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Disseminated intravascular coagulation

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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], M. Khurram Afzal, MD [3], Sogand Goudarzi, MD [4]

Synonyms and keywords: Disseminated intravascular coagulation, Disseminated intravascular coagulopathy, Consumptive coagulopathy, DIC

Overview

Overview

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

    References


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    Historical Perspective

    Historical Perspective

    Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Omer Kamal, M.D.[2]

    Overview

    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.

    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. [1]Disseminated intravascular coagulation (DIC) was first reported in the 19th century. As DIC is generally associated with an adverse outcome by most clinicians, and its acronym has been synonymous with “death is coming.”[2]

    References

    1. ↑ Levi M, van der Poll T (November 2014). “A short contemporary history of disseminated intravascular coagulation”. Semin. Thromb. Hemost. 40 (8): 874–80. doi:10.1055/s-0034-1395155. PMID 25377321.
    2. ↑ Toh CH, Dennis M (October 2003). “Disseminated intravascular coagulation: old disease, new hope”. BMJ. 327 (7421): 974–7. doi:10.1136/bmj.327.7421.974. PMC 259170. PMID 14576251.


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    Classification

    Classification

    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 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.

    Classification

    Disseminated intravascular coagulation may be classified according to the degree of fibrinolytic activation into the following subtypes/groups[1]:

    Suppressed-fibrinolytic-type DIC (DIC with suppressed fibrinolysis) [2][3][4][5]

    • Severe coagulation activation
    • Mild fibrinolytic activation
    • Seen in sepsis mostly
    • Mild bleeding complications
    • Elevated thrombin-antithrombin complex (TAT) , a coagulation activation marker
    • Mildy elevated plasmin-α2 plasmin inhibitor complex (PIC), a fibrinolysis activation marker
    • Mildly elevated Fibrin/fibrinogen degradation products (FDPs) and D-dimers
    • Normal or only slightly decreased α2 plasmin inhibitor (α2PI)

    Enhanced-fibrinolytic-type DIC (DIC with enhanced fibrinolysis)[2][3][4][5]

    • Presents with marked fibrinolysis activation corresponding to coagulation activation
    • Strong activation of fibrinolysis
    • With hardly any elevation in PAI
    • Severe bleeding severe.
    • Elevation in both TAT and PIC
    • Elevated FDPs and D-dimer
    • FDP/D-dimer ratio tends to increase (decrease when expressed as the D-dimer/FDP ratio).
    • Associated with APL, abdominal aortic aneurysm, and prostate cancer

    Balanced-fibrinolytic-type DIC (DIC with balanced fibrinolysis) [2][3][4][5]

    References

    1. ↑ Asakura H (2014). “Classifying types of disseminated intravascular coagulation: clinical and animal models”. J Intensive Care. 2 (1): 20. doi:10.1186/2052-0492-2-20. PMC 4267600. PMID 25520834.
    2. ↑ 2.0 2.1 2.2 Asakura H, Ontachi Y, Mizutani T, Kato M, Saito M, Kumabashiri I, Morishita E, Yamazaki M, Aoshima K, Nakao S (June 2001). “An enhanced fibrinolysis prevents the development of multiple organ failure in disseminated intravascular coagulation in spite of much activation of blood coagulation”. Crit. Care Med. 29 (6): 1164–8. PMID 11395595.
    3. ↑ 3.0 3.1 3.2 Takahashi H, Tatewaki W, Wada K, Hanano M, Shibata A (February 1990). “Thrombin vs. plasmin generation in disseminated intravascular coagulation associated with various underlying disorders”. Am. J. Hematol. 33 (2): 90–5. PMID 1689102.
    4. ↑ 4.0 4.1 4.2 Asakura H, Jokaji H, Saito M, Uotani C, Kumabashiri I, Morishita E, Yamazaki M, Aoshima K, Matsuda T (October 1994). “Study of the balance between coagulation and fibrinolysis in disseminated intravascular coagulation using molecular markers”. Blood Coagul. Fibrinolysis. 5 (5): 829–32. PMID 7865691.
    5. ↑ 5.0 5.1 5.2 Asakura H, Jokaji H, Saito M, Uotani C, Kumabashiri I, Morishita E, Yamazaki M, Matsuda T (March 1991). “Changes in plasma levels of tissue-plasminogen activator/inhibitor complex and active plasminogen activator inhibitor in patients with disseminated intravascular coagulation”. Am. J. Hematol. 36 (3): 176–83. PMID 1899963.

