Obada Al-Eisa Saud Bashtawy Emad Mansour

 It is an acquired condition characterized by massive activation of the coagulation system.  It is always secondary to an underlying disorder.  Systemically producing thrombosis and bleeding.  Exposure to procoagulant material and diffuse endothelial damage.

Occurs due to simultaneous action of the following 4 mechanisms 1) TF-thrombin generation 2) Impaired coagulation inhibitor systems 3) depression of the fibrino-lytic system 4) Inflammatory activation

 Sepsis and severe infection  Trauma (neurotrauma)  Organ destruction (eg, pancreatitis)  Malignancy (solid and myeloproliferative malignancies)  Severe transfusion reactions  Obstetric complications –placental abruption and eclampsia  Vascular abnormalities - large vascular aneurysms  Severe toxic reactions(venom)  Catastrophic antiphospholipid syndrome (rare)

Clinical Manifestations of DIC : The symptoms of underlying disorder is usually obvious. The patient is often acutely ill and shocked. Bleeding from different sites ( GI, mouth, epistaxis,…) -Bleeding from 3 unrelated sites  DIC Thrombotic events : - can be anywhere - mostly : skin, kidney, brain

Types AcuteChronic

Acute DIC: Acute DIC develops when sudden exposure of blood to procoagulants (eg, tissue factor [TF], or tissue thromboplastin) generates intravascular coagulation. Compensatory hemostatic mechanisms are quickly overwhelmed, and, as a consequence, a severe consumptive coagulopathy leading to hemorrhage develops

Cutaneous menifistation

Chronic DIC: chronic DIC reflects a compensated state that develops when blood is continuously or intermittently exposed to small amounts of TF. Compensatory mechanisms in the liver and bone marrow are not overwhelmed This diminish the likehood of bleeding but give rise to a hypercoagulable state

Signs and Symptoms: In addition to those of the underlying condition : -Bleeding -Thrombosis -Organ dysfunction -Shock

Complications of DIC :- Life-threatening thrombosis and hemorrhage Cardiac tamponade Hemothorax Intracerebral hematoma Acute kidney injury Change in mental status Respiratory dysfunction Hepatic dysfunction Gangrene and loss of digits Shock Death

 COMPLETE BLOOD COUNT : Severe thrombocytopenia( /µl).  PERIPHERAL BLOOD SMEAR : Schistocytes: neither sensitive nor specific for DIC but help to confirm a chronic DIC when there is normal coagulation values and increased D-dimer levels.  PROTHROMBIN TIME & aPTT : Prolonged  FIBRINOGEN LEVEL : Low

SCHISTOCYTES IN PERIPHERAL BLOOD SMEAR

 D dimer, FIBRINOGEN / FIBRIN DEGRADATION PRODUCTS : Increased (helpful for differentiating DIC from other conditions that may be associated with a low platelet count and prolonged clotting time such as chronic liver disease)  PROTEIN C & S, ANTITHROMBIN : decreased

Overt DIC Scoring System

Treatment - Therapy is primarily aimed at the underlying cause. These patients will often require intensive care to deal with concomitant issues, such as acidosis, dehydration, renal failure and hypoxia. - Blood component therapy, such as fresh frozen plasma, cryoprecipitate and platelets, should be given if the patient is bleeding, but should not be given routinely based on coagulation tests and platelet counts alone.

 GOALS: To maintain Platelet count >50000 Fibrinogen concentration >1g/L Prothrombin values less than double the normal range

 FRESH FROZEN PLASMA(FFP) :  Constituents : U/ml of factors II,V, VII, VIII, X, XI, XII, XIII and 2.5mg/ml fibrinogen.  CRYOPRECIPITATE:  Constituents ; fibrinogen 150mg/bag factor VIII units/bag factor XIII

 FRESH BLOOD: Indicated in severe trauma to replace acute massive blood loss.  ANTICOAGULANT THERAPY: Heparin to inhibit thrombin. Indicated in patients with clinically overt thromboembolism, chronic DIC and extensive fibrin deposition.

 REPLACEMENT OF NATURAL ANTICOAGULANT PATHWAY Recombinant human activated protein c 24µg/kg/hr. Adverse effects include bleeding.