Disseminated intravascular coagulation


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Disseminated intravascular coagulation

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Disseminated intravascular coagulation

  1. 1. Department of Pathophysiology (Disseminated intravascular coagulation) Name: Gustavo Duarte Viana Group: 17 3rd year 2nd semester Medical faculty Supervisor: Associated Professor Antropolskaya, E. V.
  2. 2. Contents Definition Etiology Classification Pathophysiology Symptoms and signs Laboratory diagnosis Differential Diagnosis Treatment Complications Prognosis
  3. 3. Definition  Disseminated intravascular coagulation (DIC) is characterized by systemic activation of blood coagulation, which results in generation and deposition of fibrin, leading to microvascular thrombi in various organs and contributing to multiple organ dysfunction syndrome (MODS).[1] Consumption and subsequent exhaustion of coagulation proteins and platelets (from ongoing activation of coagulation) may induce severe bleeding, though microclot formation may occur in the absence of severe clotting factor depletion and bleeding.
  4. 4.  DIC is not a kind of independent disease, but a middle process or complication of some diseases .  It is essentially an imbalance between the coagulation process and anticoagulation process. It is a syndrome characterized by massive activation and consumption of coagulation proteins, fibrinolytic proteins and platelets.  Coagulation is usually confined to a localized area by the combination of blood flow and circulating inhibitors of coagulation, especially antithrombin Ⅲ . If the stimulus to coagulation is too great, these control mechanisms can be overwhelmed, leading to the syndrome of DIC.
  5. 5. Epidemiology DIC may occur in 30-50% of patients with sepsis, and it develops in an estimated 1% of all hospitalized patients.[4] DIC occurs at all ages and in all races, and no particular sex predisposition has been noted.
  6. 6. Etiology  DIC is not a primary disease, but a disorder secondary to numerous triggering events such as serious illnesses.  Several disease states may lead to the development of DIC, generally via 1 of the following 2 pathways: 1) A systemic inflammatory response, leading to activation of the cytokine network and subsequent activation of coagulation (eg, in sepsis or major trauma) 2) Release or exposure of procoagulant material into the bloodstream (eg, in cancer, crush brain injury, or in obstetric cases)  In some situations (eg, major trauma or severe necrotizing pancreatitis), both pathways may be present.
  7. 7. Classification according to acute or chronic Etiologies
  8. 8. Pizza graph for DIC etiology infectious disease 31%~43% cancer 24%~34% obstetric complications 4%~12% severe tissue injury 1%~5% ID systemic disease Cancer O C STI SD
  9. 9. 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.
  10. 10. 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
  11. 11. Acute Infectious DIC Bacterial infection (in particular, bloodstream infection [BSI]) is commonly associated with DIC. There is no difference in the incidence of DIC between patients with gram-negative sepsis and those with gram-positive sepsis. Systemic infections with other microorganisms, such as viruses and parasites, may lead to DIC as well. Factors involved in the development of DIC in patients with infections may be specific cell membrane components of the microorganism (lipopolysaccharide or endotoxin) or bacterial exotoxins (eg, staphylococcal alpha toxin). These components cause a generalized inflammatory response, characterized by the systemic occurrence of proinflammatory cytokines.
  12. 12. Acute DIC due to trauma Severe trauma is another clinical condition frequently associated with DIC. A combination of mechanisms— including release of tissue material (eg, tissue factor [thromboplastin], fat or phospholipids) into the circulation, hemolysis, and endothelial damage—may contribute to systemic activation of coagulation. In addition, solid evidence indicates that cytokines also play a pivotal role in the occurrence of DIC in trauma patients. In fact, systemic cytokine patterns have been shown to be virtually identical in trauma patients and septic patients
  13. 13. DIC in cancer Both solid tumors and hematologic malignancies may be complicated by DIC. The mechanism by which coagulation is deranged in this situation is poorly understood. Solid tumor cells can express different procoagulant molecules, including TF and a cancer procoagulant. Cancer procoagulant is found in extracts of neoplastic cells and in the plasma of patients with solid tumors. As noted, some tumors are associated with a form of DIC that is characterized by severe hyperfibrinolysis on top of an activated coagulation system.
  14. 14. DIC in problems in obstrectics Acute DIC occurs in obstetric calamities such as placental abruption (abruptio placentae) and amniotic fluid emboli. Amniotic fluid has been shown to be able to activate coagulation in vitro, and the degree of placental separation correlates with the extent of the DIC, suggesting that leakage of thromboplastinlike material from the placental system is responsible for the occurrence of DIC.
  15. 15. DIC in vascular disease Vascular disorders, such as large aortic aneurysms or giant hemangiomas (Kasabach-Merritt syndrome), may result in local activation of coagulation. Activated coagulation factors can ultimately “overflow” to the systemic circulation and cause DIC, but systemic depletion of coagulation factors and platelets as a result of local consumption is a more common scenario.
