Jill S. Burkiewicz
LEARNING OBJECTIVES
Upon completion of the chapter, the reader will be able to:
1. Describe the pathophysiological principles associated with tissue injury and inflammation.
2. Identify the desired therapeutic goals and outcomes for a patient with musculoskeletal injury or pain.
3. Identify the factors that guide selection of an analgesic or counterirritant for a particular patient.
4. Recommend appropriate nonpharmacologic and pharmacologic therapy for a patient with musculoskeletal injury or pain.
5. Design a patient education plan including nonpharmacologic therapy and preventative strategies.
6. Develop a monitoring plan to assess treatment of a patient with musculoskeletal disorders.
KEY CONCEPTS
The two primary goals of treatment of musculoskeletal disorders are to: (a) relieve pain, and (b) maintain functionality.
The cornerstone of nonpharmacologic therapy for acute injury in the first 48 to 72 hours is known by the acronym RICE: rest, ice, compression, and elevation.
Heat should not be applied during the acute injury phase (the first 48 hours) because it promotes swelling and inflammation.
There are two main approaches to pharmacologic intervention for pain relief: oral (systemic) and topical agents.
Localized pain may be treated effectively with local topical therapy, whereas generalized pain is best treated with systemic agents.
Acetaminophen is the drug of choice for mild-to-moderate regional musculoskeletal pain without inflammation.
Aspirin is not more effective than acetaminophen, and it is not recommended for treatment of acute musculoskeletal pain because its adverse effects may be more common and severe.
Nonsteroidal anti-inflammatory drugs (NSAIDs) are preferred over acetaminophen in musculoskeletal disorders where inflammation is evident.
Patient education on proper use of counterirritants is essential to therapeutic success.
Patients using capsaicin should be advised to apply it regularly and consistently three to four times daily and that full effect may take 2 to 3 weeks or longer.
INTRODUCTION
The musculoskeletal system consists of the muscles, bones, joints, tendons, and ligaments. Disorders related to the musculoskeletal system often are classified by etiology. Acute soft-tissue injuries include strains and sprains of muscles and ligaments. Repeated movements in sports, exercise, work, or activities of daily living can lead to repetitive strain injury, where cumulative damage occurs to the muscles, ligaments, or tendons.1,2 While tendonitis and bursitis can arise from acute injury, more commonly these conditions occur as a result of chronic stress.2,3 Other forms of chronic musculoskeletal pain, such as pain from rheumatoid arthritis (see Chap. 57) or osteoarthritis (see Chap. 58), are discussed elsewhere in this textbook.
EPIDEMIOLOGY
Musculoskeletal disorders are commonly self-treated, so true estimates of the incidence of both acute and chronic injury are difficult to obtain. Musculoskeletal disorders are among the top 10 causes of ambulatory care visits in the United States for all age groups.4 These disorders account for a large portion of medical care expenditures5 and are a leading cause of work absenteeism and disability, resulting in a substantial economic burden from lost productivity and lost wages.6
In addition to chronic conditions such as arthritis and low back pain, some musculoskeletal disorders are induced by trauma at the workplace either via repetition and cumulative trauma or a one-time overexertion.7 For each reported incident, it is likely that there are at least 10 unreported work-related musculoskeletal events related to repetitive stress to the bones and joints.8 In the elderly, these injuries may not be related to work but to daily life. Instability combined with activities of daily living such as stair climbing and lifting objects may lead to strains and sprains. In pediatrics, fractures are more common than muscle and tendon injuries since the bones are weaker than the muscle-tendon unit in children and adolescents.9
Muscle injuries comprise the majority of sports-related injuries, and roughly half are related to overuse.2,10 The ankle and the knee are common sites of sports injuries.9,11 Soccer, football, basketball, track and field, and other sports that require rapid acceleration or higher speeds pose a greater risk of muscle strain.9,12 Overuse musculoskeletal injury is the phrase used to describe disorders arising from repetitive motion. This injury is common in activities such as running, particularly during periods of increased intensity or duration of training.2 It also can occur in the workplace with repeated, unvaried motion.13
PATHOPHYSIOLOGY
Skeletal muscle consists of muscle fibers linked together by connective tissue. Tendons and ligaments are composed of collagenous fibers that have a restricted capability to stretch. Tendons connect the muscle to the bone, whereas ligaments connect bone to bone (Fig. 60–1).
Muscle Strains and Sprains
A sprain is an overstretching of supporting ligaments that results in a partial or complete tear of the ligament.11 While a strain also arises from an overstretching of the muscle-tendon unit, it is marked by damage to the muscle fibers or muscle sheath without tearing of the ligament.9,14 The key difference between a sprain and a strain is that a sprain involves damage to ligaments, whereas a strain involves damage primarily to muscle. One common example of muscle strain and sprain is low back pain.15
Overloading the muscle and connective tissue results in complete or partial tears of the skeletal muscle, tendons, or ligaments.9,14 This usually occurs when the muscle is activated in an eccentric contraction, defined as a contraction in which the muscle is being lengthened.14 Examples of this type of contraction include putting down a large, heavy laundry basket or lowering oneself from a chin-up bar. Small tears can occur in the muscle because it is lengthening while also trying to contract to support the load. This leads to rupture of blood vessels at the site of the injury, resulting in the formation of a hematoma. Within 24 to 48 hours, an inflammatory response develops. In the inflammatory stage, macrophages remove necrotic fibers.10 However, there is some evidence that activated neutrophils also release free radicals and proteases that cause further damage to the area.16 Finally, capillaries grow into the area, and muscle fibers regenerate during the repair and remodeling phases of healing.10
FIGURE 60–1. Skeletal muscle fiber organization. Tendons attach muscle to bone. (From Widmaier EP, Raff H, Strang KT, et al., eds. Vander, Sherman, & Luciano’s Human Physiology: The Mechanisms of Body Function. 9th ed. New York: McGraw-Hill; 2004: Fig. 9–1.)
