Disseminated intravascular coagulation overview: Difference between revisions
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=== Prevention === | === Prevention === | ||
*There are no | *There are no established measures for the prevention of [[DIC]]. The threshold of initiation of prevention therapy for [[bleeding]] in [[DIC]] is a [[platelet count]] of ≥10,000/microL. Some studies suggest a [[platelet]] count of 20,000/microL without [[bleeding]]. There is little evidence to support [[Preventive care|preventive]] measures for [[thrombosis]] in [[DIC]]. | ||
==References== | ==References== | ||
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Latest revision as of 14:19, 25 September 2018
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Disseminated intravascular coagulation Microchapters |
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Differentiating Disseminated intravascular coagulation from other Diseases |
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Diagnosis |
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Treatment |
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Omer Kamal, M.D.[2]
Overview
Disseminated intravascular coagulation, is a pathological process in the body where the blood starts to coagulate throughout the whole body. This depletes the body of its platelets and coagulation factors, and there is a paradoxically increased risk of hemorrhage. It occurs in critically ill patients, especially those with Gram-negative sepsis (particularly meningococcal sepsis) and acute promyelocytic leukemia. DIC is a complex and highly variable disorder, whose manifestations depend upon the inciting event, the host response and underlying comorbid disease. Additionally, the morbidity and mortality in patients with DIC often depends more on the underlying disease and he specific pathophysiology. As such, well-designed studies are obviously difficult to design, and there is therefore little consensus regarding management. The term DIC has evolved from the terms ‘consumptive coagulopathy’ and later, ‘defibrination syndrome’. Although most physicians are aware of the hemorrhage that is seen in patients with DIC, the ‘coagulation’ in DIC actually refers to both hemorrhage and thrombosis. In actuality, the thrombosis, both micro and macro-vascular, with resulting ischemia, contributes more to morbidity and mortality than the hemorrhage. Bick defines DIC as ‘a systemic thrombohemorrhagic disorder seen in association with well-defined clinical situations AND laboratory evidence for procoagulant activation, fibrinolytic activation, inhibitor consumption, and evidence of end-organ damage’.
Historical Perspective
The syndrome of DIC is well known in the medical literature for centuries, although a more precise description of the underlying mechanisms had to await the 20th century. Initial ideas on a role of the contact activation system as the primary trigger for the systemic activation of coagulation as well as a presumed hyperfibrinolytic response in DIC have been found to be misconceptions.
Classification
Disseminated intravascular coagulation may be classified according to the degree of fibrinolytic activation into suppressed-fibrinolytic-type DIC (DIC with suppressed fibrinolysis), enhanced-fibrinolytic-type DIC (DIC with enhanced fibrinolysis) and balanced-fibrinolytic-type DIC (DIC with balanced fibrinolysis). Each type differs in clinical features and laboratory findings.
Pathophysiology
DIC is a hemorrhagic syndrome originating in the small blood vessels. DIC is caused by uncontrolled activation of clotting factors and fibrinolytic enzymes. Tissue necrosis and bleeding are consequences of DIC. Under homeostatic conditions, the body is maintained in a finely tuned balance of coagulation and fibrinolysis. The activation of the coagulation cascade yields thrombin that converts fibrinogen to fibrin; the stable fibrin clot being the final product of hemostasis. The fibrinolytic system then functions to break down fibrinogen and fibrin. Activation of the fibrinolytic system generates plasmin (in the presence of thrombin), which is responsible for the lysis of fibrin clots. The breakdown of fibrinogen and fibrin results in polypeptides called fibrin degradation products (FDPs) or fibrin split products (FSPs). In a state of homeostasis, the presence of thrombin is critical, as it is the central proteolytic enzyme of coagulation and is also necessary for the breakdown of clots, or fibrinolysis.
Causes
There are a variety of causes of DIC, all usually causing the release of chemicals into the blood that instigates the coagulation. Life-threatening causes include conditions which may result in death or permanent disability within 24 hours if left untreated. Disseminated intravascular coagulation in itself is a life-threatening condition and must be treated as such irrespective of the cause. Common causes include abruptio placentae, amniotic fluid embolism, aortic aneurysm, blood transfusion reaction, drugs (e.g. Amphetamines), beractant eclampsia, giant hemangioma, graft-versus-host disease, HELLP syndrome and hemolytic transfusion reaction.
Differentiating Disseminated intravascular coagulation from other Diseases
Disseminated intravascular coagulation (DIC) must be differentiated from other diseases that cause symptoms of DVT and pulmonary embolism such as: factor V Leiden mutation, protein C deficiency, protein S deficiency, prothrombin gene mutation, antithrombin III deficiency, antiphospholipid antibody syndrome.
