The Journal of Family Practice

A wet prep demonstrated clue cells in more than half of the epithelial cells and the FP diagnosed bacterial vaginosis (BV). BV is a clinical syndrome resulting from an alteration of the vaginal ecosystem. The odor of BV is caused by the aromatic amines produced by the altered bacterial flora in the vagina. Women with BV are at increased risk for human immunodeficiency virus, Neisseria gonorrhoeae, Chlamydia trachomatis, and herpes simplex virus-2, and they have an increased risk of complications after gynecologic surgery. BV is also associated with adverse pregnancy outcomes.

The FP recommended that the patient stop douching because it wouldn’t prevent or treat infections and could unfavorably influence the vaginal microscopic ecosystem. In this case, the patient had good results after being treated with oral metronidazole 500 mg bid for 7 days.

Photos and text for Photo Rounds Friday courtesy of Richard P. Usatine, MD. This case was adapted from: Mayeaux EJ. Bacterial vaginosis. In: Usatine R, Smith M, Mayeaux EJ, et al, eds. Color Atlas of Family Medicine. 2nd ed. New York, NY: McGraw-Hill; 2013:494-498.

To learn more about the Color Atlas of Family Medicine, see: http://www.amazon.com/Color-Family-Medicine-Richard-Usatine/dp/0071769641/

You can now get the second edition of the Color Atlas of Family Medicine as an app by clicking on this link: http://usatinemedia.com/

A wet prep demonstrated clue cells in more than half of the epithelial cells and the FP diagnosed bacterial vaginosis (BV). BV is a clinical syndrome resulting from an alteration of the vaginal ecosystem. The odor of BV is caused by the aromatic amines produced by the altered bacterial flora in the vagina. Women with BV are at increased risk for human immunodeficiency virus, Neisseria gonorrhoeae, Chlamydia trachomatis, and herpes simplex virus-2, and they have an increased risk of complications after gynecologic surgery. BV is also associated with adverse pregnancy outcomes.

The FP recommended that the patient stop douching because it wouldn’t prevent or treat infections and could unfavorably influence the vaginal microscopic ecosystem. In this case, the patient had good results after being treated with oral metronidazole 500 mg bid for 7 days.

Photos and text for Photo Rounds Friday courtesy of Richard P. Usatine, MD. This case was adapted from: Mayeaux EJ. Bacterial vaginosis. In: Usatine R, Smith M, Mayeaux EJ, et al, eds. Color Atlas of Family Medicine. 2nd ed. New York, NY: McGraw-Hill; 2013:494-498.

To learn more about the Color Atlas of Family Medicine, see: http://www.amazon.com/Color-Family-Medicine-Richard-Usatine/dp/0071769641/

You can now get the second edition of the Color Atlas of Family Medicine as an app by clicking on this link: http://usatinemedia.com/

A wet prep demonstrated clue cells in more than half of the epithelial cells and the FP diagnosed bacterial vaginosis (BV). BV is a clinical syndrome resulting from an alteration of the vaginal ecosystem. The odor of BV is caused by the aromatic amines produced by the altered bacterial flora in the vagina. Women with BV are at increased risk for human immunodeficiency virus, Neisseria gonorrhoeae, Chlamydia trachomatis, and herpes simplex virus-2, and they have an increased risk of complications after gynecologic surgery. BV is also associated with adverse pregnancy outcomes.

The FP recommended that the patient stop douching because it wouldn’t prevent or treat infections and could unfavorably influence the vaginal microscopic ecosystem. In this case, the patient had good results after being treated with oral metronidazole 500 mg bid for 7 days.

Photos and text for Photo Rounds Friday courtesy of Richard P. Usatine, MD. This case was adapted from: Mayeaux EJ. Bacterial vaginosis. In: Usatine R, Smith M, Mayeaux EJ, et al, eds. Color Atlas of Family Medicine. 2nd ed. New York, NY: McGraw-Hill; 2013:494-498.

To learn more about the Color Atlas of Family Medicine, see: http://www.amazon.com/Color-Family-Medicine-Richard-Usatine/dp/0071769641/

You can now get the second edition of the Color Atlas of Family Medicine as an app by clicking on this link: http://usatinemedia.com/

The patient was given a diagnosis of lichen sclerosus, which is recognized by the hour-glass configuration of the atrophy around the vulva and perianal region. (Some atrophic changes of the vulva that can be mistaken for the atrophy of estrogen deficiency.)

Lichen sclerosus is not contagious and typically affects postmenopausal women. It's unclear what causes the condition.

Lichen sclerosus is treated with a high-potency steroid ointment (such as clobetasol) rather than estrogen or topical testosterone. Studies have demonstrated that high-potency topical steroid ointments are the most effective treatment and do not cause atrophy as an adverse effect. While topical testosterone was used in the past, it has not been proven effective and should no longer be prescribed.

The topical steroid should be applied twice daily and tapered to once daily followed by an as-needed regimen based on symptoms.

There is a higher risk of vaginal intraepithelial neoplasia and squamous cell carcinoma in patients with genital lichen sclerosus. Yearly examination for premalignant and malignant changes of the external genitalia is recommended. Areas with thick leukoplakia, mucosal ulcerations, and erythroplakia should be biopsied to rule out malignancy.

Photos and text for Photo Rounds Friday courtesy of Richard P. Usatine, MD. This case was adapted from: Mayeaux EJ. Atrophic vaginitis. In: Usatine R, Smith M, Mayeaux EJ, et al, eds. Color Atlas of Family Medicine. 2nd ed. New York, NY: McGraw-Hill; 2013:489-493.

To learn more about the Color Atlas of Family Medicine, see: http://www.amazon.com/Color-Family-Medicine-Richard-Usatine/dp/0071769641/

You can now get the second edition of the Color Atlas of Family Medicine as an app by clicking on this link: http://usatinemedia.com/ 

The patient was given a diagnosis of lichen sclerosus, which is recognized by the hour-glass configuration of the atrophy around the vulva and perianal region. (Some atrophic changes of the vulva that can be mistaken for the atrophy of estrogen deficiency.)

Lichen sclerosus is not contagious and typically affects postmenopausal women. It's unclear what causes the condition.

Lichen sclerosus is treated with a high-potency steroid ointment (such as clobetasol) rather than estrogen or topical testosterone. Studies have demonstrated that high-potency topical steroid ointments are the most effective treatment and do not cause atrophy as an adverse effect. While topical testosterone was used in the past, it has not been proven effective and should no longer be prescribed.

The topical steroid should be applied twice daily and tapered to once daily followed by an as-needed regimen based on symptoms.

There is a higher risk of vaginal intraepithelial neoplasia and squamous cell carcinoma in patients with genital lichen sclerosus. Yearly examination for premalignant and malignant changes of the external genitalia is recommended. Areas with thick leukoplakia, mucosal ulcerations, and erythroplakia should be biopsied to rule out malignancy.

Photos and text for Photo Rounds Friday courtesy of Richard P. Usatine, MD. This case was adapted from: Mayeaux EJ. Atrophic vaginitis. In: Usatine R, Smith M, Mayeaux EJ, et al, eds. Color Atlas of Family Medicine. 2nd ed. New York, NY: McGraw-Hill; 2013:489-493.

To learn more about the Color Atlas of Family Medicine, see: http://www.amazon.com/Color-Family-Medicine-Richard-Usatine/dp/0071769641/

You can now get the second edition of the Color Atlas of Family Medicine as an app by clicking on this link: http://usatinemedia.com/ 

The patient was given a diagnosis of lichen sclerosus, which is recognized by the hour-glass configuration of the atrophy around the vulva and perianal region. (Some atrophic changes of the vulva that can be mistaken for the atrophy of estrogen deficiency.)

Lichen sclerosus is not contagious and typically affects postmenopausal women. It's unclear what causes the condition.

Lichen sclerosus is treated with a high-potency steroid ointment (such as clobetasol) rather than estrogen or topical testosterone. Studies have demonstrated that high-potency topical steroid ointments are the most effective treatment and do not cause atrophy as an adverse effect. While topical testosterone was used in the past, it has not been proven effective and should no longer be prescribed.

The topical steroid should be applied twice daily and tapered to once daily followed by an as-needed regimen based on symptoms.

There is a higher risk of vaginal intraepithelial neoplasia and squamous cell carcinoma in patients with genital lichen sclerosus. Yearly examination for premalignant and malignant changes of the external genitalia is recommended. Areas with thick leukoplakia, mucosal ulcerations, and erythroplakia should be biopsied to rule out malignancy.

Photos and text for Photo Rounds Friday courtesy of Richard P. Usatine, MD. This case was adapted from: Mayeaux EJ. Atrophic vaginitis. In: Usatine R, Smith M, Mayeaux EJ, et al, eds. Color Atlas of Family Medicine. 2nd ed. New York, NY: McGraw-Hill; 2013:489-493.