Bursitis and Tendonitis
Bursitis is an inflammation of the bursa, the fluid-filled sac near the joint where the tendons and muscles pass over the bone. The bursa assists with movement by reducing friction between joints. Tendonitis(also known as tendinitis) is an inflammation of the tendon or, more specifically, the fibrous sheath that attaches muscle to bone.2 Tenosynovitis is an inflammation of the tendon sheath.
Repetitive overuse of a tendon can cause cellular changes in the tissues. Specifically, collagenous tendon tissue is replaced with tissue that lacks the longitudinal structure of a normal tendon.17 As a result; the tendon progressively loses elasticity and its ability to handle stress or weight. This makes the tendon vulnerable to rupture or inflammation (tendonitis and tenosynovitis).
Repeated use also can cause degradation of collagen.18 In fact, many patients diagnosed with chronic tendonitis may not have inflammation but instead have tendinosis, a condition marked by these collagen changes. Overuse of a joint also can result in an inflamed bursa. Since the bursa serves to reduce friction within the joint space, bursitis causes stiffness and pain.
Inflammation and Peripheral Pain Sensation
Inflammation is a common pathway in soft-tissue injury of musculoskeletal disorders. Inflammatory processes lead to two outcomes: swelling and pain. Inflammatory processes traditionally are considered to be a necessary part of the remodeling process because inflammatory cells remove damaged tissue.19,20 However, inflammation also contributes to continued pain and swelling that limits range of motion.
The initial injury exposes membrane phospholipids to phospholipase A2, leading to the formation of arachidonic acid (Fig. 60–2).19,20 Next, arachidonic acid is transformed by cyclooxygenase (COX) to thromboxanes and prosta-glandins (PGs), including prostaglandin E2 (PGE2). PGE2 is the most potent inflammatory mediator; it increases vascular permeability, leading to redness, warmth, and swelling of the affected area. The increased permeability also increases pro-teolysis, or the breakdown of proteins in the damaged tissue.
Neutrophils, lymphocytes, and monocytes are attracted to the area, and monocytes are converted to macrophages.19,20 The macrophages then stimulate additional PG production. Phagocytic cells and other players in the immune system release cytokines, including interleukins, interferon, and tumor necrosis factor.
In addition to increasing vascular permeability, PGs also induce pain by sensitizing pain receptors to other substances such as bradykinin. Bradykinin, PGs, leukotrienes, and other inflammatory mediators lower the pain threshold through peripheral pain sensitization. These substances make nerve endings more excitable, and the nerve fibers are more reactive to serotonin, heat, and mechanical stimuli.20 The increased sensitization in the damaged tissue causes tenderness, soreness, and hyperalgesia or an exaggerated intensity of pain sensation.21 The process also facilitates production of additional PGs. In a cyclic fashion, the PGs then sensitize the nerves to bradykinin action.
Without interruption, the neurochemicals ultimately lead to a firing of the unmyelinated or thinly myelinated afferent neurons. This sends messages along the pain pathway in the periphery and communicates the pain message to the CNS. Interruption of this cycle occurs via anti-inflammatory agents such as aspirin and nonsteroidal anti-inflammatory drugs (NSAIDs).
FIGURE 60–2. Eicosanoid synthesis pathway. Cyclooxygenase is inhibited by nonsteroidal anti-inflammatory drugs and aspirin. (From Widmaier E P, Raff H, Strang K T, et al., eds. Vander, Sherman, & Luciano’s Human Physiology: The Mechanisms of Body Function. 9th ed. New York: McGraw-Hill; 2004: Fig. 5–11.)
Nerve receptors, or nociceptors, release substance P, a peptide that causes vasodilation when released.20,22 This dilation occurs mainly through substance P-mediated activation of neurokinin receptors. This receptor activation also increases the sensitivity of nociceptors to painful stimuli. Capsaicin relieves pain by stimulating the release of substance P from sensory nerve fibers, which ultimately depletes stores of substance P.
CLINICAL PRESENTATION AND DIAGNOSIS
See next page for information on the clinical presentation and diagnosis of musculoskeletal disorders.
TREATMENT
Desired Outcomes
The primary goals of treatment of musculoskeletal disorders are to: (a) relieve pain, and (b) maintain functionality. This is accomplished by decreasing the severity and duration of pain, shortening the recovery period, and preventing acute injury pain from becoming chronic pain. Prevention of swelling and inflammation are initial goals in acute injury because the degree of swelling is directly related to range of motion.11 If these goals are achieved, functional limitations are decreased. Ideally, a patient should be able to continue to perform activities of daily living (e.g., eating, dressing, cooking, and doing laundry) and maintain normal functions in the workplace. Children ideally should be able to maintain usual play activities and sports schedules.
Further goals include a return to usual activity and prevention of future injury. It is also important to minimize the potential for adverse drug events during treatment.
General Approach to Treatment
Treatment of musculoskeletal disorders involves three phases: (a) therapy of an acute injury using the rest, ice, compression, and elevation (RICE) principle; (b) pain relief using oral or topical agents; and (c) lifestyle and behavioral modifications for rehabilitation and to prevent recurrent injury or chronic pain (Fig. 60–3).
Clinical Presentation and Diagnosis of Musculoskeletal Disorders
General11
• Clinical presentation varies based on the etiology of the disorder.
• Repetitive strain or overuse injuries may have a gradual onset.
• Musculoskeletal disorders due to acute injury may be associated with other signs of the injury such as abrasion.
• Low back pain is often more chronic in nature.