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    Pathophysiology

    Pathophysiology

    Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Omer Kamal, M.D.[2]

    Overview

    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.

    Pathophysiology

    DIC is an acquired syndrome characterized by the intravascular activation of coagulation due to sepsis, trauma, malignancy, liver disease, obstetric disorders, envenomation, vascular anomalies and major transfusion reactions. It can originate from and cause damage to the microvasculature, which may eventually lead to organ dysfunction. Under homeostatic conditions, the body is maintained in a state of hematological equilibrium of coagulation and fibrinolysis termed as hemostasis. The activation of the coagulation cascade yields thrombin that converts fibrinogen to fibrin; the stable fibrin clot being the final product of coagulation cascade. 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).

    DIC as a disease process

    • DIC occurs secondary to a clinical disorder. The clinical spectrum includes sepsis, trauma, malignancy, liver disease, obstetric disorders, envenomation, vascular anomalies and major transfusion reactions.
    • Ocurrence of DIC in a patient should always be seen as an indicator of another life-threatening condition and warrants thorough diagnostic evaluation.

    Mediators of induction of DIC

    • DIC may be induced by either or both of the following mechanisms:
      • As a consequence of systemic inflammatory response, there is activation of cytokine network and thereby coagulation system as in sepsis or polytrauma and/or
      • Release of pro-coagulant products into the blood stream such as in malignancies or obstetrical cases.

    Activation of coagulation cascade

    Consumptive coagulopathy and bleeding sequelae

    Summary

    As a summary:[8][9][10]

    References

    1. ↑ Martinod K, Wagner DD (May 2014). “Thrombosis: tangled up in NETs”. Blood. 123 (18): 2768–76. doi:10.1182/blood-2013-10-463646. PMC 4007606. PMID 24366358.
    2. ↑ Hellum M, Øvstebø R, Brusletto BS, Berg JP, Brandtzaeg P, Henriksson CE (March 2014). “Microparticle-associated tissue factor activity correlates with plasma levels of bacterial lipopolysaccharides in meningococcal septic shock”. Thromb. Res. 133 (3): 507–14. doi:10.1016/j.thromres.2013.12.031. PMID 24423888.
    3. ↑ Gordon SG, Franks JJ, Lewis B (February 1975). “Cancer procoagulant A: a factor X activating procoagulant from malignant tissue”. Thromb. Res. 6 (2): 127–37. PMID 234638.
    4. ↑ Martinod K, Demers M, Fuchs TA, Wong SL, Brill A, Gallant M, Hu J, Wang Y, Wagner DD (May 2013). “Neutrophil histone modification by peptidylarginine deiminase 4 is critical for deep vein thrombosis in mice”. Proc. Natl. Acad. Sci. U.S.A. 110 (21): 8674–9. doi:10.1073/pnas.1301059110. PMC 3666755. PMID 23650392.
    5. ↑ Sack GH, Levin J, Bell WR (January 1977). “Trousseau’s syndrome and other manifestations of chronic disseminated coagulopathy in patients with neoplasms: clinical, pathophysiologic, and therapeutic features”. Medicine (Baltimore). 56 (1): 1–37. PMID 834136.
    6. ↑ Gordon SG, Mielicki WP (March 1997). “Cancer procoagulant: a factor X activator, tumor marker and growth factor from malignant tissue”. Blood Coagul. Fibrinolysis. 8 (2): 73–86. PMID 9518049.
    7. ↑ Xu J, Zhang X, Pelayo R, Monestier M, Ammollo CT, Semeraro F, Taylor FB, Esmon NL, Lupu F, Esmon CT (November 2009). “Extracellular histones are major mediators of death in sepsis”. Nat. Med. 15 (11): 1318–21. doi:10.1038/nm.2053. PMC 2783754. PMID 19855397.
    8. ↑ Capon SM, Goldfinger D (June 1995). “Acute hemolytic transfusion reaction, a paradigm of the systemic inflammatory response: new insights into pathophysiology and treatment”. Transfusion. 35 (6): 513–20. PMID 7770905.
    9. ↑ Levi M, Toh CH, Thachil J, Watson HG (April 2009). “Guidelines for the diagnosis and management of disseminated intravascular coagulation. British Committee for Standards in Haematology”. Br. J. Haematol. 145 (1): 24–33. doi:10.1111/j.1365-2141.2009.07600.x. PMID 19222477.
    10. ↑ Kim JE, Lee N, Gu JY, Yoo HJ, Kim HK (June 2015). “Circulating levels of DNA-histone complex and dsDNA are independent prognostic factors of disseminated intravascular coagulation”. Thromb. Res. 135 (6): 1064–9. doi:10.1016/j.thromres.2015.03.014. PMID 25843168.


