DISSEMINATED INTRAVASCULAR COAGULATION

PRESENTED BY: H. RUFUS RAJ Asst.Professor, Al Shifa College of Nursing

INTRODUCTION
Disseminated intravascular coagulation (DIC), also known as disseminated intravascular coagulopathy or consumptive coagulopathy. It is a pathological activation of coagulation (blood clotting) mechanisms that happens in response to a variety of diseases. DIC leads to the formation of small blood clots inside the blood vessels throughout the body. The small clots consume coagulation proteins and platelets, normal coagulation is disrupted and abnormal bleeding occurs from the skin, the gastrointestinal tract, the respiratory tract and surgical wounds.

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DEFINITION

Disseminated intravascular coagulation (DIC) is a serious bleeding and thrombotic disorder characterised by abnormally initiated and accelerated clotting that results from the depletion of platelets and clotting

factors.

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RISK FACTORS
Sepsis Obstetric Acute

complications

hemolysis

Trauma Shock Cancer

(especially prostate cancer and acute

promyelocytic leukemia)
Allergic

reactions
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PREDISPOSING CONDITIONS Acute DIC

Shock Hemorrhagic Cardiogenic Anaphylactic

Malignancies Acute leukemia Lymphoma Tumor lysis syndrome

Septicemia Hemolytic processes

Transfusion of mismatched blood

Acute hemolysis from infection or immunologic disorders

Obstetric conditions
Abruptio placentae Amniotic fluid embolism Septic abortion

Tissue damage Extensive burns and trauma Heatstroke Severe head injury Transplant rejections Postoperative damage, especially after extracorporeal membrane oxygenation Fat and pulmonary emboli Snakebites Glomerulonephritis Acute anoxia (e.g., after cardiac arrest) Prosthetic devices Fulminant hepatitis

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Subacute DIC
Malignant disease Myeloproliferative/lymphoprolifera tive malignancies Metastatic cancer Obstetric Retained dead fetus

Chronic DIC
Liver disease Systemic lupus erythematosus Localized malignancy

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CAUSES
Cancers of lung, pancreas, prostate and stomach, as well as acute myeloid leukemia Obstetric: abruptio placentae, pre-eclampsia, amniotic fluid embolism Massive tissue injury: Trauma, burns, extensive surgery Infections: Gram-negative sepsis, Neisseria meningitis, Streptococcuspneumoniae, malaria, histoplasmosis, a spergillosis, Rocky mountain spotted fever Miscellaneous: Liver disease, snake bite, giant hemangioma, shock, heat stroke, vasculitis, aortic aneurysm, Serotonin syndrome Viral: Arenaviruses causing Argentine hemorrhagic fever or Bolivian Hemorrhagic Fever

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PATHOPHYSIOLOGY

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PATHOLOGICAL EVENTS

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PATHOPHYSIOLOGY
Triggering mechanisms activates several steps in the coagulation cascade Tissue factor is released at the site of tissue injury and causes normal coagulation mechanisms to be enhanced. Abundant intravascular thrombin (powerful coagulant) is produced Catalyzes the conversion of fibrinogen to fibrin and enhances platelet aggregation. Widespread fibrin and platelet deposition in capillaries and arterioles, resulting in thrombosis leading to multi-organ failure. Clotting inhibitory mechanisms, such as antithrombin III (AT III) and protein C, are depressed Excessive clotting activates the fibrinolytic system, which in turn breaks down the newly formed clot, creating fibrin split (fibrin degradation) products and inhibit normal blood clotting. Fibrin split products accumulating and clotting factors are depleted Blood loses its ability to clot & predisposes to hemorrhage.

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BLEEDINGMANIFESTATIONS
Integumentary

manifestations: pallor, petechiae, purpura oozing blood, venipuncture site bleeding, hematomas, and occult hemorrhage Respiratory manifestations: tachypnea, hemoptysis, and orthopnea Cardiovascular manifestations: tachycardia and hypotension GI manifestations: upper and lower GI bleeding, abdominal distention, and bloody stools Urinary manifestations: hematuria Neurologic changes: vision changes, dizziness, headache, changes in mental status, and irritability Musculoskeletal: complaints: bone and joint pain.
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THROMBOTIC MANIFESTATIONS

Result of fibrin or platelet deposition in the microvasculature Integumentary changes- cyanosis, ischemic tissue necrosis

(e.g., gangrene), and hemorrhagic necrosis

Respiratory changes- tachypnea, dyspnea, pulmonary emboli, and acute respiratory distress syndrome

Cardiovascular changes- ECG changes and venous distention GI changes- abdominal pain and paralytic ileus; and kidney

damage and oliguria, leading to failure.

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CLINICAL MANIFESTATIONS

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DIC

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LABORATORY VALUES

COMPLICATIONS

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POTENTIAL COMPLICATIONS
Renal

failure

Gangrene Pulmonary Altered Acute Stroke

embolism or hemorrhage

level of consciousness

respiratory distress syndrome

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SITES OF ACTION FOR THERAPIES

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TREATMENT
Chronic DIC - Treatment of the underlying disease may be sufficient to reverse the DIC (e.g., antineoplastic therapy when DIC is caused by malignancy). DIC (bleeding) - providing support with necessary blood products while treating the primary disorder. Blood product support with platelets, cryoprecipitate, and fresh frozen plasma (FFP. Thrombocytopenia - platelets to correct thrombocytopenia if the platelet count is less than 20,000.Cryoprecipitate replaces factor VIII and fibrinogen and is given if the fibrinogen is below 100 mg/dl. Thrombosis - anticoagulation with heparin or low-molecularweight heparin (controversial). Recombinant human activated protein C (drotrecogin alfa [Xigris]) has both anticoagulant and antiinflammatory effects and has reduced the relative risk of death from sepsis.

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LIST OF NURSING DIAGNOSES

1.

2.

3.

4.

5. 6. 7.

8. 9.

Ineffective tissue perfusion (cerebral, cardiopulmonary, renal, GI, and peripheral) related to bleeding and sluggish or diminished blood flow secondary to thrombosis Acute pain related to bleeding into tissues and diagnostic procedures Decreased cardiac output related to fluid volume deficit and hypotension Anxiety related to fear of the unknown, disease process, diagnostic procedures, and therapy. Risk for deficient fluid volume related to bleeding. Risk for impaired skin integrity related to ischemia or bleeding Potential for excess fluid volume related to excessive blood/ factor component replacement. Ineffective tissue perfusion related to microthrombi. Anxiety and fear of the unknown and possible death.
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PROGNOSIS

Prognosis varies depending on the underlying disorder, and

the extent of the intravascular thrombosis (clotting).

Prognosis for those with DIC, regardless of cause, is often grim: between 10% and 50% of patients will die.

DIC with sepsis (infection) has a significantly higher rate of death than DIC associated with trauma.

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