Plantar Heel Pain

Plantar heel pain is a commonly encountered orthopedic problem that can cause significant discomfort and a limp because of the difficulty in bearing weight. The etiologies of this condition are multiple; therefore, a careful clinical evaluation is necessary for its appropriate management. Nonsurgical or conservative care is successful in most cases.[1, 2, 3, 4, 5, 6, 7, 8, 9, 10]

For patient education resources, see Running and Arch Pain.

The specialized soft tissue at the heel functions as a shock absorber. The subcutaneous structure consists of fibrous lamellae arranged in a complex whorl containing adipose tissues that attach with vertical fibers to the dermis and the plantar aponeurosis.[11]

The heel can absorb 110% of the body's weight during walking and 200% of the body's weight during running. The plantar fascia is a multilayered fibroaponeurotic structure that arises predominantly from the medial calcaneal tuberosity and inserts distally through several slips into the plantar plates of the metatarsophalangeal joints, the flexor tendon sheaths, and the bases of the proximal phalanges of the toes.

Dorsiflexion of the toes applies traction stress at the origin of the plantar fascia. A contracture in the triceps surae, a pes cavus, or a pes planus can increase the traction load at the origin of the plantar fascia during weightbearing activities.

Other anatomic factors that can have similar effects are overpronation, discrepancy in leg length, excessive lateral tibial torsion, and excessive femoral anteversion. However, overuse, not anatomy, is the most common cause of plantar fasciitis in athletes. The pain of plantar fasciitis is caused by collagen degeneration associated with repetitive microtrauma to the plantar fascia.

An inflammatory response and reparative process can double the thickness of the plantar fascia, which is normally approximately 3 mm. Biopsy specimens reveal collagen necrosis, angiofibroblastic hyperplasia, chondroid metaplasia, and calcification.

The heel pain can also have a neurologic basis. The tibial nerve, with nerve roots from L4-5 and S2-4, courses in the medial aspect of the hindfoot, through the tarsal tunnel, under the flexor retinaculum, and over the medial surface of the calcaneus. The calcaneal branch, arising directly from the tibial nerve, carries sensation from the medial and plantar heel dermis.

The tibial nerve divides into lateral and medial plantar nerves, which proceed into the plantar aspect of the foot through a foramen within the origin of the abductor hallucis muscles, which forms the distal tarsal tunnel. The first branch of the lateral plantar nerve changes course from a vertical to a horizontal direction around the medial plantar heel. It passes deep to the abductor hallucis muscle fascia and the plantar fascia and is the nerve supply to the abductor digiti minimi. The tibial nerve and its branches in the hindfoot can be involved with compressive neuropathies. A valgus heel can stretch in the tibial nerve.

Local causes include the following:

• Proximal plantar fasciitis
• Fat pad atrophy
• Plantar fascia rupture
• Tarsal tunnel syndrome
• Compression of the first branch of the lateral plantar nerve
• Plantar fasciitis coexisting with compression of the first branch of the lateral plantar nerve
• Stress fracture of the calcaneus
• Bone tumor or bone cyst
• Osteomyelitis

Regional causes include the following:

• Spinal stenosis
• Prolapsed intervertebral disk

Systemic causes include the following:

• Inflammatory bowel disease–associated arthritis
• Seronegative spondyloarthropathies
• Inflammatory arthritis (ie, rheumatoid arthritis)

Although the exact prevalence of plantar heel pain is unknown, it is estimated that more than 2 million Americans seek treatment for plantar heel pain each year.[12] The prevalence in active and military populations is especially high.[13] Internationally, in both athletic and nonathletic populations, the incidence of plantar fasciitis is reported to be approximately 10%.

The average age of a patient with proximal plantar fasciitis is approximately 45 years. There is a known sex-based dimorphism in presentation, with proximal plantar fasciitis being twice as common in women as in men.

Proximal plantar fasciitis is successfully managed with conservative care in approximately 90% of cases. In general, the longer the duration of symptoms, the longer it takes for the patient to obtain complete pain relief.[14]

A careful history and a thorough physical examination are valuable in identifying the etiology of heel pain. Taking a comprehensive medical and general history is important for distinguishing between various causes. Seek the history on all the characteristics of the pain, such as onset, location, radiation, modifying factors, relation to time of the day, and relation to activities.

The most common cause of plantar heel pain in both athletic and nonathletic populations is proximal plantar fasciitis.[15] Patients usually have occupations that involve spending most of their time on their feet. The pain is often unilateral, but it can manifest bilaterally, with one side being more painful than the other.

