Pain Solutions
S a fe a n d e ffe c tiv e N S A ID use
By Karen S. Abate, PhD, ANP-BC and Terry Mahan Buttaro, PhD, AIMP-BC,
toxic effects than the currently available NSAIDs.1,2
GNP-BC, FAANP, DPNAP P h a rm a c o d y n a m ic s and
Nonsteroidal anti-inflammatory drugs (NSAIDs) are pharmaceuticals used to treat fever, inflammation, and pain. There are many NSAIDs— both oral and parenteral— available over-the-counter (OTC) or by prescription. The purpose of this article is to review NSAIDs and their appropriateness to manage chronic pain.
p h a r m a c o k in e tic s
Nonselective NSAIDs inhibit COX-1 and COX-2, the enzymes responsible for formulating prostaglandin (an inflammatory mediator from arachidonic acid).3'4 NSAIDs are most often categorized as nonselective COX inhibitors or selective COX-2 inhibitors. Both categories are useful for managing inflammatory pain and
Topical NSAIDs are also a valid alternative to oral preparations because there are fewer GI effects.
There are several NSAID chemical classes with varied mechanisms of action, half-lives, efficacies, and adverse reactions. Two of the oldest classes of NSAIDs include salicylates (aspirin) and nonacetylated salicylates (choline magnesium trisalicylate). The nonselective cyclooxygenase (COX) inhibitor NSAIDs (also known as traditional NSAIDs) include several classes: acetic acids (such as diclof enac, indomethacin), fenamates (such as mefenamic acid), oxicam deriva tives (such as meloxicam), and propionic acids (such as ibuprofen and naproxen). The most recent class of NSAIDs is the COX-2 selective inhibitors (celecoxib). Nitric oxide releasing NSAIDs and hydrogen sulfide-releasing NSAIDs are newer categories that are currently under investigation and may have fewer 18 The Nurse Practitioner • Vol 40, No. 6
are well absorbed. The first pass effect of these medications is minimal. All are highly protein-bound and metabolized by the liver. The half-lives are variable, with some NSAIDs (ibuprofen) lasting only 6 hours and others (naproxen) lasting longer. Adverse reactions. NSAIDs can cause gastrointestinal (GI) bleeding, liver function test abnormalities, hematologic effects, nonallergic angioedema, bronchospasm, or urticaria and can be a significant medication-related cause of ED visits.5,6All NSAIDs cause some GI distress (pain, diarrhea, flatulence), but because COX-2 inhibitors inhibit only the COX-2 enzyme, they cause fewer gastric ulcers and bleeding than the nonselective NSAIDs.6 There is, however, a boxed warning on NSAIDs
noting that there are potential anaphylactoid reactions as well as adverse cardiovascular (CV), GI, hematological, hepatic, and renal effects. Findings from the Women’s Health Initiative indicated that postmenopausal women who regularly used selective COX-2 inhibitors and nonselective NSAIDs with COX-2 inhibition greater than COX-1 inhibition had an increased risk for CV events. Participants who used nonselective agents with COX-1 inhibition greater than COX-2 inhibition did not have an increased CV risk.7 The renal and CV effects associ ated with NSAIDs are particularly concerning in older adults, patients with kidney dysfunction, and patients with CV disease.6 NSAIDs can cause hyperkalemia, increase BP and fluid retention, and, if used in combination with aspirin, negate the antiplatelet effects of aspirin.6 Salicylates. Aspirin, an acetylated salicylate, is a non-COX selective NSAID. Aspirin is now more frequently used for its irrevers ible inhibitory action on platelet COX and its antithrombotic properties in the prevention and treatm ent of CV and cerebrovascu lar events than for pain manage ment. However, aspirin has some anti-inflammatory activity and can be used for pain, though relief will likely not be dramatic. The risks of regular aspirin, even at 75 to 100 mg a day, are well documented and include: Reyes syndrome, epigastric upset, GI bleeding, hypersensitivity, www.tnpj.com
Pain Solutions hematologic effects, hepatotoxicity, renal toxicity, and, in high doses, salicylate intoxication.5,6 Nonselective COX NSAIDs. The nonselective NSAIDs are used primarily for their analgesic and anti-inflammatory properties, but some (ibuprofen and indomethacin) are effectively used for closure of patent ductus arteriosus in infants, while others aid in treatment of gingivitis and actinic keratosis.6In theory, the nonselective NSAIDs are equally effective, but because their chemical structures are different, some are more effective than others for some types of pain. The adverse reactions can also be different with some NSAIDs, causing more toxicity than others. Selective COX-2 inhibitors. The selective COX-2 inhibitors were
