Polytrauma part 6 (DIC)
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Disseminated intravascular coagulation (DIC) is a serious acquired syndrome characterized by the abnormal activation of the coagulation cascade, which leads to both thrombosis and hemorrhage. The condition can stem from various underlying causes such as infections, trauma, or obstetric complications, and its diagnosis relies on clinical and laboratory findings. Treatment focuses on addressing the underlying condition while managing the associated complications, and the prognosis varies widely depending on these factors.
![DIC is an “Acquired” Bleeding
Disorder
• DIC is not a disease entity but an event that can
accompany various disease processes
• It is an “Acquired” Pathological process
• Widespread activation of the clotting cascade ->
formation of blood clots in small blood vessels
throughout the body
• Compromise of tissue blood flow lead to multiple
organ damage MOD
• The coagulation process consumes clotting factors
and platelets,
• Normal clotting is disrupted and severe bleeding can
occur from various sites
acute thrombotic microangiopathy,
abbreviated TMA. Kidney biopsy. PAS stain.
The differential diagnosis of TMA includes:
[1] Hemolytic uremic syndrome (HUS).
Thrombotic thrombocytopenic purpura
(TTP). HIV associated TTP. Disseminated
intravascular coagulation (DIC). Malignant
hypertension. Scleroderma renal crisis.
Antiphospholipid antibody syndrome
(APLA). Drug toxicity, e.g. calcineurin
inhibitor t](https://image.slidesharecdn.com/polytraumapart6dic-190124182227/85/Polytrauma-part-6-DIC-8-320.jpg)
Polytrauma part 6 (DIC)
- 1. Dr. Fathi Neana, MD Chief of Orthopaedics Dr. Fakhry & Dr. A. Al-Garzaie Hospital January, 24- 2019 Polytrauma Part 6 Disseminated intravascular coagulation (DIC)
- 5. Disorders causing obstruction of the Microvascular Circulation 1- Thrombotic microangiopathy (TMA) 2- Disseminated intravascular coagulation (DIC) DIC Increased fibrin formation Obstruction of the Microvascular Circulation
- 6. Other Terms: Disseminated intravascular coagulopathy Consumptive coagulopathy Disseminated intravascular coagulation (DIC) • DIC is an alteration in the blood clotting mechanism • Abnormal acceleration of the coagulation cascade -> Thrombosis • As a result of the depletion of clotting factors • Hemorrhage occurs simultaneously • DIC is s a paradoxical clinical presentation “Clotting and Hemorrhage” Porth, C.M. (2004) Essentials of Pathophysiology) & (Otto, S. (2001). Oncology Nursing
- 7. Disseminated intravascular coagulation (DIC) Definition DIC is an acquired syndrome characterized by: • The intravascular activation of coagulation with loss of localization • Arising from different causes • It can originate from and cause damage to microvasculature • Which if sufficiently severe, can produce Organ dysfunction and Bleeding disorder ISTH´s Scientific Subcommittee on DIC, July 2001
- 8. DIC is an “Acquired” Bleeding Disorder • DIC is not a disease entity but an event that can accompany various disease processes • It is an “Acquired” Pathological process • Widespread activation of the clotting cascade -> formation of blood clots in small blood vessels throughout the body • Compromise of tissue blood flow lead to multiple organ damage MOD • The coagulation process consumes clotting factors and platelets, • Normal clotting is disrupted and severe bleeding can occur from various sites acute thrombotic microangiopathy, abbreviated TMA. Kidney biopsy. PAS stain. The differential diagnosis of TMA includes: [1] Hemolytic uremic syndrome (HUS). Thrombotic thrombocytopenic purpura (TTP). HIV associated TTP. Disseminated intravascular coagulation (DIC). Malignant hypertension. Scleroderma renal crisis. Antiphospholipid antibody syndrome (APLA). Drug toxicity, e.g. calcineurin inhibitor t
- 9. Black holes - Universe Global dimming” can it counter Global warming? - Earth Wolfs - Russia Eagles - USA Osteoblast vs. Osteoclast - Bone Microbiota non pathogenic vs. pathogenic – Intestine Immunological Response Inflammatory vs. Ant inflammatory mediators Haemostatic Response Coaulatory vs. Anticoagulatory mediators Balance & Equilibrium every where from Galaxy to Atom
- 12. SIRS Injurious stimulus -Tissue Trauma – Sepsis Especially with sepsis the immunologic and haemostatic response amplify each other MODS DIC Circulating mediators Circulating mediators Haemostatic Response Immunological Response ModificationModification AmplificationAmplification Ischaemia -Ischaemia - BleedingBleeding DestructionDestruction
- 13. 1- TF (Tissue Factor) - mediated thrombin generation 2- Dysfunctional physiologic anticoagulant mechanisms (depression of Antithrombin and protein C system) 3- Impaired fibrin removal due to depression of the (impaired Fibrinolytic system ) however, in exceptional forms of DIC, Fibrinolytic activity may be increased and contribute to bleeding 4- Inflammatory activation (Hypercoagulability) Pathophysiology The hematologic derangements in DIC results from 4 simultaneously occurring mechanisms TF
