Disseminated intravascular coagulation
Background
- Abbreviation = DIC
- Widespread and inappropriate activation of the coagulation and fibrinolytic systems
- Exposure of blood to procoagulants such as tissue factor and cancer procoagulant
- Formation of fibrin within the circulation
- Fibrinolysis
- Depletion of clotting factors
- End-organ damage
- Chronic DIC occurs when hepatic/bone marrow production balances coag factor consumption
Causes
- Sepsis(most common cause)
- Carcinoma
- Leukemia
- Trauma
- Pancreatitis
- Brain injury, crush injury, burns, rhabdomyolysis, fat embolism
- Liver disease
- Pregnancy-related
- Placental Abruption, Amniotic Fluid Embolus, septic abortion, HELLP Syndrome, acute fatty liver of pregnancy
- Snake bite
- ARDS
- Transfusion reaction
- Transplant rejection
Clinical Features
Bleeding or thrombosis can predominate (bleeding is more common ~65%)
- Shock (15%)
- Acute renal failure (25-40%)
- Hepatic dysfunction (19%)
- Respiratory dysfunction (16%)
- Thromboembolism (7%)
- CNS involvement (2%)
- Purpura fulminans (widespread arterial and venous thromboses)
- Associated with significant bacteremia
Differential Diagnosis
Microangiopathic Hemolytic Anemia (MAHA)
- Disseminated Intravascular Coagulation (DIC)
- Thrombotic Thrombocytopenic Purpura (TTP)
- Hemolytic Uremic Syndrome (HUS)
- HELLP syndrome
- Heparin-Induced Thrombocytopenia (HIT)
- Hereditary spherocytosis
- Paroxysmal nocturnal hemoglobinuria (PNH)
- Malignant hypertension
- Scleroderma
- Antiphospholipid Syndrome (APS)
- Other medical causes: malignancy, renal allograft rejection, vasculitides like polyarteritis nodosa and Wegener's granulomatosis
- Drugs: chemotherapy; Clopidogrel (Plavix) associated with TTP
- Nonvascular causes: prosthetic valve (more common with mechanical, more common at aortic valve), LVAD, TIPS, coil embolization, patched AV shunt, AVM
Decreased production
- Marrow infiltration (tumor or infection)
- Viral infections (rubella, HIV)
- Marrow suppression (commonly chemotherapy or radiation)
- Congenital thrombocytopenia
- Fanconi anemia
- Alport syndrome
- Bernand Soulier
- Vitamin B12 and/or folate deficiency
Increased platelet destruction or use
- Idiopathic thrombocytopenic purpura
- Thrombotic Thrombocytopenic Purpura (TTP)
- Hemolytic Uremic Syndrome (HUS)
- Disseminated Intravascular Coagulation (DIC)
- Viral infections (HIV, mumps, varicella, EBV)
- Drugs (heparin, protamine)
- Postransfusion or Posttransplantation
- Autoimmune destruction (SLE or Sarcoidosis)
- Mechanical destruction
- Artificial valves
- ECMO
- HELLP syndrome
- Excessive hemorrhage
- Hemodialysis, extracorporeal circulation
- Splenic Sequestration
- Occurs in Sickle cell disease and Cirrhosis
Comparison by Etiology
| ITP | TTP | HUS | HIT | DIC | |
|---|---|---|---|---|---|
| ↓ PLT | Yes | Yes | Yes | Yes | Yes |
| ↑PT/INR | No | No | No | +/- | Yes |
| MAHA | No | Yes | Yes | No | Yes |
| ↓ Fibrinogen | No | No | No | No | Yes |
| Ok to give PLT | Yes | No | No | No | Yes |
Coagulopathy
Factor Related
- Acquired (Drug Related)
- Warfarin (Coumadin)
- Unfractionated heparin
- Low molecular weight heparin (i.e. enoxaparin (Lovenox), dalteparin)
- Factor Xa Inhibitors (e.g. rivaroxaban, apixaban, fondaparinux, edoxaban)
- Direct thrombin inhibitors (e.g. dabigatran, argatroban, bivalirudin)
- Illness induced
- Genetic
Vesiculobullous rashes
Febrile
- Diffuse distribution
- Localized distribution
Afebrile
- Diffuse distribution
- Bullous pemphigoid
- Drug-Induced bullous disorders
- Pemphigus vulgaris
- Phytophotodermatitis
- Erythema multiforme major
- Bullous impetigo
- Localized distribution
- Contact dermatitis
- Herpes zoster
- Dyshidrotic eczema
- Burn
- Dermatitis herpetiformis
- Erythema multiforme minor
- Poison Oak, Ivy, Sumac dermatitis
- Bullosis diabeticorum
- Bullous impetigo
- Folliculitis
Evaluation
Acute
- Platelets[1]
- Low (or dropping) in 98% of DIC patients
- Sn, not Sp
- Repeat platelets may be necessary if first level normal or if need to trend
- PT and PTT
- Fibrinogen
- Low
- <100 correlates with severe DIC
- May be normal (acute phase reactant), up to 57% in DIC patients[4]
- FDP
- Elevated
- D-dimer
- Elevated
- Sn but not Sp: may also see in patients with chronic liver or renal disease
- Combination of elevated FDP and d-dimer may increase sensitivity and specificity
- RBCs
- Fragmented (not specific)
Chronic
- FDP: Elevated
- D-dimer: Elevated
- Platelet: Variable
- Fibrinogen: Normal-elevated
- PT: Normal
- PTT: Normal
- RBCs
- Fragmented
Management
- Treat underlying illness
- Replacement treatment
- Only indicated in with documented DIC + bleeding or impending procedure
- Fibrinogen
- Consider repletion with cryoprecipitate to raise level to 100-150
- Platelets
- Consider repletion if <50K with bleeding or <20K without bleeding
- FFP
- Consider repletion to goal of PT and PTT < 1.5 times the normal limit
- Vitamin K
- Folate
- Fibrinogen
- Heparin
- Consider only if thromboembolic are predominant symptoms from chronic DIC
- Only indicated in with documented DIC + bleeding or impending procedure
Disposition
- Admit
See Also
- Coagulopathy (Main)
References
- Spero JA, Lewis JH, Hasiba U. Disseminated intravascular coagulation. Findings in 346 patients. Thromb Haemost. 1980 Feb 29. 43(1):28-33.
- Olson JD, Kaufman HH, Moake J, O'Gorman TW, Hoots K, Wagner K, et al. The incidence and significance of hemostatic abnormalities in patients with head injuries. Neurosurgery. 1989 Jun. 24(6):825-32.
- Levi M, Toh CH, Thachil J, Watson HG. Guidelines for the diagnosis and management of disseminated intravascular coagulation. British Committee for Standards in Haematology. Br J Haematol. 2009 Apr. 145(1):24-33.
- Spero JA, Lewis JH, Hasiba U. Disseminated intravascular coagulation. Findings in 346 patients. Thromb Haemost. 1980 Feb 29. 43(1):28-33.
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