Understanding Disseminated

Intravascular Coagulation (DIC)

 Objectives
Understand the pathophysiology of
Disseminated Intravascular Coagulation (DIC)
Identify risk factors and etiology of DIC
Describe the signs and symptoms of DIC
Identify treatment modalities for DIC
Define, identify and understand Acute vs
Chronic DIC
Develop understanding of diagnosing DIC (lab
interpretations)
 What is DIC?
Is considered an “acquired bleeding disorder”
Is not a disease entity but an event that can
accompany various disease processes
Is an alteration in the blood clotting
mechanism:abnormal acceleration of the
coagulation cascade, resulting in thrombosis
As a result of the depletion of clotting factors,
hemorrhage occurs simultaneously
Is a Paradoxical Clinical Presentation “clotting
and hemorrhage”
 Disseminated Intravascular Coagulation

Primarily a thrombotic process

-

– Systemic process producing both thrombosis

and hemorrhage

– Its clinical manifestation may be widespread

hemorrhage in acute, fulminant cases.
 Pathophysiology
In DIC, a systemic activation of the
coagulation system simultaneously leads
to thrombus formation (compromising
blood supply to various organs) and
exhaustion of platelets and coagulation
factors (results in hemorrhage). This is a
disruption of body homeostasis.
 Pathophysiology
Thrombosis-brief period of Fibrinolysis-period of
hypercoagulability hypocoagulability (the
1) Coagulation cascade is
hemorrhagic phase)
initiated, causing 1) Activates the complement
widespread fibrin system
formation 2) Byproducts of fibrinolysis
2) Microthrombi are (fibrin/fibrin degradation
deposited throughout he products(FDP)) further
microcirculatory enhance bleeding by
interfering with platelet
3) Fibrin deposits result in
tissue ischemia, hypoxia, aggregation, fibrin
necrosis polymerization, &
thrombin activity
4) Leads to multi organ
3) Leads to Hemorrhage
dysfunction

(Porth, 2004) & (Otto, 2001)

Pathophysiology
 Risk Factors and Etiology
Almost always a secondary event from
activation of one of the coagulation
pathways
Underlying pathology creates a triggering
event: Either-
– endothelial tissue injury (Extrinsic)
– blood vessel injury (Intrinsic)
 Pathologic Pathways
Extrinsic (endothelial)
– Shock or trauma
– Infections ( gram positive
and gram negative sepsis,
aspergillosis)
– Obstetric complications
(eclampsia, placenta
abruptio, fetal death
syndrome)
– Malignancies: APML, AML,
cancers of the lung, colon,
breast, prostate)
(Porth, 2004) & (Otto, 2001)
Intrinsic (blood vessel)
– Infectious vasculitis
(certain viral infections,
rocky mountain spotted
fever)
– Vascular disorders
– Intravascular hemolysis
(hemolytic transfusion
reactions)
– Miscellaneous: snakebite,
pancreatitis, liver disease
 Oncology Related DIC
Usually related to:
– Disease process
-APML( acute promyelocytic leukemia)
-mucin-secreting adenocarcinomas
– Treatment of cancer
-chemotherapy
-radiation
– Concomitantly with sepsis
-10-20% with gram-negative
 Clinical Features
Onset maybe Acute or Chronic
– Acute DIC
Develops rapidly over a period of hours
Presents with sudden bleeding from multiple sites
Treated as a medical emergency
– Chronic DIC
Develops over a period of months
Maybe subclinical
Eventually evolves into an acute DIC pattern
 Signs and Symptoms
Most common sign of DIC is bleeding
-manifested by ecchymosis, petechiae,and
purpura
-bleeding from multiple sites either oozing or
frank bleeding
-cool and or mottled extremities may be noted
-dyspnea and chest pain if pleura and
pericardium involvement
-hematuria
 Inflammation and DIC
Sepsis is usually underlying process for
development
Endotoxins associated with sepsis activate
factors and initiate coagulation.
Bacteria, virus also trigger the clotting cascade.
Sepsis activates complement cascade.
 Diagnosis/Lab Findings
Test Abnormality
Platelet count Decreased
Fibrin degradation product Increased
(FDP)
Factor assay Decreased
Prothrombin time (PT) Prolonged
Activated PTT Prolonged
Throbimn time Prolonged
Fibrinogen Decreased
D-dimer Increased
Antithrombin Decreased
(Otto,2001)
 Treatment Modalities
Treat the underlying cause
Provide supportive management of complications
Support organ function
Stop abnormal coagulation and control bleeding
by replacement of depleted blood and clotting
components (FFP,Platelets,PRBC)
Medications can be used and choice depends on
the patient’s condition (Heparin, Antithrombin III
(ATIII), Fibrinolytic inhibitors)
(Porth, C.M. (2004) Essentials of Pathophysiology) & (Otto, S. (2001). Oncology Nursing)
 Case Study/Post Test
D.G.,a 48-year-old, is 30 days post matched unrelated allogenic
stem cell transplant for Acute Myelegenous Leukemia. His Lab
work is as follows:
WBC 480 Sodium 130
ANC 120 Potassium 3.7
Plts 35 BUN 16
Hct 27 Creatinine 1.4
Hgb 10
(
a) Based on the above lab values, what risk factors does D.G. h
ave?
The next morning after labs are drawn, D.G. developed a fever of
101.2 and BP fell to 98/60 (normally 130/76).
(b)What may be the cause of the fever and low BP?
(c)What interventions should you as primary RN take at this time?
 Case Study cont.
D.G. is started on Vanco and Primaxin and given 1
liter fluid bolus over 2 hours. Blood cultures were
drawn prior to antibiotic RX. His fever decreased
to 99.8 and BP increased to 108/70.
Overnight D.G. again became febrile to 102.4 with
drop in BP to 70’s/50’s. Labs were drawn and
fluids started at 500cc/hr. Labs values were
significant:
ANC 100 Plts 20
Hct 9 BUN 35
Hgb 24 Creat 2.8
(a)What do the above lab values say about D.G. st
atus? (b)What interventions should be taken?
 Case Study cont.
MD orders 2 units of PRBC to be infused over 4 hours. During
infusion BP increased to 90/48 and he continues to be febrile
at 101.0.