To learn more about the Color Atlas of Family Medicine, see: http://www.amazon.com/Color-Family-Medicine-Richard-Usatine/dp/0071769641/

You can now get the second edition of the Color Atlas of Family Medicine as an app by clicking on this link: http://usatinemedia.com/ 

Foot ulcers and other lower-limb complications secondary to diabetes are common, complex, costly, and associated with increased morbidity and mortality.^1-6 Unfortunately, patients often have difficulty recognizing the heightened risk status that accompanies the diagnosis of diabetes, particularly the substantial risk for lower limb complications.⁷ In addition, loss of protective sensation (LOPS) can render patients unable to recognize damage to their lower extremities, thus creating a cycle of tissue damage and other foot complications. Strong evidence suggests that consistent provision of foot-care services and preventive care can reduce amputations among patients with diabetes.^7-9 However, routine foot examination and rapid risk stratification is often difficult to incorporate into busy primary care settings. Data suggest that the diabetic foot is adequately evaluated only 12% to 20% of the time.¹⁰

In response to the need for more consistent foot exams, an American Diabetes Association (ADA) task force lead by 2 of the authors of this article (AB and DA) created the Comprehensive Foot Examination and Risk Assessment.⁵ This set the standard for the detailed investigation of lower limb pathology by a specialist, but was not well suited for other practice settings, including primary care. One reason is that it would be difficult to complete the comprehensive examination during a typical 15-minute primary care office visit. In addition, certain examination parameters require the use of neurologic and vascular assessment equipment and training not available in all health care settings.¹¹

This exam takes substantially less time to complete than
 a comprehensive exam and eliminates common barriers to frequent assessment. With these thoughts in mind, we set out to develop an exam that could be done by a wide range of health care providers—one that takes substantially less time to complete than a comprehensive exam and eliminates common barriers to frequent assessment. The exam, which we’ll describe here, consists of 3 components: taking a patient history, performing a physical exam, and providing patient education. And best of all, it should only take 3 minutes.

The patient history (1 minute)

Patients may present with concerns about their feet, but may not be able to differentiate between benign and threatening symptoms. A thorough medical history can identify factors that may increase patients’ risk of developing lower-limb complications. Reviewing the patient’s medical history also can help guide the physical exam.

Review the patient’s diabetic history, blood glucose control, and previous diabetic complications. Ask patients about their history of peripheral vascular disease, quality of peripheral protective sensation, and previous lower-limb interventions and operations (TABLE 1^5,12). Patients with diabetes and suboptimal glycemic control have an increased risk for LOPS, chronic and recalcitrant ulcers, and wound infections.² Additionally, patients with diabetes and a previous lower extremity amputation are at high risk for reulceration.^5,12 Lastly, nicotine use and smoking are common pathogenic risk factors that contribute to peripheral artery disease (PAD).¹³

Physical examination (1 minute)

Careful inspection of the feet should be performed at every visit for patients with confirmed or suspected diabetes. Because up to 50% of patients with significant sensory loss due to neuropathy may be completely asymptomatic,¹⁴ failing to search for early signs of infection (FIGURE 1), skin breakdown, ulcer formation (FIGURE 2), skin temperature changes, and inadequate vascular perfusion may allow complications to develop.⁵ TABLE 2^5,15,16 outlines the essential components—dermatologic, neurologic, musculoskeletal, and vascular—of a rapid lower limb physical exam.

The dermatologic exam. This serves as a barometer for early intervention, and often results in a limb-saving referral to a specialist. Carefully 
examine the areas 
between the 
toes, where
 deeper lesions
 may go
 unnoticed. It should begin with a global inspection for discolorations, calluses, wounds, fissures, macerations, nail dystrophy, or paronychia.⁵ Skin discoloration or loss of hair growth may be the first signs of vascular insufficiency, while calluses and hypertrophic skin often are precursors to ulcers.^5,17-19 Inspection of the toes should include a search for fungal, ingrown, or elongated nails. Carefully examine the areas between the toes, where deeper lesions may go unnoticed.⁵

The neurologic exam. Without protective sensation, patients with neuropathy are at a heightened risk of unrecognized injury and are unlikely to mention their deformities to medical staff.^20-23 Consequently, skin deterioration may unknowingly progress to ulceration that requires extensive medical intervention or amputation.

Neuropathic LOPS is easily detectable, yet it is linked to at least 75% of all nontraumatic diabetic amputations.^20-23 Adiminished vibratory perception threshold (VPT) is one of the earliest indicators of neuropathic LOPS and is the best predictor of long-term lower extremity complications.^1,24,25 However, VPT devices are expensive and time-consuming to operate, and they require training to ensure proper use. The Semmes-Weinstein monofilament is a well-documented alternative to VPT for predicting ulcer risk^26-28 and has long been advocated as an essential component of a thorough foot exam.⁵ The 128 Hz tuning fork is another regularly used alternative.⁵ However, physicians would need to purchase one of these devices and receive training on how to use it, and, in the case of the monofilament, to regularly stock replacements to maintain accurate results.¹⁶

No testing devices are needed to conduct the Ipswich Touch Test, and it is as sensitive and specific as the monofilament test. The Ipswich Touch Test (IpTT) is an alternative neurologic test that requires only the physician’s index finger. During the IpTT, the physician instructs the patient to close his or her eyes while the physician lightly rests his or her finger on each of the patient’s first, third, and fifth toes for 1 to 2 seconds (FIGURE 3). Patients are instructed to respond with a “yes” when they feel the physician’s touch. In a head-to-head trial, diagnostic results of the IpTT directly paralleled those of the monofilament in detecting LOPS; IpTT was also equally sensitive and specific (k=.88, indicating almost perfect agreement; P<.0001).²⁹ The IpTT’s use of only 6 palpation points, constant availability, and accuracy make it a first-line neurologic test for rapidly screening the feet of a patient with diabetes.

Neuromuscular/musculoskeletal exam. Neuromuscular disturbances, such as a reduction in the strength of dorsiflexion and plantar flexion, may indicate a complicated neurologic compromise.⁵ In addition to being aesthetically problematic, musculoskeletal deformities such as a hammer toe, claw toe (FIGURE 4), or bunion can cause significant pain and/or gait disturbance, and can increase patients’ risk for ulceration.³⁰ These deformities also may compromise patients’ general health and grossly escalate their risk of falls and resultant injuries.^5,31 Therefore, patients who present with previously unreported musculoskeletal deformities should be referred to a specialist.³¹

Charcot neuroarthropathy is
 a devastating complication that classically presents as a hot, red, swollen foot; the redness resolves upon elevation. Also screen patients for Charcot neuroarthropathy (FIGURE 5), a devastating complication that classically presents as a hot, red, swollen foot; the redness resolves upon elevation.³² Charcot neuroarthropathy is hypothesized to be a dysregulation of normal bone metabolism typically occurring secondary to diabetic neuropathy and repetitive minor trauma.^33,34 This dysregulation leads to joint instability and disorganization of normal midfoot bone architecture.^31,32 Charcot neuroarthropathy is an urgent pathology that requires management by a foot specialist.³⁵

Vascular exam. PAD is particularly common in patients with diabetes and contributes to the development of impaired healing in up to half of foot ulcers.^13,18,36-39 Bilateral femoral, popliteal, posterior tibial, or dorsalis pedis pulses should be assessed by palpation; a diminished or absent pulse is a key indicator of vascular compromise.^40,41 An integrated care approach between foot specialists and vascular surgeons results in optimal treatment.

Patient education (1 minute)

It is imperative to include patients in their treatment process to reduce the likelihood of complications and, ultimately, decrease the incidence of amputations.^12,42 Patient education improves patients’ self-reported home care behaviors, even at the most fundamental levels.^43,44 TABLE 3^5,15,45 lists topics to cover during patient education.

A lack of appropriate patient education regarding diabetes is a factor in >90% of recurrent ulcers.Patients’ lack of understanding about self-care for diabetes is a common barrier to prevention.²³ El-Nahas et al⁴⁶ found a lack of appropriate education regarding diabetes was a factor in more than 90% of recurrent ulcers, which emphasizes the need for repeated education for at-risk patients.^47,48 Involve all levels of medical staff in the effort to educate patients on the importance of foot screenings, both at home and in-office. Even with proper patient education, many patients may be in various stages of coping with this all-consuming yet frequently asymptomatic condition, which makes the need for repeated patient education even more critical.

Who to refer, and when

After completing the 3-minute foot exam, create a treatment and follow-up plan, focusing on the need for referral to a specialist. TABLE 4 outlines suggested indications, priorities, and timelines for referral based on ADA guidelines.⁵ It incorporates the ADA’s patient risk categories (very low, low, moderate, and high risk) and also provides a recommended frequency for patient follow-ups.

Care for patients with lower extremity complications of diabetes mellitus is time-consuming and expensive. The brief exam described here can help you to rapidly identify patients at risk for these complications and prompt you to provide timely referrals to appropriate specialists.

