Richard P. Usatine, MD

A colleague came into the charting area and said he thought he had just seen his first case of chancroid. He asked me if I had a moment to see the patient, a 32-year-old African American man who noted the onset of painful sores on his penis 1 week ago. The patient consented to a second opinion. On further questioning, he remembered a tingling pain that started a few days prior to the sores. When asked about any previous outbreaks, he thought he may have had something like this 1 year ago. He did not remember seeing blisters before the sores appeared.

The last time the patient had sexual relations was 2 months ago, with someone he met at a party. He claimed he used a condom. He did not have any lesions at that time and had never had a sexually transmitted disease before.

He had recently fallen in love, and was concerned about these ulcers—he did not want to give her any diseases. They had only kissed so far and he wanted to know what he should tell her. He said he had never had sex with men or injected any drugs. He has had a number of serially monogamous relationships and reported no other human immunodeficiency virus (HIV) risk factors.

The patient was a healthy-looking young man. Examination of his penis (Figure 1) showed the ulcers clearly visible (Figure 2). He had only shotty inguinal adenopathy that was nontender.

FIGURE 1
Painful sores on the genitals

FIGURE 2
Close-up of ulcers on the penis

What is the diagnosis?
What is the treatment and prevention strategy?

Differential diagnosis

The most likely causes of painful genital ulcers in this case are herpes simplex, chancroid, and syphilis. Granuloma inguinale and lymphogranuloma venereum (LGV) are rare causes of genital ulceration in the United States. A zipper accident or other trauma can cause genital ulceration, but the patient should be able to give a clear history of such an event.

By epidemiology alone, the order of likelihood for the cause of any genital ulceration is herpes, syphilis, then chancroid.

This case points to herpes

Herpes simplex is by far the most common cause of painful genital ulcers in the United States; at least 50 million people have genital herpes simplex virus (HSV) infection¹ The features of this case pointing to herpes are the appearance of multiple ulcers, the tingling pain that preceded the ulcers, and the history of a possible episode in the preceding year. While it would be helpful to have a history of blisters that preceded the ulcers, the evidence still points to herpes as the most likely diagnosis.

Could it be syphilis?

While the primary chancre of syphilis is classically described as painless, the patient with syphilis may experience pain. Syphilis tends to present as a single ulcer but may cause multiple ulcers.

Why not chancroid?

Chancroid may also cause multiple small painful ulcers. However, the ulcers of chancroid tend to be deeper than those of herpes and bleed more easily.

Other characteristics to look for

All of these sexually transmitted diseases can cause tender painful adenopathy, which is particularly characteristic of chancroid and LGV. Suppurative inguinal adenopathy with painful genital ulcers is almost pathognomonic of chancroid. With LGV, there may be a self-limited genital ulcer at the site of inoculation, which is often gone by the time a patient seeks care. Granuloma inguinale causes painless, progressive ulcerative lesions without regional lymphadenopathy. These lesions are highly vascular (with a characteristic beefy red appearance) and bleed easily on contact.¹ While it would be helpful to have a history of blisters that preceded the ulcers, the evidence still points to herpes as the most likely diagnosis.

Laboratory examination

Herpes

All patients with genital ulcers thought to be from an STD should be tested for syphilis and HIV regardless of other risk factors.¹ This patient should additionally be tested for herpes simplex. A bacteriologic test for chancroid is not necessary, but the clinician who first saw the patient asked that we conduct the test for chancroid—a culture for the Haemophilus ducreyi bacterium.

Isolation of HSV in cell culture is the preferred virologic test for patients with genital ulcers.¹Unfortunately, the sensitivity of culture declines rapidly as lesions begin to heal, usually within a few days of onset. Direct fluorescent antibody tests are also available. Both herpes culture and the direct fluorescent antibody test distinguish HSV-1 from HSV-2. Polymerase chain reaction assays for HSV DNA are highly sensitive, but their role in the diagnosis of genital ulcer disease has not been well-defined.

Most cases of recurrent genital herpes are caused by HSV-2. Specific serologic testing can be expensive, and is not needed at the time of the initial virologic screening. However, consider ordering the test at a subsequent visit, because the distinction between HSV serotypes influences prognosis and counseling. Also, because false-negative HSV cultures are common—especially with recurrent infection or healing lesions—type-specific serologic tests are useful for confirming a diagnosis of genital herpes.¹ Herpes serologies can also be used to help manage sexual partners of persons with genital herpes.

Syphilis

The Venereal Disease Research Laboratory (VDRL) test or rapid plasma reagin (RPR) test should be used to detect syphilis. Both tests are used for nonspecific screening only, because they measure anticardiolipin antibodies. A positive result should be confirmed with a specific treponemal test such as a fluorescent treponemal antibody absorption test (FTA-ABS).

The results of these laboratory tests are not available immediately during the patient’s visit. If there was a high suspicion for syphilis, a dark field examination from the ulcer exudate could be used to look for spirochetes while the patient was still in the office. In this case, the suspicion for syphilis was low.

Treatment: Antivirals

The major question is whether the patient should be treated empirically with medication. The most likely diagnosis is herpes simplex. Randomized trials indicate that 3 antiviral medications— acyclovir, famciclovir, and valacyclovir—provide clinical benefit for genital herpes (level of evidence [LOE]=1a).¹

The Centers for Disease Control and Prevention (CDC) 2002 treatment guidelines for STDs recommend the following medications for the first clinical episode of genital herpes:

• Acyclovir 400 mg orally, 3 times daily for 7–10 days or until clinically resolved, OR
• Acyclovir 200 mg orally, 5 times daily for 7–10 days or until clinically resolved, OR
• Famciclovir 250 mg orally, 3 times daily for 7–10 days or until clinically resolved, OR
• Valacyclovir 1 g orally, twice daily for 7–10 days or until clinically resolved.

Topical acyclovir is less effective than the oral formulaton and its use is discouraged.

The suspicion for syphilis is too low to warrant an intramuscular shot of penicillin, which is painful and can cause anaphylaxis in some patients. The likelihood of chancroid is too low to prescribe an oral antibiotic such as erythromycin.

The patient wanted empirical treatment for herpes. He was given valacyclovir, 1 gm for 7 days, taken twice daily, with the option to call in for more if the ulcers did not resolve by day 7. He was told he might apply petrolatum and clean gauze to the ulcers to diminish the pain when open ulcers rub against underwear. Acetaminophen or other analgesics were recommended for pain, and he was advised to avoid sexual activity until the ulcers had fully healed.

Preventing transmission

The patient is appropriately concerned about the transmission of this condition to a new partner. Not having a firm diagnosis makes definitive counseling more difficult. However, general principles of safe sex and condom use were discussed. On the follow-up visit the patient was told that the result of his herpes test was positive for HSV-2. Results of his RPR, HIV antibody test, and H ducreyiculture were all negative.

Information about condom use was reinforced, and the patient was told there is definitive evidence that condom use does diminish the risk of transmission of herpes from a man to a woman (LOE=1b).² That same study did not show that condom use prevents transmission from women to men. Also, changes in sexual behavior, correlated with counseling about avoiding sex when a partner has lesions, were associated with reduction in HSV-2 acquisition over time (LOE=1b).²

One study showed that the overall risk of genital HSV transmission in couples is low (10%/year). The risk may be significantly increased in women and in seronegative individuals.³ This speaks for serologic testing for the potential partner of this patient.

When recurrences are frequent, antiviral agents can decrease the frequency (LOE=1a).¹ If this patient has frequent recurrences, antiviral agents would be appropriate and would decrease the times when the patient is shedding virus asymptomatically.

Herpes is transmitted between sexual partners during asymptomatic shedding.¹ Acyclovir 400 mg twice daily can reduce asymptomatic viral shedding significantly among women with recurrent herpes simplex (LOE=1b).⁴ While it is likely this will decrease transmission from women to men, this has not been proven. Data on decreasing viral transmission from men to women by antiviral therapy is not available. At some point, the Glycoprotein-D-adjuvant vaccine may be an option to prevent genital herpes transmission to his partner.⁵

Note. The CDC 2002 sexually transmitted diseases treatment guidelines are available for download and use on a Palm handheld computer at www.cdcnpin.org/scripts/std/pda.asp.

A colleague came into the charting area and said he thought he had just seen his first case of chancroid. He asked me if I had a moment to see the patient, a 32-year-old African American man who noted the onset of painful sores on his penis 1 week ago. The patient consented to a second opinion. On further questioning, he remembered a tingling pain that started a few days prior to the sores. When asked about any previous outbreaks, he thought he may have had something like this 1 year ago. He did not remember seeing blisters before the sores appeared.

The last time the patient had sexual relations was 2 months ago, with someone he met at a party. He claimed he used a condom. He did not have any lesions at that time and had never had a sexually transmitted disease before.

He had recently fallen in love, and was concerned about these ulcers—he did not want to give her any diseases. They had only kissed so far and he wanted to know what he should tell her. He said he had never had sex with men or injected any drugs. He has had a number of serially monogamous relationships and reported no other human immunodeficiency virus (HIV) risk factors.

The patient was a healthy-looking young man. Examination of his penis (Figure 1) showed the ulcers clearly visible (Figure 2). He had only shotty inguinal adenopathy that was nontender.

FIGURE 1
Painful sores on the genitals

FIGURE 2
Close-up of ulcers on the penis

What is the diagnosis?
What is the treatment and prevention strategy?

Differential diagnosis

The most likely causes of painful genital ulcers in this case are herpes simplex, chancroid, and syphilis. Granuloma inguinale and lymphogranuloma venereum (LGV) are rare causes of genital ulceration in the United States. A zipper accident or other trauma can cause genital ulceration, but the patient should be able to give a clear history of such an event.

By epidemiology alone, the order of likelihood for the cause of any genital ulceration is herpes, syphilis, then chancroid.

This case points to herpes

Herpes simplex is by far the most common cause of painful genital ulcers in the United States; at least 50 million people have genital herpes simplex virus (HSV) infection¹ The features of this case pointing to herpes are the appearance of multiple ulcers, the tingling pain that preceded the ulcers, and the history of a possible episode in the preceding year. While it would be helpful to have a history of blisters that preceded the ulcers, the evidence still points to herpes as the most likely diagnosis.

Could it be syphilis?

While the primary chancre of syphilis is classically described as painless, the patient with syphilis may experience pain. Syphilis tends to present as a single ulcer but may cause multiple ulcers.

Why not chancroid?

Chancroid may also cause multiple small painful ulcers. However, the ulcers of chancroid tend to be deeper than those of herpes and bleed more easily.

Other characteristics to look for

All of these sexually transmitted diseases can cause tender painful adenopathy, which is particularly characteristic of chancroid and LGV. Suppurative inguinal adenopathy with painful genital ulcers is almost pathognomonic of chancroid. With LGV, there may be a self-limited genital ulcer at the site of inoculation, which is often gone by the time a patient seeks care. Granuloma inguinale causes painless, progressive ulcerative lesions without regional lymphadenopathy. These lesions are highly vascular (with a characteristic beefy red appearance) and bleed easily on contact.¹ While it would be helpful to have a history of blisters that preceded the ulcers, the evidence still points to herpes as the most likely diagnosis.

Laboratory examination

Herpes

All patients with genital ulcers thought to be from an STD should be tested for syphilis and HIV regardless of other risk factors.¹ This patient should additionally be tested for herpes simplex. A bacteriologic test for chancroid is not necessary, but the clinician who first saw the patient asked that we conduct the test for chancroid—a culture for the Haemophilus ducreyi bacterium.

Isolation of HSV in cell culture is the preferred virologic test for patients with genital ulcers.¹Unfortunately, the sensitivity of culture declines rapidly as lesions begin to heal, usually within a few days of onset. Direct fluorescent antibody tests are also available. Both herpes culture and the direct fluorescent antibody test distinguish HSV-1 from HSV-2. Polymerase chain reaction assays for HSV DNA are highly sensitive, but their role in the diagnosis of genital ulcer disease has not been well-defined.

Most cases of recurrent genital herpes are caused by HSV-2. Specific serologic testing can be expensive, and is not needed at the time of the initial virologic screening. However, consider ordering the test at a subsequent visit, because the distinction between HSV serotypes influences prognosis and counseling. Also, because false-negative HSV cultures are common—especially with recurrent infection or healing lesions—type-specific serologic tests are useful for confirming a diagnosis of genital herpes.¹ Herpes serologies can also be used to help manage sexual partners of persons with genital herpes.

Syphilis

The Venereal Disease Research Laboratory (VDRL) test or rapid plasma reagin (RPR) test should be used to detect syphilis. Both tests are used for nonspecific screening only, because they measure anticardiolipin antibodies. A positive result should be confirmed with a specific treponemal test such as a fluorescent treponemal antibody absorption test (FTA-ABS).

The results of these laboratory tests are not available immediately during the patient’s visit. If there was a high suspicion for syphilis, a dark field examination from the ulcer exudate could be used to look for spirochetes while the patient was still in the office. In this case, the suspicion for syphilis was low.

Treatment: Antivirals

The major question is whether the patient should be treated empirically with medication. The most likely diagnosis is herpes simplex. Randomized trials indicate that 3 antiviral medications— acyclovir, famciclovir, and valacyclovir—provide clinical benefit for genital herpes (level of evidence [LOE]=1a).¹

The Centers for Disease Control and Prevention (CDC) 2002 treatment guidelines for STDs recommend the following medications for the first clinical episode of genital herpes:

• Acyclovir 400 mg orally, 3 times daily for 7–10 days or until clinically resolved, OR
• Acyclovir 200 mg orally, 5 times daily for 7–10 days or until clinically resolved, OR
• Famciclovir 250 mg orally, 3 times daily for 7–10 days or until clinically resolved, OR
• Valacyclovir 1 g orally, twice daily for 7–10 days or until clinically resolved.

Topical acyclovir is less effective than the oral formulaton and its use is discouraged.

The suspicion for syphilis is too low to warrant an intramuscular shot of penicillin, which is painful and can cause anaphylaxis in some patients. The likelihood of chancroid is too low to prescribe an oral antibiotic such as erythromycin.

The patient wanted empirical treatment for herpes. He was given valacyclovir, 1 gm for 7 days, taken twice daily, with the option to call in for more if the ulcers did not resolve by day 7. He was told he might apply petrolatum and clean gauze to the ulcers to diminish the pain when open ulcers rub against underwear. Acetaminophen or other analgesics were recommended for pain, and he was advised to avoid sexual activity until the ulcers had fully healed.