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    Causes

    Causes

    Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Ogheneochuko Ajari, MB.BS, MS [2] Omer Kamal, M.D.[3]

    Overview

    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.

    Causes

    Life Threatening Causes

    Life-threatening causes include conditions which may result in death or permanent disability within 24 hours if left untreated.[1]

    Disseminated intravascular coagulation in itself is a life-threatening condition and must be treated as such irrespective of the cause.[2][3][4]

    Common Causes

    Causes by Organ System

    Cardiovascular Aortic aneurysm, malignant hypertension, myocardial infarction, septic shock, shock, vasculitis
    Chemical / poisoning Snake bite (elapid)
    Dermatologic Purpura fulminans, Raynaud’s disease, rheumatoid arthritis, vasculitis
    Drug Side Effect Amphetamine, cocaine, indomethacin, interleukin 2, Mafenide, serotonin syndrome, Dinoprostone
    Ear Nose Throat No underlying causes
    Endocrine No underlying causes
    Environmental No underlying causes
    Gastroenterologic Acute fatty liver of pregnancy, acute hepatic failure, acute pancreatitis, Crohn disease, fulminant hepatic failure, liver disease, ulcerative colitis
    Genetic No underlying causes
    Hematologic Acute hemolytic transfusion reactions, acute myeloid leukemia, acute promyelocytic leukemia, antiphospholipid syndrome, Kasabach-Merritt syndrome, myeloproliferative syndrome, paroxysmal nocturnal hemoglobinuria, purpura fulminans, Trousseau’s syndrome
    Iatrogenic Acute renal allograft rejection, Denver shunt, extensive surgery, LeVeen shunt, liver transplantation, peritoneovenous shunt, prosthetic devices, serotonin syndrome, surgery, recent anesthesia, ventricular assist devices
    Infectious Disease Arenaviruses, Argentine hemorrhagic fever, aspergillosis, Bolivian hemorrhagic fever, capnocytophaga canimorsus, CMV, HELLP syndrome, hepatitis viruses, histoplasmosis, malaria (malignant tertian), meningococcal septicaemia, mycoplasma pneumoniae, neisseria meningiditis, osteomyelitis, rocky mountain spotted fever, sarcoidosis, sepsis, septic shock, sleeping sickness (East African), streptococcus pneumoniae, tuberculosis, typhoid fever, viral hemorrhagic fevers, VZV
    Musculoskeletal / Ortho Osteomyelitis
    Neurologic Antiphospholipid syndrome, meningococcal septicaemia, neisseria meningiditis
    Nutritional / Metabolic No underlying causes
    Obstetric/Gynecologic Abruptio placentae, amniotic fluid embolism, dead fetus syndrome, eclampsia, HELLP syndrome, intrauterine death, pre-eclampsia, retained intrauterine fetal demise, septic abortion
    Oncologic Acute myeloid leukemia, acute promyelocytic leukemia, Cancers of lung, pancreas, prostate and stomach, giant hemangioma, Kasabach-Merritt syndrome, malignancy, mucin-secreting adenocarcinoma, paraneoplastic syndrome, Trousseau’s syndrome
    Opthalmologic No underlying causes
    Overdose / Toxicity Amphetamine, cocaine
    Psychiatric No underlying causes
    Pulmonary Acute respiratory distress syndrome, empyema, mycoplasma pneumoniae, sarcoidosis, streptococcus pneumoniae, tuberculosis
    Renal / Electrolyte Renal failure
    Rheum / Immune / Allergy Acute renal allograft rejection, antiphospholipid syndrome, interleukin 2, macrophage-activation syndrome, paraneoplastic syndrome, Raynaud’s disease, rheumatoid arthritis, sarcoidosis, vasculitis
    Sexual No underlying causes
    Trauma Burns, crush syndrome, head injury, lightning strike, motor vehicle accidents, severe tissue injury, trauma
    Urologic No underlying causes
    Dental No underlying causes
    Miscellaneous Heat stroke, hyperthermia, prosthetic devices, Snake bite (elapid), venomous snakes