Signs and Symptoms of Acute Soft-Tissue Injury (Strains, Sprains)11
• Discomfort ranging from tenderness to pain; it may occur at rest or with motion
• Swelling and inflammation of the affected area
• Bruising
• Loss of motion
• Mechanical instability
Signs and Symptoms of Repetitive Strain or Overuse Injury (Tendonitis, Bursitis)3,23,24
• Pain and stiffness that occurs either at rest or with motion
• Localized tenderness on palpation
• Mild swelling of the affected area
• Decreased range of motion
• Muscle atrophy
Other Diagnostic Tests and Assessments25
• Radiograph (x-ray): Evaluate bony structures to rule out fracture, malalignment, or joint erosion as the primary cause of pain.
• MRI: Soft-tissue imaging to evaluate for tendon or ligament tears.
• Ultrasound: Superficial soft-tissue imaging to evaluate for tears in tendons or ligaments. Ultrasound does not penetrate bone, so it is of limited usefulness for assessing tendons or ligaments deep within joints.
• Pain scale: Patient self-rating of pain on a scale of zero (no pain) to 10 (worst possible pain). Used to assess pain both at rest and with movement. Determined at baseline and to assess response to therapy.
Patient Encounter 1, Part 1
A 32-year-old man presents with left ankle pain. He was playing football with friends earlier today and twisted his ankle. The pain occurs at rest and is worsened by movement and weight-bearing activities. There is moderate swelling and mild bruising of the left ankle. He states “I don’t like to take pills” and asks for a recommendation to cool the affected area.
What information is suggestive of a musculoskeletal disorder?
What is your assessment of the patient’s ankle pain?
What additional information do you need to formulate a treatment plan?
In many cases, musculoskeletal disorders are self-treated with over-the-counter (OTC) oral or topical agents. However, further evaluation may be warranted if acute pain persists longer than 7 to 10 days, symptoms worsen or subside and then return, or there are signs of a more serious condition.11,24—26 Warning signs of more serious conditions include joint deformity, dislocation, or lack of movement in a joint. Low back pain accompanied by burning, radiating pain, or difficulty urinating requires further evaluation.
In children and adolescents, treatment practices are similar to the approach in adults with a focus on nonpharmacologic therapy and oral analgesics. Children younger than 2 years of age, elderly persons, and pregnant women also may need special care. Elderly patients may be more prone to systemic effects because of thinning of the skin and increased absorption of topical agents and drug interactions from polypharmacy.
Nonpharmacologic Therapy: RICE
The cornerstone of nonpharmacologic therapy for acute injury in the first 48 to 72 hours is known by the acronym RICE: rest, ice, compression, and elevation10 (Table 60–1). Rest eases pressure on the affected area and promotes pain control during the acute inflammatory phase (the first 1–5 days after injury). Ice, compression, and elevation initially minimize bleeding from broken blood vessels. Cold causes vasoconstriction, assisting in prevention of a large hematoma and providing analgesia by slowing nerve impulses. Compression, achieved by wrapping the area with an elastic bandage, also reduces the size of the developing hematoma. Preventing hematoma formation is important because a large hematoma can limit mobility and range of motion. Both cold and compression also decrease interstitial edema and swelling that accompany the injury. Elevation decreases blood flow and increases venous return from the affected area.
In addition to minimizing the acute inflammatory response, rest prevents additional injury to the affected area.14 The properties of the muscle–tendon unit are altered during the acute injury, with limitations on the ability of the muscles and tendons to stretch. Early activity predisposes a patient to further injury, but prolonged inactivity can lengthen recovery times.
FIGURE 60–3. Treatment plan for musculoskeletal injury or disorder.
Table 60–1 RICE Therapy
Clinicians should instruct patients to use crushed ice or ice chips because the area will cool more evenly than with large pieces of ice. Patients should not apply ice directly to the affected area or leave it on for longer than the recommended 20 minutes because frostbite can occur.11 A thin sheet or napkin will protect the skin and also allow for better cold transfer than thicker material such as a towel. Alternatively, soaking the area for 20 minutes in a cool bath (13°C [55°F]) provides effective cooling.
For small areas, an ice massage for 5 to 10 minutes can cool the area and add relief.23 This is accomplished by freezing water in a paper cup and removing the top part of the cup to expose the ice. The exposed ice is rubbed on the affected area. Any ice application should be stopped if the area becomes white or blue.
Heat should not be applied during the acute injury phase (the first 48 hours) because it promotes swelling and inflammation.11 After the first 48 hours, many patients find that heat decreases pain and eases muscle stiffness associated with immobility. A heating pad, heat wrap, or warm bath can be used on day three or later as long as no swelling develops after heat is applied. Heat should be discontinued if increased swelling occurs. Clinicians should educate patients to avoid sleeping with, or sitting or lying on heating pads because this can result in burns. Low-level heat, such as that supplied by therapeutic heat wraps (e.g., ThermaCare) may provide a safer means of heat application.27 However, the elderly should still be cautioned about the risk of burns and be advised to wear the wrap over thin clothing.
Pharmacologic Therapy
There are two main approaches to pharmacologic intervention for pain relief: oral (systemic) and topical agents. The choice between systemic or topical options is often guided by patient preference. For example, many topical products have a medicinal odor and require frequent applications. The extent of musculoskeletal pain also guides treatment choice.
Localized pain may be treated effectively with local topical therapy, whereas generalized pain is best treated with systemic agents Factors such as alcohol use, liver function, renal function, allergies, age, and comorbid conditions should be considered when choosing among therapeutic options.