CORRESPONDENCE
David G. Armstrong, DPM, MD, PhD, Professor, Department of Surgery, Director, Southern Arizona Limb Salvage Alliance (SALSA), 1501 N. Campbell Avenue, Tucson, AZ 85724-5072; armstrong@usa.net

Foot ulcers and other lower-limb complications secondary to diabetes are common, complex, costly, and associated with increased morbidity and mortality.^1-6 Unfortunately, patients often have difficulty recognizing the heightened risk status that accompanies the diagnosis of diabetes, particularly the substantial risk for lower limb complications.⁷ In addition, loss of protective sensation (LOPS) can render patients unable to recognize damage to their lower extremities, thus creating a cycle of tissue damage and other foot complications. Strong evidence suggests that consistent provision of foot-care services and preventive care can reduce amputations among patients with diabetes.^7-9 However, routine foot examination and rapid risk stratification is often difficult to incorporate into busy primary care settings. Data suggest that the diabetic foot is adequately evaluated only 12% to 20% of the time.¹⁰

In response to the need for more consistent foot exams, an American Diabetes Association (ADA) task force lead by 2 of the authors of this article (AB and DA) created the Comprehensive Foot Examination and Risk Assessment.⁵ This set the standard for the detailed investigation of lower limb pathology by a specialist, but was not well suited for other practice settings, including primary care. One reason is that it would be difficult to complete the comprehensive examination during a typical 15-minute primary care office visit. In addition, certain examination parameters require the use of neurologic and vascular assessment equipment and training not available in all health care settings.¹¹

This exam takes substantially less time to complete than
 a comprehensive exam and eliminates common barriers to frequent assessment. With these thoughts in mind, we set out to develop an exam that could be done by a wide range of health care providers—one that takes substantially less time to complete than a comprehensive exam and eliminates common barriers to frequent assessment. The exam, which we’ll describe here, consists of 3 components: taking a patient history, performing a physical exam, and providing patient education. And best of all, it should only take 3 minutes.

The patient history (1 minute)

Patients may present with concerns about their feet, but may not be able to differentiate between benign and threatening symptoms. A thorough medical history can identify factors that may increase patients’ risk of developing lower-limb complications. Reviewing the patient’s medical history also can help guide the physical exam.

Review the patient’s diabetic history, blood glucose control, and previous diabetic complications. Ask patients about their history of peripheral vascular disease, quality of peripheral protective sensation, and previous lower-limb interventions and operations (TABLE 1^5,12). Patients with diabetes and suboptimal glycemic control have an increased risk for LOPS, chronic and recalcitrant ulcers, and wound infections.² Additionally, patients with diabetes and a previous lower extremity amputation are at high risk for reulceration.^5,12 Lastly, nicotine use and smoking are common pathogenic risk factors that contribute to peripheral artery disease (PAD).¹³

Physical examination (1 minute)

Careful inspection of the feet should be performed at every visit for patients with confirmed or suspected diabetes. Because up to 50% of patients with significant sensory loss due to neuropathy may be completely asymptomatic,¹⁴ failing to search for early signs of infection (FIGURE 1), skin breakdown, ulcer formation (FIGURE 2), skin temperature changes, and inadequate vascular perfusion may allow complications to develop.⁵ TABLE 2^5,15,16 outlines the essential components—dermatologic, neurologic, musculoskeletal, and vascular—of a rapid lower limb physical exam.

The dermatologic exam. This serves as a barometer for early intervention, and often results in a limb-saving referral to a specialist. Carefully 
examine the areas 
between the 
toes, where
 deeper lesions
 may go
 unnoticed. It should begin with a global inspection for discolorations, calluses, wounds, fissures, macerations, nail dystrophy, or paronychia.⁵ Skin discoloration or loss of hair growth may be the first signs of vascular insufficiency, while calluses and hypertrophic skin often are precursors to ulcers.^5,17-19 Inspection of the toes should include a search for fungal, ingrown, or elongated nails. Carefully examine the areas between the toes, where deeper lesions may go unnoticed.⁵

The neurologic exam. Without protective sensation, patients with neuropathy are at a heightened risk of unrecognized injury and are unlikely to mention their deformities to medical staff.^20-23 Consequently, skin deterioration may unknowingly progress to ulceration that requires extensive medical intervention or amputation.

Neuropathic LOPS is easily detectable, yet it is linked to at least 75% of all nontraumatic diabetic amputations.^20-23 Adiminished vibratory perception threshold (VPT) is one of the earliest indicators of neuropathic LOPS and is the best predictor of long-term lower extremity complications.^1,24,25 However, VPT devices are expensive and time-consuming to operate, and they require training to ensure proper use. The Semmes-Weinstein monofilament is a well-documented alternative to VPT for predicting ulcer risk^26-28 and has long been advocated as an essential component of a thorough foot exam.⁵ The 128 Hz tuning fork is another regularly used alternative.⁵ However, physicians would need to purchase one of these devices and receive training on how to use it, and, in the case of the monofilament, to regularly stock replacements to maintain accurate results.¹⁶

No testing devices are needed to conduct the Ipswich Touch Test, and it is as sensitive and specific as the monofilament test. The Ipswich Touch Test (IpTT) is an alternative neurologic test that requires only the physician’s index finger. During the IpTT, the physician instructs the patient to close his or her eyes while the physician lightly rests his or her finger on each of the patient’s first, third, and fifth toes for 1 to 2 seconds (FIGURE 3). Patients are instructed to respond with a “yes” when they feel the physician’s touch. In a head-to-head trial, diagnostic results of the IpTT directly paralleled those of the monofilament in detecting LOPS; IpTT was also equally sensitive and specific (k=.88, indicating almost perfect agreement; P<.0001).²⁹ The IpTT’s use of only 6 palpation points, constant availability, and accuracy make it a first-line neurologic test for rapidly screening the feet of a patient with diabetes.

Neuromuscular/musculoskeletal exam. Neuromuscular disturbances, such as a reduction in the strength of dorsiflexion and plantar flexion, may indicate a complicated neurologic compromise.⁵ In addition to being aesthetically problematic, musculoskeletal deformities such as a hammer toe, claw toe (FIGURE 4), or bunion can cause significant pain and/or gait disturbance, and can increase patients’ risk for ulceration.³⁰ These deformities also may compromise patients’ general health and grossly escalate their risk of falls and resultant injuries.^5,31 Therefore, patients who present with previously unreported musculoskeletal deformities should be referred to a specialist.³¹

Charcot neuroarthropathy is
 a devastating complication that classically presents as a hot, red, swollen foot; the redness resolves upon elevation. Also screen patients for Charcot neuroarthropathy (FIGURE 5), a devastating complication that classically presents as a hot, red, swollen foot; the redness resolves upon elevation.³² Charcot neuroarthropathy is hypothesized to be a dysregulation of normal bone metabolism typically occurring secondary to diabetic neuropathy and repetitive minor trauma.^33,34 This dysregulation leads to joint instability and disorganization of normal midfoot bone architecture.^31,32 Charcot neuroarthropathy is an urgent pathology that requires management by a foot specialist.³⁵

Vascular exam. PAD is particularly common in patients with diabetes and contributes to the development of impaired healing in up to half of foot ulcers.^13,18,36-39 Bilateral femoral, popliteal, posterior tibial, or dorsalis pedis pulses should be assessed by palpation; a diminished or absent pulse is a key indicator of vascular compromise.^40,41 An integrated care approach between foot specialists and vascular surgeons results in optimal treatment.

Patient education (1 minute)

It is imperative to include patients in their treatment process to reduce the likelihood of complications and, ultimately, decrease the incidence of amputations.^12,42 Patient education improves patients’ self-reported home care behaviors, even at the most fundamental levels.^43,44 TABLE 3^5,15,45 lists topics to cover during patient education.

A lack of appropriate patient education regarding diabetes is a factor in >90% of recurrent ulcers.Patients’ lack of understanding about self-care for diabetes is a common barrier to prevention.²³ El-Nahas et al⁴⁶ found a lack of appropriate education regarding diabetes was a factor in more than 90% of recurrent ulcers, which emphasizes the need for repeated education for at-risk patients.^47,48 Involve all levels of medical staff in the effort to educate patients on the importance of foot screenings, both at home and in-office. Even with proper patient education, many patients may be in various stages of coping with this all-consuming yet frequently asymptomatic condition, which makes the need for repeated patient education even more critical.

Who to refer, and when

After completing the 3-minute foot exam, create a treatment and follow-up plan, focusing on the need for referral to a specialist. TABLE 4 outlines suggested indications, priorities, and timelines for referral based on ADA guidelines.⁵ It incorporates the ADA’s patient risk categories (very low, low, moderate, and high risk) and also provides a recommended frequency for patient follow-ups.

Care for patients with lower extremity complications of diabetes mellitus is time-consuming and expensive. The brief exam described here can help you to rapidly identify patients at risk for these complications and prompt you to provide timely referrals to appropriate specialists.

