Learning Objectives
By the end of this section, you will be able to:
- Discuss pathophysiology, risk factors, and clinical manifestations associated with thrombotic disorders
- Describe the diagnostics and laboratory values in thrombotic disorders
- Apply nursing concepts and plan associated nursing care for the patient with a thrombotic disorder
- Evaluate the efficacy of nursing care for the patient with a thrombotic disorder
- Describe the medical therapies for thrombotic disorders
A thrombotic disorder is a condition that interferes with hemostasis, which is the body’s ability to clot or stop the flow of blood. A thrombus is a clot that forms inside a blood vessel. To effectively treat thrombotic disorders, nurses must understand the complex mechanisms of coagulation, which is the process of a liquid changing into a semi-solid or solid state. For blood, coagulation depends on platelet aggregation, which is the clumping together of platelets around RBCs (Figure 16.3). This process is supported by complex cascade of enzymatic reactions and essential proteins that combine to form a stable blood clot.
Pathophysiology of Thrombotic Disorders
Understanding the pathophysiology of thrombotic disorders is vital to an accurate diagnosis and successful management. There are three main types of clotting disorders: vascular, platelet, and coagulation.
Vascular disorders are conditions that may lead to bleeding. Examples include aneurysms and vasculitis, or inflammation of blood vessels; disruptions in blood flow due to blood vessel structure can also lead to vascular disorders. Constricted blood vessels can restrict the lumen of a vessel, provoking RBC aggregation and creation a blood clot.
Platelet disorders are caused by abnormalities in the quantity or quality of the platelets (Yale Medicine, n.d.). Internal conditions of the bone, such as bone marrow cancer or tumors, can disrupt the normal production and quality of platelets. As previously discussed in 16.4 Thrombocytopenia, thrombocytopenia, or low quantities of platelets, can result in impaired clot formation. Irregular or abnormal qualities of platelets also disrupt normal coagulation.
Coagulation disorders stem from disruptions to the cascade of reactions that happens during clotting. Vitamin K deficiency is essential for clot formation; if not properly absorbed or deficient, clotting cannot occur. Because vitamin K is processed in the liver, people with liver disease may not be able to metabolize vitamin K and can be at increased risk for impaired clotting. An acquired disorder of coagulation is disseminated intravascular coagulation (DIC), which triggers activation of the clotting cascade using up all the clotting factors, resulting in a mix of clotting and bleeding. Sepsis, trauma, and other diseases can trigger DIC.
Another pathology of coagulation disorders is due to fibrinolytic disorders. The breaking down of blood clots, or fibrinolysis, is needed to return the blood to homeostasis. Disorders in the ability to create a clot and then dissolve it are grouped in the pathology of fibrinolytic disorders.
Hereditary Thrombotic Disorders
Hereditary thrombotic disorders can often be detected when there is a family history of repeated venous thromboembolism. Genetic testing can confirm their presence and provide vital data for risk analysis as well as managing appropriate strategies such as anticoagulant treatment. It is crucial that individuals with family histories of blood clots seek appropriate medical care as soon as they experience repeated blood clots, so they can mitigate increased risks efficiently and avoid bleeding events. Two of the most common hereditary thrombotic disorders are factor V Leiden mutation and prothrombin G20210A mutation. Each occurs due to deficiencies in clotting factors from a genetic mutation in a particular gene (Stevens et al., 2018).
A factor V Leiden mutation is caused by a mutation in the F5 gene, which prevents normal production of the factor V needed for clotting. The factor V Leiden mutation is one of the most frequently hereditary thrombotic disorders. The pathophysiology of F5 gene mutation leads to the production of a factor V Leiden variant that resists inactivation by protein C, which is an anticoagulant protein. It acts as its own barrier against inactivation by anticoagulants such as warfarin. Individuals carrying a factor V Leiden mutation are more at risk of DVT and PE than people without this mutation.
A prothrombin G20210A mutation is a mutation that involves changes to the prothrombin (F2) gene, resulting in higher prothrombin levels, an essential clotting factor. High prothrombin levels contribute to blood clot formation by amplifying the coagulation cascade. Individuals carrying the prothrombin G20210A mutation have an increased risk of venous thromboembolism. Prothrombin G20210A carriers may also have an increased chance of DVT and PE, often in response to environmental influences like oral contraceptive use or pregnancy.
Venous Thromboembolism
In deep vein thrombosis (DVT), a type of venous thromboembolism (VTE), a blood clot forms within a deep vein, most commonly in the leg or pelvis. This happens when blood clots form within the vessels of muscles as opposed to superficial veins of the skin. Pooling of the blood within the veins occurs, creating soreness, redness, and pain (Figure 16.4). Risk factors include immobility; surgery or trauma; certain medical conditions such as cancer, obesity, and inflammatory disorders; and other conditions that damage vessels. An unprovoked occurrence of DVT is typically linked to an inherited disorder. Genetic mutations involving factor V Leiden or prothrombin can increase the risk of incorrect clotting (Ginsberg et al., 2019).