Preventing transmission

The patient is appropriately concerned about the transmission of this condition to a new partner. Not having a firm diagnosis makes definitive counseling more difficult. However, general principles of safe sex and condom use were discussed. On the follow-up visit the patient was told that the result of his herpes test was positive for HSV-2. Results of his RPR, HIV antibody test, and H ducreyiculture were all negative.

Information about condom use was reinforced, and the patient was told there is definitive evidence that condom use does diminish the risk of transmission of herpes from a man to a woman (LOE=1b).² That same study did not show that condom use prevents transmission from women to men. Also, changes in sexual behavior, correlated with counseling about avoiding sex when a partner has lesions, were associated with reduction in HSV-2 acquisition over time (LOE=1b).²

One study showed that the overall risk of genital HSV transmission in couples is low (10%/year). The risk may be significantly increased in women and in seronegative individuals.³ This speaks for serologic testing for the potential partner of this patient.

When recurrences are frequent, antiviral agents can decrease the frequency (LOE=1a).¹ If this patient has frequent recurrences, antiviral agents would be appropriate and would decrease the times when the patient is shedding virus asymptomatically.

Herpes is transmitted between sexual partners during asymptomatic shedding.¹ Acyclovir 400 mg twice daily can reduce asymptomatic viral shedding significantly among women with recurrent herpes simplex (LOE=1b).⁴ While it is likely this will decrease transmission from women to men, this has not been proven. Data on decreasing viral transmission from men to women by antiviral therapy is not available. At some point, the Glycoprotein-D-adjuvant vaccine may be an option to prevent genital herpes transmission to his partner.⁵

Note. The CDC 2002 sexually transmitted diseases treatment guidelines are available for download and use on a Palm handheld computer at www.cdcnpin.org/scripts/std/pda.asp.

A colleague came into the charting area and said he thought he had just seen his first case of chancroid. He asked me if I had a moment to see the patient, a 32-year-old African American man who noted the onset of painful sores on his penis 1 week ago. The patient consented to a second opinion. On further questioning, he remembered a tingling pain that started a few days prior to the sores. When asked about any previous outbreaks, he thought he may have had something like this 1 year ago. He did not remember seeing blisters before the sores appeared.

The last time the patient had sexual relations was 2 months ago, with someone he met at a party. He claimed he used a condom. He did not have any lesions at that time and had never had a sexually transmitted disease before.

He had recently fallen in love, and was concerned about these ulcers—he did not want to give her any diseases. They had only kissed so far and he wanted to know what he should tell her. He said he had never had sex with men or injected any drugs. He has had a number of serially monogamous relationships and reported no other human immunodeficiency virus (HIV) risk factors.

The patient was a healthy-looking young man. Examination of his penis (Figure 1) showed the ulcers clearly visible (Figure 2). He had only shotty inguinal adenopathy that was nontender.

FIGURE 1
Painful sores on the genitals

FIGURE 2
Close-up of ulcers on the penis

What is the diagnosis?
What is the treatment and prevention strategy?

Differential diagnosis

The most likely causes of painful genital ulcers in this case are herpes simplex, chancroid, and syphilis. Granuloma inguinale and lymphogranuloma venereum (LGV) are rare causes of genital ulceration in the United States. A zipper accident or other trauma can cause genital ulceration, but the patient should be able to give a clear history of such an event.

By epidemiology alone, the order of likelihood for the cause of any genital ulceration is herpes, syphilis, then chancroid.

This case points to herpes

Herpes simplex is by far the most common cause of painful genital ulcers in the United States; at least 50 million people have genital herpes simplex virus (HSV) infection¹ The features of this case pointing to herpes are the appearance of multiple ulcers, the tingling pain that preceded the ulcers, and the history of a possible episode in the preceding year. While it would be helpful to have a history of blisters that preceded the ulcers, the evidence still points to herpes as the most likely diagnosis.

Could it be syphilis?

While the primary chancre of syphilis is classically described as painless, the patient with syphilis may experience pain. Syphilis tends to present as a single ulcer but may cause multiple ulcers.

Why not chancroid?

Chancroid may also cause multiple small painful ulcers. However, the ulcers of chancroid tend to be deeper than those of herpes and bleed more easily.

Other characteristics to look for

All of these sexually transmitted diseases can cause tender painful adenopathy, which is particularly characteristic of chancroid and LGV. Suppurative inguinal adenopathy with painful genital ulcers is almost pathognomonic of chancroid. With LGV, there may be a self-limited genital ulcer at the site of inoculation, which is often gone by the time a patient seeks care. Granuloma inguinale causes painless, progressive ulcerative lesions without regional lymphadenopathy. These lesions are highly vascular (with a characteristic beefy red appearance) and bleed easily on contact.¹ While it would be helpful to have a history of blisters that preceded the ulcers, the evidence still points to herpes as the most likely diagnosis.

Laboratory examination

Herpes

All patients with genital ulcers thought to be from an STD should be tested for syphilis and HIV regardless of other risk factors.¹ This patient should additionally be tested for herpes simplex. A bacteriologic test for chancroid is not necessary, but the clinician who first saw the patient asked that we conduct the test for chancroid—a culture for the Haemophilus ducreyi bacterium.

Isolation of HSV in cell culture is the preferred virologic test for patients with genital ulcers.¹Unfortunately, the sensitivity of culture declines rapidly as lesions begin to heal, usually within a few days of onset. Direct fluorescent antibody tests are also available. Both herpes culture and the direct fluorescent antibody test distinguish HSV-1 from HSV-2. Polymerase chain reaction assays for HSV DNA are highly sensitive, but their role in the diagnosis of genital ulcer disease has not been well-defined.

Most cases of recurrent genital herpes are caused by HSV-2. Specific serologic testing can be expensive, and is not needed at the time of the initial virologic screening. However, consider ordering the test at a subsequent visit, because the distinction between HSV serotypes influences prognosis and counseling. Also, because false-negative HSV cultures are common—especially with recurrent infection or healing lesions—type-specific serologic tests are useful for confirming a diagnosis of genital herpes.¹ Herpes serologies can also be used to help manage sexual partners of persons with genital herpes.

Syphilis

The Venereal Disease Research Laboratory (VDRL) test or rapid plasma reagin (RPR) test should be used to detect syphilis. Both tests are used for nonspecific screening only, because they measure anticardiolipin antibodies. A positive result should be confirmed with a specific treponemal test such as a fluorescent treponemal antibody absorption test (FTA-ABS).

The results of these laboratory tests are not available immediately during the patient’s visit. If there was a high suspicion for syphilis, a dark field examination from the ulcer exudate could be used to look for spirochetes while the patient was still in the office. In this case, the suspicion for syphilis was low.

Treatment: Antivirals

The major question is whether the patient should be treated empirically with medication. The most likely diagnosis is herpes simplex. Randomized trials indicate that 3 antiviral medications— acyclovir, famciclovir, and valacyclovir—provide clinical benefit for genital herpes (level of evidence [LOE]=1a).¹

The Centers for Disease Control and Prevention (CDC) 2002 treatment guidelines for STDs recommend the following medications for the first clinical episode of genital herpes:

• Acyclovir 400 mg orally, 3 times daily for 7–10 days or until clinically resolved, OR
• Acyclovir 200 mg orally, 5 times daily for 7–10 days or until clinically resolved, OR
• Famciclovir 250 mg orally, 3 times daily for 7–10 days or until clinically resolved, OR
• Valacyclovir 1 g orally, twice daily for 7–10 days or until clinically resolved.

Topical acyclovir is less effective than the oral formulaton and its use is discouraged.

The suspicion for syphilis is too low to warrant an intramuscular shot of penicillin, which is painful and can cause anaphylaxis in some patients. The likelihood of chancroid is too low to prescribe an oral antibiotic such as erythromycin.

The patient wanted empirical treatment for herpes. He was given valacyclovir, 1 gm for 7 days, taken twice daily, with the option to call in for more if the ulcers did not resolve by day 7. He was told he might apply petrolatum and clean gauze to the ulcers to diminish the pain when open ulcers rub against underwear. Acetaminophen or other analgesics were recommended for pain, and he was advised to avoid sexual activity until the ulcers had fully healed.

Preventing transmission

The patient is appropriately concerned about the transmission of this condition to a new partner. Not having a firm diagnosis makes definitive counseling more difficult. However, general principles of safe sex and condom use were discussed. On the follow-up visit the patient was told that the result of his herpes test was positive for HSV-2. Results of his RPR, HIV antibody test, and H ducreyiculture were all negative.

Information about condom use was reinforced, and the patient was told there is definitive evidence that condom use does diminish the risk of transmission of herpes from a man to a woman (LOE=1b).² That same study did not show that condom use prevents transmission from women to men. Also, changes in sexual behavior, correlated with counseling about avoiding sex when a partner has lesions, were associated with reduction in HSV-2 acquisition over time (LOE=1b).²

One study showed that the overall risk of genital HSV transmission in couples is low (10%/year). The risk may be significantly increased in women and in seronegative individuals.³ This speaks for serologic testing for the potential partner of this patient.

When recurrences are frequent, antiviral agents can decrease the frequency (LOE=1a).¹ If this patient has frequent recurrences, antiviral agents would be appropriate and would decrease the times when the patient is shedding virus asymptomatically.

Herpes is transmitted between sexual partners during asymptomatic shedding.¹ Acyclovir 400 mg twice daily can reduce asymptomatic viral shedding significantly among women with recurrent herpes simplex (LOE=1b).⁴ While it is likely this will decrease transmission from women to men, this has not been proven. Data on decreasing viral transmission from men to women by antiviral therapy is not available. At some point, the Glycoprotein-D-adjuvant vaccine may be an option to prevent genital herpes transmission to his partner.⁵

Note. The CDC 2002 sexually transmitted diseases treatment guidelines are available for download and use on a Palm handheld computer at www.cdcnpin.org/scripts/std/pda.asp.

A 43-year-old African-American woman was seen for a rash on her right hand and neck. The rash appeared 2 weeks earlier, and was itchy. The patient had been applying alcohol directly to the affected skin.

The patient said she had experienced rashes on and off during her adult life. She has not worn necklaces for years because they irritate the skin around her neck. She also cannot wear wool clothing or any shirts with bright colors. She had not discussed this with a physician before, and she did not know why her skin is so sensitive.

The patient was not taking any new medications, using new bath products, or wearing new clothing before the rash appeared. However, she did remember getting new perfume 2 weeks earlier. She did not have asthma, but did have a mild hay fever. She was adopted and therefore did not know her biologic family’s medical history.

On close inspection, prominent erythema was seen around her neck and on the dorsum of her right hand (Figures 1 and 2).

FIGURE 1
Itchy rash on the neck…

FIGURE 2
…and the right hand

What is the diagnosis?
What are the management options?

Diagnosis: contact dermatitis

The patient demonstrated how she applied perfume to her neck using the back of her right hand. She has acute contact dermatitis on top of previously undiagnosed eczema. Her history is positive for contact dermatitis in reaction to metal (probably nickel) in necklaces and to various fabrics.

Contact dermatitis is a common inflammatory skin condition in which erythematous and pruritic skin lesions result from contact with a foreign substance. The term describes 2 diagnostic categories—allergic contact dermatitis and irritant contact dermatitis. In this case, the chemicals in the perfume may have acted as irritants. The alcohol she used to treat the rash was probably an irritant as well.

A hypersensitivity reaction to irritants and allergens

The mechanism of allergic contact dermatitis is a delayed hypersensitivity reaction. A foreign substance comes into contact with skin and links to skin protein, forming an antigen complex recognized by the immune system. In the skin, the major antigen-presenting cell is the Langerhans cell. When the epidermis is re-exposed to the antigen, the sensitized T-cells initiate an inflammatory cascade leading to changes in the skin. The reaction generally occurs within 12 to 48 hours in a sensitized person. The differential diagnoses for this patient include atopic dermatitis, psoriasis, and fungal infection.

Cosmetics, perfumes, and chemicals in cleaning solutions are known to cause irritant contact dermatitis. The most typical locations are hands or feet, with the dorsum affected more often than the palm or the sole. The lesions are usually erythematous and not well demarcated. The lesions may be macular, papular, or vesicular.

Allergic contact dermatitis often occurs after contact with allergens such as nickel in jewelry, or resins in plants such as poison ivy or poison oak. Vesicles may appear, and the hands are most commonly affected. The lesions may form a linear pattern, as in the case of plant dermatitis.

Evaluation: tests usually not needed

A diagnosis of contact dermatitis usually requires nothing more than findings in the patient’s history and physical exam. If a fungal infection is suspected, use a potassium hydroxide (KOH) preparation to look for hyphae or spores (see page 854 in this issue). Patch testing—placing common antigens on the patient’s skin and observing for reactions—is used to confirm the diagnosis of contact dermatitis and to determine the offending agent.

In this case, neither test was necessary or warranted because the history and physical exam led to a clear diagnosis that was treatable without having to analyze the chemicals in the perfume.

Treatment: remove the irritant, stop the swelling

Whether this is irritant or allergic contact dermatitis, the first line of treatment is to stop further exposure to the offending substance. A mid- to high-potency topical corticosteroid is recommended to stopping the inflammatory process (level of evidence [LOE]=5). (For an explanation of evidence-based medicine ratings, see page 000.) Ointments are more potent and particularly useful when the affected skin is dry and scaly.

Oral steroids are often used for severe local dermatitis, such as that caused by poison ivy (LOE=5). Topical tacrolimus ointment 0.1% is a more expensive option for the treatment of allergic contact dermatitis induced by nickel (LOE=2b).¹ Oral H1 blocking sedating anti-histamines (such as diphenhydramine and hydroxyzine) provide relief from itching and help with sleep. Sedating antihistamines may be more effective for itching, but are probably inadvisable for persons who must drive or operate machinery. Newer nonsedating anti-histamines are an option when sedating agents should be avoided.

Conclusion of visit

The patient was given 0.1% triamcinolone ointment (a generic mid-potency steroid) to apply 2 to 3 times a day to the affected areas. She did not want any oral medications for the itching, but understood that diphenhydramine is available without a prescription if needed. She planned to give the perfume away and understood it was now on her list of items to avoid. Her physician explained her underlying eczema and what could be done to prevent rashes.

A 43-year-old African-American woman was seen for a rash on her right hand and neck. The rash appeared 2 weeks earlier, and was itchy. The patient had been applying alcohol directly to the affected skin.

The patient said she had experienced rashes on and off during her adult life. She has not worn necklaces for years because they irritate the skin around her neck. She also cannot wear wool clothing or any shirts with bright colors. She had not discussed this with a physician before, and she did not know why her skin is so sensitive.