- 14. Pathophysiology The hematologic derangements in DIC results from 4 simultaneously occurring mechanisms 2- Dysfunctional physiologic Anticoagulant mechanisms 3- Impaired fibrin removal Fibrinolytic system 1- TF- mediated Thrombin generation 4- Inflammatory activation Hypercoagulability
- 15. Endothelialdamage Haemostatic mechanisms SYSTEMIC INFLAMMATION TF TF TF Monocyte Monocytes Activation TF TF Cytokines Intravascular clot formation NORMAL HAEMOSTASIS Activated monocyte
- 16. SYSTEMIC ACTIVATION OF COAGULATION Intravascular deposition of fibrin Depletion of platelets and coagulation factors Thrombosis of small and midsize vessels Bleeding Organ failure DEATHDEATH
- 17. The combination of widespread tissue ischemia and simultaneous bleeding carry an increased risk of death In addition to that posed by the underlying disease DIC can be overt and severe in some cases, but milder and insidious in others The diagnosis of DIC depends on the findings of characteristic laboratory tests and clinical background Treatment is mainly geared towards the underlying condition DIC does not occur by itself A complication from another underlying condition Usually in critical illness
- 18. • Extrinsic ( tissue) – Shock or trauma – Infections gram positive & gram negative sepsis, aspergillosis – Obstetric complications (eclampsia, placenta abruptio, fetal death syndrome) – Malignancies APML, AML, cancers of the lung, colon, breast, prostate) • Intrinsic (blood vessel) – Infectious vasculitis (certain viral infections, rocky mountain spotted fever) – Vascular disorders – Intravascular hemolysis (hemolytic transfusion reactions) – Miscellaneous snakebite pancreatitis liver disease Risk factors and etiology of DIC (Porth, 2004) & (Otto, 2001) Almost always a secondary event from activation of one of the coagulation pathways. Underlying pathology creates a triggering event either 1- Tissue injury (Extrinsic) or 2- Blood vessel injury (Intrinsic)
- 19. Infections Sepsis • Gram negative (endotoxin) • Gram positive(polysaccharides, peptides) Viremias • Varicella • Hepatitis • Cytomegalovirus • HIV Causes of DIC
- 20. Sepsis Pro-inflammatory cytokines IL-6 TF- activation of coagulation TNF-α Inhibition of physiological anticoagulant pathways Depression of fibrinolysis due to high levels of PAI-1. Enhanced Fibrin formation Impaired Fibrin removal Microvascular thrombosis
- 22. Trauma • Crush injuries • Other trauma with tissue necrosis • Severe burns • Extensive surgery Causes of DIC
- 24. Obstetric complications • Amniotic fluid embolism • Placental abruption • (Pre)eclampsia • Dead fetus syndrome Causes of DIC
- 25. Other causes of DIC Hemolysis • Hemolytic transfusion reaction • Massive transfusions • Malaria • Other severe hemolysis Malignant disorders • Metastatic malignancy • Tumors producing cancer procoagulant • Tumor with tissue necrosis Vascular abnormalities • Giant hemangioma • Heriditary teleangiectasis • Prosthetic devices • Aortic balloon assist devices • Denver shunts Other conditions • Pancreatitis • Acute liver necrosis • Transplant rejection • Heat stroke
- 26. 1- Thrombosis 2- Organ dysfunction 3- Hemorrahage 4- Do not forget The underlying cause Clinical manifestations of DIC
- 27. Clinical manifestations of DIC Thromosis, Organ dysfunction, Hemorrahage
- 28. 1- The underlying cause 2- Thrombosis 3- Dysfunction of multiple organs MODS 4- The most common sign of DIC is Bleeding Signs and symptoms
- 29. Signs and symptoms The underlying cause • The underlying cause usually leads to symptoms and signs, and DIC is discovered on laboratory testing • The onset of DIC can be sudden, as in endotoxic shock or amniotic fluid embolism • or it may be insidious and chronic, as in cases of malignancy • Overt DIC can further lead to, multiorgan failure and widespread hemorrhage from various sites
- 31. • Microvascular clot formation is the primary event • Signs of Organ dysfunction Indistinguishable from SIRS, Sepsis and MODS • Lung dysfunction i. Acute pulmonary micro embolism syndrome ii. Late pulmonary micro embolism syndrome → ARDS , Microatelectasis and capillary leakage • Acute renal failure i. Oliguria or anuria ii. Microscopic or macroscopic haematuria Signs and symptoms Dysfunction of multiple organs (MODS)
- 32. • Cerebral dysfunction i. Confusion & Blurring of consciousness • Dermal changes :micro thrombosis / bleedings i. Focal hemorrhagic necroses : face & peripheral extremities ii. Petechiae and/or Ecchymoses • Additional symptoms i. from dysfunction of the liver, endocrine glands and other organs Signs and symptoms Dysfunction of multiple organs (MODS)