Epidemiology and Demographics
The incidence of DIC is different in different diseases as it is almost always related to a life threatening condition. It depends on the cause of DIC such as cancer, infection, trauma and Obstetrical complications. The incidence of DIC is different in different diseases as it is almost always related to a life threatening condition. It depends on the cause of DIC such as cancer, infection, trauma and obstetrical complications. The prevalence of DIC depends on the clinical settings, higher versus low acquity settings. The data sometimes may underestimate the incidence of trasient or mild cases of DIC.
Risk Factors
Common risk factors in the development of DIC include trauma, sepsis, obstetric complications, cancers, and immunologic reactions
Natural History, Complications and Prognosis
If left untreated, 40-80% patients with DIC may progress to develop organ dysfunction. Common complications of DIC include renal failure, hepatic dysfunction, acute lung injury, neurologic dysfunction and adrenal failure. Low levels of antithrombin at the onset if shock may predict an unfavorable prognosis.
Diagnosis
Diagnostic Study of Choice
There is no single diagnostic study of choice for DIC. DIC is a clinical as well as a laboratory diagnosis. DIC may be diagnosed based on the diagnostic criteria established by Japanese Society on Thrombosis and Hemostasis.
History and Symptoms
Patients with DIC may have a history of abruptio placentae, amniotic fluid embolism, aortic aneurysm, blood transfusion reaction, drugs (e.g. Amphetamines), beractant eclampsia, giant hemangioma, graft-versus-host disease, HELLP syndrome, hemolytic transfusion reaction, liver disease, malignancy (especially APL), sepsis (esp. gram-negative bacteria), severe allergic reaction, transplant rejection, trauma (e.g. Fat embolism, head injury), venomous snake and viral hemorrhagic fever.
Physical Examination
Common physical examination findings of DIC include signs of spontaneous and life-threatening hemorrhage, signs of subacute bleeding, signs of diffuse or localized thrombosis, bleeding into serouscavities, nonspecific altered consciousness or stupor, transient focal neurologic deficits, hypotension, tachycardia, circulatory collapse, pleural friction rub, signs of acute respiratory distress syndrome(ARDS), hematemesis, hematochezia, signs of azotemia and renal failure, acidosis, hematuria, oliguria, metrorrhagia and uterine hemorrhage.
Laboratory Findings
Laboratory findings consistent with the diagnosis of DIC include decreased platelets, fibrin degradation products or D-dimer tests (markers of fibrinolysis), bleeding time and fibrinogen levels. Peripheral smear shows schistocytes and RBC fragments in ~ 50%, mild reticulocytosis, leukocytosis, and thrombocytopenia with an increased population of young platelets (due to increased destruction and turnover). Clotting factors include normal prothrombin time and partial thromboplastin time in up to 50% of patients (due to higher circulating levels of clotting factors such as factor Xa and thrombin), elevated fibrin and fibrinogen degradation products. D-dimer more sensitive and specific for DIC. Antithrombin levels have become a key test for diagnosing and monitoring therapy in DIC.
Electrocardiogram
There are no specific ECG findings associated with DIC but it may cause thrombosis which may lead to recurrent ST-segment elevations in leads II, III, and aVF.
X-ray
There are no x-ray findings associated with DIC.
Echocardiography and Ultrasound
There are no echocardiography/ultrasound findings associated with DIC. However, an echocardiography/ultrasound may be helpful in the diagnosis of complications of DIC, which include myocardial infarction, pulmonary artery mass etc.
CT scan
There are no CT scan findings associated with DIC. CT scanning of the chest may reveal blood in the tracheobronchial tree or clots elsewhere in the body.
MRI
There are no MRI findings associated with DIC. However, sepsis induced DIC may show lesions predominated in the white matter, suggesting increased blood-brain barrier permeability.
Treatment
Medical Therapy
- There is no treatment for [disease name]; the mainstay of therapy is supportive care.
- The mainstay of therapy for [disease name] is [medical therapy 1] and [medical therapy 2].
- [Medical therapy 1] acts by [mechanism of action 1].
- Response to [medical therapy 1] can be monitored with [test/physical finding/imaging] every [frequency/duration].
Surgery
- Surgery is not the mainstay of therapy for DIC.
Prevention
- There are no established measures for the prevention of DIC. The threshold of initiation of prevention therapy for bleeding in DIC is a platelet count of ≥10,000/microL. Some studies suggest a platelet count of 20,000/microL without bleeding. There is little evidence to support preventive measures for thrombosis in DIC.
References