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disseminated intravascular coagulation


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Disseminated intravascular coagulation

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disseminated intravascular coagulation

  1. 1. Disseminated Intravascular Coagulation DR.M.KRISHNA VASUDEV
  3. 3. Disseminated intravascular coagulation (DIC) is a clinicopathologic syndrome characterized by widespread intravascular fibrin formation in response to excessive blood protease activity that overcomes the natural anticoagulant mechanisms.
  4. 4. CAUSES
  5. 5. ACUTE DIC Type Infectious Cause Bacterial (eg, gram-negative sepsis, gram-positive infections, rickettsial) Viral (eg, HIV, cytomegalovirus [CMV], varicella-zoster virus [VZV], and hepatitis virus) Fungal (eg, Histoplasma) Parasitic (eg, malaria) Malignancy Hematologic (eg, acute myelocytic leukemia) Metastatic (eg, mucin-secreting adenocarcinoma) Obstetric Placental abruption Amniotic fluid embolism Acute fatty liver of pregnancy Eclampsia Trauma Burns Motor vehicle accidents Snake envenomation Transfusion Hemolytic reactions Transfusion Other Liver disease/acute hepatic failure* Prosthetic devices Shunts (Denver or LeVeen) Ventricular assist devices *Some do not classify this as DIC; rather, it is liver disease with reduced blood coagulation factor synthesis and reduced clearance of activate products of coagulation.
  6. 6. CHRONIC DIC Type Malignancies Cause Solid tumors Leukemia Obstetric Retained dead fetus syndrome Retained products of conception Hematologic Vascular Myeloproliferative syndromes Rheumatoid arthritis Raynaud disease Cardiovascular Inflammatory Myocardial infarction Ulcerative colitis Crohn disease Sarcoidosis Localized DIC Aortic aneurysms Giant hemangioma (Kasabach-Merritt syndrome) Acute renal allograft rejection
  8. 8. 1. Increased thrombin generation: Mediated predominantly by tissue factor/factor VIIa pathway 2. Impaired function of physiological anticoagulant pathway a) Reduction of antithrombin levels -- The result of a combination of increased consumption, enzyme degradation, impaired liver synthesis and vascular leakage b) Depression of protein C system -- The result of a combination of increased consumption, impaired liver synthesis, vascular leakage and down- regulation of thrombomodulin c) Insufficient tissue factor pathway inhibitor (TFPI) 3. Impaired fibrinolysis: Mediated by release of plasminogen activators from endothelial cells immediately followed by an increase in the plasma levels of plasminogen activator inhibitor type 1 (PAI-1) 4. Activation of inflammatory pathway: Mediated by activated coagulation proteins and by depression of the protein C system
  10. 10. HISTORY The symptoms of disseminated intravascular coagulation (DIC) are often those of the underlying inciting condition 1. Bleeding • GI bleed • petechiae and ecchymosis, • intravenous (IV) lines and catheters bleed • surgical sites, drains, and tracheostomies and within serous cavities. 2. Renal Failure 3. Pulmonary involvement • dyspnea, hemoptysis, and cough 4. Jaundice
  11. 11. SYMPTOMS Circulatory signs include the following: 1. Signs of spontaneous and life-threatening hemorrhage 2. Signs of subacute bleeding 3. Signs of diffuse or localized thrombosis 4. Bleeding into serous cavities Central nervous system signs include the following: 1. Nonspecific altered consciousness or stupor 2. Transient focal or neurologic deficits Cardiovascular signs include the following: 1. Hypotension 2. Tachycardia 3. Circulatory collapse Respiratory signs include the following: 1. Pleural friction rub 2. Signs of acute respiratory distress syndrome (ARDS)
  12. 12. GI signs include the following: 1. Hematemesis 2. Hematochezia Genitourinary signs include the following: 1. Signs of azotemia and renal failure 2. Acidosis 3. Hematuria 4. Oliguria 5. Metrorrhagia 6. Uterine hemorrhage Dermatologic signs include the following: 1. Petechiae 2. Jaundice (liver dysfunction or hemolysis) 3. Purpura 4. Hemorrhagic bullae 5. Acral cyanosis 6. Skin necrosis of lower limbs (purpura fulminans) 7. Localized infarction and gangrene 8. Wound bleeding and deep subcutaneous hematomas 9. Thrombosis
  13. 13. Features Affected Patients, % Bleeding 64% Renal dysfunction 25% Hepatic dysfunction 19% Respiratory dysfunction 16% Shock 14% Central nervous system dysfunction 2%