CORRESPONDENCE
David G. Armstrong, DPM, MD, PhD, Professor, Department of Surgery, Director, Southern Arizona Limb Salvage Alliance (SALSA), 1501 N. Campbell Avenue, Tucson, AZ 85724-5072; armstrong@usa.net

Foot ulcers and other lower-limb complications secondary to diabetes are common, complex, costly, and associated with increased morbidity and mortality.^1-6 Unfortunately, patients often have difficulty recognizing the heightened risk status that accompanies the diagnosis of diabetes, particularly the substantial risk for lower limb complications.⁷ In addition, loss of protective sensation (LOPS) can render patients unable to recognize damage to their lower extremities, thus creating a cycle of tissue damage and other foot complications. Strong evidence suggests that consistent provision of foot-care services and preventive care can reduce amputations among patients with diabetes.^7-9 However, routine foot examination and rapid risk stratification is often difficult to incorporate into busy primary care settings. Data suggest that the diabetic foot is adequately evaluated only 12% to 20% of the time.¹⁰

In response to the need for more consistent foot exams, an American Diabetes Association (ADA) task force lead by 2 of the authors of this article (AB and DA) created the Comprehensive Foot Examination and Risk Assessment.⁵ This set the standard for the detailed investigation of lower limb pathology by a specialist, but was not well suited for other practice settings, including primary care. One reason is that it would be difficult to complete the comprehensive examination during a typical 15-minute primary care office visit. In addition, certain examination parameters require the use of neurologic and vascular assessment equipment and training not available in all health care settings.¹¹

This exam takes substantially less time to complete than
 a comprehensive exam and eliminates common barriers to frequent assessment. With these thoughts in mind, we set out to develop an exam that could be done by a wide range of health care providers—one that takes substantially less time to complete than a comprehensive exam and eliminates common barriers to frequent assessment. The exam, which we’ll describe here, consists of 3 components: taking a patient history, performing a physical exam, and providing patient education. And best of all, it should only take 3 minutes.

The patient history (1 minute)

Patients may present with concerns about their feet, but may not be able to differentiate between benign and threatening symptoms. A thorough medical history can identify factors that may increase patients’ risk of developing lower-limb complications. Reviewing the patient’s medical history also can help guide the physical exam.

Review the patient’s diabetic history, blood glucose control, and previous diabetic complications. Ask patients about their history of peripheral vascular disease, quality of peripheral protective sensation, and previous lower-limb interventions and operations (TABLE 1^5,12). Patients with diabetes and suboptimal glycemic control have an increased risk for LOPS, chronic and recalcitrant ulcers, and wound infections.² Additionally, patients with diabetes and a previous lower extremity amputation are at high risk for reulceration.^5,12 Lastly, nicotine use and smoking are common pathogenic risk factors that contribute to peripheral artery disease (PAD).¹³

Physical examination (1 minute)

Careful inspection of the feet should be performed at every visit for patients with confirmed or suspected diabetes. Because up to 50% of patients with significant sensory loss due to neuropathy may be completely asymptomatic,¹⁴ failing to search for early signs of infection (FIGURE 1), skin breakdown, ulcer formation (FIGURE 2), skin temperature changes, and inadequate vascular perfusion may allow complications to develop.⁵ TABLE 2^5,15,16 outlines the essential components—dermatologic, neurologic, musculoskeletal, and vascular—of a rapid lower limb physical exam.

The dermatologic exam. This serves as a barometer for early intervention, and often results in a limb-saving referral to a specialist. Carefully 
examine the areas 
between the 
toes, where
 deeper lesions
 may go
 unnoticed. It should begin with a global inspection for discolorations, calluses, wounds, fissures, macerations, nail dystrophy, or paronychia.⁵ Skin discoloration or loss of hair growth may be the first signs of vascular insufficiency, while calluses and hypertrophic skin often are precursors to ulcers.^5,17-19 Inspection of the toes should include a search for fungal, ingrown, or elongated nails. Carefully examine the areas between the toes, where deeper lesions may go unnoticed.⁵

The neurologic exam. Without protective sensation, patients with neuropathy are at a heightened risk of unrecognized injury and are unlikely to mention their deformities to medical staff.^20-23 Consequently, skin deterioration may unknowingly progress to ulceration that requires extensive medical intervention or amputation.

Neuropathic LOPS is easily detectable, yet it is linked to at least 75% of all nontraumatic diabetic amputations.^20-23 Adiminished vibratory perception threshold (VPT) is one of the earliest indicators of neuropathic LOPS and is the best predictor of long-term lower extremity complications.^1,24,25 However, VPT devices are expensive and time-consuming to operate, and they require training to ensure proper use. The Semmes-Weinstein monofilament is a well-documented alternative to VPT for predicting ulcer risk^26-28 and has long been advocated as an essential component of a thorough foot exam.⁵ The 128 Hz tuning fork is another regularly used alternative.⁵ However, physicians would need to purchase one of these devices and receive training on how to use it, and, in the case of the monofilament, to regularly stock replacements to maintain accurate results.¹⁶

No testing devices are needed to conduct the Ipswich Touch Test, and it is as sensitive and specific as the monofilament test. The Ipswich Touch Test (IpTT) is an alternative neurologic test that requires only the physician’s index finger. During the IpTT, the physician instructs the patient to close his or her eyes while the physician lightly rests his or her finger on each of the patient’s first, third, and fifth toes for 1 to 2 seconds (FIGURE 3). Patients are instructed to respond with a “yes” when they feel the physician’s touch. In a head-to-head trial, diagnostic results of the IpTT directly paralleled those of the monofilament in detecting LOPS; IpTT was also equally sensitive and specific (k=.88, indicating almost perfect agreement; P<.0001).²⁹ The IpTT’s use of only 6 palpation points, constant availability, and accuracy make it a first-line neurologic test for rapidly screening the feet of a patient with diabetes.

Neuromuscular/musculoskeletal exam. Neuromuscular disturbances, such as a reduction in the strength of dorsiflexion and plantar flexion, may indicate a complicated neurologic compromise.⁵ In addition to being aesthetically problematic, musculoskeletal deformities such as a hammer toe, claw toe (FIGURE 4), or bunion can cause significant pain and/or gait disturbance, and can increase patients’ risk for ulceration.³⁰ These deformities also may compromise patients’ general health and grossly escalate their risk of falls and resultant injuries.^5,31 Therefore, patients who present with previously unreported musculoskeletal deformities should be referred to a specialist.³¹

Charcot neuroarthropathy is
 a devastating complication that classically presents as a hot, red, swollen foot; the redness resolves upon elevation. Also screen patients for Charcot neuroarthropathy (FIGURE 5), a devastating complication that classically presents as a hot, red, swollen foot; the redness resolves upon elevation.³² Charcot neuroarthropathy is hypothesized to be a dysregulation of normal bone metabolism typically occurring secondary to diabetic neuropathy and repetitive minor trauma.^33,34 This dysregulation leads to joint instability and disorganization of normal midfoot bone architecture.^31,32 Charcot neuroarthropathy is an urgent pathology that requires management by a foot specialist.³⁵

Vascular exam. PAD is particularly common in patients with diabetes and contributes to the development of impaired healing in up to half of foot ulcers.^13,18,36-39 Bilateral femoral, popliteal, posterior tibial, or dorsalis pedis pulses should be assessed by palpation; a diminished or absent pulse is a key indicator of vascular compromise.^40,41 An integrated care approach between foot specialists and vascular surgeons results in optimal treatment.

Patient education (1 minute)

It is imperative to include patients in their treatment process to reduce the likelihood of complications and, ultimately, decrease the incidence of amputations.^12,42 Patient education improves patients’ self-reported home care behaviors, even at the most fundamental levels.^43,44 TABLE 3^5,15,45 lists topics to cover during patient education.

A lack of appropriate patient education regarding diabetes is a factor in >90% of recurrent ulcers.Patients’ lack of understanding about self-care for diabetes is a common barrier to prevention.²³ El-Nahas et al⁴⁶ found a lack of appropriate education regarding diabetes was a factor in more than 90% of recurrent ulcers, which emphasizes the need for repeated education for at-risk patients.^47,48 Involve all levels of medical staff in the effort to educate patients on the importance of foot screenings, both at home and in-office. Even with proper patient education, many patients may be in various stages of coping with this all-consuming yet frequently asymptomatic condition, which makes the need for repeated patient education even more critical.

Who to refer, and when

After completing the 3-minute foot exam, create a treatment and follow-up plan, focusing on the need for referral to a specialist. TABLE 4 outlines suggested indications, priorities, and timelines for referral based on ADA guidelines.⁵ It incorporates the ADA’s patient risk categories (very low, low, moderate, and high risk) and also provides a recommended frequency for patient follow-ups.

Care for patients with lower extremity complications of diabetes mellitus is time-consuming and expensive. The brief exam described here can help you to rapidly identify patients at risk for these complications and prompt you to provide timely referrals to appropriate specialists.

CORRESPONDENCE
David G. Armstrong, DPM, MD, PhD, Professor, Department of Surgery, Director, Southern Arizona Limb Salvage Alliance (SALSA), 1501 N. Campbell Avenue, Tucson, AZ 85724-5072; armstrong@usa.net

A 61-year-old Caucasian man sought care for a rash that he’d had on and off for the past 5 years. He’d seen several physicians, but none had been able to make a diagnosis. Topical antifungal creams and steroids provided some improvement, but the rash would always come back.

The patient was otherwise healthy and had no personal or family history of atopy or skin disease.

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

A clinical diagnosis of Grover’s disease (transient acantholytic dermatosis) was confirmed by skin biopsy.

