Disseminated intravascular coagulation: Difference between revisions

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==Background==
==Background==
#Widespread and inappropriate activation of the coagulation and fibrinolytic systems
*Abbreviation = DIC
##Thrombosis
*Widespread and inappropriate activation of the coagulation and fibrinolytic systems
###Tissue factor activation -> thrombin -> fibrin clots in microcirculation
**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
**Formation of fibrin within the circulation
##Bleeding
**Fibrinolysis
###Thrombin/fibrin actives tPA and the fibrinolytic system
**Depletion of clotting factors
####Degree of fibrinolysis can be excessive -> bleeding
**End-organ damage
*Chronic DIC occurs when hepatic/bone marrow production balances coag factor consumption


==Causes==
===Causes===
#Infection
*[[Sepsis]](most common cause)
##Most common cause of DIC
*Carcinoma
##10%–20% of pts w/ Gram-neg sepsis have DIC
*[[Leukemia]]
###Septic pts more likely to have bleeding than thrombosis
*[[Trauma]]
##More likely to develop in asplenic pts or cirrhosis
*[[Pancreatitis]]
#Carcinoma
**Brain injury, [[crush injury]], [[burns]], [[rhabdomyolysis]], [[fat embolism]]
##DIC is often chronic and compensated
*[[hepatic failure|Liver disease]]
##Thrombosis is more common than bleeding
*[[Pregnancy]]-related
#Leukemia
**[[Placental Abruption]], [[Amniotic Fluid Embolus]], [[septic abortion]], [[HELLP Syndrome]], [[acute fatty liver of pregnancy]]
##More likely to have bleeding than thrombosis
*[[Snake bite]]
#Trauma
*[[ARDS]]
##Brain injury, crush injury, burns, rhabdo, fat embolism
*[[Transfusion reaction]]
#Liver disease
*[[Transplant complications|Transplant rejection]]
##May have chronic compensated DIC; acute DIC may occur in setting of acute liver failure
#Pregnancy
##Abruption, amniotic fluid embolus, septic abortion, HELLP syndrome
#Envenomation
##Rattlesnakes and other vipers
##Bleeding not as serious as expected from lab values
#ARDS
##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%)
*Respiratory dysfunction (16%)
*[[Thromboembolism]] (7%)
*CNS involvement (2%)
*[[Purpura fulminans]] (widespread arterial and venous thromboses)
**Associated with significant [[bacteremia]]


==Diagnosis==
==Differential Diagnosis==
#PT high
{{Hemolytic anemia DDX}}
#PTT high
{{Thrombocytopenia}}
#Platlet low
{{Increased bleeding DDX}}
#Fibrinogen low
{{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
**Repeat platelets may be necessary if first level normal or if need to trend
*PT and PTT
**[[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
**Low
**<100 correlates with severe DIC
**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
**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)


==Treatment==
===Chronic===
See Heme: Bleeding Treatment
*FDP: Elevated
*[[D-dimer]]: Elevated
*Platelet: Variable
*Fibrinogen: Normal-elevated
*PT: Normal
*PTT: Normal
*RBCs
**Fragmented


==Source ==
==Management==
1/26/06 DONALDSON (addapted from Tintinalli)
*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]]
**[[Heparin]]
***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.