The Journal of Family Practice

The patient was given a diagnosis of widespread tinea corporis. This diagnosis may not fit with the common paradigm of tinea as thin, scaly annular patches, often known as ringworm. However, a skin scraping was performed on the red scaly patches, and the diagnosis was confirmed.

A skin scraping is a simple procedure that takes minutes to yield actionable information. A scalpel blade is used in a scraping motion and skin flakes are caught on a slide as they fall from the skin. (Another glass slide can be used in place of the scalpel, which is slightly less frightening for children.) The sample is then covered with 1 to 2 drops of potassium hydroxide (KOH), in 1 of various available formulations, and covered with a coverslip. Gently heating the slide, or simply waiting a few minutes, will allow the KOH to begin dissolving some keratinocyte membranes and stain any fungal walls light purple.

Hyphae, which may be linear (see Figure) or branched, will cross multiple cell membranes and are themselves about the thickness of a cell membrane. A high-powered view of hyphae should reveal nuclei and septa.

Skin biopsy, culture, and a skin scraping sent to an outside lab are all alternatives to the aforementioned approach but take days or weeks to yield a result. Fungal polymerase chain reaction is a novel diagnostic approach that can be both sensitive and specific, but still requires several days for results and incurs additional cost to the patient.

In this case, the diagnosis was made at the patient’s bedside and terbinafine 250 mg/d for 3 weeks was chosen as systemic therapy because of the extent of disease. At the follow-up visit 2 months later, the patient’s rash had completely cleared.

‌

Text and photos courtesy of Jonathan Karnes, MD, medical director, MDFMR Dermatology Services, Augusta, ME. (Photo copyright retained.)

The patient was given a diagnosis of widespread tinea corporis. This diagnosis may not fit with the common paradigm of tinea as thin, scaly annular patches, often known as ringworm. However, a skin scraping was performed on the red scaly patches, and the diagnosis was confirmed.

A skin scraping is a simple procedure that takes minutes to yield actionable information. A scalpel blade is used in a scraping motion and skin flakes are caught on a slide as they fall from the skin. (Another glass slide can be used in place of the scalpel, which is slightly less frightening for children.) The sample is then covered with 1 to 2 drops of potassium hydroxide (KOH), in 1 of various available formulations, and covered with a coverslip. Gently heating the slide, or simply waiting a few minutes, will allow the KOH to begin dissolving some keratinocyte membranes and stain any fungal walls light purple.

Hyphae, which may be linear (see Figure) or branched, will cross multiple cell membranes and are themselves about the thickness of a cell membrane. A high-powered view of hyphae should reveal nuclei and septa.

Skin biopsy, culture, and a skin scraping sent to an outside lab are all alternatives to the aforementioned approach but take days or weeks to yield a result. Fungal polymerase chain reaction is a novel diagnostic approach that can be both sensitive and specific, but still requires several days for results and incurs additional cost to the patient.

In this case, the diagnosis was made at the patient’s bedside and terbinafine 250 mg/d for 3 weeks was chosen as systemic therapy because of the extent of disease. At the follow-up visit 2 months later, the patient’s rash had completely cleared.

‌

Text and photos courtesy of Jonathan Karnes, MD, medical director, MDFMR Dermatology Services, Augusta, ME. (Photo copyright retained.)

The patient was given a diagnosis of widespread tinea corporis. This diagnosis may not fit with the common paradigm of tinea as thin, scaly annular patches, often known as ringworm. However, a skin scraping was performed on the red scaly patches, and the diagnosis was confirmed.

A skin scraping is a simple procedure that takes minutes to yield actionable information. A scalpel blade is used in a scraping motion and skin flakes are caught on a slide as they fall from the skin. (Another glass slide can be used in place of the scalpel, which is slightly less frightening for children.) The sample is then covered with 1 to 2 drops of potassium hydroxide (KOH), in 1 of various available formulations, and covered with a coverslip. Gently heating the slide, or simply waiting a few minutes, will allow the KOH to begin dissolving some keratinocyte membranes and stain any fungal walls light purple.

Hyphae, which may be linear (see Figure) or branched, will cross multiple cell membranes and are themselves about the thickness of a cell membrane. A high-powered view of hyphae should reveal nuclei and septa.

Skin biopsy, culture, and a skin scraping sent to an outside lab are all alternatives to the aforementioned approach but take days or weeks to yield a result. Fungal polymerase chain reaction is a novel diagnostic approach that can be both sensitive and specific, but still requires several days for results and incurs additional cost to the patient.

In this case, the diagnosis was made at the patient’s bedside and terbinafine 250 mg/d for 3 weeks was chosen as systemic therapy because of the extent of disease. At the follow-up visit 2 months later, the patient’s rash had completely cleared.

‌

Text and photos courtesy of Jonathan Karnes, MD, medical director, MDFMR Dermatology Services, Augusta, ME. (Photo copyright retained.)

The findings of follicular-based papules, pustules, and scars led to the diagnosis of early folliculitis keloidalis nuchae (FKN).

FKN, also called acne keloidalis nuchae, is more common in patients with darker skin types (Fitzpatrick skin types IV-VI) and is the most common form of scarring alopecia in men of African descent. The pathogenesis is unclear, but the condition may arise from mechanical occlusion with a retained short hair that leads to follicular destruction. Patients should lengthen their hair to at least a quarter of an inch to minimize this process. Military personnel may receive a waiver from standard grooming requirements. FKN may also occur as a primary disorder arising from bacterial infection and subsequent vigorous inflammation.

For early disease, topical therapy with either clindamycin 1% lotion or chlorhexidine solution are acceptable options. Should these options and hair lengthening fail over 3 to 4 months, consider a 6- to 12-week course of doxycycline or minocycline 100 mg once or twice daily. Intralesional triamcinolone with 5 to 10 mg/mL injected into fixed papules every 4 to 8 weeks is another option to reduce scar formation. The most severe cases may require combination oral antibiotics, isotretinoin, or plastic surgery.

In this case, the patient grew out his hair and applied clindamycin 1% lotion twice daily for a year. As a result, he had no further disease.

‌

Text and photos courtesy of Jonathan Karnes, MD, medical director, MDFMR Dermatology Services, Augusta, ME. (Photo copyright retained.)

The findings of follicular-based papules, pustules, and scars led to the diagnosis of early folliculitis keloidalis nuchae (FKN).

FKN, also called acne keloidalis nuchae, is more common in patients with darker skin types (Fitzpatrick skin types IV-VI) and is the most common form of scarring alopecia in men of African descent. The pathogenesis is unclear, but the condition may arise from mechanical occlusion with a retained short hair that leads to follicular destruction. Patients should lengthen their hair to at least a quarter of an inch to minimize this process. Military personnel may receive a waiver from standard grooming requirements. FKN may also occur as a primary disorder arising from bacterial infection and subsequent vigorous inflammation.

For early disease, topical therapy with either clindamycin 1% lotion or chlorhexidine solution are acceptable options. Should these options and hair lengthening fail over 3 to 4 months, consider a 6- to 12-week course of doxycycline or minocycline 100 mg once or twice daily. Intralesional triamcinolone with 5 to 10 mg/mL injected into fixed papules every 4 to 8 weeks is another option to reduce scar formation. The most severe cases may require combination oral antibiotics, isotretinoin, or plastic surgery.

In this case, the patient grew out his hair and applied clindamycin 1% lotion twice daily for a year. As a result, he had no further disease.

‌

Text and photos courtesy of Jonathan Karnes, MD, medical director, MDFMR Dermatology Services, Augusta, ME. (Photo copyright retained.)

The findings of follicular-based papules, pustules, and scars led to the diagnosis of early folliculitis keloidalis nuchae (FKN).

FKN, also called acne keloidalis nuchae, is more common in patients with darker skin types (Fitzpatrick skin types IV-VI) and is the most common form of scarring alopecia in men of African descent. The pathogenesis is unclear, but the condition may arise from mechanical occlusion with a retained short hair that leads to follicular destruction. Patients should lengthen their hair to at least a quarter of an inch to minimize this process. Military personnel may receive a waiver from standard grooming requirements. FKN may also occur as a primary disorder arising from bacterial infection and subsequent vigorous inflammation.

For early disease, topical therapy with either clindamycin 1% lotion or chlorhexidine solution are acceptable options. Should these options and hair lengthening fail over 3 to 4 months, consider a 6- to 12-week course of doxycycline or minocycline 100 mg once or twice daily. Intralesional triamcinolone with 5 to 10 mg/mL injected into fixed papules every 4 to 8 weeks is another option to reduce scar formation. The most severe cases may require combination oral antibiotics, isotretinoin, or plastic surgery.

In this case, the patient grew out his hair and applied clindamycin 1% lotion twice daily for a year. As a result, he had no further disease.

‌

Text and photos courtesy of Jonathan Karnes, MD, medical director, MDFMR Dermatology Services, Augusta, ME. (Photo copyright retained.)

REFERENCES

1. Oliver SE, Gargano JW, Marin M; et al. The Advisory Committee on Immunization Practices’ interim recommendation for use of Pfizer-BioNTech COVID-19 vaccine—United States, December 2020. MMWR Morbid Mortal Wkly Rep. 2020;69:1922-1924. Accessed January 13, 2021. www.cdc.gov/mmwr/volumes/69/wr/mm6950e2.htm
2. 2. Oliver SE, Gargano JW, Marin M; et al. The Advisory Committee on Immunization Practices’ interim recommendation for use of Moderna COVID-19 vaccine—United States, December 2020. MMWR Morbid Mortal Wkly Rep. 2021;69:1653-1656. Accessed January 13, 2021. www.cdc.gov/mmwr/volumes/69/wr/mm695152e1.htm
3. CDC. COVID-19 vaccines: update on allergic reactions, contraindications, and precautions [webinar]. December 30, 2020. Accessed January 6, 2021. https://emergency.cdc.gov/coca/calls/2020/callinfo_123020.asp
4. CDC. What clinicians need to know about the Pfizer-BioNTech and Moderna COVID-19 vaccines [webinar]. December 18, 2020. Accessed January 6, 2021. https://emergency.cdc.gov/coca/calls/2020/callinfo_121820.asp
5. CDC COVID-19 Response Team; Food and Drug Administration. Allergic reactions including anaphylaxis after receipt of the first dose of Pfizer-BioNTech COVID-19 vaccine—United States, December 14-23, 2020. MMWR Morb Mortal Wkly Rep. ePub: January 6, 2021. Accessed January 13, 2021. www.cdc.gov/mmwr/volumes/70/wr/mm7002e1.htm

