Difference between revisions of "Disseminated intravascular coagulation"
 
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==Background==
 
==Background==
−
#Widespread and inappropriate activation of the coagulation and fibrinolytic systems
+
*Abbreviation = DIC
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##Thrombosis
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*Widespread and inappropriate activation of the coagulation and fibrinolytic systems
−
###Tissue factor activation -> thrombin -> fibrin clots in microcirculation
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**Exposure of blood to procoagulants such as tissue factor and cancer procoagulant
−
####Activation of the coagulation system leads to consumption of plts and coag factors
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**Formation of fibrin within the circulation
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##Bleeding
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**Fibrinolysis
−
###Thrombin/fibrin actives tPA and the fibrinolytic system
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**Depletion of clotting factors
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####Degree of fibrinolysis can be excessive -> bleeding
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**End-organ damage
 +
*Chronic DIC occurs when hepatic/bone marrow production balances coag factor consumption
  
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==Causes==
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===Causes===
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#Infection
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*[[Sepsis]](most common cause)
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##Most common cause of DIC
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*Carcinoma
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##10%–20% of pts w/ Gram-neg sepsis have DIC
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*[[Leukemia]]
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###Septic pts more likely to have bleeding than thrombosis
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*[[Trauma]]
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##More likely to develop in asplenic pts or cirrhosis
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*[[Pancreatitis]]
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#Carcinoma
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**Brain injury, [[crush injury]], [[burns]], [[rhabdomyolysis]], [[fat embolism]]
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##DIC is often chronic and compensated
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*[[hepatic failure|Liver disease]]
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##Thrombosis is more common than bleeding
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*[[Pregnancy]]-related
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#Leukemia
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**[[Placental Abruption]], [[Amniotic Fluid Embolus]], [[septic abortion]], [[HELLP Syndrome]], [[acute fatty liver of pregnancy]]
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##More likely to have bleeding than thrombosis
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*[[Snake bite]]
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#Trauma
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*[[ARDS]]
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##Brain injury, crush injury, burns, rhabdo, fat embolism
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*[[Transfusion reaction]]
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#Liver disease
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*[[Transplant complications|Transplant rejection]]
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##May have chronic compensated DIC; acute DIC may occur in setting of acute liver failure
 
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#Pregnancy
 
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##Abruption, amniotic fluid embolus, septic abortion, HELLP syndrome
 
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#Envenomation
 
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##Rattlesnakes and other vipers
 
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##Bleeding not as serious as expected from lab values
 
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#ARDS
 
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##20% of pts with ARDS develop DIC; 20% of pts with DIC develop ARDS
 
−
#Transfusion reactions
 
  
 
==Clinical Features==
 
==Clinical Features==
 +
''[[hemorrhage|Bleeding]] or [[thromboembolism|thrombosis]] can predominate (bleeding is more common ~65%)''
 +
*[[Shoc]]k (15%)
 +
*[[Acute renal failure]] (25-40%)
 +
*[[hepatic failure|Hepatic dysfunction]] (19%)
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*Respiratory dysfunction (16%)
 +
*[[Thromboembolism]] (7%)
 +
*CNS involvement (2%)
 +
*[[Purpura fulminans]] (widespread arterial and venous thromboses)
 +
**Associated with significant [[bacteremia]]
  
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==Diagnosis==
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==Differential Diagnosis==
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#PT high
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{{Hemolytic anemia DDX}}
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#PTT high
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{{Thrombocytopenia}}
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#Platlet low
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{{Increased bleeding DDX}}
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#Fibrinogen low
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{{Bullous rashes DDX}}
−
#FDP high
 
−
#D-dimer high
 
−
#RBCs fragmented
 
  
 +
==Evaluation==
 +
===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>
 +
**[[thrombocytopenia|Low]] (or dropping) in 98% of DIC patients
 +
**Sn, not Sp
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**Repeat platelets may be necessary if first level normal or if need to trend
 +
*PT and PTT
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**[[coagulopathy|Prolonged]]
 +
**May be normal in as many as 50% of DIC patients<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
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**Low
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**<100 correlates with severe DIC
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**May be normal (acute phase reactant), up to 57% in  DIC patients<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
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**Elevated
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*[[D-dimer]]
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**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)
  
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==Treatment==
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===Chronic===
−
See Heme: Bleeding Treatment
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*FDP: Elevated
 +
*[[D-dimer]]: Elevated
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*Platelet: Variable
 +
*Fibrinogen: Normal-elevated
 +
*PT: Normal
 +
*PTT: Normal
 +
*RBCs
 +
**Fragmented
  
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==Source ==
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==Management==
−
1/26/06 DONALDSON (addapted from Tintinalli)
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*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]]
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****Consider repletion if <50K with bleeding or <20K without bleeding
 +
***[[FFP]]
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****Consider repletion to goal of PT and PTT < 1.5 times the normal limit
 +
***[[Vitamin K]]
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***[[Folate]]
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**[[Heparin]]
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***Consider only if thromboembolic are predominant symptoms from chronic DIC
  
 +
==Disposition==
 +
*Admit
 +
 +
==See Also==
 +
*[[Coagulopathy (Main)]]
 +
 +
==References==
 +
<references/>
 
[[Category:Heme/Onc]]
 
[[Category:Heme/Onc]]

Latest revision as of 00:24, 1 October 2019

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

Clinical Features

Bleeding or thrombosis can predominate (bleeding is more common ~65%)

Differential Diagnosis

Microangiopathic Hemolytic Anemia (MAHA)

Thrombocytopenia

Decreased production

Increased platelet destruction or use

Drug Induced

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

Factor Related

Vesiculobullous rashes

Febrile

Afebrile

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
    • Prolonged
    • May be normal in as many as 50% of DIC patients[2]
    • Serial coagulation testing may be necessary
    • PT, not INR, is used for monitoring[3]
  • 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
      • 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
    • Heparin
      • Consider only if thromboembolic are predominant symptoms from chronic DIC

Disposition

  • Admit

See Also

References

  1. ↑ Spero JA, Lewis JH, Hasiba U. Disseminated intravascular coagulation. Findings in 346 patients. Thromb Haemost. 1980 Feb 29. 43(1):28-33.
  2. ↑ 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.
  3. ↑ 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.
  4. ↑ 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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