Nonsteroidal Anti-inflammatory Drugs (NSAIDs)


Article Author:
Ida Ghlichloo


Article Editor:
Valerie Gerriets


Editors In Chief:
Sisira Reddy
Joseph Nahas
Chokkalingam Siva


Managing Editors:
Avais Raja
Orawan Chaigasame
Khalid Alsayouri
Kyle Blair
Radia Jamil
Erin Hughes
Patrick Le
Anoosh Zafar Gondal
Saad Nazir
William Gossman
Hassam Zulfiqar
Navid Mahabadi
Hussain Sajjad
Steve Bhimji
Muhammad Hashmi
John Shell
Matthew Varacallo
Heba Mahdy
Ahmad Malik
Abbey Smiley
Sarosh Vaqar
Mark Pellegrini
James Hughes
Beenish Sohail
Hajira Basit
Phillip Hynes
Sandeep Sekhon


Updated:
9/28/2019 11:28:47 PM

Indications

Nonsteroidal anti-inflammatory drugs (NSAIDs) are a drug class FDA-approved for use as antipyretic, anti-inflammatory, and analgesic agents.[1] These effects make NSAIDs useful for the treatment of muscle pain, dysmenorrhea, arthritic conditions, pyrexia, gout, migraines, and used as opioid-sparing agents in certain acute trauma cases.[2][3][4]

NSAIDs are typically divided into groups based on their chemical structure and selectivity: acetylated salicylates (aspirin), non-acetylated salicylates (diflunisal, salsalate), propionic acids (naproxen, ibuprofen, acetic acids (diclofenac, indomethacin), enolic acids (meloxicam, piroxicam) anthranilic acids (meclofenamate, mefenamic acid), naphthylalanine (nabumetone), and selective COX-2 inhibitors (celecoxib, etoricoxib).   

Topical NSAIDs (diclofenac gel) are also available for use in acute tenosynovitis, ankle sprains, and soft tissue injuries.[5][6][7][8]

Listed below are the FDA-approved NSAIDs (organized alphabetically):

Non-selective NSAIDs

  • Diclofenac
  • Diflunisal
  • Etodolac
  • Fenoprofen
  • Flurbiprofen
  • Ibuprofen
  • Indomethacin
  • Ketoprofen
  • Ketorolac
  • Mefenamic acid
  • Meloxicam
  • Nabumetone
  • Naproxen
  • Oxaprozin
  • Piroxicam
  • Sulindac
  • Tolmetin

COX-2 Selective NSAIDs

  • Celecoxib
  • Rofecoxib
  • Valdecoxib

(However, rofecoxib and valdecoxib were withdrawn from the market in 2004 and 2005, respectively)

Mechanism of Action

The main mechanism of action of NSAIDs is the inhibition of the enzyme cyclooxygenase (COX). Cyclooxygenase is required to convert arachidonic acid into thromboxanes, prostaglandins, and prostacyclins.[9] The therapeutic effects of NSAIDs are attributed to the lack of these eicosanoids. Specifically, thromboxanes play a role in platelet adhesion, prostaglandins cause vasodilation, increase the temperature set-point in the hypothalamus, and play a role in anti-nociception. 

There are two cyclooxygenase isoenzymes, COX-1 and COX-2. COX-1 gets constitutively expressed in the body, and it plays a role in maintaining gastrointestinal mucosa lining, kidney function, and platelet aggregation. COX-2 is not constitutively expressed in the body, and instead it inducibly expresses during an inflammatory response. Most of the NSAIDs are nonselective and inhibit both COX-1 and COX-2. However, COX-2 selective NSAIDs (ex. celecoxib) only target COX-2 and therefore have a different side effect profile. Importantly, because COX-1 is the prime mediator for ensuring gastric mucosal integrity and COX-2 is mainly involved in inflammation, COX-2 selective NSAIDs should provide anti-inflammatory relief without compromising the gastric mucosa.[10]

Administration

Most commonly, NSAIDs are available as oral tablets. According to the package insert, the dosage for the most common over-the-counter NSAIDs are as follows:

  • Ibuprofen: for 200 mg tablets, 1 to 2 tablets every 4 to 6 hours while symptoms persist. The daily limit for ibuprofen is 1200 mg. 
  • Aspirin regular strength: for 325 mg tablets, 1 to 2 tablets every 4 hours or 3 tablets every 6 hours. The daily limit for aspirin is 4000 mg.
  • Naproxen sodium: for 220 mg tablets, 1 to 2 tablets every 8 to 12 hours. The daily limit for naproxen sodium is 660 mg. 

Topical NSAIDs are also available (diclofenac sodium 1.5% topical solution, diclofenac hydroxyethyl pyrrolidine 1.3% patch, and diclofenac sodium gel 1%). They are most useful for treating pain due to soft-tissue injuries and osteoarthritis.[8]

Specific NSAIDs can also be administered parenterally, for example, intravenous ibuprofen is available, given as a 30-minute infusion; this can be used as a non-opioid analgesic to manage pain and can also reduce fever. Trials have shown that using intravenous ibuprofen along with morphine in postoperative adult patients has the potential to lower the total use of morphine. For treating pyrexia an initial 400mg dose then 400 or 100 to 200 mg every 4 to 6 hours as needed. For the treatment of pain, 400 to 800 mg, every 6 hours as needed is the recommendation.[11]  Ketorolac is also available for parenteral administration.  

