Ch. 37 Flashcards
is a condition characterized by systemic activation of coagulation, potentially leading to thrombotic obstruction of small and midsize vessels, thereby contributing to organ dysfunction.
Consumptive coagulopathy, DIC is characterized by bleeding and thrombosis, both of which result from depletion of clotting factors, platelets, and RBCs. If not treated quickly, DIC will progress to multiple organ failure and death.
is always secondary to an underlying condition, such as severe infection, solid or hematologic malignancies, trauma, or obstetric calamities
Description and Etiology - Disseminated Intravascular Coagulation (DIC)
the common thread in the development of DIC is damage to the endothelium that results in activation of the coagulation mechanism extrinsic coagulation pathway plays a major role in the development of DIC
damage to the endothelium results in the release of tissue factor and activation of this pathway.
Excessive thrombin formation results in rapid consumption of coagulation factors and depletion of regulatory substances
In response to the formation of clots, the fibrinolytic system is activated.
Pathophysiology - Disseminated Intravascular Coagulation (DIC)
the formation of thrombi and bleeding. Thrombi in peripheral capillaries can lead to cyanosis, particularly in the fingers, toes, ears, and nose.
severe, untreated cases, this peripheral ischemia may progress to gangrene
The result of this more central ischemia can be respiratory insufficiency and failure, acute kidney injury, bowel infarction, and ischemic stroke.
As coagulation factors are depleted, bleeding from intravenous and other puncture sites is observed. Ecchymoses may result from routine interventions such as the use of a manual blood pressure cuff, bathing, or turning. Bloody drainage may also occur from surgical sites, drains, and urinary catheters.
Clinical Manifestations - Disseminated Intravascular Coagulation (DIC)
used to diagnose DIC essentially assess the four basic characteristics of this syndrome: (1) increased coagulant activity, (2) increased fibrinolytic activity, (3) impaired regulatory function, and (4) end-organ failure
Continuous activation of the coagulation pathways results in the consumption of coagulation factors. Because of this, prothrombin time, activated partial thromboplastin time, and international normalized ratio values are elevated.
response to the excess clotting activity, the fibrinolytic process accelerates, and levels of byproducts increase
Another key laboratory test used to evaluate the degree of clot dissolution and the severity of the coagulopathy is the D-dimer level
Common findings in advanced DIC include respiratory failure, indicated by abnormal arterial blood gas (ABG) levels; liver failure, indicated by increasing liver enzymes; and renal impairment, indicated by increasing blood urea nitrogen (BUN) and creatinine levels.
Laboratory Findings - Disseminated Intravascular Coagulation (DIC)
After DIC is identified, maintaining organ perfusion and slowing consumption of coagulation factors are paramount to achieving a favorable outcome.
Multiple organ dysfunction syndrome (MODS) frequently results from DIC and exacerbates the underlying pathology. It is essential to prevent end-organ ischemia and damage by supporting blood pressure and circulating volume.
Replacement of clotting factors in a patient with DIC is thought by some authorities to perpetuate the coagulopathy; however, there is little scientific evidence to support this theory
Slowing consumption of coagulation factors by inhibiting the processes involved in clot formation is another strategy used to treat DIC.
Thrombin production in DIC surpasses production of antithrombins and other regulatory factors that would normally be present to inactivate thrombin and its subsequent actions.
Medical Management - Disseminated Intravascular Coagulation (DIC)
Assessment and monitoring are the primary weapons in the arsenal against DIC.
Nursing actions are driven by the specific cause of the DIC, although some common interventions are appropriate for all patients with DIC.
Support Vital Functions
Initiate Bleeding Precautions
Provide Comfort and Emotional Support
Nursing Management - Disseminated Intravascular Coagulation (DIC)
is critical to the outcome of the patient. The administration of intravenous fluids, blood products, and medications is essential to providing adequate hemodynamic support and ensuring adequate tissue oxygenation to combat DIC and prevent end-organ damage
The patient should be closely monitored for any adverse reaction to blood products.
Close monitoring of vital signs, hemodynamic parameters, intake and output, and appropriate laboratory values assists in the administration and titration of appropriate agents.
Support Vital Functions
Awareness of the patient’s bleeding potential necessitates adjustments to normal nursing interventions. Unnecessary venipunctures or arterial punctures that may result in bleeding, bruising, or hematomas are avoided.
The use of manual or automatic blood pressure cuffs is avoided whenever possible.
The patient is continually assessed for signs of bleeding, petechiae, and ecchymosis.
Initiate Bleeding Precautions
The development of DIC in an already critically ill patient can be stressful for the patient and his or her family members.
imperative to provide psychosocial support throughout this crisis
Calm reassurance and uncomplicated explanations of the care the patient is receiving can help allay much of the anxiety experienced.
Provide Comfort and Emotional Support
The clinical manifestations of HIT are related to the formation of thrombi and subsequent vessel occlusion.
Thrombotic events typically include deep vein thrombosis, pulmonary embolism, limb ischemia thrombosis, thrombotic stroke, and myocardial infarction.
Neurologic signs and symptoms such as confusion, headache, and impaired speech can signal the onset of cerebral artery occlusion and stroke. Acute myocardial infarction may be heralded by dyspnea, chest pain, pallor, and alterations in blood pressure. Thrombi in the pulmonary vasculature may be evidenced by pleuritic pain, rales, and dyspnea.
Clinical Manifestations - Heparin-Induced Thrombocytopenia (HIT)
The key indicator for identifying HIT is the platelet count. General consensus in the literature considers a platelet count of less than 100,000/mm3 or a sudden drop of 50% from the patient’s baseline after initiation of heparin therapy to strongly indicate HIT.
Laboratory Findings - Heparin-Induced Thrombocytopenia (HIT)
Early identification is critical When a decrease in the platelet count is detected, heparin therapy is discontinued immediately, and the patient is tested for the presence of heparin antibodies.
Direct Thrombin Inhibitors
Medical Management - Heparin-Induced Thrombocytopenia (HIT)
Direct thrombin inhibitors (DTIs) are being used with increasing frequency to treat HIT. DTIs bind directly to the thrombin molecule, inhibiting its action
Direct Thrombin Inhibitors
The patient care management plan for a patient with HIT incorporates a variety of patient problems
Prevention of HIT is a major nursing focus, because most critically ill patients receive heparin as part of their plan of care and thus are at risk for this disorder.
A medical history that includes previous heparin therapy, deep vein thrombosis, or cardiovascular surgery
Decrease Incidence of Heparin Exposure
Maintain Surveillance for Complications
Educate the Patient and Family
Nursing Management - Heparin-Induced Thrombocytopenia (HIT)
Ensuring that all heparin has been removed from the patient’s hemodynamic pressure monitoring system, avoiding the use of heparin-coated catheters, and discontinuing heparin flushes
Decrease Incidence of Heparin Exposure
