Etiology

Relative Frequencies of Etiologies of Disseminated Intravascular Coagulation (DIC)
Hematologic Disorder
- COVID-19 Vaccine-Induced Immune Thrombotic Thrombocytopenia
- Hemophagocytic Lymphohistiocytosis (HLH) (see Hemophagocytic Lymphohistiocytosis)
- Protein C Deficiency (see Protein C Deficiency)
- Epidemiology
- Hereditary Homozygous Protein C Deficiency Commonly Presents in Early Infancy with Purpura Fulminans, But Older Patients are Also Occasionally Seen
- In Contrast, Heterozygous Protein C Deficiency with Venous Thromboembolism Typically Does Not Have Disseminated Intravascular Coagulation (DIC) as a Component of its Pathogenesis
- Severe Acquired Protein C Deficiency (Such as May Cases Associated with Severe Meningococcal Infection) May Also Present with Purpura Fulminans
- Hereditary Homozygous Protein C Deficiency Commonly Presents in Early Infancy with Purpura Fulminans, But Older Patients are Also Occasionally Seen
- Clinical Features of Purpura Fulminans (see Purpura Fulminans)
- Disseminated Intravascular Coagulation (DIC)
- Extensive Tissue Thrombosis and Hemorrhagic Skin Necrosis
- Retiform Purpura with Branched or Angular Purpuric Lesions
- Epidemiology
- Heparin-Induced Thrombocytopenia (HIT) (Specific Types) (see Heparin-Induced Thrombocytopenia)
Infection
- Sepsis (see Sepsis)
- Viral Infection
- Severe Acute Respiratory Syndrome Coronavirus-2 (SARS-CoV-2) (see Severe Acute Respiratory Syndrome Coronavirus-2) (J Thromb Haemost, 2020) [MEDLINE]
- Bacterial Infection
- Fungal Infection
- Parasitic Infection
- Malaria (see Malaria) (Parasitol Res, 2008) [MEDLINE]
- Visceral Leishmaniasis (see Leishmaniasis) (Trop Doct, 2021) [MEDLINE]
- Viral Infection
Intravascular Hemolysis (see Hemolytic Anemia)
- Acute Hemolytic Transfusion Reaction (see Acute Hemolytic Transfusion Reaction)
- Malaria (see Malaria) (Parasitol Res, 2008) [MEDLINE]
Intravascular Device
- Cardiopulmonary Bypass (CPB) (see Cardiopulmonary Bypass)
- Diagnosis
- The Diagnosis of Disseminated Intravascular Coagulation (DIC) Post-Cardiopulmonary Bypass is Clinically Difficult (Since the Identification of Microthrombi is Difficult and Hemolysis and Consumption of Coagulation Factors May Be Commonly Observed Following Cardiopulmonary Bypass)
- Diagnosis
- Extracorporeal Membrane Oxygenation (ECMO) (see Extracorporeal Membrane Oxygenation)
Malignancy
- Acute Promyelocytic Leukemia (APML) (see Acute Promyelocytic Leukemia)
- Epidemiology
- Patient May Present with Disseminated Intravascular Coagulation (DIC) Acutely or After Initiation of Chemotherapy
- Epidemiology
- Brain Tumors
- NK Cell Leukemia (aka Aggressive NK Cell Leukemia, ANKL) (see NK Cell Leukemia)
- Mucinous Tumors
- Breast Cancer (see Breast Cancer)
- Gastric Cancer (see Gastric Cancer)
- Lung Cancer (see Lung Cancer)
- Ovarian Cancer (see Ovarian Cancer)
- Pancreatic Cancer (see Pancreatic Cancer)
- Prostate Cancer (see Prostate Cancer)
Obstetric Complications
- Acute Fatty Liver of Pregnancy (see Acute Fatty Liver of Pregnancy)
- Amniotic Fluid Embolism (see Amniotic Fluid Embolism)
- HELLP Syndrome (see HELLP Syndrome)
- Pre-Eclampsia/Eclampsia (see Pre-Eclampsia,Eclampsia)
- Retained Dead Fetus
Toxic
- Amphetamine Intoxication (see Amphetamine)
- Serotonin Syndrome (see Serotonin Syndrome)
- Snake Bite
- Rattlesnake Bite (see Rattlesnake Bite)
- However, Some Consider This to Be a Coagulopathy/Thrombotic Microangiopathy Which is Distinct from Disseminated Intravascular Coagulation (DIC) (Semin Thromb Hemost, 2010) [MEDLINE]