D.G. is becoming more confused, complaining of GI pain and

cramping, developing a moist cough with rapid respiratory
rate.

(a)What maybe causing the new symptoms?

(b)What interventions do you take at this time?

(c)What maybe the underlying process? What else is he at risk f

or?
 Case Study cont.
O2 sats on RA measure 84% and lung sounds are coarse
throughout. STAT ABG’s and CXR are done. X-ray results
show diffuse consolidation and the ABGs demonstrate
respiratory acidosis with hypoxemia. D.G. is placed on
oxygen, O2 sats improve to 91%. Urine and stool output at
this time test heme positive. You also note he has small
lower extremity bruising and scattered petechia. A
bronchoscophy is ordered and performed. Results show
diffuse alveolar hemorrhage.

(
a) Based on D.G. history and the current clinical picture, what
are potential causes for symptoms (GI, Respiratory, GU)?
(b) What information would be useful at this time for diagnosis?
 Case Study Cont.
MD orders CBC and coagulation screen. The results are as
follows:
WBC <100 PT 34 sec
ANC 0 PTT 72
Plts 12 Fibrinogen <100
Hct 23 FSP >1000
Hgb 9 D-dimer >500

(
c)What secondary process is possibly occurring based on
above values?
(
d)What interventions are appropriate? What should be the
focus of your assessments?
 Case Study Cont.
D.G. Continues to be hypotensive. Lung sounds
remain course, hemoptysis develops and CXR
continues with diffuse consolidation. Urine and
stool remain heme positive. After transfusion,
labs redrawn. Values as follows:
Plts 22 Pt 28
Hct 26 PTT 54
Hgb 10 Fibrin <100
FSP >1000
(
a)What is the results of treatment based on abov
e values?
(b)What interventions should be done?
 Case Study cont.
D.G. status continues to deteriorate and
needed to be intubated 2 days after
developing DIC. The sepsis remained
unresolved and he went into acute renal
failure. Family decided not to dialyze due
to the multi-organ involvement. D.G.
expired 2 days later from the gram neg
sepsis and secondary DIC.
 Answers for Case Study
(a)Risk for infection, renal insufficiency,
neutropenia, bleeding based on lab
values. WBC low along with the ANC
makes patient more susceptible to
infection. The BUN and creatinine are
elevated leading to possible renal
problems
 Answers for Case Study
(b) Possible septic shock as a result of an
underlying infection. Neutropenic patients
are at high risk for development of
infections.
(c) Patient will need blood cultures and labs
drawn, a fluid challenge is needed to help
with low BP’s. Will need to be started on
antibiotics. Patient will need to be
monitored closely, VS, I&O’s …
 Answers for Case Study
(a) D.G.’s labs cont to show anemia,
neutropenia, renal insuffiency/failure.
BUN and creatinine have increased and
the H&H has falling since previous draw.
The ANC conts to drop.
(b) Fluids, PRBC transfusion, monitoring of
urine output and VS are needed at this
time. The transfusion and fluids will help
with hypotension and anemia.
 Answers for Case Study
(a) Pt possibly developing hypoxemia as a
result of the infection process,
hypotension.
(b) Need to monitor O2 sats and apply
oxygen. Need to get orders for CXR and
cont to monitor Vital signs closely.
 Answers for Case Study
(c) Patient maybe developing pneumonia
and is at an increased risk for ARDS
(acute respiratory distress syndrome).
The moist cough with rapid resp. rate is
good indication of pulmonary
involvement.
The patient also has increased risk of
developing DIC based on the clinical
presentation and risk factors presented.
 Answers for Case Study
(a) The clinical presentation leads to the
diagnosis of DIC (effects every system of
the body); Lungs- hypoxemia,
hemorrhage, tachypnea Cardiac-
acidosis, tachycardia GI- cramping,
abdominal pain Renal- hematuria
Integument- bruising, petechiae Mental
status changes- confusion
 Answer for Case Study
(b) A DIC panel results would be helpful at
this time. Lab abnormalities along with
clinical presentation is used to confirm a
diagnosis of DIC. If abnormal results are
obtained for PT, PTT, platelets, and
fibrinogen, then the D-dimer and FDPs
levels are used to confirm DIC...FDPs
abnormal in 75% and D-dimer in 95%.
(Otto, 2001)
 Answers for Case Study
(a) Based on the lab values, DIC is confirmed for
the patient. The Platelet count is decreased,
the fibrinogen level is decreased, PT and PTT
levels increased and prolonged, FDPs level is
increased and the D-dimer is increased
(usually together, levels are 100% specificity
and sensitive). If a factor assay was done one
would expect the levels to show a decrease in
factors VI, VIII, and IX
(Otto, 2001)
 Answers for Case Study
(b) The immediate goal for the overall
management of DIC is the treat the underlying
disorder and to stop the patient from actively
bleeding and clotting with the need to give
transfusions and anticoagulation therapy if
needed.* Focus of assessments is to monitor
for more bleeding and changes.
*Heparin therapy has met with controversy for the
treatment of DIC
(Porth, 2004) & (Otto, 2001)
 Answers for Case Study
(a) Based on the lab values, DG shows
slight improvement. The PT and PTT
numbers are better, platelet level has
increased.
(b) The patient will cont to need to be
monitored very closely. Will need to cont
with treatment, monitor lab values
frequently. Patient remains critically ill.
 References
Otto, Shirley E. (2001). Oncology
Nursing. Mosby: St. Louis.
Porth, Carol M. (2004). Essentials of
Pathophysiology: Concepts of Altered
Health States. Lippncott Williams &
Wilkins: Philadelphia.

