CH71 Nsaids KEY Points Nursing Implications PDF

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It a great summary with key points for drugs categorized as NSAIDs including the nursing consideration for Nurs 123 class....

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CHAPTER 71 NSAIDS_COX-INHIBITORS_ACETAMINOPHEN Key Points 

■ All of the drugs discussed in this chapter inhibit cyclooxygenase (COX), an enzyme that converts arachidonic acid into prostanoids (prostaglandins and related compounds).

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■ Cyclooxygenase has two forms: COX-1 and COX-2.

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■ The cyclooxygenase inhibitors fall into two major groups: nonsteroidal anti-inflammatory drugs (NSAIDs) and acetaminophen (in a group by itself).

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■ The NSAIDs can be subdivided into two groups: (1) first-generation NSAIDs, which inhibit COX1 and COX-2, and (2) second-generation NSAIDs, which selectively inhibit COX-2.

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■ Inhibition of COX-1 can cause gastric ulceration, renal impairment, and bleeding.

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■ Inhibition of COX-2 suppresses inflammation, pain, and fever, but can also cause renal impairment.

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■ Aspirin is the prototype of the first-generation NSAIDs.

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■ Aspirin has four major beneficial actions: suppression of inflammation, relief of mild to moderate pain, reduction of fever, and prevention of MI and stroke (secondary to suppressing platelet aggregation). All of these benefits result from inhibiting COX-2, except for prevention of MI and stroke, which results from inhibiting COX-1 (in platelets).

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■ Because aspirin inhibits COX-1 as well as COX-2, it cannot cause beneficial effects without posing a risk of gastric ulceration, bleeding, and renal impairment.

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■ Aspirin causes irreversible inhibition of cyclooxygenase. As a result, the effects of aspirin persist until cells can make more cyclooxygenase.

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■ Because platelets are unable to synthesize new cyclooxygenase, the antiplatelet effects of a single dose of aspirin persist for the life of the platelet (about 8 days).

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■ Anti-inflammatory doses of aspirin are much higher than analgesic or antipyretic doses.

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■ Aspirin is a useful drug for rheumatoid arthritis and other chronic inflammatory conditions.

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■ Aspirin is a very effective analgesic. It can be as effective as opioids for some types of postoperative pain.

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■ The risk of aspirin-induced gastric ulcers can be reduced by (1) testing for and eliminating H. pylori before starting therapy and by (2) giving a proton pump inhibitor or histamine receptor antagonist. 2

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■ Because of its antiplatelet actions, aspirin can protect against MI, stroke, and other thrombotic events.

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■ When taken for primary prevention, the benefits of aspirin must be weighed against the potential for harm. Ibuprofen, naproxen, and other nonaspirin NSAIDs can antagonize the antiplatelet actions of aspirin and can thereby decrease protection against MI and stroke. To minimize this interaction, patients should take aspirin about 2 hours before other NSAIDs.

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■ Because of its antiplatelet actions, high-dose aspirin should be discontinued 1 week before elective surgery or parturition. In most cases, low-dose aspirin taken to protect against thrombosis can be continued.

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■ Because of its antiplatelet actions, aspirin can increase the risk of bleeding in patients taking warfarin, heparin, and other anticoagulants.

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■ By impairing renal function, aspirin can cause sodium and water retention, edema, and elevation of blood pressure. However, adverse outcomes are likely only in patients with additional risk factors: advanced age, pre-existing renal dysfunction, hypovolemia, hypertension, hepatic cirrhosis, or heart failure. Long-term aspirin use may lead to renal papillary necrosis and other forms of renal injury.

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■ Because of the risk of Reye's syndrome, aspirin should be avoided by children with influenza or chickenpox.

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■ Use of aspirin during labor and delivery can suppress spontaneous uterine contractions, induce premature closure of the ductus arteriosus, and intensify uterine bleeding.

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■ Although rarely fatal in adults, aspirin poisoning may prove lethal in children.

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■ Aspirin can cause hypersensitivity reactions, especially in adults with asthma, rhinitis, and nasal polyps. Severe reactions (anaphylaxis) can be treated with epinephrine.

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■ All of the nonaspirin first-generation NSAIDs are much like aspirin itself. All of these drugs inhibit COX-1 and COX-2; they all can suppress inflammation, pain, and fever; and they all can cause gastric ulceration, renal impairment, and bleeding.

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■ The nonaspirin NSAIDs differ from aspirin in three important ways. First, nonaspirin NSAIDs cause reversible inhibition of COX, and hence their effects decline as soon as their blood levels decline. Second, although they can suppress platelet aggregation, these drugs are not used to prevent MI and stroke. Third, these drugs actually increase the risk of MI and stroke, and hence should be used in the lowest effective dosage for the shortest possible time.