The discomfort commonly manifests spontaneously and insidiously without an antecedent trauma or fever. Occasionally, some patients state they might have stepped on a small object such as a pebble or they may have recently started an exercise regimen involving walking or running. Some patients may have a history of recent weight gain.

The pain is localized to the plantar and medial aspects of the heel. It is worse typically with the first few steps in the morning. The pain causes patients to limp for approximately half an hour. It is also worse after a period of rest, such as after standing up from a chair or getting out of a car.

The pain then improves with walking and stretching, but it is aggravated by prolonged walking and standing. The pain can be present with every step, causing a limp, and patients tend to walk bearing weight on the forefoot and the outer aspect of the foot, which can exacerbate the problem.

An acute onset of pain, especially after a vigorous or sudden athletic activity, can be indicative of traumatic rupture of the plantar fascia.

Fat pad atrophy in elderly patients and in persons who have received multiple steroid injections manifests with pain under the heel that is more diffuse, involving most of the weightbearing surface. The pain worsens when the patients walk on hard surfaces and when they wear hard-soled footwear. The initial improvement in walking observed in patients with plantar fasciitis is not observed in patients with fat pad atrophy.

Pain radiating from the heel distally or proximally and associated with numbness, paresthesia, or a burning sensation after activity and continuing even after rest is likely to be neurologic in origin. This is usually due to a compressive neuropathy locally, as in tarsal tunnel syndrome, or proximally at the level of the nerve root, in which case low back pain may be associated.

Bilateral heel pain and pain at the tendon insertions (or enthesopathy), especially associated with general symptoms such as malaise, recurrent fever, multiple joint pains, or bowel dysfunction, may indicate an association with inflammatory disorders such as rheumatoid arthritis, spondyloarthropathies, Reiter syndrome, or Behcet syndrome. Significant loss of appetite and weight or pain at night can be indicative of a neoplasm. Heel pain in elderly patients or patients with atypical presentations should be investigated for deficiency fractures or for tumors.

A general examination is necessary to rule out systemic causes of heel pain. A spine examination is required if the pain radiates or if the history is suggestive of radiculopathy.

In the local examination, inspect the foot and the heel for any abnormalities such as swelling, lumps, scars, bruising, or foot deformities such as pes planus or pes cavus.

Palpation is performed to elicit the site of maximum tenderness. Practitioners should be cognizant of the "windlass mechanism" of the plantar fascia.[16, 17] Check the condition of the fad pad, feel for defects or lumps in the plantar fascia, and identify any bony deformity due to previous fractures.

Percussion over the tibial nerve in the tarsal tunnel and its distal branches is performed to check for hypersensitivity or tingling. Percussion over any previous scars in the region can be performed to detect a neuroma in the scar.

Examining the range of motion at the ankle joint and a performing a Silfverskiöld test reveals any stiffness in the gastrocnemius and/or the triceps surae complex.[18]

The association between plantar fasciitis and isolated contracture of the gastrocnemius was studied by Patel et al in a prospective evaluation of patients with either acute or chronic plantar fasciitis (N = 254). Of the 254 patients, 211 (83%) had limited ankle dorsiflexion, 145 (57%) had an isolated contracture of the gastrocnemius, 66 (26%) had a contracture of the gastrocnemius-soleus complex, and only 43 (17%) did not have a dorsiflexion limitation. Equinus contracture was noted in 83% (129/155) of acute cases and 82% (82/99) of chronic cases. An isolated contracture of the gastrocnemius was found in 60% (93/155) of acute cases and 52% (52/99) of chronic cases.[19]

In persons with proximal plantar fasciitis, the tenderness is typically localized over the medial calcaneal tuberosity at the origin of the plantar fascia. Associated features may include a triceps surae contracture, decreased subtalar mobility, pes cavus, or pes planus. These conditions can create increased tension on the plantar fascia. However, when a clinical test is performed to stretch the plantar fascia by dorsiflexion of the toes, patients do not experience any aggravation of pain. On the other hand, pain may be aggravated by this maneuver in persons with an acute plantar fascia rupture, which may be accompanied by localized bruising or even a palpable defect.

Tenderness upon squeezing both the medial and lateral sides of the posterior calcaneal tuberosity is highly indicative of a stress fracture in the calcaneus, and this may be associated with local edema (see the image below).[20]

In persons with compressive neuropathy, either of the tibial nerve in the tarsal tunnel or of the first branch of the lateral plantar nerve, the point of maximal tenderness in the heel is located more medially in the posterior heel.