- Viper Bite
- Rattlesnake Bite (see Rattlesnake Bite)
Other
- Acute Solid Organ Transplant Rejection
- Liver Transplant Rejection (see Liver Transplant)
- Adult-Onset Still’s Disease (see Adult-Onset Still’s Disease)
- Aortic Aneurysm
- Abdominal Aortic Aneurysm (AAA) (see Abdominal Aortic Aneurysm)
- Thoracic Aortic Aneurysm (see Thoracic Aortic Aneurysm)
- Catastrophic Antiphospholipid Antibody Syndrome (see Antiphospholipid Antibody Syndrome)
- Crush Injury
- Cytokine Release Syndrome (see Cytokine Release Syndrome)
- Fat Embolism (see Fat Embolism)
- Heat Stroke (see Heat Stroke)
- Kaposiform Hemangioendothelioma
- Peritoneovenous Shunt (LeVeen Shunt) (see Peritoneovenous Shunt)
- Surgery
- Trauma
- Epidemiology
- Especially Trauma to the Central Nervous System
- Traumatic Brain Injury (TBI) (see Traumatic Brain Injury)
- Especially Trauma to the Central Nervous System
- Epidemiology
Physiology
XXXXXXXXXXXXXXXXXXXX
- xxxx
- xxxx
Diagnosis
General Comments
- Findings Such as Thrombocytopenia, Hypofibrinogenemia, and Elevated D-Dimer are Considered to Be Relatively Sensitive for the Diagnosis of Disseminated Intravascular Coagulation (DIC), But Not Specific
- However, Data from Clinical Trials Addressing Sensitivity and Specificity are Lacking
- Many of the Laboratory Abnormalities Used to Diagnose Disseminated Intravascular Coagulation (DIC) are Present in Normal Pregnancy
- Testing is Often Repeated Serially to Determine if Coagulation and Fibrinolysis are Worsening or Improving
- The Frequency of Repeat Testing Depends on the Severity of Clinical Findings
International Society of Thrombosis and Hemostasis Disseminated Intravascular Coagulation (DIC) Scoring System (Thromb Res, 2015) [MEDLINE] (Ann Lab Med, 2016) [MEDLINE]

General Comments
- The International Society of Thrombosis and Hemostasis (ISTH) Disseminated Intravascular Coagulation (DIC) Scoring System Utilizes Laboratory Features, Including the International Normalized Ratio (INR), Platelet Count, Fibrinogen Level, and D-Dimer
- Scoring System Has Been Validated, But is Not Widely Used
International Society of Thrombosis and Hemostasis Disseminated Intravascular Coagulation (DIC) Scoring System Adapted for Use in Pregnancy (PLoS One, 2014) [MEDLINE]
- Parameters
- Platelets <50k or 100-185k or Fibrinogen 400-450 mg/dL: 1 points
- Platelets 50k-100k: 2 points
- PT Difference 0.5-1.0: 5 points
- Fibrinogen 300-400 mg/dL): 6 points
- PT Difference 1-1.5: 12 points
- PT Difference >1.5 or Fibrinogen ≤300 mg/dL: 25 points
- Score
- Cutoff Point of ≥26 Had a Sensitivity of 88%, a Specificity of 96%, Positive Likelihood Ratio of 22, and a Negative Likelihood Ratio of 0.125 for the Diagnosis of Disseminated Intravascular Coagulation (DIC)
Differentiation of Disseminated Intravascular Coagulation (DIC) from Severe Liver Disease (see Cirrhosis)
- Liver Disease Severe Enough to Impair the Hepatic Synthesis of Coagulation Factors Can Result in a Severe Coagulopathy
- Severe Liver Disease is Associated with Decreases in Both Procoagulant and Anticoagulant Factors as Well as Thrombocytopenia (and Therefore, May Result in Bleeding or Thrombosis)
- Similar to Disseminated Intravascular Coagulation (DIC)
- The Decrease in Coagulation Factors and Thrombocytopenia in Severe Liver Disease are Due to a Combination of Hypersplenism and Thrombopoietin Deficiency
- Liver is the Primary Site of Thrombopoietin Synthesis