    Causes in Alphabetical Order

    References

    1. ↑ Spero JA, Lewis JH, Hasiba U (February 1980). “Disseminated intravascular coagulation. Findings in 346 patients”. Thromb. Haemost. 43 (1): 28–33. PMID 6773170.
    2. ↑ Levi M, Toh CH, Thachil J, Watson HG (April 2009). “Guidelines for the diagnosis and management of disseminated intravascular coagulation. British Committee for Standards in Haematology”. Br. J. Haematol. 145 (1): 24–33. doi:10.1111/j.1365-2141.2009.07600.x. PMID 19222477.
    3. ↑ Ghosh K, Shetty S (March 2008). “Blood coagulation in falciparum malaria–a review”. Parasitol. Res. 102 (4): 571–6. doi:10.1007/s00436-007-0832-0. PMID 18066597.
    4. ↑ Siegal T, Seligsohn U, Aghai E, Modan M (February 1978). “Clinical and laboratory aspects of disseminated intravascular coagulation (DIC): a study of 118 cases”. Thromb. Haemost. 39 (1): 122–34. PMID 580488.
    5. ↑ 5.0 5.1 5.2 5.3 5.4 Lurie S, Feinstein M, Mamet Y (2000). “Disseminated intravascular coagulopathy in pregnancy: thorough comprehension of etiology and management reduces obstetricians’ stress”. Arch Gynecol Obstet. 263 (3): 126–30. PMID 10763841.


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    Differentiating Disseminated intravascular coagulation from other Diseases

    Differentiating Disseminated intravascular coagulation from other Diseases

    Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: M. Khurram Afzal, MD [2], Sogand Goudarzi, MD [3], Omer Kamal, M.D.[4]

    Overview

    Disseminated intravascular coagulation (DIC) must be differentiated from other diseases that cause symptoms of DVTand pulmonary embolismsuch as: factor V Leiden mutation, protein C deficiency, protein S deficiency, prothrombin gene mutation, antithrombin III deficiency, antiphospholipid antibody syndrome.

    Differential Diagnosis

    Differentiating different thrombophilias on the basis of symptoms, physical examination, and laboratory findings

    Disseminated intravascular coagulation (DIC) must be differentiated from other diseases that cause symptoms of DVT and pulmonary embolism such as:

    Diseases Clinical manifestations Para-clinical findings Gold standard Additional findings
    Symptoms Physical examination
    Lab Findings Imaging
    Symptoms of DVT Symptoms of Pulmonary Embolism Symptoms of Myocardial Infarction Tenderness in extremities Edema in extremities Warmth in extremities PT aPTT Doppler ultrasound Chest CT scan
    Antithrombin III deficiency[1][2][3] + + – + + + Normal
    • Normal
    • Reduces the Increase in PTT after administration of heparin
    Factor V Leiden mutation[4][5][6][7][8] + + + + + + N/A ↑
    • N/A
    • Inactivates factor Va and factor VIIIa
    Protein C deficiency[9][10][11] + + – + + + Normal Normal / ↑
    Protein S deficiency[11][12][13] + + – + + + Normal Normal / ↑
    Prothrombin gene mutation[14][15][16] + + – + + + ↑ N/A
    Disseminated intravascular coagulation (DIC)[17][18][19] + + +/- + + + ↑ ↑
    • N/A
    Antiphospholipid antibody syndrome[20][21][22][23][24] + + +/- + + + N/A ↑