Oral Analgesics
Nonopioid analgesics, including acetaminophen, aspirin, and NSAIDs, are used commonly for musculoskeletal disorders. All these agents provide analgesia, but aspirin and NSAIDs also work peripherally to decrease production of the principal mediator of acute inflammation, PGE2.19 NSAIDs and aspirin inhibit the enzyme COX. While the mechanism of action of acetaminophen is less clear, it appears that acetaminophen acts as a weak inhibitor of PG production. In contrast to aspirin and NSAIDs that inhibit PG production peripherally, acetaminophen exerts its effect centrally with little or no anti-inflammatory effect.28
Acetaminophen
Acetaminophen is the drug of choice for mild-to-moderate regional musculoskeletal pain without inflammation.29,30 Comparative trials between acetaminophen and oral NSAIDs demonstrate equivalent analgesia in some situations, but NSAIDs may be preferred in others.30 Therefore, if adequate analgesia is not achieved with acetaminophen, switching to an NSAID is a reasonable approach. Acetaminophen offers the advantage of less GI toxicity than NSAIDs. While tolerability of acetaminophen is high at therapeutic doses, hepatotoxicity has been reported after overdose and at therapeutic doses, especially in combination with other factors.31 Acetaminophen should be used with caution in patients who have liver disease or consume alcohol because of the risk of hepatotoxicity.25
Salicylates
Aspirin is not more effective than acetaminophen, and it is not recommended for treatment of acute musculoskeletal pain because its adverse effects may be more common and severe.30 Gastric irritation is more common with aspirin, and bleeding risk is increased because aspirin irreversibly inhibits platelet aggregation.30 Patients with aspirin-induced asthma should avoid aspirin and other salicylates.31 Aspirin should be avoided in children younger than age 16 due to the risk of Reye’s syndrome.
Some salicylates are specifically marketed for musculoskeletal back pain, such as magnesium salicylate. However, no studies specifically support use of these salicylates over other systemic analgesics. Magnesium salicylate should be used with caution in cases of renal impairment because hypermagnesemia can occur.32
NSAIDs
Oral NSAIDs are used commonly for musculoskeletal pain because of their availability without a prescription and anti-inflammatory effects.21,32
NSAIDs are a preferred choice over acetaminophen in musculoskeletal disorders where inflammation is evident.29 Most experts recommend the early use of NSAIDs following acute injury to control inflammation and the range-of-motion limitations that may accompany swelling.29
NSAIDs are particularly beneficial for chronic overuse injury, where inflammation is central to the pain and loss of motion. While NSAIDs may be helpful in relieving pain and inflammation in tendonitis, many tendonopathies are not associated with inflammation. Therefore, use of a simple analgesic such as acetaminophen may relieve pain adequately.24,32
The analgesic effects of NSAIDs are attributed to inhibition of the COX-2 enzyme, whereas the negative GI effects are due to inhibition of COX-1.30 Patients taking oral anticoagulants, those with a history of peptic ulcer disease, or others at high risk for GI complications may be considered candidates for a COX-2 inhibitor (e.g., celecoxib) or a combination of a nonselective NSAID with a gastroprotective agent such as a proton pump inhibitor (see Chap. 58).
COX-2 inhibitors are associated with adverse effects such as nephrotoxicity and a potential increased risk of myocardial infarction (see Chap. 58). Combination of COX-2 inhibitors with alcohol can increase GI adverse effects. All NSAIDs should be used with caution in patients with aspirin-induced asthma.32
Opioids
Opioid analgesics can be used for patients not responding adequately to nonopioid analgesics or for moderate-to-severe pain.30 These agents generally are given alone or in combination with simple analgesics such as acetaminophen. Tolerance and physical dependence are considerations but less of a concern when treating acute pain. When used in equivalent doses, opioids produce similar pain relief and adverse effects such as sedation, nausea, constipation, and respiratory depression (see Chap. 33).
Topical (External) Analgesics
Topically (or externally) applied drugs that exert a local analgesic, anesthetic, or antipruritic effect by either suppressing cutaneous sensory receptors or by stimulating these receptors in a counterirritant fashion are termed external analgesics.26 These medications are applied directly to the affected area to create high local concentrations of the drug.33,34 Formulations include gel, cream, lotion, patch, liquid, liniment, or aerosol spray. Negligible systemic concentrations are achieved with intact skin, minimizing systemic adverse effects. Topical application should not be confused with transdermal delivery, where drug absorption into the bloodstream produces a systemic effect. Musculoskeletal disorders often are treated with topical (but not transdermal) medications.
After application, the topical medication penetrates the skin to the soft tissue and peripheral nerves.26 Here, the drug suppresses the sensitization of pain receptors, thus reducing pain and burning. Examples include topical NSAIDs and local anesthetics, such as lidocaine. External analgesics also include counterirritant products that, in contrast, stimulate cutaneous sensory receptors, producing a burning, warming, or cooling sensation that masks the underlying pain. In effect, the irritation or inflammation caused by the counterirritant distracts from the underlying pain. For example, counterirritants include menthol and capsaicin.
Some patients prefer external analgesics to systemic analgesics because the rubbing during application can be comforting. External analgesics are useful adjuvants to nonpharmacologic therapy and systemic analgesic therapy to provide additional relief.35 These agents also offer a therapeutic option in patients who cannot tolerate systemic analgesics. Because these agents are not in pill form and many are available without a prescription, they may be overused or misused. This prompted the FDA to issue a warning to consumers.36 Clinicians should advise patients to always read and follow directions on the labels of OTC products.
Topical NSAIDs
Topical NSAIDs have been available commercially in Canada and Europe, and topical diclofenac is now available in gel and patch form in the United States.37,38 These agents exert a local anti-inflammatory and analgesic effect.39,40In soft-tissue injury such as strains and sprains, topical NSAIDs have efficacy that is superior to placebo and similar to oral NSAIDs. Tissue concentrations of topical NSAIDs are high enough to produce anti-inflammatory effects, but systemic concentrations after application remain low.37−40
Diclofenac gel (Voltaren Gel) is indicated for joint pain in the knees and hands secondary to osteoarthritis; it is applied up to four times daily. Diclofenac patch (Flector Patch) is indicated specifically for the topical treatment of acute pain from minor sprains and strains.37,38 The patch is applied to the most painful area twice daily. Patient education for topical NSAIDs is outlined in Table 60–2.
