Thromboembolic disorders and their associated long-term complications place a burden on patients, healthcare systems and society. Non-vitamin K antagonist (VKA) oral anticoagulants (OACs), including rivaroxaban, dabigatran, apixaban and edoxaban, are effective for the prevention of stroke in patients with non-valvular atrial fibrillation and for the treatment and secondary prevention of venous thromboembolism. The increasing uptake of the non-VKA OACs in primary care lessens the burden of care and allows for an easier transition of treatment from hospital to home. This transformation in terms of patient management has resulted in the need to empower nurses working in this field to endorse management strategies with a focus on patient education and long-term management ( i.e. assessment of compliance, scheduling follow-up visits). Management of both venous thromboembolism and stroke prevention in patients with non-valvular atrial fibrillation requires a multidisciplinary team approach and, looking to the future, nurses are likely to have a key role at the heart of the thrombosis team. This review aims to provide nurses with the confidence to manage patients with thromboembolic disorders, and highlights the importance of responsible non-VKA OAC use and the impact that this can have on improving patient care and outcomes.
Thromboembolic diseases are often life-threatening but can be prevented with effective anticoagulation treatment. Venous thromboembolism (VTE)―the formation of a thrombus within a vein―comprises deep vein thrombosis (DVT) and pulmonary embolism (PE) and is associated with significant morbidity and mortality [
Chronic thromboembolic pulmonary hypertension (CTEPH) is a long-term complication in patients with PE and is caused by chronic major pulmonary vascular obstruction [
Atrial fibrillation (AF) is a common cardiac arrhythmia with a prevalence of about 1.5% - 2.0% in the general population [
Consequently, there is an increasing awareness that these thromboembolic disorders and their associated long-term complications contribute substantially to the healthcare burden on patients, healthcare systems and society.
Long-term anticoagulant therapy in both VTE and AF has historically involved oral vitamin K antagonists (VKAs), which have remained the mainstay of oral anticoagulation therapy for many years. Patients with VTE have typically received anticoagulant treatment with a parenteral heparin overlapping with a VKA, before transitioning to a VKA [
Although VKAs have proven efficacy in both indications, they lack many of the properties of an ideal anticoagulant, including a wide therapeutic window, predictable dose-response, low risk of drug-drug and food-drug interactions and no need for routine coagulation monitoring [
The increasing uptake of non-VKA OACs in primary care is transforming the management of patients and the transition from hospital to home. Non-VKA OAC therapy was associated with a significantly shorter length of hospital stay compared with warfarin in patients hospitalized for non-valvular AF, DVT or PE [
There is an increasing need to empower primary care workers in the management of chronic conditions such as VTE and AF. Therefore, this review aims to provide nurses with the understanding, required skills and confidence to manage non-VKA OAC therapy in these patient populations, subsequently improving outcomes.
The regulatory approvals of apixaban, dabigatran and rivaroxaban (EU, US and several other countries worldwide) and edoxaban (EU, US and Japan) in these indications derive from the successful completion of large phase III randomized clinical trials. An overview of the non-VKA OACs and their approved dosing regimens across licensed indications in Europe is shown in
Overall, these agents have shown the potential to improve the benefit-risk profile in patients treated for acute VTE, with efficacy profiles as good as those observed in patients treated with standard of care, and similar/su- perior safety profiles [
Similarly, in phase III studies in patients with non-valvular AF, non-VKA OACs were better or equivalent to warfarin for stroke prevention, but with significant improvements in safety profile. In a meta-analysis of these trials, non-VKA OACs significantly reduced the risk of stroke or systemic embolism in patients with non-valvular AF by 19% compared with warfarin, mainly driven by a significant 51% reduction in the risk of haemorrhagic stroke [
All non-VKA OACs are administered orally at fixed doses once or twice daily. They have shorter half-lives than VKAs (such as warfarin) as well as a faster onset of action, with peak anticoagulant effect within a few hours after drug administration. Of particular benefit, non-VKA OACs have significantly fewer food and drug interactions than the VKAs. As opposed to the indirect mode of action of the VKAs, non-VKA OACs target single, specific molecules i.e. Factor Xa and thrombin, which are critical components of the coagulation process. This is particularly true for Factor Xa, which is a crucial site of amplification in the coagulation process; the central role of Factor Xa in thrombus formation is now well recognized, with one molecule of Factor Xa being able to catalyse the formation of approximately 1000 thrombin molecules [
The increasing number of patients diagnosed with VTE/AF, combined with the complexities and patient co-morbidities that accompany these disorders, necessitates a multidisciplinary approach to patient management.
