The Journal of Family Practice

This patient was given a diagnosis of xerosis of the feet, commonly called fissured or cracked heels. Scaling and fissuring are also common in tinea pedis, but the location is often between the toes and there are finer splits and scale.

Xerosis is severely dry skin with hyperkeratosis due to abnormal keratinization;¹ it leads to inflexibility and subsequent fissuring of the heel pads. The cracks can be painful and even bleed.

Although the condition is common, well-controlled trials and definitive evidence in the literature are sparse. The authors of one systematic review were unable to draw conclusions regarding the efficacy of various treatments due to wide variation in research methodologies and outcome measures; they did, however, note that urea-containing products (followed by ammonium lactate products) were studied the most.²

In clinical practice, frequently applied topical emollients are recommended. Exfoliating products, including prescription Lac-Hydrin (ammonium lactate 12% cream) and the over-the-counter version, Am-Lactin, may be helpful. Mechanical debridement with a file or pumice stone can be used (with caution) to reduce the hyperkeratotic plaques. If these measures fail, topical steroids may be added to the emollients. In addition, patients have used cyanoacrylate glues to hold the fissures together with a reported reduction in pain.³

This patient had already tried standard topical emollients. She was prescribed ammonium lactate cream to be used as an exfoliating moisturizer topically twice daily along with triamcinolone acetonide (TAC) 0.1% ointment to be applied twice daily. She was instructed to wean off the TAC once the xerosis was controlled with the ammonium lactate cream.

‌

Photo and text courtesy of Daniel Stulberg, MD, FAAFP, Professor and Chair, Department of Family and Community Medicine, Western Michigan University Homer Stryker, MD School of Medicine, Kalamazoo.

This patient was given a diagnosis of xerosis of the feet, commonly called fissured or cracked heels. Scaling and fissuring are also common in tinea pedis, but the location is often between the toes and there are finer splits and scale.

Xerosis is severely dry skin with hyperkeratosis due to abnormal keratinization;¹ it leads to inflexibility and subsequent fissuring of the heel pads. The cracks can be painful and even bleed.

Although the condition is common, well-controlled trials and definitive evidence in the literature are sparse. The authors of one systematic review were unable to draw conclusions regarding the efficacy of various treatments due to wide variation in research methodologies and outcome measures; they did, however, note that urea-containing products (followed by ammonium lactate products) were studied the most.²

In clinical practice, frequently applied topical emollients are recommended. Exfoliating products, including prescription Lac-Hydrin (ammonium lactate 12% cream) and the over-the-counter version, Am-Lactin, may be helpful. Mechanical debridement with a file or pumice stone can be used (with caution) to reduce the hyperkeratotic plaques. If these measures fail, topical steroids may be added to the emollients. In addition, patients have used cyanoacrylate glues to hold the fissures together with a reported reduction in pain.³

This patient had already tried standard topical emollients. She was prescribed ammonium lactate cream to be used as an exfoliating moisturizer topically twice daily along with triamcinolone acetonide (TAC) 0.1% ointment to be applied twice daily. She was instructed to wean off the TAC once the xerosis was controlled with the ammonium lactate cream.

‌

Photo and text courtesy of Daniel Stulberg, MD, FAAFP, Professor and Chair, Department of Family and Community Medicine, Western Michigan University Homer Stryker, MD School of Medicine, Kalamazoo.

This patient was given a diagnosis of xerosis of the feet, commonly called fissured or cracked heels. Scaling and fissuring are also common in tinea pedis, but the location is often between the toes and there are finer splits and scale.

Xerosis is severely dry skin with hyperkeratosis due to abnormal keratinization;¹ it leads to inflexibility and subsequent fissuring of the heel pads. The cracks can be painful and even bleed.

Although the condition is common, well-controlled trials and definitive evidence in the literature are sparse. The authors of one systematic review were unable to draw conclusions regarding the efficacy of various treatments due to wide variation in research methodologies and outcome measures; they did, however, note that urea-containing products (followed by ammonium lactate products) were studied the most.²

In clinical practice, frequently applied topical emollients are recommended. Exfoliating products, including prescription Lac-Hydrin (ammonium lactate 12% cream) and the over-the-counter version, Am-Lactin, may be helpful. Mechanical debridement with a file or pumice stone can be used (with caution) to reduce the hyperkeratotic plaques. If these measures fail, topical steroids may be added to the emollients. In addition, patients have used cyanoacrylate glues to hold the fissures together with a reported reduction in pain.³

This patient had already tried standard topical emollients. She was prescribed ammonium lactate cream to be used as an exfoliating moisturizer topically twice daily along with triamcinolone acetonide (TAC) 0.1% ointment to be applied twice daily. She was instructed to wean off the TAC once the xerosis was controlled with the ammonium lactate cream.

‌

Photo and text courtesy of Daniel Stulberg, MD, FAAFP, Professor and Chair, Department of Family and Community Medicine, Western Michigan University Homer Stryker, MD School of Medicine, Kalamazoo.

A 62-YEAR-OLD HISPANIC WOMAN with a history of well-controlled diabetes and hypertension presented with an intensely pruritic rash of 3 months’ duration. She reported poor sleep due to scratching throughout the night. She denied close contact with individuals with similar rashes or itching, new intimate partners, or recent travel. She worked in an office setting and had stable, noncrowded housing.

A physical exam revealed brown and purple scaly papules and many excoriation marks. The rash was concentrated along clothing lines, around intertriginous areas, and on her ankles, wrists, and the interdigital spaces (FIGURE 1A and 1B).

WHAT IS YOUR DIAGNOSIS?
HOW WOULD YOU TREAT THIS PATIENT?

Scabies is a diagnosis that should be considered in any patient with new-onset, widespread, nocturnal-dominant pruritus¹ and it was suspected, in this case, after the initial history taking and physical exam. (See “Consider these diagnoses in cases of pruritic skin conditions” for more on lichen planus and prurigo nodularis, which were also included in the differential diagnosis.)

To minimize the likelihood of reinfestion, we advised the patient to decontaminate her bedding, clothing, and towels.

The use of a handheld dermatoscope confirmed the diagnosis by revealing white to yellow scales following the serpiginous lines. These serpiginous lines resembled scabies burrows, and at the end of some burrows, small triangular and hyperpigmented structures resembling “delta-winged jets” were seen. These “delta-winged jets” were the mite’s pigmented mouth parts and anterior legs. The burrows, which contain eggs and feces, have been described as the “contrails” behind the jets (FIGURE 2).

The use of a new UV illumination feature on our dermatoscope (which we’ll describe shortly) made for an even more dramatic diagnostic visual. With the click of a button, the mites fluoresced green to yellow and the burrows fluoresced white to blue (FIGURE 3).

Meeting the criteria. The clinical and dermoscopic findings met the 2020 International Alliance for the Control of Scabies (IACS) Consensus Criteria for the Diagnosis of Scabies,² confirming the diagnosis in this patient. Scabies infestation poses a significant public health burden globally, with an estimated incidence of more than 454 million in 2016.³

Visualization is key to the diagnosis

Traditionally, the diagnosis of scabies infestation is made by direct visualization of mites via microscopy of skin scrapings.⁴ However, this approach is seldom feasible in a family medicine office. Fortunately, the 2020 IACS criteria included dermoscopy as a Level A diagnostic method for confirmed scabies.

Continue to: The pros and cons of dermoscopy

The pros and cons of dermoscopy. A handheld dermatoscope is an accessible, convenient tool for any clinician who treats the skin. It has been demonstrated that, in the hands of experts and novices alike, dermoscopy has a sensitivity of 91% and specificity of 86% for the diagnosis of scabies.⁵

However, accurate identification of the dermoscopic findings can depend on the operator and can be harder to achieve in patients who have skin of color.² This is largely because the mite’s brown-to-black triangular head is small (sometimes hidden under skin scales) and easy to miss, especially against darker skin.

A new technologic feature helps. In this case, we used the built-in 365-nm UV illumination feature of our handheld dermatoscope (Dermlite-5) and both mites and burrows fluoresced intensely (FIGURE 3). A skin scraping at the location of the fluorescent body under microscopic examination confirmed that the organism was a Sarcoptes scabiei mite (FIGURE 4).

UV light dermoscopy can decrease operator error and ameliorate the challenge of diagnosing scabies in skin of color. Specifically, when using UV dermoscopy it’s easier to:

• locate mites, regardless of the patient’s skin color
• see the mite’s entire body, rather than just a small portion (thus increasing diagnostic certainty).

New diagnostic feature, classic treatment

Due to the severity of the patient’s scabies, she was prescribed both permethrin 5% cream and oral ivermectin 200 mcg/kg, both to be used immediately and repeated in 1 week. Notably, a systematic review indicated that topical permethrin is a superior treatment to oral ivermectin.⁶ However, in cases of widespread scabies and crusted scabies, it is standard of care to treat with both medications.

The patient’s pruritus was treated with cetirizine as needed. She was told that the itching might persist for a few weeks after treatment was completed.

Reinfestation was a concern with this patient because she was unable to identify a source for the mites. To minimize the likelihood of reinfestation, we advised her to decontaminate her bedding, clothing, and towels by washing them in hot water (≥ 122° F) or placing in a sealed plastic bag for at least 1 week.¹ For crusted scabies cases, thorough vacuuming of a patient’s furniture and carpets is recommended.

A 62-YEAR-OLD HISPANIC WOMAN with a history of well-controlled diabetes and hypertension presented with an intensely pruritic rash of 3 months’ duration. She reported poor sleep due to scratching throughout the night. She denied close contact with individuals with similar rashes or itching, new intimate partners, or recent travel. She worked in an office setting and had stable, noncrowded housing.

A physical exam revealed brown and purple scaly papules and many excoriation marks. The rash was concentrated along clothing lines, around intertriginous areas, and on her ankles, wrists, and the interdigital spaces (FIGURE 1A and 1B).

WHAT IS YOUR DIAGNOSIS?
HOW WOULD YOU TREAT THIS PATIENT?