    References

    1. ↑ Patnaik MM, Moll S (November 2008). “Inherited antithrombin deficiency: a review”. Haemophilia. 14 (6): 1229–39. doi:10.1111/j.1365-2516.2008.01830.x. PMID 19141163.
    2. ↑ Al Hadidi, Samer; Wu, Kristi; Aburahma, Ahmed; Alamarat, Zain (2017). “Family with clots: antithrombin deficiency”. BMJ Case Reports: bcr-2017–221556. doi:10.1136/bcr-2017-221556. ISSN 1757-790X.
    3. ↑ Konecny F (January 2009). “Inherited trombophilic states and pulmonary embolism”. J Res Med Sci. 14 (1): 43–56. PMC 3129068. PMID 21772860.
    4. ↑ Mannucci PM, Asselta R, Duga S, Guella I, Spreafico M, Lotta L, Merlini PA, Peyvandi F, Kathiresan S, Ardissino D (October 2010). “The association of factor V Leiden with myocardial infarction is replicated in 1880 patients with premature disease”. J. Thromb. Haemost. 8 (10): 2116–21. doi:10.1111/j.1538-7836.2010.03982.x. PMID 20626623.
    5. ↑ Campello E, Spiezia L, Simioni P (December 2016). “Diagnosis and management of factor V Leiden”. Expert Rev Hematol. 9 (12): 1139–1149. doi:10.1080/17474086.2016.1249364. PMID 27797270.
    6. ↑ Van Rooden CJ, Rosendaal FR, Meinders AE, Van Oostayen JA, Van Der Meer FJ, Huisman MV (February 2004). “The contribution of factor V Leiden and prothrombin G20210A mutation to the risk of central venous catheter-related thrombosis”. Haematologica. 89 (2): 201–6. PMID 15003896.
    7. ↑ Dentali F, Pomero F, Borretta V, Gianni M, Squizzato A, Fenoglio L; et al. (2013). “Location of venous thrombosis in patients with FVL or prothrombin G20210A mutations: systematic review and meta-analysis”. Thromb Haemost. 110 (1): 191–4. doi:10.1160/TH13-02-0163. PMID 23615845.
    8. ↑ Press RD, Bauer KA, Kujovich JL, Heit JA (November 2002). “Clinical utility of factor V leiden (R506Q) testing for the diagnosis and management of thromboembolic disorders”. Arch. Pathol. Lab. Med. 126 (11): 1304–18. doi:10.1043/0003-9985(2002)126<1304:CUOFVL>2.0.CO;2. PMID 12421138.
    9. ↑ Bernard Khor & Elizabeth M. Van Cott (2010). “Laboratory tests for protein C deficiency”. American journal of hematology. 85 (6): 440–442. doi:10.1002/ajh.21679. PMID 20309856. Unknown parameter |month= ignored (help)
    10. ↑ Pescatore SL (March 2001). “Clinical management of protein C deficiency”. Expert Opin Pharmacother. 2 (3): 431–9. doi:10.1517/14656566.2.3.431. PMID 11336597.
    11. ↑ 11.0 11.1 Gustavo A. Rodriguez-Leal, Segundo Moran, Roberto Corona-Cedillo & Rocio Brom-Valladares (2014). “Portal vein thrombosis with protein C-S deficiency in a non-cirrhotic patient”. World journal of hepatology. 6 (7): 532–537. doi:10.4254/wjh.v6.i7.532. PMID 25068006. Unknown parameter |month= ignored (help)
    12. ↑ Kristi J. Smock, Elizabeth A. Plumhoff, Piet Meijer, Peihong Hsu, Nicole D. Zantek, Nahla M. Heikal & Elizabeth M. Van Cott (2016). “Protein S testing in patients with protein S deficiency, factor V Leiden, and rivaroxaban by North American Specialized Coagulation Laboratories”. Thrombosis and haemostasis. 116 (1): 50–57. doi:10.1160/TH15-12-0918. PMID 27075008. Unknown parameter |month= ignored (help)