REFERENCES

1. Oliver SE, Gargano JW, Marin M; et al. The Advisory Committee on Immunization Practices’ interim recommendation for use of Pfizer-BioNTech COVID-19 vaccine—United States, December 2020. MMWR Morbid Mortal Wkly Rep. 2020;69:1922-1924. Accessed January 13, 2021. www.cdc.gov/mmwr/volumes/69/wr/mm6950e2.htm
2. 2. Oliver SE, Gargano JW, Marin M; et al. The Advisory Committee on Immunization Practices’ interim recommendation for use of Moderna COVID-19 vaccine—United States, December 2020. MMWR Morbid Mortal Wkly Rep. 2021;69:1653-1656. Accessed January 13, 2021. www.cdc.gov/mmwr/volumes/69/wr/mm695152e1.htm
3. CDC. COVID-19 vaccines: update on allergic reactions, contraindications, and precautions [webinar]. December 30, 2020. Accessed January 6, 2021. https://emergency.cdc.gov/coca/calls/2020/callinfo_123020.asp
4. CDC. What clinicians need to know about the Pfizer-BioNTech and Moderna COVID-19 vaccines [webinar]. December 18, 2020. Accessed January 6, 2021. https://emergency.cdc.gov/coca/calls/2020/callinfo_121820.asp
5. CDC COVID-19 Response Team; Food and Drug Administration. Allergic reactions including anaphylaxis after receipt of the first dose of Pfizer-BioNTech COVID-19 vaccine—United States, December 14-23, 2020. MMWR Morb Mortal Wkly Rep. ePub: January 6, 2021. Accessed January 13, 2021. www.cdc.gov/mmwr/volumes/70/wr/mm7002e1.htm

REFERENCES

1. Oliver SE, Gargano JW, Marin M; et al. The Advisory Committee on Immunization Practices’ interim recommendation for use of Pfizer-BioNTech COVID-19 vaccine—United States, December 2020. MMWR Morbid Mortal Wkly Rep. 2020;69:1922-1924. Accessed January 13, 2021. www.cdc.gov/mmwr/volumes/69/wr/mm6950e2.htm
2. 2. Oliver SE, Gargano JW, Marin M; et al. The Advisory Committee on Immunization Practices’ interim recommendation for use of Moderna COVID-19 vaccine—United States, December 2020. MMWR Morbid Mortal Wkly Rep. 2021;69:1653-1656. Accessed January 13, 2021. www.cdc.gov/mmwr/volumes/69/wr/mm695152e1.htm
3. CDC. COVID-19 vaccines: update on allergic reactions, contraindications, and precautions [webinar]. December 30, 2020. Accessed January 6, 2021. https://emergency.cdc.gov/coca/calls/2020/callinfo_123020.asp
4. CDC. What clinicians need to know about the Pfizer-BioNTech and Moderna COVID-19 vaccines [webinar]. December 18, 2020. Accessed January 6, 2021. https://emergency.cdc.gov/coca/calls/2020/callinfo_121820.asp
5. CDC COVID-19 Response Team; Food and Drug Administration. Allergic reactions including anaphylaxis after receipt of the first dose of Pfizer-BioNTech COVID-19 vaccine—United States, December 14-23, 2020. MMWR Morb Mortal Wkly Rep. ePub: January 6, 2021. Accessed January 13, 2021. www.cdc.gov/mmwr/volumes/70/wr/mm7002e1.htm

A shave biopsy of the lesion confirmed a nodular and pigmented basal cell carcinoma (BCC). In the United States, BCC is the most common cancer and accounts for 80% of all skin cancer diagnoses. BCC is also the most widespread cancer in White, Hispanic, and Asian patients and the second most common skin cancer in Black patients.

In all patients, BCC presents as a shiny growing macule, papule, or plaque, usually in areas of sun exposure. Much less is known about the role of UV exposure in skin of color because of the lack of high-quality studies in this population. Despite this, BCC in skin of color most often presents on the head and neck, as it does in non-Hispanic White patients. There is a correlation between lighter skin tones in Black patients and increased numbers of BCC diagnoses.

When assessing a suspicious skin lesion in skin of color, be on the lookout for the following visual cues. Pigmentation, clinically and on dermoscopy, is a more common feature of BCCs in non-White patients—occurring in more than half of all BCCs in skin of color.¹ While pigmentation in a skin tumor may be mistaken for melanoma, the blue ovoid nests, brown dots in focus, and brown leaf-like areas on dermoscopy are BCC-specific clues that can alert the clinician to the diagnosis. In all patients, telangiectasias are another hallmark of BCC but may be the only feature in White patients and just one of many features in non-White patients.

In small data sets, there is no difference in tumor-related morbidity and prognosis between White and Black patients with BCC. Additionally, BCCs in White, Asian, and Hispanic patients have had no differences in preoperative tumor size, number of Mohs stages, and outcome.¹

In this case, the patient underwent a complete excision with a 5-mm margin. She remained free of new or recurrent BCCs over the next 2 years, with surveillance exams twice a year.

‌

Text and photos courtesy of Jonathan Karnes, MD, medical director, MDFMR Dermatology Services, Augusta, ME. (Photo copyright retained.)

A shave biopsy of the lesion confirmed a nodular and pigmented basal cell carcinoma (BCC). In the United States, BCC is the most common cancer and accounts for 80% of all skin cancer diagnoses. BCC is also the most widespread cancer in White, Hispanic, and Asian patients and the second most common skin cancer in Black patients.

In all patients, BCC presents as a shiny growing macule, papule, or plaque, usually in areas of sun exposure. Much less is known about the role of UV exposure in skin of color because of the lack of high-quality studies in this population. Despite this, BCC in skin of color most often presents on the head and neck, as it does in non-Hispanic White patients. There is a correlation between lighter skin tones in Black patients and increased numbers of BCC diagnoses.

When assessing a suspicious skin lesion in skin of color, be on the lookout for the following visual cues. Pigmentation, clinically and on dermoscopy, is a more common feature of BCCs in non-White patients—occurring in more than half of all BCCs in skin of color.¹ While pigmentation in a skin tumor may be mistaken for melanoma, the blue ovoid nests, brown dots in focus, and brown leaf-like areas on dermoscopy are BCC-specific clues that can alert the clinician to the diagnosis. In all patients, telangiectasias are another hallmark of BCC but may be the only feature in White patients and just one of many features in non-White patients.

In small data sets, there is no difference in tumor-related morbidity and prognosis between White and Black patients with BCC. Additionally, BCCs in White, Asian, and Hispanic patients have had no differences in preoperative tumor size, number of Mohs stages, and outcome.¹

In this case, the patient underwent a complete excision with a 5-mm margin. She remained free of new or recurrent BCCs over the next 2 years, with surveillance exams twice a year.

‌

Text and photos courtesy of Jonathan Karnes, MD, medical director, MDFMR Dermatology Services, Augusta, ME. (Photo copyright retained.)

A shave biopsy of the lesion confirmed a nodular and pigmented basal cell carcinoma (BCC). In the United States, BCC is the most common cancer and accounts for 80% of all skin cancer diagnoses. BCC is also the most widespread cancer in White, Hispanic, and Asian patients and the second most common skin cancer in Black patients.

In all patients, BCC presents as a shiny growing macule, papule, or plaque, usually in areas of sun exposure. Much less is known about the role of UV exposure in skin of color because of the lack of high-quality studies in this population. Despite this, BCC in skin of color most often presents on the head and neck, as it does in non-Hispanic White patients. There is a correlation between lighter skin tones in Black patients and increased numbers of BCC diagnoses.

When assessing a suspicious skin lesion in skin of color, be on the lookout for the following visual cues. Pigmentation, clinically and on dermoscopy, is a more common feature of BCCs in non-White patients—occurring in more than half of all BCCs in skin of color.¹ While pigmentation in a skin tumor may be mistaken for melanoma, the blue ovoid nests, brown dots in focus, and brown leaf-like areas on dermoscopy are BCC-specific clues that can alert the clinician to the diagnosis. In all patients, telangiectasias are another hallmark of BCC but may be the only feature in White patients and just one of many features in non-White patients.

In small data sets, there is no difference in tumor-related morbidity and prognosis between White and Black patients with BCC. Additionally, BCCs in White, Asian, and Hispanic patients have had no differences in preoperative tumor size, number of Mohs stages, and outcome.¹

In this case, the patient underwent a complete excision with a 5-mm margin. She remained free of new or recurrent BCCs over the next 2 years, with surveillance exams twice a year.

‌

Text and photos courtesy of Jonathan Karnes, MD, medical director, MDFMR Dermatology Services, Augusta, ME. (Photo copyright retained.)

The acute rash with minute pustules and associated leukocytosis with neutrophilia and eosinophilia led to a diagnosis of acute generalized exanthematous pustulosis (AGEP), which may have been triggered by azithromycin—the patient’s only recent medication. AGEP is a severe cutaneous eruption that may be associated with systemic involvement. Medications are usually implicated, and patients often seek urgent evaluation.

AGEP typically begins as an acute eruption in the intertriginous sites of the axilla, groin, and neck, but often becomes more generalized. The diagnosis is strongly suggested by the condition’s key features: fever (97% of cases) and leukocytosis (87%) with neutrophilia (91%) and eosinophilia (30%). Leukocytosis peaks 4 days after pustulosis occurs and lasts for about 12 days. Although common, fever is not always documented in patients with AGEP. (This patient was a case in point.)

In approximately 90% of AGEP cases, medications such as antibiotics and calcium channel blockers are implicated; however, the lack of such an association does not preclude the diagnosis. In cases of drug reactions, the eruption typically develops 1 to 2 days after a medication is begun, and the pustules typically resolve in fewer than 15 days. In 17% of patients, systemic involvement can occur and can include the liver, kidneys, bone marrow, and lungs. A physical exam, review of systems, and a laboratory evaluation can help rule out systemic involvement and guide additional testing.

AGEP has an incidence of 1 to 5 cases per million people per year, affecting women slightly more frequently than men. While the pathophysiology is not well understood, AGEP and its differential diagnoses are categorized as T cell-related inflammatory responses.

There are at least 4 severe cutaneous eruptions that might be confused with AGEP, all of which may be associated with fever. They include a drug reaction with eosinophilia and systemic symptoms, Stevens-Johnson syndrome, toxic epidermal necrolysis, and pustular psoriasis. The clinical features that may help differentiate these conditions from AGEP include timeline, mucocutaneous features, organ system involvement, and histopathologic findings.

Patients who have AGEP, including those with systemic involvement, generally improve after the offending drug is discontinued and treatment with topical corticosteroids is initiated. A brief course of systemic corticosteroids can also be considered for patients with severe skin involvement or systemic involvement.

This patient was prescribed topical corticosteroid wet dressing treatments twice daily for 2 weeks. At the 2-week follow-up visit, the rash had completely cleared and only minimal residual erythema was noted. The patient was instructed to avoid azithromycin.

This case was adapted from: Tolkachjov SN, Wetter DA, Sandefur BJ. Generalized pustular eruption. J Fam Pract. 2018;67:309-310,312.

The acute rash with minute pustules and associated leukocytosis with neutrophilia and eosinophilia led to a diagnosis of acute generalized exanthematous pustulosis (AGEP), which may have been triggered by azithromycin—the patient’s only recent medication. AGEP is a severe cutaneous eruption that may be associated with systemic involvement. Medications are usually implicated, and patients often seek urgent evaluation.