Scabies is a diagnosis that should be considered in any patient with new-onset, widespread, nocturnal-dominant pruritus¹ and it was suspected, in this case, after the initial history taking and physical exam. (See “Consider these diagnoses in cases of pruritic skin conditions” for more on lichen planus and prurigo nodularis, which were also included in the differential diagnosis.)

To minimize the likelihood of reinfestion, we advised the patient to decontaminate her bedding, clothing, and towels.

The use of a handheld dermatoscope confirmed the diagnosis by revealing white to yellow scales following the serpiginous lines. These serpiginous lines resembled scabies burrows, and at the end of some burrows, small triangular and hyperpigmented structures resembling “delta-winged jets” were seen. These “delta-winged jets” were the mite’s pigmented mouth parts and anterior legs. The burrows, which contain eggs and feces, have been described as the “contrails” behind the jets (FIGURE 2).

The use of a new UV illumination feature on our dermatoscope (which we’ll describe shortly) made for an even more dramatic diagnostic visual. With the click of a button, the mites fluoresced green to yellow and the burrows fluoresced white to blue (FIGURE 3).

Meeting the criteria. The clinical and dermoscopic findings met the 2020 International Alliance for the Control of Scabies (IACS) Consensus Criteria for the Diagnosis of Scabies,² confirming the diagnosis in this patient. Scabies infestation poses a significant public health burden globally, with an estimated incidence of more than 454 million in 2016.³

Visualization is key to the diagnosis

Traditionally, the diagnosis of scabies infestation is made by direct visualization of mites via microscopy of skin scrapings.⁴ However, this approach is seldom feasible in a family medicine office. Fortunately, the 2020 IACS criteria included dermoscopy as a Level A diagnostic method for confirmed scabies.

Continue to: The pros and cons of dermoscopy

The pros and cons of dermoscopy. A handheld dermatoscope is an accessible, convenient tool for any clinician who treats the skin. It has been demonstrated that, in the hands of experts and novices alike, dermoscopy has a sensitivity of 91% and specificity of 86% for the diagnosis of scabies.⁵

However, accurate identification of the dermoscopic findings can depend on the operator and can be harder to achieve in patients who have skin of color.² This is largely because the mite’s brown-to-black triangular head is small (sometimes hidden under skin scales) and easy to miss, especially against darker skin.

A new technologic feature helps. In this case, we used the built-in 365-nm UV illumination feature of our handheld dermatoscope (Dermlite-5) and both mites and burrows fluoresced intensely (FIGURE 3). A skin scraping at the location of the fluorescent body under microscopic examination confirmed that the organism was a Sarcoptes scabiei mite (FIGURE 4).

UV light dermoscopy can decrease operator error and ameliorate the challenge of diagnosing scabies in skin of color. Specifically, when using UV dermoscopy it’s easier to:

• locate mites, regardless of the patient’s skin color
• see the mite’s entire body, rather than just a small portion (thus increasing diagnostic certainty).

New diagnostic feature, classic treatment

Due to the severity of the patient’s scabies, she was prescribed both permethrin 5% cream and oral ivermectin 200 mcg/kg, both to be used immediately and repeated in 1 week. Notably, a systematic review indicated that topical permethrin is a superior treatment to oral ivermectin.⁶ However, in cases of widespread scabies and crusted scabies, it is standard of care to treat with both medications.

The patient’s pruritus was treated with cetirizine as needed. She was told that the itching might persist for a few weeks after treatment was completed.

Reinfestation was a concern with this patient because she was unable to identify a source for the mites. To minimize the likelihood of reinfestation, we advised her to decontaminate her bedding, clothing, and towels by washing them in hot water (≥ 122° F) or placing in a sealed plastic bag for at least 1 week.¹ For crusted scabies cases, thorough vacuuming of a patient’s furniture and carpets is recommended.

A 62-YEAR-OLD HISPANIC WOMAN with a history of well-controlled diabetes and hypertension presented with an intensely pruritic rash of 3 months’ duration. She reported poor sleep due to scratching throughout the night. She denied close contact with individuals with similar rashes or itching, new intimate partners, or recent travel. She worked in an office setting and had stable, noncrowded housing.

A physical exam revealed brown and purple scaly papules and many excoriation marks. The rash was concentrated along clothing lines, around intertriginous areas, and on her ankles, wrists, and the interdigital spaces (FIGURE 1A and 1B).

WHAT IS YOUR DIAGNOSIS?
HOW WOULD YOU TREAT THIS PATIENT?

Scabies is a diagnosis that should be considered in any patient with new-onset, widespread, nocturnal-dominant pruritus¹ and it was suspected, in this case, after the initial history taking and physical exam. (See “Consider these diagnoses in cases of pruritic skin conditions” for more on lichen planus and prurigo nodularis, which were also included in the differential diagnosis.)

To minimize the likelihood of reinfestion, we advised the patient to decontaminate her bedding, clothing, and towels.

The use of a handheld dermatoscope confirmed the diagnosis by revealing white to yellow scales following the serpiginous lines. These serpiginous lines resembled scabies burrows, and at the end of some burrows, small triangular and hyperpigmented structures resembling “delta-winged jets” were seen. These “delta-winged jets” were the mite’s pigmented mouth parts and anterior legs. The burrows, which contain eggs and feces, have been described as the “contrails” behind the jets (FIGURE 2).

The use of a new UV illumination feature on our dermatoscope (which we’ll describe shortly) made for an even more dramatic diagnostic visual. With the click of a button, the mites fluoresced green to yellow and the burrows fluoresced white to blue (FIGURE 3).

Meeting the criteria. The clinical and dermoscopic findings met the 2020 International Alliance for the Control of Scabies (IACS) Consensus Criteria for the Diagnosis of Scabies,² confirming the diagnosis in this patient. Scabies infestation poses a significant public health burden globally, with an estimated incidence of more than 454 million in 2016.³

Visualization is key to the diagnosis

Traditionally, the diagnosis of scabies infestation is made by direct visualization of mites via microscopy of skin scrapings.⁴ However, this approach is seldom feasible in a family medicine office. Fortunately, the 2020 IACS criteria included dermoscopy as a Level A diagnostic method for confirmed scabies.

Continue to: The pros and cons of dermoscopy

The pros and cons of dermoscopy. A handheld dermatoscope is an accessible, convenient tool for any clinician who treats the skin. It has been demonstrated that, in the hands of experts and novices alike, dermoscopy has a sensitivity of 91% and specificity of 86% for the diagnosis of scabies.⁵

However, accurate identification of the dermoscopic findings can depend on the operator and can be harder to achieve in patients who have skin of color.² This is largely because the mite’s brown-to-black triangular head is small (sometimes hidden under skin scales) and easy to miss, especially against darker skin.

A new technologic feature helps. In this case, we used the built-in 365-nm UV illumination feature of our handheld dermatoscope (Dermlite-5) and both mites and burrows fluoresced intensely (FIGURE 3). A skin scraping at the location of the fluorescent body under microscopic examination confirmed that the organism was a Sarcoptes scabiei mite (FIGURE 4).

UV light dermoscopy can decrease operator error and ameliorate the challenge of diagnosing scabies in skin of color. Specifically, when using UV dermoscopy it’s easier to:

• locate mites, regardless of the patient’s skin color
• see the mite’s entire body, rather than just a small portion (thus increasing diagnostic certainty).

New diagnostic feature, classic treatment

Due to the severity of the patient’s scabies, she was prescribed both permethrin 5% cream and oral ivermectin 200 mcg/kg, both to be used immediately and repeated in 1 week. Notably, a systematic review indicated that topical permethrin is a superior treatment to oral ivermectin.⁶ However, in cases of widespread scabies and crusted scabies, it is standard of care to treat with both medications.

The patient’s pruritus was treated with cetirizine as needed. She was told that the itching might persist for a few weeks after treatment was completed.

Reinfestation was a concern with this patient because she was unable to identify a source for the mites. To minimize the likelihood of reinfestation, we advised her to decontaminate her bedding, clothing, and towels by washing them in hot water (≥ 122° F) or placing in a sealed plastic bag for at least 1 week.¹ For crusted scabies cases, thorough vacuuming of a patient’s furniture and carpets is recommended.

Evidence summary

Small studies offer mixed evidence of benefit

Seven RCTs using manual therapies to treat chronic tension headaches have reported the change in headache frequency (TABLE^1-7). Most, but not all, manual therapies significantly improved headache frequency.

Participants ranged in age from 18 to 65 years, with mean age ranges of 33 to 42 years in each study. At baseline, patients had 10 or more tension-type headaches per month. The manual therapies varied in techniques, duration, and the training of the person performing the intervention:

• Twice-weekly chiropractic spinal manipulation for 6 weeks¹
• Soft-tissue therapy plus spinal manipulation (8 treatments over 4 weeks)²
• Chiropractic spinal manipulation with or without amitriptyline for 14 weeks³
• Corrective osteopathic manipulation treatment (OMT) techniques tailored for each patient for 1 month⁴
• High-velocity low-amplitude manipulation (HVLA) plus exercise or myofascial release plus exercise twice weekly for 8 weeks⁵
• Manual therapy treatment consisting of a combination of mobilizations of the cervical and thoracic spine, exercises, and postural correction for up to 9 sessions of 30 minutes each⁶
• One hour of direct or indirect myofascial release treatment twice weekly for 12 weeks.⁷

Three studies involved chiropractic providers.^1-3 One study (n = 19) found a positive effect, in which chiropractic manipulation augmented with amitriptyline performed better than chiropractic manipulation alone.³ Another chiropractic study did not find an immediate posttreatment benefit but did report significant headache reduction at the 4-week follow-up interval.¹ The third chiropractic study did not show additional benefit from HVLA manipulation.²

One small study involving osteopathic physicians using OMT found reduced headache frequency after 12 weeks but not at 4 weeks.⁴ Another study, comparing HVLA or myofascial release with exercise to exercise alone, found benefit for the HVLA group but not for myofascial release; interventions in this study were performed by a physician with at least 6 years of unspecified manual therapy experience.⁵ A small study of manual therapists found improvement at the end of manual therapy but not at 18 months.⁶ Another small study using providers with 10 months’ experience with myofascial release found reduced headache frequency 4 weeks after a course of direct and indirect myofascial release (compared with sham release).⁷

Editor’s takeaway

It isn’t hard to imagine why muscle tension headaches might respond to certain forms of manual therapy. However, all available studies of these modalities have been small (< 100 patients) or lacked blinding, introducing the potential for significant bias. Nevertheless, for now it appears reasonable to refer interested patients with tension headache to an osteopathic physician for OMT or myofascial release to reduce headache frequency.