pain, dysmenorrhea, and other inflammatory conditions. Unfortu nately, they also cause untoward effects in multiple organ systems. Peptic ulcer disease is a documented risk in NSAID therapy, but lower GI bleeding is also a concern. Bleeding is a definite consideration for patients taking nonselective NSAIDs; thus, it is important to avoid prescribing nonselective NSAIDs if there is a past medical history of GI bleeding.2 However, GI bleeding is possibly moderated by a concurrent administration of a proton pump inhibitor or histamine H, blocker antagonist.2 According to McGettigan and Henry, naproxen and ibuprofen (in small doses) for a short amount of time can be an option if the patient understands the risks—even in
For all patients, using the least toxic medications in any drug category constitutes good practice. designed specifically to decrease the adverse GI effects associated with the nonselective NSAIDs.6 Initial studies suggested that patients incurred less GI ulceration and bleeding when taking a COX-2 inhibitor. More recently, however, the benefits of COX-2 inhibition on the GI system are less clear, and the concerns regarding the increased risk of CV events warrant careful consideration for all healthcare providers.6 Celecoxib is the only available purely selective COX-2 inhibitor in the U.S. at this time. Meloxicam is a revers ible inhibitor of both COX-1 and COX-2 enzymes, but it is a greater inhibitor of the COX-2 enzyme. P a in m a n a g e m e n t re c o m m e n d a tio n s
NSAIDs are an effective treatment for musculoskeletal pain, arthritic 20 The Nurse Practitioner • Vol. 40, No. 6
patients with CV disease.8In another large, retrospective study, naproxen was a safer alternative than other NSAIDs for patients with a recent hospital stay for a myocardial infarction, revascularization, or unstable angina.9 For all patients, using the least toxic medications in any drug category constitutes good practice. Topical NSAIDs are also a valid alter native to oral preparations because there are fewer GI effects.10Accord ing to Derry, topical NSAIDs— especially in gel form—provide relief for patients with chronic musculo skeletal pain.11 For patients with hand or knee pain associated with osteoarthritis, topical diclofenac can ease the pain associated with osteoarthritis, and at least short term (less than 12 weeks) seems less likely to cause GI bleeding.11
Other NSAID pain management recommendations include: • Enteric or extended-release medications should not be prescribed for treating acute pain because the drug formulation will delay the rate of absorption, thus impacting pain management • NSAIDs are effective for biliary and renal colic12 • Nonselective NSAIDs can poten tially increase GI bleeding and should not be used in combination with aspirin • NSAIDs should not be used if the patient is taking aspirin for cardioprotective reasons. Concur rent NSAID and aspirin use negates antiplatelet action of aspirin and increases risk for thromboembolic events13 • NSAIDs should be avoided in patients with atrial fibrillation due to increased risk of bleeding and thromboembolism when patients are also taking an antiplatelet or anticoagulant agent14 • COX-2 inhibitor NSAIDs for patients at risk for stroke should be avoided15 • NSAIDs are associated with continued microvascular damage and inflammation in patients with inflammatory bowel disease and should be avoided12 P ra c tic e re c o m m e n d a tio n s
It is imperative for the provider to complete a comprehensive history and thorough physical exam prior and during NSAID prescribing. The adverse reactions of NSAID use are often associated with manifestations in the GI, renal, and CV systems. As such, a focused history and physical exam of these organ systems should be performed. Subjective complaints such as gastric discomfort, dyspepsia, burning, or gastric discomfort and bloating should be evaluated.16Hepatic www.tnpj.com