Theoretically, the risk of serious GI adverse events should be less than with oral NSAIDs, but long-term studies evaluating these events are lacking.39,40 Like oral NSAIDs, topical NSAIDs should be used with caution in patients with a history of GI bleeding or ulcer.37,38 Studies comparing topical NSAIDs with other topical products, including counterirritants, are also needed. Local cutaneous adverse reactions (e.g., erythema, pruritus, and irritation) occur in up to 4% of the patients and may be due in part to the vehicle used.37–40
Table 60–2 Patient Education for Topical NSAIDs
Local Anesthetics
Nonprescription topical anesthetics such as lidocaine and benzocaine are available in many types of products. Local anesthetics decrease discharges in superficial somatic nerves and cause numbness on the skin surface but do not penetrate deeper structures such as muscle where the pain often lies.
However, local anesthetics are helpful when abrasion accompanies the injury.41 Application of an OTC antibiotic ointment containing an anesthetic provides soothing relief, promotes healing of abrasions, and prevents soft-tissue infection. Minor abrasions should be cleansed thoroughly with mild soap and water before application. More severe abrasions may require removal of debris or foreign bodies by a clinician followed by irrigation with normal saline.
Counterirritants
Counterirritants are categorized by the FDA into four groups (groups A–D) based on their primary actions (Table 60–3). They produce a feeling of warmth, cooling, or irritation that diverts sensation from the primary source of pain. Because these irritant effects are central to the beneficial actions, counterirritants should not be combined with topical anesthetics or topical analgesics.
Counterirritants are indicated for the temporary relief of minor aches and pains related to muscles and joints.26 These symptoms may be associated with simple backache, arthritis, strains, sprains, or bruises. Many are available commercially as combination products with ingredients from different counterirritant groups. Active ingredients in marketed products sometimes change; clinicians should be aware of the current ingredients before providing a product recommendation.Patient education on proper use of counterirritants is essential to therapeutic success (Table 60–4).
Rubefacients (group A) are counterirritants that produce redness on application. Topical rubefacients containing salicylates (e.g., methyl salicylate) are used most commonly. Turpentine oil is no longer judged as either safe or effective but remains in a few products.26 Clinical trial data evaluating the effect of rubefacients on acute pain from strains, sprains, sports injuries, and chronic musculoskeletal pain are lacking.42 A systematic review of available evidence concluded that topical salicylates are effective for acute pain but have limited effectiveness in chronic pain.42
Table 60–3 Nonprescription Counterirritant External Analgesics
Methyl salicylate and trolamine salicylate are topical salicylates. Methyl salicylate is considered a counterirritant, but trolamine salicylate is not considered a counterirritant because it does not produce localized irritation after application. Application of both topical salicylates can lead to systemic effects, especially if the product is applied liberally.43 Repeated application and occlusion with a wrap or bandage also can increase systemic concentrations. Salicylate-containing products should be used with caution in patients in whom systemic salicylates are contraindicated, such as patients with severe asthma or aspirin allergy.43 Topical salicylates have been reported to increase prothrombin time in patients on warfarin and should be used with caution in patients on oral anticoagulants.43 Methyl salicylate, including oil of wintergreen, is one of the most common sources of pediatric poisonings.44 Clinicians should advise patients to keep products out of the reach of children.
The FDA advises that there is insufficient evidence to support the effectiveness of trolamine salicylate contained in products such as Aspercreme.26 However, many patients choose trolamine products because of the lack of medicinal odor.
Table 60–4 Patient Education for Counterirritants
Apply up to 3–5 times daily to affected area
Only for external use on the skin; do not ingest
Do not apply to broken or damaged skin or cover large areas
Wash hands immediately after application
Avoid contact with the eyes and mouth
Do not use with heating pads or other methods of heat application, because burning or blistering can occur
Do not wrap or bandage the area tightly after application
Consult a physician if:
• Symptoms worsen
• Symptoms persist for more than 7 daysa
• Symptoms resolve but then recur
a Capsaicin may be used for chronic pain and must be applied consistently for efficacy.
From Ref. 26.
The group B counterirritants menthol and camphor exert a sensation of cooling through direct action on sensory nerve endings.43,45 A sensation of warmth follows the cooling effect. The agents also have mild anesthetic activity at low concentrations.45 In higher concentrations, they act as counterirritants and cause a burning sensation by stimulating cutaneous nociceptors. Menthol and camphor are used often in combination with rubefacients.
Menthol, also known as peppermint oil, is used widely in toothpastes, mouthwashes, gum, sore-throat lozenges, lip balms, and nasal decongestants. For topical analgesic use, it is available in creams, lotions, ointment, and patches. The patches can be trimmed to fit the affected area.
Menthol and camphor have caused respiratory distress in infants and should not be used in children under 2 years of age. Despite limits on the concentration of available products, camphor can be toxic to children even in small amounts.46 Patients should be advised to keep the products out of the reach of children.
The group C counterirritants methyl nicotinate and histamine dihydrochloride produce vasodilation.26 Methyl nicotinate is a nicotinic acid derivative that produces PG-mediated vasodilation.47 NSAIDs and aspirin block the production of PGs and decrease methyl nicotinate–induced vasodilation. Application over a large area has been reported to cause systemic symptoms and syncope, possibly due to vasodilation and a decrease in blood pressure.48Patients should be educated to apply only scant amounts to the affected area to avoid this effect.