Evidence summary

Small studies offer mixed evidence of benefit

Seven RCTs using manual therapies to treat chronic tension headaches have reported the change in headache frequency (TABLE^1-7). Most, but not all, manual therapies significantly improved headache frequency.

Participants ranged in age from 18 to 65 years, with mean age ranges of 33 to 42 years in each study. At baseline, patients had 10 or more tension-type headaches per month. The manual therapies varied in techniques, duration, and the training of the person performing the intervention:

• Twice-weekly chiropractic spinal manipulation for 6 weeks¹
• Soft-tissue therapy plus spinal manipulation (8 treatments over 4 weeks)²
• Chiropractic spinal manipulation with or without amitriptyline for 14 weeks³
• Corrective osteopathic manipulation treatment (OMT) techniques tailored for each patient for 1 month⁴
• High-velocity low-amplitude manipulation (HVLA) plus exercise or myofascial release plus exercise twice weekly for 8 weeks⁵
• Manual therapy treatment consisting of a combination of mobilizations of the cervical and thoracic spine, exercises, and postural correction for up to 9 sessions of 30 minutes each⁶
• One hour of direct or indirect myofascial release treatment twice weekly for 12 weeks.⁷

Three studies involved chiropractic providers.^1-3 One study (n = 19) found a positive effect, in which chiropractic manipulation augmented with amitriptyline performed better than chiropractic manipulation alone.³ Another chiropractic study did not find an immediate posttreatment benefit but did report significant headache reduction at the 4-week follow-up interval.¹ The third chiropractic study did not show additional benefit from HVLA manipulation.²

One small study involving osteopathic physicians using OMT found reduced headache frequency after 12 weeks but not at 4 weeks.⁴ Another study, comparing HVLA or myofascial release with exercise to exercise alone, found benefit for the HVLA group but not for myofascial release; interventions in this study were performed by a physician with at least 6 years of unspecified manual therapy experience.⁵ A small study of manual therapists found improvement at the end of manual therapy but not at 18 months.⁶ Another small study using providers with 10 months’ experience with myofascial release found reduced headache frequency 4 weeks after a course of direct and indirect myofascial release (compared with sham release).⁷

Editor’s takeaway

It isn’t hard to imagine why muscle tension headaches might respond to certain forms of manual therapy. However, all available studies of these modalities have been small (< 100 patients) or lacked blinding, introducing the potential for significant bias. Nevertheless, for now it appears reasonable to refer interested patients with tension headache to an osteopathic physician for OMT or myofascial release to reduce headache frequency.

Evidence summary

Small studies offer mixed evidence of benefit

Seven RCTs using manual therapies to treat chronic tension headaches have reported the change in headache frequency (TABLE^1-7). Most, but not all, manual therapies significantly improved headache frequency.

Participants ranged in age from 18 to 65 years, with mean age ranges of 33 to 42 years in each study. At baseline, patients had 10 or more tension-type headaches per month. The manual therapies varied in techniques, duration, and the training of the person performing the intervention:

• Twice-weekly chiropractic spinal manipulation for 6 weeks¹
• Soft-tissue therapy plus spinal manipulation (8 treatments over 4 weeks)²
• Chiropractic spinal manipulation with or without amitriptyline for 14 weeks³
• Corrective osteopathic manipulation treatment (OMT) techniques tailored for each patient for 1 month⁴
• High-velocity low-amplitude manipulation (HVLA) plus exercise or myofascial release plus exercise twice weekly for 8 weeks⁵
• Manual therapy treatment consisting of a combination of mobilizations of the cervical and thoracic spine, exercises, and postural correction for up to 9 sessions of 30 minutes each⁶
• One hour of direct or indirect myofascial release treatment twice weekly for 12 weeks.⁷

Three studies involved chiropractic providers.^1-3 One study (n = 19) found a positive effect, in which chiropractic manipulation augmented with amitriptyline performed better than chiropractic manipulation alone.³ Another chiropractic study did not find an immediate posttreatment benefit but did report significant headache reduction at the 4-week follow-up interval.¹ The third chiropractic study did not show additional benefit from HVLA manipulation.²

One small study involving osteopathic physicians using OMT found reduced headache frequency after 12 weeks but not at 4 weeks.⁴ Another study, comparing HVLA or myofascial release with exercise to exercise alone, found benefit for the HVLA group but not for myofascial release; interventions in this study were performed by a physician with at least 6 years of unspecified manual therapy experience.⁵ A small study of manual therapists found improvement at the end of manual therapy but not at 18 months.⁶ Another small study using providers with 10 months’ experience with myofascial release found reduced headache frequency 4 weeks after a course of direct and indirect myofascial release (compared with sham release).⁷

Editor’s takeaway

It isn’t hard to imagine why muscle tension headaches might respond to certain forms of manual therapy. However, all available studies of these modalities have been small (< 100 patients) or lacked blinding, introducing the potential for significant bias. Nevertheless, for now it appears reasonable to refer interested patients with tension headache to an osteopathic physician for OMT or myofascial release to reduce headache frequency.

AN OTHERWISE HEALTHY 53-YEAR-OLD MAN presented with a 6-month history of an acneiform eruption on his face. There was no history of teenage acne or allergic contact dermatitis.

Scattered papules and pustules were present on the forehead, nose, and cheeks, with background erythema and telangiectasias (FIGURE 1). A few pinpoint crusted excoriations were noted. A sample was taken from the papules and pustules using a #15 blade and submitted for examination.

WHAT IS YOUR DIAGNOSIS?
HOW WOULD YOU TREAT THIS PATIENT?

Under light microscopy, the scraping revealed Demodex mites (FIGURE 2). It has been proposed that these mites play a role in the inflammatory process seen in rosacea, although studies have yet to determine whether the inflammatory symptoms of rosacea cause the mites to proliferate or if the mites contribute to the initial inflammatory process.^1,2

Demodex folliculorum and D brevis are part of normal skin flora; they are found in about 12% of all follicles and most commonly involve the face.³ They often become abundant in the presence of numerous sebaceous glands. Men have more sebaceous glands than women do, and thus run a greater risk for infestation with mites. An abnormal proliferation of Demodex mites can lead to demodicosis.

A proliferation of Demodex is seen in almost all cases of papulopustular rosacea and more than 60% of cases of erythematotelangiectatic rosacea.

Demodex mites can be examined microscopically via the skin surface sampling technique known as scraping, which was done in this case. Samples taken from the papules and pustules utilizing a #15 blade are placed in immersion oil on a glass slide, cover-slipped, and examined by light microscopy.

Rosacea is thought to be an inflammatory disease in which the immune system is triggered by a variety of factors, including UV light, heat, stress, alcohol, hormonal influences, and microorganisms.^1,4 The disease is found in up to 10% of the population worldwide.¹

The diagnosis of rosacea requires at least 1 of the 2 “core features”—persistent central facial erythema or phymatous changes—or 2 of 4 “major features”: papules/pustules, ocular manifestation, flushing, and telangiectasias. There are 3 phenotypes: ocular, papulopustular, and erythematotelangiectatic.^5,6

Continue to: The connection

The connection. Papulopustular and erythematotelangiectatic rosacea may be caused by a proliferation of Demodex mites and increased vascular endothelial growth factor production.² In fact, a proliferation of Demodex is seen in almost all cases of papulopustular rosacea and more than 60% of cases of erythematotelangiectatic rosacea.²

Patient age and distribution of lesions narrowed the differential

Acne vulgaris is an inflammatory disease of the pilosebaceous units caused by increased sebum production, inflammation, and bacterial colonization (Propionibacterium acnes) of hair follicles on the face, neck, chest, and other areas. Both inflammatory and noninflammatory lesions can be present, and in serious cases, scarring can result.⁷ The case patient’s age and accompanying broad erythema were more consistent with rosacea than acne vulgaris.

Seborrheic dermatitis is a common skin condition usually stemming from an inflammatory reaction to a common yeast. Classic symptoms include scaling and erythema of the scalp and central face, as well as pruritus. Topical antifungals such as ketoconazole 2% cream and 2% shampoo are the mainstay of treatment.⁸ The broad distribution and papulopustules in this patient argue against the diagnosis of seborrheic dermatitis.

Systemic lupus erythematosus is a systemic inflammatory disease that often has cutaneous manifestations. Acute lupus manifests as an erythematous “butterfly rash” across the face and cheeks. Chronic discoid lupus involves depigmented plaques, erythematous macules, telangiectasias, and scarring with loss of normal hair follicles. These findings classically are photodistributed.⁹ The classic broad erythema extending from the cheeks over the bridge of the nose was not present in this patient.

Treatment is primarily topical

Mild cases of rosacea often can be managed with topical antibiotic creams. More severe cases may require systemic antibiotics such as tetracycline or doxycycline, although these are used with caution due to the potential for antibiotic resistance.

Ivermectin 1% cream is a US Food and Drug Administration–approved medication that is applied once daily for up to a year to treat the inflammatory pustules associated with Demodex mites. Although it is costly, studies have shown better results with topical ivermectin than with other topical medications (eg, metronidazole 0.75% gel or cream). However, metronidazole 0.75% gel applied twice daily and oral tetracycline 250 mg or doxycycline 100 mg daily or twice daily for at least 2 months often are utilized when the cost of topical ivermectin is prohibitive.¹⁰

Our patient was treated with a combination of doxycycline 100 mg daily for 30 days and ivermectin 1% cream daily. He was also instructed to apply sunscreen daily. He improved rapidly, and the daily topical ivermectin was discontinued after 6 months.