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■ By inhibiting COX-2, the second-generation NSAIDs (coxibs) can suppress inflammation, pain, and fever.

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■ By sparing COX-1, the coxibs may cause less gastric ulceration than the first-generation NSAIDs.

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■ Coxibs do not inhibit platelet aggregation, and hence do not pose a risk of bleeding.

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■ Like all first-generation NSAIDs (except aspirin), coxibs pose a risk of MI and stroke.

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■ Currently, celecoxib [Celebrex] is the only coxib on the market.

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■ Acetaminophen reduces pain and fever, but not inflammation.

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■ Acetaminophen inhibits prostaglandin synthesis in the CNS, but not in the periphery. As a result, acetaminophen differs from the NSAIDs in four ways: it (1) lacks anti-inflammatory actions, (2) does not cause gastric ulceration, (3) does not suppress platelet aggregation, and (4) does not impair renal function.

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■ Hepatic necrosis from acetaminophen overdose results from the accumulation of a toxic metabolite. Risk is increased by undernourishment, alcohol consumption, and pre-existing liver disease.

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■ Chronic alcohol consumption increases the risk of liver damage from acetaminophen overdose, but probably not from therapeutic doses. Two major mechanisms are involved: induction of cytochrome P450 (which increases production of the toxic metabolite of acetaminophen) and depletion of glutathione stores (which reduces detoxification of the metabolite).

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■ Acetaminophen may increase the risk of warfarin-induced bleeding by inhibiting the metabolism of warfarin.

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■ Acetaminophen is associated with SJS, AGEP, and TEN. If rash appears, this may be a medical emergency.

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■ Acetaminophen overdose is treated with PO or IV acetylcysteine, a drug that substitutes for depleted glutathione in the reaction that clears the toxic metabolite of acetaminophen.

Summary of Major Nursing Implications

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Nonsteroidal Anti-Inflammatory Drugs First-Generation NSAIDs                      

Aspirin Diclofenac Diflunisal Etodolac Fenoprofen Flurbiprofen Ibuprofen Indomethacin Ketoprofen Ketorolac Magnesium salicylate Meclofenamate Mefenamic acid Meloxicam Nabumetone Naproxen Oxaprozin Piroxicam Salsalate Sodium salicylate Sulindac Tolmetin

Second-Generation NSAIDs (Coxibs)  Celecoxib  Except where noted, the nursing implications described here apply to aspirin and all other NSAIDs.

Preadministration Assessment Therapeutic Goal Major indications for the NSAIDs are inflammatory disorders (e.g., rheumatoid arthritis, osteoarthritis), mild to moderate pain, fever, and primary dysmenorrhea. In addition, aspirin is used to prevent MI and stroke. Applications of individual NSAIDs are shown in Table 71.4.

Identifying High-Risk Patients NSAIDs are contraindicated for patients with a history of severe NSAID hypersensitivity. NSAIDs (especially aspirin) are contraindicated for children with chickenpox or influenza. Celecoxib is contraindicated for patients with sulfa allergy. NSAIDs should be used with extreme caution by pregnant women and patients with peptic ulcer disease and bleeding disorders (e.g., hemophilia, vitamin K deficiency, hypoprothrombinemia) and patients taking anticoagulants (e.g., warfarin, heparin), glucocorticoids, ACE inhibitors, or ARBs. Caution is also needed when treating older adult patients and patients with heart failure, angina pectoris, history of MI, hypertension, hypovolemia, hepatic cirrhosis, renal dysfunction, asthma, hay fever, chronic urticaria, nasal polyps, or a history of alcoholism or heavy smoking.

Implementation: Administration Routes Oral. All NSAIDs. Topical. Diclofenac (patch, solution, and gel). Intranasal. Ketorolac. Intramuscular. Ketorolac.

Intravenous. Ibuprofen, ketorolac. Rectal Suppository. Aspirin, indomethacin.

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• Advise patients to take oral NSAIDs with food, milk, or a glass of water to reduce gastric upset. • Warn patients not to crush or chew enteric-coated or sustained-release formulations. • Advise patients to discard aspirin preparations that smell like vinegar. • Advise patients using topical diclofenac to apply the gel 4 times a day or to apply a new patch twice a day.