Indication | Apixaban | Dabigatran | Edoxaban | Rivaroxaban |
---|---|---|---|---|
VTE prevention after major orthopaedic surgery* | ||||
Hip | 2.5 mg bid | 220 mg od | O | 10 mg od |
Knee | 2.5 mg bid | 220 mg od | O | 10 mg od |
VTE treatment† | ||||
DVT | 10 mg bid for 7 days and 5 mg bid thereafter | 150 mg bid, following treatment with a parenteral anticoagulant for ≥5 days | 60 mg od, following treatment with a parenteral anticoagulant for ≥5 days | 15 mg bid for 21 days and 20 mg od thereafter |
PE | ||||
VTE secondary prevention | 2.5 mg bid | |||
Stroke prevention in patients with AF‡ | 5 mg bid | 150 mg bid | 60 mg od | 20 mg od |
Acute coronary syndrome§ | O | O | O | 2.5 mg bid |
*No dose adjustment is necessary in rivaroxaban- or apixaban-treated patients with mild (CrCl 50 - 80 ml/min) or moderate (CrCl 30 - 49 ml/min) renal impairment. Rivaroxaban and apixaban are to be used with caution in patients with severe renal impairment (CrCl 15 - 29 ml/min) and are not recommended in patients with CrCl < 15 ml/min. Dabigatran should only be used with caution in patients with moderate renal impairment (CrCl 30 - 50 ml/min). These patients should initiate their treatment within 1 - 4 hours following surgery with a single capsule of dabigatran 75 mg and continuing with two capsules (150 mg) od thereafter for a total of 10 days (knee replacement surgery) or 28 - 35 days (hip replacement surgery). Dabigatran is contraindicated in patients with CrCl < 30 ml/min. †Rivaroxaban-treated patients with moderate (CrCl 30 - 49 ml/min) or severe (CrCl 15 - 29 ml/min, rivaroxaban is to be used with caution in these patients) renal impairment should receive a reduced dose (15 mg od) if the patient’s assessed risk for bleeding outweighs the risk of recurrent DVT and PE (no dose adjustment is necessary in patients with mild renal impairment [CrCl 50 - 80 ml/min]). No dose adjustment is necessary in apixaban-treated patients with mild (CrCl 50 - 80 ml/min) or moderate (CrCl 30 - 49 ml/min) renal impairment, whereas in patients with severe renal impairment (CrCl 15 - 29 ml/min) apixaban should be used with caution. Dabigatran-treated patients with moderate renal impairment (CrCl 30 - 49 ml/min) should receive either a total daily dose of 300 mg or 220 mg based on bleeding risk, whereas no dose adjustment is necessary in patients with mild renal impairment. A reduced dose is also recommended or should be considered in other special patient populations. A reduced dose of edoxaban (30 mg od) is recommended in patients with one or more of the following: CrCl 15 - 50 ml/min, bodyweight ≤ 60 kg, patients receiving certain P-glycoprotein inhibitors. ‡Rivaroxaban-treated patients with moderate (CrCl 30 - 49 ml/min) or severe (CrCl 15 - 29 ml/min) renal impairment should receive 15 mg od. The recommended dose of apixaban is 2.5 mg bid in patients with severe renal impairment (CrCl 15 - 29 ml/min) or with two or more of the following: age ≥ 80 years, bodyweight ≤ 60 kg or serum creatinine ≥ 1.5 mg/dl. Dabigatran-treated patients with moderate renal impairment (CrCl 30 - 49 ml/min) should receive a total daily dose of 300 mg or 220 mg based on the benefit-risk ratio. A reduced dose of edoxaban (30 mg od) is recommended in patients with one or more of the following: CrCl 15 - 50 ml/min, bodyweight ≤ 60 kg, patients receiving certain P-glycoprotein inhibitors. §No dose adjustment is necessary in rivaroxaban-treated patients with mild (CrCl 50 - 80 ml/min) or moderate (CrCl 30 - 49 ml/min) renal impairment. Approved for patients with elevated cardiac biomarkers also receiving a daily dose of 75 - 100 mg ASA or a daily dose of 75 - 100 mg ASA in addition to either a daily dose of 75 mg clopidogrel or a standard daily dose of ticlopidine. AF, atrial fibrillation; ASA, acetylsalicylic acid; bid, twice daily; CrCl, creatinine clearance; DVT, deep vein thrombosis; EU, European Union; od, once daily; PE, pulmonary embolism; VTE, venous thromboembolism.