Adverse Effects

NSAIDs have well-known adverse effects affecting the gastric mucosa, renal system, cardiovascular system, hepatic system, and hematologic system.

Gastric adverse effects are likely due to the inhibition of COX-1, preventing the creation of prostaglandins that protect the gastric mucosa. The damage is more likely in a patient that has a prior history of peptic ulcers. Since it is COX-1 specific, the use of COX-2 selective NSAIDs is a lower risk alternative.[12]

Renal adverse effects are because COX-1 and COX-2 facilitate the production of prostaglandins that play a role in renal hemodynamics. In a patient with normal renal function, inhibition of prostaglandin synthesis does not pose a large problem; however, in a patient with renal dysfunction, these prostaglandins play a greater role and can be the source of problems when reduced via NSAIDs. Complications that can occur due to this are acute renal dysfunction, fluid and electrolyte disorders, renal papillary necrosis, and nephrotic syndrome/ interstitial nephritis.[13]

Cardiovascular adverse effects can also be increased with NSAID use; these include MI, thromboembolic events, and atrial fibrillation. Diclofenac seems to be the NSAID with the highest reported increase in adverse cardiovascular events.[14]

Hepatic adverse effects are less common; NSAID-associated risk of hepatotoxicity (raised aminotransferase levels) is not very common, and liver-related hospitalization is very rare. Among the various NSAIDs, Diclofenac has a higher rate of hepatotoxic effects.[15] 

Hematologic adverse effects are possible, particularly with nonselective NSAIDs due to their antiplatelet activity. This antiplatelet effect typically only poses a problem if the patient has a history of GI ulcers, diseases that impair platelet activity (hemophilia, thrombocytopenia, von Willebrand, etc.), and in some perioperative cases.[16]

Other minor adverse effects include anaphylactoid reactions that involve the skin and pulmonary systems, like urticaria and aspirin-exacerbated respiratory disease.[17][18]

For a complete list of adverse effects for an individual NSAID, please see the StatPearls article for that particular drug. 

Contraindications

According to the package insert NSAIDs are contraindicated in patients:

  • With NSAID hypersensitivity or salicylate hypersensitivity, as well as in patients who have experienced an allergic reaction (urticaria, asthma, etc.) after taking NSAIDs 
  • Who have undergone coronary artery bypass graft surgery
  • During the third trimester of pregnancy

Monitoring

Recommended monitoring includes a CBC, renal tests, and hepatic panel. These recommendations are from the American College of Rheumatology for use in rheumatoid arthritis patients who use NSAIDs chronically and who have no comorbidities nor history of complications. Monitoring is less common in patients not considered high risk for NSAID toxicity. However, NSAIDs are either contraindicated, or their use requires monitoring, in patients with liver or renal problems.[19]

Toxicity

NSAID toxicity can manifest as GI bleeding, hypertension, hepatotoxicity, and renal damage. [19] Typically, acute NSAID overdose is asymptomatic or has negligible gastrointestinal symptoms. However, other symptoms of toxicity complications may include anion gap metabolic acidosis, coma, convulsions, and acute renal failure. Also, NSAIDs can confer gastrointestinal damage by inhibiting COX-1, which causes decrease gastric mucosa production. Nephrotoxicity can also occur with NSAID use because these medications reduce prostaglandin levels, which are essential for the vasodilation of the renal arterioles.  Lastly, neurologic toxicity can present with drowsiness, confusion, nystagmus, blurred vision, diplopia, headache, and tinnitus.[20]

Enhancing Healthcare Team Outcomes

The general public widely uses NSAIDs because of their wide range of commonly encountered indications. Patient education on the use of NSAIDs is an important piece of care that providers need to pay attention to because of the many possible adverse effects on multiple different organ systems. Because these adverse effects occur at a much higher rate in patients with specific comorbidities, it is crucial for physicians, nurses, and pharmacists to pay close attention to a patient's history and to educate the patient accordingly on risks and dosing. The treating clinician will initiate therapy, whether for a short or long-term regimen. The pharmacist will need to verify the dosing and administration, as well as checking for potential drug-drug interactions. Pharmacists should also offer patient counseling on how to best use their NSAID and minimize adverse events; this is particularly the case when the patient uses NSAIDs as an OTC agent. Nursing must also take a careful medication history, and include OTC NSAID use, so the clinician can make an informed choice for prescribing NSAID therapy. MUrses, pharmacists, and clinicians all need to be cognizant of the signs and symptoms of NSAID toxicity or adverse effects, so that changes can be made to the patient's regimen as needed.