    13. ↑ Ji M, Yoon SN, Lee W, Jang S, Park SH, Kim DY, Chun S, Min WK (October 2011). “Protein S deficiency with a PROS1 gene mutation in a patient presenting with mesenteric venous thrombosis following total colectomy”. Blood Coagul. Fibrinolysis. 22 (7): 619–21. doi:10.1097/MBC.0b013e32834a0421. PMID 21799399.
    14. ↑ Cooper PC, Rezende SM (2007). “An overview of methods for detection of factor V Leiden and the prothrombin G20210A mutations”. Int J Lab Hematol. 29 (3): 153–62. doi:10.1111/j.1751-553X.2007.00892.x. PMID 17474891.
    15. ↑ McGlennen RC, Key NS (2002). “Clinical and laboratory management of the prothrombin G20210A mutation”. Arch Pathol Lab Med. 126 (11): 1319–25. doi:10.1043/0003-9985(2002)126<1319:CALMOT>2.0.CO;2. PMID 12421139.
    16. ↑ Dentali F, Pomero F, Borretta V, Gianni M, Squizzato A, Fenoglio L; et al. (2013). “Location of venous thrombosis in patients with FVL or prothrombin G20210A mutations: systematic review and meta-analysis”. Thromb Haemost. 110 (1): 191–4. doi:10.1160/TH13-02-0163. PMID 23615845.
    17. ↑ Venugopal A (September 2014). “Disseminated intravascular coagulation”. Indian J Anaesth. 58 (5): 603–8. doi:10.4103/0019-5049.144666. PMC 4260307. PMID 25535423.
    18. ↑ Makruasi N (November 2015). “Treatment of Disseminated Intravascular Coagulation”. J Med Assoc Thai. 98 Suppl 10: S45–51. PMID 27276832.
    19. ↑ Cui S, Fu Z, Feng Y, Xie X, Ma X, Liu T; et al. (2018). “The disseminated intravascular coagulation score is a novel predictor for portal vein thrombosis in cirrhotic patients with hepatitis B.” Thromb Res. 161: 7–11. doi:10.1016/j.thromres.2017.11.010. PMID 29178991.
    20. ↑ Lim W (2013). “Antiphospholipid syndrome”. Hematology Am Soc Hematol Educ Program. 2013: 675–80. doi:10.1182/asheducation-2013.1.675. PMID 24319251.
    21. ↑ Pengo V, Tripodi A, Reber G, Rand JH, Ortel TL, Galli M, De Groot PG (October 2009). “Update of the guidelines for lupus anticoagulant detection. Subcommittee on Lupus Anticoagulant/Antiphospholipid Antibody of the Scientific and Standardisation Committee of the International Society on Thrombosis and Haemostasis”. J. Thromb. Haemost. 7 (10): 1737–40. doi:10.1111/j.1538-7836.2009.03555.x. PMID 19624461.
    22. ↑ Lim W (2013). “Antiphospholipid syndrome”. Hematology Am Soc Hematol Educ Program. 2013: 675–80. doi:10.1182/asheducation-2013.1.675. PMID 24319251.
    23. ↑ Garcia D, Erkan D (2018). “Diagnosis and Management of the Antiphospholipid Syndrome”. N Engl J Med. 378 (21): 2010–2021. doi:10.1056/NEJMra1705454. PMID 29791828.
    24. ↑ Kornacki J, Wirstlein P, Skrzypczak J (2012). “[Assessment of uterine arteries Doppler in the first half of pregnancy in women with thrombophilia]”. Ginekol Pol. 83 (12): 916–21. PMID 23488294.