AN OTHERWISE HEALTHY 53-YEAR-OLD MAN presented with a 6-month history of an acneiform eruption on his face. There was no history of teenage acne or allergic contact dermatitis.

Scattered papules and pustules were present on the forehead, nose, and cheeks, with background erythema and telangiectasias (FIGURE 1). A few pinpoint crusted excoriations were noted. A sample was taken from the papules and pustules using a #15 blade and submitted for examination.

WHAT IS YOUR DIAGNOSIS?
HOW WOULD YOU TREAT THIS PATIENT?

Under light microscopy, the scraping revealed Demodex mites (FIGURE 2). It has been proposed that these mites play a role in the inflammatory process seen in rosacea, although studies have yet to determine whether the inflammatory symptoms of rosacea cause the mites to proliferate or if the mites contribute to the initial inflammatory process.^1,2

Demodex folliculorum and D brevis are part of normal skin flora; they are found in about 12% of all follicles and most commonly involve the face.³ They often become abundant in the presence of numerous sebaceous glands. Men have more sebaceous glands than women do, and thus run a greater risk for infestation with mites. An abnormal proliferation of Demodex mites can lead to demodicosis.

A proliferation of Demodex is seen in almost all cases of papulopustular rosacea and more than 60% of cases of erythematotelangiectatic rosacea.

Demodex mites can be examined microscopically via the skin surface sampling technique known as scraping, which was done in this case. Samples taken from the papules and pustules utilizing a #15 blade are placed in immersion oil on a glass slide, cover-slipped, and examined by light microscopy.

Rosacea is thought to be an inflammatory disease in which the immune system is triggered by a variety of factors, including UV light, heat, stress, alcohol, hormonal influences, and microorganisms.^1,4 The disease is found in up to 10% of the population worldwide.¹

The diagnosis of rosacea requires at least 1 of the 2 “core features”—persistent central facial erythema or phymatous changes—or 2 of 4 “major features”: papules/pustules, ocular manifestation, flushing, and telangiectasias. There are 3 phenotypes: ocular, papulopustular, and erythematotelangiectatic.^5,6

Continue to: The connection

The connection. Papulopustular and erythematotelangiectatic rosacea may be caused by a proliferation of Demodex mites and increased vascular endothelial growth factor production.² In fact, a proliferation of Demodex is seen in almost all cases of papulopustular rosacea and more than 60% of cases of erythematotelangiectatic rosacea.²

Patient age and distribution of lesions narrowed the differential

Acne vulgaris is an inflammatory disease of the pilosebaceous units caused by increased sebum production, inflammation, and bacterial colonization (Propionibacterium acnes) of hair follicles on the face, neck, chest, and other areas. Both inflammatory and noninflammatory lesions can be present, and in serious cases, scarring can result.⁷ The case patient’s age and accompanying broad erythema were more consistent with rosacea than acne vulgaris.

Seborrheic dermatitis is a common skin condition usually stemming from an inflammatory reaction to a common yeast. Classic symptoms include scaling and erythema of the scalp and central face, as well as pruritus. Topical antifungals such as ketoconazole 2% cream and 2% shampoo are the mainstay of treatment.⁸ The broad distribution and papulopustules in this patient argue against the diagnosis of seborrheic dermatitis.

Systemic lupus erythematosus is a systemic inflammatory disease that often has cutaneous manifestations. Acute lupus manifests as an erythematous “butterfly rash” across the face and cheeks. Chronic discoid lupus involves depigmented plaques, erythematous macules, telangiectasias, and scarring with loss of normal hair follicles. These findings classically are photodistributed.⁹ The classic broad erythema extending from the cheeks over the bridge of the nose was not present in this patient.

Treatment is primarily topical

Mild cases of rosacea often can be managed with topical antibiotic creams. More severe cases may require systemic antibiotics such as tetracycline or doxycycline, although these are used with caution due to the potential for antibiotic resistance.

Ivermectin 1% cream is a US Food and Drug Administration–approved medication that is applied once daily for up to a year to treat the inflammatory pustules associated with Demodex mites. Although it is costly, studies have shown better results with topical ivermectin than with other topical medications (eg, metronidazole 0.75% gel or cream). However, metronidazole 0.75% gel applied twice daily and oral tetracycline 250 mg or doxycycline 100 mg daily or twice daily for at least 2 months often are utilized when the cost of topical ivermectin is prohibitive.¹⁰

Our patient was treated with a combination of doxycycline 100 mg daily for 30 days and ivermectin 1% cream daily. He was also instructed to apply sunscreen daily. He improved rapidly, and the daily topical ivermectin was discontinued after 6 months.

AN OTHERWISE HEALTHY 53-YEAR-OLD MAN presented with a 6-month history of an acneiform eruption on his face. There was no history of teenage acne or allergic contact dermatitis.

Scattered papules and pustules were present on the forehead, nose, and cheeks, with background erythema and telangiectasias (FIGURE 1). A few pinpoint crusted excoriations were noted. A sample was taken from the papules and pustules using a #15 blade and submitted for examination.

WHAT IS YOUR DIAGNOSIS?
HOW WOULD YOU TREAT THIS PATIENT?

Under light microscopy, the scraping revealed Demodex mites (FIGURE 2). It has been proposed that these mites play a role in the inflammatory process seen in rosacea, although studies have yet to determine whether the inflammatory symptoms of rosacea cause the mites to proliferate or if the mites contribute to the initial inflammatory process.^1,2

Demodex folliculorum and D brevis are part of normal skin flora; they are found in about 12% of all follicles and most commonly involve the face.³ They often become abundant in the presence of numerous sebaceous glands. Men have more sebaceous glands than women do, and thus run a greater risk for infestation with mites. An abnormal proliferation of Demodex mites can lead to demodicosis.

A proliferation of Demodex is seen in almost all cases of papulopustular rosacea and more than 60% of cases of erythematotelangiectatic rosacea.

Demodex mites can be examined microscopically via the skin surface sampling technique known as scraping, which was done in this case. Samples taken from the papules and pustules utilizing a #15 blade are placed in immersion oil on a glass slide, cover-slipped, and examined by light microscopy.

Rosacea is thought to be an inflammatory disease in which the immune system is triggered by a variety of factors, including UV light, heat, stress, alcohol, hormonal influences, and microorganisms.^1,4 The disease is found in up to 10% of the population worldwide.¹

The diagnosis of rosacea requires at least 1 of the 2 “core features”—persistent central facial erythema or phymatous changes—or 2 of 4 “major features”: papules/pustules, ocular manifestation, flushing, and telangiectasias. There are 3 phenotypes: ocular, papulopustular, and erythematotelangiectatic.^5,6

Continue to: The connection

The connection. Papulopustular and erythematotelangiectatic rosacea may be caused by a proliferation of Demodex mites and increased vascular endothelial growth factor production.² In fact, a proliferation of Demodex is seen in almost all cases of papulopustular rosacea and more than 60% of cases of erythematotelangiectatic rosacea.²

Patient age and distribution of lesions narrowed the differential

Acne vulgaris is an inflammatory disease of the pilosebaceous units caused by increased sebum production, inflammation, and bacterial colonization (Propionibacterium acnes) of hair follicles on the face, neck, chest, and other areas. Both inflammatory and noninflammatory lesions can be present, and in serious cases, scarring can result.⁷ The case patient’s age and accompanying broad erythema were more consistent with rosacea than acne vulgaris.

Seborrheic dermatitis is a common skin condition usually stemming from an inflammatory reaction to a common yeast. Classic symptoms include scaling and erythema of the scalp and central face, as well as pruritus. Topical antifungals such as ketoconazole 2% cream and 2% shampoo are the mainstay of treatment.⁸ The broad distribution and papulopustules in this patient argue against the diagnosis of seborrheic dermatitis.

Systemic lupus erythematosus is a systemic inflammatory disease that often has cutaneous manifestations. Acute lupus manifests as an erythematous “butterfly rash” across the face and cheeks. Chronic discoid lupus involves depigmented plaques, erythematous macules, telangiectasias, and scarring with loss of normal hair follicles. These findings classically are photodistributed.⁹ The classic broad erythema extending from the cheeks over the bridge of the nose was not present in this patient.

Treatment is primarily topical

Mild cases of rosacea often can be managed with topical antibiotic creams. More severe cases may require systemic antibiotics such as tetracycline or doxycycline, although these are used with caution due to the potential for antibiotic resistance.

Ivermectin 1% cream is a US Food and Drug Administration–approved medication that is applied once daily for up to a year to treat the inflammatory pustules associated with Demodex mites. Although it is costly, studies have shown better results with topical ivermectin than with other topical medications (eg, metronidazole 0.75% gel or cream). However, metronidazole 0.75% gel applied twice daily and oral tetracycline 250 mg or doxycycline 100 mg daily or twice daily for at least 2 months often are utilized when the cost of topical ivermectin is prohibitive.¹⁰

Our patient was treated with a combination of doxycycline 100 mg daily for 30 days and ivermectin 1% cream daily. He was also instructed to apply sunscreen daily. He improved rapidly, and the daily topical ivermectin was discontinued after 6 months.

Ruptured abdominal aortic aneurysms (AAAs) caused about 6000 deaths annually in the United States between 2014 and 2020¹ and are associated with a pooled mortality rate of 81%.² They result from a distinct degenerative process of the layers of the aortic wall.² An AAA is defined as an abdominal aorta whose dilation is > 50% normal (more commonly, a diameter > 3 cm).^3,4 The risk for rupture correlates closely with size; most ruptures occur in aneurysms > 5.5 cm^3,4 (TABLE 1⁵).

Most AAAs are asymptomatic and often go undetected until rupture, resulting in poor outcomes. Because of a low and declining prevalence of AAA and ruptured AAA in developed countries, screening recommendations target high-risk groups rather than the general population.^4,6-8 This review summarizes risk factors, prevalence, and current evidence-based screening and management recommendations for AAA.

