Disseminated Intravascular Coagulation (DIC) for Nursing Students with case study

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					Disseminated Intravascular Coagulation (DIC)
“An Oncologic Emergency”

What is DIC?
Is considered an “acquired bleeding disorder”
Is not a disease entity but an event that can accompany various disease
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
Is a Paradoxical Clinical Presentation “clotting and hemorrhage”
(Porth, C.M. (2004) Essentials of Pathophysiology) & (Otto, S. (2001). Oncology
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.

(Porth, 2001)

Thrombosis-brief period of hypercoagulability
Coagulation cascade is initiated, causing widespread fibrin formation
Microthrombi are deposited throughout he microcirculatory
Fibrin deposits result in tissue ischemia, hypoxia, necrosis
Leads to multi organ dysfunction

(Porth, 2004) & (Otto, 2001)

Fibrinolysis-period of hypocoagulability (the hemorrhagic phase)
Activates the complement system
Byproducts of fibrinolysis (fibrin/fibrin degradation products(FDP)) further
enhance bleeding by interfering with platelet aggregation, fibrin
polymerization, & thrombin activity
Leads to Hemorrhage


(Porth, 2004)
Risk Factors and Etiology
Almost always a secondary event from activation of one of the coagulation
Underlying pathology creates a triggering event: Either-
– endothelial tissue injury (Extrinsic)
– blood vessel injury (Intrinsic)
(Porth, 2004)

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
–Concomitantly with sepsis
          -10-20% with gram-negative
(Otto, S. (2001). Oncology Nursing)
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
(Otto, 2001)
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
(Porth, 2004) & (Otto, 2001)
Genetic Component
None associated with DIC
Genetic mutations to the clotting cascade can lead to coagulation disorders:
              Hemophilla A and B
              von Willebrand Factor
           Impaired Synthesis of Coagulation                 Factors
tutorial on homeostasis
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.

http://tutorial on inflammation
P.Bowne, Alverno College

Diagnosis/Lab Findings
Platelet count
Fibrin degradation product (FDP)
Factor assay
Prothrombin time (PT)
Activated PTT
Throbimn time


             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. have?
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. status? (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 for?
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

 (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
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 above 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

Answers for Case Study
-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
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.
 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
Pt possibly developing hypoxemia as a result of the infection process,
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
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
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
(Otto, 2001)
Answers for Case Study
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
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
Based on the lab values, DG shows slight improvement. The PT and PTT
numbers are better, platelet level has increased.
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.
       Otto, Shirley E. (2001). Oncology                      Nursing. Mosby: St.
   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.

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)
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)
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)

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
       -Fresh frozen plasma (FFPs): used for volume expansion and contains
clotting factors V,VIII,XIII and antithrombinIII.

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

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)

Description: Disseminated Intravascular Coagulation (DIC) for Nursing Students with case study