- Patients with Severe Liver Disease Typically Present with a Known Source of Liver Injury (Such as Acute Hepatitis or Alcoholic Cirrhosis) and Abnormal Liver Function Tests (Although the Transaminases May Appear to Normalize if Liver Synthetic Function is Severely Impaired)
- Dissimilar to Disseminated Intravascular Coagulation (DIC)
- Some Clinicians Utilize the Measurement of Factor VIII Levels to Aid in the Differentiation of Disseminated Intravascular Coagulation (DIC) from Severe Liver Disease, Since Factor VIII is Not Produced by Hepatocytes and Therefore, is Frequently Decreased in Disseminated Intravascular Coagulation (DIC) and Increased in Severe Liver Disease
- Severe Liver Disease is Associated with Decreases in Both Procoagulant and Anticoagulant Factors as Well as Thrombocytopenia (and Therefore, May Result in Bleeding or Thrombosis)
Differentiation of Disseminated Intravascular Coagulation (DIC) from Thrombotic Microangiopathy (TMA) (see xxxx)
- XXX
Differentiation of Disseminated Intravascular Coagulation (DIC) from Hemophagocytic Lymphohistiocytosis (HLH) (see Hemophagocytic Lymphohistiocytosis)
- Hemophagocytic Lymphohistiocytosis is an Aggressive, Life-Threatening Syndrome of Excessive Immune Activation Which, Untreated, Can Result in Tissue Damage and a High Mortality Rate
- Acute Illness with Cytopenias, Prolonged Clotting Times, Hypofibrinogenemia, and Increased D-Dimer May Be Present
- Similar to Disseminated Intravascular Coagulation (DIC)
- Patients May Also Have Fever, Hepatic Dysfunction, Neurologic Deficits, and Severe Hyperferritinemia
- Patients with Hemophagocytic Lymphohistiocytosis (HLH) Have Evidence of Immune Activation, with Pathogenic Variants in One of Several Immune Regulatory Genes and Often Including Low/Absent Natural Killer (NK) Cell Activity, Increased Soluble Interleukin 2 (IL-2) Receptor α (sCD25) and/or CXCL19
- Dissimilar to Disseminated Intravascular Coagulation (DIC)
- Patients with Hemophagocytic Lymphohistiocytosis (HLH) Typically Require Treatment Directed at the Underlying Etiology (if Present), as Well as Treatment Directed at Stopping the Immune Activation
- Dissimilar to Disseminated Intravascular Coagulation (DIC)
- Acute Illness with Cytopenias, Prolonged Clotting Times, Hypofibrinogenemia, and Increased D-Dimer May Be Present
Clinical Manifestations-Acute (Decompensated) Disseminated Intravascular Coagulation (DIC)
Candidate Precipitating Etiologies
- Acute Hemolytic Transfusion Reaction (see Acute Hemolytic Transfusion Reaction)
- Malignancy (Especially the Following)
- Acute Promyelocytic Leukemia (see Acute Promyelocytic Leukemia)
- Sepsis (see Sepsis)
- Trauma
Diagnosis
- General Comments
- The Most Impaired Coagulation Tests are the Prothrombin Iime/International Normalized Ratio (INR), Partial Thromboplastin Time, Thrombin Time, and the Platelet Count
- The Degree of Abnormality of These Coagulation Tests is Correlated to the Degree of Organ Involvement
- The Most Impaired Coagulation Tests are the Prothrombin Iime/International Normalized Ratio (INR), Partial Thromboplastin Time, Thrombin Time, and the Platelet Count
- Platelet Count (see Complete Blood Count)
- Decreased (see Thrombocytopenia)
- Platelet Count is Typically Mildly-Moderately Decreased
- Platelet Counts <20,000/μL are Less Commonly Observed
- Platelet Count is Typically Mildly-Moderately Decreased
- Decreased (see Thrombocytopenia)
- Prothrombin Time/International Normalized Ratio (INR) (see Prothrombin Time)
- Increased