Pain Solutions function assessment by means of liver function tests and determination of liver span should be completed. Assessment of kidney function by means of creati nine clearance along with a renal function panel is recommended in older adults as well as those with polypharmacy concerns, as these are risk factors for NSAID-associated kidney failure. 16 CV assessment should include the evaluation of heart sounds, peripheral edema, and BP, as arterial hypertension is an associated adverse reaction related to chronic NSAID use. 16 Antiplatelet hematologic effects associated with NSAIDs use can be evaluated with a periodic complete blood count. A comprehensive health history, including comor bidities and additional risk factors, should be consid ered relative to the risk benefit ratio of NSAID use with patients. In addition, OTC preparation and herbal supplement use should be appraised for potential interactions. Routine clinical follow up is recommended for patients with regular NSAID use. Monitoring of any NSAID use, risks, benefits, and adverse reactions should be ongoing. 16 NSAIDs should be promptly discontinued should any of the aforementioned factors, assessment
findings, or blood work indicate an actual or potential adverse reaction relative to NSAID use. 16 Clinician referral would be appropriate at that time. NSAIDs are frequently used to treat fever, inflammation, and pain; however, they are not without patient risk. As such, both OTC and prescription-based usage should be carefully monitored by healthcare providers. C D REFERENCES 1. Atkinson TJ, Fudin J, Jahn HL, Kubotera N, Rennick AL, Rhorer M. What’s new in NSAID pharmacotherapy: oral agents to injectables. Pain Med. 2013;14(suppl 1):S11-S17. 2. Gargallo CJ, Lanas A. Is NSAIDs-related gastrointestinal damage prevent able? J Dig Dis. 2013; 14(2):55-61. 3. Smyth EM, Fitzgerald GA. Chapter 18. The eicosanoids, prostaglandins, leukotrienes 8c related compounds. In: Katsung BG, Masters SB, Trevor AJ, eds. Basic & Clinical Pharmacology. 12th ed. New York: McGraw Hill Lange. 4. Ricciotti E, Fitzgerald GA. Prostaglandins and inflammation. Arterioscler Thromb Vase Biol. 2011 ;31(5):986-1000. 5. Aun MV, Blanca M, Garro LS, et al. Nonsteroidal anti-inflammatory drugs are major causes of drug-induced anaphylaxis. / Allergy Clin Immunol Pract. 2014;2(4):414-20. 6. Furst DE, Ulrich RW, Prakash S. Chapter 36. Nonsteroidal anti-inflammatory drugs, disease-modifying antirheumatic drugs, nonopioid analgesics and drugs used in gout. In Katsung BG, Masters SB, Trevor AJ, eds. Basic & Clinical Pharmacology. 12th ed. New York: McGraw Hill; 2012. 7. Bavry AA, Thomas F, Allison M, et al. Nonsteroidal anti-inflammatory drugs and cardiovascular outcomes in women: results from the women’s health initiative. Circ Cardiovasc Qual Outcomes. 2014;7(4):603-610.
S ta y u p to d a te w it h th e p e e r -r e v ie w e d
journal of clinical excellence N u rs in g 2 0 1 5 is the award-winning, how-to journal that provides practical, handson information for all nurses. Readers say this peer-reviewed journal is their first choice for quick-read updates on the most comprehensive range of nursing topics.
11. Derry S, Moore RA, Rabbie R. Topical NSAIDs for chronic musculoskeletal pain in adults. Cochrane Database Syst Rev. 2012;9:CD007400. 12. Davis MP. Drug management o f visceral pain: concepts from basic research. Pain Res Treat. 2012;2012:265605. 13. Stepensky D, Rimon G. Competition between low-dose aspirin and other NSAIDs for COX-1 binding and its clinical consequences for the drugs’ antiplatelet effects. Expert Opin DrugMetab Toxicol. 2015;11(1 ):41-52. 14. Lamberts M, Lip GY, Hansen ML, et al. Relation of nonsteroidal anti-inflam matory drugs to serious bleeding and thromboembolism risk in patients with atrial fibrillation receiving antithrombotic therapy: a nationwide cohort study. Ann Intern Med. 2014;161(10):690-698.
— Published m onthly
• O n lin e a c c e s s • M o b ile v ie w • iP a d App
— Including the fu ll archives at Nursing2015.com
— Full-text access via most internet-enabled devices
— Available for download from the App StoreSM
Subscribe today at LWW.com or call 1-800-638-3030 N u r s in g 2 0 1 5 .c o m
A ppS tore
W o lte rs K lu w e r Apple and iPad are tradem arks of Apple Inc., registered in the U. S. and other countries. App Store is a service m ark of Apple Inc.