AGEP typically begins as an acute eruption in the intertriginous sites of the axilla, groin, and neck, but often becomes more generalized. The diagnosis is strongly suggested by the condition’s key features: fever (97% of cases) and leukocytosis (87%) with neutrophilia (91%) and eosinophilia (30%). Leukocytosis peaks 4 days after pustulosis occurs and lasts for about 12 days. Although common, fever is not always documented in patients with AGEP. (This patient was a case in point.)

In approximately 90% of AGEP cases, medications such as antibiotics and calcium channel blockers are implicated; however, the lack of such an association does not preclude the diagnosis. In cases of drug reactions, the eruption typically develops 1 to 2 days after a medication is begun, and the pustules typically resolve in fewer than 15 days. In 17% of patients, systemic involvement can occur and can include the liver, kidneys, bone marrow, and lungs. A physical exam, review of systems, and a laboratory evaluation can help rule out systemic involvement and guide additional testing.

AGEP has an incidence of 1 to 5 cases per million people per year, affecting women slightly more frequently than men. While the pathophysiology is not well understood, AGEP and its differential diagnoses are categorized as T cell-related inflammatory responses.

There are at least 4 severe cutaneous eruptions that might be confused with AGEP, all of which may be associated with fever. They include a drug reaction with eosinophilia and systemic symptoms, Stevens-Johnson syndrome, toxic epidermal necrolysis, and pustular psoriasis. The clinical features that may help differentiate these conditions from AGEP include timeline, mucocutaneous features, organ system involvement, and histopathologic findings.

Patients who have AGEP, including those with systemic involvement, generally improve after the offending drug is discontinued and treatment with topical corticosteroids is initiated. A brief course of systemic corticosteroids can also be considered for patients with severe skin involvement or systemic involvement.

This patient was prescribed topical corticosteroid wet dressing treatments twice daily for 2 weeks. At the 2-week follow-up visit, the rash had completely cleared and only minimal residual erythema was noted. The patient was instructed to avoid azithromycin.

This case was adapted from: Tolkachjov SN, Wetter DA, Sandefur BJ. Generalized pustular eruption. J Fam Pract. 2018;67:309-310,312.

The acute rash with minute pustules and associated leukocytosis with neutrophilia and eosinophilia led to a diagnosis of acute generalized exanthematous pustulosis (AGEP), which may have been triggered by azithromycin—the patient’s only recent medication. AGEP is a severe cutaneous eruption that may be associated with systemic involvement. Medications are usually implicated, and patients often seek urgent evaluation.

AGEP typically begins as an acute eruption in the intertriginous sites of the axilla, groin, and neck, but often becomes more generalized. The diagnosis is strongly suggested by the condition’s key features: fever (97% of cases) and leukocytosis (87%) with neutrophilia (91%) and eosinophilia (30%). Leukocytosis peaks 4 days after pustulosis occurs and lasts for about 12 days. Although common, fever is not always documented in patients with AGEP. (This patient was a case in point.)

In approximately 90% of AGEP cases, medications such as antibiotics and calcium channel blockers are implicated; however, the lack of such an association does not preclude the diagnosis. In cases of drug reactions, the eruption typically develops 1 to 2 days after a medication is begun, and the pustules typically resolve in fewer than 15 days. In 17% of patients, systemic involvement can occur and can include the liver, kidneys, bone marrow, and lungs. A physical exam, review of systems, and a laboratory evaluation can help rule out systemic involvement and guide additional testing.

AGEP has an incidence of 1 to 5 cases per million people per year, affecting women slightly more frequently than men. While the pathophysiology is not well understood, AGEP and its differential diagnoses are categorized as T cell-related inflammatory responses.

There are at least 4 severe cutaneous eruptions that might be confused with AGEP, all of which may be associated with fever. They include a drug reaction with eosinophilia and systemic symptoms, Stevens-Johnson syndrome, toxic epidermal necrolysis, and pustular psoriasis. The clinical features that may help differentiate these conditions from AGEP include timeline, mucocutaneous features, organ system involvement, and histopathologic findings.

Patients who have AGEP, including those with systemic involvement, generally improve after the offending drug is discontinued and treatment with topical corticosteroids is initiated. A brief course of systemic corticosteroids can also be considered for patients with severe skin involvement or systemic involvement.

This patient was prescribed topical corticosteroid wet dressing treatments twice daily for 2 weeks. At the 2-week follow-up visit, the rash had completely cleared and only minimal residual erythema was noted. The patient was instructed to avoid azithromycin.

This case was adapted from: Tolkachjov SN, Wetter DA, Sandefur BJ. Generalized pustular eruption. J Fam Pract. 2018;67:309-310,312.

The mainstay of treatment for many musculoskeletal (MSK) complaints is physical or occupational therapy. But often an individual’s underlying biomechanical issue is one that can be easily addressed with a home exercise plan, and, in light of the COVID-19 pandemic, patients may wish to avoid in-person physical therapy. This article describes the rationale for, and methods of providing, home exercises for several MSK conditions commonly seen in the primary care setting.

General rehabilitation principles: First things first

With basic MSK complaints, focus on controlling pain and swelling before undertaking restoration of function. Tailor pharmacologic and nonpharmacologic options to the patient’s needs, using first-line modalities such as ice and compression to reduce inflammation, and prescribing scheduled doses of an anti-inflammatory medication to help with both pain and inflammation.

Once pain is sufficiently controlled, have patients begin basic rehabilitation with simple range-of-motion exercises that move the injured region through normal patterns, as tolerated. Later, the patient can progress through more specific exercises to return the injured region to full functional capacity.

Explain to patients that it takes about 7 to 10 days of consistent care to decrease inflammation, but that they should begin prescribed exercises once they are able to tolerate them. Plan a follow-up visit in 2 to 3 weeks to check on the patient’s response to prescribed care.

Which is better, ice or heat?

Ice and heat are both commonly used to treat MSK injuries and pain, although scrutiny of the use of either intervention has increased. Despite the widespread use of these modalities, there is little evidence to support their effect on patient outcomes. The historical consensus has been that ice decreases pain, inflammation, and edema,while heat can facilitate movement in rehabilitation by improving blood flow and decreasing stiffness.^1-3 In our practice, we encourage use of both topical modalities as a way to start exercise therapy when pain from the acute injury limits participation. Patients often ask which modality they should use. Ice is generally applied in the acute injury phase (48-72 hours after injury), while heat has been thought to be more beneficial in the chronic stages.

Ccontinue to: When and how to apply ice

When and how to apply ice. Applying an ice pack or a bag of frozen vegetables directly to the affected area will help control pain and swelling. Ice should be applied for 15 to 20 minutes at a time, once an hour. If a patient has sensitivity to cold or if the ice pack is a gel-type, have the patient place a layer (eg, towel) between the ice and skin to avoid injury to the skin. Additional caution should be exercised in patients with peripheral vascular disease, cryoglobulinemia, Raynaud disease, or a history of frostbite at the site.⁴

An alternative method we sometimes recommend is ice-cup massage. The patient can fill a small paper cup with water and freeze it. The cup is then used to massage the injured area, providing a more active method of icing whereby the cold can penetrate more quickly. Ice-cup massage should be done for 5 to 10 minutes, 3 to 4 times a day.

When and how to apply heat. Heat will help relax and loosen muscles and is a preferred treatment for older injuries, chronic pain, muscle tension, and spasms.⁵ Because heat can increase blood flow and, likely, inflammation, it should not be used in the acute injury phase. A heating pad or a warm, wet towel can be applied for up to 20 minutes at a time to help relieve pain and tension. Heat is also beneficial before participating in rehab activities as a method of “warming up” a recently injured area.⁶ However, ice should still be used following activity to prevent any new inflammation.

Anti-inflammatory medications

For an acute injury, nonsteroidal anti-­inflammatory drugs (NSAIDs) not only can decrease inflammation and aid in healing but can alleviate pain. We typically start with over-the-counter (OTC) NSAIDs taken on a schedule. A good suggestion is to have the patient take the scheduled NSAID with food for 7 to 10 days or until symptoms subside.

Topical analgesics

Because oral medications can occasionally cause adverse effects or be contraindicated in some patients, topical analgesics can be a good substitute due to their minimal adverse effects. Acceptable topical medications include NSAIDs, lidocaine, menthol, and arnica. Other than prescribed topical NSAIDs, these products can be applied directly to the painful area on an as-needed basis. Often, a topical patch is a nice option to recommend for use during work or school, and a topical cream or ointment can be used at bedtime.

Continue to: Graduated rehabilitation

Graduated rehabilitation

The following 4 common MSK injuries are ones that can benefit from a graduated approach to rehabilitation at home.

Lateral ankle sprain

Lateral ankle sprain, usually resulting from an inversion mechanism, is the most common type of acute ankle sprain seen in primary care and sports medicine settings.^7-9 The injury causes lateral ankle pain and swelling, decreased range of motion and strength, and pain with weight-bearing activities.

Have patients avoid using heat in the acute injury phase because it can increase inflammation due to increased blood flow.

Treatment and rehabilitation after this type of injury are critical to restoring normal function and increasing the likelihood of returning to pre-injury levels of activity.^9,10 Goals for an acute ankle sprain include controlling swelling, regaining full range of motion, increasing muscle strength and power, and improving balance.

Phase 1: Immediately following injury, have the patient protect the injured area with rest, ice, compression, and elevation (RICE). This will help to decrease swelling and pain. Exercises to regain range of motion, such as stretching and doing ankle “ABCs,” should begin within 48 to 72 hours of the initial injury (TABLE 1).^9-11

Continue to: Phase 2

Phase 2: Once the patient has achieved full range of motion and pain is controlled, begin the process of regaining strength. The 4-way ankle exercise program (with elastic tubing) is an easy at-home exercise that has been shown to improve strength in plantar flexion, dorsiflexion, eversion, and inversion (TABLE 1).^9-11

Phase 3: Once your patient is able to bear full weight with little to no pain, begin a balance program (TABLE 1^9-11). This is the most frequently neglected component of rehabilitation and the most common reason patients return with chronic ankle pain or repeat ankle injuries. Deficits in postural stability and balance have been reported in unstable ankles following acute ankle sprains,^10,12-15 and studies have shown that individuals with poor stability are at a greater risk of injury.^13-16

For most lateral ankle sprains, patients can expect time to recovery to range from 2 to 8 weeks. Longer recoveries are associated with more severe injuries or those that involve the syndesmosis.

Plantar fasciitis

Plantar fasciitis (PF) of the foot can be frustrating for a patient due to its chronic nature. Most patients will present with pain in the heel that is aggravated by weight-bearing activities. A conservative management program that focuses on reducing pain and inflammation, reducing tissue stress, and restoring strength and flexibility has been shown to be effective for this type of injury.^17,18

Step 1: Reduce pain and inflammation. Deep-tissue massage and cryotherapy are easy ways to help with pain and inflammation. Deep-tissue massage can be accomplished by rolling the bottom of the foot on a golf or lacrosse ball. A favorite recommendation of ours to reduce inflammation is to use the ice-cup massage, mentioned earlier, for 5 minutes. Or rolling the bottom of the foot on a frozen water bottle will accomplish both tasks at once (TABLE 2^17,18).