- Partial Thromboplastin Time (PTT) (see Partial Thromboplastin Time)
- Increased
- Thrombin Time (see Thrombin Time)
- Increased
- Serum Fibrinogen (see Serum Fibrinogen)
- Decreased (see Hypofibrinogenemia)
- However, Since Patients with Sepsis/Malignancy/Other Inflammatory Disorders May Have Significantly Increased Fibrinogen Synthesis (as Fibrinogen is an Acute Phase Reactant), a Normal Plasma Fibrinogen Level May Represent a Substantial Consumption (and a Significant Abnormality) for that Patient Despite the Value Being in the Normal Range
- Decreased (see Hypofibrinogenemia)
- Decreased Procoagulant Factors
- Plasma Factor II (Thrombin)
- Decreased
- Plasma Factor V (see Plasma Factor V)
- Decreased
- Plasma Factor VIII (see Plasma Factor VIII)
- Decreased (see Decreased Plasma Factor VIII)
- Since Factor VIII is Not Synthesized by the Liver, it is Often High in the Setting of Liver Disease, But is Decreased in the Setting of Disseminated Intravascular Coagulation (DIC)
- Decreased (see Decreased Plasma Factor VIII)
- Plasma Factor X (see Plasma Factor X)
- Decreased
- Plasma Factor II (Thrombin)
- Decreased Coagulation Inhibitors
- Antithrombin (see Plasma Antithrombin)
- Decreased
- Protein C
- Decreased
- Protein S
- Decreased
- Antithrombin (see Plasma Antithrombin)
- Fibrin Degradation Products (FDP)
- Increased (Due to Fibrinolysis) (see Increased Fibrin Degradation Products)
- Plasma D-Dimers (see Plasma D-Dimers)
- Increased (Due to Fibrinolysis) (see Increased Plasma D-Dimers)
- Peripheral Blood Smear (see Peripheral Blood Smear)
- Changes Consistent with Microangiopathic Hemolytic Anemia (MAHA) (see Hemolytic Anemia): schistocytes, helmet cells, etc
- Microangiopathic Changes May Be Less Pronounced than Those Observed in Other Thrombotic Microangiopathies (such as Thrombotic Thrombocytopenic Purpura, TTP)
- Severe Anemia Due to Microangiopathic Hemolytic Anemia is Uncommon (Although Most of the Underlying Etiologies of Disseminated Intravascular Coagulation Can Cause Anemia by Other Mechanisms, Such as Bone Marrow Suppression, Anemia of Chronic Disease/Inflammation, etc)
- Changes Consistent with Microangiopathic Hemolytic Anemia (MAHA) (see Hemolytic Anemia): schistocytes, helmet cells, etc

Clinical
General Comments
- In Trauma-Associated Cases, Pulmonary Dysfunction is Common, While Hepatic/Renal Dysfunction are Rare (Thromb Haemost, 1978) [MEDLINE]
- In Contrast, in Infection-Associated Cases, Hepatic/Renal Dysfunction are Common, While Pulmonary Dysfunction is Rare (Thromb Haemost, 1978) [MEDLINE]
- This Variability Indicates that the Clinical Manifestations are Affected Not Only by the Process of Intravascular Coagulation, But Also by the Underlying Clinical Disorder
Hemorrhage
- General Comments
- Hemorrhage is More Common in Acute Disseminated Intravascular Coagulation (DIC) Than in Chronic Disseminated Intravascular Coagulation (DIC)
- Hemorrhage Occurs in 64% of Acute Disseminated Intravascular Coagulation (DIC) Cases (Thromb Haemost, 1978) [MEDLINE]
- Hemorrhage is More Common in Acute Disseminated Intravascular Coagulation (DIC) Than in Chronic Disseminated Intravascular Coagulation (DIC)
- Sites of Hemorrhage
- Diffuse Alveolar Hemorrhage (DAH) (see Diffuse Alveolar Hemorrhage)
- Due to Damage to the Pulmonary Vascular Endothelium
- Ecchymosis (see Ecchymosis)
- Gastrointestinal Hemorrhage (see Gastrointestinal Hemorrhage)
- Hemorrhage from Wound/Trauma/Catheter/Drain Sites
- Hemorrhage into Serous Cavity (in Cases of Postoperative Disseminated Intravascular Coagulation)
