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Understanding Disseminated Intravascular Coagulation (DIC)


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Title: Understanding Disseminated Intravascular Coagulation (DIC)

Understanding Disseminated Intravascular
Coagulation (DIC) An Oncologic Emergency
  • Deborah Kwasneske RN, BSN, OCN
  • MSN 621, Spring 2006
  • Alverno College
  • Email debbiern_at_wi.rr.com

  • This tutorial is self guided by using buttons to
    move about screens. You can return to the main
    screen at anytime by using the home button.
    The arrow buttons allow you to move forward or
  • To return to previous spot you may use the
    return button
  • To navigate through different topics of this
    tutorial, use the
  • button.
  • There are multiple hyperlinks to outside learning
    sources to help with the understanding of DIC .
    To get back to DIC tutorial use back button on
  • For the case study answers, just click on the
    question for answers to appear. You can return
    to the case study using the return key.

Understanding Disseminated Intravascular
Coagulation (DIC) An Oncologic Emergency
DIC What isDIC
Case Study
  • 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
  • Develop understanding of diagnosing DIC (lab

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
    mechanismabnormal 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
  • (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)

  • 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
  • Leads to Hemorrhage
  • Thrombosis-brief period of hypercoagulability
  • Coagulation cascade is initiated, causing
    widespread fibrin formation
  • Microthrombi are deposited throughout he
  • Fibrin deposits result in tissue ischemia,
    hypoxia, necrosis
  • Leads to multi organ dysfunction
  • (Porth, 2004) (Otto, 2001)

  • (Porth, 2004)

Risk Factors and Etiology
  • Almost always a secondary event from activation
    of one of the coagulation pathways
  • Underlying pathology creates a triggering event
  • 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
  • Miscellaneous snakebite, pancreatitis, liver

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
  • (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
  • -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
  • (Porth, 2004) (Otto, 2001)

Genetic Component
  • None associated with DIC
  • BUT-------
  • Genetic mutations to the clotting cascade can
    lead to coagulation disorders
  • Hemophilla A and B
  • von Willebrand Factor
  • Impaired Synthesis of Coagulation
  • tutorial on homeostasis
  • http//alverno.edu.bownep

Inflammation and DIC
  • Sepsis is usually underlying process for
  • Endotoxins associated with sepsis activate
    factors and initiate coagulation.
  • Bacteria, virus also trigger the clotting
  • Sepsis activates complement cascade.
  • http//tutorial on inflammation
  • P.Bowne, Alverno College

Diagnosis/Lab Findings
  • Test
  • Platelet count
  • Fibrin degradation product (FDP)
  • Factor assay
  • Prothrombin time (PT)
  • Activated PTT
  • Throbimn time
  • Fibrinogen
  • D-dimer
  • Antithrombin
  • Abnormality
  • Decreased
  • Increased
  • Decreased
  • Prolonged
  • Prolonged
  • Prolonged
  • Decreased
  • Increased
  • 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
    patients condition (Heparin, Antithrombin III
    (ATIII), Fibrinolytic inhibitors)
  • (Porth, C.M. (2004) Essentials of
    Pathophysiology) (Otto, S. (2001). Oncology

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
  • 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 70s/50s. Labs were drawn and
    fluids started at 500cc/hr. Labs values were
  • 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 ABGs 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 lt100 PT 34 sec
  • ANC 0 PTT 72
  • Plts 12 Fibrinogen lt100
  • Hct 23 FSP gt1000
  • Hgb 9 D-dimer gt500
  • (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 lt100
  • FSP gt1000
  • (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

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
  • 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 BPs. Will need to be started on
    antibiotics. Patient will need to be monitored
    closely, VS, IOs

Answers for Case Study
  1. D.G.s labs cont to show anemia, neutropenia,
    renal insuffiency/failure. BUN and creatinine
    have increased and the HH has falling since
    previous draw. The ANC conts to drop.
  2. 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, hypotension.
  • 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
  • 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-

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 95.
  • (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
  • Heparin therapy has met with controversy for the
    treatment of DIC
  • (Porth, 2004) (Otto, 2001)

Answers for Case Study
  1. Based on the lab values, DG shows slight
    improvement. The PT and PTT numbers are better,
    platelet level has increased.
  2. 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. 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.

  • 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.
  • Fs (factors) of Coagulationfactors 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(pla
    sminogen) 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 plug
  • -Fresh frozen plasma (FFPs) used for volume
    expansion and contains clotting factors
    V,VIII,XIII and antithrombinIII.
  • (Otto, S. (2001) Oncology Nursing.)

  • Blood Components contd
  • Packed Red Blood Cells (PRBCs) used to
    increase RBCs and clotting factors. Used
    instead of whole blood to help with fluid
    overload and reduce development of antibodies.
  • Cryoprecpitate contains fibrinogen and factor
  • (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_at_wi.rr.com
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