Percussion over the tibial nerve branches elicits tingling, burning, or numbness. A valgus heel associated with pes planus or acquired flatfoot can put increased stretch on the tibial nerve and can cause tarsal tunnel syndrome.

In elderly patients or persons who have had multiple steroid injections in the heel, the pain and tenderness is maximal over the central weightbearing area of the heel. Dorsiflexion of the toes does not aggravate the pain. The heel does not have the usual firmness; it feels soft, and the underlying calcaneus is more readily palpable.

Generally, plantar fasciitis is a clinical diagnosis; laboratory and imaging studies are rarely indicated. However, heel pain, especially when it is bilateral, can be a rare primary presenting sign of systemic inflammatory disorders. If a patient presents with bilateral heel pain in association with systemic symptoms, the blood should be screened for inflammatory markers, such as the erythrocyte sedimentation rate (ESR), human leukocyte antigen (HLA)-B27, rheumatoid factor (RF), and antinuclear antibodies (ANA).

Radiography

Heel spurs develops in the origin of the flexor digitorum brevis in approximately 50% of patients with proximal plantar fasciitis. The etiology is thought to be repetitive traction that leads to collagen degeneration, angiofibroblastic hyperplasia, and matrix calcification. Plain weightbearing radiographs can show calcaneal spurs in approximately 50% of patients with plantar fasciitis, but, because spurs are frequently noted in patients without heel pain, the presence of calcaneal spurs is not considered contributory to the pain, and it does not affect the diagnosis or treatment.[23, 24]  (See the image below.)

However, a report by Johal and Milner suggests a significant association between plantar fasciitis and calcaneal spur formation. In their study, the lateral heel radiographs of 19 patients with a diagnosis of plantar fasciitis and 19 comparison subjects with a lateral ankle ligament sprain matched for age and sex, were reviewed independently by two observers. Objective measurements of calcaneal spur length and a subjective grading of spur size were recorded. There was a significantly higher prevalence of calcaneal spurs in the plantar fasciitis group than in the comparison group (89% vs 32%). There was good interobserver and intraobserver agreement.[25]

Plain radiographs showing the lateral view of the calcaneus can be useful in detecting a stress fracture, which appears as a double-dense sclerotic line. However, 3-4 weeks may pass from the onset of symptoms until the injury is detectable on plain radiographs. Bony infections or tumors can also be detected on plain radiographs.

Ultrasonography

Ultrasonographic examination of the plantar heel can identify a thickened plantar fascia, but this investigation and the interpretation of the results depend on the expertise of the person performing the procedure.[6, 26]

Magnetic resonance imaging

Magnetic resonance imaging (MRI) can be used to confirm a diagnosis, such as a stress fracture, especially in the early stages before it is detectable with plain radiography. MRI is also used to investigate further for soft-tissue or bone lesions in the hindfoot. In persons with plantar fasciitis, this modality demonstrates edema and thickening of the plantar fascia, but MRI is not used to diagnose this condition. Any space-occupying lesions in the tarsal tunnel that could cause a tarsal tunnel syndrome are also revealed.[27]

Proximal plantar fasciitis is successfully managed with conservative care in approximately 90% of cases. In general, the longer the duration of symptoms, the longer it takes for the patient to obtain complete pain relief; patients should be counseled regarding this correlation so that their expectations can be managed more effectively.

Various modalities of treatment are available, and patient education is important to improve the understanding of the condition and to obtain compliance with various treatment regimens. The important aims of the treatment are to limit impact stresses on the heel, to alleviate inflammation, and to stretch the triceps surae muscle.

Impact reduction

Means of decreasing the effects of impacts include the following:

• Activity modification - Avoiding impact activities is especially important in athletes, who can cross-train with nonimpact sports such as cycling or swimming
• Reduction of body weight (consultation with a nutritionist, if available, should be considered)
• Use of soft cushions or insoles and soft-heeled footwear (see the first and second images below) ^[28]
• Taping, ^[29] arch supports, and custom-molded orthotics (see the third image below) ^{[30, 31]}

Anti-inflammatory measures

Application of ice, iontophoresis, or both may be helpful.[32]  Anti-inflammatory medication is useful in the early stages, especially if the patient has begun stretching exercises, which initially can worsen the pain (see Medication).