Who’s at risk?

Age is the most significant nonmodifiable risk factor, with AAA rupture uncommon in patients younger than 55 years.⁹ One retrospective study found the odds ratio (OR) for diagnosing AAA was 9.41 in adults ages 65 to 69 years (95% CI, 8.76-10.12; P < .0001) and 14.46 (95% CI, 13.45-15.55; P < .0001) in adults ages 70 to 74 years, compared to adults younger than 55 years.¹⁰

Smoking is the most potent modifiable risk factor for AAA. Among patients with AAA, > 90% have a history of smoking.⁴ The association between smoking and AAA is dose dependent, with an OR of 2.61 (95% CI, 2.47-2.74) in patients with a pack-per-year history < 5 years and 12.13 (95% CI, 11.66-12.61) in patients with a pack-per-year history > 35 years, compared to nonsmokers.¹⁰ The risk for AAA increases with smoking duration but decreases with cessation duration.^4,10 Smoking cessation remains an important intervention, as active smokers have higher AAA rupture rates.¹¹

Other risk factors for AAA include concomitant cardiovascular disease (CVD) such as coronary artery disease (CAD), cerebrovascular disease, atherosclerosis, dyslipidemia, and hypertension.¹⁰ Factors associated with reduced risk for AAA include African American race, Hispanic ethnicity, Asian ethnicity, diabetes, smoking cessation, consuming fruits and vegetables > 3 times per week, and exercising more than once per week.^6,10

Prevalence declines but sex-based disparities in outcomes persist

The prevalence of AAA has declined in the United States and Europe in recent decades, correlating with declining rates of smoking.^4,12 Reports published between 2011 and 2019 estimate that AAA prevalence in men older than 60 years has declined over time, with a prevalence of 1.2% to 3.3%.⁶ The prevalence of AAA has also decreased in women,^6,13,14 estimated in 1 study to be as low as 0.74%.¹³ Similarly, deaths from ruptured AAA have declined markedly in the United States—by 70% between 1999 and 2016 according to 1 analysis.⁹

One striking difference in the male-female data is that although AAAs are more common in men, there is a 2- to 4-fold higher risk for rupture in women, who account for nearly half of all AAA-related deaths.^9,10,15-17 The reasons for this heightened risk to women despite lower prevalence are not fully understood but are likely multifactorial and related to a general lack of screening for AAA in women, tendency for AAA to rupture at smaller diameters in women, rupture at an older age in women, and a history of worse surgical outcomes in women than men (though the gap in surgical outcomes appears to be closing).^9,10,18

Continue to: While declines in AAA and AAA-related...

While declines in AAA and AAA-related death are largely attributed to lower smoking rates, other likely contributing factors include the implementation of screening programs, incidental detection during cross-sectional imaging, and improved surgical techniques and management of CV risk factors (eg, hypertension, hyperlipidemia).^9,10

The benefits of screening older men

Randomized controlled trials (RCTs) have demonstrated the benefits of AAA screening programs. A meta-analysis of 4 population­based RCTs of AAA screening in men ≥ 65 years demonstrated statistically significant reductions in AAA rupture (OR = 0.62; 95% CI, 0.55-0.70) and death from AAA (OR = 0.65; 95% CI, 0.57-0.74) over 12 to 15 years, with a number needed to screen (NNS) of 305 (95% CI, 248-411) to prevent 1 AAA-related death.¹⁸ The study also found screening decreases the rate of emergent surgeries for AAA (OR = 0.57; 95% CI, 0.48-0.68) while increasing the number of elective surgeries (OR = 1.44; 95% CI, 1.34-1.55) over 4 to 15 years.¹⁸

Only 1 study has demonstrated an improvement in all-cause mortality with screening programs, with a relatively small benefit (OR = 0.97; 95% CI, 0.94-0.99).¹⁹ Only 1 of the studies included women and, while underpowered, showed no difference in AAA-related death or rupture.²⁰ Guidelines and recommendations of various countries and professional societies focus screening on subgroups at highest risk for AAA.^4,6-8,18

Screening recommendations from USPSTF and others

The US Preventive Services Task Force ­(USPSTF) currently recommends one-time ultrasound screening for AAA in men ages 65 to 75 years who have ever smoked (commonly defined as having smoked > 100 cigarettes) in their lifetime.⁶ This grade “B” recommendation, initially made in 2005 and reaffirmed in the 2014 and 2019 ­USPSTF updates, recommends screening the ­highest-risk segment of the population (ie, older male smokers).⁶

In men ages 65 to 75 years with no smoking history, rather than routine screening, the USPSTF recommends selectively offering screening based on the patient’s medical history, family history, risk factors, and personal values (with a “C” grade).⁶ The USPSTF continues to recommend against screening for AAA in women with no smoking history and no family history of AAA.⁶ According to the USPSTF, the evidence is insufficient to recommend for or against screening women ages 65 to 75 years who have ever smoked or have a family history of AAA (“I” statement).⁶

Continue to: One critique of the USPSTF recommendations

One critique of the USPSTF recommendations is that they fail to detect a significant portion of patients with AAA and AAA rupture. For example, in a retrospective analysis of 55,197 patients undergoing AAA repair, only 33% would have been detected by the USPSTF grade “B” recommendation to screen male smokers ages 65 to 75 years, and an analysis of AAA-related fatalities found 43% would be missed by USPSTF criteria.^9,21

Screening guidelines from the Society for Vascular Surgery (SVS) are broader than those of the USPSTF, in an attempt to capture a larger percentage of the population at risk for AAA-related disease by extrapolating from epidemiologic data. The SVS guidelines include screening for women ages 65 to 75 years with a smoking history, screening men and women ages 65 to 75 years who have a first-degree relative with AAA, and consideration of screening patients older than 75 years if they are in good health and have a first-degree relative with AAA or a smoking history and have not been previously screened.⁴ However, these expanded recommendations are not supported by patient-oriented evidence.⁶

Attempts to broaden screening guidelines must be tempered by potential risks for harm, primarily overdiagnosis (ie, diagnosing AAAs that would not otherwise rise to clinical significance) and overtreatment (ie, resulting in unnecessary imaging, appointments, anxiety, or surgery). Negative psychological effects on quality of life after a diagnosis of AAA have not been shown to cause significant harm.^6,18

A recent UK analysis found that screening programs for AAA in women modeled after those in men are not cost effective, with an NNS to prevent 1 death of 3900 in women vs 700 in men.^15,18 Another recent trial of ultrasound screening in 5200 high-risk women ages 65 to 74 years found an AAA incidence of 0.29% (95% CI, 0.18%-0.48%) in which only 3 large aneurysms were identified.²²

Smoking is the most potent modifiable risk factor for abdominal aortic aneurysm.

In the United States, rates of screening for AAA remain low.²³ One study has shown electronic medical record–based reminders increased screening rates from 48% to 80%.²⁴ Point-of-care bedside ultrasound performed by clinicians also could improve screening rates. Multiple studies have demonstrated that screening and diagnosis of AAA can be performed safely and effectively at the bedside by nonradiologists such as family physicians and emergency physicians.^25-28 In 1 study, such exams added < 4 minutes to the patient encounter.²⁶ Follow-up surveillance schedules for those identified as having a AAA are summarized in TABLE 2.⁴

Continue to: Management options

Management options: Immediate repair or surveillance?

After diagnosing AAA, important decisions must be made regarding management, including indications for surgical repair, appropriate follow-up surveillance, and medications for secondary prevention and cardiovascular risk reduction.

EVAR vs open repair

The 2 main surgical strategies for aneurysm repair are open repair and endovascular repair (EVAR). In the United States, EVAR is becoming the more common approach and was used to repair asymptomatic aneurysms in > 80% of patients and ruptured aneurysms in 50% of patients.⁶ There have been multiple RCTs assessing EVAR and open repair for large and small aneurysms.^29-34 Findings across these studies consistently show EVAR is associated with lower immediate (ie, ­30-day) morbidity and mortality but no ­longer-term survival benefit compared to open repair.

EVAR procedures require ongoing long-term surveillance for endovascular leakage and other complications, resulting in an increased need for re-intervention.^31,33,35 For these reasons, the National Institute for Health and Care Excellence (NICE) guidelines suggest open repair as the preferred modality.⁷ However, SVS and the American College of Cardiology Foundation/American Heart Association guidance support either EVAR or open repair, noting that open repair may be preferable in patients unable to engage in long-term follow-up surveillance.³⁶

Indications for repair. In general, repair is indicated when an aneurysm reaches or exceeds 5.5 cm.^4,7 Both SVS and NICE also recommend clinicians consider surgical repair of smaller, rapidly expanding aneurysms (> 1 cm over a 1-year period).^4,7 Based on evidence suggesting a higher risk for rupture in women with smaller aneurysms,^14,37 SVS recommends clinicians consider surgical repair in women with an AAA ≥ 5.0 cm. Several RCTs evaluating the benefits of immediate repair for smaller-sized aneurysms (4.0-5.5 cm) favored surveillance.^38,39 Accepted indications for surgical repair are summarized in TABLE 3.^4,7,34Surgical repair recommendations also are based on aneurysm morphology, which can be fusiform or saccular (FIGURE). More than 90% of AAAs are fusiform.⁴⁰ Although saccular AAAs are less common, some studies suggest they are more prone to rupture than fusiform AAAs, and SVS guidelines suggest surgical repair of saccular aneurysms regardless of size.^4,41,42

Perioperative and long-term risks. Both EVAR and open repair of AAA carry a high perioperative and long-term risk for death, as patients often have multiple comorbidities. A 2019 trial comparing EVAR to open repair with 14 years of follow-up reported death in 68% of patients in the EVAR group and 70% in the open repair group. ³¹ Among these deaths, 2.7% in the EVAR group and 3.7% in the open repair group were aneurysm related.³¹ The study also found a second surgical intervention was required in 19.8% of patients in the open repair group and 26.7% in the EVAR group.³¹

Continue to: When assessing perioperative risk...