The patient was not taking any new medications, using new bath products, or wearing new clothing before the rash appeared. However, she did remember getting new perfume 2 weeks earlier. She did not have asthma, but did have a mild hay fever. She was adopted and therefore did not know her biologic family’s medical history.

On close inspection, prominent erythema was seen around her neck and on the dorsum of her right hand (Figures 1 and 2).

FIGURE 1
Itchy rash on the neck…

FIGURE 2
…and the right hand

What is the diagnosis?
What are the management options?

Diagnosis: contact dermatitis

The patient demonstrated how she applied perfume to her neck using the back of her right hand. She has acute contact dermatitis on top of previously undiagnosed eczema. Her history is positive for contact dermatitis in reaction to metal (probably nickel) in necklaces and to various fabrics.

Contact dermatitis is a common inflammatory skin condition in which erythematous and pruritic skin lesions result from contact with a foreign substance. The term describes 2 diagnostic categories—allergic contact dermatitis and irritant contact dermatitis. In this case, the chemicals in the perfume may have acted as irritants. The alcohol she used to treat the rash was probably an irritant as well.

A hypersensitivity reaction to irritants and allergens

The mechanism of allergic contact dermatitis is a delayed hypersensitivity reaction. A foreign substance comes into contact with skin and links to skin protein, forming an antigen complex recognized by the immune system. In the skin, the major antigen-presenting cell is the Langerhans cell. When the epidermis is re-exposed to the antigen, the sensitized T-cells initiate an inflammatory cascade leading to changes in the skin. The reaction generally occurs within 12 to 48 hours in a sensitized person. The differential diagnoses for this patient include atopic dermatitis, psoriasis, and fungal infection.

Cosmetics, perfumes, and chemicals in cleaning solutions are known to cause irritant contact dermatitis. The most typical locations are hands or feet, with the dorsum affected more often than the palm or the sole. The lesions are usually erythematous and not well demarcated. The lesions may be macular, papular, or vesicular.

Allergic contact dermatitis often occurs after contact with allergens such as nickel in jewelry, or resins in plants such as poison ivy or poison oak. Vesicles may appear, and the hands are most commonly affected. The lesions may form a linear pattern, as in the case of plant dermatitis.

Evaluation: tests usually not needed

A diagnosis of contact dermatitis usually requires nothing more than findings in the patient’s history and physical exam. If a fungal infection is suspected, use a potassium hydroxide (KOH) preparation to look for hyphae or spores (see page 854 in this issue). Patch testing—placing common antigens on the patient’s skin and observing for reactions—is used to confirm the diagnosis of contact dermatitis and to determine the offending agent.

In this case, neither test was necessary or warranted because the history and physical exam led to a clear diagnosis that was treatable without having to analyze the chemicals in the perfume.

Treatment: remove the irritant, stop the swelling

Whether this is irritant or allergic contact dermatitis, the first line of treatment is to stop further exposure to the offending substance. A mid- to high-potency topical corticosteroid is recommended to stopping the inflammatory process (level of evidence [LOE]=5). (For an explanation of evidence-based medicine ratings, see page 000.) Ointments are more potent and particularly useful when the affected skin is dry and scaly.

Oral steroids are often used for severe local dermatitis, such as that caused by poison ivy (LOE=5). Topical tacrolimus ointment 0.1% is a more expensive option for the treatment of allergic contact dermatitis induced by nickel (LOE=2b).¹ Oral H1 blocking sedating anti-histamines (such as diphenhydramine and hydroxyzine) provide relief from itching and help with sleep. Sedating antihistamines may be more effective for itching, but are probably inadvisable for persons who must drive or operate machinery. Newer nonsedating anti-histamines are an option when sedating agents should be avoided.

Conclusion of visit

The patient was given 0.1% triamcinolone ointment (a generic mid-potency steroid) to apply 2 to 3 times a day to the affected areas. She did not want any oral medications for the itching, but understood that diphenhydramine is available without a prescription if needed. She planned to give the perfume away and understood it was now on her list of items to avoid. Her physician explained her underlying eczema and what could be done to prevent rashes.

A 43-year-old African-American woman was seen for a rash on her right hand and neck. The rash appeared 2 weeks earlier, and was itchy. The patient had been applying alcohol directly to the affected skin.

The patient said she had experienced rashes on and off during her adult life. She has not worn necklaces for years because they irritate the skin around her neck. She also cannot wear wool clothing or any shirts with bright colors. She had not discussed this with a physician before, and she did not know why her skin is so sensitive.

The patient was not taking any new medications, using new bath products, or wearing new clothing before the rash appeared. However, she did remember getting new perfume 2 weeks earlier. She did not have asthma, but did have a mild hay fever. She was adopted and therefore did not know her biologic family’s medical history.

On close inspection, prominent erythema was seen around her neck and on the dorsum of her right hand (Figures 1 and 2).

FIGURE 1
Itchy rash on the neck…

FIGURE 2
…and the right hand

What is the diagnosis?
What are the management options?

Diagnosis: contact dermatitis

The patient demonstrated how she applied perfume to her neck using the back of her right hand. She has acute contact dermatitis on top of previously undiagnosed eczema. Her history is positive for contact dermatitis in reaction to metal (probably nickel) in necklaces and to various fabrics.

Contact dermatitis is a common inflammatory skin condition in which erythematous and pruritic skin lesions result from contact with a foreign substance. The term describes 2 diagnostic categories—allergic contact dermatitis and irritant contact dermatitis. In this case, the chemicals in the perfume may have acted as irritants. The alcohol she used to treat the rash was probably an irritant as well.

A hypersensitivity reaction to irritants and allergens

The mechanism of allergic contact dermatitis is a delayed hypersensitivity reaction. A foreign substance comes into contact with skin and links to skin protein, forming an antigen complex recognized by the immune system. In the skin, the major antigen-presenting cell is the Langerhans cell. When the epidermis is re-exposed to the antigen, the sensitized T-cells initiate an inflammatory cascade leading to changes in the skin. The reaction generally occurs within 12 to 48 hours in a sensitized person. The differential diagnoses for this patient include atopic dermatitis, psoriasis, and fungal infection.

Cosmetics, perfumes, and chemicals in cleaning solutions are known to cause irritant contact dermatitis. The most typical locations are hands or feet, with the dorsum affected more often than the palm or the sole. The lesions are usually erythematous and not well demarcated. The lesions may be macular, papular, or vesicular.

Allergic contact dermatitis often occurs after contact with allergens such as nickel in jewelry, or resins in plants such as poison ivy or poison oak. Vesicles may appear, and the hands are most commonly affected. The lesions may form a linear pattern, as in the case of plant dermatitis.

Evaluation: tests usually not needed

A diagnosis of contact dermatitis usually requires nothing more than findings in the patient’s history and physical exam. If a fungal infection is suspected, use a potassium hydroxide (KOH) preparation to look for hyphae or spores (see page 854 in this issue). Patch testing—placing common antigens on the patient’s skin and observing for reactions—is used to confirm the diagnosis of contact dermatitis and to determine the offending agent.

In this case, neither test was necessary or warranted because the history and physical exam led to a clear diagnosis that was treatable without having to analyze the chemicals in the perfume.

Treatment: remove the irritant, stop the swelling

Whether this is irritant or allergic contact dermatitis, the first line of treatment is to stop further exposure to the offending substance. A mid- to high-potency topical corticosteroid is recommended to stopping the inflammatory process (level of evidence [LOE]=5). (For an explanation of evidence-based medicine ratings, see page 000.) Ointments are more potent and particularly useful when the affected skin is dry and scaly.

Oral steroids are often used for severe local dermatitis, such as that caused by poison ivy (LOE=5). Topical tacrolimus ointment 0.1% is a more expensive option for the treatment of allergic contact dermatitis induced by nickel (LOE=2b).¹ Oral H1 blocking sedating anti-histamines (such as diphenhydramine and hydroxyzine) provide relief from itching and help with sleep. Sedating antihistamines may be more effective for itching, but are probably inadvisable for persons who must drive or operate machinery. Newer nonsedating anti-histamines are an option when sedating agents should be avoided.

Conclusion of visit

The patient was given 0.1% triamcinolone ointment (a generic mid-potency steroid) to apply 2 to 3 times a day to the affected areas. She did not want any oral medications for the itching, but understood that diphenhydramine is available without a prescription if needed. She planned to give the perfume away and understood it was now on her list of items to avoid. Her physician explained her underlying eczema and what could be done to prevent rashes.

A 28-year-old man came to the office with a rash on his face. He reported he has had this rash on and off for 3 years. The rash sometimes itches around his moustache, and it gets worse with stress—he has been under increasing stress for the past 2 months. He is in good health and does not have any other symptoms, and he denies any risk factors for human immunodeficiency virus (HIV).

Physical examination reveals erythema and scale across his eyebrows, cheeks, and near his moustache. On close inspection, the scale is visible under his moustache and eyebrows as well.

FIGURE 1
Erythema on the face

FIGURE 2
Close-up of erythema

What is the diagnosis?
What are the management options?

DIAGNOSIS

This young man has seborrhea (seborrheic dermatitis), a superficial inflammatory dermatitis. It is a common condition characterized by patches of erythema and scaling, usually on the scalp (ie, dandruff), eyebrows, nasolabial creases, forehead, cheeks, around the nose, behind the ears, and under facial hair. Seborrhea can also occur over the sternum and in the axillae, submammary folds, umbilicus, groin, and gluteal creases. These areas are regions with a greater number of pilosebaceous units, which produce sebum.

Seborrhea is thought to be caused by an inflammatory hypersensitivity to epidermal, bacterial, or yeast antigens. Persons with seborrhea have a profusion of Pityrosporum yeast on the skin. This yeast can be a normal part of skin flora; seborrhea is an inflammatory reaction to its presence. Seborrhea is characterized by remissions and exacerbations. The most common precipitating factors are stress, immuno suppression, and cold weather. The treatment of seborrhea should be directed at the inflammation and the Pityrosporum.

Epidemiology

Seborrhea is most commonly seen in patients aged 20 and 50 years, and mostly in males. The prevalence of seborrhea is approximately 3% to 5% in young adults who are HIV-negative. The prevalence of seborrhea is as high as 36% in HIV-positive persons, although the vast majority of persons with seborrhea have a normal immune system. No lab tests are required to make the diagnosis.

Treatment: antifungals and topical steroids

Treat seborrhea with a 2-pronged plan: antifungal agents for the yeast and topical corticosteroids for the inflammation. The antifungals can also be used to prevent exacerbations; steroids should only be applied to active areas of inflammation.

Fortunately, seborrhea on the face responds well to low-potency topical corticosteroids, such as 1% hydrocortisone cream or lotion. Still, corticosteroids should not be used on the face for prolonged periods to avoid skin atrophy and other side effects. The lotion is better for hair-covered areas as it is less messy to apply than a cream.

Antifungal shampoos

Over-the-counter dandruff shampoos have been the mainstay of therapy for seborrhea of the scalp. These products often contain selenium (ie, Selsun Blue) or zinc (ie, Head and Shoulders), both of which are toxic to Pityrosporum. Often patients have both seborrhea on the scalp and the face, and using these shampoos can cut down the amount of Pityrosporumon both. Instruct patients with facial hair to lather their beards and moustache with shampoo as well.

Both ketoconazole (Nizoral) 2% shampoo and selenium sulfide 2.5% shampoo are effective in the treatment of moderate to severe dandruff (level of evidence [LOE]: 1b).¹ Ketoconazole 2% shampoo is highly effective not only for clearing seborrheic dermatitis on the scalp but also for preventing relapse when used prophylactically once weekly (LOE: 1b).² Ketoconazole has become available in a 1% over-the-counter dandruff shampoo, but the 2% shampoo still requires a prescription.

Treating severe cases

When seborrhea of the scalp becomes more severe, add a higher-potency steroid solution or lotion to the treatment until the exacerbation is under control. Ketoconazole cream is also a good treatment for seborrheic dermatitis in areas other than the scalp. Other antifungal creams such as miconazole can be used to treat seborrhea of the face.

One trial demonstrated the effectiveness of topical 1% metronidazole gel in seborrheic dermatitis (LOE: 1b). At the 8-week follow-up, 14 patients in the metronidazole group showed a marked to complete improvement compared with 2 in the placebo group (P<.001; number needed to treat=2).³ This is not an approved indication for metronidazole gel, but it may be considered when other topical medications fail. In a randomized controlled trial using crossover design, treatment with a low-dose homeopathic preparation provided significant improvement in seborrheic dermatitis and dandruff after 10 weeks of dosing (LOE: 2b).⁴

Most seborrheic dermatitis is fully treatable with topical agents. When topical medications are not providing adequate results, oral antifungal agents may be considered. In 1 study, oral terbinafine was found to be effective in the treatment of moderate to severe seborrheic dermatitis. Clinical improvement following 4 weeks treatment with terbinafine was maintained 8 weeks after completing treatment (LOE: 1b).⁵

Conclusion of visit

The patient was given a prescription for 1% hydrocortisone lotion and 2% ketoconazole cream, both to be applied twice daily to the affected areas. He also planned to investigate the homeopathy option for the future. It was explained to the patient that these treatments may not be curative, and seborrhea may come back when he is under stress.

A 28-year-old man came to the office with a rash on his face. He reported he has had this rash on and off for 3 years. The rash sometimes itches around his moustache, and it gets worse with stress—he has been under increasing stress for the past 2 months. He is in good health and does not have any other symptoms, and he denies any risk factors for human immunodeficiency virus (HIV).

Physical examination reveals erythema and scale across his eyebrows, cheeks, and near his moustache. On close inspection, the scale is visible under his moustache and eyebrows as well.

FIGURE 1
Erythema on the face

FIGURE 2
Close-up of erythema

What is the diagnosis?
What are the management options?

DIAGNOSIS

This young man has seborrhea (seborrheic dermatitis), a superficial inflammatory dermatitis. It is a common condition characterized by patches of erythema and scaling, usually on the scalp (ie, dandruff), eyebrows, nasolabial creases, forehead, cheeks, around the nose, behind the ears, and under facial hair. Seborrhea can also occur over the sternum and in the axillae, submammary folds, umbilicus, groin, and gluteal creases. These areas are regions with a greater number of pilosebaceous units, which produce sebum.

Seborrhea is thought to be caused by an inflammatory hypersensitivity to epidermal, bacterial, or yeast antigens. Persons with seborrhea have a profusion of Pityrosporum yeast on the skin. This yeast can be a normal part of skin flora; seborrhea is an inflammatory reaction to its presence. Seborrhea is characterized by remissions and exacerbations. The most common precipitating factors are stress, immuno suppression, and cold weather. The treatment of seborrhea should be directed at the inflammation and the Pityrosporum.