An untreated DVT may lead to serious health complications, including PE, and become a medical emergency. A clot that migrates from the deep veins and occludes the pulmonary arteries has a mortality risk of 25 percent (CDC, 2023).
A pulmonary embolism (PE) is a medical emergency caused when a blood clot from DVT migrates through the circulatory system and lodges itself within a pulmonary artery in a lung, blocking off oxygen and potentially leading to life-threatening consequences (Figure 16.5). Risk factors for PE include a previous history of PE or DVT, as well as immobility, prolonged bedrest after surgery, surgery itself, cancer, and chemotherapy; genetic mutations and medications that can cause blood clots are also risk factors for PE.
Clinical Manifestations of VTE
Common symptoms of DVT include pain or tenderness of the leg or calf on the affected side, as well as swelling, edema, warmth, and redness. Complications can happen if the blood clot loosens and travels through the bloodstream as an embolism. This can cause a pulmonary embolism in the lung, stroke if lodged in the brain or carotid arteries, or heart attack if lodged in the coronary artery.
The clinical presentation of a PE needs to be recognized quickly by a nurse because the prognosis is poor if oxygen is blocked within the lung and cannot perfuse into the main circulation. Symptoms include sudden shortness of breath, anxiety, chest pain that is sharper with inhalation, tachycardia, exertional dyspnea, cough with possible bloody sputum, sweating, dizziness, and disorientation (Ouellette, 2020). The complications from PE can be life-threatening because the clot blocks blood flow to the lungs, creating an increase in pulmonary artery pressure, which affects the right heart. Consequently, PE can exacerbate right-sided heart failure, leading to poor cardiac output and death.
Diagnostics and Laboratory Values of VTE
The most common diagnostic imaging tool for identifying DVT is ultrasound, which is noninvasive and allows providers to visualize the blood flow within a patient. A venous duplex is an ultrasound that examines for patency of veins in the legs. Coagulation laboratory studies can also look at the following factors relevant to clotting:
- partial thromboplastic time (PTT): measures the intrinsic clotting cascade and the time it takes blood to clot. It is often used to measure the therapeutic effectiveness of heparin treatment. The normal range is 18–24 seconds.
- prothrombin time (PT): uses extrinsic clotting factors to measure the time it takes for blood to clot. The normal range is generally 9–12 seconds.
- international normalized ratio (INR): a standard measurement of PT that is used across different laboratories, because many laboratory values for PT and PTT may vary. The INR is also used to measure the therapeutic range of coagulation. The normal ratio is 1:2 (Favaloro, 2017).
Diagnosis of a PE should be quick for best patient outcomes. Imaging studies are helpful in visualizing the blood clot within the lungs. Computed tomography pulmonary angiography can visualize the pulmonary arteries within minutes to help expedite a diagnosis. Other laboratory work is slower but can include clotting factors, CBC count, PT, PTT, and INR. A laboratory test that has been done for decades but is now known to be less specific is the D-dimer test, which measures a protein in the blood created when a clot dissolves. A normal D-dimer result is considered less than 0.50 (Bounds & Kok, 2023). An elevated D-dimer result may indicate the presence of a blood clot or clotting disorder (Cleveland Clinic, n.d.). Current recommendations endorse using this test simply as a qualitative test when there is a low suspicion of PE (Bounds & Kok, 2023).
Nursing Care of the Patient with VTE
Treatment goals include managing the symptoms of existing clots and preventing further clot formation. Common interventions include administering anticoagulant medicines (blood thinners) to avoid additional clotting (Peck & Brown, 2020). Nursing interventions also include monitoring the patient’s vital signs, assisting with airway and breathing, sitting the patient up in bed, and educating the patient about their condition.
Recognizing and Analyzing Cues
Nurses must remain diligent when it comes to monitoring patients for cues of excess blood clotting. To obtain cues, the nurse should complete a medical history, including any family history of clotting disorders, and examining risk factors—especially for those undergoing surgical procedures and for high-risk populations. Timely recognition of signs and symptoms along with collaboration among health-care providers allows prompt diagnosis and intervention in individuals at higher risks of blood clots. Education and preventive measures are also essential components of nursing care for these high-risk groups.