First described in 1970,¹ Grover’s disease is characterized by a monomorphic papulovesicular eruption that is limited to the trunk and is seen mainly among middle-aged² Caucasian men.³ Most cases of Grover’s disease are benign and self-limiting, lasting weeks to months, but it can be difficult to manage and has been reported to be recurrent or persistent.⁴

Some researchers have proposed that Grover’s disease is caused by obstructed sweat glands that lead to pooled sweat urea coming out of the epidermis, resulting in acantholysis.⁵ However, patients typically present during the winter months when presumably they perspire less frequently.²

There is some evidence linking infection, infestation, ionizing radiation, drugs such as sulfadoxine/pyrimethamine, and recombinant human interleukin-4 with the development of Grover’s disease;³ however, the evidence is weak. Patients with recurrent Grover’s disease often report a history of asteatotic eczema, atopic dermatitis, or contact dermatitis.³

The differential diagnosis 
includes truncal acne, folliculitis

Because the clinical features of Grover’s disease are often subtle (macules and papules are not florid) and variable (may be red or brown and usually papular but can be acneiform, vesicular, pustular, and even bullous), diagnosis requires a high degree of clinical suspicion. There are many potential differential diagnoses, including:

Truncal acne may present as inflammatory papules. Patient may complain of itchiness. Comedones and pustules are telltale signs of truncal acne, and are not present in Grover’s disease.

Seborrheic dermatitis often presents as greasy, scaly, eczematous patches, and papules. It can be found on the hair-bearing area on the scalp, forehead, eyebrows, nasolabial folds, postauricular skin, and anterior chest wall. Grover’s disease typically presents on the trunk.

Folliculitis may look very similar to Grover’s disease, and its erythematous papules are often found on the trunk. Distinguishing the 2 can be done on biopsy.

Exanthematous drug eruptions, also called maculopapular eruptions, are not limited to the trunk. They are often associated with the use of a new medication within the previous 4 to 21 days.⁶

Biopsy can confirm the diagnosis

A diagnosis of Grover’s disease is usually made clinically based on the appearance of the rash and the patient’s age and sex (typically seen in middle-aged men). The diagnosis can be confirmed by biopsy. Under a microscope, Grover’s disease has a characteristic appearance of acantholytic dyskeratosis (FIGURE 2); it can be similar in appearance to Darier’s disease, Hailey-Hailey disease, or pemphigus.⁷

Steroids, other meds are used
 to reduce itching and inflammation

There are no curative treatments for Grover’s disease. Treatment usually is symptomatic. Local application twice a day of topical steroids, such as triamcinolone acetonide or fluticasone propionate, is often used to relieve the itching and reduce inflammation. Oral steroids, oral retinoids, calcipotriol, phototherapy with ultraviolet B or psoralen plus ultraviolet A light, Grenz radiation, and methotrexate may help clear the eruption in patients with severe itch or extensive or refractory disease.^3,8 Antibiotics such as topical fucidin 2 to 3 times a day or oral cloxacillin 500 mg 4 times a day are indicated only if there is secondary impetiginization.

Advise patients to avoid excessive sweating, excessive sun exposure, occlusive clothing, and contact with topical irritants because all of these things are likely to make an outbreak worse.

Our patient was instructed to apply a topical clobetasone butyrate 0.05% cream twice a day. He was also told to take an oral antihistamine, fexofenadine, 180 mg bid for 2 months. The lesions healed, leaving hyperpigmentation. He was advised that the lesions might return in the future.

CORRESPONDENCE
Ch’ng Chin Chwen, MBBS, MRCP, Department of Medicine, Faculty of Medicine, University of Malaya, Lembah Pantai, 50603 Kuala Lumpur, Malaysia; chinchwen@gmail.com

A 61-year-old Caucasian man sought care for a rash that he’d had on and off for the past 5 years. He’d seen several physicians, but none had been able to make a diagnosis. Topical antifungal creams and steroids provided some improvement, but the rash would always come back.

The patient was otherwise healthy and had no personal or family history of atopy or skin disease.

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

A clinical diagnosis of Grover’s disease (transient acantholytic dermatosis) was confirmed by skin biopsy.

First described in 1970,¹ Grover’s disease is characterized by a monomorphic papulovesicular eruption that is limited to the trunk and is seen mainly among middle-aged² Caucasian men.³ Most cases of Grover’s disease are benign and self-limiting, lasting weeks to months, but it can be difficult to manage and has been reported to be recurrent or persistent.⁴

Some researchers have proposed that Grover’s disease is caused by obstructed sweat glands that lead to pooled sweat urea coming out of the epidermis, resulting in acantholysis.⁵ However, patients typically present during the winter months when presumably they perspire less frequently.²

There is some evidence linking infection, infestation, ionizing radiation, drugs such as sulfadoxine/pyrimethamine, and recombinant human interleukin-4 with the development of Grover’s disease;³ however, the evidence is weak. Patients with recurrent Grover’s disease often report a history of asteatotic eczema, atopic dermatitis, or contact dermatitis.³

The differential diagnosis 
includes truncal acne, folliculitis

Because the clinical features of Grover’s disease are often subtle (macules and papules are not florid) and variable (may be red or brown and usually papular but can be acneiform, vesicular, pustular, and even bullous), diagnosis requires a high degree of clinical suspicion. There are many potential differential diagnoses, including:

Truncal acne may present as inflammatory papules. Patient may complain of itchiness. Comedones and pustules are telltale signs of truncal acne, and are not present in Grover’s disease.

Seborrheic dermatitis often presents as greasy, scaly, eczematous patches, and papules. It can be found on the hair-bearing area on the scalp, forehead, eyebrows, nasolabial folds, postauricular skin, and anterior chest wall. Grover’s disease typically presents on the trunk.

Folliculitis may look very similar to Grover’s disease, and its erythematous papules are often found on the trunk. Distinguishing the 2 can be done on biopsy.

Exanthematous drug eruptions, also called maculopapular eruptions, are not limited to the trunk. They are often associated with the use of a new medication within the previous 4 to 21 days.⁶

Biopsy can confirm the diagnosis

A diagnosis of Grover’s disease is usually made clinically based on the appearance of the rash and the patient’s age and sex (typically seen in middle-aged men). The diagnosis can be confirmed by biopsy. Under a microscope, Grover’s disease has a characteristic appearance of acantholytic dyskeratosis (FIGURE 2); it can be similar in appearance to Darier’s disease, Hailey-Hailey disease, or pemphigus.⁷

Steroids, other meds are used
 to reduce itching and inflammation

There are no curative treatments for Grover’s disease. Treatment usually is symptomatic. Local application twice a day of topical steroids, such as triamcinolone acetonide or fluticasone propionate, is often used to relieve the itching and reduce inflammation. Oral steroids, oral retinoids, calcipotriol, phototherapy with ultraviolet B or psoralen plus ultraviolet A light, Grenz radiation, and methotrexate may help clear the eruption in patients with severe itch or extensive or refractory disease.^3,8 Antibiotics such as topical fucidin 2 to 3 times a day or oral cloxacillin 500 mg 4 times a day are indicated only if there is secondary impetiginization.

Advise patients to avoid excessive sweating, excessive sun exposure, occlusive clothing, and contact with topical irritants because all of these things are likely to make an outbreak worse.

Our patient was instructed to apply a topical clobetasone butyrate 0.05% cream twice a day. He was also told to take an oral antihistamine, fexofenadine, 180 mg bid for 2 months. The lesions healed, leaving hyperpigmentation. He was advised that the lesions might return in the future.

CORRESPONDENCE
Ch’ng Chin Chwen, MBBS, MRCP, Department of Medicine, Faculty of Medicine, University of Malaya, Lembah Pantai, 50603 Kuala Lumpur, Malaysia; chinchwen@gmail.com

A 61-year-old Caucasian man sought care for a rash that he’d had on and off for the past 5 years. He’d seen several physicians, but none had been able to make a diagnosis. Topical antifungal creams and steroids provided some improvement, but the rash would always come back.

The patient was otherwise healthy and had no personal or family history of atopy or skin disease.

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

A clinical diagnosis of Grover’s disease (transient acantholytic dermatosis) was confirmed by skin biopsy.

First described in 1970,¹ Grover’s disease is characterized by a monomorphic papulovesicular eruption that is limited to the trunk and is seen mainly among middle-aged² Caucasian men.³ Most cases of Grover’s disease are benign and self-limiting, lasting weeks to months, but it can be difficult to manage and has been reported to be recurrent or persistent.⁴

Some researchers have proposed that Grover’s disease is caused by obstructed sweat glands that lead to pooled sweat urea coming out of the epidermis, resulting in acantholysis.⁵ However, patients typically present during the winter months when presumably they perspire less frequently.²

There is some evidence linking infection, infestation, ionizing radiation, drugs such as sulfadoxine/pyrimethamine, and recombinant human interleukin-4 with the development of Grover’s disease;³ however, the evidence is weak. Patients with recurrent Grover’s disease often report a history of asteatotic eczema, atopic dermatitis, or contact dermatitis.³

The differential diagnosis 
includes truncal acne, folliculitis

Because the clinical features of Grover’s disease are often subtle (macules and papules are not florid) and variable (may be red or brown and usually papular but can be acneiform, vesicular, pustular, and even bullous), diagnosis requires a high degree of clinical suspicion. There are many potential differential diagnoses, including:

Truncal acne may present as inflammatory papules. Patient may complain of itchiness. Comedones and pustules are telltale signs of truncal acne, and are not present in Grover’s disease.

Seborrheic dermatitis often presents as greasy, scaly, eczematous patches, and papules. It can be found on the hair-bearing area on the scalp, forehead, eyebrows, nasolabial folds, postauricular skin, and anterior chest wall. Grover’s disease typically presents on the trunk.