Ongoing Evaluation and Interventions Minimizing Adverse Effects Gastrointestinal Effects. NSAIDs frequently cause mild GI reactions (dyspepsia, abdominal pain, nausea). To minimize GI effects, advise patients to take NSAIDs with food, milk, or water. Long-term therapy, even at moderate doses, can cause gastric ulceration, perforation, and hemorrhage. Several measures can reduce risk:

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• Avoid NSAIDs in patients with a recent history of peptic ulcer disease, and use NSAIDs with caution in patients with other risk factors (advanced age, previous intolerance to NSAIDs, heavy cigarette smoking, history of alcoholism). • Test for and eliminate H. pylori before starting long-term therapy. • Give a proton pump inhibitor (PPI) or histamine receptor antagonist (H RA) for prophylaxis in highrisk patients. • Use celecoxib instead of a traditional NSAID in high-risk patients. • Warn patients not to consume alcohol. • Instruct patients to notify the prescriber if gastric irritation is severe or persistent. 2

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Manage ulcers by giving an antiulcer medication (e.g., H2RA, PPI). Bleeding. Aspirin promotes bleeding by causing irreversible suppression of platelet aggregation. High-dose aspirin should be discontinued 7 to 10 days before elective surgery or anticipated date of parturition, but need not be stopped before minor dental, dermatologic, or cataract surgeries. Discontinuation of low-dose aspirin depends on circumstances. Specifically, low-dose aspirin should be discontinued in:

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• Patients considered at low risk of a cardiovascular event who require noncardiac surgery. Dosing should stop 7 to 10 days before surgery and can resume 24 hours after the procedure. • Patients undergoing intracranial surgery.

Conversely, low-dose aspirin should be continued in:

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• Patients undergoing coronary artery bypass surgery (CABG). • Patients facing surgery within 6 weeks of receiving a bare-metal coronary stent or within 12 months of receiving a drug-eluting coronary stent. • Patients considered at high risk of a cardiovascular event who require noncardiac surgery or a percutaneous coronary intervention. • Patients undergoing cataract surgery, minor dental procedures, or minor dermatologic procedures.

Exercise caution when using aspirin in conjunction with warfarin, heparin, and other anticoagulants. Avoid aspirin in patients with bleeding disorders (e.g., hemophilia, vitamin K deficiency, hypoprothrombinemia).

Discontinue ibuprofen and other nonaspirin NSAIDs five half-lives before elective surgery and childbirth. The nonacetylated salicylates—sodium salicylate, magnesium salicylate, and salsalate—have minimal effects on platelet aggregation. Accordingly, these drugs are preferred for use in surgical patients and patients with bleeding disorders. The risk of bleeding can be minimized by using celecoxib instead of a traditional NSAID. Renal Impairment. NSAIDs can cause acute renal insufficiency in older adult patients and in patients with heart failure, hypovolemia, hepatic cirrhosis, or preexisting renal dysfunction. Keep NSAID dosages as low as possible in these patients. Monitor high-risk patients for indications of renal impairment (reduced urine output, weight gain despite diuretic therapy, rapid elevation of serum creatinine and blood urea nitrogen). Discontinue NSAIDs if these signs occur. Prolonged NSAID therapy can cause renal papillary necrosis. Avoid prolonged NSAID use whenever possible. Myocardial Infarction and Stroke. Nonaspirin NSAIDs—but not aspirin itself—increase the risk of MI and stroke. To minimize cardiovascular risk, nonaspirin NSAIDs should be used in the lowest effective dosage for the shortest time needed, and they should not be used before CABG surgery or for 14 days after. In patients with cardiovascular risk factors, use all NSAIDs (except aspirin) with caution, and use celecoxib only as a last resort. Hypersensitivity Reactions. Hypersensitivity reactions are most likely in adults with a history of asthma, rhinitis, and nasal polyps. Use NSAIDs with caution in these patients. If a severe hypersensitivity reaction occurs, parenteral epinephrine is the treatment of choice. As a rule, avoid NSAIDs in patients with a history of NSAID hypersensitivity. However, if an NSAID-like drug must be used, four are probably safe: celecoxib, salsalate, meloxicam (in low doses), and acetaminophen. Salicylism. Aspirin and other salicylates can cause salicylism. Educate patients about manifestations of salicylism (tinnitus, sweating, headache, dizziness), and advise them to notify the prescriber if these occur. Aspirin should be withheld until symptoms subside, after which therapy can resume but at a slightly reduced dosage. Reye's Syndrome. Use of NSAIDs, especially aspirin, by children with chickenpox or influenza may precipitate Reye's syndrome. Advise parents to avoid aspirin in these children and to use acetaminophen instead. Use in Pregnancy. NSAIDs can cause maternal anemia and can prolong labor. In addition, they can promote premature closure of the ductus arteriosus. NSAIDs should be avoided by expectant mothers unless the potential benefits outweigh the risks. If NSAIDs are employed during pregnancy, they should be discontinued at least five half-lives before the anticipated day of delivery. Liver Injury. Diclofenac can cause severe liver injury. Patients should receive periodic liver function tests. Inform patients about signs of liver damage (e.g., jaundice, fatigue, nausea), and instruct them to report these immediately. If liver injury is diagnosed, diclofenac should be discontinued. Sulfonamide Allergy. Celecoxib can cause severe allergic reactions in patients with sulfa allergy, and hence must not be given to these people.