Stretching and strengthening

A variety of exercises can help the patient achieve active and passive ankle dorsiflexion with the knee kept straight and the subtalar joint in inversion, which helps achieve maximum stretch of the triceps surae.[10] The foot can be rolled over a tennis ball or a can to massage and stretch the plantar fascia. The exercises can be performed at home or can be guided by a physical therapist (see the images below).[33]

Plantar fascia–specific stretching exercises

To perform the exercise, the patient crosses the affected leg over the contralateral leg. While placing the fingers across the base of the toes, the patient pulls the toes back toward the shin until he or she feels a stretch in the arch or plantar fascia. The patient confirms that the stretch was correct by palpating tension in the plantar fascia (see the image below).

A randomized, prospective study with 2-year follow up compared Achilles tendon stretching with plantar fascia–specific exercises.[34] The authors found plantar fascia–specific stretching exercises to be superior.

Rompe et al,[35]  randomly assigned 102 patients with acute plantar fasciopathy to perform an 8-week plantar fascia–specific stretching program (n = 54) or to receive repetitive low-energy radial shock-wave therapy without local anesthesia, administered weekly for 3 weeks (n = 48).[35] The primary outcome measures were a mean change in the Foot Function Index (FFI) sum score at 2 months after baseline, a mean change in item 2 on the FFI (pain during the first few steps of walking in the morning), and satisfaction with treatment. The stretching program was superior to repetitive shockwave therapy for treating acute symptoms of proximal plantar fasciopathy.

Intrinsic muscle strengthening

Exercises include toe curls or other activities, such as picking up marbles with the toes.

Resting splints

During the night, the relaxed posture of plantarflexion at the ankle tends to favor contracture of the triceps surae. To prevent this, night splints that hold the ankle in dorsiflexion can be worn.[36] Patients who wear a posterior night splint should be warned to take it off before getting out of bed. As an anecdotal example, one patient walked to the toilet while wearing the splint, slipped, and sustained a humeral fracture. However, a dorsally applied splint, as opposed to a posterior splint, need not be taken off before the patient gets out of bed (see images below).

Attard et al compared the effectiveness of the posterior night splint, which dorsiflexes the foot, with that of the anterior night splint, which maintains the foot in a plantigrade position.[37] In this study, two thirds of all participants confirmed that morning pain and stiffness was less after wearing the night splints; both types were relatively easy to don and doff, but the posterior orthosis was more uncomfortable and disrupted sleep. On average, the anterior night splint reduced heel pain more significantly than the posterior orthosis did.

Treatment of recalcitrant pain

If the pain persists persists for longer than 2 months despite the above treatment, then the following modalities can be offered.

Casting

A short leg walking cast for 6 weeks is generally effective in relieving pain, but the pain can recur after the cast is removed.[38] To prevent this, the patient should use the previously mentioned treatment modalities, such as activity modification, stretching exercises, and insoles, until recovery is complete.

Corticosteroids

Iontophoresis is administered by a physical therapist and uses low-voltage galvanic current stimulation to distribute topical corticosteroids. It is performed two or three times per week. This therapy can provide short-term relief but is usually reserved for patients in whom other therapies are unsuccessful or who have occupations that involve spending most of their time on their feet. Depot injections can provide good short-term relief, but multiple injections can cause plantar fascia rupture and fat pad atrophy—and, later, a flatfoot deformity—especially if the injection is not administered deep into the fascia.[39]

Extracorporeal shockwave therapy

Extracorporeal shockwave therapy (ESWT)[4, 40, 41, 39, 42] was approved by the US Food and Drug Administration (FDA) in 2005; it had been used in Europe for more than a decade previously. Animal study data suggest that this modality creates microdisruption and stimulates new bone and tissue formation. Shockwaves may be delivered in three ways: (1) electrohydraulically (high power), (2) electromagnetically, or (3) piezoelectrically. The FDA approved electrohydraulic and electromagnetic devices for the treatment of chronic plantar heel pain that has persisted for longer than 6 months despite other treatment.

Platelet-rich plasma injections

Platelets-rich plasma (PRP) is derived from autologous blood and contains high concentrations of growth factors necessary for tissue healing. The use of PRP in the treatment of plantar fasciitis is an evolving approach that is not yet widely accepted or practiced.[43]

A prospective study by Ragab et al evaluated 25 patients with chronic plantar fasciitis (mean age, 44 years) who were treated by means of PRP injection.[44] All patients were assessed for pain on the Visual Analogue Scale (VAS) before and after injection. The thickness of the plantar fascia was measured ultrasonographically before injection and at each postinjection follow-up visit (mean follow-up, 10.3 months). Average preinjection pain was 9.1 on the VAS (range, 8-10). Before injection, 72% of patients had severe limitation of activities, and 28% of patients had moderate limitation of activities.