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    Epidemiology and Demographics

    Epidemiology and Demographics

    Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1];Associate Editor(s)-in-Chief: Omer Kamal, M.D.[2]

    Overview

    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.

    Epidemiology and Demographics

    Incidence

    • 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[1][2]
    • In 2010, the incidence of DIC was estimated to be 26.2 cases per 100,000 individuals worldwide.[3][4][5]

    Prevalence

    • The prevalence of DIC depends on the clinical settings, higher versus low acquity settings.
    • In 2013, the prevalence of DIC was estimated to be 46.8% (292/624) [6][7][8][9]

    Age

    • Patients of all age groups may develop DIC.

    Race

    • There is no racial predilection to DIC

    Gender

    • DIC affects men and women equally

    Developing Countries

    • The prevalence of DIC depends on the clinical settings, higher versus low acquity settings.

    References

    1. ↑ Levi M, Ten Cate H (August 1999). “Disseminated intravascular coagulation”. N. Engl. J. Med. 341 (8): 586–92. doi:10.1056/NEJM199908193410807. PMID 10451465.
    2. ↑ Sallah S, Wan JY, Nguyen NP, Hanrahan LR, Sigounas G (September 2001). “Disseminated intravascular coagulation in solid tumors: clinical and pathologic study”. Thromb. Haemost. 86 (3): 828–33. PMID 11583315.
    3. ↑ Singh B, Hanson AC, Alhurani R, Wang S, Herasevich V, Cartin-Ceba R, Kor DJ, Gangat N, Li G (May 2013). “Trends in the incidence and outcomes of disseminated intravascular coagulation in critically ill patients (2004-2010): a population-based study”. Chest. 143 (5): 1235–1242. doi:10.1378/chest.12-2112. PMID 23139140.
    4. ↑ Smith OP, White B, Vaughan D, Rafferty M, Claffey L, Lyons B, Casey W (November 1997). “Use of protein-C concentrate, heparin, and haemodiafiltration in meningococcus-induced purpura fulminans”. Lancet. 350 (9091): 1590–3. PMID 9393338.
    5. ↑ Gando S, Nanzaki S, Kemmotsu O (January 1999). “Disseminated intravascular coagulation and sustained systemic inflammatory response syndrome predict organ dysfunctions after trauma: application of clinical decision analysis”. Ann. Surg. 229 (1): 121–7. PMC 1191617. PMID 9923809.
    6. ↑ Gando S, Saitoh D, Ogura H, Fujishima S, Mayumi T, Araki T, Ikeda H, Kotani J, Kushimoto S, Miki Y, Shiraishi S, Suzuki K, Suzuki Y, Takeyama N, Takuma K, Tsuruta R, Yamaguchi Y, Yamashita N, Aikawa N (June 2013). “A multicenter, prospective validation study of the Japanese Association for Acute Medicine disseminated intravascular coagulation scoring system in patients with severe sepsis”. Crit Care. 17 (3): R111. doi:10.1186/cc12783. PMC 4056654. PMID 23787004.
    7. ↑ Hulka F, Mullins RJ, Frank EH (September 1996). “Blunt brain injury activates the coagulation process”. Arch Surg. 131 (9): 923–7, discussion 927–8. PMID 8790176.
    8. ↑ Gilbert WM, Danielsen B (June 1999). “Amniotic fluid embolism: decreased mortality in a population-based study”. Obstet Gynecol. 93 (6): 973–7. PMID 10362165.
    9. ↑ Sibai BM, Ramadan MK, Usta I, Salama M, Mercer BM, Friedman SA (October 1993). “Maternal morbidity and mortality in 442 pregnancies with hemolysis, elevated liver enzymes, and low platelets (HELLP syndrome)”. Am. J. Obstet. Gynecol. 169 (4): 1000–6. PMID 8238109.


