CASEA 70-year-old man was admitted to the hospital

because of generalized ecchymoses.He had been diagnosed with prostate cancer

metastatic to bone 5 years earlier. Subsequently, he had slowly progressive disease

He also received radiation therapy to his left shoulder and to epidural disease in the lower thoracic spine

Three months before this admission, he

underwent posterolateral decompression and fusion for thoracic spinal cord compression.

Within 24 hours of surgery, his platelet count dropped from 230,000/µL to 69,000/µL, and

his prothrombin time increased to 19.1 seconds (International Normalized Ratio [INR] = 1.56). He was given packed red cells,

platelets, and fresh frozen plasma, and he showed improvement in all hematologic parameters. Five weeks before this admission, his platelet count was 149,000/µL.

The most striking physical finding on this admission was multiple large confluent ecchymoses primarily involving the flanks and

lower extremities

His platelet count was 62,000/µL, and his prothrombin time was 14.8 seconds (INR = 1.21). The activated partial thromboplastin

time was 32.6 seconds, the serum fibrinogen was 87 mg/dL. Shortly after admission, the fibrinogen dropped to 55 mg/dL.

OverviewDisseminated Intravascular Coagulation - clinicopathologic syndrome that is not a

specific disease but a manifestation of an underlying disorder.- loss of balance between procoagulant and fibrinolytic capacities.

Types of DIC1. Acute2. Chronic

Diagnostic exams1.Prothrombin Time (11-16 seconds)2.Prothrombin / International normalized ratio

(1.2 – 2.5 seconds)3. Activated partial thromboplastin time

(25-38 seconds)4. Fibrinogen (200 – 400 g/dL)

Manifestations1. Thrombosis

- petechiae or ecchymoses2. Hemorrhage

Causes1. Obstetric conditions2. Cancers3. Infections4. Trauma or surgery5. Shock

Anatomy and Physiology

PlateletsPlatelets (see fig. 18.1) are not cells but small

fragments ofmegakaryocyte cytoplasm. They are 2 to 4 m in

diameterand possess lysosomes, endoplasmic reticulum,

a Golgicomplex, and Golgi vesicles, or “granules,” that

contain avariety of factors involved in platelet function.

Events in Hemostasis1. Vascular constriction2. Formation of a platelet plug3. Formation of a blood clot as a result of

blood coagulation4. Eventual growth of fibrous tissue into the

blood clot to close the hole in the blood vessel permanently

Lysis of Blood ClotsPlasmin

- Digest fibrin fibers

t-PA

Plasminogen

Plasmin

Pathophysiology

Stimulus

Tissue destruction Endothelial Injury

Tissue factorExtrinsic pathwaysFactor XII activation (intrinsic pathway)

Thrombin generation

Intravascular fibrin deposition

Plasminogen activation

Plasmin generation

Fibrinolysis

Platelet consumption

Thrombocytopenia

Clotting factor degradation

Fibrin degradation products (inhibit thrombin and platelet

aggregation)

Bleeding

Thrombosis

Hemolytic anemia

Tissue ischemia

Organ Failure

dec circulating blood

dec O2 transportation

Tissue hypoxia

RBCs damaged

Nursing Problems1. High Risk for Altered Tissue Perfusion2. High Risk for Fluid Volume Deficit3. Impaired Tissue Integrity

Bibliography

XimelagatranA promising new oral anticoagulantby Lee P. Skrupky and Karen Kopacek , RPh

References1. Wintrobe’s Clinical Hematology 9th ed. by Lee2. Internal Medicine by Jay Stein3. Kelley’s Internal Medicine by H. David Humes4. Anatomy and Physiology 6th ed. By Thibodeau &

Patton5. Pathophysiology: The Biological Principles of

Disease by Smith & Thier6. Textbook of Medical Physiology by Guyton &

Hall7. Pathophysiology for the Health Professions 3rd

ed. by Gould8. Pathophysiology: Concepts of Altered Health

States 6th ed. by Porth