Although abdominal aortic aneurysms are more common in men, there is a 2- to 4-fold higher risk for rupture in women.

When assessing perioperative risk, SVS guidelines recommend clinicians employ a shared decision-making approach with patients that incorporates Vascular Quality Initiative (VQI) mortality risk score.⁴ (VQI risk calculators are available at https://qxmd.com/vascular-study-group-new-england-decision-support-tools.⁴³)

Medication management

Based on the close association of aortic aneurysm with atherosclerotic CVD (ASCVD), professional societies such as the European Society of Cardiology and European Atherosclerosis Society (ESC/EAS) have suggested aortic aneurysm is equivalent to ASCVD and should be managed medically in a similar manner to peripheral arterial disease.⁴⁴ Indeed, many patients with AAA may have concomitant CAD or other arterial vascular diseases (eg, carotid, lower extremity).

Statins. In its guidelines, the ESC/EAS consider patients with AAA at “very high risk” for adverse CV events and suggest pharmacotherapy with high-intensity statins, adding ezetimibe or proprotein convertase ­subtilisin/kexin type 9 (PCSK9) inhibitors if needed, to reduce low-density lipoprotein cholesterol ≥ 50% from baseline, with a goal of < 55 mg/dL.⁴⁴ Statin therapy additionally lowers all-cause postoperative mortality in patients undergoing AAA repair but does not affect the rate of aneurysm expansion.⁴⁵

Aspirin and other anticoagulants. Although aspirin therapy may be indicated for the secondary prevention of other cardiovascular events that may coexist with AAA, it does not appear to affect the rate of growth or prevent rupture of aneurysms.^46,47 In addition to aspirin, anticoagulants such as clopidogrel, enoxaparin, and warfarin are not recommended when the presence of AAA is the only indication.⁴

The USPSTF continues to recommend against screening in women with no smoking history and no family history of abdominal aortic aneurysm.

Other medications. Angiotensin-­converting enzyme inhibitors, angiotensin receptor blockers, beta-blockers, and antibiotics (eg, doxycycline) have been studied as a treatment for AAA. However, none has shown benefit in reducing aneurysm growth or rupture and they are not recommended for that sole purpose.^4,48

Metformin. There is a negative association between diabetes and AAA expansion and rupture. Several cohort studies have indicated that this may be an independent effect driven primarily by exposure to metformin. While it is not unreasonable to consider this another important indication for metformin use in patients with diabetes, RCT evidence has yet to establish a role for metformin in patients without diabetes who have AAA.^48,49

ACKNOWLEDGEMENT
The authors thank Gwen Wilson, MLS, AHIP, for her assistance with the literature searches performed in the preparation of this manuscript.

CORRESPONDENCE
Nicholas LeFevre, MD, Family and Community Medicine, University of Missouri–Columbia School of Medicine, One Hospital Drive, M224 Medical Science Building, Columbia, MO 65212; [email protected]

Ruptured abdominal aortic aneurysms (AAAs) caused about 6000 deaths annually in the United States between 2014 and 2020¹ and are associated with a pooled mortality rate of 81%.² They result from a distinct degenerative process of the layers of the aortic wall.² An AAA is defined as an abdominal aorta whose dilation is > 50% normal (more commonly, a diameter > 3 cm).^3,4 The risk for rupture correlates closely with size; most ruptures occur in aneurysms > 5.5 cm^3,4 (TABLE 1⁵).

Most AAAs are asymptomatic and often go undetected until rupture, resulting in poor outcomes. Because of a low and declining prevalence of AAA and ruptured AAA in developed countries, screening recommendations target high-risk groups rather than the general population.^4,6-8 This review summarizes risk factors, prevalence, and current evidence-based screening and management recommendations for AAA.

Who’s at risk?

Age is the most significant nonmodifiable risk factor, with AAA rupture uncommon in patients younger than 55 years.⁹ One retrospective study found the odds ratio (OR) for diagnosing AAA was 9.41 in adults ages 65 to 69 years (95% CI, 8.76-10.12; P < .0001) and 14.46 (95% CI, 13.45-15.55; P < .0001) in adults ages 70 to 74 years, compared to adults younger than 55 years.¹⁰

Smoking is the most potent modifiable risk factor for AAA. Among patients with AAA, > 90% have a history of smoking.⁴ The association between smoking and AAA is dose dependent, with an OR of 2.61 (95% CI, 2.47-2.74) in patients with a pack-per-year history < 5 years and 12.13 (95% CI, 11.66-12.61) in patients with a pack-per-year history > 35 years, compared to nonsmokers.¹⁰ The risk for AAA increases with smoking duration but decreases with cessation duration.^4,10 Smoking cessation remains an important intervention, as active smokers have higher AAA rupture rates.¹¹

Other risk factors for AAA include concomitant cardiovascular disease (CVD) such as coronary artery disease (CAD), cerebrovascular disease, atherosclerosis, dyslipidemia, and hypertension.¹⁰ Factors associated with reduced risk for AAA include African American race, Hispanic ethnicity, Asian ethnicity, diabetes, smoking cessation, consuming fruits and vegetables > 3 times per week, and exercising more than once per week.^6,10

Prevalence declines but sex-based disparities in outcomes persist

The prevalence of AAA has declined in the United States and Europe in recent decades, correlating with declining rates of smoking.^4,12 Reports published between 2011 and 2019 estimate that AAA prevalence in men older than 60 years has declined over time, with a prevalence of 1.2% to 3.3%.⁶ The prevalence of AAA has also decreased in women,^6,13,14 estimated in 1 study to be as low as 0.74%.¹³ Similarly, deaths from ruptured AAA have declined markedly in the United States—by 70% between 1999 and 2016 according to 1 analysis.⁹

One striking difference in the male-female data is that although AAAs are more common in men, there is a 2- to 4-fold higher risk for rupture in women, who account for nearly half of all AAA-related deaths.^9,10,15-17 The reasons for this heightened risk to women despite lower prevalence are not fully understood but are likely multifactorial and related to a general lack of screening for AAA in women, tendency for AAA to rupture at smaller diameters in women, rupture at an older age in women, and a history of worse surgical outcomes in women than men (though the gap in surgical outcomes appears to be closing).^9,10,18

Continue to: While declines in AAA and AAA-related...

While declines in AAA and AAA-related death are largely attributed to lower smoking rates, other likely contributing factors include the implementation of screening programs, incidental detection during cross-sectional imaging, and improved surgical techniques and management of CV risk factors (eg, hypertension, hyperlipidemia).^9,10

The benefits of screening older men

Randomized controlled trials (RCTs) have demonstrated the benefits of AAA screening programs. A meta-analysis of 4 population­based RCTs of AAA screening in men ≥ 65 years demonstrated statistically significant reductions in AAA rupture (OR = 0.62; 95% CI, 0.55-0.70) and death from AAA (OR = 0.65; 95% CI, 0.57-0.74) over 12 to 15 years, with a number needed to screen (NNS) of 305 (95% CI, 248-411) to prevent 1 AAA-related death.¹⁸ The study also found screening decreases the rate of emergent surgeries for AAA (OR = 0.57; 95% CI, 0.48-0.68) while increasing the number of elective surgeries (OR = 1.44; 95% CI, 1.34-1.55) over 4 to 15 years.¹⁸

Only 1 study has demonstrated an improvement in all-cause mortality with screening programs, with a relatively small benefit (OR = 0.97; 95% CI, 0.94-0.99).¹⁹ Only 1 of the studies included women and, while underpowered, showed no difference in AAA-related death or rupture.²⁰ Guidelines and recommendations of various countries and professional societies focus screening on subgroups at highest risk for AAA.^4,6-8,18

Screening recommendations from USPSTF and others

The US Preventive Services Task Force ­(USPSTF) currently recommends one-time ultrasound screening for AAA in men ages 65 to 75 years who have ever smoked (commonly defined as having smoked > 100 cigarettes) in their lifetime.⁶ This grade “B” recommendation, initially made in 2005 and reaffirmed in the 2014 and 2019 ­USPSTF updates, recommends screening the ­highest-risk segment of the population (ie, older male smokers).⁶

In men ages 65 to 75 years with no smoking history, rather than routine screening, the USPSTF recommends selectively offering screening based on the patient’s medical history, family history, risk factors, and personal values (with a “C” grade).⁶ The USPSTF continues to recommend against screening for AAA in women with no smoking history and no family history of AAA.⁶ According to the USPSTF, the evidence is insufficient to recommend for or against screening women ages 65 to 75 years who have ever smoked or have a family history of AAA (“I” statement).⁶

Continue to: One critique of the USPSTF recommendations

One critique of the USPSTF recommendations is that they fail to detect a significant portion of patients with AAA and AAA rupture. For example, in a retrospective analysis of 55,197 patients undergoing AAA repair, only 33% would have been detected by the USPSTF grade “B” recommendation to screen male smokers ages 65 to 75 years, and an analysis of AAA-related fatalities found 43% would be missed by USPSTF criteria.^9,21

Screening guidelines from the Society for Vascular Surgery (SVS) are broader than those of the USPSTF, in an attempt to capture a larger percentage of the population at risk for AAA-related disease by extrapolating from epidemiologic data. The SVS guidelines include screening for women ages 65 to 75 years with a smoking history, screening men and women ages 65 to 75 years who have a first-degree relative with AAA, and consideration of screening patients older than 75 years if they are in good health and have a first-degree relative with AAA or a smoking history and have not been previously screened.⁴ However, these expanded recommendations are not supported by patient-oriented evidence.⁶

Attempts to broaden screening guidelines must be tempered by potential risks for harm, primarily overdiagnosis (ie, diagnosing AAAs that would not otherwise rise to clinical significance) and overtreatment (ie, resulting in unnecessary imaging, appointments, anxiety, or surgery). Negative psychological effects on quality of life after a diagnosis of AAA have not been shown to cause significant harm.^6,18

A recent UK analysis found that screening programs for AAA in women modeled after those in men are not cost effective, with an NNS to prevent 1 death of 3900 in women vs 700 in men.^15,18 Another recent trial of ultrasound screening in 5200 high-risk women ages 65 to 74 years found an AAA incidence of 0.29% (95% CI, 0.18%-0.48%) in which only 3 large aneurysms were identified.²²

Smoking is the most potent modifiable risk factor for abdominal aortic aneurysm.