Step 2: Reduce tissue stress. Management tools commonly used to reduce tissue stress are OTC orthotics and night splints. The night splint has been shown to improve symptoms,but patients often stop using it due to discomfort.¹⁹ Many kinds of night splints are available, but we have found that the sock variety with a strap to keep the foot in dorsiflexion is best tolerated, and it should be covered by most care plans.

Continue to: Step 3

Step 3: Restore muscle strength and flexibility. Restoring flexibility of the gastrocnemius and soleus is most frequently recommended for treating PF. Strengthening exercises that involve intrinsic and extrinsic muscles of the foot and ankle are also essential.^17,18 Helpful exercises include those listed in TABLE 1.^9-11 Additionally, an eccentric heel stretch can help to alleviate PF symptoms (TABLE 2^17,18).

A reasonable timeline for follow-up on newly diagnosed PF is 4 to 6 weeks. While many patients will not have recovered in that time, the goal is to document progress in recovery. If no progress is made, consider other treatment modalities.

Patellofemoral pain syndrome

Patellofemoral pain syndrome (PFPS) is one of the most common orthopedic complaints, estimated to comprise 7.3% of all orthopedic visits.²⁰ Commonly called “runner’s knee,” PFPS is the leading cause of anterior knee pain in active individuals. Studies suggest a gender bias, with PFPS being diagnosed more frequently in females than in males, particularly between the ages of 10 and 19.²⁰ Often, there is vague anterior knee pain, or pain that worsens with activities such as climbing hills or stairs, or with long sitting or when fatigued.

In general, unbalanced patellar tracking within the trochlear groove likely leads to this pain. Multiple contributory factors have been described; however, evidence increasingly has shown that deficiencies in hip strength may contribute significantly to maltracking of the patella with resultant pain. Specifically, weakness in hip external rotators and abductors is associated with abnormal lower extremity mechanics.²¹ One randomized controlled trial by Ferber et al found that therapy protocols directed at hip and core strength showed earlier resolution of pain and greater strength when compared with knee protocols alone.²²

We routinely talk to patients about how the knee is the “victim” caught between weak hips and/or flat feet. It is prudent to look for both in the office visit. This can be done with one simple maneuver: Ask your patient to do a squat followed by 3 or 4 single-leg squats on each side. This will often reveal dysfunction at the foot/ankle or weakness in the hips/core as demonstrated by pronated feet (along with valgus tracking of the knees inward) or loss of balance upon squatting.

There is general consensus that a nonsurgical approach is the mainstay of treatment for PFPS.²³ Pelvic stabilization and hip strengthening are standard components along with treatment protocols of exercises tailored to one’s individual weaknesses.

Numerous types of exercises do not require specialized equipment and can be taught in the office (TABLE 3²⁴). Explain to patients that the recovery process may take several months. Monthly follow-up to document progress is essential and helps to ensure compliance with one’s home program.

Continue to : Neck pain

Neck pain

The annual prevalence of nonspecific neck pain ranges from 27% to 48%, with 70% of individuals being afflicted at some time in their lives.²⁵ First rule out any neurologic factors that might suggest cervical disc disease or spinal stenosis. If a patient describes weakness or sensory changes along one or both upper extremities, obtain imaging and consider more formalized therapy with a physical therapist.

In patients without any red flags, investigate possible biomechanical causes. It is essential to review the patient’s work and home habits, particularly in light of COVID-19, to determine if adjustments may be needed. Factors to consider are desk and computer setups at work or home, reading or laptop use in bed, sleep habits, and frequency of cellular phone calls/texting.²⁶ A formal ergonomic assessment of the patient’s workplace may be helpful.

A mainstay in treating mechanical neck pain is alleviating trapezial tightness or spasm. Manipulative therapies such as osteopathic manipulation, massage, and chiropractic care can provide pain relief in the acute setting as well as help with control of chronic symptoms.²⁷ A simple self-care tool is using a tennis ball to massage the trapezial muscles. This can be accomplished by having the patient position the tennis ball along the upper trapezial muscles, holding it in place by leaning against a wall, and initiating self-massage. Another method of self-massage is to put 2 tennis balls in an athletic tube sock and tie off the end, place the sock on the floor, and lie on it in the supine position.

There is also evidence that exercise of any kind can help control neck pain.^28,29 The easiest exercises one can offer a patient with neck stiffness, or even mild cervical strains, is self-directed stretching through gentle pressure applied in all 4 directions on the neck. This technique can be repeated hourly both at work and at home (TABLE 4).

Reminders that can help ensure success

You can use the approaches described here for numerous other MSK conditions in helping patients on the road to recovery.

After the acute phase, advise patients to

• apply heat to the affected area before exercising. This can help bring blood flow to the region and promote ease of movement.

• continue icing the area following rehabilitation exercises in order to control exercise-induced inflammation.

• report any changing symptoms such as worsening pain, numbness, or weakness.


These techniques are one step in the recovery process. A home program can benefit the patient either alone or in combination with more advanced techniques that are best accomplished under the watchful eye of a physical or occupational therapist.
 

CORRESPONDENCE

Carrie A. Jaworski, MD, FAAFP, FACSM, 2180 Pfingsten Road, Suite 3100, Glenview, IL 60026; cjaworski@northshore.org

The mainstay of treatment for many musculoskeletal (MSK) complaints is physical or occupational therapy. But often an individual’s underlying biomechanical issue is one that can be easily addressed with a home exercise plan, and, in light of the COVID-19 pandemic, patients may wish to avoid in-person physical therapy. This article describes the rationale for, and methods of providing, home exercises for several MSK conditions commonly seen in the primary care setting.

General rehabilitation principles: First things first

With basic MSK complaints, focus on controlling pain and swelling before undertaking restoration of function. Tailor pharmacologic and nonpharmacologic options to the patient’s needs, using first-line modalities such as ice and compression to reduce inflammation, and prescribing scheduled doses of an anti-inflammatory medication to help with both pain and inflammation.

Once pain is sufficiently controlled, have patients begin basic rehabilitation with simple range-of-motion exercises that move the injured region through normal patterns, as tolerated. Later, the patient can progress through more specific exercises to return the injured region to full functional capacity.

Explain to patients that it takes about 7 to 10 days of consistent care to decrease inflammation, but that they should begin prescribed exercises once they are able to tolerate them. Plan a follow-up visit in 2 to 3 weeks to check on the patient’s response to prescribed care.

Which is better, ice or heat?

Ice and heat are both commonly used to treat MSK injuries and pain, although scrutiny of the use of either intervention has increased. Despite the widespread use of these modalities, there is little evidence to support their effect on patient outcomes. The historical consensus has been that ice decreases pain, inflammation, and edema,while heat can facilitate movement in rehabilitation by improving blood flow and decreasing stiffness.^1-3 In our practice, we encourage use of both topical modalities as a way to start exercise therapy when pain from the acute injury limits participation. Patients often ask which modality they should use. Ice is generally applied in the acute injury phase (48-72 hours after injury), while heat has been thought to be more beneficial in the chronic stages.

Ccontinue to: When and how to apply ice

When and how to apply ice. Applying an ice pack or a bag of frozen vegetables directly to the affected area will help control pain and swelling. Ice should be applied for 15 to 20 minutes at a time, once an hour. If a patient has sensitivity to cold or if the ice pack is a gel-type, have the patient place a layer (eg, towel) between the ice and skin to avoid injury to the skin. Additional caution should be exercised in patients with peripheral vascular disease, cryoglobulinemia, Raynaud disease, or a history of frostbite at the site.⁴

An alternative method we sometimes recommend is ice-cup massage. The patient can fill a small paper cup with water and freeze it. The cup is then used to massage the injured area, providing a more active method of icing whereby the cold can penetrate more quickly. Ice-cup massage should be done for 5 to 10 minutes, 3 to 4 times a day.

When and how to apply heat. Heat will help relax and loosen muscles and is a preferred treatment for older injuries, chronic pain, muscle tension, and spasms.⁵ Because heat can increase blood flow and, likely, inflammation, it should not be used in the acute injury phase. A heating pad or a warm, wet towel can be applied for up to 20 minutes at a time to help relieve pain and tension. Heat is also beneficial before participating in rehab activities as a method of “warming up” a recently injured area.⁶ However, ice should still be used following activity to prevent any new inflammation.

Anti-inflammatory medications

For an acute injury, nonsteroidal anti-­inflammatory drugs (NSAIDs) not only can decrease inflammation and aid in healing but can alleviate pain. We typically start with over-the-counter (OTC) NSAIDs taken on a schedule. A good suggestion is to have the patient take the scheduled NSAID with food for 7 to 10 days or until symptoms subside.

Topical analgesics

Because oral medications can occasionally cause adverse effects or be contraindicated in some patients, topical analgesics can be a good substitute due to their minimal adverse effects. Acceptable topical medications include NSAIDs, lidocaine, menthol, and arnica. Other than prescribed topical NSAIDs, these products can be applied directly to the painful area on an as-needed basis. Often, a topical patch is a nice option to recommend for use during work or school, and a topical cream or ointment can be used at bedtime.

Continue to: Graduated rehabilitation

Graduated rehabilitation

The following 4 common MSK injuries are ones that can benefit from a graduated approach to rehabilitation at home.

Lateral ankle sprain

Lateral ankle sprain, usually resulting from an inversion mechanism, is the most common type of acute ankle sprain seen in primary care and sports medicine settings.^7-9 The injury causes lateral ankle pain and swelling, decreased range of motion and strength, and pain with weight-bearing activities.

Have patients avoid using heat in the acute injury phase because it can increase inflammation due to increased blood flow.

Treatment and rehabilitation after this type of injury are critical to restoring normal function and increasing the likelihood of returning to pre-injury levels of activity.^9,10 Goals for an acute ankle sprain include controlling swelling, regaining full range of motion, increasing muscle strength and power, and improving balance.

Phase 1: Immediately following injury, have the patient protect the injured area with rest, ice, compression, and elevation (RICE). This will help to decrease swelling and pain. Exercises to regain range of motion, such as stretching and doing ankle “ABCs,” should begin within 48 to 72 hours of the initial injury (TABLE 1).^9-11

Continue to: Phase 2

Phase 2: Once the patient has achieved full range of motion and pain is controlled, begin the process of regaining strength. The 4-way ankle exercise program (with elastic tubing) is an easy at-home exercise that has been shown to improve strength in plantar flexion, dorsiflexion, eversion, and inversion (TABLE 1).^9-11

Phase 3: Once your patient is able to bear full weight with little to no pain, begin a balance program (TABLE 1^9-11). This is the most frequently neglected component of rehabilitation and the most common reason patients return with chronic ankle pain or repeat ankle injuries. Deficits in postural stability and balance have been reported in unstable ankles following acute ankle sprains,^10,12-15 and studies have shown that individuals with poor stability are at a greater risk of injury.^13-16

For most lateral ankle sprains, patients can expect time to recovery to range from 2 to 8 weeks. Longer recoveries are associated with more severe injuries or those that involve the syndesmosis.