Epidemiology

Seborrhea is most commonly seen in patients aged 20 and 50 years, and mostly in males. The prevalence of seborrhea is approximately 3% to 5% in young adults who are HIV-negative. The prevalence of seborrhea is as high as 36% in HIV-positive persons, although the vast majority of persons with seborrhea have a normal immune system. No lab tests are required to make the diagnosis.

Treatment: antifungals and topical steroids

Treat seborrhea with a 2-pronged plan: antifungal agents for the yeast and topical corticosteroids for the inflammation. The antifungals can also be used to prevent exacerbations; steroids should only be applied to active areas of inflammation.

Fortunately, seborrhea on the face responds well to low-potency topical corticosteroids, such as 1% hydrocortisone cream or lotion. Still, corticosteroids should not be used on the face for prolonged periods to avoid skin atrophy and other side effects. The lotion is better for hair-covered areas as it is less messy to apply than a cream.

Antifungal shampoos

Over-the-counter dandruff shampoos have been the mainstay of therapy for seborrhea of the scalp. These products often contain selenium (ie, Selsun Blue) or zinc (ie, Head and Shoulders), both of which are toxic to Pityrosporum. Often patients have both seborrhea on the scalp and the face, and using these shampoos can cut down the amount of Pityrosporumon both. Instruct patients with facial hair to lather their beards and moustache with shampoo as well.

Both ketoconazole (Nizoral) 2% shampoo and selenium sulfide 2.5% shampoo are effective in the treatment of moderate to severe dandruff (level of evidence [LOE]: 1b).¹ Ketoconazole 2% shampoo is highly effective not only for clearing seborrheic dermatitis on the scalp but also for preventing relapse when used prophylactically once weekly (LOE: 1b).² Ketoconazole has become available in a 1% over-the-counter dandruff shampoo, but the 2% shampoo still requires a prescription.

Treating severe cases

When seborrhea of the scalp becomes more severe, add a higher-potency steroid solution or lotion to the treatment until the exacerbation is under control. Ketoconazole cream is also a good treatment for seborrheic dermatitis in areas other than the scalp. Other antifungal creams such as miconazole can be used to treat seborrhea of the face.

One trial demonstrated the effectiveness of topical 1% metronidazole gel in seborrheic dermatitis (LOE: 1b). At the 8-week follow-up, 14 patients in the metronidazole group showed a marked to complete improvement compared with 2 in the placebo group (P<.001; number needed to treat=2).³ This is not an approved indication for metronidazole gel, but it may be considered when other topical medications fail. In a randomized controlled trial using crossover design, treatment with a low-dose homeopathic preparation provided significant improvement in seborrheic dermatitis and dandruff after 10 weeks of dosing (LOE: 2b).⁴

Most seborrheic dermatitis is fully treatable with topical agents. When topical medications are not providing adequate results, oral antifungal agents may be considered. In 1 study, oral terbinafine was found to be effective in the treatment of moderate to severe seborrheic dermatitis. Clinical improvement following 4 weeks treatment with terbinafine was maintained 8 weeks after completing treatment (LOE: 1b).⁵

Conclusion of visit

The patient was given a prescription for 1% hydrocortisone lotion and 2% ketoconazole cream, both to be applied twice daily to the affected areas. He also planned to investigate the homeopathy option for the future. It was explained to the patient that these treatments may not be curative, and seborrhea may come back when he is under stress.

A 28-year-old man came to the office with a rash on his face. He reported he has had this rash on and off for 3 years. The rash sometimes itches around his moustache, and it gets worse with stress—he has been under increasing stress for the past 2 months. He is in good health and does not have any other symptoms, and he denies any risk factors for human immunodeficiency virus (HIV).

Physical examination reveals erythema and scale across his eyebrows, cheeks, and near his moustache. On close inspection, the scale is visible under his moustache and eyebrows as well.

FIGURE 1
Erythema on the face

FIGURE 2
Close-up of erythema

What is the diagnosis?
What are the management options?

DIAGNOSIS

This young man has seborrhea (seborrheic dermatitis), a superficial inflammatory dermatitis. It is a common condition characterized by patches of erythema and scaling, usually on the scalp (ie, dandruff), eyebrows, nasolabial creases, forehead, cheeks, around the nose, behind the ears, and under facial hair. Seborrhea can also occur over the sternum and in the axillae, submammary folds, umbilicus, groin, and gluteal creases. These areas are regions with a greater number of pilosebaceous units, which produce sebum.

Seborrhea is thought to be caused by an inflammatory hypersensitivity to epidermal, bacterial, or yeast antigens. Persons with seborrhea have a profusion of Pityrosporum yeast on the skin. This yeast can be a normal part of skin flora; seborrhea is an inflammatory reaction to its presence. Seborrhea is characterized by remissions and exacerbations. The most common precipitating factors are stress, immuno suppression, and cold weather. The treatment of seborrhea should be directed at the inflammation and the Pityrosporum.

Epidemiology

Seborrhea is most commonly seen in patients aged 20 and 50 years, and mostly in males. The prevalence of seborrhea is approximately 3% to 5% in young adults who are HIV-negative. The prevalence of seborrhea is as high as 36% in HIV-positive persons, although the vast majority of persons with seborrhea have a normal immune system. No lab tests are required to make the diagnosis.

Treatment: antifungals and topical steroids

Treat seborrhea with a 2-pronged plan: antifungal agents for the yeast and topical corticosteroids for the inflammation. The antifungals can also be used to prevent exacerbations; steroids should only be applied to active areas of inflammation.

Fortunately, seborrhea on the face responds well to low-potency topical corticosteroids, such as 1% hydrocortisone cream or lotion. Still, corticosteroids should not be used on the face for prolonged periods to avoid skin atrophy and other side effects. The lotion is better for hair-covered areas as it is less messy to apply than a cream.

Antifungal shampoos

Over-the-counter dandruff shampoos have been the mainstay of therapy for seborrhea of the scalp. These products often contain selenium (ie, Selsun Blue) or zinc (ie, Head and Shoulders), both of which are toxic to Pityrosporum. Often patients have both seborrhea on the scalp and the face, and using these shampoos can cut down the amount of Pityrosporumon both. Instruct patients with facial hair to lather their beards and moustache with shampoo as well.

Both ketoconazole (Nizoral) 2% shampoo and selenium sulfide 2.5% shampoo are effective in the treatment of moderate to severe dandruff (level of evidence [LOE]: 1b).¹ Ketoconazole 2% shampoo is highly effective not only for clearing seborrheic dermatitis on the scalp but also for preventing relapse when used prophylactically once weekly (LOE: 1b).² Ketoconazole has become available in a 1% over-the-counter dandruff shampoo, but the 2% shampoo still requires a prescription.

Treating severe cases

When seborrhea of the scalp becomes more severe, add a higher-potency steroid solution or lotion to the treatment until the exacerbation is under control. Ketoconazole cream is also a good treatment for seborrheic dermatitis in areas other than the scalp. Other antifungal creams such as miconazole can be used to treat seborrhea of the face.

One trial demonstrated the effectiveness of topical 1% metronidazole gel in seborrheic dermatitis (LOE: 1b). At the 8-week follow-up, 14 patients in the metronidazole group showed a marked to complete improvement compared with 2 in the placebo group (P<.001; number needed to treat=2).³ This is not an approved indication for metronidazole gel, but it may be considered when other topical medications fail. In a randomized controlled trial using crossover design, treatment with a low-dose homeopathic preparation provided significant improvement in seborrheic dermatitis and dandruff after 10 weeks of dosing (LOE: 2b).⁴

Most seborrheic dermatitis is fully treatable with topical agents. When topical medications are not providing adequate results, oral antifungal agents may be considered. In 1 study, oral terbinafine was found to be effective in the treatment of moderate to severe seborrheic dermatitis. Clinical improvement following 4 weeks treatment with terbinafine was maintained 8 weeks after completing treatment (LOE: 1b).⁵

Conclusion of visit

The patient was given a prescription for 1% hydrocortisone lotion and 2% ketoconazole cream, both to be applied twice daily to the affected areas. He also planned to investigate the homeopathy option for the future. It was explained to the patient that these treatments may not be curative, and seborrhea may come back when he is under stress.

A 25-year-old woman visited her family doctor for treatment of skin lesions on her left leg, which had developed over the previous 8 weeks. The patient had just returned to the US after working with the Peace Corps in the Amazon rain forest for 3 months. During that time, she slept outside in the jungle without any skin protection—no mosquito netting, no insect repellent, no protective clothing on her extremities. She reported no recent history of trauma, burns, or chemical exposure to the leg, and she had been healthy prior to this skin condition. She reported that she was taking no medications, and was not using alcohol or tobacco.

The lesions started with the development of small pustules on her left leg and ankle. Over the next 3 weeks, these grew into larger, ulcerated lesions. The ulcers persisted for 5 more weeks despite multiple attempts at local topical treatments in Ecuador. No pain or itching were associated with the lesions.

The physical examination revealed a generally healthy woman, remarkable only for the 2 skin ulcers on her left lower leg and ankle (Figure 1 and Figure 2). The patient was afebrile, and had no lymphadenopathy or hepatosplenomegaly.

FIGURE 1
Cutaneous ulceration with indurated border.

Differential diagnosis of tropical skin ulcers

The woman’s family physician used the Internet to determine that the differential diagnosis of tropical skin ulcers includes localized cutaneous leishmaniasis, foreign body reaction, impetigo, pyoderma gangrenosum, bacterial or deep fungal infection, atypical mycobacterial infection, sarcoidosis, squamous and basal cell carcinoma, and superinfected insect bites. The combination of the patient’s history of potential exposure, clinical presentation, and epidemiology of leishmaniasis within the region in which she was working supports a presumptive diagnosis of localized cutaneous leishmaniasis.

Leishmaniasis

Leishmaniasis is comprised of several diverse diseases with varying degrees of severity, ranging from spontaneously healing skin ulcers to a disfiguring mucocutaneous disease, and even to fatal visceral illness. Endemic worldwide except Australia, Oceania, and Antarctica, leishmaniasis is found in the tropics and subtropics.

Approximately 2 million new cases occur each year, with markedly increasing incidence in several parts of the world resulting from international travel, immigration, military deployment, and human immunodeficiency virus coinfection.¹

An estimated 10% of the world’s population is at risk for contracting leishmaniasis. Most cases reported in the US are in travelers to countries where the disease is endemic, although sporadic cases have been reported in Texas and Oklahoma.²

Characteristics

Leishmaniasis is a vector-borne disease, caused by obligate intracellular protozoa of the genus Leishmaniaand transmitted by the bite of infected female sandflies. The disease may take several forms, including cutaneous, mucocutaneous, and visceral leishmaniasis, depending on the particular Leishmaniaspecies and host response.

Localized cutaneous leishmaniasis is characterized clinically by the appearance of skin lesions at the site of the sandfly bite, which typically present as inflammatory papules before progressing to nodules and ulcers. Local lymphadenopathy may occur. Sores may be painless or painful.

Both cutaneous and mucocutaneous forms generally yield normal laboratory values, although complete blood counts may show mild anemia, leukopenia, or thrombocytopenia.³ US travelers may consult numerous physicians before leishmaniasis is diagnosed. The median time from recognition of skin lesions to drug treatment is 112 days.⁴

Lab results

The patient’s complete blood count with differential, electrolytes, creatinine, liver function tests, and electrocardiogram were within normal limits. An infectious disease consultant suggested direct microscopic visualization of skin biopsies, dermal scrapings, and needle aspirates using Giemsa and Leishman stains, but these failed to reveal any parasitic organisms. It was thought these results were most likely false negatives.

In the best situation, the diagnosis of leishmaniasis is confirmed by isolating, visualizing, and culturing the parasite from infected tissue. Dermal scrapings or needle aspirates may reveal Leishmania amastigotes using a Giemsa stain. Early in the course of localized disease, Leishmania organisms may be numerous and found readily within the cytoplasm of macrophages. However, biopsy specimens from old lesions (>6 months), partially or incompletely treated, are frequently negative.

In vitro culture of the parasite from tissue samples using Nicolle-Noy-McNeal medium is often obtained to aid in diagnosis and to identify Leishmania species. With successful culture, the parasite can be sent to the Centers for Disease Control for speciation. New, rapid tests for leishmaniasis are being developed.

Treatment

Although 90% of skin lesions caused by cutaneous leishmaniasis heal spontaneously to form atrophic scars, the infectious disease consultant recommended treatment to prevent development of disfiguring mucocutaneous disease (level of evidence [LOE]=5)—otherwise, immunity may not be complete and skin ulcers can recur.

Experts believe it is important to treat cutaneous leishmaniasis if a species known or suspected of being capable of converting to the mucocutaneous disease form—eg, New World L braziliensis—is present. These lesions may appear months or even years after the initial exposure, and can be refractory to further treatment. However, surgical excision usually is not recommended because of the risk of relapse and further cosmetic disfigurement.³

Yearly follow-up to evaluate for recurrence or evolution of mucocutaneous leishmaniasis is crucial; early treatment of this form of the disease is more efficacious and can yield more favorable outcomes by limiting potential facial involvement (LOE=5).

Meglumine antimonate

The patient’s initial treatment included gluteal injections of meglumine antimonate at a dosage of 20 mg antimony/kg/d intramuscularly for a total course of 21 days (LOE=5). In addition, one tenth of each dose was injected directly into skin lesions under the peripheral margins, as shown in Figure 3 (LOE=5).

Side effects. The patient’s side effects from the meglumine antimonate therapy included insomnia, lightheadedness, increased fatigue, pain at the gluteal injection sites, bone aches, painful splenomegaly, and left leg myoclonic spasms. These signs and symptoms resolved shortly after completion of the course of therapy with no apparent sequelae. Monitoring cardiac, renal, and hepatic function before and during treatment is important, as meglumine antimonate has significant potential to cause renal and hepatic toxicity.

Outcome

The patient’s skin lesions began to show signs of healing after a few days of treatment. Healed lesions can be seen in Figure 4 Of course, we don’t know that these lesions would not have healed without treatment.

Follow-up diagnostic tests including electrocardiograms, liver function tests, and renal function showed normal values at the conclusion of the 21-day course of therapy.

Fluconazole studied

Since this patient was treated, a Saudi Arabian study was published on use of oral fluconazole 200 mg/d for 6 weeks in patients with cutaneous leishmaniasis (L major).⁵ At the 3-month followup, healing of lesions was complete for 79% of patients in the fluconazole group and 34% patients in the placebo group (LOE=2b).