In the United States, rates of screening for AAA remain low.²³ One study has shown electronic medical record–based reminders increased screening rates from 48% to 80%.²⁴ Point-of-care bedside ultrasound performed by clinicians also could improve screening rates. Multiple studies have demonstrated that screening and diagnosis of AAA can be performed safely and effectively at the bedside by nonradiologists such as family physicians and emergency physicians.^25-28 In 1 study, such exams added < 4 minutes to the patient encounter.²⁶ Follow-up surveillance schedules for those identified as having a AAA are summarized in TABLE 2.⁴

Continue to: Management options

Management options: Immediate repair or surveillance?

After diagnosing AAA, important decisions must be made regarding management, including indications for surgical repair, appropriate follow-up surveillance, and medications for secondary prevention and cardiovascular risk reduction.

EVAR vs open repair

The 2 main surgical strategies for aneurysm repair are open repair and endovascular repair (EVAR). In the United States, EVAR is becoming the more common approach and was used to repair asymptomatic aneurysms in > 80% of patients and ruptured aneurysms in 50% of patients.⁶ There have been multiple RCTs assessing EVAR and open repair for large and small aneurysms.^29-34 Findings across these studies consistently show EVAR is associated with lower immediate (ie, ­30-day) morbidity and mortality but no ­longer-term survival benefit compared to open repair.

EVAR procedures require ongoing long-term surveillance for endovascular leakage and other complications, resulting in an increased need for re-intervention.^31,33,35 For these reasons, the National Institute for Health and Care Excellence (NICE) guidelines suggest open repair as the preferred modality.⁷ However, SVS and the American College of Cardiology Foundation/American Heart Association guidance support either EVAR or open repair, noting that open repair may be preferable in patients unable to engage in long-term follow-up surveillance.³⁶

Indications for repair. In general, repair is indicated when an aneurysm reaches or exceeds 5.5 cm.^4,7 Both SVS and NICE also recommend clinicians consider surgical repair of smaller, rapidly expanding aneurysms (> 1 cm over a 1-year period).^4,7 Based on evidence suggesting a higher risk for rupture in women with smaller aneurysms,^14,37 SVS recommends clinicians consider surgical repair in women with an AAA ≥ 5.0 cm. Several RCTs evaluating the benefits of immediate repair for smaller-sized aneurysms (4.0-5.5 cm) favored surveillance.^38,39 Accepted indications for surgical repair are summarized in TABLE 3.^4,7,34Surgical repair recommendations also are based on aneurysm morphology, which can be fusiform or saccular (FIGURE). More than 90% of AAAs are fusiform.⁴⁰ Although saccular AAAs are less common, some studies suggest they are more prone to rupture than fusiform AAAs, and SVS guidelines suggest surgical repair of saccular aneurysms regardless of size.^4,41,42

Perioperative and long-term risks. Both EVAR and open repair of AAA carry a high perioperative and long-term risk for death, as patients often have multiple comorbidities. A 2019 trial comparing EVAR to open repair with 14 years of follow-up reported death in 68% of patients in the EVAR group and 70% in the open repair group. ³¹ Among these deaths, 2.7% in the EVAR group and 3.7% in the open repair group were aneurysm related.³¹ The study also found a second surgical intervention was required in 19.8% of patients in the open repair group and 26.7% in the EVAR group.³¹

Continue to: When assessing perioperative risk...

Although abdominal aortic aneurysms are more common in men, there is a 2- to 4-fold higher risk for rupture in women.

When assessing perioperative risk, SVS guidelines recommend clinicians employ a shared decision-making approach with patients that incorporates Vascular Quality Initiative (VQI) mortality risk score.⁴ (VQI risk calculators are available at https://qxmd.com/vascular-study-group-new-england-decision-support-tools.⁴³)

Medication management

Based on the close association of aortic aneurysm with atherosclerotic CVD (ASCVD), professional societies such as the European Society of Cardiology and European Atherosclerosis Society (ESC/EAS) have suggested aortic aneurysm is equivalent to ASCVD and should be managed medically in a similar manner to peripheral arterial disease.⁴⁴ Indeed, many patients with AAA may have concomitant CAD or other arterial vascular diseases (eg, carotid, lower extremity).

Statins. In its guidelines, the ESC/EAS consider patients with AAA at “very high risk” for adverse CV events and suggest pharmacotherapy with high-intensity statins, adding ezetimibe or proprotein convertase ­subtilisin/kexin type 9 (PCSK9) inhibitors if needed, to reduce low-density lipoprotein cholesterol ≥ 50% from baseline, with a goal of < 55 mg/dL.⁴⁴ Statin therapy additionally lowers all-cause postoperative mortality in patients undergoing AAA repair but does not affect the rate of aneurysm expansion.⁴⁵

Aspirin and other anticoagulants. Although aspirin therapy may be indicated for the secondary prevention of other cardiovascular events that may coexist with AAA, it does not appear to affect the rate of growth or prevent rupture of aneurysms.^46,47 In addition to aspirin, anticoagulants such as clopidogrel, enoxaparin, and warfarin are not recommended when the presence of AAA is the only indication.⁴

The USPSTF continues to recommend against screening in women with no smoking history and no family history of abdominal aortic aneurysm.

Other medications. Angiotensin-­converting enzyme inhibitors, angiotensin receptor blockers, beta-blockers, and antibiotics (eg, doxycycline) have been studied as a treatment for AAA. However, none has shown benefit in reducing aneurysm growth or rupture and they are not recommended for that sole purpose.^4,48

Metformin. There is a negative association between diabetes and AAA expansion and rupture. Several cohort studies have indicated that this may be an independent effect driven primarily by exposure to metformin. While it is not unreasonable to consider this another important indication for metformin use in patients with diabetes, RCT evidence has yet to establish a role for metformin in patients without diabetes who have AAA.^48,49

ACKNOWLEDGEMENT
The authors thank Gwen Wilson, MLS, AHIP, for her assistance with the literature searches performed in the preparation of this manuscript.

CORRESPONDENCE
Nicholas LeFevre, MD, Family and Community Medicine, University of Missouri–Columbia School of Medicine, One Hospital Drive, M224 Medical Science Building, Columbia, MO 65212; [email protected]

Ruptured abdominal aortic aneurysms (AAAs) caused about 6000 deaths annually in the United States between 2014 and 2020¹ and are associated with a pooled mortality rate of 81%.² They result from a distinct degenerative process of the layers of the aortic wall.² An AAA is defined as an abdominal aorta whose dilation is > 50% normal (more commonly, a diameter > 3 cm).^3,4 The risk for rupture correlates closely with size; most ruptures occur in aneurysms > 5.5 cm^3,4 (TABLE 1⁵).

Most AAAs are asymptomatic and often go undetected until rupture, resulting in poor outcomes. Because of a low and declining prevalence of AAA and ruptured AAA in developed countries, screening recommendations target high-risk groups rather than the general population.^4,6-8 This review summarizes risk factors, prevalence, and current evidence-based screening and management recommendations for AAA.

Who’s at risk?

Age is the most significant nonmodifiable risk factor, with AAA rupture uncommon in patients younger than 55 years.⁹ One retrospective study found the odds ratio (OR) for diagnosing AAA was 9.41 in adults ages 65 to 69 years (95% CI, 8.76-10.12; P < .0001) and 14.46 (95% CI, 13.45-15.55; P < .0001) in adults ages 70 to 74 years, compared to adults younger than 55 years.¹⁰

Smoking is the most potent modifiable risk factor for AAA. Among patients with AAA, > 90% have a history of smoking.⁴ The association between smoking and AAA is dose dependent, with an OR of 2.61 (95% CI, 2.47-2.74) in patients with a pack-per-year history < 5 years and 12.13 (95% CI, 11.66-12.61) in patients with a pack-per-year history > 35 years, compared to nonsmokers.¹⁰ The risk for AAA increases with smoking duration but decreases with cessation duration.^4,10 Smoking cessation remains an important intervention, as active smokers have higher AAA rupture rates.¹¹

Other risk factors for AAA include concomitant cardiovascular disease (CVD) such as coronary artery disease (CAD), cerebrovascular disease, atherosclerosis, dyslipidemia, and hypertension.¹⁰ Factors associated with reduced risk for AAA include African American race, Hispanic ethnicity, Asian ethnicity, diabetes, smoking cessation, consuming fruits and vegetables > 3 times per week, and exercising more than once per week.^6,10

Prevalence declines but sex-based disparities in outcomes persist

The prevalence of AAA has declined in the United States and Europe in recent decades, correlating with declining rates of smoking.^4,12 Reports published between 2011 and 2019 estimate that AAA prevalence in men older than 60 years has declined over time, with a prevalence of 1.2% to 3.3%.⁶ The prevalence of AAA has also decreased in women,^6,13,14 estimated in 1 study to be as low as 0.74%.¹³ Similarly, deaths from ruptured AAA have declined markedly in the United States—by 70% between 1999 and 2016 according to 1 analysis.⁹

One striking difference in the male-female data is that although AAAs are more common in men, there is a 2- to 4-fold higher risk for rupture in women, who account for nearly half of all AAA-related deaths.^9,10,15-17 The reasons for this heightened risk to women despite lower prevalence are not fully understood but are likely multifactorial and related to a general lack of screening for AAA in women, tendency for AAA to rupture at smaller diameters in women, rupture at an older age in women, and a history of worse surgical outcomes in women than men (though the gap in surgical outcomes appears to be closing).^9,10,18

Continue to: While declines in AAA and AAA-related...