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    Risk Factors

    Risk Factors

    Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Omer Kamal, M.D.[2]

    Overview

    Common risk factors in the development of DIC include trauma, sepsis, obstetric complications, cancers, and immunologic reactions

    Risk Factors

    Common risk factors in the development of DIC include:[1][2].[3][4][5]

    References

    1. ↑ Levi M, Ten Cate H (August 1999). “Disseminated intravascular coagulation”. N. Engl. J. Med. 341 (8): 586–92. doi:10.1056/NEJM199908193410807. PMID 10451465.
    2. ↑ Sallah S, Wan JY, Nguyen NP, Hanrahan LR, Sigounas G (September 2001). “Disseminated intravascular coagulation in solid tumors: clinical and pathologic study”. Thromb. Haemost. 86 (3): 828–33. PMID 11583315.
    3. ↑ Singh B, Hanson AC, Alhurani R, Wang S, Herasevich V, Cartin-Ceba R, Kor DJ, Gangat N, Li G (May 2013). “Trends in the incidence and outcomes of disseminated intravascular coagulation in critically ill patients (2004-2010): a population-based study”. Chest. 143 (5): 1235–1242. doi:10.1378/chest.12-2112. PMID 23139140.
    4. ↑ Smith OP, White B, Vaughan D, Rafferty M, Claffey L, Lyons B, Casey W (November 1997). “Use of protein-C concentrate, heparin, and haemodiafiltration in meningococcus-induced purpura fulminans”. Lancet. 350 (9091): 1590–3. PMID 9393338.
    5. ↑ Gando S, Nanzaki S, Kemmotsu O (January 1999). “Disseminated intravascular coagulation and sustained systemic inflammatory response syndrome predict organ dysfunctions after trauma: application of clinical decision analysis”. Ann. Surg. 229 (1): 121–7. PMC 1191617. PMID 9923809.


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    Screening

    Screening

    Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Omer Kamal, M.D.[2]

    Overview

    There is insufficient evidence to recommend routine screening for DIC as it does not suggest any changes in mortality except in sepsis

    Screening

    There is insufficient evidence to recommend routine screening for DIC as it does not suggest any changes in mortality except in sepsis [1]

    References

    1. ↑ Umemura Y, Yamakawa K, Hayakawa M, Hamasaki T, Fujimi S (January 2018). “Screening itself for disseminated intravascular coagulation may reduce mortality in sepsis: A nationwide multicenter registry in Japan”. Thromb. Res. 161: 60–66. doi:10.1016/j.thromres.2017.11.023. PMID 29202320.
    Natural History, Complications and Prognosis

    Natural History, Complications and Prognosis

    Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Omer Kamal, M.D.[2]

    Overview

    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.

    Natural History, Complications, and Prognosis

    Natural History

    • If left untreated, 40-80% patients with DIC may progress to develop organ dysfunction

    Complications

    Common complications of DIC include:

    Prognosis

    References

    1. ↑ Hulka F, Mullins RJ, Frank EH (September 1996). “Blunt brain injury activates the coagulation process”. Arch Surg. 131 (9): 923–7, discussion 927–8. PMID 8790176.
    2. ↑ Fourrier F, Chopin C, Goudemand J, Hendrycx S, Caron C, Rime A, Marey A, Lestavel P (March 1992). “Septic shock, multiple organ failure, and disseminated intravascular coagulation. Compared patterns of antithrombin III, protein C, and protein S deficiencies”. Chest. 101 (3): 816–23. PMID 1531791.
    3. ↑ Gando S, Nanzaki S, Kemmotsu O (January 1999). “Disseminated intravascular coagulation and sustained systemic inflammatory response syndrome predict organ dysfunctions after trauma: application of clinical decision analysis”. Ann. Surg. 229 (1): 121–7. PMC 1191617. PMID 9923809.
    4. ↑ Siegal T, Seligsohn U, Aghai E, Modan M (February 1978). “Clinical and laboratory aspects of disseminated intravascular coagulation (DIC): a study of 118 cases”. Thromb. Haemost. 39 (1): 122–34. PMID 580488.


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    Diagnosis

    Diagnosis

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    Treatment

    Treatment

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    See also

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