The treatment of VTE and prevention of stroke in patients with AF is not restricted to the medical aspects (i.e. diagnosis and choice of medication), but also encompasses patient education, ongoing communication and organization of scheduled follow-up visits. Owing to constraints on their time, physicians focus predominately on the essential aspects of diagnosis and treatment, with less emphasis on non-medical aspects (e.g. patient education) [
Although a nurse-led multidisciplinary AF clinic can be implemented safely [
Warfarin | Dabigatran | Rivaroxaban | Apixaban | Edoxaban | What does it mean for my patient? | |
---|---|---|---|---|---|---|
Mechanism of action | Indirect mode of action (inhibits the production of blood procoagulant factors (i.e. prothrombin and Factors VII, IX and X), as well as of protein C and protein S | Direct Factor IIa (thrombin) inhibitor (prevents thrombin from converting fibrinogen into fibrin) | Direct Factor Xa inhibitors (prevent Factor Xa from converting prothrombin to thrombin) | Not applicable | ||
Needs to be taken with food | With or without food | With or without food | With or without food for the 10 mg dose; to be taken with food for the 15 and 20 mg doses | With or without food | With or without food | Establishing the most suitable time of day for the patient to take their medication |
Time to peak activity | Generally 24 h but can be delayed by 72 - 96 h | 0.5 - 2 h | 2 - 4 h | 3 - 4 h | 1 - 2 h | Non-VKA OACs have quicker onset of action compared with warfarin |
Half-life | 20 - 60 h | 12 - 14 h | 5 - 9 h (young individuals); 11 - 13 h (elderly individuals) | ~12 h | 10 - 14 h | Warfarin has a slower offset of action, meaning it needs to be stopped earlier before surgery |
GI tolerability* | No problem | Dyspepsia | No problem | No problem | No problem | Dabigatran is not appropriate for patients suffering from dyspepsia |
Drug interactions (important examples) | Numerous drugs | Contraindicated in patients receiving systemic ketoconazole, ciclosporin, itraconazole and dronedarone; caution needed with amiodarone, posaconazole, quinidine, verapamil, ticagrelor; should be avoided in patients receiving rifampicin, St John’s wort, carbamazepine or phenytoin; contraindicated in patients receiving concomitant anticoagulants | Not recommended in patients receiving azole-antimycotics (such as ketoconazole, itraconazole, voriconazole, posaconazole) or HIV protease inhibitors (e.g. ritonavir); care to be taken with concomitant use of NSAIDs, ASA and PAIs; contraindicated in patients receiving concomitant anticoagulants | Contraindicated (DVT/PE indication)/caution needed (prevention of VTE in patients undergoing elective hip or knee replacement surgery/stroke prevention in AF/VTE secondary prevention indications) in patients receiving rifampicin, phenytoin, carbamazepine, phenobarbital, St John’s wort; not recommended in patients receiving ketoconazole, itraconazole, voriconazole, posaconazole and HIV protease inhibitors (e.g. ritonavir); contraindicated in patients receiving concomitant anticoagulants | Should be used with caution in patients receiving rifampicin; dose reduction in patients receiving ciclosporin, dronedarone, erythromycin, ketoconazole; close scrutiny for bleeding in patients who require chronic treatment with low-dose ASA and/or NSAIDs; contraindicated in patients receiving concomitant anticoagulants | Close surveillance of patients receiving co-medications |
Renal excretion | Negligible | 85% | ~33% as active metabolite | ~27% | ~50% | Close surveillance of renal function and evaluation of drug choice/dose in patients with renal impairment |
*Relating to issues other than bleeding. AF, atrial fibrillation; ASA, acetylsalicylic acid; DVT, deep vein thrombosis; GI, gastrointestinal; NSAID; non-steroidal anti-inflammatory drug; OAC, oral anticoagulant; PAI, platelet aggregation inhibitor; PE, pulmonary embolism; VKA, vitamin K antagonist, VTE, venous thromboembolism.