  16. 16. Pathophysiology DIC occurs when monocytes and endothelial cells are activated or injured by toxic substances elaborated in the course of certain diseases. The response of monocytes and endothelial cells to injury is to generate tissue factor on the cell surface, activating the coagulation cascade . In acute DIC, an explosive generation of thrombin depletes clotting factors and platelets and activates the fibrinolytic system. Bleeding into the subcutaneous tissues, skin, and mucous membranes occurs, along with occlusion of blood vessels caused by fibrin in the microcirculation.
  17. 17. In chronic DIC, the process is the same, but it is less explosive. Usually there is time for compensatory responses to take place, which diminish the likelihood of bleeding but give rise to a hypercoagulable state. These changes in the blood can be detected by testing the coagulation system. Thromboembolism occurs in this setting, and when oral anticoagulants are given following heparin therapy, there is a tendency for it to recur. Long-term therapy with low-molecular-weight heparin may be a solution to this problem until the underlying cause can be brought under control.
  18. 18. Stimulation of Coagulation Intravascular thrombosis Consumption of coagulation factors Secondary activation of thrombolysis Hypoperfusion to tissues and organs Inability to form a stable clot Release of anticoagulants Ischemic damage Bleeding Bleeding
  19. 19. Symptoms and sings Acute DIC      Clinical findings Multiple bleeding sites Ecchymoses of skin, mucous membranes Visceral hemorrhage Ischemic tissue
  20. 20. Chronic DIC  Clinical findings  Signs of deep venous or arterial thrombosis or embolism  Superficial venous thrombosis, especially without varicose veins  Multiple thrombotic sites at the same time  Serial thrombotic episodes
  21. 21. Symptoms and signs  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
  22. 22. 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)
  23. 23. 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
  24. 24. Features Affected Patients, % Bleeding 64% Renal dysfunction 25% Hepatic dysfunction 19% Respiratory dysfunction 16% Shock 14% Central nervous system dysfunction 2%
  25. 25. Meningococcemia on the Calves
  26. 26. Necrosis of the toes
  27. 27. Purpura Fulminans  Purpura fulminans that is also known as "Purpura gangrenosa“ is a haemorrhagic condition usually associated with sepsis or previous infection, it is the cutaneous manifestation of disseminated intravascular coagulation. Occurs mainly in babies and small children, but there are also rare cases reported among adults. Specially caused by gram-negative bacteria.
  28. 28. Purpura fulminans
  29. 29. Purpura fulminans of a child's leg
  30. 30. Laboratory diagnosis
  31. 31. Test Result Platelet count Markedly decreased Prothrombin time (PT) Increased Activated partial thromboplastin time (APTT) Increased Fibrin degradation products (FDP) Markedly increased Fibrinogen Normal or decreased Antithrombin III (AT III) Markedly decreased
  32. 32. Different Diagnosis  Liver disease: Liver disease may prolong both the PT and PTT, but fibrinogen levels are usually normal, and the platelet count is usually normal or only slightly reduced. Severe liver disease may be difficult to distinguish from DIC.  Vitamin K deficiency: Vitamin K deficiency will not affect the fibrinogen level or platelet count, but will decrease the coagulation factors and will be completely corrected by vitamin K replacement.  Sepsis: Sepsis may produce thrombo-cytopenia, and coagulopathy may be present because of vitamin K deficiency. However, in these cases, the fibrinogen level should be normal.  TTP (thrombotic thrombocytopenic purpura): TTP may produce fever and MAHA (microangiopathic hemolytic anemia). However, fibrinogen levels and other coagulation studies should be normal.
  33. 33. Treatment Treatment of the underlying disorder Replacement therapy Heparin therapy Other Treatment
  34. 34.    Acute DIC Without bleeding or evidence of ischemia No treatment With bleeding Blood components as needed Fresh frozen plasma Cryoprecipitate Platelet transfusions With ischemia Anticoagulants after bleeding risk is corrected with blood products
  35. 35. Chronic DIC  Without thromboembolism  No specific therapy needed but prophylactic drugs (eg, low-dose heparin, low-molecularweight heparin) may be used for patients at high risk of thrombosis  With thromboembolism  Heparin or low-molecular-weight heparin, trial of warfarin sodium (Coumadin). (If warfarin is unsuccessful, long-term use of lowmolecular-weight heparin may be helpful.)
  36. 36. Complications Severe bleeding Stroke Ischemia of extremities or organs
  37. 37. Prognosis  Since DIC is a result of an acute medical illness, prognoses depends almost entirely upon the speed of the intensive in handing the bleeding emergency, as well as the ability to treat the underling disorder  The underlying disease that causes the disorder will usually predict the probable outcome.
  38. 38. References  Lecture of Kursk State Medical university on the     theme Disseminated intravascular coagulation Robbins, Stanley L.; Cotran, Ramzi S.; Kumar, Vinay; Collins, Tucker (1999). Robbins' Pathologic Basis of Disease (6 ed.). Philadelphia: Saunders. Davidson's Principles and Practice of Medicine (19 ed.). Churchill Livingstone. 2002 http://emedicine.medscape.com/article/199627overview http://www.slideshare.net/deepak15/disseminatedintravascular-coagulation
  39. 39. Thank you