Disseminated intravascular coagulation overview: Difference between revisions
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==Classification== | ==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== | ==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 [[Homeostasis|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 [[Fibrinolysis|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== | ==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 [disease name] from other Diseases== | ==Differentiating [disease name] from other Diseases== | ||
*[Disease name] must be differentiated from other diseases that cause [clinical feature 1], [clinical feature 2], and [clinical feature 3], such as: | *[Disease name] must be differentiated from other diseases that cause [clinical feature 1], [clinical feature 2], and [clinical feature 3], such as: | ||
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==Epidemiology and Demographics== | ==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== | ==Risk Factors== | ||
Common risk factors in the development of [[DIC]] include [[trauma]], [[sepsis]], [[obstetric]] complications, [[cancers]], and [[Immunological|immunologic]] reactions | |||
== Natural History, Complications and Prognosis== | == 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 == | == Diagnosis == | ||
===Diagnostic | ===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 bites|venomous snake]] and [[viral hemorrhagic fever]]. | |||
=== Symptoms === | |||
===Physical Examination=== | |||
===Laboratory Findings=== | |||
===Electrocardiogram=== | |||
===X-ray=== | |||
=== | ===Echocardiography and Ultrasound=== | ||
===CT scan=== | |||
===MRI=== | |||
===Other Imaging Findings=== | |||
===Other Diagnostic Studies=== | |||
* | |||
=== Other Diagnostic Studies === | |||
* | |||
== Treatment == | == Treatment == | ||
Revision as of 14:16, 5 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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Disseminated intravascular coagulation overview On the Web |
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Risk calculators and risk factors for Disseminated intravascular coagulation overview |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
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.[1] [2] [3] [4]
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
- [Disease name] was first discovered by [scientist name], a [nationality + occupation], in [year] during/following [event].
- In [year], [gene] mutations were first identified in the pathogenesis of [disease name].
- In [year], the first [discovery] was developed by [scientist] to treat/diagnose [disease name].
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 [disease name] from other Diseases
- [Disease name] must be differentiated from other diseases that cause [clinical feature 1], [clinical feature 2], and [clinical feature 3], such as:
- [Differential dx1]
- [Differential dx2]
- [Differential dx3]
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
Laboratory Findings
Electrocardiogram
X-ray
Echocardiography and Ultrasound
CT scan
MRI
Other Imaging Findings
Other Diagnostic Studies
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 the mainstay of therapy for [disease name].
- [Surgical procedure] in conjunction with [chemotherapy/radiation] is the most common approach to the treatment of [disease name].
- [Surgical procedure] can only be performed for patients with [disease stage] [disease name].
Prevention
- There are no primary preventive measures available for [disease name].
- Effective measures for the primary prevention of [disease name] include [measure1], [measure2], and [measure3].
- Once diagnosed and successfully treated, patients with [disease name] are followed-up every [duration]. Follow-up testing includes [test 1], [test 2], and [test 3].
References
- ↑ Baglin, T., Disseminated intravascular coagulation: diagnosis and treatment, BMJ 1996; 312: 683-686.
- ↑ Bick, R.L., Disseminated intravascular coagulation: pathophysiological mechanisms and manifestations, Sem Thromb Hemostasis 1998; 24: 3-18.
- ↑ Penner, J.A., Disseminated intravascular coagulation in patients with multiple organ failure of non-septic origin, Sem Thromb Hemostasis 1998, 24: 45-52.
- ↑ Riewald, M., Riess, H., Treatment options for clinically recognized disseminated intravascular coagulation, Sem Thromb Hemostasis 1998; 24: 53-59.