2 2 The Nurse Practitioner • Vol. 40, No. 6
9. Ray WA, Varas-Lorenzo C, Chung CP, et al. Cardiovascular risks of nonsteroidal antiinflammatory drugs in patients after hospitalization for serious coronary heart disease. Circ Cardiovasc Qual Outcomes. 2009;2(3): 155-163. 10. Klinge SA, Sawyer GA. Effectiveness and safety of topical versus oral nonste roidal anti-inflammatory drugs: a comprehensive review. Phys Sportsmed. 2013;41(2):64-74.
Y o u r p e rs o n a l s u b s c rip tio n in c lu d e s : • P rin t
8. McGettigan P, Henry D. Cardiovascular risk with non-steroidal anti inflammatory drugs: systematic review of population-based controlled observational studies. PLoS Med. 2011;8(9):el001098.
KID
15. Schmidt M, Hovath-Puho E, Christiansen CF, Petersen KL, Botker HE, So rensen HT. Preadmission use of nonaspirin nonsteroidal anti-inflammatory drugs and 30-day stroke mortality. Neurology. 2014;83(22):2013-2022. 16. Wehling M. Non-steroidal anti-inflammatory drug use in chronic pain conditions with special emphasis on the elderly and patients with relevant comorbidities: management and mitigation o f risks and adverse effects. Eur J Clin Pharmacol. 2014;70( 10): 1159-1172. Karen S. Abate is adjunct faculty at Simmons College, Boston, Mass and mentor (online course instructor) at Thomas Edison State College, W. Cary Edwards School of Nursing, Trenton, N.J. Terry Mahan Buttaro is an assistant clinical professor at University of Massachusetts, Boston, Mass. The authors have disclosed that they have no financial relationships related to this article. D O I-10.1097/01.NPR.0000465125.35030.3a
www.tnpj.com
Copyright of Nurse Practitioner is the property of Springhouse Corporation and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use.
S a fe a n d e ffe c tiv e N S A ID use
By Karen S. Abate, PhD, ANP-BC and Terry Mahan Buttaro, PhD, AIMP-BC,
toxic effects than the currently available NSAIDs.1,2
GNP-BC, FAANP, DPNAP P h a rm a c o d y n a m ic s and
Nonsteroidal anti-inflammatory drugs (NSAIDs) are pharmaceuticals used to treat fever, inflammation, and pain. There are many NSAIDs— both oral and parenteral— available over-the-counter (OTC) or by prescription. The purpose of this article is to review NSAIDs and their appropriateness to manage chronic pain.
p h a r m a c o k in e tic s
Nonselective NSAIDs inhibit COX-1 and COX-2, the enzymes responsible for formulating prostaglandin (an inflammatory mediator from arachidonic acid).3'4 NSAIDs are most often categorized as nonselective COX inhibitors or selective COX-2 inhibitors. Both categories are useful for managing inflammatory pain and
Topical NSAIDs are also a valid alternative to oral preparations because there are fewer GI effects.