Average postinjection pain in this study was 1.6 on the VAS.[44] Twenty-two patients (88%) were completely satisfied, two (8%) were satisfied with reservations, and one (4%) was unsatisfied. Fifteen patients (60%) had no functional limitations post injection, and eight (32%) had minimal functional limitations. Two patients (8%) had moderate functional limitations post injection. Ultrasonography showed significant changes not only in thickness but also in the signal intensity of the plantar fascia after injection. None of these patients experienced any complications from PRP injection at the end of the follow-up period.

Percutaneous radiofrequency nerve ablation

Percutaneous radiofrequency nerve ablation (RFNA) of the calcaneal branches of the inferior calcaneal nerve in patients with chronic heel pain associated with plantar fasciitis has also been used successfully in a few reports. However, there are no prospective randomized controlled studies comparing RFNA with other treatment modalities.

A prospective study by Erken et al reported their 2-year follow-up results of RFNA of the calcaneal branches of the inferior calcaneal nerve in 35 feet in 29 patients with chronic plantar heel pain associated with plantar fasciitis between 2008 and 2011.[45]  All of the patients who were treated had been complaining of heel pain for more than 6 months and had failed conservative treatment. The average VAS score of the feet was 9.2±1.9 before treatment, and the average American Orthopaedic Foot and Ankle Society (AOFAS) score was 66.9±8.1 (range, 44-80).

After treatment, the average VAS scores were 0.5 ± 1.3 at 1 month, 1.5 ± 2.1 at 1 year, and 1.3 ± 1.8 at 2 years.[45] The average AOFAS scores were 95.2 ± 6.1 (range, 77-100) at 1 month, 93 ± 7.5 (range, 71-100) at 1-year follow-up, and 93.3 ± 7.9 (range, 69-100) at 2-year follow-up. At the 1- and 2-year follow-up, 85.7% of the patients rated their treatment as very successful or successful.

Low-level laser therapy

Low-level laser therapy (LLLT) has demonstrated some early promising results for the treatment of acute and chronic pain. Jastifer et al reported on a study of 30 patients who received LLLT and completed 12 months of follow-up.[46] Patients were treated twice a week for 3 weeks for a total of six treatments. Patients demonstrated a mean improvement in heel pain VAS from 67.8 of 100 at baseline to 6.9 of 100 at the 12-month follow-up period. Total FFI score improved from a mean of 106.2 at baseline to 32.3 at 12 months post procedure.

Micronized dehydrated human amnion/chorion membrane injection

In a randomized controlled trial, Cazzell et al compared micronized dehydrated human amnion/chorion membrane (dHACM) injection (one injection in the affected area; n = 73) with 0.9% sodium chloride placebo (n = 72) for the treatment of plantar fasciitis.[47] They assessed safety and efficacy at 4 weeks, 8 weeks, 3 months, 6 months, and 12 months post injection, using the Visual Analogue Scale (VAS) for pain, the Foot Function Index–Revised (FFI-R) score, and the presence or absence of adverse events. The primary outcome was mean change in VAS score between baseline and 3 months; the secondary outcome was mean change in FFI-R score between baseline and 3 months.

Baseline VAS scores in this study were similar between groups.[47] At 3 months, VAS scores in the treatment group had a mean reduction of 76% versus baseline, whereas those in the control group had a mean reduction of 45%. FFI-R scores in the treatment group had a mean reduction of 60% versus baseline, whereas those in the control group had a mean reduction of 40%. Of the four serious adverse events noted, none were related to study procedures. The authors concluded that the pain reduction and functional improvement outcomes were statistically significant and clinically relevant, supporting the use of micronized dHACM injection as a safe and effective treatment for plantar fasciitis.

Other measures

Fat pad atrophy is managed conservatively with the use of heel cups, soft insoles, and soft-soled footwear. The heel cup helps to centralize and increase the bulk of the soft tissue under the calcaneus.

In patients with planovalgus deformity, if the valgus hindfoot is thought to be the cause of tarsal tunnel syndrome through traction on the tibial nerve, the initial treatment can be placement of a medial longitudinal arch support and a medial lift.

Stress fractures of the calcaneus and traumatic rupture of the plantar fascia are managed with conservative measures. Avoiding the offending activity and a 6- to 8-week period in a cast may be required to alleviate the symptoms.