The primary counterirritant in group D is capsaicin, a natural substance found in red chili peppers and responsible for the hot, spicy characteristic when used in foods.33,34,49 Capsaicin stimulates the release of substance P from local sensory nerve fibers, depleting substance P stores over time. A period of reduced sensitivity to painful stimuli follows, and transmission of pain impulses to the CNS is reduced.33
As with other counterirritants, capsaicin and its derivatives (i.e., capsicum and capsicum oleoresin) exert a warming or burning sensation. With repeated application, desensitization occurs, and the burning sensation subsides. This typically occurs within the first 1 to 2 weeks. After discontinuation, resensitization occurs gradually and returns completely within a few weeks.49
Because of the lag time between initiation and effect, capsaicin is not used for treatment of acute pain from injury. Instead, topical capsaicin is used for chronic pain from musculoskeletal and neuropathic disorders. Capsaicin preparations have been studied in the treatment of pain from diabetic neuropathy, osteoarthritis, rheumatoid arthritis, postherpetic neuralgia, and other disorders.49 It is often used as an adjuvant to systemic analgesics in these chronic pain conditions.
While systemic adverse effects to capsaicin are rare, local adverse effects are expected and common.50 Patient education regarding consistent use of capsaicin products is essential to achieving desired outcomes. Product should be applied in a thin layer and rubbed into the skin thoroughly until little remains on the surface.43 Patients using capsaicin should be advised to apply it regularly and consistently three to four times daily and that full effect may take 1 to 2 weeks or longer. Patients should be assured that the burning effects will diminish with repeated application. Adherence to therapy is essential because the burning sensation persists if applications are less frequent than recommended. Because the burning sensation is enhanced with heat, patients should avoid hot showers or baths immediately before or after application. Wearing gloves during application can decrease the potential for unintended contact with eyes or mucous membranes.50 Dried product residue has been reported to cause respiratory effects on inhalation,49 and caution should be used in patients with asthma or other respiratory illnesses.
Patient Encounter 1, Part 2: Medical History, Physical Examination, and Diagnostic Tests
PMH: Asthma, well controlled with current medication regimen; allergic rhinitis
SH: Denies smoking; drinks alcoholic beverages on most days
Meds: Fluticasone 220 mcg one puff twice daily; albuterol (salbutamol) two to four puffs 4 times daily as needed
Allergies: Aspirin (difficulty breathing)
Diagnostic Tests: Radiographs of left ankle show no evidence of fracture
What are your treatment goals and desired outcomes?
What nonpharmacologic and pharmacologic treatments options are available? Are there treatment options that should be avoided? If so, which options and why?
Muscle Relaxants
Where pain is worsened by muscle spasm, oral muscle relaxants serve as a useful adjunct to therapy.51 These agents include baclofen, metaxalone, methocarbamol, carisoprodol, and cyclobenzaprine. Muscle relaxants decrease spasm and stiffness associated with either acute or chronic musculoskeletal disorders. These agents should be used with caution because they all may cause sedation, especially in combination with alcohol or narcotic analgesics.
Lifestyle and Behavioral Modifications
After treatment of the acute injury with RICE and pharmacologic therapy, the final phase of therapy is rehabilitation and prevention of future injury. For most injuries, prolonged immobilization can lengthen the recovery time by causing wasting of the healthy muscle fibers.10,52 Rehabilitation starts with the development of range of motion via stretching exercises. Patient should warm the muscle first with light activity or moderate heat.10 Warmth produces relaxation and increases elasticity. Next, the patient should start general strengthening exercises.11,52 Resistance exercises using resistance bands available at sporting goods stores are an effective method of strengthening.11Strengthening exercises should be continued beyond the healing phase to prevent future injury.
After rehabilitation, the patient should be educated about behavior changes to prevent reinjury or the development of chronic pain.2,9,25 The warm-up and strengthening routines learned in the rehabilitation phase should be continued. For overuse injury, correction of biomechanical abnormalities with proper footwear and changes in technique may correct misalignments and imbalances.2 Repetitive trauma can be decreased with proper training (e.g., by implementing a gradual increase in mileage in a running plan).
Patient Encounter 1, Part 3: Creating a Care Plan
Based on the information presented, create a care plan to treat this patient’s ankle injury. Your plan should include:
(a) the goals of therapy and desired outcomes,
(b) a patient-specific therapeutic plan, including nonpharmacologic therapy, and (c) a plan to monitor the outcome of therapy to determine if goals of therapy have been met and adverse effects avoided.
Patient Encounter 2
A 40-year-old woman presents with right elbow pain. On questioning, you determine that she works in a factory performing repetitive tasks with her right arm. She reports the gradual onset of pain over the last few months. When she wakes in the morning, she has minimal pain after rest, but the pain intensifies after a few hours at work. She tends to have less pain on weekends. She reports decreased range of motion compared with the left side. She is a nonsmoker and does not drink. She has no significant past medical history or allergies. She takes no medications.
Given this information, what is your assessment of the patient’s elbow pain?
What is the likely etiology of the pain?
What nonpharmacologic and pharmacologic treatments options should be considered?
Based on the information presented, create a care plan for this patient’s elbow injury. Your plan should include: (a) the goals of therapy and desired outcomes, (b) a patient-specific therapeutic plan, including nonpharmacologic therapy, and (c) a monitoring plan to determine if goals of therapy have been met and adverse effects avoided.
Proper lifting techniques can decrease low back pain.15 Lifting methods include standing with legs shoulder-width apart, lifting with the legs and not the back, and keeping the object close to the body. In the workplace, repetitive motion can be decreased through proper ergonomic design and diversification of job tasks.13 In pain of the lower extremity, weight loss in overweight or obese patients can assist in reduction of further inflammation and help to prevent reinjury or repetitive strain injuries.23 Nonweight-bearing activities, such as swimming or bicycling, can be recommended for initial return to activity.25
Patient Care and Monitoring
1. Assess the patient’s symptoms to determine if empirical care is appropriate or whether diagnostic evaluation is warranted. Determine the timing of injury (if applicable), duration of pain, type and degree of pain, and exacerbating factors. Determine if the musculoskeletal disorder interferes with usual activities or range of motion.