There are several NSAID chemical classes with varied mechanisms of action, half-lives, efficacies, and adverse reactions. Two of the oldest classes of NSAIDs include salicylates (aspirin) and nonacetylated salicylates (choline magnesium trisalicylate). The nonselective cyclooxygenase (COX) inhibitor NSAIDs (also known as traditional NSAIDs) include several classes: acetic acids (such as diclof enac, indomethacin), fenamates (such as mefenamic acid), oxicam deriva tives (such as meloxicam), and propionic acids (such as ibuprofen and naproxen). The most recent class of NSAIDs is the COX-2 selective inhibitors (celecoxib). Nitric oxide releasing NSAIDs and hydrogen sulfide-releasing NSAIDs are newer categories that are currently under investigation and may have fewer 18 The Nurse Practitioner • Vol 40, No. 6
are well absorbed. The first pass effect of these medications is minimal. All are highly protein-bound and metabolized by the liver. The half-lives are variable, with some NSAIDs (ibuprofen) lasting only 6 hours and others (naproxen) lasting longer. Adverse reactions. NSAIDs can cause gastrointestinal (GI) bleeding, liver function test abnormalities, hematologic effects, nonallergic angioedema, bronchospasm, or urticaria and can be a significant medication-related cause of ED visits.5,6All NSAIDs cause some GI distress (pain, diarrhea, flatulence), but because COX-2 inhibitors inhibit only the COX-2 enzyme, they cause fewer gastric ulcers and bleeding than the nonselective NSAIDs.6 There is, however, a boxed warning on NSAIDs
noting that there are potential anaphylactoid reactions as well as adverse cardiovascular (CV), GI, hematological, hepatic, and renal effects. Findings from the Women’s Health Initiative indicated that postmenopausal women who regularly used selective COX-2 inhibitors and nonselective NSAIDs with COX-2 inhibition greater than COX-1 inhibition had an increased risk for CV events. Participants who used nonselective agents with COX-1 inhibition greater than COX-2 inhibition did not have an increased CV risk.7 The renal and CV effects associ ated with NSAIDs are particularly concerning in older adults, patients with kidney dysfunction, and patients with CV disease.6 NSAIDs can cause hyperkalemia, increase BP and fluid retention, and, if used in combination with aspirin, negate the antiplatelet effects of aspirin.6 Salicylates. Aspirin, an acetylated salicylate, is a non-COX selective NSAID. Aspirin is now more frequently used for its irrevers ible inhibitory action on platelet COX and its antithrombotic properties in the prevention and treatm ent of CV and cerebrovascu lar events than for pain manage ment. However, aspirin has some anti-inflammatory activity and can be used for pain, though relief will likely not be dramatic. The risks of regular aspirin, even at 75 to 100 mg a day, are well documented and include: Reyes syndrome, epigastric upset, GI bleeding, hypersensitivity, www.tnpj.com
Pain Solutions hematologic effects, hepatotoxicity, renal toxicity, and, in high doses, salicylate intoxication.5,6 Nonselective COX NSAIDs. The nonselective NSAIDs are used primarily for their analgesic and anti-inflammatory properties, but some (ibuprofen and indomethacin) are effectively used for closure of patent ductus arteriosus in infants, while others aid in treatment of gingivitis and actinic keratosis.6In theory, the nonselective NSAIDs are equally effective, but because their chemical structures are different, some are more effective than others for some types of pain. The adverse reactions can also be different with some NSAIDs, causing more toxicity than others. Selective COX-2 inhibitors. The selective COX-2 inhibitors were
pain, dysmenorrhea, and other inflammatory conditions. Unfortu nately, they also cause untoward effects in multiple organ systems. Peptic ulcer disease is a documented risk in NSAID therapy, but lower GI bleeding is also a concern. Bleeding is a definite consideration for patients taking nonselective NSAIDs; thus, it is important to avoid prescribing nonselective NSAIDs if there is a past medical history of GI bleeding.2 However, GI bleeding is possibly moderated by a concurrent administration of a proton pump inhibitor or histamine H, blocker antagonist.2 According to McGettigan and Henry, naproxen and ibuprofen (in small doses) for a short amount of time can be an option if the patient understands the risks—even in
For all patients, using the least toxic medications in any drug category constitutes good practice. designed specifically to decrease the adverse GI effects associated with the nonselective NSAIDs.6 Initial studies suggested that patients incurred less GI ulceration and bleeding when taking a COX-2 inhibitor. More recently, however, the benefits of COX-2 inhibition on the GI system are less clear, and the concerns regarding the increased risk of CV events warrant careful consideration for all healthcare providers.6 Celecoxib is the only available purely selective COX-2 inhibitor in the U.S. at this time. Meloxicam is a revers ible inhibitor of both COX-1 and COX-2 enzymes, but it is a greater inhibitor of the COX-2 enzyme. P a in m a n a g e m e n t re c o m m e n d a tio n s