Non-VKA OACs should not be used in patients who |
---|
Have active clinically significant bleeding |
Have CrCl < 15 ml/min* |
Are receiving concomitant treatment with any other anticoagulant |
Have hepatic disease associated with coagulopathy and/or clinically relevant bleeding risk† |
Are < 18 years of age |
Are pregnant or breastfeeding |
Have prosthetic heart valves |
Have haemodynamically unstable pulmonary embolism or require thrombolysis or pulmonary embolectomy |
Guidance provided by the European Medicines Agency-approved Summary of Product Characteristics regarding the main contraindications of the non-VKA OACs for stroke prevention in patients with atrial fibrillation and for treatment and secondary prevention of venous thromboembolism [
Patient education, improved adherence to guideline recommendations, time spent with patients, and teamwork between the nurse and the cardiologist were put forward as the essential elements behind the benefits of the nurse-led approach [
Patients with thromboembolic diseases commonly have additional medical conditions that may complicate their management. Challenging-to-treat patient groups often encountered in primary care include patients with renal impairment, diabetes, prior stroke/transient ischaemic attack or heart failure, and elderly patients. Anticoagulant therapy with VKAs can be challenging in such patients owing to numerous drug-drug interactions [
Patients likely to benefit from the non-VKA OACs include those poorly controlled on VKAs (i.e. those with a time in therapeutic range < 70%) [
Convenience, costs, risk factors for bleeding and concerns about reversibility are some of the reasons why patients may wish to switch OAC agents. Switching between OACs is mainly based on the pharmacodynamic/ pharmacokinetic properties of these agents and recommendations derived from the results of the clinical trial programmes of each drug. Nurses should take a holistic view when considering whether a patient should be switched from a VKA to a non-VKA OAC or vice versa, ensuring that the patient is made aware of the reasons why a switch may be beneficial so that they can make an informed decision.
The need for appropriate follow-up of patients receiving non-VKA OACs to ensure safe and effective anticoagulation treatment remains, despite the lack of a need for routine coagulation monitoring. For the treatment of VTE, a follow-up appointment or call would also help to ensure that the patient transitions smoothly from the acute to the longer-term phase of treatment, i.e. after the first 21 days of rivaroxaban or the first 7 days of apixaban treatment (
Nurses should always advise patients to bring their remaining medication to appointments, which will allow for an estimation of patient adherence. The assessment of compliance/adherence can be made by asking the patient specific questions about missed doses (or by inspecting the prescribed medication in blister packs), while making sure that the patient has not been switched to another anticoagulant by another healthcare provider. To further evaluate the understanding of the need for habitual taking of the medication as prescribed, the nurse could ask the patient, “If you missed a tablet, what did you do?” and “When did you take your next tablet?”. A more in-depth assessment of how a patient takes their medication can identify where compliance/adherence issues are arising. The nurse can then have a constructive discussion with the patient and provide suggestions as to how these issues could be prevented in the future (e.g. by changing the time of day the medication is taken, by making it part of the patient’s daily routine, by the patient carrying the medication with them if they are often out of the house). This provides the patient with the knowledge that they need in order to take responsibility and ownership of their disease state. For patients in whom poor adherence is suspected, technological aids may help, for example smartphone applications that remind the patient about the next drug intake. Nurses also need to ensure that the patient is aware of the over-the-counter medications associated with an increased risk of bleeding (i.e. non-steroidal anti-inflammatory drugs, acetylsalicylic acid) and highlight which medications are contraindicated and which should be used with caution. Thromboembolic and bleeding complications constitute crucial elements of the nurse’s checklist during follow-up and, if confirmed, these patients should be seen by a cardiologist and/or haematologist as soon as possible. In addition, caution should be taken to reduce the risk of falling, and the need for medications associated with an increased risk of falls (e.g. psychotropics, antidepressants and antipsychotics) should be reassessed [
