolution of the underlying condition

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