DIC – The Unknown
Gunjan Patangay, MD, Tonya Fancher, MD, Jerry Powell, MD
University of California, Davis Medical Center; Sacramento, CA
Introduction:
Disseminated Intravascular Coagulation, DIC, is poorly
understood, difficult to manage, and associated with high mortality
rates of 31-86%. Causes associated with higher survival rates are
the better understood etiologies of septic abortion, neisseria
infection, and acute promyelocytic leukemia.
Figure 2: Platelets
Figure 1: Hemoglobin
120
18
16
100
14
80
12
10
Learning Objectives:
1) Management of DIC when the cause is unknown
2) Discussing if there should be limits on aggressive
resuscitation of DIC with extensive use of blood products
at the risks of high cost and significant resource depletion
60
1
8
2
6
2
2 units
PRBC
4
Hemoglobin
Hemoglobin goal
Units of
N
PRBCs
1
40
Units of
N Platelets
2
20
2
1 unit
platelets
1
Platelets
Platelet goal
2
0
0
Conclusion:
• Despite medical advances, DIC remains difficult to treat, and
research is ongoing to understand its pathophysiology, the
effectiveness of blood products in its management, and other
treatments that may decrease morbidity and mortality.
• The patient required at least 110 units of cryoprecipitate to
bring his fibrinogen level above 150, and he would have
likely required more FFP to correct the INR and aPTT if he
was not made comfort care, but it is unclear if he would have
survived even with these interventions.
Case:
51 yo male who recently traveled to North Carolina, presented with
pain, urinary retention, and penile and scrotal swelling after coitus.
Figure 4: INR
Figure 3: Fibrinogen
Labs:
Hb, INR, aPTT, fibrinogen, D-dimer, and platelets suggested severe
anemia, thrombocytopenia, and DIC.
350
3
300
2.5
250
Hospital course:
During his 5-day hospitalization, the patient was given:
- 7 units PRBC (goal hemoglobin >10) (Figure 1)
- 7 units of platelets (goal platelet count >50,000) (Figure 2)
- 210 units cryoprecipitate (goal fibrinogen >150) (Figure 3)
- 16 jumbo units FFP to correct his INR and aPTT (Figure 4)
- Low dose heparin, 5mg/kg/hr to interrupt the coagulation
cascade. (shown to benefit patients in DIC with severe sepsis)
- Antithrombin concentrate when antithrombin III levels were
low
Fibrinogen, antithrombin III, hemoglobin, and platelet count
normalized, but INR, aPTT, and D-dimer remained elevated.
• Had hematuria and signs of thrombosis, including tender
ecchymoses, mottled skin, blisters, and necrotic tissue throughout
his extremities (Figures 5 and 6).
• Developed multiorgan failure with acute renal failure, confusion,
intubation for airway protection, and heartblock with periods of
sustained asystole.
• On HD5, his family decided on comfort care.
• After autopsy, the underlying cause of DIC remained unclear,
with the most likely etiology considered to be overwhelming
systemic inflammatory response due to vibrio infection.
2
50
200
1.5
50
Fibrinogen
Fibrinogen goal
150
100
50
1
1 unit 1
FFP
2
2
2
2
2 2
2
0
5 cryo 5
5
10
15
20
Figure 5: DIC sequelae - mottled skin
INR
INR goal
N
Single units of
N cryoprecipitate
0.5
50
Discussion:
• Most research indicates that effective treatment of DIC is to
treat its underlying cause.
• The patient was treated for presumed vibrio infection (blood
cultures were negative) with antibiotics, this did not control his
overwhelming systemic inflammatory response already
underway that caused the hemorrhagic and thrombotic sequelae
of DIC.
• DIC was treated with PRBCs, platelets, FFP, cryoprecipitate,
low dose heparin, and antithrombin. Other treatment
considerations were activated protein C and factor VIIa.
0
Units
of FFP
For further discussion:
1) Since mortality in most causes of DIC is so high, should
there be limits on aggressive resuscitation of DIC with
extensive use of blood products at the risks of high cost
and significant resource depletion?
2) Should families be allowed to switch to comfort care after
starting down this road of aggressive resuscitation in DIC?
Figure 6: DIC sequelae - necrotic tissue
References:
1) Levi, M. “Disseminated intravascular coagulation” Critical Care
Medicine 2007, vol 35, No 9, pp 2191-2195.
2) “Guidelines for the diagnosis and management of disseminated
intravascular coagulation,” British Journal of Haematology, vol
145, 2009, pp 24-33.
3) Labelle, C.A., Kitchens, C.S. “Disseminated intravascular
coagulation: Treat the cause, not the lab values,” Cleveland
Clinic Journal of Medicine, vol 72, No 5, May 2005, pp 377-397.
4) Callum, J.L., Karkouti, K., and Lin, Y. “Cryoprecipitate: The
Current State of Knowledge,” Tranfusion Medicine Reviews, Vol
23, No 3 (July), 2009: pp 177-188.
5) Sihler, K.C., Napolitano, L.M. “Massive Transfusion: New
Insights,” Chest 2009; vol 136; pp1654-1667.