  15. 15. 1. 2. 3. 4. 5. 6. 7. Atypical hemolytic-uremic syndrome Hemolytic-Uremic Syndrome Heparin-induced thrombocytopenia and thrombosis syndrome Idiopathic Thrombocytopenic Purpura Liver disease Primary hemostatic disorders (eg, dysfibrinogenemias; inhibitors to factors II, V, X) Thrombotic Thrombocytopenic Purpura
  16. 16. DIAGNOSIS
  17. 17. •Platelet -- moderate-to-severe thrombocytopenia is present in DIC. •Activated partial thromboplastin time [aPTT] and prothrombin time [PT]) are typically prolonged. •Protein C and antithrombin are 2 natural anticoagulants that are frequently decreased in DIC. •Elevated levels D-dimer and FDPs •Thrombomodulin is elevated in DIC, a marker for early identification and monitoring of DIC. •Chronic DIC diagnosis when the schistocytes are seen in concert with normal coagulation values and increased D-dimer levels.
  18. 18. Clinical conditions that should be ruled out Thrombocytopenia Dilution and abnormal distribution Massive blood loss, massive infusion ITP, TTP-HUS, HIT, HELLP syndrome Disorders of hematopoiesis Liver disease Hypothermia Spurious laboratory results Diagnostic algorithm for SIRS Temperature >38°C or < 36°C Heart rate >90 beats/min Respiratory rate >20 breaths/min or PaCO2 < 32 mm Hg (< 4.3 kPa) WBC count >12,000 cells/µL, < 4000 cells/ µL, or 10% immature (band) forms Diagnostic algorithm SIRS criteria Score >3 1 0-2 0 Platelet count (× 109/L) < 80 or >50 % decrease within 24 hours 3 >80 and < 120 or >30% decrease within 24 hours 1 >120 0 Prothrombin time (value of patient/normal value) >1.2 1 < 1.2 0 Fibrin/FDPs (mg/L) >25 3 >10 and < 25 1 < 10 0 Diagnosis 4 points or more DIC
  19. 19. TREATMENT
  20. 20. 1) Replacement therapy - Fresh-frozen plasma 2) Anticoagulants - Unfractionated and low-molecular-weight heparin - Danaparoid sodium - Recombinant hirudin - Recombinant tissue factor pathway inhibitor - Recombinant nematode anticoagulant protein c2 3) Restoration of anticoagulant pathways - Antithrombin - Recombinant human activated protein C 4) Other agents - Recombinant activated factor VII - Antifibrinolytic agents - Antiselectin antibodies - Recombinant interleukin-10 - Monoclonal antibodies against TNF and CD14
  21. 21. Management of Underlying Disease •The management of acute and chronic forms of disseminated intravascular coagulation (DIC) should primarily be directed at treatment of the underlying disorder. Administration of Blood Components and Coagulation Factors •Platelet transfusion may be considered in patients with DIC and severe thrombocytopenia, in particular, in patients with bleeding or in patients at risk for bleeding •The PT (>1.5 times the normal) Replacement with FFP is indicated •Low levels of fibrinogen (<100 mg/dL) or brisk hyperfibrinolysis will require infusion of cryoprecipitate. The replacement of 10 U of cryoprecipitate for every 2–3 U of FFP is sufficient to correct the hemostasis. •In case of a (relative) vitamin K deficiency in the face of consumption, administration of vitamin K may be required.
  22. 22. Anticoagulation •Experimental studies have suggested that heparin can at least partly inhibit the activation of coagulation in cases of sepsis and other causes of DIC. However, a beneficial effect of heparin on clinically important outcome events in patients with DIC has not yet been demonstrated in controlled clinical trials. •Therapeutic doses of heparin are indicated in cases of obvious thromboembolic disease or where fibrin deposition predominates (eg, purpura fulminans or acral ischemia). • A dose of 4-5 U/kg constant infusion without a 80-U/kg bolus is a safe means to deliver heparin to the DIC without increasing the bleeding risk. Restoration of Anticoagulant Pathways •Antithrombin concentrate, recombinant human APC, tissue factor (TF) pathway inhibitor (TFPI) and recombinant thrombomodulin (rTM)
  23. 23. Antifibrinolytic treatment In the coagulopathy associated with acute promyelocytic leukemia (AML-M3) and in some cases of DIC secondary to malignancies (e.g. prostate carcinoma) lysine analogues such as tranexamic acid can be utilized Investigational Treatments Tissue factor (TF)-VIIa complex include inactivated factor VII and recombinant nematode anticoagulant peptide (NAPc2)