Apixaban | Dabigatran | Edoxaban | Rivaroxaban | |
---|---|---|---|---|
Switching from a VKA to a non-VKA OAC | Discontinue the VKA and start apixaban at INR < 2.0 | Discontinue the VKA and start dabigatran at INR < 2.0 | Discontinue the VKA and start edoxaban at INR ≤ 2.5 | Discontinue the VKA and start rivaroxaban at INR ≤ 3.0 for stroke prevention in patients with non-valvular AF and ≤2.5 for treatment and secondary prevention of VTE |
Switching to a VKA from a non-VKA OAC | Continue apixaban for at least 2 days after beginning VKA therapy. After 2 days of co-administration, obtain an INR prior to the next scheduled dose of apixaban, and continue co-administration until the INR is ≥2.0 | If CrCl is ≥50 ml/min, start VKA 3 days before discontinuing dabigatran If CrCl is 30 - 49 ml/min, start VKA 2 days before discontinuing dabigatran | Ensure continuous adequate anticoagulation during any transition to an alternate anticoagulant Oral option: For patients currently on a 60 mg od or 30 mg od dose, administer edoxaban together with VKA Patients should not take a loading dose of VKA in order to promptly achieve a stable INR between 2.0 and 3.0. It is recommended to take into account the maintenance dose of VKA and if the patient was previously taking a VKA or to use a valid INR-driven VKA treatment algorithm, in accordance with local practice Once an INR ≥ 2.0 is achieved, edoxaban should be discontinued. Most patients (85%) should be able to achieve an INR ≥ 2.0 within 14 days of concomitant administration. After 14 days it is recommended that edoxaban is discontinued and the VKA continued to achieve an INR between 2.0 and 3.0 It is recommended that during the first 14 days of concomitant therapy the INR is measured at least three times just prior to taking the daily dose of edoxaban. Concomitant edoxaban and VKA can increase the INR post edoxaban dose by up to 46% Parenteral option: Discontinue edoxaban and administer a parenteral anticoagulant and VKA at the time of the next scheduled edoxaban dose. Once a stable INR of ≥2.0 is achieved, the parenteral anticoagulant should be discontinued and the VKA continued | Give the VKA and rivaroxaban concurrently until the INR is ≥2.0; standard initial VKA dosing should be given for the first 2 days of the conversion period, followed by INR-guided VKA dosing; INR should not be tested earlier than 24 h after the previous rivaroxaban dose |
Switching from a parenteral anticoagulant to a non-VKA OAC | Switch at the next scheduled dose | Stop the parenteral agent and start dabigatran 0 - 2 h prior to the time that the next dose of the parenteral therapy would be due, or at the time of discontinuation in case of continuous treatment (e.g. intravenous UFH) | s.c. anticoagulant (e.g. LMWH, fondaparinux): discontinue s.c. anticoagulant and start edoxaban at the time of the next scheduled s.c. dose Intravenous UFH: discontinue the infusion and start edoxaban 4 h later | Stop the parenteral agent and start rivaroxaban 0 - 2 h before the time of the next scheduled administration of the parenteral agent (e.g. for LMWH) would be due, or at the time of discontinuation of a continuously administered parenteral medicinal product (e.g. UFH) |
Switching to a parenteral anticoagulant from a non-VKA OAC | Switch at the next scheduled dose. These agents should not be administered simultaneously | Wait 12 h after the last dose before switching from dabigatran to a parenteral anticoagulant (non-valvular AF, treatment and secondary prevention of DVT/PE); wait 24 h after the last dose before switching from dabigatran to a parenteral anticoagulant for VTE prevention after major orthopaedic surgery | Discontinue edoxaban and start the parenteral anticoagulant at the time of the next scheduled dose | Give the first dose of parenteral anticoagulant at the time the next rivaroxaban dose would be taken |
Switching between non-VKA OACs [ | Discontinue the current non-VKA OAC and begin the other non-VKA OAC at the next scheduled dose (except in situations in which higher-than-therapeutic plasma concentrations are expected, e.g. in a patient with impaired renal function) |
AF, atrial fibrillation; CrCl, creatinine clearance; DVT, deep vein thrombosis; INR, international normalized ratio; LMWH, low molecular weight heparin; OAC, oral anticoagulant; od, once daily; PE, pulmonary embolism; s.c., subcutaneous; UFH, unfractionated heparin; VKA, vitamin K antagonist; VTE, venous thromboembolism.