Plantar fasciitis

Plantar fasciitis (PF) of the foot can be frustrating for a patient due to its chronic nature. Most patients will present with pain in the heel that is aggravated by weight-bearing activities. A conservative management program that focuses on reducing pain and inflammation, reducing tissue stress, and restoring strength and flexibility has been shown to be effective for this type of injury.^17,18

Step 1: Reduce pain and inflammation. Deep-tissue massage and cryotherapy are easy ways to help with pain and inflammation. Deep-tissue massage can be accomplished by rolling the bottom of the foot on a golf or lacrosse ball. A favorite recommendation of ours to reduce inflammation is to use the ice-cup massage, mentioned earlier, for 5 minutes. Or rolling the bottom of the foot on a frozen water bottle will accomplish both tasks at once (TABLE 2^17,18).

Step 2: Reduce tissue stress. Management tools commonly used to reduce tissue stress are OTC orthotics and night splints. The night splint has been shown to improve symptoms,but patients often stop using it due to discomfort.¹⁹ Many kinds of night splints are available, but we have found that the sock variety with a strap to keep the foot in dorsiflexion is best tolerated, and it should be covered by most care plans.

Continue to: Step 3

Step 3: Restore muscle strength and flexibility. Restoring flexibility of the gastrocnemius and soleus is most frequently recommended for treating PF. Strengthening exercises that involve intrinsic and extrinsic muscles of the foot and ankle are also essential.^17,18 Helpful exercises include those listed in TABLE 1.^9-11 Additionally, an eccentric heel stretch can help to alleviate PF symptoms (TABLE 2^17,18).

A reasonable timeline for follow-up on newly diagnosed PF is 4 to 6 weeks. While many patients will not have recovered in that time, the goal is to document progress in recovery. If no progress is made, consider other treatment modalities.

Patellofemoral pain syndrome

Patellofemoral pain syndrome (PFPS) is one of the most common orthopedic complaints, estimated to comprise 7.3% of all orthopedic visits.²⁰ Commonly called “runner’s knee,” PFPS is the leading cause of anterior knee pain in active individuals. Studies suggest a gender bias, with PFPS being diagnosed more frequently in females than in males, particularly between the ages of 10 and 19.²⁰ Often, there is vague anterior knee pain, or pain that worsens with activities such as climbing hills or stairs, or with long sitting or when fatigued.

In general, unbalanced patellar tracking within the trochlear groove likely leads to this pain. Multiple contributory factors have been described; however, evidence increasingly has shown that deficiencies in hip strength may contribute significantly to maltracking of the patella with resultant pain. Specifically, weakness in hip external rotators and abductors is associated with abnormal lower extremity mechanics.²¹ One randomized controlled trial by Ferber et al found that therapy protocols directed at hip and core strength showed earlier resolution of pain and greater strength when compared with knee protocols alone.²²

We routinely talk to patients about how the knee is the “victim” caught between weak hips and/or flat feet. It is prudent to look for both in the office visit. This can be done with one simple maneuver: Ask your patient to do a squat followed by 3 or 4 single-leg squats on each side. This will often reveal dysfunction at the foot/ankle or weakness in the hips/core as demonstrated by pronated feet (along with valgus tracking of the knees inward) or loss of balance upon squatting.

There is general consensus that a nonsurgical approach is the mainstay of treatment for PFPS.²³ Pelvic stabilization and hip strengthening are standard components along with treatment protocols of exercises tailored to one’s individual weaknesses.

Numerous types of exercises do not require specialized equipment and can be taught in the office (TABLE 3²⁴). Explain to patients that the recovery process may take several months. Monthly follow-up to document progress is essential and helps to ensure compliance with one’s home program.

Continue to : Neck pain

Neck pain

The annual prevalence of nonspecific neck pain ranges from 27% to 48%, with 70% of individuals being afflicted at some time in their lives.²⁵ First rule out any neurologic factors that might suggest cervical disc disease or spinal stenosis. If a patient describes weakness or sensory changes along one or both upper extremities, obtain imaging and consider more formalized therapy with a physical therapist.

In patients without any red flags, investigate possible biomechanical causes. It is essential to review the patient’s work and home habits, particularly in light of COVID-19, to determine if adjustments may be needed. Factors to consider are desk and computer setups at work or home, reading or laptop use in bed, sleep habits, and frequency of cellular phone calls/texting.²⁶ A formal ergonomic assessment of the patient’s workplace may be helpful.

A mainstay in treating mechanical neck pain is alleviating trapezial tightness or spasm. Manipulative therapies such as osteopathic manipulation, massage, and chiropractic care can provide pain relief in the acute setting as well as help with control of chronic symptoms.²⁷ A simple self-care tool is using a tennis ball to massage the trapezial muscles. This can be accomplished by having the patient position the tennis ball along the upper trapezial muscles, holding it in place by leaning against a wall, and initiating self-massage. Another method of self-massage is to put 2 tennis balls in an athletic tube sock and tie off the end, place the sock on the floor, and lie on it in the supine position.

There is also evidence that exercise of any kind can help control neck pain.^28,29 The easiest exercises one can offer a patient with neck stiffness, or even mild cervical strains, is self-directed stretching through gentle pressure applied in all 4 directions on the neck. This technique can be repeated hourly both at work and at home (TABLE 4).

Reminders that can help ensure success

You can use the approaches described here for numerous other MSK conditions in helping patients on the road to recovery.

After the acute phase, advise patients to

• apply heat to the affected area before exercising. This can help bring blood flow to the region and promote ease of movement.

• continue icing the area following rehabilitation exercises in order to control exercise-induced inflammation.

• report any changing symptoms such as worsening pain, numbness, or weakness.


These techniques are one step in the recovery process. A home program can benefit the patient either alone or in combination with more advanced techniques that are best accomplished under the watchful eye of a physical or occupational therapist.
 

CORRESPONDENCE

Carrie A. Jaworski, MD, FAAFP, FACSM, 2180 Pfingsten Road, Suite 3100, Glenview, IL 60026; cjaworski@northshore.org

The mainstay of treatment for many musculoskeletal (MSK) complaints is physical or occupational therapy. But often an individual’s underlying biomechanical issue is one that can be easily addressed with a home exercise plan, and, in light of the COVID-19 pandemic, patients may wish to avoid in-person physical therapy. This article describes the rationale for, and methods of providing, home exercises for several MSK conditions commonly seen in the primary care setting.

General rehabilitation principles: First things first

With basic MSK complaints, focus on controlling pain and swelling before undertaking restoration of function. Tailor pharmacologic and nonpharmacologic options to the patient’s needs, using first-line modalities such as ice and compression to reduce inflammation, and prescribing scheduled doses of an anti-inflammatory medication to help with both pain and inflammation.

Once pain is sufficiently controlled, have patients begin basic rehabilitation with simple range-of-motion exercises that move the injured region through normal patterns, as tolerated. Later, the patient can progress through more specific exercises to return the injured region to full functional capacity.

Explain to patients that it takes about 7 to 10 days of consistent care to decrease inflammation, but that they should begin prescribed exercises once they are able to tolerate them. Plan a follow-up visit in 2 to 3 weeks to check on the patient’s response to prescribed care.

Which is better, ice or heat?

Ice and heat are both commonly used to treat MSK injuries and pain, although scrutiny of the use of either intervention has increased. Despite the widespread use of these modalities, there is little evidence to support their effect on patient outcomes. The historical consensus has been that ice decreases pain, inflammation, and edema,while heat can facilitate movement in rehabilitation by improving blood flow and decreasing stiffness.^1-3 In our practice, we encourage use of both topical modalities as a way to start exercise therapy when pain from the acute injury limits participation. Patients often ask which modality they should use. Ice is generally applied in the acute injury phase (48-72 hours after injury), while heat has been thought to be more beneficial in the chronic stages.

Ccontinue to: When and how to apply ice

When and how to apply ice. Applying an ice pack or a bag of frozen vegetables directly to the affected area will help control pain and swelling. Ice should be applied for 15 to 20 minutes at a time, once an hour. If a patient has sensitivity to cold or if the ice pack is a gel-type, have the patient place a layer (eg, towel) between the ice and skin to avoid injury to the skin. Additional caution should be exercised in patients with peripheral vascular disease, cryoglobulinemia, Raynaud disease, or a history of frostbite at the site.⁴

An alternative method we sometimes recommend is ice-cup massage. The patient can fill a small paper cup with water and freeze it. The cup is then used to massage the injured area, providing a more active method of icing whereby the cold can penetrate more quickly. Ice-cup massage should be done for 5 to 10 minutes, 3 to 4 times a day.

When and how to apply heat. Heat will help relax and loosen muscles and is a preferred treatment for older injuries, chronic pain, muscle tension, and spasms.⁵ Because heat can increase blood flow and, likely, inflammation, it should not be used in the acute injury phase. A heating pad or a warm, wet towel can be applied for up to 20 minutes at a time to help relieve pain and tension. Heat is also beneficial before participating in rehab activities as a method of “warming up” a recently injured area.⁶ However, ice should still be used following activity to prevent any new inflammation.

Anti-inflammatory medications

For an acute injury, nonsteroidal anti-­inflammatory drugs (NSAIDs) not only can decrease inflammation and aid in healing but can alleviate pain. We typically start with over-the-counter (OTC) NSAIDs taken on a schedule. A good suggestion is to have the patient take the scheduled NSAID with food for 7 to 10 days or until symptoms subside.

Topical analgesics

Because oral medications can occasionally cause adverse effects or be contraindicated in some patients, topical analgesics can be a good substitute due to their minimal adverse effects. Acceptable topical medications include NSAIDs, lidocaine, menthol, and arnica. Other than prescribed topical NSAIDs, these products can be applied directly to the painful area on an as-needed basis. Often, a topical patch is a nice option to recommend for use during work or school, and a topical cream or ointment can be used at bedtime.

Continue to: Graduated rehabilitation

Graduated rehabilitation

The following 4 common MSK injuries are ones that can benefit from a graduated approach to rehabilitation at home.

Lateral ankle sprain

Lateral ankle sprain, usually resulting from an inversion mechanism, is the most common type of acute ankle sprain seen in primary care and sports medicine settings.^7-9 The injury causes lateral ankle pain and swelling, decreased range of motion and strength, and pain with weight-bearing activities.

Have patients avoid using heat in the acute injury phase because it can increase inflammation due to increased blood flow.

Treatment and rehabilitation after this type of injury are critical to restoring normal function and increasing the likelihood of returning to pre-injury levels of activity.^9,10 Goals for an acute ankle sprain include controlling swelling, regaining full range of motion, increasing muscle strength and power, and improving balance.