- Hemoperitoneum (see Hemoperitoneum)
- Retroperitoneal Hemorrhage (see Retroperitoneal Hemorrhage)
- Intracranial Hemorrhage
- Mucosal Hemorrhage
- Petechiae (see Petechiae)
- Diffuse Alveolar Hemorrhage (DAH) (see Diffuse Alveolar Hemorrhage)
Thrombosis
- General Comments
- Thrombosis is More Common in Chronic Disseminated Intravascular Coagulation (DIC) than in Acute Disseminated Intravascular Coagulation (DIC)
- Thrombosis Occurs in Only 7% of Acute Disseminated Intravascular Coagulation (DIC) Cases (Thromb Haemost, 1978) [MEDLINE]
- Thrombosis is More Common in Chronic Disseminated Intravascular Coagulation (DIC) than in Acute Disseminated Intravascular Coagulation (DIC)
- Clinical Types
- Arterial Thrombosis (Especially without a Clear Precipitating Factor) with Organ Ischemia
- Nonbacterial Thrombotic Endocarditis (Marantic Endocarditis, Libman-Sacks Endocarditis, Verrucous Endocarditis) (see Nonbacterial Thrombotic Endocarditis)
- Superficial Migratory Thrombophlebitis (Trousseau’s Syndrome) (see Superficial Venous Thrombosis)
- Venous Thromboembolism (Especially without a Clear Precipitating Factor)
- Acute Pulmonary Embolism (PE) (see Acute Pulmonary Embolism)
- Deep Venous Thrombosis (DVT) (see Deep Venous Thrombosis)
Organ Dysfunction
- Cardiovascular Dysfunction
- Shock
- Epidemiology
- Shock Occurs in 14% of Acute Disseminated Intravascular Coagulation (DIC) Cases (Thromb Haemost, 1978) [MEDLINE]
- Clinical
- Hypotension (see Hypotension)
- Epidemiology
- Shock
- Central Nervous System Dysfunction (Coma, Delirium, Transient Focal Neurologic Symptoms)
- Epidemiology
- Central Nervous System Dysfunction Occurs in 2% of Acute Disseminated Intravascular Coagulation (DIC) Cases (Thromb Haemost, 1978) [MEDLINE]
- Mechanisms
- Central Nervous System Microthrombi
- Hemorrhage
- Hypoperfusion
- Clinical
- Coma (see Obtundation-Coma)
- Delirium (see Delirium)
- Transient Focal Neurologic Deficits
- Epidemiology
- Endocrine Dysfunction
- Clinical
- Adrenal Dysfunction/Waterhouse-Friderichsen Syndrome (see Adrenal Insufficiency)
- Mechanism
- Adrenal Hemorrhage or Infarction
- Adrenal Dysfunction/Waterhouse-Friderichsen Syndrome (see Adrenal Insufficiency)
- Clinical
- Hepatic Dysfunction
- Epidemiology
- Hepatic Dysfunction Occurs in 19% of Acute Disseminated Intravascular Coagulation (DIC) Cases (Thromb Haemost, 1978) [MEDLINE]
- Clinical
- Preexisting Liver Disease Can Exacerbate Disseminated Intravascular Coagulation (DIC) by Impairing Hepatic Synthesis and/or Clearance of Coagulation Factors
- Epidemiology
- Pulmonary Dysfunction
- Mechanism
- Pulmonary Microthrombi
- Clinical
- Acute Respiratory Distress Syndrome (ARDS) (see Acute Respiratory Distress Syndrome)
- Acute Respiratory Distress Syndrome (ARDS) Occurs in 16% of Acute Disseminated Intravascular Coagulation (DIC) Cases (Thromb Haemost, 1978) [MEDLINE]
- Hypoxemia (see Hypoxemia)
- Acute Respiratory Distress Syndrome (ARDS) (see Acute Respiratory Distress Syndrome)
- Mechanism
- Renal Dysfunction
- Clinical
- Acute Kidney Injury (AKI) (see Acute Kidney Injury)
- Acute Kidney Injury Occurs in 25% of Acute Disseminated Intravascular Coagulation (DIC) Cases (Thromb Haemost, 1978) [MEDLINE]
- Clinical
Prognosis
- The mortality (overall 54.7%) increased independently with age, with the number of clinical manifestations and with the degree of abnormality of the above-mentioned four most impaired coagulation tests (Thromb Haemost, 1978) [MEDLINE]