Web Sites:
Pat Bowne, faculty Alverno College Milwaukee Wis.
 Glossary
Complement-a heat-labile cascade system of at least 20
glycoproteins in normal serum that interacts to provide
manu of the effector functions of humoral immunity and
inflammation, including vasodilation and increases of
vascular permeability, facilitation of phagocyte activity
and lysis of certain foreign cells.
F’s (factors) of Coagulation:factors essential to normal
blood-clotting, whose absence, diminution, or excess
may lead to abnormality of clotting mechanisms. There
are 12 Factors-designated by Roman Numerals.

(Porth, 2004) & (Otto, 2001)

 Glossary
Fibrin- an insoluble protein that is essential to clotting of blood,
formed from fibrinogen by action of thrombin
Fibrinogen- a coagulation factor I, a glycoprotein; administered to
increase the coagulability of the blood
Fibrinolysin- plasmin, a preparation of proteolytic enzyme formed
from profibrinolysin(plasminogen); to promote dissolution of
thrombi
Hemostasis-the condition in which the external and internal
environment of a cell remains relatively constant
Thrombin- an enzyme resulting from activation of prothrombin,
which catalyzes the conversion of fibrinogen to fibrin.
Thrombosis-formation,development or presences of a thrombus
Thrombus-an aggregation of blood factors, primarily platlets and
fibrin with entrapment of cellular elements, frequently causing
vascular obstruction at the point of formation.

(Porth, 2004) & (Otto, 2001)

 Glossary
Activated PTT- aPTT tests the intrinsic and
common pathways
D-dimer- an antigen formed as a result of plasmin
lysis of cross-linked fibrin clots, documents the
presence of thrombin
Fibrin degradation product(FDP)- degradation
products increase as plasmin biodegrades
fibrinogen and fibrin,levels are elevated in 85-
100% of patients with DIC
Prothrombin Time(PT)- tests the extrinsic and
common pathways
(Porth, 2004) & (Otto, 2001)
 Glossary
Blood Components: used to correct abnormal
homeostasis. Used to correct the clotting
deficiencies caused by the consumption of
blood components during the DIC process.
-Platelets: contain platelet factor III, which
functions as a mechanical plug
-Fresh frozen plasma (FFPs): used for volume
expansion and contains clotting factors
V,VIII,XIII and antithrombinIII.

(Otto, S. (2001) Oncology Nursing.)

 Glossary
Blood Components cont’d:
Packed Red Blood Cells (PRBC’s): used
to increase RBC’s and clotting factors.
Used instead of whole blood to help with
fluid overload and reduce development of
antibodies.
Cryoprecpitate: contains fibrinogen and
factor VIII.
(Otto, S. (2001). Oncology Nursing)
 Thank you
This completes the DIC tutorial. Any and all
comments regarding your learning
experience are greatly appreciated.
Please send any correspondence to my
email address listed below:

debbiern@wi.rr.com