The toxicity of this treatment is much lower than the antimonials; we should be looking for further evidence of its benefits in other countries with other species of Leishmania.

FIGURE 3
Perilesional infiltration of leishmaniasis lesion using meglumine antimonate.

FIGURE 4
Healed cutaneous leishmaniasis lesions on left leg.

Preventing sandfly bites

Leishmaniasis is preventable by avoiding contact with the vector—the sandfly—while living or traveling in endemic areas. Sandflies are most active from dusk to dawn. Though relatively poor fliers, they are small enough to fit through standard mosquito netting and make no audible noise. Effective prevention may be achieved by avoiding nighttime outdoor activities, using topical insecticides (eg, N, N diethyl-m-toluamide [DEET]) on exposed skin surfaces, using insecticide-impregnated clothing (permethrin stays in material for many washings), using fine-mesh mosquito netting, and sleeping with a fan.³

In this time of the globalization of infectious diseases, family doctors in the US should be aware of the tropical diseases that our patients may bring to their offices.

A 25-year-old woman visited her family doctor for treatment of skin lesions on her left leg, which had developed over the previous 8 weeks. The patient had just returned to the US after working with the Peace Corps in the Amazon rain forest for 3 months. During that time, she slept outside in the jungle without any skin protection—no mosquito netting, no insect repellent, no protective clothing on her extremities. She reported no recent history of trauma, burns, or chemical exposure to the leg, and she had been healthy prior to this skin condition. She reported that she was taking no medications, and was not using alcohol or tobacco.

The lesions started with the development of small pustules on her left leg and ankle. Over the next 3 weeks, these grew into larger, ulcerated lesions. The ulcers persisted for 5 more weeks despite multiple attempts at local topical treatments in Ecuador. No pain or itching were associated with the lesions.

The physical examination revealed a generally healthy woman, remarkable only for the 2 skin ulcers on her left lower leg and ankle (Figure 1 and Figure 2). The patient was afebrile, and had no lymphadenopathy or hepatosplenomegaly.

FIGURE 1
Cutaneous ulceration with indurated border.

Differential diagnosis of tropical skin ulcers

The woman’s family physician used the Internet to determine that the differential diagnosis of tropical skin ulcers includes localized cutaneous leishmaniasis, foreign body reaction, impetigo, pyoderma gangrenosum, bacterial or deep fungal infection, atypical mycobacterial infection, sarcoidosis, squamous and basal cell carcinoma, and superinfected insect bites. The combination of the patient’s history of potential exposure, clinical presentation, and epidemiology of leishmaniasis within the region in which she was working supports a presumptive diagnosis of localized cutaneous leishmaniasis.

Leishmaniasis

Leishmaniasis is comprised of several diverse diseases with varying degrees of severity, ranging from spontaneously healing skin ulcers to a disfiguring mucocutaneous disease, and even to fatal visceral illness. Endemic worldwide except Australia, Oceania, and Antarctica, leishmaniasis is found in the tropics and subtropics.

Approximately 2 million new cases occur each year, with markedly increasing incidence in several parts of the world resulting from international travel, immigration, military deployment, and human immunodeficiency virus coinfection.¹

An estimated 10% of the world’s population is at risk for contracting leishmaniasis. Most cases reported in the US are in travelers to countries where the disease is endemic, although sporadic cases have been reported in Texas and Oklahoma.²

Characteristics

Leishmaniasis is a vector-borne disease, caused by obligate intracellular protozoa of the genus Leishmaniaand transmitted by the bite of infected female sandflies. The disease may take several forms, including cutaneous, mucocutaneous, and visceral leishmaniasis, depending on the particular Leishmaniaspecies and host response.

Localized cutaneous leishmaniasis is characterized clinically by the appearance of skin lesions at the site of the sandfly bite, which typically present as inflammatory papules before progressing to nodules and ulcers. Local lymphadenopathy may occur. Sores may be painless or painful.

Both cutaneous and mucocutaneous forms generally yield normal laboratory values, although complete blood counts may show mild anemia, leukopenia, or thrombocytopenia.³ US travelers may consult numerous physicians before leishmaniasis is diagnosed. The median time from recognition of skin lesions to drug treatment is 112 days.⁴

Lab results

The patient’s complete blood count with differential, electrolytes, creatinine, liver function tests, and electrocardiogram were within normal limits. An infectious disease consultant suggested direct microscopic visualization of skin biopsies, dermal scrapings, and needle aspirates using Giemsa and Leishman stains, but these failed to reveal any parasitic organisms. It was thought these results were most likely false negatives.

In the best situation, the diagnosis of leishmaniasis is confirmed by isolating, visualizing, and culturing the parasite from infected tissue. Dermal scrapings or needle aspirates may reveal Leishmania amastigotes using a Giemsa stain. Early in the course of localized disease, Leishmania organisms may be numerous and found readily within the cytoplasm of macrophages. However, biopsy specimens from old lesions (>6 months), partially or incompletely treated, are frequently negative.

In vitro culture of the parasite from tissue samples using Nicolle-Noy-McNeal medium is often obtained to aid in diagnosis and to identify Leishmania species. With successful culture, the parasite can be sent to the Centers for Disease Control for speciation. New, rapid tests for leishmaniasis are being developed.

Treatment

Although 90% of skin lesions caused by cutaneous leishmaniasis heal spontaneously to form atrophic scars, the infectious disease consultant recommended treatment to prevent development of disfiguring mucocutaneous disease (level of evidence [LOE]=5)—otherwise, immunity may not be complete and skin ulcers can recur.

Experts believe it is important to treat cutaneous leishmaniasis if a species known or suspected of being capable of converting to the mucocutaneous disease form—eg, New World L braziliensis—is present. These lesions may appear months or even years after the initial exposure, and can be refractory to further treatment. However, surgical excision usually is not recommended because of the risk of relapse and further cosmetic disfigurement.³

Yearly follow-up to evaluate for recurrence or evolution of mucocutaneous leishmaniasis is crucial; early treatment of this form of the disease is more efficacious and can yield more favorable outcomes by limiting potential facial involvement (LOE=5).

Meglumine antimonate

The patient’s initial treatment included gluteal injections of meglumine antimonate at a dosage of 20 mg antimony/kg/d intramuscularly for a total course of 21 days (LOE=5). In addition, one tenth of each dose was injected directly into skin lesions under the peripheral margins, as shown in Figure 3 (LOE=5).

Side effects. The patient’s side effects from the meglumine antimonate therapy included insomnia, lightheadedness, increased fatigue, pain at the gluteal injection sites, bone aches, painful splenomegaly, and left leg myoclonic spasms. These signs and symptoms resolved shortly after completion of the course of therapy with no apparent sequelae. Monitoring cardiac, renal, and hepatic function before and during treatment is important, as meglumine antimonate has significant potential to cause renal and hepatic toxicity.

Outcome

The patient’s skin lesions began to show signs of healing after a few days of treatment. Healed lesions can be seen in Figure 4 Of course, we don’t know that these lesions would not have healed without treatment.

Follow-up diagnostic tests including electrocardiograms, liver function tests, and renal function showed normal values at the conclusion of the 21-day course of therapy.

Fluconazole studied

Since this patient was treated, a Saudi Arabian study was published on use of oral fluconazole 200 mg/d for 6 weeks in patients with cutaneous leishmaniasis (L major).⁵ At the 3-month followup, healing of lesions was complete for 79% of patients in the fluconazole group and 34% patients in the placebo group (LOE=2b).

The toxicity of this treatment is much lower than the antimonials; we should be looking for further evidence of its benefits in other countries with other species of Leishmania.

FIGURE 3
Perilesional infiltration of leishmaniasis lesion using meglumine antimonate.

FIGURE 4
Healed cutaneous leishmaniasis lesions on left leg.

Preventing sandfly bites

Leishmaniasis is preventable by avoiding contact with the vector—the sandfly—while living or traveling in endemic areas. Sandflies are most active from dusk to dawn. Though relatively poor fliers, they are small enough to fit through standard mosquito netting and make no audible noise. Effective prevention may be achieved by avoiding nighttime outdoor activities, using topical insecticides (eg, N, N diethyl-m-toluamide [DEET]) on exposed skin surfaces, using insecticide-impregnated clothing (permethrin stays in material for many washings), using fine-mesh mosquito netting, and sleeping with a fan.³

In this time of the globalization of infectious diseases, family doctors in the US should be aware of the tropical diseases that our patients may bring to their offices.

A 25-year-old woman visited her family doctor for treatment of skin lesions on her left leg, which had developed over the previous 8 weeks. The patient had just returned to the US after working with the Peace Corps in the Amazon rain forest for 3 months. During that time, she slept outside in the jungle without any skin protection—no mosquito netting, no insect repellent, no protective clothing on her extremities. She reported no recent history of trauma, burns, or chemical exposure to the leg, and she had been healthy prior to this skin condition. She reported that she was taking no medications, and was not using alcohol or tobacco.

The lesions started with the development of small pustules on her left leg and ankle. Over the next 3 weeks, these grew into larger, ulcerated lesions. The ulcers persisted for 5 more weeks despite multiple attempts at local topical treatments in Ecuador. No pain or itching were associated with the lesions.

The physical examination revealed a generally healthy woman, remarkable only for the 2 skin ulcers on her left lower leg and ankle (Figure 1 and Figure 2). The patient was afebrile, and had no lymphadenopathy or hepatosplenomegaly.

FIGURE 1
Cutaneous ulceration with indurated border.

Differential diagnosis of tropical skin ulcers

The woman’s family physician used the Internet to determine that the differential diagnosis of tropical skin ulcers includes localized cutaneous leishmaniasis, foreign body reaction, impetigo, pyoderma gangrenosum, bacterial or deep fungal infection, atypical mycobacterial infection, sarcoidosis, squamous and basal cell carcinoma, and superinfected insect bites. The combination of the patient’s history of potential exposure, clinical presentation, and epidemiology of leishmaniasis within the region in which she was working supports a presumptive diagnosis of localized cutaneous leishmaniasis.

Leishmaniasis

Leishmaniasis is comprised of several diverse diseases with varying degrees of severity, ranging from spontaneously healing skin ulcers to a disfiguring mucocutaneous disease, and even to fatal visceral illness. Endemic worldwide except Australia, Oceania, and Antarctica, leishmaniasis is found in the tropics and subtropics.

Approximately 2 million new cases occur each year, with markedly increasing incidence in several parts of the world resulting from international travel, immigration, military deployment, and human immunodeficiency virus coinfection.¹

An estimated 10% of the world’s population is at risk for contracting leishmaniasis. Most cases reported in the US are in travelers to countries where the disease is endemic, although sporadic cases have been reported in Texas and Oklahoma.²

Characteristics

Leishmaniasis is a vector-borne disease, caused by obligate intracellular protozoa of the genus Leishmaniaand transmitted by the bite of infected female sandflies. The disease may take several forms, including cutaneous, mucocutaneous, and visceral leishmaniasis, depending on the particular Leishmaniaspecies and host response.

Localized cutaneous leishmaniasis is characterized clinically by the appearance of skin lesions at the site of the sandfly bite, which typically present as inflammatory papules before progressing to nodules and ulcers. Local lymphadenopathy may occur. Sores may be painless or painful.

Both cutaneous and mucocutaneous forms generally yield normal laboratory values, although complete blood counts may show mild anemia, leukopenia, or thrombocytopenia.³ US travelers may consult numerous physicians before leishmaniasis is diagnosed. The median time from recognition of skin lesions to drug treatment is 112 days.⁴

Lab results

The patient’s complete blood count with differential, electrolytes, creatinine, liver function tests, and electrocardiogram were within normal limits. An infectious disease consultant suggested direct microscopic visualization of skin biopsies, dermal scrapings, and needle aspirates using Giemsa and Leishman stains, but these failed to reveal any parasitic organisms. It was thought these results were most likely false negatives.

In the best situation, the diagnosis of leishmaniasis is confirmed by isolating, visualizing, and culturing the parasite from infected tissue. Dermal scrapings or needle aspirates may reveal Leishmania amastigotes using a Giemsa stain. Early in the course of localized disease, Leishmania organisms may be numerous and found readily within the cytoplasm of macrophages. However, biopsy specimens from old lesions (>6 months), partially or incompletely treated, are frequently negative.

In vitro culture of the parasite from tissue samples using Nicolle-Noy-McNeal medium is often obtained to aid in diagnosis and to identify Leishmania species. With successful culture, the parasite can be sent to the Centers for Disease Control for speciation. New, rapid tests for leishmaniasis are being developed.

Treatment

Although 90% of skin lesions caused by cutaneous leishmaniasis heal spontaneously to form atrophic scars, the infectious disease consultant recommended treatment to prevent development of disfiguring mucocutaneous disease (level of evidence [LOE]=5)—otherwise, immunity may not be complete and skin ulcers can recur.

Experts believe it is important to treat cutaneous leishmaniasis if a species known or suspected of being capable of converting to the mucocutaneous disease form—eg, New World L braziliensis—is present. These lesions may appear months or even years after the initial exposure, and can be refractory to further treatment. However, surgical excision usually is not recommended because of the risk of relapse and further cosmetic disfigurement.³

Yearly follow-up to evaluate for recurrence or evolution of mucocutaneous leishmaniasis is crucial; early treatment of this form of the disease is more efficacious and can yield more favorable outcomes by limiting potential facial involvement (LOE=5).

Meglumine antimonate

The patient’s initial treatment included gluteal injections of meglumine antimonate at a dosage of 20 mg antimony/kg/d intramuscularly for a total course of 21 days (LOE=5). In addition, one tenth of each dose was injected directly into skin lesions under the peripheral margins, as shown in Figure 3 (LOE=5).

Side effects. The patient’s side effects from the meglumine antimonate therapy included insomnia, lightheadedness, increased fatigue, pain at the gluteal injection sites, bone aches, painful splenomegaly, and left leg myoclonic spasms. These signs and symptoms resolved shortly after completion of the course of therapy with no apparent sequelae. Monitoring cardiac, renal, and hepatic function before and during treatment is important, as meglumine antimonate has significant potential to cause renal and hepatic toxicity.

Outcome

The patient’s skin lesions began to show signs of healing after a few days of treatment. Healed lesions can be seen in Figure 4 Of course, we don’t know that these lesions would not have healed without treatment.

Follow-up diagnostic tests including electrocardiograms, liver function tests, and renal function showed normal values at the conclusion of the 21-day course of therapy.