Completing a thorough physical exam can help the nurse identify cues such as warmth or redness in the lower legs or sudden respiratory problems that may be indicative of a DVT or PE. Laboratory work should be reviewed for clotting levels, including PT, PTT, and INR. Nurses should assess for changes in skin color and temperature, sudden chest pain worsened by deep breathing or movement, tachycardia, cough, hemoptysis, and laboratory studies (Anderson et al., 2021). One endorsed mnemonic to consider when assessing for the possible presence of DVT are the 6Ps: pulselessness, pallor, pain, perishingly cold, paresthesia (numbness), and paralysis. Capillary refill may be delayed by longer than 2 seconds. For recognizing PEs, a combination of subjective and objective complaints should be analyzed. The patient may appear pale, work harder to breathe at rest, appear anxious, or have a drop in their oxygen saturation level during ambulation. Vital signs may demonstrate tachycardia and may or may not show hypoxia.
Prioritizing Hypotheses, Generating Solutions, and Taking Action
The priority of care in patients with VTE is maintenance of hemodynamic stability and oxygenation. Patients with DVT should maintain bed rest and avoid further ambulation; the latter may promote clot migration. The nurse should avoid massage or rubbing the affected extremity, and the patient should be instructed to abstain from this also. The nurse should also perform a neurovascular assessment (using the 6Ps) and monitor capillary refill every shift—more frequently if the patient underwent an interventional procedure to surgically break down the clot.
Patients with acute PE tend to have a higher degree of symptom burden in regard to airway and breathing. Supplemental oxygen and putting the head of the bed up to high Fowler’s position (i.e., sitting up with spine straight) can assist with ventilation and oxygenation.
First-line therapies for acute VTE management include the initiation of blood thinners, either through the IV infusion of heparin or the administration of subcutaneous, low-molecular-weight heparins or direct oral anticoagulants (DOACs). Patients with a PE may require step-down or intensive care unit (ICU) level of care, with cardiac telemetry and frequent hemodynamic monitoring if there is a significant clot. Identification and treatment of atrial dysrhythmias put patients at risk for VTE occurrence.
Patients who have potential risks for thrombotic disorders should be educated about the risks of smoking while taking oral contraceptives or undergoing hormone replacement therapy, and should be discouraged from smoking while using oral contraceptive therapy. The vasoconstriction from nicotine in addition to the increased viscosity of blood from hormonal contraceptives may put a woman at risk for a pulmonary embolism or DVT. Patients with a hereditary thrombotic disorder may need to explore other methods of birth control to reduce risk of a thrombotic event. During assessment, nurses must interview patients to determine if there is any family history of thrombotic disorders. Patients with factor V Leiden will require lifelong anticoagulant therapy.
VTE prophylaxis is considered a standard of care in medical-surgical nursing. To decrease the risk of VTE occurrence, nurses may use a sequential compression device (SCD), which uses sleeves that fit over a patient’s legs and intermittently inflate and deflate to assist with blood mobilization in the legs (Figure 16.6). SCDs should never be used if the patient already has a DVT, because the pressure could dislodge the clot into circulation and increase the risk for PE, stroke, or heart attack. Prophylaxis also includes applying compression hose that help with venous return and decreasing edema. Early mobilization is also a part of the nursing care plan, along with frequent ambulation or with passive range of motion exercises. Adequate hydration and frequent mobilization also help prevent VTE occurrence. Nurses should also provide education on pharmacological therapies, which may be short term (e.g., 6 months) or longer.
Evaluation of Nursing Care for the Patient with VTE
As part of the nursing process, reevaluation is an important step to identify how the plan of care should be modified, if needed, based on the patient’s response to treatments and interventions. The nurse should evaluate the progress and patient response to nursing interventions for common problems seen in thrombotic disorders. Evaluating trends for impaired gas exchange, pain, impaired mobility, and risks of infection and bleeding can alert the nurse to take action.
Evaluating Outcomes
Evaluation of nursing care may depend on the acuity or chronicity of the VTE. Examples of improvement include
- Patient will report decreased shortness of breath and exhibit normalization of respiratory rate and oxygen saturation levels.
- The patient will identify risk factors that promote VTE occurrence, such as smoking and concurrent use of oral contraceptives or hormone replacement therapy.
- The patient will report decreased pain, swelling, warmth, and redness of the affected extremity.
- The patient will verbalize the importance of adherence to anticoagulation therapy.
Medical Therapies and Related Care
Treatment involves targeting the root cause of the thrombotic disorder, providing replacement clotting factors if applicable, or taking anticoagulant drugs as appropriate based on each disorder’s individual presentation. The most frequently used anticoagulants include heparin, warfarin, and apixiban. For chronic management, the choice of medication should be made collaboratively with the patient to ensure compliance and ease of administration, as well as consideration of cost. Historically, warfarin was the common drug of choice; however, it requires frequent blood monitoring. Newer DOACs do not require surveillance with bloodwork, but they may be more expensive.