Phase 1: Immediately following injury, have the patient protect the injured area with rest, ice, compression, and elevation (RICE). This will help to decrease swelling and pain. Exercises to regain range of motion, such as stretching and doing ankle “ABCs,” should begin within 48 to 72 hours of the initial injury (TABLE 1).^9-11

Continue to: Phase 2

Phase 2: Once the patient has achieved full range of motion and pain is controlled, begin the process of regaining strength. The 4-way ankle exercise program (with elastic tubing) is an easy at-home exercise that has been shown to improve strength in plantar flexion, dorsiflexion, eversion, and inversion (TABLE 1).^9-11

Phase 3: Once your patient is able to bear full weight with little to no pain, begin a balance program (TABLE 1^9-11). This is the most frequently neglected component of rehabilitation and the most common reason patients return with chronic ankle pain or repeat ankle injuries. Deficits in postural stability and balance have been reported in unstable ankles following acute ankle sprains,^10,12-15 and studies have shown that individuals with poor stability are at a greater risk of injury.^13-16

For most lateral ankle sprains, patients can expect time to recovery to range from 2 to 8 weeks. Longer recoveries are associated with more severe injuries or those that involve the syndesmosis.

Plantar fasciitis

Plantar fasciitis (PF) of the foot can be frustrating for a patient due to its chronic nature. Most patients will present with pain in the heel that is aggravated by weight-bearing activities. A conservative management program that focuses on reducing pain and inflammation, reducing tissue stress, and restoring strength and flexibility has been shown to be effective for this type of injury.^17,18

Step 1: Reduce pain and inflammation. Deep-tissue massage and cryotherapy are easy ways to help with pain and inflammation. Deep-tissue massage can be accomplished by rolling the bottom of the foot on a golf or lacrosse ball. A favorite recommendation of ours to reduce inflammation is to use the ice-cup massage, mentioned earlier, for 5 minutes. Or rolling the bottom of the foot on a frozen water bottle will accomplish both tasks at once (TABLE 2^17,18).

Step 2: Reduce tissue stress. Management tools commonly used to reduce tissue stress are OTC orthotics and night splints. The night splint has been shown to improve symptoms,but patients often stop using it due to discomfort.¹⁹ Many kinds of night splints are available, but we have found that the sock variety with a strap to keep the foot in dorsiflexion is best tolerated, and it should be covered by most care plans.

Continue to: Step 3

Step 3: Restore muscle strength and flexibility. Restoring flexibility of the gastrocnemius and soleus is most frequently recommended for treating PF. Strengthening exercises that involve intrinsic and extrinsic muscles of the foot and ankle are also essential.^17,18 Helpful exercises include those listed in TABLE 1.^9-11 Additionally, an eccentric heel stretch can help to alleviate PF symptoms (TABLE 2^17,18).

A reasonable timeline for follow-up on newly diagnosed PF is 4 to 6 weeks. While many patients will not have recovered in that time, the goal is to document progress in recovery. If no progress is made, consider other treatment modalities.

Patellofemoral pain syndrome

Patellofemoral pain syndrome (PFPS) is one of the most common orthopedic complaints, estimated to comprise 7.3% of all orthopedic visits.²⁰ Commonly called “runner’s knee,” PFPS is the leading cause of anterior knee pain in active individuals. Studies suggest a gender bias, with PFPS being diagnosed more frequently in females than in males, particularly between the ages of 10 and 19.²⁰ Often, there is vague anterior knee pain, or pain that worsens with activities such as climbing hills or stairs, or with long sitting or when fatigued.

In general, unbalanced patellar tracking within the trochlear groove likely leads to this pain. Multiple contributory factors have been described; however, evidence increasingly has shown that deficiencies in hip strength may contribute significantly to maltracking of the patella with resultant pain. Specifically, weakness in hip external rotators and abductors is associated with abnormal lower extremity mechanics.²¹ One randomized controlled trial by Ferber et al found that therapy protocols directed at hip and core strength showed earlier resolution of pain and greater strength when compared with knee protocols alone.²²

We routinely talk to patients about how the knee is the “victim” caught between weak hips and/or flat feet. It is prudent to look for both in the office visit. This can be done with one simple maneuver: Ask your patient to do a squat followed by 3 or 4 single-leg squats on each side. This will often reveal dysfunction at the foot/ankle or weakness in the hips/core as demonstrated by pronated feet (along with valgus tracking of the knees inward) or loss of balance upon squatting.

There is general consensus that a nonsurgical approach is the mainstay of treatment for PFPS.²³ Pelvic stabilization and hip strengthening are standard components along with treatment protocols of exercises tailored to one’s individual weaknesses.

Numerous types of exercises do not require specialized equipment and can be taught in the office (TABLE 3²⁴). Explain to patients that the recovery process may take several months. Monthly follow-up to document progress is essential and helps to ensure compliance with one’s home program.

Continue to : Neck pain

Neck pain

The annual prevalence of nonspecific neck pain ranges from 27% to 48%, with 70% of individuals being afflicted at some time in their lives.²⁵ First rule out any neurologic factors that might suggest cervical disc disease or spinal stenosis. If a patient describes weakness or sensory changes along one or both upper extremities, obtain imaging and consider more formalized therapy with a physical therapist.

In patients without any red flags, investigate possible biomechanical causes. It is essential to review the patient’s work and home habits, particularly in light of COVID-19, to determine if adjustments may be needed. Factors to consider are desk and computer setups at work or home, reading or laptop use in bed, sleep habits, and frequency of cellular phone calls/texting.²⁶ A formal ergonomic assessment of the patient’s workplace may be helpful.

A mainstay in treating mechanical neck pain is alleviating trapezial tightness or spasm. Manipulative therapies such as osteopathic manipulation, massage, and chiropractic care can provide pain relief in the acute setting as well as help with control of chronic symptoms.²⁷ A simple self-care tool is using a tennis ball to massage the trapezial muscles. This can be accomplished by having the patient position the tennis ball along the upper trapezial muscles, holding it in place by leaning against a wall, and initiating self-massage. Another method of self-massage is to put 2 tennis balls in an athletic tube sock and tie off the end, place the sock on the floor, and lie on it in the supine position.

There is also evidence that exercise of any kind can help control neck pain.^28,29 The easiest exercises one can offer a patient with neck stiffness, or even mild cervical strains, is self-directed stretching through gentle pressure applied in all 4 directions on the neck. This technique can be repeated hourly both at work and at home (TABLE 4).

Reminders that can help ensure success

You can use the approaches described here for numerous other MSK conditions in helping patients on the road to recovery.

After the acute phase, advise patients to

• apply heat to the affected area before exercising. This can help bring blood flow to the region and promote ease of movement.

• continue icing the area following rehabilitation exercises in order to control exercise-induced inflammation.

• report any changing symptoms such as worsening pain, numbness, or weakness.


These techniques are one step in the recovery process. A home program can benefit the patient either alone or in combination with more advanced techniques that are best accomplished under the watchful eye of a physical or occupational therapist.
 

CORRESPONDENCE

Carrie A. Jaworski, MD, FAAFP, FACSM, 2180 Pfingsten Road, Suite 3100, Glenview, IL 60026; cjaworski@northshore.org

Peripheral arterial disease (PAD), the progressive disorder that results in ischemia to distal vascular territories as a result of atherosclerosis, spans a wide range of presentations, from minimally symptomatic disease to limb ischemia secondary to acute or chronic occlusion.

The prevalence of PAD is variable, due to differing diagnostic criteria used in studies, but PAD appears to affect 1 in every 22 people older than age 40.¹ However, since PAD incidence increases with age, it is increasing in prevalence as the US population ages.^1-3

PAD is associated with increased hospitalizations and decreased quality of life.⁴ Patients with PAD have an estimated 30% 5-year risk for myocardial infarction, stroke, or death from a vascular cause.³

Screening. Although PAD is underdiagnosed and appears to be undertreated,³ population-based screening for PAD in asymptomatic patients is not recommended. A Cochrane review found no studies evaluating the benefit of ­asymptomatic population-based screening.⁵ Similarly, in 2018, the USPSTF performed a comprehensive review and found no studies to support routine screening and determined there was insufficient evidence to recommend it.^6,7

Risk factors and associated comorbidities

PAD risk factors, like the ones detailed below, have a potentiating effect. The presence of 2 risk factors doubles PAD risk, while 3 or more risk factors increase PAD risk by a factor of 10.¹

Increasing age is the greatest single risk factor for PAD.^1,2,8,9 Researchers using data from the National Health and Nutrition Examination Survey (NHANES) found that the prevalence of PAD increased from 1.4% in individuals ages 40 to 49 years to almost 17% in those age 70 or older.¹

© kostudios

Patients with PAD have an estimated 30% 5-year risk for myocardial infarction, stroke, or death from a vascular cause.

Demographic characteristics. Most studies demonstrate a higher risk for PAD in men.^1-3,10 African-American patients have more than twice the risk for PAD, compared with Whites, even after adjustment for the increased prevalence of associated diseases such as hypertension and diabetes in this population.^1-3,10

Continue to: Genetics...

Genetics. A study performed by the National Heart Lung and Blood Institute suggested that genetic correlations between twins were more important than environmental factors in the development of PAD.¹¹

Smoking. Most population studies show smoking to be the greatest modifiable risk factor for PAD. An analysis of the NHANES data yielded an odds ratio (OR) of 4.1 for current smokers and of 1.8 for former smokers.¹ Risk increases linearly with cumulative years of smoking.^1,2,9,10

Diabetes is another significant modifiable risk factor, increasing PAD risk by 2.5 times.² Diabetes is also associated with increases in functional limitation from claudication, risk for acute coronary syndrome, and progression to amputation.¹

Hypertension nearly doubles the risk for PAD, and poor control further increases this risk.^2,9,10

Chronic kidney disease (CKD). Patients with CKD have a progressively higher prevalence of PAD with worsening renal function.¹ There is also an association between CKD and increased morbidity, revascularization failure, and increased mortality.¹

Two additional risk factors that are less well understood are dyslipidemia and chronic inflammation. There is conflicting data regarding the role of individual components of cholesterol and their effect on PAD, although lipoprotein (a) has been shown to be an independent risk factor for both the development and progression of PAD.¹² Similarly, chronic inflammation has been shown to play a role in the initiation and progression of the disease, although the role of inflammatory markers in evaluation and treatment is unclear and assessment for these purposes is not currently recommended.^12,13

Continue to: Diagnosis...

Diagnosis

Clinical presentation

Lower extremity pain is the hallmark symptom of PAD, but presentation varies. The classic presentation is claudication, pain within a defined muscle group that occurs with exertion and is relieved by rest. Claudication is most common in the calf but also occurs in the buttock/thigh and the foot.

African- American patients have more than twice the risk for PAD, compared with Whites, even after adjustment for the increased prevalence of associated diseases in this population.