- 33. • Ecchymoses, petechiae, and purpura • Cool and or mottled extremities • Bleeding from multiple sites either oozing or frank bleeding (hematemesis) • Dyspnea and chest pain if pleura and pericardium involvement • Haematuria (Porth, 2004) & (Otto, 2001) Signs and symptoms Most common sign of DIC is Bleeding
- 36. Fibrinolysis Hypocoagulability Thrombosis Hypercoagulability Diagnostic criteria of DIC Pathophysiology
- 37. Pathophysiology Thrombosis Hypercoagulability 1) Coagulation cascade is initiated, -> widespread fibrin formation 2) Micro thrombi throughout the microcirculatory system 3) Fibrin deposits result in tissue ischemia, hypoxia, necrosis 4) Leads to multi organ dysfunction MODS 5) Exhaustion of platelets and coagulation factors (results in Hemorrhage) consumption coagulopathy (Porth, 2004) & Otto, 2001 Fibrinolysis Hypocoagulability 1) Activates the Complement system 2) Byproducts of fibrinolysis (fibrin/fibrin degradation products(FDP)) further enhance bleeding by interfering with platelet aggregation, fibrin polymerization, & thrombin activity 3) Leads to Hemorrhage
- 40. Laboratory Diagnosis Analysis Early changes Late changes Platelets / APTT Fibrinogen D-dimer F:II,VII,X Protein C Anti-thrombin TAT complex Soluble fibrin
- 41. Blood tests when DIC is suspected Simple screening Platelet count Activated partial thromboplastintime (APTT) Prothrombin time (PT) Extended screening Fibrin D-dimer fragment Antithrombin (AT) Fibrinogen Supplementary tests Further evidence for activation of coagulation & fibrinolysis *Prothrombin fragment 1.2 *Thrombin-antithrombin complexes (TAT) (↑ procoagulation) *Fibrinopeptid A (FPA) or soluble fibrin *Protein C *Fibrinolytic activity (Clot lysis time) *Thrombin time *Plasmin-antiplasmin complexes (PAP)
- 42. Treatment of DIC
- 43. Treatment of DIC General Guidelines Patients with DIC should be treated at hospitals with appropriate critical care units (ICU) Available Subspecialty expertise, such as hematology, blood bank, or surgery. Patients who present to hospitals without those capabilities and who are stable enough for transfer should be referred expeditiously to a hospital that has those resources.
- 44. Etiological factors Infections Trauma Obstetric complications Pathogenetic factors Toxic O- and OH-free radicals Complement activation Cytokine formation Thrombus formation Treatment of DIC General Guidelines 1- Treatment of underlying disorder 2- Supportive Treatment 3- Hemostatic Therapy
- 45. Treatment of DIC Treatment of underlying disorder • Antibiotic treatment of infections • Surgical debridement and drainage of infected foci • Immobilization of fractures • Evacuation of uterus in obstetric DIC
- 46. Treatment of DIC Supportive Treatment Supportive treatment of MODS • Shock : fluids, catecholamines • Hypoxemia : oxygen, mechanical ventilation • Renal failure : diuretics, renal replacement therapy • Severe anemia : blood transfusion
- 47. Treatment of DIC Hemostatic Therapy • Antithrombotic treatment • Antithrombin concentrate (AT concentrate) • Concurrent treatment with heparin should be avoided, heparin worsens thrombocytopenia • Fresh frozen plasma (FFP) When bleeding; administer after antithrombin • Platelets : severe thrombocytopenia + bleeding antifibrinolytic treatment Should be avoided
- 49. Management of DIC Medication Summary Anticoagulants, Hematologic • Heparin • extensive fibrin deposition without evidence of substantial hemorrhage, reserved for cases of chronic DIC.. limited use in acute hemorrhagic DIC acral cyanosis and digital ischemia • Antithrombin(Atryn, Thrombate III) • Recombinant Human Activated Protein C • Withdrawn from the worldwide market on October 25, 2011.was approved for the reduction of mortality in patients who have severe sepsis • Tissue factor pathway inhibitor (Recombinant thrombomodulin) Blood Components • Packed red blood cells (PRBCs; washed) • Platelets • Fresh frozen plasma (FFP) • Cryoprecipitate or fibrinogen concentrates Antifibrinolytic Agents • Aminocaproic acid (Amicar) • Tranexamic acid (Cyklokapron, Lysteda)
- 50. Prognosis
- 51. Prognosis of DIC •Prognosis varies depending on The underlying disorder The extent of the intravascular thrombosis •The mortality rate with DIC, regardless of cause is 10% to 50% •DIC with Sepsis has a significantly higher rate of death compared to DIC associated with Trauma
Editor's Notes
- #32: The most common symptoms are those described for SIRS (Systemic Inflammatory Response Syndrome) and MODS (Multiple Organ Dysfunction Syndrome) and cerebral dysfunction. As Microvascular clot formation is the primary event, signs of organ dysfunction determine the clinical symptoms in most DIC patients. Thus making the presentation of DIC rather indistinguishable from SIRS/Sepsis and MODS.
- #33: Characteristic changes in skin :micro thrombosis / bleedings
- #41:
- #48: because heparin increases the degradation of antithrombin, worsens thrombocytopenia and increases bleeding complications.