The healthcare team should communicate and work together to ensure that each patient receives the proper dose for their specific condition and comorbidities; high enough for efficacy but as low as possible to reduce the incidence of adverse effects. Through collaborative interprofessional teamwork, NSAID therapy can confer maximum benefit with minimal downside. [Level V]


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Nonsteroidal Anti-inflammatory Drugs (NSAIDs) - Questions

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A 64-year-old female patient visits her primary care physician after her rheumatoid arthritis has flared up. She is currently on warfarin for atrial fibrillation and wants to go on anti-inflammatory medication to help with her arthritis symptoms. Which of the following cyclooxygenase inhibitors causes the least amount of gastrointestinal upset?



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A 48-year-old female present to your clinic with complaints of abdominal pain that started about a week ago. She states that she has not had any recent trauma. But she notes that she has been having joint pain for 3 weeks which she has been taking ibuprofen for. Her past medical history is significant for peptic ulcer disease. All other physical exam findings are not remarkable. Which of the following anti-inflammatory agents will you recommend that she replaces ibuprofen with?



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What is the nonsteroidal anti-inflammatory drug with the longest duration of activity?



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A 17-year-old female patient presents to the emergency department with a fever and a productive cough. She is complaining of chest pain when she breathes. Upon physical examination, her vitals include a temperature of 100 degrees fahrenheit, respiration of 18 breaths per minute, bp 130/78 mmHg, and pulse of 90 beats per minute. On further evaluation, you find egophony in the right lung. Suspecting pneumonia, you order a chest X-ray and sputum cultures. While awaiting results which of the following medications would be most appropriate in managing the patient's pain and fever?



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A patient experiencing tendinitis is to receive naproxen sodium 500 mg, po, bid. Which of the following is true of this medication?



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What is the most likely adverse effect of chronic use of nonsteroidal anti-inflammatory drugs (NSAIDs)?



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Which of the following is a non-selective cyclooxygenase inhibitor?



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A 65-year-old female presents to the clinician for a follow-up of her rheumatoid arthritis. She feels fine but states that she has been taking ibuprofen daily for many years to manage the pain secondary to her rheumatoid arthritis. Physical examination is unremarkable. The clinician wants to monitor her chronic use of ibuprofen. Which of the following laboratory studies sets will be ordered to monitor her chronic NSAID use?



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A 46-year-old female patient is seen for physical therapy (PT) on her shoulder that involves moderate-intensity exercise in a pool at the facility. She is noted to be on an angiotensin-converting enzyme (ACE) inhibitor and thiazide diuretic for hypertension. The patient has also been taking over-the-counter cyclooxygenase (COX) inhibitors for pain. Which of the following is the most likely side effect that the patient may be experiencing during her PT appointment due to her choice of pain medications?



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A 16-year-old male complains of a headache that occurs once a week and is exacerbated when he has to study for his final exams. The headache feels like a band around his head. He denies blurry vision, nausea, vomiting, recent head trauma, and numbness or tingling in his body. He is given a medication that inhibits the conversion of arachidonic acid to cyclic endoperoxides and is told that it can help alleviate the headache. Which of the following is a potential side effect of this medication?



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Which of the following medications is not in the NSAID classification?



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A client is postoperative day 3 following hip replacement surgery. He is weaned off of opioids and started on a short course of an NSAID for pain control. He is in stable condition and denies any significant past medical history. Which of the following is appropriate before medication administration? Select all that apply.



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A 45-year-old man presents to the emergency department. He reports ingesting a large amount of “some pain medication." He brought the pill bottle, which shows that it is a drug that inhibits thromboxane synthesis. Which of the following best describes how the drug inhibits thromboxane synthesis?



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A 68-year-old woman complains of pain in her knee that started after a car accident several weeks ago. She has a history of angina and hypertension. She reports swelling of the joint but no deformity and describes her pain as a 3 or 4 on a scale of 1 to 10. She reports taking celecoxib for the pain. The provider explains her increased cardiovascular risk with this drug. Which of the following best explains why her cardiovascular risk is increased?



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A 16-year-old girl presents to the clinic complaining about menstrual cramp pain. She had menarche at age 13, and her cycles are normal in duration. For the first several days of her menses, she reports severe pain. She has no significant medical history, takes no medications regularly, and is not sexually active. The provider prescribes a medication that is FDA-approved for dysmenorrhea, is taken orally, and reversibly inhibits the enzyme cyclooxygenase. Which of the following best describes the prescribed medication?



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Nonsteroidal Anti-inflammatory Drugs (NSAIDs) - References

References

Vane JR, Inhibition of prostaglandin synthesis as a mechanism of action for aspirin-like drugs. Nature: New biology. 1971 Jun 23;     [PubMed]
Phillips WJ,Currier BL, Analgesic pharmacology: II. Specific analgesics. The Journal of the American Academy of Orthopaedic Surgeons. 2004 Jul-Aug;     [PubMed]
Dawood MY, Primary dysmenorrhea: advances in pathogenesis and management. Obstetrics and gynecology. 2006 Aug;     [PubMed]
Shekelle PG,Newberry SJ,FitzGerald JD,Motala A,O'Hanlon CE,Tariq A,Okunogbe A,Han D,Shanman R, Management of Gout: A Systematic Review in Support of an American College of Physicians Clinical Practice Guideline. Annals of internal medicine. 2017 Jan 3;     [PubMed]
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