However, most patients with PAD present with pain that does not fit the definition of claudication. Patients with comorbidities, physical inactivity, and neuropathy are more likely to present with atypical pain.¹⁴ These patients may demonstrate critical or acute limb ischemia, characterized by pain at rest and most often localized to the forefoot and toes. Patients with critical limb ischemia may also present with nonhealing wounds/ulcers or gangrene.¹⁵

Physical exam findings can support the diagnosis of PAD, but none are reliable enough to rule the diagnosis in or out. Findings suggestive of PAD include cool skin, presence of a bruit (iliac, femoral, or popliteal), and palpable pulse abnormality. Multiple abnormal physical exam findings increase the likelihood of PAD, while the absence of a bruit or palpable pulse abnormality makes PAD less likely.¹⁶ In patients with PAD, an associated wound/ulcer is most often distal in the foot and usually appears dry.¹⁷

The differential diagnosis for intermittent leg pain is broad and includes neurologic, musculoskeletal, and venous etiologies. Table 1¹⁸ lists some common alternate diagnoses for patients presenting with leg pain or claudication.

Continue to: Diagnostic testing...

Diagnostic testing

An ankle-brachial index (ABI) test should be performed in patients with history or physical exam findings suggestive of PAD. A resting ABI is performed with the patient in the supine position, with measurement of systolic blood pressure in both arms and ankles using a Doppler ultrasound device. Table 2¹³ outlines ABI scoring and interpretation.

An ABI > 1.4 is an invalid measurement, indicating that the arteries are too calcified to be compressed. These highly elevated ABI measurements are common in patients with diabetes and/or advanced CKD. In these patients, a toe-brachial index (TBI) test should be performed, because the digital arteries are almost always compressible.¹³

Patients with symptomatic PAD who are under consideration for revascularization may benefit from radiologic imaging of the lower extremities with duplex ultrasound, computed tomography angiography, or magnetic resonance angiography to determine the anatomic location and severity of stenosis.¹³

Management of PAD

Lifestyle interventions

For patients with PAD, lifestyle modifications are an essential—but challenging—component of disease management.

Continue to: Smoking cessation...

Smoking cessation. As with other atherosclerotic diseases, PAD progression is strongly correlated with smoking. A trial involving 204 active smokers with PAD showed that 5-year mortality and amputation rates dropped by more than half in those who quit smoking within a year, with numbers needed to treat (NNT) of 6 for mortality and 5 for amputation.¹⁹ Because of this dramatic effect, American College of Cardiology/American Heart Association (ACC/AHA) guidelines encourage providers to address smoking at every visit and use cessation programs and medication to increase quit rates.¹³

Exercise may be the most important intervention for PAD. A 2017 Cochrane review found that supervised, structured exercise programs increase pain-free and maximal walking distances by at least 20% and also improve physical and mental quality of life.²⁰ In a trial involving 111 patients with aortoiliac PAD, supervised exercise plus medical care led to greater functional improvement than either revascularization plus medical care or medical care alone.²¹ In a 2018 Cochrane review, neither revascularization or revascularization added to supervised exercise were better than supervised exercise alone.²² ACC/AHA guidelines recommend supervised exercise programs for claudication prior to considering revascularization.¹³TABLE 3¹³ outlines the components of a structured exercise program.

Unfortunately, the benefit of these programs has been difficult to reproduce without supervision. Another 2018 Cochrane review demonstrated significant improvement with supervised exercise and no clear improvement in patients given home exercise or advice to walk.²³ A recent study examined the effect of having patients use a wearable fitness tracker for home exercise and demonstrated no benefit over usual care.²⁴

Diet. There is some evidence that dietary interventions can prevent and possibly improve PAD. A large randomized controlled trial showed that a Mediterranean diet lowered rates of PAD over 1 year compared to a low-fat diet, with an NNT of 336 if supplemented with extra-virgin olive oil and 448 if supplemented with nuts.²⁵ A small trial of 25 patients who consumed non-soy legumes daily for 8 weeks showed average ABI improvement of 6%, although there was no control group.²⁶

Medical therapy to address peripheral and cardiovascular events

Standard medical therapy for coronary artery disease (CAD) is recommended for patients with PAD to reduce cardiovascular and limb events. For example, treatment of hypertension reduces cardiovascular and cerebrovascular events, and studies verify that lowering blood pressure does not worsen claudication or limb perfusion.

A trial involving 204 active smokers with PAD showed that 5-year mortality and amputation rates dropped by more than half in those who quit smoking within a year.

¹³TABLE 4^13,27-30 outlines the options for medical therapy.

Continue to: Statins...

Statins reduce cardiovascular events in PAD patients. A large study demonstrated that 40 mg of simvastatin has an NNT of 21 to prevent a coronary or cerebrovascular event in PAD, similar to the NNT of 23 seen in treatment of CAD.²⁷ Statins also reduce adverse limb outcomes. A registry of atherosclerosis patients showed that statins have an NNT of 56 to prevent amputation in PAD and an NNT of 28 to prevent worsening claudication, critical limb ischemia, revascularization, or amputation.²⁸

Antiplatelet therapy with low-dose aspirin or clopidogrel is recommended for symptomatic patients and for asymptomatic patients with an ABI ≤ 0.9.¹³ A Cochrane review demonstrated significantly reduced mortality with nonaspirin antiplatelet agents vs aspirin (NNT = 94) without increase in major bleeding.²⁹ Only British guidelines specifically recommend clopidogrel over aspirin.³¹

Dual antiplatelet therapy has not shown consistent benefits over aspirin alone. ACC/AHA guidelines state that dual antiplatelet therapy is not well established for PAD but may be reasonable after revascularization.¹³

Voraxapar is a novel antiplatelet agent that targets the thrombin-binding receptor on platelets. However, trials show no significant coronary benefit, and slight reductions in acute limb ischemia are offset by increases in major bleeding.¹³

For patients receiving medical therapy, ongoing evaluation and treatment should be based on claudication symptoms and clinical assessment.

Medical therapy for claudication

Several medications have been proposed for symptomatic treatment of intermittent claudication. Cilostazol is a phosphodiesterase inhibitor with the best risk-benefit ratio. A Cochrane review showed improvements in maximal and pain-free walking distances compared to placebo and improvements in quality of life with cilostazol 100 mg taken twice daily.³² Adverse effects included headache, dizziness, palpitations, and diarrhea.²⁹

Continue to: Pentoxifylline...

Pentoxifylline is another phosphodiesterase inhibitor with less evidence of improvement, higher adverse effect rates, and more frequent dosing. It is not recommended for treatment of intermittent claudication.^13,33

Supplements. Padma 28, a Tibetan herbal formulation, appears to improve maximal walking distance with adverse effect rates similar to placebo.³⁴ Other supplements, including vitamin E, ginkgo biloba, and omega-3 fatty acids, have no evidence of benefit.^35-37

When revascularizationis needed

Patients who develop limb ischemia or lifestyle-limiting claudication despite conservative therapy are candidates for revascularization. Endovascular techniques include angioplasty, stenting, atherectomy, and precise medication delivery. Surgical approaches mainly consist of thrombectomy and bypass grafting. For intermittent claudication despite conservative care, ACC/AHA guidelines state endovascular procedures are appropriate for aortoiliac disease and reasonable for femoropopliteal disease, but unproven for infrapopliteal disease.¹³

Acute limb ischemia is an emergency requiring immediate intervention. Two trials revealed identical overall and amputation-free survival rates for percutaneous thrombolysis and surgical thrombectomy.^38,39 ACC/AHA guidelines recommend anticoagulation with heparin followed by the revascularization technique that will most rapidly restore arterial flow.¹³

For chronic limb ischemia, a large trial showed angioplasty had lower initial morbidity, length of hospitalization, and cost than surgical repair. However, surgical mortality was lower after 2 years.⁴⁰ ACC/AHA guidelines recommend either surgery or endovascular procedures and propose initial endovascular treatment followed by surgery if needed.¹³ After revascularization, the patient should be followed periodically with a clinical evaluation and ABI measurement with further consideration for routine duplex ultrasound surveillance.¹³

For chronic limb ischemia, a large trial showed angioplasty had lower initial morbidity, length of hospitalization, and cost than surgical repair. Surgical mortality was lower after 2 years.

Outcomes

Patients with PAD have variable outcomes. About 70% to 80% of patients with this diagnosis will have a stable disease process with no worsening of symptoms, 10% to 20% will experience worsening symptoms over time, 5% to 10% will require revascularization within 5 years of diagnosis, and 1% to 5% will progress to critical limb ischemia, which has a 5-year amputation rate of 1% to 4%.² Patients who require amputation have poor outcomes: Within 2 years, 30% are dead and 15% have had further amputations.¹⁸

In addition to the morbidity and mortality from its own progression, PAD is an important predictor of CAD and is associated with a significant elevation in morbidity and mortality from CAD. One small but well-designed prospective cohort study found that patients with PAD had a more than 6-fold increased risk of death from CAD than did patients without PAD.⁴¹

Acknowledgement
The authors thank Francesca Cimino, MD, FAAFP, for her help in reviewing this manuscript.

CORRESPONDENCE
Dustin K. Smith, DO, 2080 Child Street, Jacksonville, FL 32214; dustinksmith@yahoo.com

Peripheral arterial disease (PAD), the progressive disorder that results in ischemia to distal vascular territories as a result of atherosclerosis, spans a wide range of presentations, from minimally symptomatic disease to limb ischemia secondary to acute or chronic occlusion.

The prevalence of PAD is variable, due to differing diagnostic criteria used in studies, but PAD appears to affect 1 in every 22 people older than age 40.¹ However, since PAD incidence increases with age, it is increasing in prevalence as the US population ages.^1-3

PAD is associated with increased hospitalizations and decreased quality of life.⁴ Patients with PAD have an estimated 30% 5-year risk for myocardial infarction, stroke, or death from a vascular cause.³

Screening. Although PAD is underdiagnosed and appears to be undertreated,³ population-based screening for PAD in asymptomatic patients is not recommended. A Cochrane review found no studies evaluating the benefit of ­asymptomatic population-based screening.⁵ Similarly, in 2018, the USPSTF performed a comprehensive review and found no studies to support routine screening and determined there was insufficient evidence to recommend it.^6,7

Risk factors and associated comorbidities

PAD risk factors, like the ones detailed below, have a potentiating effect. The presence of 2 risk factors doubles PAD risk, while 3 or more risk factors increase PAD risk by a factor of 10.¹

Increasing age is the greatest single risk factor for PAD.^1,2,8,9 Researchers using data from the National Health and Nutrition Examination Survey (NHANES) found that the prevalence of PAD increased from 1.4% in individuals ages 40 to 49 years to almost 17% in those age 70 or older.¹

© kostudios

Patients with PAD have an estimated 30% 5-year risk for myocardial infarction, stroke, or death from a vascular cause.

Demographic characteristics. Most studies demonstrate a higher risk for PAD in men.^1-3,10 African-American patients have more than twice the risk for PAD, compared with Whites, even after adjustment for the increased prevalence of associated diseases such as hypertension and diabetes in this population.^1-3,10

Continue to: Genetics...