Fluconazole studied

Since this patient was treated, a Saudi Arabian study was published on use of oral fluconazole 200 mg/d for 6 weeks in patients with cutaneous leishmaniasis (L major).⁵ At the 3-month followup, healing of lesions was complete for 79% of patients in the fluconazole group and 34% patients in the placebo group (LOE=2b).

The toxicity of this treatment is much lower than the antimonials; we should be looking for further evidence of its benefits in other countries with other species of Leishmania.

FIGURE 3
Perilesional infiltration of leishmaniasis lesion using meglumine antimonate.

FIGURE 4
Healed cutaneous leishmaniasis lesions on left leg.

Preventing sandfly bites

Leishmaniasis is preventable by avoiding contact with the vector—the sandfly—while living or traveling in endemic areas. Sandflies are most active from dusk to dawn. Though relatively poor fliers, they are small enough to fit through standard mosquito netting and make no audible noise. Effective prevention may be achieved by avoiding nighttime outdoor activities, using topical insecticides (eg, N, N diethyl-m-toluamide [DEET]) on exposed skin surfaces, using insecticide-impregnated clothing (permethrin stays in material for many washings), using fine-mesh mosquito netting, and sleeping with a fan.³

In this time of the globalization of infectious diseases, family doctors in the US should be aware of the tropical diseases that our patients may bring to their offices.

A 74-year-old Caucasian woman visited an outpatient clinic at a homeless shelter. Her chief concern was itching all over her body. Her chart revealed a history of chronic scabies and mental illness. She had been seen in the clinic on 4 separate occasions over a 2-year period for scabies. She claimed on this visit that she could not get rid of the scabies because people kept taking away her medication. She also stated she could see the creatures feed on her and move in and out of her skin.

The physical exam revealed that she was unwashed and disheveled. She had multiple excoriations on her extremities, hands, abdomen, back, and the nape of her neck (Figure 1).

FIGURE 1
Excoriations on the abdomen

FIGURE 2
Adult body lice and nymphs on clothing seams

Diagnosis

The woman’s appearance and mental status are consistent with schizophrenia; however, a diagnosis of scabies is not possible if she is really seeing the “bugs” on her body, as opposed to just imagining them. The scabies mite can only be seen with the aid of a microscope.

We looked for the bugs to confirm her story. While this could have been a case of delusions of parasitosis, on close inspection small “bugs” were indeed visible on her abdomen and along the seams of her pants. Multiple nits appeared attached to the hairs of her head, and a “bug” is noted to be feeding on the nape of her neck. This homeless woman has a massive infestation of body and head lice (Figure 2).

In the past she may have had a scabies infestation, but there was no documentation in the chart of any skin scrapings looked at under the microscope for diagnosis. It is more likely that she has been chronically infested with lice. Due to her mental illness, this patient may have been misdiagnosed with scabies based on the assumption that her claim to see the bugs was a hallucination. A close exam may not have been performed due to her mental illness and poor hygiene, along with the health care providers’ fears of catching scabies. Repeated documentation of scabies may have discouraged further investigation into another cause.

Pediculosis

Lice are bloodsucking obligate parasites. There are hundreds of millions of cases of pediculosis worldwide affecting men, women, and children from all socioeconomic classes.

Three types of lice infest humans: the head louse (Pediculus humanus capitis), the body louse (Pediculus humanus corporis), and the pubic louse (Phthirus pubis). Lice cling to hairs with their clawlike legs and pierce the skin, inject saliva, and then defecate while obtaining their blood meal. When exposed to lice, people clinically experience little irritation from the first bite, but after a short period they become sensitized. A hypersensitivity reaction—producing reddening of the skin, itching, and overall inflammation— subsequently develops.

Body lice are similar to head lice, except they are slightly larger. They are primarily seen in the homeless and indigent populations, with transmission occurring with direct body contact or sharing of contaminated clothes or bedding.

The body louse, contrary to popular belief, does not live on the body. It lives in the seams of clothing, clinging to the fibers. It will feed, remaining on the clothes, and only in massive infestations are they typically seen moving about the body. The axillae, groin, and truncal areas are the most severely affected. Patients have severe itching and tend to excoriate these regions. In chronically infested patients a postinflammatory hyperpigmentation can be observed.

Treatment

Persons infested with body lice need to discard or launder their clothing using hot water, and then bathe themselves. In cases of massive infestation—such as this case, in which head lice were also found—a pediculicide should be applied to the hair and entire body from head to toe. This can then be washed off in the shower (level of evidence [LOE]=1a, from Cochrane Review). This same Cochrane systematic review of the treatment of head lice found no evidence that any one pediculicide has greater effect than another (LOE=1a).¹

In this case, the patient did not want to get rid of her green pants because she was able to find the “bugs” easily in its seams, which she thought helped keep them under control. When we explained that the full treatment of this condition required her to be given new clothes, she finally accepted this course of action.

Arrangements were made for her to shower at the shelter and obtain new clothes, and she was given permethrin shampoo to apply over her entire body from head to toe. She was scheduled to follow up in 1 week but unfortunately never returned to the clinic.

A 74-year-old Caucasian woman visited an outpatient clinic at a homeless shelter. Her chief concern was itching all over her body. Her chart revealed a history of chronic scabies and mental illness. She had been seen in the clinic on 4 separate occasions over a 2-year period for scabies. She claimed on this visit that she could not get rid of the scabies because people kept taking away her medication. She also stated she could see the creatures feed on her and move in and out of her skin.

The physical exam revealed that she was unwashed and disheveled. She had multiple excoriations on her extremities, hands, abdomen, back, and the nape of her neck (Figure 1).

FIGURE 1
Excoriations on the abdomen

FIGURE 2
Adult body lice and nymphs on clothing seams

Diagnosis

The woman’s appearance and mental status are consistent with schizophrenia; however, a diagnosis of scabies is not possible if she is really seeing the “bugs” on her body, as opposed to just imagining them. The scabies mite can only be seen with the aid of a microscope.

We looked for the bugs to confirm her story. While this could have been a case of delusions of parasitosis, on close inspection small “bugs” were indeed visible on her abdomen and along the seams of her pants. Multiple nits appeared attached to the hairs of her head, and a “bug” is noted to be feeding on the nape of her neck. This homeless woman has a massive infestation of body and head lice (Figure 2).

In the past she may have had a scabies infestation, but there was no documentation in the chart of any skin scrapings looked at under the microscope for diagnosis. It is more likely that she has been chronically infested with lice. Due to her mental illness, this patient may have been misdiagnosed with scabies based on the assumption that her claim to see the bugs was a hallucination. A close exam may not have been performed due to her mental illness and poor hygiene, along with the health care providers’ fears of catching scabies. Repeated documentation of scabies may have discouraged further investigation into another cause.

Pediculosis

Lice are bloodsucking obligate parasites. There are hundreds of millions of cases of pediculosis worldwide affecting men, women, and children from all socioeconomic classes.

Three types of lice infest humans: the head louse (Pediculus humanus capitis), the body louse (Pediculus humanus corporis), and the pubic louse (Phthirus pubis). Lice cling to hairs with their clawlike legs and pierce the skin, inject saliva, and then defecate while obtaining their blood meal. When exposed to lice, people clinically experience little irritation from the first bite, but after a short period they become sensitized. A hypersensitivity reaction—producing reddening of the skin, itching, and overall inflammation— subsequently develops.

Body lice are similar to head lice, except they are slightly larger. They are primarily seen in the homeless and indigent populations, with transmission occurring with direct body contact or sharing of contaminated clothes or bedding.

The body louse, contrary to popular belief, does not live on the body. It lives in the seams of clothing, clinging to the fibers. It will feed, remaining on the clothes, and only in massive infestations are they typically seen moving about the body. The axillae, groin, and truncal areas are the most severely affected. Patients have severe itching and tend to excoriate these regions. In chronically infested patients a postinflammatory hyperpigmentation can be observed.

Treatment

Persons infested with body lice need to discard or launder their clothing using hot water, and then bathe themselves. In cases of massive infestation—such as this case, in which head lice were also found—a pediculicide should be applied to the hair and entire body from head to toe. This can then be washed off in the shower (level of evidence [LOE]=1a, from Cochrane Review). This same Cochrane systematic review of the treatment of head lice found no evidence that any one pediculicide has greater effect than another (LOE=1a).¹

In this case, the patient did not want to get rid of her green pants because she was able to find the “bugs” easily in its seams, which she thought helped keep them under control. When we explained that the full treatment of this condition required her to be given new clothes, she finally accepted this course of action.

Arrangements were made for her to shower at the shelter and obtain new clothes, and she was given permethrin shampoo to apply over her entire body from head to toe. She was scheduled to follow up in 1 week but unfortunately never returned to the clinic.

A 74-year-old Caucasian woman visited an outpatient clinic at a homeless shelter. Her chief concern was itching all over her body. Her chart revealed a history of chronic scabies and mental illness. She had been seen in the clinic on 4 separate occasions over a 2-year period for scabies. She claimed on this visit that she could not get rid of the scabies because people kept taking away her medication. She also stated she could see the creatures feed on her and move in and out of her skin.

The physical exam revealed that she was unwashed and disheveled. She had multiple excoriations on her extremities, hands, abdomen, back, and the nape of her neck (Figure 1).

FIGURE 1
Excoriations on the abdomen

FIGURE 2
Adult body lice and nymphs on clothing seams

Diagnosis

The woman’s appearance and mental status are consistent with schizophrenia; however, a diagnosis of scabies is not possible if she is really seeing the “bugs” on her body, as opposed to just imagining them. The scabies mite can only be seen with the aid of a microscope.

We looked for the bugs to confirm her story. While this could have been a case of delusions of parasitosis, on close inspection small “bugs” were indeed visible on her abdomen and along the seams of her pants. Multiple nits appeared attached to the hairs of her head, and a “bug” is noted to be feeding on the nape of her neck. This homeless woman has a massive infestation of body and head lice (Figure 2).

In the past she may have had a scabies infestation, but there was no documentation in the chart of any skin scrapings looked at under the microscope for diagnosis. It is more likely that she has been chronically infested with lice. Due to her mental illness, this patient may have been misdiagnosed with scabies based on the assumption that her claim to see the bugs was a hallucination. A close exam may not have been performed due to her mental illness and poor hygiene, along with the health care providers’ fears of catching scabies. Repeated documentation of scabies may have discouraged further investigation into another cause.

Pediculosis

Lice are bloodsucking obligate parasites. There are hundreds of millions of cases of pediculosis worldwide affecting men, women, and children from all socioeconomic classes.

Three types of lice infest humans: the head louse (Pediculus humanus capitis), the body louse (Pediculus humanus corporis), and the pubic louse (Phthirus pubis). Lice cling to hairs with their clawlike legs and pierce the skin, inject saliva, and then defecate while obtaining their blood meal. When exposed to lice, people clinically experience little irritation from the first bite, but after a short period they become sensitized. A hypersensitivity reaction—producing reddening of the skin, itching, and overall inflammation— subsequently develops.

Body lice are similar to head lice, except they are slightly larger. They are primarily seen in the homeless and indigent populations, with transmission occurring with direct body contact or sharing of contaminated clothes or bedding.

The body louse, contrary to popular belief, does not live on the body. It lives in the seams of clothing, clinging to the fibers. It will feed, remaining on the clothes, and only in massive infestations are they typically seen moving about the body. The axillae, groin, and truncal areas are the most severely affected. Patients have severe itching and tend to excoriate these regions. In chronically infested patients a postinflammatory hyperpigmentation can be observed.

Treatment

Persons infested with body lice need to discard or launder their clothing using hot water, and then bathe themselves. In cases of massive infestation—such as this case, in which head lice were also found—a pediculicide should be applied to the hair and entire body from head to toe. This can then be washed off in the shower (level of evidence [LOE]=1a, from Cochrane Review). This same Cochrane systematic review of the treatment of head lice found no evidence that any one pediculicide has greater effect than another (LOE=1a).¹

In this case, the patient did not want to get rid of her green pants because she was able to find the “bugs” easily in its seams, which she thought helped keep them under control. When we explained that the full treatment of this condition required her to be given new clothes, she finally accepted this course of action.

Arrangements were made for her to shower at the shelter and obtain new clothes, and she was given permethrin shampoo to apply over her entire body from head to toe. She was scheduled to follow up in 1 week but unfortunately never returned to the clinic.

A 47-year-old man had severe itching that started the previous day and kept him up all night. We examined his rash (Figure ) as we inquired about his history. He had no previous skin problems and no known allergies. He had no fever, pain, or malaise.

We discovered that a month ago he had started taking 1 trimethoprim-sulfamethoxazole double-strength tablet twice daily for chronic prostatitis. He was told he would need to take the medication for 3 months. Other than prostatitis, he had no other medical problems and was not taking any other medications.

FIGURE

What is the diagnosis?
What is the best course of management?

Diagnosis

This patient has urticaria (hives), presenting as variously shaped wheals on his chest and arms, resulting from a drug allergy.

These wheals are erythematous, nonpitting, edematous plaques that change size and shape by peripheral extension or regression. Urticaria is a dynamic process in which new wheals evolve as old ones resolve. Wheals result from localized capillary vasodilation, followed by transudation of protein-rich fluid into the surrounding skin. The wheals resolve when the fluid is slowly reabsorbed.

Urticaria symptoms and signs

Itching is the hallmark symptom of urticaria. Patients may also experience burning or stinging. Acute urticaria may exhibit a rapid or gradual onset. The onset and resolution of wheals vary with the cause, and vary even among persons who have the same underlying cause.

It is easier to determine the precipitating factor—a drug allergy in this case—with acute urticaria than chronic urticaria (lasting 6 or more weeks). Angioedema causes a deeper edematous area that involves transudation of fluid into the dermis and subcutaneous tissue.

Wheals vary in size from the small, 2-mm papules of cholinergic urticaria to giant hives that may cover an extremity or part of the abdomen in a single wheal. The wheal may be all red or white, or the border may be red with the remainder of the surface white. Wheals may be surrounded by a red halo. The larger lesions (over 5 mm in diameter) are called plaques. In patients with darker skin, the wheals may be skin-colored only, with no visible erythema.

Differential diagnosis

The full differential diagnosis of urticaria includes angioedema, insect bites, food allergies, erythema multiforme, bullous pemphigoid, dermatitis herpetiformis, urticarial contact dermatitis, pruritic urticarial papules and plaques of pregnancy (known as PUPPP), mast cell releasability syndromes, and urticarial vasculitis.

