Difference between revisions of "Disseminated intravascular coagulation"
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==Diagnosis== | ==Diagnosis== | ||
===Acute=== | ===Acute=== | ||
| − | * | + | *Platelets<ref>Spero JA, Lewis JH, Hasiba U. Disseminated intravascular coagulation. Findings in 346 patients. Thromb Haemost. 1980 Feb 29. 43(1):28-33.</ref> |
| − | **Low (or dropping) | + | **Low (or dropping) in 98% of DIC pts |
**Sn, not Sp | **Sn, not Sp | ||
| − | *PT | + | **Repeat platelets may be necessary if first level normal or if need to trend |
| + | *PT and PTT | ||
**Prolonged | **Prolonged | ||
| + | **May be normal in as many as 50% of DIC pts<ref>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.</ref> | ||
| + | **Serial coagulation testing may be necessary | ||
| + | **PT, not INR, is used for monitoring<ref>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.</ref> | ||
*Fibrinogen | *Fibrinogen | ||
**Low | **Low | ||
**<100 correlates w/ severe DIC | **<100 correlates w/ severe DIC | ||
| − | **May be normal (acute phase reactant) | + | **May be normal (acute phase reactant), up to 57% in DIC pts<ref>Spero JA, Lewis JH, Hasiba U. Disseminated intravascular coagulation. Findings in 346 patients. Thromb Haemost. 1980 Feb 29. 43(1):28-33.</ref> |
| − | |||
| − | |||
*FDP | *FDP | ||
**Elevated | **Elevated | ||
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**Elevated | **Elevated | ||
**Sn but not Sp: may also see in pts w/ chronic liver or renal disease | **Sn but not Sp: may also see in pts w/ chronic liver or renal disease | ||
| + | **Combination of elevated FDP and d-dimer may increase sensitivity and specificity | ||
*RBCs | *RBCs | ||
**Fragmented (not specific) | **Fragmented (not specific) | ||
Revision as of 21:25, 20 February 2016
Contents
Background
- 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
- Infection (most common cause)
- Carcinoma
- Leukemia
- Trauma
- Brain injury, crush injury, burns, rhabdo, fat embolism
- Liver disease
- Pregnancy
- Abruption, Amniotic Fluid Embolus, septic abortion, HELLP syndrome
- Snake bite
- ARDS
- Transfusion reaction
Clinical Features
In given pt either bleeding or thrombosis will 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
- Severe liver disease
- Also a/w prolonged PT/PTT, thrombocytopenia, incr D-dimer, incr FDPs
- However, D-dimer is usually only mildly elevated
- Also a/w prolonged PT/PTT, thrombocytopenia, incr D-dimer, incr FDPs
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
Thrombocytopenia
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
Drug Induced
- sulfa antibiotics, ETOH, ASA, thiazide diuretics/furosemide
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
Platelet Related
- Too few
- Nonfunctional
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
Diagnosis
Acute
- Platelets[1]
- Low (or dropping) in 98% of DIC pts
- Sn, not Sp
- Repeat platelets may be necessary if first level normal or if need to trend
- PT and PTT
- Fibrinogen
- Low
- <100 correlates w/ severe DIC
- May be normal (acute phase reactant), up to 57% in DIC pts[4]
- FDP
- Elevated
- D-dimer
- Elevated
- Sn but not Sp: may also see in pts w/ 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
Treatment
- 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 w/ bleeding or <20K without bleeding
- FFP
- 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
See Also
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.