Genetics. A study performed by the National Heart Lung and Blood Institute suggested that genetic correlations between twins were more important than environmental factors in the development of PAD.¹¹

Smoking. Most population studies show smoking to be the greatest modifiable risk factor for PAD. An analysis of the NHANES data yielded an odds ratio (OR) of 4.1 for current smokers and of 1.8 for former smokers.¹ Risk increases linearly with cumulative years of smoking.^1,2,9,10

Diabetes is another significant modifiable risk factor, increasing PAD risk by 2.5 times.² Diabetes is also associated with increases in functional limitation from claudication, risk for acute coronary syndrome, and progression to amputation.¹

Hypertension nearly doubles the risk for PAD, and poor control further increases this risk.^2,9,10

Chronic kidney disease (CKD). Patients with CKD have a progressively higher prevalence of PAD with worsening renal function.¹ There is also an association between CKD and increased morbidity, revascularization failure, and increased mortality.¹

Two additional risk factors that are less well understood are dyslipidemia and chronic inflammation. There is conflicting data regarding the role of individual components of cholesterol and their effect on PAD, although lipoprotein (a) has been shown to be an independent risk factor for both the development and progression of PAD.¹² Similarly, chronic inflammation has been shown to play a role in the initiation and progression of the disease, although the role of inflammatory markers in evaluation and treatment is unclear and assessment for these purposes is not currently recommended.^12,13

Continue to: Diagnosis...

Diagnosis

Clinical presentation

Lower extremity pain is the hallmark symptom of PAD, but presentation varies. The classic presentation is claudication, pain within a defined muscle group that occurs with exertion and is relieved by rest. Claudication is most common in the calf but also occurs in the buttock/thigh and the foot.

African- American patients have more than twice the risk for PAD, compared with Whites, even after adjustment for the increased prevalence of associated diseases in this population.

However, most patients with PAD present with pain that does not fit the definition of claudication. Patients with comorbidities, physical inactivity, and neuropathy are more likely to present with atypical pain.¹⁴ These patients may demonstrate critical or acute limb ischemia, characterized by pain at rest and most often localized to the forefoot and toes. Patients with critical limb ischemia may also present with nonhealing wounds/ulcers or gangrene.¹⁵

Physical exam findings can support the diagnosis of PAD, but none are reliable enough to rule the diagnosis in or out. Findings suggestive of PAD include cool skin, presence of a bruit (iliac, femoral, or popliteal), and palpable pulse abnormality. Multiple abnormal physical exam findings increase the likelihood of PAD, while the absence of a bruit or palpable pulse abnormality makes PAD less likely.¹⁶ In patients with PAD, an associated wound/ulcer is most often distal in the foot and usually appears dry.¹⁷

The differential diagnosis for intermittent leg pain is broad and includes neurologic, musculoskeletal, and venous etiologies. Table 1¹⁸ lists some common alternate diagnoses for patients presenting with leg pain or claudication.

Continue to: Diagnostic testing...

Diagnostic testing

An ankle-brachial index (ABI) test should be performed in patients with history or physical exam findings suggestive of PAD. A resting ABI is performed with the patient in the supine position, with measurement of systolic blood pressure in both arms and ankles using a Doppler ultrasound device. Table 2¹³ outlines ABI scoring and interpretation.

An ABI > 1.4 is an invalid measurement, indicating that the arteries are too calcified to be compressed. These highly elevated ABI measurements are common in patients with diabetes and/or advanced CKD. In these patients, a toe-brachial index (TBI) test should be performed, because the digital arteries are almost always compressible.¹³

Patients with symptomatic PAD who are under consideration for revascularization may benefit from radiologic imaging of the lower extremities with duplex ultrasound, computed tomography angiography, or magnetic resonance angiography to determine the anatomic location and severity of stenosis.¹³

Management of PAD

Lifestyle interventions

For patients with PAD, lifestyle modifications are an essential—but challenging—component of disease management.

Continue to: Smoking cessation...

Smoking cessation. As with other atherosclerotic diseases, PAD progression is strongly correlated with smoking. A trial involving 204 active smokers with PAD showed that 5-year mortality and amputation rates dropped by more than half in those who quit smoking within a year, with numbers needed to treat (NNT) of 6 for mortality and 5 for amputation.¹⁹ Because of this dramatic effect, American College of Cardiology/American Heart Association (ACC/AHA) guidelines encourage providers to address smoking at every visit and use cessation programs and medication to increase quit rates.¹³

Exercise may be the most important intervention for PAD. A 2017 Cochrane review found that supervised, structured exercise programs increase pain-free and maximal walking distances by at least 20% and also improve physical and mental quality of life.²⁰ In a trial involving 111 patients with aortoiliac PAD, supervised exercise plus medical care led to greater functional improvement than either revascularization plus medical care or medical care alone.²¹ In a 2018 Cochrane review, neither revascularization or revascularization added to supervised exercise were better than supervised exercise alone.²² ACC/AHA guidelines recommend supervised exercise programs for claudication prior to considering revascularization.¹³TABLE 3¹³ outlines the components of a structured exercise program.

Unfortunately, the benefit of these programs has been difficult to reproduce without supervision. Another 2018 Cochrane review demonstrated significant improvement with supervised exercise and no clear improvement in patients given home exercise or advice to walk.²³ A recent study examined the effect of having patients use a wearable fitness tracker for home exercise and demonstrated no benefit over usual care.²⁴

Diet. There is some evidence that dietary interventions can prevent and possibly improve PAD. A large randomized controlled trial showed that a Mediterranean diet lowered rates of PAD over 1 year compared to a low-fat diet, with an NNT of 336 if supplemented with extra-virgin olive oil and 448 if supplemented with nuts.²⁵ A small trial of 25 patients who consumed non-soy legumes daily for 8 weeks showed average ABI improvement of 6%, although there was no control group.²⁶

Medical therapy to address peripheral and cardiovascular events

Standard medical therapy for coronary artery disease (CAD) is recommended for patients with PAD to reduce cardiovascular and limb events. For example, treatment of hypertension reduces cardiovascular and cerebrovascular events, and studies verify that lowering blood pressure does not worsen claudication or limb perfusion.

A trial involving 204 active smokers with PAD showed that 5-year mortality and amputation rates dropped by more than half in those who quit smoking within a year.

¹³TABLE 4^13,27-30 outlines the options for medical therapy.

Continue to: Statins...

Statins reduce cardiovascular events in PAD patients. A large study demonstrated that 40 mg of simvastatin has an NNT of 21 to prevent a coronary or cerebrovascular event in PAD, similar to the NNT of 23 seen in treatment of CAD.²⁷ Statins also reduce adverse limb outcomes. A registry of atherosclerosis patients showed that statins have an NNT of 56 to prevent amputation in PAD and an NNT of 28 to prevent worsening claudication, critical limb ischemia, revascularization, or amputation.²⁸

Antiplatelet therapy with low-dose aspirin or clopidogrel is recommended for symptomatic patients and for asymptomatic patients with an ABI ≤ 0.9.¹³ A Cochrane review demonstrated significantly reduced mortality with nonaspirin antiplatelet agents vs aspirin (NNT = 94) without increase in major bleeding.²⁹ Only British guidelines specifically recommend clopidogrel over aspirin.³¹

Dual antiplatelet therapy has not shown consistent benefits over aspirin alone. ACC/AHA guidelines state that dual antiplatelet therapy is not well established for PAD but may be reasonable after revascularization.¹³

Voraxapar is a novel antiplatelet agent that targets the thrombin-binding receptor on platelets. However, trials show no significant coronary benefit, and slight reductions in acute limb ischemia are offset by increases in major bleeding.¹³

For patients receiving medical therapy, ongoing evaluation and treatment should be based on claudication symptoms and clinical assessment.

Medical therapy for claudication

Several medications have been proposed for symptomatic treatment of intermittent claudication. Cilostazol is a phosphodiesterase inhibitor with the best risk-benefit ratio. A Cochrane review showed improvements in maximal and pain-free walking distances compared to placebo and improvements in quality of life with cilostazol 100 mg taken twice daily.³² Adverse effects included headache, dizziness, palpitations, and diarrhea.²⁹

Continue to: Pentoxifylline...

Pentoxifylline is another phosphodiesterase inhibitor with less evidence of improvement, higher adverse effect rates, and more frequent dosing. It is not recommended for treatment of intermittent claudication.^13,33

Supplements. Padma 28, a Tibetan herbal formulation, appears to improve maximal walking distance with adverse effect rates similar to placebo.³⁴ Other supplements, including vitamin E, ginkgo biloba, and omega-3 fatty acids, have no evidence of benefit.^35-37

When revascularizationis needed

Patients who develop limb ischemia or lifestyle-limiting claudication despite conservative therapy are candidates for revascularization. Endovascular techniques include angioplasty, stenting, atherectomy, and precise medication delivery. Surgical approaches mainly consist of thrombectomy and bypass grafting. For intermittent claudication despite conservative care, ACC/AHA guidelines state endovascular procedures are appropriate for aortoiliac disease and reasonable for femoropopliteal disease, but unproven for infrapopliteal disease.¹³

Acute limb ischemia is an emergency requiring immediate intervention. Two trials revealed identical overall and amputation-free survival rates for percutaneous thrombolysis and surgical thrombectomy.^38,39 ACC/AHA guidelines recommend anticoagulation with heparin followed by the revascularization technique that will most rapidly restore arterial flow.¹³

For chronic limb ischemia, a large trial showed angioplasty had lower initial morbidity, length of hospitalization, and cost than surgical repair. However, surgical mortality was lower after 2 years.⁴⁰ ACC/AHA guidelines recommend either surgery or endovascular procedures and propose initial endovascular treatment followed by surgery if needed.¹³ After revascularization, the patient should be followed periodically with a clinical evaluation and ABI measurement with further consideration for routine duplex ultrasound surveillance.¹³

For chronic limb ischemia, a large trial showed angioplasty had lower initial morbidity, length of hospitalization, and cost than surgical repair. Surgical mortality was lower after 2 years.

Outcomes

Patients with PAD have variable outcomes. About 70% to 80% of patients with this diagnosis will have a stable disease process with no worsening of symptoms, 10% to 20% will experience worsening symptoms over time, 5% to 10% will require revascularization within 5 years of diagnosis, and 1% to 5% will progress to critical limb ischemia, which has a 5-year amputation rate of 1% to 4%.² Patients who require amputation have poor outcomes: Within 2 years, 30% are dead and 15% have had further amputations.¹⁸

In addition to the morbidity and mortality from its own progression, PAD is an important predictor of CAD and is associated with a significant elevation in morbidity and mortality from CAD. One small but well-designed prospective cohort study found that patients with PAD had a more than 6-fold increased risk of death from CAD than did patients without PAD.⁴¹

Acknowledgement
The authors thank Francesca Cimino, MD, FAAFP, for her help in reviewing this manuscript.

CORRESPONDENCE
Dustin K. Smith, DO, 2080 Child Street, Jacksonville, FL 32214; dustinksmith@yahoo.com

Peripheral arterial disease (PAD), the progressive disorder that results in ischemia to distal vascular territories as a result of atherosclerosis, spans a wide range of presentations, from minimally symptomatic disease to limb ischemia secondary to acute or chronic occlusion.