(e.g. proton pump inhibitors) or drug-dose adjustments might be needed to reduce the risk of bleeding, especially when considering ongoing anticoagulation [
Patients receiving a non-VKA OAC need to understand why regular kidney function monitoring is important. All of the non-VKA OACs are eliminated by the kidneys to some extent, unlike the VKAs, and periodic checks of CrCl levels are advised. It is of critical importance for patients to understand that they can continue their treatment safely providing their kidneys are functional and able to eliminate the drug. Patients receiving a non-VKA OAC and with CrCl ≥ 60 ml/min are recommended to have their renal function monitored on a yearly basis, whereas patients with CrCl 30 - 60 ml/min or CrCl ≤ 30 ml/min should be monitored every 6 and 3 months, respectively [
For a man aged 65 years, weighing 85 kg with a serum creatinine of 74 µmol/l:
For a woman aged 70 years, weighing 50 kg with a serum creatinine of 80 µmol/l:
Exclusion of thrombocytopenia or anaemia (especially in elderly patients), assessment of other adverse events (i.e. dyspepsia and/or vomiting), advice on red flags (i.e. what happens if symptoms get worse and when to go to the Emergency Room [ER]) and optimal management of hypertension are aspects of patient management that need to be reviewed on a regular basis. Nurses should also keep track of difficult-to-manage patients (e.g. patients with substance dependency or intravenous drug users) because it is very likely that they will be in need of more frequent follow-up visits. Of note, close supervision by family members or caregivers will be required for patients with cognitive or memory deficits to ensure adherence/compliance.
Continuous patient education on their condition as well as treatment options and duration is of utmost importance (see Section 3.5). Various approaches could be employed in this regard, including face-to-face educational sessions and supplying leaflets/brochures with detailed instructions on how to initiate anticoagulation therapy and what is involved from the patient’s perspective. It is important that information is provided to patients at a level they can understand, in a manner that is timely and without overwhelming them. Nurses should avoid giving all the available information at once and should allow time for patients to digest and comprehend the most critical aspects of their disease and management. Patients also need to be given opportunities to ask questions such as, “Why has this happened to me?”, “When will the pain in my leg/lungs go away?”, “When will the clot go away?”, “Will my condition affect my everyday activities?” and “Why do I have to be on an anticoagulant and for how long?” Patients will often seek answers to practical issues concerning their everyday life such as whether they can drink alcohol, exercise or fly abroad. Much of the nurse’s role is also centred on educating patients to seek help when symptoms worsen or do not improve as expected. For example, ongoing shortness of breath, chest pain, coughing or vomiting blood for the newly diagnosed PE patient, or for the AF patient, ongoing shortness of breath or tachycardia that may indicate the need for further evaluation by a specialist. Further examination is also warranted in the case of ongoing pain, swelling or redness, or the appearance of new symptoms of shortness of breath or chest pain in patients with a current event of DVT. Nurses need to be confident in explaining to their patients how non-VKA OACs work, as well as the existing differences between them. All patients’ questions, fears and anxieties must be adequately addressed; unanswered or partially answered questions can cause misunderstandings with regard to treatment plan and duration. The most commonly reported fear associated with the use of anticoagulation is bleeding; therefore, as part of the ongoing education process, bleeding risk should be considered in context.