- In addition, older patients were more likely to have an increased number of clinical manifestations and more impaired coagulation tests
- Mortality was similar in the various etiologies except for trauma patients in whom it was lower (30%)
Clinical Manifestations-Chronic (Compensated) Disseminated Intravascular Coagulation (DIC)
Candidate Precipitating Etiology
- Malignancy (Especially the Following)
- Brain Tumors
- XXXX (see xxxx)
- Gastric Cancer (see Gastric Cancer)
- Ovarian Cancer (see Ovarian Cancer)
- Pancreatic Cancer (see Pancreatic Cancer)
- Brain Tumors
Diagnosis
- Platelet Count
- Variable
- Prothrombin Time/International Normalized Ratio (INR) (see Prothrombin Time)
- Normal
- Partial Thromboplastin Time (PTT) (see Partial Thromboplastin Time)
- Normal
- Thrombin Time (see Thrombin Time)
- Normal-Slightly Increased
- Thrombin Time is More Sensitive than INR/PTT to the Effects of Increased D-Dimers and Fibrin Degradation Products in Chronic Disseminated Intravascular Coagulation (DIC)
- Serum Fibrinogen (see Serum Fibrinogen)
- Normal-Slightly Increased (see Hyperfibrinogenemia)
- Plasma Factor V (see Plasma Factor V)
- Normal
- Plasma Factor VIII (see Plasma Factor VIII)
- Normal
- Fibrin Degradation Products (FDP)
- Increased (Due to Fibrinolysis) (see Increased Fibrin Degradation Products)
- Plasma D-Dimers (see Plasma D-Dimers)
- Increased (Due to Fibrinolysis) (see Increased Plasma D-Dimers)
- Peripheral Blood Smear (see Peripheral Blood Smear)
- Changes Consistent with Microangiopathic Hemolytic Anemia (MAHA) (see Hemolytic Anemia): schistocytes, helmet cells, etc
- Microangiopathic Changes May Be Less Pronounced than Those Observed in Other Thrombotic Microangiopathies (such as Thrombotic Thrombocytopenic Purpura, TTP)
- Severe Anemia Due to Microangiopathic Hemolytic Anemia is Uncommon (Although Most of the Underlying Etiologies of Disseminated Intravascular Coagulation Can Cause Anemia by Other Mechanisms, Such as Bone Marrow Suppression, Anemia of Chronic Disease/Inflammation, etc)
- Changes Consistent with Microangiopathic Hemolytic Anemia (MAHA) (see Hemolytic Anemia): schistocytes, helmet cells, etc
Clinical
Chronic Disseminated Intravascular Coagulation (DIC) May Be Asymptomatic
- xx
Hemorrhage
- General Comments
- Hemorrhage is More Common in Acute Disseminated Intravascular Coagulation (DIC) Than in Chronic Disseminated Intravascular Coagulation (DIC)
Thrombosis
- General Comments
- Thrombosis is More Common in Chronic Disseminated Intravascular Coagulation (DIC) Than in Acute Disseminated Intravascular Coagulation (DIC)
- Typically in the Setting of a Solid Tumor
- Thrombosis is More Common in Chronic Disseminated Intravascular Coagulation (DIC) Than in Acute Disseminated Intravascular Coagulation (DIC)
- Clinical Types
- Arterial Thrombosis (Especially without a Clear Precipitating Factor) with Organ Ischemia
- Nonbacterial Thrombotic Endocarditis (Marantic Endocarditis, Libman-Sacks Endocarditis, Verrucous Endocarditis) (see Nonbacterial Thrombotic Endocarditis)
- Superficial Migratory Thrombophlebitis (Trousseau’s Syndrome) (see Superficial Venous Thrombosis)
- Venous Thromboembolism (Especially without a Clear Precipitating Factor)
- Acute Pulmonary Embolism (PE) (see Acute Pulmonary Embolism)
- Deep Venous Thrombosis (DVT) (see Deep Venous Thrombosis)
Treatment
Treat Underlying Etiology
- Most Important Treatment Modality
Supportive Care
- Hemodynamic Support (Pressors, Intravenous Fluids): as required