Folliculitis may look very similar to Grover’s disease, and its erythematous papules are often found on the trunk. Distinguishing the 2 can be done on biopsy.

Exanthematous drug eruptions, also called maculopapular eruptions, are not limited to the trunk. They are often associated with the use of a new medication within the previous 4 to 21 days.⁶

Biopsy can confirm the diagnosis

A diagnosis of Grover’s disease is usually made clinically based on the appearance of the rash and the patient’s age and sex (typically seen in middle-aged men). The diagnosis can be confirmed by biopsy. Under a microscope, Grover’s disease has a characteristic appearance of acantholytic dyskeratosis (FIGURE 2); it can be similar in appearance to Darier’s disease, Hailey-Hailey disease, or pemphigus.⁷

Steroids, other meds are used
 to reduce itching and inflammation

There are no curative treatments for Grover’s disease. Treatment usually is symptomatic. Local application twice a day of topical steroids, such as triamcinolone acetonide or fluticasone propionate, is often used to relieve the itching and reduce inflammation. Oral steroids, oral retinoids, calcipotriol, phototherapy with ultraviolet B or psoralen plus ultraviolet A light, Grenz radiation, and methotrexate may help clear the eruption in patients with severe itch or extensive or refractory disease.^3,8 Antibiotics such as topical fucidin 2 to 3 times a day or oral cloxacillin 500 mg 4 times a day are indicated only if there is secondary impetiginization.

Advise patients to avoid excessive sweating, excessive sun exposure, occlusive clothing, and contact with topical irritants because all of these things are likely to make an outbreak worse.

Our patient was instructed to apply a topical clobetasone butyrate 0.05% cream twice a day. He was also told to take an oral antihistamine, fexofenadine, 180 mg bid for 2 months. The lesions healed, leaving hyperpigmentation. He was advised that the lesions might return in the future.

CORRESPONDENCE
Ch’ng Chin Chwen, MBBS, MRCP, Department of Medicine, Faculty of Medicine, University of Malaya, Lembah Pantai, 50603 Kuala Lumpur, Malaysia; chinchwen@gmail.com

Despite a high vaccination rate, pertussis is the only vaccine-preventable disease whose incidence is on the rise.^1-3 The Centers for Disease Control and Prevention (CDC) reported 48,277 laboratory-confirmed cases in 2012—the most since 1955—and 20 pertussis-related deaths.⁴ And while only 28,639 pertussis cases were reported in 2013, more than 17,000 cases had already been reported through August 15, 2014, suggesting that the incidence may again be on the rise this year.⁴

This uptick is likely due to a combination of factors, including a growing awareness of pertussis, and therefore a lower threshold for physicians to test for it. In addition, there’s some evidence that the immunity provided by the currently used pertussis vaccines may wane over time. Recently reported epidemics, including those in California this year and in 2010, as well as in Washington in 2011, have added to this concern.⁵ This article outlines what you can do to improve prevention, diagnosis, and treatment of pertussis.

A 3-stage course of disease

Bordetella pertussis is an aerobic, gram-negative bacterium that causes symptoms by producing multiple antigenic and biologically active components, including pertussis toxin, filamentous hemagglutinin, and agglutinogens. The bacteria adhere to the cilia in the respiratory tract and initiate an inflammatory cascade that paralyzes the cilia and inhibits the respiratory functions responsible for clearing secretions, largely through an immune-mediated response.

Pertussis has an incubation period of approximately 7 days, but this can last as long as 3 to 6 weeks. The 3 stages in the course of the disease are:⁶

• Catarrhal. This stage lasts 1 to 2 weeks and is characterized by coryza, sneezing, and a mild, occasional cough.
• Paroxysmal. This stage lasts 1 to 6 weeks, and is characterized by periods of severe coughing “fits” that include the inspiratory "whoop." These coughing episodes may occur more often at night and may worsen in intensity and frequency in the first 2 to 3 weeks and then gradually decrease. This stage also may include posttussive vomiting.
• Convalescent. During this stage, the cough begins to wane.

Vaccination: Don’t forget adults

The 2 vaccines used to prevent pertussis are DTaP (diphtheria-tetanus-acellular pertussis) and Tdap (tetanus-diphtheria-acellular pertussis). The difference between the 2 is that the Tdap vaccine contains a reduced dose of the diphtheria and acellular pertussis vaccines. DTaP is designed primarily for children younger than 7 years of age. Tdap is given to older children and adults. The CDC and Advisory Committee on Immunization Practices recommend that children receive 5 doses of DTaP, one dose at each of the following ages: 2, 4, 6, and 15 to 18 months and at 4 to 6 years.⁷ All adults 19 years of age and older who have not yet received a dose of Tdap should receive a single dose regardless of when they last received any immunization for tetanus or diphtheria.^7-10 A one-time Tdap booster should be given to all adults in place of a tetanus booster (TABLE 1).^7-10

What about pregnant women? Tdap should be administered to every pregnant woman between 27 to 36 weeks gestation regardless of Tdap history.^7,11 This strategy allows maternal antibodies to transfer to the infant, thus providing some protection to the newborn prior to pediatric vaccinations.

All adults ages ≥19 years who have not yet received a dose of Tdap should receive a single dose regardless of when they last received any immunization for tetanus or diphtheria. Is the vaccine becoming less effective? Since 1991, the number of cases of pertussis reported in previously vaccinated adolescents and adults has increased, which suggests waning immunity.^12,13 Another recent trial investigating the acellular pertussis vaccine found that immunity decreases dramatically 5 years after the fifth dose.¹⁴

Recommendations on who should receive pertussis vaccination have been expanded to include adolescents and adults, including pregnant women and those ages 65 and older in close contact with infants, and this should decrease the overall incidence of disease through decreased communicability.¹⁵ Current recommendations call for a single adult vaccination; however, ongoing studies are evaluating whether a booster later in life might be necessary.¹⁵

Diagnosis needs to be
 confirmed by lab testing


Any patient who reports having a persistent cough should be considered for pertussis testing and treatment, and any clinician who triages such patients should ask detailed questions about the characteristics and duration of the patient’s symptoms. Antibiotics do not appear 
to shorten the duration of pertussis symptoms unless given 
in the catarrhal phase. However, while a prolonged cough is the hallmark of pertussis, there are many other potential causes of this symptom. Therefore, diagnosis of pertussis requires a combination of clinical and laboratory testing, because clinical parameters alone are neither sensitive nor specific enough for pertussis infection.

TABLE 2¹⁶ outlines the clinical and laboratory diagnostic criteria for pertussis from the CDC and the World Health Organization. Suspect pertussis in a patient who’s had a cough for more than 14 days that includes an inspiratory “whoop.” In infants, pertussis should be suspected in those with symptoms that suggest cough and associated apnea.¹⁶ Order laboratory testing for any patients who have clinical signs or symptoms of pertussis.

Four methods of lab testing for pertussis infection are polymerase chain reaction (PCR), direct fluorescent antibody (DFA) testing, serologic testing, and culture (TABLE 3).^17-19 The sensitivity of these tests is as follows: PCR, 90% to 95%; DFA, 50% to 60%; serologic testing, 70% to 80%; and culture, 50% to 70%. The specificity is: PCR, 95% to 98%; DFA, 90% to 100%; serologic testing, 90% to 100%; and culture, 100%.

PCR is the preferred method because of its rapid turnaround and fairly high sensitivity. The reliability of PCR decreases, however, for a patient who’s had a cough for more than 2 weeks because the individual may have transitioned to the convalescent phase, when less bacterial DNA remain.

Results from DFA testing also are rapidly available, but the need for specialized equipment and a well-trained examiner of the specimen limits widespread use of this test. It also is not particularly sensitive for pertussis.

Serologic testing is less reliable in patients who have received an acellular pertussis vaccine and is not helpful in the first few weeks of infection.

The sensitivity of culture is best if the sample is collected appropriately (more on this in a bit) and within the first 2 weeks of symptoms (catarrhal stage). Culture is also very specific.

Given the strengths and weakness of the different tests, an acceptable method of laboratory confirmation is to obtain PCR and/or culture within the first 2 weeks of symptoms in all age groups.^17-20 Testing after 2 weeks should include a combination of PCR and serology.¹⁷ It is essential that the clinical specimen used for PCR or culture testing for pertussis is properly collected. (See “Collecting a swab for pertussis testing” below.²¹)

Collecting a swab for pertussis testing

The illustration below shows the correct swab and sampling method. Swab tips may be polyester (such as Dacron or rayon) or they may be nylon-flocked. Cotton-tipped or
calcium alginate swabs are not acceptable because the residue will inhibit DNA assays.²¹
The specimen must be obtained from the posterior nasopharynx and not the nares or oropharynx. The Centers for Disease Control and Prevention offers a video that demonstrates how to properly collect a specimen for testing at http://www.cdc.gov/pertussis/clinical/diagnostic-testing/specimen-collection.html.