While declines in AAA and AAA-related death are largely attributed to lower smoking rates, other likely contributing factors include the implementation of screening programs, incidental detection during cross-sectional imaging, and improved surgical techniques and management of CV risk factors (eg, hypertension, hyperlipidemia).^9,10

The benefits of screening older men

Randomized controlled trials (RCTs) have demonstrated the benefits of AAA screening programs. A meta-analysis of 4 population­based RCTs of AAA screening in men ≥ 65 years demonstrated statistically significant reductions in AAA rupture (OR = 0.62; 95% CI, 0.55-0.70) and death from AAA (OR = 0.65; 95% CI, 0.57-0.74) over 12 to 15 years, with a number needed to screen (NNS) of 305 (95% CI, 248-411) to prevent 1 AAA-related death.¹⁸ The study also found screening decreases the rate of emergent surgeries for AAA (OR = 0.57; 95% CI, 0.48-0.68) while increasing the number of elective surgeries (OR = 1.44; 95% CI, 1.34-1.55) over 4 to 15 years.¹⁸

Only 1 study has demonstrated an improvement in all-cause mortality with screening programs, with a relatively small benefit (OR = 0.97; 95% CI, 0.94-0.99).¹⁹ Only 1 of the studies included women and, while underpowered, showed no difference in AAA-related death or rupture.²⁰ Guidelines and recommendations of various countries and professional societies focus screening on subgroups at highest risk for AAA.^4,6-8,18

Screening recommendations from USPSTF and others

The US Preventive Services Task Force ­(USPSTF) currently recommends one-time ultrasound screening for AAA in men ages 65 to 75 years who have ever smoked (commonly defined as having smoked > 100 cigarettes) in their lifetime.⁶ This grade “B” recommendation, initially made in 2005 and reaffirmed in the 2014 and 2019 ­USPSTF updates, recommends screening the ­highest-risk segment of the population (ie, older male smokers).⁶

In men ages 65 to 75 years with no smoking history, rather than routine screening, the USPSTF recommends selectively offering screening based on the patient’s medical history, family history, risk factors, and personal values (with a “C” grade).⁶ The USPSTF continues to recommend against screening for AAA in women with no smoking history and no family history of AAA.⁶ According to the USPSTF, the evidence is insufficient to recommend for or against screening women ages 65 to 75 years who have ever smoked or have a family history of AAA (“I” statement).⁶

Continue to: One critique of the USPSTF recommendations

One critique of the USPSTF recommendations is that they fail to detect a significant portion of patients with AAA and AAA rupture. For example, in a retrospective analysis of 55,197 patients undergoing AAA repair, only 33% would have been detected by the USPSTF grade “B” recommendation to screen male smokers ages 65 to 75 years, and an analysis of AAA-related fatalities found 43% would be missed by USPSTF criteria.^9,21

Screening guidelines from the Society for Vascular Surgery (SVS) are broader than those of the USPSTF, in an attempt to capture a larger percentage of the population at risk for AAA-related disease by extrapolating from epidemiologic data. The SVS guidelines include screening for women ages 65 to 75 years with a smoking history, screening men and women ages 65 to 75 years who have a first-degree relative with AAA, and consideration of screening patients older than 75 years if they are in good health and have a first-degree relative with AAA or a smoking history and have not been previously screened.⁴ However, these expanded recommendations are not supported by patient-oriented evidence.⁶

Attempts to broaden screening guidelines must be tempered by potential risks for harm, primarily overdiagnosis (ie, diagnosing AAAs that would not otherwise rise to clinical significance) and overtreatment (ie, resulting in unnecessary imaging, appointments, anxiety, or surgery). Negative psychological effects on quality of life after a diagnosis of AAA have not been shown to cause significant harm.^6,18

A recent UK analysis found that screening programs for AAA in women modeled after those in men are not cost effective, with an NNS to prevent 1 death of 3900 in women vs 700 in men.^15,18 Another recent trial of ultrasound screening in 5200 high-risk women ages 65 to 74 years found an AAA incidence of 0.29% (95% CI, 0.18%-0.48%) in which only 3 large aneurysms were identified.²²

Smoking is the most potent modifiable risk factor for abdominal aortic aneurysm.

In the United States, rates of screening for AAA remain low.²³ One study has shown electronic medical record–based reminders increased screening rates from 48% to 80%.²⁴ Point-of-care bedside ultrasound performed by clinicians also could improve screening rates. Multiple studies have demonstrated that screening and diagnosis of AAA can be performed safely and effectively at the bedside by nonradiologists such as family physicians and emergency physicians.^25-28 In 1 study, such exams added < 4 minutes to the patient encounter.²⁶ Follow-up surveillance schedules for those identified as having a AAA are summarized in TABLE 2.⁴

Continue to: Management options

Management options: Immediate repair or surveillance?

After diagnosing AAA, important decisions must be made regarding management, including indications for surgical repair, appropriate follow-up surveillance, and medications for secondary prevention and cardiovascular risk reduction.

EVAR vs open repair

The 2 main surgical strategies for aneurysm repair are open repair and endovascular repair (EVAR). In the United States, EVAR is becoming the more common approach and was used to repair asymptomatic aneurysms in > 80% of patients and ruptured aneurysms in 50% of patients.⁶ There have been multiple RCTs assessing EVAR and open repair for large and small aneurysms.^29-34 Findings across these studies consistently show EVAR is associated with lower immediate (ie, ­30-day) morbidity and mortality but no ­longer-term survival benefit compared to open repair.

EVAR procedures require ongoing long-term surveillance for endovascular leakage and other complications, resulting in an increased need for re-intervention.^31,33,35 For these reasons, the National Institute for Health and Care Excellence (NICE) guidelines suggest open repair as the preferred modality.⁷ However, SVS and the American College of Cardiology Foundation/American Heart Association guidance support either EVAR or open repair, noting that open repair may be preferable in patients unable to engage in long-term follow-up surveillance.³⁶

Indications for repair. In general, repair is indicated when an aneurysm reaches or exceeds 5.5 cm.^4,7 Both SVS and NICE also recommend clinicians consider surgical repair of smaller, rapidly expanding aneurysms (> 1 cm over a 1-year period).^4,7 Based on evidence suggesting a higher risk for rupture in women with smaller aneurysms,^14,37 SVS recommends clinicians consider surgical repair in women with an AAA ≥ 5.0 cm. Several RCTs evaluating the benefits of immediate repair for smaller-sized aneurysms (4.0-5.5 cm) favored surveillance.^38,39 Accepted indications for surgical repair are summarized in TABLE 3.^4,7,34Surgical repair recommendations also are based on aneurysm morphology, which can be fusiform or saccular (FIGURE). More than 90% of AAAs are fusiform.⁴⁰ Although saccular AAAs are less common, some studies suggest they are more prone to rupture than fusiform AAAs, and SVS guidelines suggest surgical repair of saccular aneurysms regardless of size.^4,41,42

Perioperative and long-term risks. Both EVAR and open repair of AAA carry a high perioperative and long-term risk for death, as patients often have multiple comorbidities. A 2019 trial comparing EVAR to open repair with 14 years of follow-up reported death in 68% of patients in the EVAR group and 70% in the open repair group. ³¹ Among these deaths, 2.7% in the EVAR group and 3.7% in the open repair group were aneurysm related.³¹ The study also found a second surgical intervention was required in 19.8% of patients in the open repair group and 26.7% in the EVAR group.³¹

Continue to: When assessing perioperative risk...

Although abdominal aortic aneurysms are more common in men, there is a 2- to 4-fold higher risk for rupture in women.

When assessing perioperative risk, SVS guidelines recommend clinicians employ a shared decision-making approach with patients that incorporates Vascular Quality Initiative (VQI) mortality risk score.⁴ (VQI risk calculators are available at https://qxmd.com/vascular-study-group-new-england-decision-support-tools.⁴³)

Medication management

Based on the close association of aortic aneurysm with atherosclerotic CVD (ASCVD), professional societies such as the European Society of Cardiology and European Atherosclerosis Society (ESC/EAS) have suggested aortic aneurysm is equivalent to ASCVD and should be managed medically in a similar manner to peripheral arterial disease.⁴⁴ Indeed, many patients with AAA may have concomitant CAD or other arterial vascular diseases (eg, carotid, lower extremity).

Statins. In its guidelines, the ESC/EAS consider patients with AAA at “very high risk” for adverse CV events and suggest pharmacotherapy with high-intensity statins, adding ezetimibe or proprotein convertase ­subtilisin/kexin type 9 (PCSK9) inhibitors if needed, to reduce low-density lipoprotein cholesterol ≥ 50% from baseline, with a goal of < 55 mg/dL.⁴⁴ Statin therapy additionally lowers all-cause postoperative mortality in patients undergoing AAA repair but does not affect the rate of aneurysm expansion.⁴⁵

Aspirin and other anticoagulants. Although aspirin therapy may be indicated for the secondary prevention of other cardiovascular events that may coexist with AAA, it does not appear to affect the rate of growth or prevent rupture of aneurysms.^46,47 In addition to aspirin, anticoagulants such as clopidogrel, enoxaparin, and warfarin are not recommended when the presence of AAA is the only indication.⁴

The USPSTF continues to recommend against screening in women with no smoking history and no family history of abdominal aortic aneurysm.

Other medications. Angiotensin-­converting enzyme inhibitors, angiotensin receptor blockers, beta-blockers, and antibiotics (eg, doxycycline) have been studied as a treatment for AAA. However, none has shown benefit in reducing aneurysm growth or rupture and they are not recommended for that sole purpose.^4,48

Metformin. There is a negative association between diabetes and AAA expansion and rupture. Several cohort studies have indicated that this may be an independent effect driven primarily by exposure to metformin. While it is not unreasonable to consider this another important indication for metformin use in patients with diabetes, RCT evidence has yet to establish a role for metformin in patients without diabetes who have AAA.^48,49

ACKNOWLEDGEMENT
The authors thank Gwen Wilson, MLS, AHIP, for her assistance with the literature searches performed in the preparation of this manuscript.

CORRESPONDENCE
Nicholas LeFevre, MD, Family and Community Medicine, University of Missouri–Columbia School of Medicine, One Hospital Drive, M224 Medical Science Building, Columbia, MO 65212; [email protected]