Food allergies and insect bites can sometimes cause urticarial reactions. Angioedema is seen more often on the face and is especially found around the mouth and eyes.

Management

First-generation antihistamines

H₁ antihistamines, which compete with histamine for the H₁ receptor sites, are the first-line therapy for urticaria. First-generation antihistamines—such as diphenhydramine, chlorpheniramine, and hydroxyzine—can be very effective, particularly in acute cases. Diphenhydramine and chlorpheniramine are available over-the-counter and are relatively inexpensive. Hydroxyzine still requires a prescription, and it is thought to be more potent than diphenhydramine and chlorpheniramine.

The sedation experienced with these agents may help reduce pruritus, but it may also be a danger when a patient is driving or operating machinery. Because people respond to these medicines differently, you must weigh the bene fits and risks for each person based on their response to the medicine.

Second-generation antihistamines

Second-generation H₁ antihistamines—such as astemizole, loratadine, desloratadine, and cetirizine—cause less sedation and are better for long-term daytime use. While more expensive, they are valuable in the management of chronic urticaria.

In the most refractory cases, combinations of various antihistamines may be useful in suppressing symptomatology. A nonsedating H₁ antihistamine in the daytime can be combined with a sedating H₁antihistamine and doxepin at night. An H₂antihistamine can be added to this regimen before starting oral prednisone (level of evidence=5 for all the treatment regimes cited, based on expert opinion without explicit critical appraisal and based on physiology).

This patient’s treatment

The patient understood that he must stop taking the trimethoprim-sulfamethoxazole tablets and was given a fluoroquinolone for his chronic prostatitis. He took 1 dose of diphenhydramine (Benadryl, in this case) in the office, and the itching and wheals began to subside.

He was also told the could purchase diphenhydramine over the counter to continue to relieve his itching and wheals. He was advised that if it made him sleepy, he could call the office for a prescription for a nonsedating antihistamine.

This patient’s outcome

The patient was significantly better the next day and never needed additional medications for urticaria. His chronic prostatitis did resolve with a 2-month course of fluoroquinolone.

A 47-year-old man had severe itching that started the previous day and kept him up all night. We examined his rash (Figure ) as we inquired about his history. He had no previous skin problems and no known allergies. He had no fever, pain, or malaise.

We discovered that a month ago he had started taking 1 trimethoprim-sulfamethoxazole double-strength tablet twice daily for chronic prostatitis. He was told he would need to take the medication for 3 months. Other than prostatitis, he had no other medical problems and was not taking any other medications.

FIGURE

What is the diagnosis?
What is the best course of management?

Diagnosis

This patient has urticaria (hives), presenting as variously shaped wheals on his chest and arms, resulting from a drug allergy.

These wheals are erythematous, nonpitting, edematous plaques that change size and shape by peripheral extension or regression. Urticaria is a dynamic process in which new wheals evolve as old ones resolve. Wheals result from localized capillary vasodilation, followed by transudation of protein-rich fluid into the surrounding skin. The wheals resolve when the fluid is slowly reabsorbed.

Urticaria symptoms and signs

Itching is the hallmark symptom of urticaria. Patients may also experience burning or stinging. Acute urticaria may exhibit a rapid or gradual onset. The onset and resolution of wheals vary with the cause, and vary even among persons who have the same underlying cause.

It is easier to determine the precipitating factor—a drug allergy in this case—with acute urticaria than chronic urticaria (lasting 6 or more weeks). Angioedema causes a deeper edematous area that involves transudation of fluid into the dermis and subcutaneous tissue.

Wheals vary in size from the small, 2-mm papules of cholinergic urticaria to giant hives that may cover an extremity or part of the abdomen in a single wheal. The wheal may be all red or white, or the border may be red with the remainder of the surface white. Wheals may be surrounded by a red halo. The larger lesions (over 5 mm in diameter) are called plaques. In patients with darker skin, the wheals may be skin-colored only, with no visible erythema.

Differential diagnosis

The full differential diagnosis of urticaria includes angioedema, insect bites, food allergies, erythema multiforme, bullous pemphigoid, dermatitis herpetiformis, urticarial contact dermatitis, pruritic urticarial papules and plaques of pregnancy (known as PUPPP), mast cell releasability syndromes, and urticarial vasculitis.

Food allergies and insect bites can sometimes cause urticarial reactions. Angioedema is seen more often on the face and is especially found around the mouth and eyes.

Management

First-generation antihistamines

H₁ antihistamines, which compete with histamine for the H₁ receptor sites, are the first-line therapy for urticaria. First-generation antihistamines—such as diphenhydramine, chlorpheniramine, and hydroxyzine—can be very effective, particularly in acute cases. Diphenhydramine and chlorpheniramine are available over-the-counter and are relatively inexpensive. Hydroxyzine still requires a prescription, and it is thought to be more potent than diphenhydramine and chlorpheniramine.

The sedation experienced with these agents may help reduce pruritus, but it may also be a danger when a patient is driving or operating machinery. Because people respond to these medicines differently, you must weigh the bene fits and risks for each person based on their response to the medicine.

Second-generation antihistamines

Second-generation H₁ antihistamines—such as astemizole, loratadine, desloratadine, and cetirizine—cause less sedation and are better for long-term daytime use. While more expensive, they are valuable in the management of chronic urticaria.

In the most refractory cases, combinations of various antihistamines may be useful in suppressing symptomatology. A nonsedating H₁ antihistamine in the daytime can be combined with a sedating H₁antihistamine and doxepin at night. An H₂antihistamine can be added to this regimen before starting oral prednisone (level of evidence=5 for all the treatment regimes cited, based on expert opinion without explicit critical appraisal and based on physiology).

This patient’s treatment

The patient understood that he must stop taking the trimethoprim-sulfamethoxazole tablets and was given a fluoroquinolone for his chronic prostatitis. He took 1 dose of diphenhydramine (Benadryl, in this case) in the office, and the itching and wheals began to subside.

He was also told the could purchase diphenhydramine over the counter to continue to relieve his itching and wheals. He was advised that if it made him sleepy, he could call the office for a prescription for a nonsedating antihistamine.

This patient’s outcome

The patient was significantly better the next day and never needed additional medications for urticaria. His chronic prostatitis did resolve with a 2-month course of fluoroquinolone.

A 47-year-old man had severe itching that started the previous day and kept him up all night. We examined his rash (Figure ) as we inquired about his history. He had no previous skin problems and no known allergies. He had no fever, pain, or malaise.

We discovered that a month ago he had started taking 1 trimethoprim-sulfamethoxazole double-strength tablet twice daily for chronic prostatitis. He was told he would need to take the medication for 3 months. Other than prostatitis, he had no other medical problems and was not taking any other medications.

FIGURE

What is the diagnosis?
What is the best course of management?

Diagnosis

This patient has urticaria (hives), presenting as variously shaped wheals on his chest and arms, resulting from a drug allergy.

These wheals are erythematous, nonpitting, edematous plaques that change size and shape by peripheral extension or regression. Urticaria is a dynamic process in which new wheals evolve as old ones resolve. Wheals result from localized capillary vasodilation, followed by transudation of protein-rich fluid into the surrounding skin. The wheals resolve when the fluid is slowly reabsorbed.

Urticaria symptoms and signs

Itching is the hallmark symptom of urticaria. Patients may also experience burning or stinging. Acute urticaria may exhibit a rapid or gradual onset. The onset and resolution of wheals vary with the cause, and vary even among persons who have the same underlying cause.

It is easier to determine the precipitating factor—a drug allergy in this case—with acute urticaria than chronic urticaria (lasting 6 or more weeks). Angioedema causes a deeper edematous area that involves transudation of fluid into the dermis and subcutaneous tissue.

Wheals vary in size from the small, 2-mm papules of cholinergic urticaria to giant hives that may cover an extremity or part of the abdomen in a single wheal. The wheal may be all red or white, or the border may be red with the remainder of the surface white. Wheals may be surrounded by a red halo. The larger lesions (over 5 mm in diameter) are called plaques. In patients with darker skin, the wheals may be skin-colored only, with no visible erythema.

Differential diagnosis

The full differential diagnosis of urticaria includes angioedema, insect bites, food allergies, erythema multiforme, bullous pemphigoid, dermatitis herpetiformis, urticarial contact dermatitis, pruritic urticarial papules and plaques of pregnancy (known as PUPPP), mast cell releasability syndromes, and urticarial vasculitis.

Food allergies and insect bites can sometimes cause urticarial reactions. Angioedema is seen more often on the face and is especially found around the mouth and eyes.

Management

First-generation antihistamines

H₁ antihistamines, which compete with histamine for the H₁ receptor sites, are the first-line therapy for urticaria. First-generation antihistamines—such as diphenhydramine, chlorpheniramine, and hydroxyzine—can be very effective, particularly in acute cases. Diphenhydramine and chlorpheniramine are available over-the-counter and are relatively inexpensive. Hydroxyzine still requires a prescription, and it is thought to be more potent than diphenhydramine and chlorpheniramine.

The sedation experienced with these agents may help reduce pruritus, but it may also be a danger when a patient is driving or operating machinery. Because people respond to these medicines differently, you must weigh the bene fits and risks for each person based on their response to the medicine.

Second-generation antihistamines

Second-generation H₁ antihistamines—such as astemizole, loratadine, desloratadine, and cetirizine—cause less sedation and are better for long-term daytime use. While more expensive, they are valuable in the management of chronic urticaria.

In the most refractory cases, combinations of various antihistamines may be useful in suppressing symptomatology. A nonsedating H₁ antihistamine in the daytime can be combined with a sedating H₁antihistamine and doxepin at night. An H₂antihistamine can be added to this regimen before starting oral prednisone (level of evidence=5 for all the treatment regimes cited, based on expert opinion without explicit critical appraisal and based on physiology).

This patient’s treatment

The patient understood that he must stop taking the trimethoprim-sulfamethoxazole tablets and was given a fluoroquinolone for his chronic prostatitis. He took 1 dose of diphenhydramine (Benadryl, in this case) in the office, and the itching and wheals began to subside.

He was also told the could purchase diphenhydramine over the counter to continue to relieve his itching and wheals. He was advised that if it made him sleepy, he could call the office for a prescription for a nonsedating antihistamine.

This patient’s outcome

The patient was significantly better the next day and never needed additional medications for urticaria. His chronic prostatitis did resolve with a 2-month course of fluoroquinolone.

This Photo Rounds aims to help you hone your visual diagnostic skills to recognize the 3 most common types of skin cancer (in order of prevalence): basal cell carcinoma, squamous cell carcinoma, and melanoma. (See also “Diagnosis of skin malignancy,”.)

Pattern recognition informs us about the initial differential diagnosis and the appropriate biopsy method.

Basal cell carcinoma

The most common basal cell carcinoma is nodular. Figure 1 shows nodular basal cell carcinoma with a raised pearly pink and white nodule with a smooth, shiny, translucent surface. The smooth surface reflects a loss of the normal pore pattern. Telangiectasias can be seen within the lesion, and the border may appear to be rolled.

Figure 2 shows a nodular basal cell carcinoma that is both pigmented and has some central ulceration. This figure demonstrates how difficult it is to distinguish a melanoma from a pigmented basal cell carcinoma.

Figure 3 shows the next most frequently seen basal cell carcinoma, the superficial basal cell carcinoma. These lesions are found most often on the trunk and extremities rather than the face, and may appear as a pink scaling plaque. Sometimes shallow crusts or erosions may be seen within the lesion. Note the thready border present around this scaling plaque. This slightly elevated border is the best tip-off to recognizing this scaling plaque as a skin cancer rather than a plaque of psoriasis or nummular eczema.

Figure 4 shows the least prevalent basal cell carcinoma, the sclerosing type. These lesions are often ivory-colored or colorless. The skin may be appear atrophic and feel indurated. A sclerosing basal cell carcinoma may resemble a scar and can be easily overlooked. These carcinomas are often called morpheaform because of the resemblance to localized scleroderma (morphea). They are also called infiltrating basal cell carcinoma because they infiltrate into the surrounding normal skin in a way not easily visible to the naked eye.

FIGURE 1

Squamous cell carcinoma

The next most common type of skin cancer is squamous cell carcinoma. These cancers are most often found on the lips, ears, and scalp. Figure 5 shows a squamous cell carcinoma on the lower lip. The lower lip catches more ultraviolet rays from the sun than the upper lip, and therefore is the more prevalent site for this carcinoma.

Figure 6 shows a squamous cell carcinoma on the face in an area of sun exposure. This carcinoma looks very much like the superficial basal cell carcinoma in Figure 3, except that the squamous cell carcinoma has one area of crusting. The only way to make a definitive diagnosis is to perform biopsy and get a pathologic reading.

FIGURE 5

There are many different types of melanomas. Figure 7 shows one version of the most common melanoma, the superficial spreading melanoma. The dark pigmentation around the outside of this melanoma is where the lesion is superficially spreading away from the center (which has lost its pigmentation). This lesion meets all of the ABCDE criteria for malignant melanoma.

Figure 8 shows a melanoma arising in a lentigo maligna on the face of an older patient. It is not necessary to know the type of melanoma before the biopsy, but you should recognize that the lesion may be melanoma and perform a full-thickness biopsy. What may have started off as a simple age spot in this patient has become a malignant melanoma (see page 214).

Figure 9 shows a very thick and deadly nodular melanoma. One can recognize a nodular melanoma by the increased thickness and its darker pigmentation.

Figure 10 shows an uncommon type of melanoma but one of the deadliest—the acrallentiginous melanoma. This melanoma is often not detected until it has metastasized. Any pigmented lesion on the hands, feet, or under the fingernails that looks like melanoma should be biopsied early before it gets to this deadly stage.

FIGURE 7

Choice of biopsy technique

Choice of biopsy technique depends on the type of skin lesion. Most basal cell and squamous cell carcinomas can be adequately biopsied by the shave technique because the pathology is superficial and the prognosis is not determined by thickness. Exceptions include sclerosing basal cell carcinomas and very flat superficial basal cell carcinomas, which are best biopsied with a full-thickness specimen in the form of a punch biopsy or excisional biopsy.

All lesions you suspect may be melanoma should be biopsied with a full-thickness specimen. Very small and very large lesions can initially be biopsied using a punch instrument. The excisional biopsy is preferred when the lesion can be removed with one surgical procedure. Depending upon the depth of the melanoma, you may need to perform a second surgery to get adequate margins.

This Photo Rounds aims to help you hone your visual diagnostic skills to recognize the 3 most common types of skin cancer (in order of prevalence): basal cell carcinoma, squamous cell carcinoma, and melanoma. (See also “Diagnosis of skin malignancy,”.)