Tx is effective when started early

Antibiotics are an effective treatment for pertussis, but they need to be started within the first few weeks of developing symptoms. Studies have not found evidence that antibiotics shorten the duration of pertussis symptoms unless they are given in the catarrhal phase.^22,23 It can be challenging to get treatment started during this window, however, because patients may put off seeking care for symptoms they perceive as only minor, such as a cough, until the disease progresses. In addition, physicians may not suspect pertussis in patients who present with a cough they have had for only a short time, and therefore may not test for it.

It may be necessary to rely on clinical suspicion when deciding whether to initiate treatment for pertussis before testing to confirm the diagnosis. For patients in whom clinical suspicion of pertussis is high and who may be in contact with high-risk individuals, it may be acceptable to begin treatment before receiving lab test results.^24,25 A recent Cochrane meta-analysis²⁶ recommended initiating treatment to render a patient who has pertussis “noninfectious” but without an expectation of diminishing symptoms.

Limited role for prophylaxis. There is little evidence that prophylactic treatment for pertussis can decrease the spread of the disease. Studies that investigated potential benefits of prophylactic treatment for pertussis have been inconclusive, except for individuals who are in close contact with an infant younger than 6 months of age who has not been fully immunized.^27,28

A macrolide antibiotic is generally used to treat pertussis (TABLE 4).^25-30 Consider starting treatment before lab results are
 in when clinicial suspicion is high and the patient may be in contact with high-risk individuals. Erythromycin had been the drug of choice, but recent studies have found similar efficacy for azithromycin and clarithromycin.²⁹ For infants younger than one month of age, azithromycin is preferred because in addition to being as effective as other macrolides, it has a better adverse effect profile.²⁹ For patients who are at least 2 months of age, trimethoprim-sulfamethoxazole is an acceptable alternative to a macrolide.

The CDC recommends that any adolescent or adult who has a cough and has had close contact with an individual with a laboratory-confirmed case of pertussis within the past 21 days should be treated.³⁰ Close contacts younger than 7 years of age who have not received the first 4 doses of the pertussis vaccine should be offered treatment.

CORRESPONDENCE
Gary Rivard, DO, Family Medicine Residency Program, Central Maine Medical Center, 76 High Street, Lewiston, ME 04282; rivardga@cmhc.org

Despite a high vaccination rate, pertussis is the only vaccine-preventable disease whose incidence is on the rise.^1-3 The Centers for Disease Control and Prevention (CDC) reported 48,277 laboratory-confirmed cases in 2012—the most since 1955—and 20 pertussis-related deaths.⁴ And while only 28,639 pertussis cases were reported in 2013, more than 17,000 cases had already been reported through August 15, 2014, suggesting that the incidence may again be on the rise this year.⁴

This uptick is likely due to a combination of factors, including a growing awareness of pertussis, and therefore a lower threshold for physicians to test for it. In addition, there’s some evidence that the immunity provided by the currently used pertussis vaccines may wane over time. Recently reported epidemics, including those in California this year and in 2010, as well as in Washington in 2011, have added to this concern.⁵ This article outlines what you can do to improve prevention, diagnosis, and treatment of pertussis.

A 3-stage course of disease

Bordetella pertussis is an aerobic, gram-negative bacterium that causes symptoms by producing multiple antigenic and biologically active components, including pertussis toxin, filamentous hemagglutinin, and agglutinogens. The bacteria adhere to the cilia in the respiratory tract and initiate an inflammatory cascade that paralyzes the cilia and inhibits the respiratory functions responsible for clearing secretions, largely through an immune-mediated response.

Pertussis has an incubation period of approximately 7 days, but this can last as long as 3 to 6 weeks. The 3 stages in the course of the disease are:⁶

• Catarrhal. This stage lasts 1 to 2 weeks and is characterized by coryza, sneezing, and a mild, occasional cough.
• Paroxysmal. This stage lasts 1 to 6 weeks, and is characterized by periods of severe coughing “fits” that include the inspiratory "whoop." These coughing episodes may occur more often at night and may worsen in intensity and frequency in the first 2 to 3 weeks and then gradually decrease. This stage also may include posttussive vomiting.
• Convalescent. During this stage, the cough begins to wane.

Vaccination: Don’t forget adults

The 2 vaccines used to prevent pertussis are DTaP (diphtheria-tetanus-acellular pertussis) and Tdap (tetanus-diphtheria-acellular pertussis). The difference between the 2 is that the Tdap vaccine contains a reduced dose of the diphtheria and acellular pertussis vaccines. DTaP is designed primarily for children younger than 7 years of age. Tdap is given to older children and adults. The CDC and Advisory Committee on Immunization Practices recommend that children receive 5 doses of DTaP, one dose at each of the following ages: 2, 4, 6, and 15 to 18 months and at 4 to 6 years.⁷ All adults 19 years of age and older who have not yet received a dose of Tdap should receive a single dose regardless of when they last received any immunization for tetanus or diphtheria.^7-10 A one-time Tdap booster should be given to all adults in place of a tetanus booster (TABLE 1).^7-10

What about pregnant women? Tdap should be administered to every pregnant woman between 27 to 36 weeks gestation regardless of Tdap history.^7,11 This strategy allows maternal antibodies to transfer to the infant, thus providing some protection to the newborn prior to pediatric vaccinations.

All adults ages ≥19 years who have not yet received a dose of Tdap should receive a single dose regardless of when they last received any immunization for tetanus or diphtheria. Is the vaccine becoming less effective? Since 1991, the number of cases of pertussis reported in previously vaccinated adolescents and adults has increased, which suggests waning immunity.^12,13 Another recent trial investigating the acellular pertussis vaccine found that immunity decreases dramatically 5 years after the fifth dose.¹⁴

Recommendations on who should receive pertussis vaccination have been expanded to include adolescents and adults, including pregnant women and those ages 65 and older in close contact with infants, and this should decrease the overall incidence of disease through decreased communicability.¹⁵ Current recommendations call for a single adult vaccination; however, ongoing studies are evaluating whether a booster later in life might be necessary.¹⁵

Diagnosis needs to be
 confirmed by lab testing


Any patient who reports having a persistent cough should be considered for pertussis testing and treatment, and any clinician who triages such patients should ask detailed questions about the characteristics and duration of the patient’s symptoms. Antibiotics do not appear 
to shorten the duration of pertussis symptoms unless given 
in the catarrhal phase. However, while a prolonged cough is the hallmark of pertussis, there are many other potential causes of this symptom. Therefore, diagnosis of pertussis requires a combination of clinical and laboratory testing, because clinical parameters alone are neither sensitive nor specific enough for pertussis infection.

TABLE 2¹⁶ outlines the clinical and laboratory diagnostic criteria for pertussis from the CDC and the World Health Organization. Suspect pertussis in a patient who’s had a cough for more than 14 days that includes an inspiratory “whoop.” In infants, pertussis should be suspected in those with symptoms that suggest cough and associated apnea.¹⁶ Order laboratory testing for any patients who have clinical signs or symptoms of pertussis.

Four methods of lab testing for pertussis infection are polymerase chain reaction (PCR), direct fluorescent antibody (DFA) testing, serologic testing, and culture (TABLE 3).^17-19 The sensitivity of these tests is as follows: PCR, 90% to 95%; DFA, 50% to 60%; serologic testing, 70% to 80%; and culture, 50% to 70%. The specificity is: PCR, 95% to 98%; DFA, 90% to 100%; serologic testing, 90% to 100%; and culture, 100%.

PCR is the preferred method because of its rapid turnaround and fairly high sensitivity. The reliability of PCR decreases, however, for a patient who’s had a cough for more than 2 weeks because the individual may have transitioned to the convalescent phase, when less bacterial DNA remain.

Results from DFA testing also are rapidly available, but the need for specialized equipment and a well-trained examiner of the specimen limits widespread use of this test. It also is not particularly sensitive for pertussis.

Serologic testing is less reliable in patients who have received an acellular pertussis vaccine and is not helpful in the first few weeks of infection.

The sensitivity of culture is best if the sample is collected appropriately (more on this in a bit) and within the first 2 weeks of symptoms (catarrhal stage). Culture is also very specific.

Given the strengths and weakness of the different tests, an acceptable method of laboratory confirmation is to obtain PCR and/or culture within the first 2 weeks of symptoms in all age groups.^17-20 Testing after 2 weeks should include a combination of PCR and serology.¹⁷ It is essential that the clinical specimen used for PCR or culture testing for pertussis is properly collected. (See “Collecting a swab for pertussis testing” below.²¹)

Collecting a swab for pertussis testing

The illustration below shows the correct swab and sampling method. Swab tips may be polyester (such as Dacron or rayon) or they may be nylon-flocked. Cotton-tipped or
calcium alginate swabs are not acceptable because the residue will inhibit DNA assays.²¹
The specimen must be obtained from the posterior nasopharynx and not the nares or oropharynx. The Centers for Disease Control and Prevention offers a video that demonstrates how to properly collect a specimen for testing at http://www.cdc.gov/pertussis/clinical/diagnostic-testing/specimen-collection.html.

Tx is effective when started early

Antibiotics are an effective treatment for pertussis, but they need to be started within the first few weeks of developing symptoms. Studies have not found evidence that antibiotics shorten the duration of pertussis symptoms unless they are given in the catarrhal phase.^22,23 It can be challenging to get treatment started during this window, however, because patients may put off seeking care for symptoms they perceive as only minor, such as a cough, until the disease progresses. In addition, physicians may not suspect pertussis in patients who present with a cough they have had for only a short time, and therefore may not test for it.