- Mechanical Ventilation: as required
Treatment of Thrombotic Complications
- Anticoagulation: as required to treat thrombotic complications
Treatment of Bleeding Complications
- Antifibrinolytic Agents (Tranexamic Acid, Epsilon-Aminocaproic Acid, Aprotinin): contraindicated (since blockade of the fibrinolytic system may increase the risk of thrombosis)
- However, these agents may be used in patients who have severe bleeding associated with a hyperfibrinolytic state
- Antithombin: trials have shown this to be ineffective in DIC
- Cryoprecipitate (see Cryoprecipitate)
- Indication: fibrinogen <100 mg/dL
- One unit of cryoprecipitate (10-20 ml) contains the cold insoluble protein from one unit of FFP (contains vWF, factor VIII, factor XIII, fibrinogen, and fibrinonectin)
- Some blood suppliers now provide one bag of pre-pooled cryoprecipitate which contains 5 (or more) units in 120-160 mL: use two bags of pre-pooled cryoprecipitate (ie: from 10 units of FFP)
- Fresh Frozen Plasma (FFP) (see Fresh Frozen Plasma): as required to treat coagulopathy in the setting of significant hemorrhage or need for invasive procedures
- Packed Red Blood Cells (see Packed Red Blood Cells): as required to treat hemorrhage-related anemia
- Platelet Transfusion (see Platelet Transfusion)
- Transfuse for Platelet Count <50k: in the setting of significant hemorrhage or need for invasive procedures
- Transfuse for Platelet Count <10k: in all patients (due to the risk of spontaneous hemorrhage)
- Prothrombin Complex Concentrates: likely contraindicated (due to risk of more thrombotic complications in the setting of an already hypercoagulable state)
Treatment of Purpura Fulminans (see Purpura Fulminans)
- Fresh Frozen Plasma (FFP) (see Fresh Frozen Plasma): the administration of FFP as a source of protein C is problematic because of the short plasma half-life of protein C
- Due to short plasma protein C half-life, FFP 2-3 units may be administered approximately every 6 hrs
- Protein C Concentrate (see Protein C Concentrate): proven to decrease mortality rate in purpura fulminans
Expected Course of Resolution
- Factors Impacting the Rate of DIC Resolution: DIC does not usually resolve immediately once the inciting factor is corrected
- Resolution requires the synthesis of coagulant factors (which are synthesized at different rates)
- Resolution requires hepatic clearance of anticoagulant factors and fibrin degradation products
- Resolution requires bone marrow production of new platelets (which may take several days)
- Resolution of DIC-Related Laboratory abnormalities: usually improve within a few days after the inciting stimulus is removed
- Impact of Renal Failure on the Rate of DIC Resolution: does not impact the rate DIC resolution (unless there is a component of hepatorenal syndrome or if the kidneys are a major site of thrombosis)
References
General
- xxx
Diagnosis
- Clinical and laboratory aspects of disseminated intravascular coagulation (DIC): a study of 118 cases. Thromb Haemost. 1978;39(1):122 [MEDLINE]
- Management of disseminated intravascular coagulation: a survey of the International Society on Thrombosis and Haemostasis. Thromb Res. 2015;136(2):239 [MEDLINE]
- Current Pathological and Laboratory Considerations in the Diagnosis of Disseminated Intravascular Coagulation. Ann Lab Med. 2016;36(6):505 [MEDLINE]
Clinical
- Clinical and laboratory aspects of disseminated intravascular coagulation (DIC): a study of 118 cases. Thromb Haemost. 1978;39(1):122 [MEDLINE]