2. Assess exacerbating or alleviating factors. Ask if the patient has tried any nonpharmacologic or pharmacologic treatments.
3. Obtain a complete medication history, including history of prescription drug, nonprescription drug, and dietary supplement use. Determine if the patient has used any successful or unsuccessful treatments for this condition in the past.
4. Gather patient history. Assess factors involved in drug selection. Inquire about social history and alcohol use. Ask the patient about drug allergies and chronic health problems such as asthma.
5. Educate the patient on nonpharmacologic therapy, including each of the steps in RICE. If injury is the source of the pain and it occurred more than 48 hours ago, consider heat instead of ice.
6. Assess patient preference for systemic (oral) or local (topical) therapy. Would frequent application of topical medications be possible? Would the patient accept topical medications with a medicinal odor?
7. Recommend appropriate pharmacologic therapy and educate on proper use. If a counterirritant is recommended, counsel patients on the irritant effect of the product and recommend washing hands immediately after use and to avoid heating pads. For patients using a capsaicin product, emphasize that adherence to regular application is required for effectiveness.
8. Develop a plan to assess effectiveness of pharmacologic therapy. If pain is from an acute injury, assess effectiveness within 7 to 10 days. For chronic pain treated with capsaicin, begin to assess pain control in 2 weeks.
9. Evaluate for adverse effects and drug interactions. For patients on topical therapy, evaluate for local adverse effects. For patients on acetaminophen or NSAIDs, inquire about alcohol use.
10. Stress lifestyle modifications for rehabilitation and prevention. Recommend strength training, range-of-motion exercises, and a warm-up period before exercise. In repetitive-motion injury, recommend methods to correct biomechanical abnormalities and vary work tasks as applicable. Refer to a physical therapist or sports trainer as needed.
OUTCOME EVALUATION
• Use a pain scale to monitor treatment interventions to ensure that pain relief is achieved. Ask the patient to rate pain on a scale of zero (no pain) to 10 (worst possible pain) both at rest and with movement. Compare the results with baseline pain assessment to monitor the response to therapy. In pediatric patients, use a visual pain scale with facial expressions depicting various degrees of pain.
• Assess range of motion at baseline and after treatment by comparing movement with the unaffected limb and functionality before the injury. Assess functionality by asking patients if they are able to perform activities of daily living or participate in exercise as desired.
• If pain from acute injury does not decrease greatly within 7 to 10 days, further diagnostic evaluation is warranted.
• For patients using capsaicin products, assess adherence to regular application for therapeutic benefit. Assess chronic pain control in 2 weeks.
• Assess medication adverse effects on a regular basis. When NSAIDs and aspirin are used, ask about GI tolerability, bruising, and bleeding. Inquire about local adverse effects, such as burning, when topical counterirritants are used for treatment.
• Evaluate adherence to preventative rehabilitation measures such as proper footwear, warm-up before activity, strength training, and proper lifting technique.
Abbreviations Introduced in This Chapter
Self-assessment questions and answers are available at http://www.mhpharmacotherapy.com/pp.html.
REFERENCES
1. Abasolo L, Blanco M, Bachiller J, et al. A health system program to reduce work disability related to musculoskeletal disorders. Ann Intern Med 2005; 143:404–414.
2. Wilder RP, Sethi S. Overuse injuries: Tendinopathies, stress fractures, compartment syndrome, and shin splints. Clin Sports Med 2004;23:55–81.
3. Biundo Jr. JJ, Irwin RW, Umpierre E. Sports and other soft tissue injuries, tendinitis, bursitis, and occupation-related syndromes. Curr Opin Rheumatol 2001;13:146–149.
4. Schappert SM, Burt CW. Ambulatory care visits to physician offices, hospital outpatient departments, and emergency departments: United States, 2001–02. Vital Health Stat 13. 2006;159:1–66.
5. Yellin E, Herrndorf A, Trupin L, Sonneborn D. A national study of medical care expenditures for musculoskeletal conditions. Arthritis Rheum 2001;44:1160–1169.
6. National Research Council, The Institute of Medicine. Musculoskeletal Disorders and the Workplace: Low Back and Upper Extremities. Washington, DC: National Academy Press, 2001.
7. Mani L, Gerr F. Work-related upper extremity musculoskeletal disorders. Prim Care 2000;27:845–864.
8. Morse T, Dillon C, Kenta-Bibi E, et al. Trends in work-related musculoskeletal disorder reports by year, type, and industrial sector: A capture-recapture analysis. Am J Ind Med 2005;48:40–49.
9. Audette J, Frotera W. Assessment and treatment of pain in sports injuries. In: Warfield CA, Bajwa ZH, eds. Principles and Practice of Pain Medicine, 2nd ed. New York: McGraw-Hill, 2004:35–48.
10. Jarvinen TA, Kaariainen M, Jarvinen M, et al. Muscle strain injuries. Curr Opin Rheumatol 2000;12:155–161.
11. Wolfe MW, Uhl TL, Mattacola CG, et al. Management of ankle sprains. Am Fam Physician 2001;63:93–104.
12. Ivins D. Acute ankle sprain: An update. Am Fam Physician 2006; 74:1714–1720, 1723–1726.
13. Amell T, Kumar S. Work-related musculoskeletal disorders: Design as a prevention strategy: A review. J Occup Rehabil 2001;11:255–265.