It may be necessary to rely on clinical suspicion when deciding whether to initiate treatment for pertussis before testing to confirm the diagnosis. For patients in whom clinical suspicion of pertussis is high and who may be in contact with high-risk individuals, it may be acceptable to begin treatment before receiving lab test results.^24,25 A recent Cochrane meta-analysis²⁶ recommended initiating treatment to render a patient who has pertussis “noninfectious” but without an expectation of diminishing symptoms.

Limited role for prophylaxis. There is little evidence that prophylactic treatment for pertussis can decrease the spread of the disease. Studies that investigated potential benefits of prophylactic treatment for pertussis have been inconclusive, except for individuals who are in close contact with an infant younger than 6 months of age who has not been fully immunized.^27,28

A macrolide antibiotic is generally used to treat pertussis (TABLE 4).^25-30 Consider starting treatment before lab results are
 in when clinicial suspicion is high and the patient may be in contact with high-risk individuals. Erythromycin had been the drug of choice, but recent studies have found similar efficacy for azithromycin and clarithromycin.²⁹ For infants younger than one month of age, azithromycin is preferred because in addition to being as effective as other macrolides, it has a better adverse effect profile.²⁹ For patients who are at least 2 months of age, trimethoprim-sulfamethoxazole is an acceptable alternative to a macrolide.

The CDC recommends that any adolescent or adult who has a cough and has had close contact with an individual with a laboratory-confirmed case of pertussis within the past 21 days should be treated.³⁰ Close contacts younger than 7 years of age who have not received the first 4 doses of the pertussis vaccine should be offered treatment.

CORRESPONDENCE
Gary Rivard, DO, Family Medicine Residency Program, Central Maine Medical Center, 76 High Street, Lewiston, ME 04282; rivardga@cmhc.org

Despite a high vaccination rate, pertussis is the only vaccine-preventable disease whose incidence is on the rise.^1-3 The Centers for Disease Control and Prevention (CDC) reported 48,277 laboratory-confirmed cases in 2012—the most since 1955—and 20 pertussis-related deaths.⁴ And while only 28,639 pertussis cases were reported in 2013, more than 17,000 cases had already been reported through August 15, 2014, suggesting that the incidence may again be on the rise this year.⁴

This uptick is likely due to a combination of factors, including a growing awareness of pertussis, and therefore a lower threshold for physicians to test for it. In addition, there’s some evidence that the immunity provided by the currently used pertussis vaccines may wane over time. Recently reported epidemics, including those in California this year and in 2010, as well as in Washington in 2011, have added to this concern.⁵ This article outlines what you can do to improve prevention, diagnosis, and treatment of pertussis.

A 3-stage course of disease

Bordetella pertussis is an aerobic, gram-negative bacterium that causes symptoms by producing multiple antigenic and biologically active components, including pertussis toxin, filamentous hemagglutinin, and agglutinogens. The bacteria adhere to the cilia in the respiratory tract and initiate an inflammatory cascade that paralyzes the cilia and inhibits the respiratory functions responsible for clearing secretions, largely through an immune-mediated response.

Pertussis has an incubation period of approximately 7 days, but this can last as long as 3 to 6 weeks. The 3 stages in the course of the disease are:⁶

• Catarrhal. This stage lasts 1 to 2 weeks and is characterized by coryza, sneezing, and a mild, occasional cough.
• Paroxysmal. This stage lasts 1 to 6 weeks, and is characterized by periods of severe coughing “fits” that include the inspiratory "whoop." These coughing episodes may occur more often at night and may worsen in intensity and frequency in the first 2 to 3 weeks and then gradually decrease. This stage also may include posttussive vomiting.
• Convalescent. During this stage, the cough begins to wane.

Vaccination: Don’t forget adults

The 2 vaccines used to prevent pertussis are DTaP (diphtheria-tetanus-acellular pertussis) and Tdap (tetanus-diphtheria-acellular pertussis). The difference between the 2 is that the Tdap vaccine contains a reduced dose of the diphtheria and acellular pertussis vaccines. DTaP is designed primarily for children younger than 7 years of age. Tdap is given to older children and adults. The CDC and Advisory Committee on Immunization Practices recommend that children receive 5 doses of DTaP, one dose at each of the following ages: 2, 4, 6, and 15 to 18 months and at 4 to 6 years.⁷ All adults 19 years of age and older who have not yet received a dose of Tdap should receive a single dose regardless of when they last received any immunization for tetanus or diphtheria.^7-10 A one-time Tdap booster should be given to all adults in place of a tetanus booster (TABLE 1).^7-10

What about pregnant women? Tdap should be administered to every pregnant woman between 27 to 36 weeks gestation regardless of Tdap history.^7,11 This strategy allows maternal antibodies to transfer to the infant, thus providing some protection to the newborn prior to pediatric vaccinations.

All adults ages ≥19 years who have not yet received a dose of Tdap should receive a single dose regardless of when they last received any immunization for tetanus or diphtheria. Is the vaccine becoming less effective? Since 1991, the number of cases of pertussis reported in previously vaccinated adolescents and adults has increased, which suggests waning immunity.^12,13 Another recent trial investigating the acellular pertussis vaccine found that immunity decreases dramatically 5 years after the fifth dose.¹⁴

Recommendations on who should receive pertussis vaccination have been expanded to include adolescents and adults, including pregnant women and those ages 65 and older in close contact with infants, and this should decrease the overall incidence of disease through decreased communicability.¹⁵ Current recommendations call for a single adult vaccination; however, ongoing studies are evaluating whether a booster later in life might be necessary.¹⁵

Diagnosis needs to be
 confirmed by lab testing


Any patient who reports having a persistent cough should be considered for pertussis testing and treatment, and any clinician who triages such patients should ask detailed questions about the characteristics and duration of the patient’s symptoms. Antibiotics do not appear 
to shorten the duration of pertussis symptoms unless given 
in the catarrhal phase. However, while a prolonged cough is the hallmark of pertussis, there are many other potential causes of this symptom. Therefore, diagnosis of pertussis requires a combination of clinical and laboratory testing, because clinical parameters alone are neither sensitive nor specific enough for pertussis infection.

TABLE 2¹⁶ outlines the clinical and laboratory diagnostic criteria for pertussis from the CDC and the World Health Organization. Suspect pertussis in a patient who’s had a cough for more than 14 days that includes an inspiratory “whoop.” In infants, pertussis should be suspected in those with symptoms that suggest cough and associated apnea.¹⁶ Order laboratory testing for any patients who have clinical signs or symptoms of pertussis.

Four methods of lab testing for pertussis infection are polymerase chain reaction (PCR), direct fluorescent antibody (DFA) testing, serologic testing, and culture (TABLE 3).^17-19 The sensitivity of these tests is as follows: PCR, 90% to 95%; DFA, 50% to 60%; serologic testing, 70% to 80%; and culture, 50% to 70%. The specificity is: PCR, 95% to 98%; DFA, 90% to 100%; serologic testing, 90% to 100%; and culture, 100%.

PCR is the preferred method because of its rapid turnaround and fairly high sensitivity. The reliability of PCR decreases, however, for a patient who’s had a cough for more than 2 weeks because the individual may have transitioned to the convalescent phase, when less bacterial DNA remain.

Results from DFA testing also are rapidly available, but the need for specialized equipment and a well-trained examiner of the specimen limits widespread use of this test. It also is not particularly sensitive for pertussis.

Serologic testing is less reliable in patients who have received an acellular pertussis vaccine and is not helpful in the first few weeks of infection.

The sensitivity of culture is best if the sample is collected appropriately (more on this in a bit) and within the first 2 weeks of symptoms (catarrhal stage). Culture is also very specific.

Given the strengths and weakness of the different tests, an acceptable method of laboratory confirmation is to obtain PCR and/or culture within the first 2 weeks of symptoms in all age groups.^17-20 Testing after 2 weeks should include a combination of PCR and serology.¹⁷ It is essential that the clinical specimen used for PCR or culture testing for pertussis is properly collected. (See “Collecting a swab for pertussis testing” below.²¹)

Collecting a swab for pertussis testing

The illustration below shows the correct swab and sampling method. Swab tips may be polyester (such as Dacron or rayon) or they may be nylon-flocked. Cotton-tipped or
calcium alginate swabs are not acceptable because the residue will inhibit DNA assays.²¹
The specimen must be obtained from the posterior nasopharynx and not the nares or oropharynx. The Centers for Disease Control and Prevention offers a video that demonstrates how to properly collect a specimen for testing at http://www.cdc.gov/pertussis/clinical/diagnostic-testing/specimen-collection.html.

Tx is effective when started early

Antibiotics are an effective treatment for pertussis, but they need to be started within the first few weeks of developing symptoms. Studies have not found evidence that antibiotics shorten the duration of pertussis symptoms unless they are given in the catarrhal phase.^22,23 It can be challenging to get treatment started during this window, however, because patients may put off seeking care for symptoms they perceive as only minor, such as a cough, until the disease progresses. In addition, physicians may not suspect pertussis in patients who present with a cough they have had for only a short time, and therefore may not test for it.