4 Disseminated Intravascular Coagulation Nursing Care Plans

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Disseminated intravascular coagulation (DIC) is a coagulation disorder that prompts overstimulation of the normal clotting cascade and results in simultaneous thrombosis and hemorrhage. The formation of microclots affects tissue perfusion in the major organs, causing hypoxia, ischemia, and tissue damage. Coagulation occurs in two different pathways: intrinsic and extrinsic. These pathways are responsible for the formation of fibrin clots and blood clotting, which maintains homeostasis. In the intrinsic pathway, endothelial cell damage commonly occurs because of sepsis or infection. The extrinsic pathway is initiated by tissue injury such as from malignancy, trauma, or obstetrical complications. DIC may present as an acute or chronic condition.

An essential medical management of DIC is primarily aimed at treating the underlying cause, managing complications from both primary and secondary cause, supporting organ function, and stopping abnormal coagulation and controlling bleeding. Morbidity and mortality depend on underlying cause and severity of coagulopathy.

Nursing Care Plans

The following are the common nursing care planning and goals for clients with DIC: maintenance of hemodynamic status, maintenance of intact skin and oral mucosa, maintenance of fluid balance, maintenance of tissue perfusion, prevention of complications.

Here are four (4) nursing care plans (NCP) and nursing diagnosis for patients with disseminated intravascular coagulation:

  1. Impaired Gas Exchange
  2. Ineffective Tissue Perfusion
  3. Deficient Knowledge
  4. Risk for Bleeding
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Risk for Bleeding

Nursing Diagnosis

May be related to

  • Abnormal blood profile (depleted coagulation factors)
  • Drug therapy (adverse effects of heparin)

Possibly evidenced by

  • [not applicable]

Desired Outcomes

  • Client will experience reduced episode of bleeding and hematomas.
  • Client will experience reduced side effects of medication therapy.
  • Client will maintain therapeutic levels of coagulation laboratory profiles (prothrombin, partial prothrombin time, fibrinogen, fibrin split products, bleeding time).
Nursing Interventions Rationale
Assess for the underlying cause of DIC. DIC is not a primary disease but occurs in response to a precipitating factor such as an infection or tumor. Successful treatment of DIC includes management of the underlying disorder.
Assess the client’s heart rate and blood pressure. Observe for signs of orthostatic hypotension. Tachycardia and hypotension are signs of decreased cardiac output. Orthostasis (a drop of more than 15 mm Hg when changing from a supine to a sitting position) indicates reduced circulating fluids.
Observe for signs of internal bleeding, such as pain or changes in the level of consciousness. Institute a neurological checklist. Changes in the level of consciousness may occur with the decreased fluid volume or with decreasing hemoglobin.
Observe for signs of external bleeding from the gastrointestinal (GI) and genitourinary (GU) tracts. One of the diagnostic hallmarks of acute DIC can be manifested as bleeding simultaneously from at least three unrelated sites associated with shock, respiratory failure, or renal failure. For example, the client may have increased skin bruising, hemoptysis, and hematuria.
Note any hemoptysis or blood obtained during suctioning. These are the common manifestation of acute DIC.
Examine the skin surface for signs of bleeding. Note petechiae; purpura; hematomas; oozing of blood from IV sites, drains, and wounds; and bleeding from the mucous membranes. Prolonged oozing of blood from injection sites or venipuncture sites could be the first indication of DIC.
Monitor hemoglobin and hematocrit levels. Decreased hemoglobin and hematocrit levels are associated with bleeding from DIC.
Monitor serial coagulation profiles. Initially, accelerated clotting is noted. As the clotting then stimulates the fibrinolytic system, clotting factors become depleted and large quantities of proteins are produced as part of the fibrin degradation process. Common laboratory values in DIC are PT greater than 15 seconds, PTT greater than 60 to 90 seconds, hypofibrinogenemia, thrombocytopenia, elevated fibrin split products (FSPs), elevated d-dimers, and prolonged bleeding time. All put the client at risk for increased bleeding. Specific deficiencies guide treatment therapy.
If heparin therapy is initiated, observe for:

  • An increase in bleeding from IV sites, GI/GU tracts, respiratory tract, or wounds.
  • New purpura, petechiae, or hematoma.
Heparin is used for milder cases when clotting is more of a problem than bleeding. It aborts the clotting process by blocking thrombin production.
Institute precautionary measures:

  • Avoid intramuscular injections.
  • Avoid unnecessary venipunctures; draw all laboratory specimens through an existing line: arterial line or venous heparin lock line.
  • Apply pressure to any oozing sites.
  • Minimize the number of cuff BPs.
  • Pad the side rails (for agitated and confused clients).
  • Provide gentle oral care, using saline and water rinses instead of toothbrushes.
  • Prevent trauma to the catheters and tubes by proper taping; minimize pulling.
  • Use only compressible vessels for IV sites.
  • Use an electric rather than safety razor for shaving.
  • Use gentle suctioning.
  • Use gentle chest physiotherapy, such as turning, repositioning, coughing, deep breathing, percussion, and vibration.
Nursing interventions should be planned and implemented to eliminate potential sources of bleeding and to control the amount of potential bleeding and tissue injury.
Administer heparin therapy as prescribed. The dose may be titrated based on laboratory values and the clinical situation. If bleeding is increased, notify the physician of the possible need to decrease the IV drip. Heparin is used for milder cases when clotting is more of a problem than bleeding. Heparin augments antithrombin III activity that interrupts the clotting cycle and conversion of fibrinogen to fibrin. It also blocks the intrinsic and extrinsic pathways by inhibiting factor X, which slows clot formation. As the clinical situation improves, the need for heparin decreases. The challenge lies in differentiating the blood loss as an untoward effect of heparin therapy from a worsening DIC.
Administer parenteral fluids as prescribed. Anticipate the need for an IV fluid challenge with the immediate infusion of fluids for clients with hypotension. Maintenance of an adequate blood volume is vital for maintaining cardiac output and systemic perfusion.
Administer blood products as prescribed: red blood cells (RBCs), fresh frozen plasma (FFP), cryoprecipitate, and platelets. Blood and plasma transfusions replace blood clotting factors. RBCs increase oxygen carrying capacity; FFP replaces clotting factors and inhibitors; platelet and cryoprecipitate provide proteins for coagulation.
Administer additional medications or investigational drugs as ordered:
  • Antithrombin III concentration
This is a cofactor of heparin used for more severe cases. The anti-inflammatory properties may be of benefit when sepsis is the causative factor.
  • Epsilon-aminocaproic acid (Amicar)
This antifibrinolytic agent is reserved for when other measures have failed. Its use can lead to organ failure from large vessel thrombosis, and thus its use is controversial.
  • Hirudin
This is a thrombin inhibitor and neutralizer; Limited clinical experience exists with this drug.
  • Recombinant human activated protein C
This inhibits factors Va and VIIIa of the coagulation cascade.
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