Multiple clinical recommendations, including the clinical consensus statement by the American Orthopaedic Foot and Ankle Society on the diagnosis and treatment of adult acquired infracalcaneal heel pain,[48] are available and are widely accepted.[10]

Because 90% of patients with plantar fasciitis respond favorably to conservative care, conservative methods should be tried for at least 6, or preferably 12, months before surgery is considered. Furthermore, full counseling regarding the risks and benefits must be administered because complete satisfaction after surgery is observed in only 50% of patients.

The surgery can be performed by open or endoscopic methods. However, if plantar fasciitis is suspected to coexist with compression of the first branch of the lateral plantar nerve, then the endoscopic method is not recommended.

Electromyography and nerve conduction studies are not necessary to diagnose compressive neuropathy of the first branch of the lateral plantar nerve; rather, the diagnosis of entrapment of the first branch of the lateral plantar nerve is made on a clinical basis. Testing nerve conduction across the site of entrapment in the heel is technically demanding. Motor weakness in the abductor digiti quinti may not be detected because of the dynamic nature of the compression.

By either the open or the endoscopic method, only 50% of the plantar fascia is released because a complete release can lead to collapse of the medial and lateral longitudinal arches.

Excision of a plantar heel spur is performed only if it is significantly large and it is compressing the first branch of the lateral plantar nerve.

Surgery for tarsal tunnel syndrome or for decompression of the first branch of the lateral plantar nerve requires release of the tibial nerve and its branches and overlying fascia, including the deep fascia of the abductor hallucis.

Of patients with plantar fasciitis, 90% respond favorably to conservative care. Conservative methods should be tried for at least 6 months (preferably 12 months) before surgery is considered. Furthermore, patients should be fully counseled regarding the risks and benefits because complete satisfaction after surgery is observed in only 50% of patients.

For nonsurgical treatment, depot steroid injections can provide good short-term relief of symptoms; however, multiple injections can cause the plantar fascia to rupture and the fat pad to atrophy, especially if the injection is not administered deep into the fascia.[49, 50, 51]

Regardless of whether an open or endoscopic method is used for surgical correction, only 50% of the plantar fascia should be released, because a complete release can lead to collapse of the medial and lateral longitudinal arches.

Endoscopic plantar fascia release can be associated with a higher incidence of nerve damage and painful and hypersensitive neuroma.[52, 53]

Because overuse is the most common cause of plantar fasciitis in athletes, avoiding overuse can help prevent this problem.[54]

Medication is useful in the early stages, especially if the patient has begun stretching exercises, because, initially, these can worsen the pain.

Class Summary

Pain control is essential to quality patient care. Analgesics ensure patient comfort, promote pulmonary toilet, and have sedating properties, which are beneficial for patients who have sustained trauma or who have sustained injuries.

Acetaminophen (Aspirin Free Anacin, Feverall, Tylenol)

DOC for pain in patients with documented hypersensitivity to aspirin or NSAIDs, with upper GI disease, or who are taking PO anticoagulants.

Effective in relieving mild to moderate acute pain; however, it has no peripheral anti-inflammatory effects. May be preferred in elderly patients because of fewer adverse GI and renal effects.

Class Summary

NSAIDs have analgesic and antipyretic activities. The mechanism of action of these agents is not known, but NSAIDs may inhibit cyclooxygenase activity and prostaglandin synthesis. Other mechanisms may exist as well, such as inhibition of leukotriene synthesis, lysosomal enzyme release, lipoxygenase activity, neutrophil aggregation and various cell membrane functions. Treatment of pain tends to be patient specific.

Ibuprofen (Advil, Excedrin IB, Motrin, Ibuprin)

DOC for patients with mild to moderate pain. Inhibits inflammatory reactions and pain by decreasing prostaglandin synthesis.

Ketoprofen (Actron, Orudis, Oruvail)

For the relief of mild to moderate pain and inflammation. Small initial dosages are indicated in small and elderly patients and in those with renal or liver disease.

Doses >75 mg do not increase therapeutic effects.

Administer high doses with caution and closely observe patient for response.

Naproxen (Aleve, Anaprox, Naprelan, Naprosyn)

For the relief of mild to moderate pain; inhibits inflammatory reactions and pain by decreasing the activity of cyclooxygenase, which is responsible for prostaglandin synthesis. NSAIDs decrease intraglomerular pressure and decrease proteinuria.