NSAIDs are an effective treatment for musculoskeletal pain, arthritic 20 The Nurse Practitioner • Vol. 40, No. 6
patients with CV disease.8In another large, retrospective study, naproxen was a safer alternative than other NSAIDs for patients with a recent hospital stay for a myocardial infarction, revascularization, or unstable angina.9 For all patients, using the least toxic medications in any drug category constitutes good practice. Topical NSAIDs are also a valid alter native to oral preparations because there are fewer GI effects.10Accord ing to Derry, topical NSAIDs— especially in gel form—provide relief for patients with chronic musculo skeletal pain.11 For patients with hand or knee pain associated with osteoarthritis, topical diclofenac can ease the pain associated with osteoarthritis, and at least short term (less than 12 weeks) seems less likely to cause GI bleeding.11
Other NSAID pain management recommendations include: • Enteric or extended-release medications should not be prescribed for treating acute pain because the drug formulation will delay the rate of absorption, thus impacting pain management • NSAIDs are effective for biliary and renal colic12 • Nonselective NSAIDs can poten tially increase GI bleeding and should not be used in combination with aspirin • NSAIDs should not be used if the patient is taking aspirin for cardioprotective reasons. Concur rent NSAID and aspirin use negates antiplatelet action of aspirin and increases risk for thromboembolic events13 • NSAIDs should be avoided in patients with atrial fibrillation due to increased risk of bleeding and thromboembolism when patients are also taking an antiplatelet or anticoagulant agent14 • COX-2 inhibitor NSAIDs for patients at risk for stroke should be avoided15 • NSAIDs are associated with continued microvascular damage and inflammation in patients with inflammatory bowel disease and should be avoided12 P ra c tic e re c o m m e n d a tio n s
It is imperative for the provider to complete a comprehensive history and thorough physical exam prior and during NSAID prescribing. The adverse reactions of NSAID use are often associated with manifestations in the GI, renal, and CV systems. As such, a focused history and physical exam of these organ systems should be performed. Subjective complaints such as gastric discomfort, dyspepsia, burning, or gastric discomfort and bloating should be evaluated.16Hepatic www.tnpj.com
Pain Solutions function assessment by means of liver function tests and determination of liver span should be completed. Assessment of kidney function by means of creati nine clearance along with a renal function panel is recommended in older adults as well as those with polypharmacy concerns, as these are risk factors for NSAID-associated kidney failure. 16 CV assessment should include the evaluation of heart sounds, peripheral edema, and BP, as arterial hypertension is an associated adverse reaction related to chronic NSAID use. 16 Antiplatelet hematologic effects associated with NSAIDs use can be evaluated with a periodic complete blood count. A comprehensive health history, including comor bidities and additional risk factors, should be consid ered relative to the risk benefit ratio of NSAID use with patients. In addition, OTC preparation and herbal supplement use should be appraised for potential interactions. Routine clinical follow up is recommended for patients with regular NSAID use. Monitoring of any NSAID use, risks, benefits, and adverse reactions should be ongoing. 16 NSAIDs should be promptly discontinued should any of the aforementioned factors, assessment
findings, or blood work indicate an actual or potential adverse reaction relative to NSAID use. 16 Clinician referral would be appropriate at that time. NSAIDs are frequently used to treat fever, inflammation, and pain; however, they are not without patient risk. As such, both OTC and prescription-based usage should be carefully monitored by healthcare providers. C D REFERENCES 1. Atkinson TJ, Fudin J, Jahn HL, Kubotera N, Rennick AL, Rhorer M. What’s new in NSAID pharmacotherapy: oral agents to injectables. Pain Med. 2013;14(suppl 1):S11-S17. 2. Gargallo CJ, Lanas A. Is NSAIDs-related gastrointestinal damage prevent able? J Dig Dis. 2013; 14(2):55-61. 3. Smyth EM, Fitzgerald GA. Chapter 18. The eicosanoids, prostaglandins, leukotrienes 8c related compounds. In: Katsung BG, Masters SB, Trevor AJ, eds. Basic & Clinical Pharmacology. 12th ed. New York: McGraw Hill Lange. 4. Ricciotti E, Fitzgerald GA. Prostaglandins and inflammation. Arterioscler Thromb Vase Biol. 2011 ;31(5):986-1000. 5. Aun MV, Blanca M, Garro LS, et al. Nonsteroidal anti-inflammatory drugs are major causes of drug-induced anaphylaxis. / Allergy Clin Immunol Pract. 2014;2(4):414-20. 6. Furst DE, Ulrich RW, Prakash S. Chapter 36. Nonsteroidal anti-inflammatory drugs, disease-modifying antirheumatic drugs, nonopioid analgesics and drugs used in gout. In Katsung BG, Masters SB, Trevor AJ, eds. Basic & Clinical Pharmacology. 12th ed. New York: McGraw Hill; 2012. 7. Bavry AA, Thomas F, Allison M, et al. Nonsteroidal anti-inflammatory drugs and cardiovascular outcomes in women: results from the women’s health initiative. Circ Cardiovasc Qual Outcomes. 2014;7(4):603-610.
