disseminated intravascular coagulation with pathophysiology
DESCRIPTION
This is a presentation made for Advanced Medical Surgical Nursing 1 (Pathophysiology) University of Santo Tomas - Graduate School, Manila, PhilippinesTRANSCRIPT
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