14. Noonan TJ, Garrett WE Jr. Muscle strain injury: Diagnosis and treatment. J Am Acad Orthop Surg 1999;7:262–269.
15. Patel AT, Ogle AA. Diagnosis and management of acute low back pain. Am Fam Physician, 2000;61:1779–1786, 1789–1790.
16. Toumi H, Best TM. The inflammatory response: Friend or enemy for muscle injury? Br J Sports Med 2003;37:284–286.
17. Murrell GA. Understanding tendinopathies. Br J Sports Med 2002;36:392–393.
18. Wilson JJ, Best TM. Common overuse tendon problems: A review and recommendations for treatment. Am Fam Physician 2005;72:881–888.
19. Baldwin Lanier A. Use of nonsteroidal anti-inflammatory drugs following exercise-induced muscle injury. Sports Med 2003;33:177–185.
20. Cohen SA. Pathophysiology of pain. In: Warfield CA, Bajwa ZH, eds. Principles and Practice of Pain Medicine, 2nd ed. New York: McGraw-Hill, 2004:35–48.
21. Fields HL, Martin JB. Pain: Pathophysiology and management. In: Kasper DL, Fauci AS, Braunwald E, et al., eds. Harrison’s Principles of Internal Medicine, 17th ed. New York City: McGraw-Hill, 2008:81–87.
22. DeVane CL. Substance P: A new era, a new role. Pharmacotherapy 2001; 21:1061–1069.
23. Mazzone MF, McCue T. Common conditions of the Achilles tendon. Am Fam Physician 2002;65:1805–1810.
24. Wilson JJ, Best TM. Common overuse tendon problems: A review and recommendations for treatment. Am Fam Physician 2005;72:811–818.
25. Palmer T, Toombs JD. Managing joint pain in primary care. J Am Board Fam Pract 2004;17(suppl):S32–S42.
26. External analgesics drug products for over-the-counter human use: Tentative final monograph. Fed Regist 1983;48:5851–5869.
27. Pray WS. Treating sore muscles and tendons. US Pharm 2006;5:18–24.
28. Graham GG, Scott KF. Mechanism of action of paracetamol. Am J Ther 2005;12:46–55.
29. Kvien TK, Viktil K. Pharmacotherapy for regional musculoskeletal pain. Best Pract Res Clin Rheumatol 2003;17:137–150.
30. Sachs CJ. Oral analgesics for acute nonspecific pain. Am Fam Physician 2005;71:913–918.
31. Graham GG, Scott KF, Day RO. Tolerability of paracetamol. Drug Saf 2005;28:227–240.
32. Peterson GM. Selecting nonprescription analgesics. Am J Ther 2005;12:67–79.
33. Galer BS. Topical medications. In: Loeser JD, Bonica JJ, eds. Bonica’s Management of Pain, 3rd ed. Philadelphia: Lippincott Williams & Wilkins, 2001:1736–1741.
34. Sawynok J. Topical and peripherally acting analgesics. Pharmacol Rev 2003;55:1–20.
35. Tramer MR. It’s not just about rubbing—Topical capsaicin and topical salicylates may be useful as adjuvants to conventional pain treatment. BMJ 2004;328:998.
36. FDA Consumer Health Information. Use Caution with Over-the-Counter Creams, Ointments. http://www.fda.gov/consumer/updates/otc_creams040108.html.
37. Voltaren Gel (diclofenac sodium topical gel 1%) product information. Novartis Consumer Health. Parsippany, NJ: October 2007.
38. Flector Patch (diclofenac epolamine patch 1.3%). Alpharma Pharmaceuticals. Piscataway, NJ: November 2007.
39. Zacher J, Altman R, Bellamy N, et al. Topical diclofenac and its role in pain and inflammation: An evidence-based review. Curr Med Res Opin 2008;24:925–950.
40. Mason L, Moore RA, Edwards JE, et al. Topical NSAIDs for acute pain: A meta-analysis. BMC Fam Pract 2004;5:10.
41. Blasen LS. Soft tissue injuries. Management of common presentations. Adv Nurse Pract 2000;8:65–66, 84.
42. Mason L, Moore RA, Edwards JE, et al. Systematic review of efficacy of topical rubefacients containing salicylates for the treatment of acute and chronic pain. BMJ 2004;328:995.
43. Martindale: The complete drug reference. London: Pharma-ceutical Press. Electronic version, Thomson Healthcare, Greenwood Village, CO. http://www.thomsonhc.com.
44. Davis JE. Are one or two dangerous? Methyl salicylate exposure in toddlers. J Emerg Med 2007;32:63–69.
45. Patel T, Ishiuji Y, Yosipovitch G. Menthol: A refreshing look at this ancient compound. J Am Acad Dermatol 2007;57:873–878.
46. Michael JB, Sztajnkrycer MD. Deadly pediatric poisons: Nine common agents that kill at low doses. Emerg Med Clin North Am 2004;22:1019–1050.
47. Wilkin JK, Fortner G, Reinhardt LA, et al. Prostaglandins and nicotinate-provoked increase in cutaneous blood flow. Clin Pharmacol Ther 1985;38:273–277.
48. Fergusson DA. Systemic symptoms associated with a rubefacient. BMJ 1988;297:1339.
49. Mason L, Moore RA, Derry S, et al. Systematic review of topical capsaicin for the treatment of chronic pain. BMJ 2004;328:991.
50. Rosenstein ED. Topical agents in the treatment of rheumatic disorders. Rheum Dis Clin North Am 1999;25:899–918.
51. Beebe FA, Barkin RL, Barkin S. A clinical and pharmacologic review of skeletal muscle relaxants for musculoskeletal conditions. Am J Ther 2005;12:151–171.
52. Schramm-Bloodworth D, Grabois M. Physical medicine and rehabilitation. In: Warfield CA, Bajwa ZH, eds. Principles and Practice of Pain Medicine, 2nd ed. New York: McGraw-Hill; 2004:35–48.