S ta y u p to d a te w it h th e p e e r -r e v ie w e d
journal of clinical excellence N u rs in g 2 0 1 5 is the award-winning, how-to journal that provides practical, handson information for all nurses. Readers say this peer-reviewed journal is their first choice for quick-read updates on the most comprehensive range of nursing topics.
11. Derry S, Moore RA, Rabbie R. Topical NSAIDs for chronic musculoskeletal pain in adults. Cochrane Database Syst Rev. 2012;9:CD007400. 12. Davis MP. Drug management o f visceral pain: concepts from basic research. Pain Res Treat. 2012;2012:265605. 13. Stepensky D, Rimon G. Competition between low-dose aspirin and other NSAIDs for COX-1 binding and its clinical consequences for the drugs’ antiplatelet effects. Expert Opin DrugMetab Toxicol. 2015;11(1 ):41-52. 14. Lamberts M, Lip GY, Hansen ML, et al. Relation of nonsteroidal anti-inflam matory drugs to serious bleeding and thromboembolism risk in patients with atrial fibrillation receiving antithrombotic therapy: a nationwide cohort study. Ann Intern Med. 2014;161(10):690-698.
— Published m onthly
• O n lin e a c c e s s • M o b ile v ie w • iP a d App
— Including the fu ll archives at Nursing2015.com
— Full-text access via most internet-enabled devices
— Available for download from the App StoreSM
Subscribe today at LWW.com or call 1-800-638-3030 N u r s in g 2 0 1 5 .c o m
A ppS tore
W o lte rs K lu w e r Apple and iPad are tradem arks of Apple Inc., registered in the U. S. and other countries. App Store is a service m ark of Apple Inc.
2 2 The Nurse Practitioner • Vol. 40, No. 6
9. Ray WA, Varas-Lorenzo C, Chung CP, et al. Cardiovascular risks of nonsteroidal antiinflammatory drugs in patients after hospitalization for serious coronary heart disease. Circ Cardiovasc Qual Outcomes. 2009;2(3): 155-163. 10. Klinge SA, Sawyer GA. Effectiveness and safety of topical versus oral nonste roidal anti-inflammatory drugs: a comprehensive review. Phys Sportsmed. 2013;41(2):64-74.
Y o u r p e rs o n a l s u b s c rip tio n in c lu d e s : • P rin t
8. McGettigan P, Henry D. Cardiovascular risk with non-steroidal anti inflammatory drugs: systematic review of population-based controlled observational studies. PLoS Med. 2011;8(9):el001098.
KID
15. Schmidt M, Hovath-Puho E, Christiansen CF, Petersen KL, Botker HE, So rensen HT. Preadmission use of nonaspirin nonsteroidal anti-inflammatory drugs and 30-day stroke mortality. Neurology. 2014;83(22):2013-2022. 16. Wehling M. Non-steroidal anti-inflammatory drug use in chronic pain conditions with special emphasis on the elderly and patients with relevant comorbidities: management and mitigation o f risks and adverse effects. Eur J Clin Pharmacol. 2014;70( 10): 1159-1172. Karen S. Abate is adjunct faculty at Simmons College, Boston, Mass and mentor (online course instructor) at Thomas Edison State College, W. Cary Edwards School of Nursing, Trenton, N.J. Terry Mahan Buttaro is an assistant clinical professor at University of Massachusetts, Boston, Mass. The authors have disclosed that they have no financial relationships related to this article. D O I-10.1097/01.NPR.0000465125.35030.3a
www.tnpj.com
Copyright of Nurse Practitioner is the property of Springhouse Corporation and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use.