Minimizing Adverse Interactions Anticoagulants. NSAIDs can increase the risk of bleeding in patients taking warfarin, heparin, and other anticoagulants. Monitor patients for signs of bleeding. Glucocorticoids. Glucocorticoids increase the risk of gastric ulceration in patients taking NSAIDs. Prophylactic therapy with a PPI or H 2RA can decrease the risk. Alcohol. Alcohol increases the risk of gastric ulceration from NSAIDs. Exercise caution. Aspirin-NSAID Interactions. Ibuprofen, naproxen, and other nonaspirin NSAIDs can antagonize the antiplatelet actions of aspirin and can thereby decrease protection against MI and stroke. Advise patients to take aspirin about 2 hours before taking another NSAID.

ACE Inhibitors and ARBs. These drugs increase the risk of acute renal failure in patients taking NSAIDs. If possible, avoid all NSAIDs—except low-dose aspirin—in patients taking ACE inhibitors or ARBs. Vaccines. NSAIDs may blunt the immune response to vaccines. Advise parents to avoid routine use of NSAIDs to prevent vaccination-associated fever and pain.

Managing Aspirin Toxicity Aspirin poisoning is an acute medical emergency that requires hospitalization. Treatment is largely supportive and consists of external cooling (e.g., sponging with tepid water), infusion of fluids (to correct dehydration and electrolyte loss), infusion of bicarbonate (to reverse acidosis and promote renal excretion of salicylates), and mechanical ventilation (if respiration is severely depressed). Absorption of aspirin can be reduced by gastric lavage and by giving activated charcoal. If necessary, hemodialysis or peritoneal dialysis can accelerate salicylate removal.

Acetaminophen Preadministration Assessment Therapeutic Goal Acetaminophen is indicated to relieve pain and to reduce fever. The drug is preferred to NSAIDs for use in children with chickenpox or influenza, and for all patients with peptic ulcer disease.

Identifying High-Risk Patients Use with caution in chronic alcohol abusers, patients who consume moderate amounts of alcohol daily, and patients taking warfarin.

Implementation: Administration Routes Oral, rectal, intravenous.

Administration Do not exceed recommended doses.

Ongoing Evaluation and Interventions Minimizing Adverse Effects Acetaminophen is largely devoid of significant adverse effects at usual therapeutic doses, except possibly in people who routinely consume alcohol. Overdose can cause liver damage (discussed later). Hypertension. Taking at least 500 mg of acetaminophen per day is associated with an increased risk of hypertension, although studies have demonstrated conflicting data. Nonetheless, prudence dictates the monitoring of blood pressure in patients who take acetaminophen each day. Asthma. Acetaminophen is associated with an increased risk of asthma, although a causal relationship has not been established. Anaphylaxis. Rarely, acetaminophen causes anaphylaxis. Inform patients about symptoms—breathing difficulty associated with swelling of the face, mouth, and throat—and advise them to seek immediate medical help if these develop. Skin Reactions. Acetaminophen has been associated with SJS, AGEP, and TEN. If rash develops, the patient should stop the medication and seek medical attention. Liver Damage. Overdose can cause hepatic necrosis. Risk is increased by consuming high doses (more than 4000 mg/day), as well as by undernourishment, alcohol consumption, and pre-existing liver disease. To reduce risk:

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• Inform patients about the risk of liver injury. • Advise patients to consume no more than 4000 mg of acetaminophen a day, including the amount in combination prescription products (e.g., Vicodin, Percocet) as well as OTC products. • Advise patients who are undernourished (e.g., owing to fasting or illness) to consume no more than 3000 mg of acetaminophen a day. • Advise patients not to drink alcohol while taking acetaminophen. • Advise patients who won't stop drinking alcohol (more than 3 drinks a day) to take no more than 2000 mg of acetaminophen a day. • Advise patients with liver disease to ask their prescribers whether acetaminophen is safe.

Acetylcysteine—given PO or IV—is a specific antidote to acetaminophen overdose. Oral acetylcysteine has an extremely unpleasant odor and may induce vomiting. If vomiting interferes with oral dosing, there are two options: give acetylcysteine IV or through an oroduodenal tube.

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