Disseminated Intravascular Coagulation
Objectives: To provide a review of the definition, pathophysiology, differential diagnosis, and treatment of disseminated intravascular coagulation (DIC). Methods: A case scenario and a review of the literature related to the pertinent facts concerning DIC are provided. Results: DIC is a systemic pa...
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| Published in: | American journal of clinical pathology Vol. 146; no. 6; pp. 670 - 680 |
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| Main Authors: | , , |
| Format: | Journal Article |
| Language: | English |
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England
Oxford University Press
01-12-2016
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| Abstract | Objectives: To provide a review of the definition, pathophysiology, differential diagnosis, and treatment of disseminated intravascular coagulation (DIC).
Methods: A case scenario and a review of the literature related to the pertinent facts concerning DIC are provided.
Results: DIC is a systemic pathophysiologic process and not a single disease entity, resulting from an overwhelming activation of coagulation that consumes platelets and coagulation factors and causes microvascular fibrin thrombi, which can result in multiorgan dysfunction syndrome from tissue ischemia. Some conditions associated with acute DIC include septic shock, exsanguinating trauma, burns, or acute promyelocytic leukemia.
Conclusions: The massive tissue factor stimulus results in excess intravascular thrombin, which overcomes the anticoagulant systems and leads to thrombosis. Because of consumption of coagulation factors and platelets, DIC also has a hemorrhagic phase. Treatment of the bleeding patient with DIC is supportive with the use of blood components. |
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| AbstractList | Key Words: Coagulopathy; DIC; Thrombi; Hemorrhage; Thrombocytopenia; Thrombin Am J Clin Pathol December 2016;146:670-680 ABSTRACT Objectives: To provide a review of the definition, patho-physiology, differential diagnosis, and treatment of disseminated intravascular coagulation (DIC). Results: DIC is a systemic pathophysiologic process and not a single disease entity, resulting from an overwhelming activation ofcoagulation that consumes platelets and coagulation factors and causes microvascular fibrin thrombi, which can result in multiorgan dysfunction syndrome from tissue ischemia. Conclusions: The massive tissue factor stimulus results in excess intravascular thrombin, which overcomes the anticoagulant systems and leads to thrombosis. Because ofconsumption ofcoagulation factors and platelets, DIC also has a hemorrhagic phase. Case History A 44-year-old man with a medical history of hepatitis C, cirrhosis, and chronic kidney disease sought treatment at the emergency room for altered mental status and an ammonia level over 400 mmol/L (11-51 mmol/L). Vital signs on admission to the intensive care unit (ICU) on October 23 were as follows: blood pressure, 120/84 mm Hg; heart rate, 107 beats/min; respiratory rate, 18/min; and temperature, 97.8°F. The following laboratory results were obtained (reference range is in parentheses) on admission: WBC, 20.1 x 109/L (3.7-10.3 x 109/L); sodium, 111 mmol/L (136-145 mmol/L); potassium, 5.7mmol/L (3.7-4.8 mmol/L); hemoglobin (Hb), 13.5 g/dL (13.7-17.5 g/dL in males); platelet count, 253 x 109/L (155-369 x 109/L); international normalized ratio (INR), 1.4 (0.9-1.2); prothrombin time (PT), 13.5 seconds (9.6-12.5 seconds); activated thromboplastin time (aPTT), 34 seconds (19-30 seconds); and creatinine, 5.8mg/dL (0.8-1.3mg/dL). Normal hemostasis is a localized process that results... OBJECTIVESTo provide a review of the definition, pathophysiology, differential diagnosis, and treatment of disseminated intravascular coagulation (DIC).METHODSA case scenario and a review of the literature related to the pertinent facts concerning DIC are provided.RESULTSDIC is a systemic pathophysiologic process and not a single disease entity, resulting from an overwhelming activation of coagulation that consumes platelets and coagulation factors and causes microvascular fibrin thrombi, which can result in multiorgan dysfunction syndrome from tissue ischemia. Some conditions associated with acute DIC include septic shock, exsanguinating trauma, burns, or acute promyelocytic leukemia.CONCLUSIONSThe massive tissue factor stimulus results in excess intravascular thrombin, which overcomes the anticoagulant systems and leads to thrombosis. Because of consumption of coagulation factors and platelets, DIC also has a hemorrhagic phase. Treatment of the bleeding patient with DIC is supportive with the use of blood components. Objectives: To provide a review of the definition, pathophysiology, differential diagnosis, and treatment of disseminated intravascular coagulation (DIC). Methods: A case scenario and a review of the literature related to the pertinent facts concerning DIC are provided. Results: DIC is a systemic pathophysiologic process and not a single disease entity, resulting from an overwhelming activation of coagulation that consumes platelets and coagulation factors and causes microvascular fibrin thrombi, which can result in multiorgan dysfunction syndrome from tissue ischemia. Some conditions associated with acute DIC include septic shock, exsanguinating trauma, burns, or acute promyelocytic leukemia. Conclusions: The massive tissue factor stimulus results in excess intravascular thrombin, which overcomes the anticoagulant systems and leads to thrombosis. Because of consumption of coagulation factors and platelets, DIC also has a hemorrhagic phase. Treatment of the bleeding patient with DIC is supportive with the use of blood components. To provide a review of the definition, pathophysiology, differential diagnosis, and treatment of disseminated intravascular coagulation (DIC). A case scenario and a review of the literature related to the pertinent facts concerning DIC are provided. DIC is a systemic pathophysiologic process and not a single disease entity, resulting from an overwhelming activation of coagulation that consumes platelets and coagulation factors and causes microvascular fibrin thrombi, which can result in multiorgan dysfunction syndrome from tissue ischemia. Some conditions associated with acute DIC include septic shock, exsanguinating trauma, burns, or acute promyelocytic leukemia. The massive tissue factor stimulus results in excess intravascular thrombin, which overcomes the anticoagulant systems and leads to thrombosis. Because of consumption of coagulation factors and platelets, DIC also has a hemorrhagic phase. Treatment of the bleeding patient with DIC is supportive with the use of blood components. |
| Author | Boral, Leonard I. Boral, Benjamin M. Williams, Dennis J. |
| Author_xml | – sequence: 1 givenname: Benjamin M. surname: Boral fullname: Boral, Benjamin M. organization: From the Departments of 1Medicine – sequence: 2 givenname: Dennis J. surname: Williams fullname: Williams, Dennis J. organization: 2Pathology and Laboratory MedicineUniversity of Kentucky Medical Center, Lexington – sequence: 3 givenname: Leonard I. surname: Boral fullname: Boral, Leonard I. email: libora2@uky.edu organization: 2Pathology and Laboratory MedicineUniversity of Kentucky Medical Center, Lexington |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/28013226$$D View this record in MEDLINE/PubMed |
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| Keywords | Thrombocytopenia Thrombin Thrombi Hemorrhage Coagulopathy DIC |
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| SubjectTerms | Adult Blood Coagulation - physiology Blood platelets Diagnosis, Differential Disseminated intravascular coagulation Disseminated Intravascular Coagulation - blood Disseminated Intravascular Coagulation - diagnosis Emergency medical care Endothelium Family medical history Hematology Hemorrhage Humans Intensive care Laboratories Liver cirrhosis Male Patients Physiology Sepsis Thrombosis Vital signs |
| Title | Disseminated Intravascular Coagulation |
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