jslum.
com | Medicine
Disseminated Intravascular Coagulation (DIC)
Definition Pathophysiol ogy (Acute DIC)
Acquired syndrome Acute DIC occur when Normal Compensatory Mechanisms of Hemostasis have
Characterized by Systemic Intravascular Coagulation been overcome
(Systemic Activation of Blood Coagulation System) Triggered by
Coagulation (always the initial event) Entry of Tissue Thromboplastin into circulation
Results in Generation and Deposition of Fibrin Widespread endothelial damage & collagen exposure
Leads to Microvascular Thrombi in various organs (multi-organ failure) Direct activation of FX or F11 by specific proteolytic enzymes (snake bite)
Consumption & Subsequently Exhaustion of coagulation protein, platelets Final consequences, following excessive abnormal activation of coagulation by
(ongoing activation of coagulation system)(severe bleeding complications) triggering mechanism is Thrombin Generation
Evidence of In excess, Normal Inhibitory Effe ct of Natural Anticoagulant is overcome
Coagulant activation Generation of Thrombin leads to
Fibrinolytic activation Conversion of Fibrinogen → Fibrin
Natural inhibitor (anticoagulant) consumption Activation of Platelets
Platelet consumption Activation of Factors – FV, FVIII
Biochemi cal evidence of end organ damage or failure Activation of Endothelial cells
Disseminated micro/ macrothrombosis (Fully Obstructed)
Associated DIC Conditions Intravascular Haemolysis (Partially Obstructed)
Thrombosis leads to activation of Fibrinolytic Pathway
Plasmin breaks down cross-link Fibrin, Circulating Fibrinogen
(lead to formation of Fibrin/ Fibrinogen Degradation Products (FDP))
Fibrinogen – Fragment D, E
Cross-link Fibrin – D-Dimer
FDP
Inhibit Thrombin Action → Bleeding
Interferes Fibrin Monomer Polymerization → Impair Hemostasis → Bleeding
Bind to Platelet Membranes → Platelet Function Defect → Bleeding
Biodegrades Factor V, VIII, IX, XI → Bleeding
With continual Excessive Activation of Coagulation system
Liver cell synthesis of coagulation – unable to compensate for consumption
Bone Marrow Megakaryocytes – production of platelet unable to maintain
platelet count
Widespread Blee ding Tendency
Consumption of Coagulation Factors, Platelets
Inhibitory action of ↑ FDP
Classification of DIC Activation of complements by Plasmin, Kinin system through XIIa
Acute (Decompensated) Chronic (Compensated) ↑ Vascular Permeability
Clinically life threatening Not critical Shock, Hypotension
Recognize/ diagnose fast Not easily diagnosed
Haematological emergency Can convert to Acute
Treat 1° Disorder Treat 1° Disorder
Give Blood Transfusion supp ort Blood Transfusion not indicated
Etiology Etiology
Infection/ Sepsis Malignancy
Obstetric Complications Retained Dead Fetus
Trauma – Severe Severe localised intravascular
Transfusion of ABO In compatible coagulation
Haematological disorders
Autoimmune diseases
Clinical Findings
Acute DIC Chronic DIC
Thrombosis (5 -10%) Compensated
Renal Failure Few/ No Clinical Signs
Coma Non-Obvious Multiple Small Microthrombosis
Liver Failure No/ Few Bleeding
Respiratory Failure Risk of Decompe nsation
Skin Necrosis/ Gangrene
Venous Thromboembolism (common)
Haemorrhage
Spontaneous Bruising
Petechiae
GIT Bleeding
Respiratory Tract Bleeding
Persistent Bleeding
(Oozing at Venipuncture sites)
Bleeding at Surgical Wounds
ICB
Cytokine, Kinin Generation
Tachycardia
Shock
Hypotension
Edema
jslum.com | Medicine
Diagnosis
Laboratory tests
No single test for confirmation
Panel of tests needed in coagulation study
Screening tests
More specific tests
Screening Tests More Specific Assay
PT Suggest presence of
aPTT Abnormally ↑ Thrombin
Thrombin Time FDPs
Fibrinogen Level Fibrin Monomer
Blood Cou nt, FBP D-Dimer
Coagulation Factor Assay
Acute Phase Protein
Laboratory Findings
Acute DIC Chronic DIC
PT/PTT ↑ Normal
Platelets ↓ Normal
Fibrinogen ↓ Normal
Fibrin Monomer +ve +ve
FDP +ve +ve (↓ concentration)
D-Dimer +ve +ve
TT ↑ Normal (often)
Antithrombin ↓ Normal
Factor Assay ↓ FV, FVIII
Morphologic Findi ngs
Schistocytes (Red Cell Fragments) seen in 50% patients with DIC
Absence of RBC Fragments does not rule out diagnosis of DIC
Mild Reticulocytosis
Mild Leucocytosis
Left Shift
Management
Supportive Measures
Removal of Triggering Mechanism
Outcome depe nds 1° on ability to deal with trigger
not on direct attempts to correct coagulation deficit
Replacement Therapy
Indication
Patients with active bleeding
Patient require Invasive Procedures (otherwise risk for bleeding complication)
Should not instituted on bases of laboratory results alone
Blood Pr oducts
Packed Red Cells
Platelet Concentrate
FFP
Cryoprecipitate
AT Concentrates
Factor Concentrates