For example, the nurse might reassure a patient with AF who is taking an anticoagulant for stroke prevention by saying, “Yes, bleeding can be a frightening experience, but regardless of which anticoagulant you are taking, we (the doctors and nurses) will treat it using standard methods until it is under control. Bleeding is generally not caused by the anticoagulant and, therefore, it is important we investigate what else might have caused the bleeding.”
“Yes, it is true that VKAs have a reversal agent, but even that takes time to work. Non-VKA OACs do not remain in your body for very long, and ER physicians are able to manage your bleeding until the drug is eliminated from your body. If you are bleeding and need emergency care, it is important for the ER physician that you try to remember when your last dose was taken. This will help them to determine how much of the drug may still be circulating. There is a difference in the amount of circulating drug if you happened to take it an hour ago compared with 10 hours ago.”
The number of patients experiencing a serious bleeding event is low, whereas a stroke or PE can be fatal or permanently disabling. Real-world experience indicates that major bleeding rates in rivaroxaban- and dabigatran-treated patients are generally similar to or lower than those seen in VKA-treated patients [
Factors affecting the risk of bleeding in patients with AF receiving an oral anticoagulant [ | Baseline risk factors for fatal bleeding during VTE treatment [ |
---|---|
Intensity of anticoagulation | Age > 75 years |
Age | Metastatic cancer |
History of stroke | Immobility ≥ 4 days |
Previous bleeding | Major bleeding event within the past 30 days |
Anaemia | Abnormal prothrombin time |
Co-morbidities (e.g. hypertension, renal insufficiency, hepatic disease) | Platelet count < 100 × 109/l |
Co-medications (e.g. antiplatelets, NSAIDs) | CrCl < 30 ml/min |
Lifestyle (e.g. alcohol consumption) | Anaemia |
AF, atrial fibrillation; CrCl, creatinine clearance; NSAID; non-steroidal anti-inflammatory drug; VTE, venous thromboembolism.
Consider the following patient scenario: An 83-year-old female patient with a history of non-valvular AF who suffered a stroke resulting in left hemiparesis. She had not previously received treatment with an OAC. Her age and hypertension gave her a CHADS2 score of 4 and her echocardiogram was normal. It was decided that the patient should initiate warfarin therapy. Over a period of 6 months, she had supratherapeutic INRs (without any obvious cause) of 7.4, 7.0 and 9.3 on three separate occasions. Regular laboratory attendance for INR monitoring was difficult owing to her physical limitations. Follow-up visits showed that her time in therapeutic range was suboptimal, at approximately 30%. Her kidney function was checked and she had a CrCl of 65 ml/min. Clearly, warfarin was not working for this patient, so she was switched to a non-VKA OAC.
And a second patient scenario: A 78-year-old patient with a history of non-valvular AF who was familiar and comfortable with warfarin therapy. His cardiologist wanted to switch him to a non-VKA OAC, highlighting the advantages of no INR testing. His INR was followed in the clinic and he had a time in therapeutic range of approximately 85%, so was well controlled on warfarin. The patient was uncertain about switching but offered to try the new drug based on the recommendation of the cardiologist. Within a few weeks, it was found that the patient was having trouble adjusting to the new way of managing his condition. He did not have a problem with the new medication itself, but for years had had an understanding that having his INR measured regularly and knowing the range within which this value should fall kept him safe from stroke. This patient was subsequently switched back to warfarin.
The increasing uptake of non-VKA OACs in primary care is gradually transforming the management of patients and transitioning care from hospital to home. This provides the opportunity and vision for an integrated approach to disease management, with the nurse at the heart of a multidisciplinary thrombosis team. This forward thinking enables the nurse specialist to become actively involved in all aspects of the patient’s non-VKA OAC journey. This redefined role for the nurse is key to patient care and contributes greatly to patient outcomes.
The author would like to acknowledge Sarah Atkinson, who provided editorial support with funding from Bayer HealthCare Pharmaceuticals.
Marlene Robinson acts as a consultant for Bayer, Pfizer and Boehringer Ingelheim.
MarleneRobinson, (2015) Non-Vitamin K Antagonist Oral Anticoagulants: Redefining the Role of the Nurse to Improve Patient Care. Open Journal of Nursing,05,1142-1157. doi: 10.4236/ojn.2015.512121