Pattern recognition informs us about the initial differential diagnosis and the appropriate biopsy method.

Basal cell carcinoma

The most common basal cell carcinoma is nodular. Figure 1 shows nodular basal cell carcinoma with a raised pearly pink and white nodule with a smooth, shiny, translucent surface. The smooth surface reflects a loss of the normal pore pattern. Telangiectasias can be seen within the lesion, and the border may appear to be rolled.

Figure 2 shows a nodular basal cell carcinoma that is both pigmented and has some central ulceration. This figure demonstrates how difficult it is to distinguish a melanoma from a pigmented basal cell carcinoma.

Figure 3 shows the next most frequently seen basal cell carcinoma, the superficial basal cell carcinoma. These lesions are found most often on the trunk and extremities rather than the face, and may appear as a pink scaling plaque. Sometimes shallow crusts or erosions may be seen within the lesion. Note the thready border present around this scaling plaque. This slightly elevated border is the best tip-off to recognizing this scaling plaque as a skin cancer rather than a plaque of psoriasis or nummular eczema.

Figure 4 shows the least prevalent basal cell carcinoma, the sclerosing type. These lesions are often ivory-colored or colorless. The skin may be appear atrophic and feel indurated. A sclerosing basal cell carcinoma may resemble a scar and can be easily overlooked. These carcinomas are often called morpheaform because of the resemblance to localized scleroderma (morphea). They are also called infiltrating basal cell carcinoma because they infiltrate into the surrounding normal skin in a way not easily visible to the naked eye.

FIGURE 1

Squamous cell carcinoma

The next most common type of skin cancer is squamous cell carcinoma. These cancers are most often found on the lips, ears, and scalp. Figure 5 shows a squamous cell carcinoma on the lower lip. The lower lip catches more ultraviolet rays from the sun than the upper lip, and therefore is the more prevalent site for this carcinoma.

Figure 6 shows a squamous cell carcinoma on the face in an area of sun exposure. This carcinoma looks very much like the superficial basal cell carcinoma in Figure 3, except that the squamous cell carcinoma has one area of crusting. The only way to make a definitive diagnosis is to perform biopsy and get a pathologic reading.

FIGURE 5

There are many different types of melanomas. Figure 7 shows one version of the most common melanoma, the superficial spreading melanoma. The dark pigmentation around the outside of this melanoma is where the lesion is superficially spreading away from the center (which has lost its pigmentation). This lesion meets all of the ABCDE criteria for malignant melanoma.

Figure 8 shows a melanoma arising in a lentigo maligna on the face of an older patient. It is not necessary to know the type of melanoma before the biopsy, but you should recognize that the lesion may be melanoma and perform a full-thickness biopsy. What may have started off as a simple age spot in this patient has become a malignant melanoma (see page 214).

Figure 9 shows a very thick and deadly nodular melanoma. One can recognize a nodular melanoma by the increased thickness and its darker pigmentation.

Figure 10 shows an uncommon type of melanoma but one of the deadliest—the acrallentiginous melanoma. This melanoma is often not detected until it has metastasized. Any pigmented lesion on the hands, feet, or under the fingernails that looks like melanoma should be biopsied early before it gets to this deadly stage.

FIGURE 7

Choice of biopsy technique

Choice of biopsy technique depends on the type of skin lesion. Most basal cell and squamous cell carcinomas can be adequately biopsied by the shave technique because the pathology is superficial and the prognosis is not determined by thickness. Exceptions include sclerosing basal cell carcinomas and very flat superficial basal cell carcinomas, which are best biopsied with a full-thickness specimen in the form of a punch biopsy or excisional biopsy.

All lesions you suspect may be melanoma should be biopsied with a full-thickness specimen. Very small and very large lesions can initially be biopsied using a punch instrument. The excisional biopsy is preferred when the lesion can be removed with one surgical procedure. Depending upon the depth of the melanoma, you may need to perform a second surgery to get adequate margins.

This Photo Rounds aims to help you hone your visual diagnostic skills to recognize the 3 most common types of skin cancer (in order of prevalence): basal cell carcinoma, squamous cell carcinoma, and melanoma. (See also “Diagnosis of skin malignancy,”.)

Pattern recognition informs us about the initial differential diagnosis and the appropriate biopsy method.

Basal cell carcinoma

The most common basal cell carcinoma is nodular. Figure 1 shows nodular basal cell carcinoma with a raised pearly pink and white nodule with a smooth, shiny, translucent surface. The smooth surface reflects a loss of the normal pore pattern. Telangiectasias can be seen within the lesion, and the border may appear to be rolled.

Figure 2 shows a nodular basal cell carcinoma that is both pigmented and has some central ulceration. This figure demonstrates how difficult it is to distinguish a melanoma from a pigmented basal cell carcinoma.

Figure 3 shows the next most frequently seen basal cell carcinoma, the superficial basal cell carcinoma. These lesions are found most often on the trunk and extremities rather than the face, and may appear as a pink scaling plaque. Sometimes shallow crusts or erosions may be seen within the lesion. Note the thready border present around this scaling plaque. This slightly elevated border is the best tip-off to recognizing this scaling plaque as a skin cancer rather than a plaque of psoriasis or nummular eczema.

Figure 4 shows the least prevalent basal cell carcinoma, the sclerosing type. These lesions are often ivory-colored or colorless. The skin may be appear atrophic and feel indurated. A sclerosing basal cell carcinoma may resemble a scar and can be easily overlooked. These carcinomas are often called morpheaform because of the resemblance to localized scleroderma (morphea). They are also called infiltrating basal cell carcinoma because they infiltrate into the surrounding normal skin in a way not easily visible to the naked eye.

FIGURE 1

Squamous cell carcinoma

The next most common type of skin cancer is squamous cell carcinoma. These cancers are most often found on the lips, ears, and scalp. Figure 5 shows a squamous cell carcinoma on the lower lip. The lower lip catches more ultraviolet rays from the sun than the upper lip, and therefore is the more prevalent site for this carcinoma.

Figure 6 shows a squamous cell carcinoma on the face in an area of sun exposure. This carcinoma looks very much like the superficial basal cell carcinoma in Figure 3, except that the squamous cell carcinoma has one area of crusting. The only way to make a definitive diagnosis is to perform biopsy and get a pathologic reading.

FIGURE 5

There are many different types of melanomas. Figure 7 shows one version of the most common melanoma, the superficial spreading melanoma. The dark pigmentation around the outside of this melanoma is where the lesion is superficially spreading away from the center (which has lost its pigmentation). This lesion meets all of the ABCDE criteria for malignant melanoma.

Figure 8 shows a melanoma arising in a lentigo maligna on the face of an older patient. It is not necessary to know the type of melanoma before the biopsy, but you should recognize that the lesion may be melanoma and perform a full-thickness biopsy. What may have started off as a simple age spot in this patient has become a malignant melanoma (see page 214).

Figure 9 shows a very thick and deadly nodular melanoma. One can recognize a nodular melanoma by the increased thickness and its darker pigmentation.

Figure 10 shows an uncommon type of melanoma but one of the deadliest—the acrallentiginous melanoma. This melanoma is often not detected until it has metastasized. Any pigmented lesion on the hands, feet, or under the fingernails that looks like melanoma should be biopsied early before it gets to this deadly stage.

FIGURE 7

Choice of biopsy technique

Choice of biopsy technique depends on the type of skin lesion. Most basal cell and squamous cell carcinomas can be adequately biopsied by the shave technique because the pathology is superficial and the prognosis is not determined by thickness. Exceptions include sclerosing basal cell carcinomas and very flat superficial basal cell carcinomas, which are best biopsied with a full-thickness specimen in the form of a punch biopsy or excisional biopsy.

All lesions you suspect may be melanoma should be biopsied with a full-thickness specimen. Very small and very large lesions can initially be biopsied using a punch instrument. The excisional biopsy is preferred when the lesion can be removed with one surgical procedure. Depending upon the depth of the melanoma, you may need to perform a second surgery to get adequate margins.

A 48-year-old African American woman came to our office because the discoloration of one fingernail that began months earlier had spread to a second finger, and the first finger to become discolored had begun to hurt.

The patient had initially seen another physician, who prescribed itraconazole for presumptive onychomycosis. The patient received a pulse therapy course of itraconazole for 3 months and had no improvement. Therapy ended 4 months ago, and a month ago the end of her left index finger began to ache.

The patient works at a computer, and typing causes pain in the left index finger. A review of her chart reveals she is taking a diuretic for hypertension; there are no other health problems.

What is the diagnosis?

Before taking a more extensive history, it is appropriate to look at her fingers more closely to collect data that will inform questioning. By applying pattern recognition skills first, you can form hypotheses and use the remainder of the exam to test them.

How would you describe the abnormalities seen in Figure 1 and Figure 2 (pattern recognition), and what would be the differential diagnosis (hypotheses)?

What further history, physical exam, or laboratory tests should be completed (hypothesis testing)?

FIGURE 1
This patient’s fingernail had been discolored for months and the fingertip had recently begun to hurt.

Figure 1 shows a brownish discoloration of the fingernail, with small pits particularly prominent around the lunula (the semicircular light area adjacent to the proximal nail fold). There is also evidence of onycholysis (separation of the nail from the nail bed). The vertical ridging is not abnormal.

Figure 2 shows a well-circumscribed brown discoloration in the proximal nail called an oil spot. These nail findings are classic for psoriasis.¹

Figure 1 also shows subtle swelling of the distal interphalangeal (DIP) joint. It is this area the patient said was painful, and she had joint tenderness to palpation over this DIP joint only.

Hypotheses

The 2 most likely diagnoses are:

• psoriasis causing nail changes while psoriatic arthritis is developing
• onychomycosis with incidental joint pain of the DIP joint.

Other causes of nail changes include lichen planus, chronic candida paronychia, and Reiter’s disease. Epidemiologically the most likely diagnosis is onychomycosis, which is far more prevalent than the other conditions. However, this patient has already failed a course of an oral antifungal agent, and her nail changes are more consistent with psoriasis.

Hypothesis testing

Questions and physical examination focus on collecting data to determine the more likely of the two diagnoses, psoriasis and fungal nail disease. The patient denied having any skin lesions and a history of psoriasis. She also said she had no athlete’s foot or problems with her toenails or other hand. Her knees ache from time to time, which she attributed to aging.

Physical exam revealed no evidence of psoriasis on the skin and no tinea pedis or onychomycosis of the toenails. She had no other skin findings suggestive of lichen planus or Reiter’s disease. Looking more closely at the fingernails, we saw no evidence of subungual keratoses, which are frequently found in onychomycosis.

A scraping and clipping of the fingernail was sent for fungal culture, and an x-ray film of that digit revealed no bony changes. The fungal culture results 2 weeks later were negative.

Patient follow-up

We made a presumptive diagnosis of psoriatic nail changes and psoriatic arthritis, and the patient was sent to a rheumatologist for consultation. The rheumatologist agreed with the diagnosis and placed the patient on nonsteroidal anti-inflammatory drugs to treat the early psoriatic arthritis.

The patient developed more areas of psoriatic arthritis involvement over the subsequent years and became less concerned about the appearance of her nails. Eventually the psoriatic arthritis progressed to the point where the patient was taking remititive agents for inflammatory arthropathy. She never did develop the skin lesions of psoriasis.

Nail changes of psoriasis

It has been reported that 30% of patients with psoriasis have nail changes, the most common being pitting. Onycholysis is the next most frequent change, and the oil spot is less frequent but not rare.

Not everyone with nail pitting has psoriasis; however, there is a high correlation between psoriatic arthritis and nail pitting.

Patients with psoriasis and psoriatic arthritis have a higher percentage of nail changes than patients with psoriasis of the skin only. In 1 study, nail changes were noted in 86.5% of patients affected by arthropathic psoriasis, and the most common fingernail change was pitting.²

This particular case shows it is possible to have psoriatic arthritis and psoriatic nail changes without psoriasis of the skin. Fortunately, the patient did not have an adverse reaction to the itraconazole prescribed for the incorrectly diagnosed onychomycosis.

It is debatable whether fungal cultures are needed before prescribing oral antifungal agents for onychomycosis. This was 1 case in which the nail findings may have steered the clinician toward getting a nail scraping for microscopic analysis using potassium hydroxide or a fungal culture. Negative findings would have spared the patient the treatment with an expensive agent with known liver toxicity.

The onset of pain, swelling, and tenderness of the DIP joint of the affected nail helped to make the diagnosis. It is the finger joint most commonly affected by psoriatic arthritis.

Treatment of psoriasis of the nails

There is no good treatment for psoriasis of the nails. Treatment regimens that have been studied include injection of steroids into the nail matrix and use of topical retinoids. Intralesional steroid injections are very painful, and the results are not adequate to recommend this treatment.

A study of topical retinoid tazorotene showed some promise.³ The study size was small, however, and the measured change was not great. But for patients desperately looking for help for psoriatic nail changes, the topical treatment may be worth a try.

Figure 3 shows a different patient with an interesting connection between involvement of psoriatic arthritis in the finger and accompanying nail changes. This man had psoriatic plaques over his fingers and a severely swollen DIP joint of the middle finger with significant accompanying nail changes. The inflammatory reaction in the DIP joint is accompanied by abnormal changes in the nail matrix, producing a psoriatic nail on the same finger.

FIGURE 3
Another patient’s hand, with psoriatic plaques and swollen distal interphalangeal joint.

A 48-year-old African American woman came to our office because the discoloration of one fingernail that began months earlier had spread to a second finger, and the first finger to become discolored had begun to hurt.

The patient had initially seen another physician, who prescribed itraconazole for presumptive onychomycosis. The patient received a pulse therapy course of itraconazole for 3 months and had no improvement. Therapy ended 4 months ago, and a month ago the end of her left index finger began to ache.

The patient works at a computer, and typing causes pain in the left index finger. A review of her chart reveals she is taking a diuretic for hypertension; there are no other health problems.

What is the diagnosis?

Before taking a more extensive history, it is appropriate to look at her fingers more closely to collect data that will inform questioning. By applying pattern recognition skills first, you can form hypotheses and use the remainder of the exam to test them.

How would you describe the abnormalities seen in Figure 1 and Figure 2 (pattern recognition), and what would be the differential diagnosis (hypotheses)?

What further history, physical exam, or laboratory tests should be completed (hypothesis testing)?

FIGURE 1
This patient’s fingernail had been discolored for months and the fingertip had recently begun to hurt.

Figure 1 shows a brownish discoloration of the fingernail, with small pits particularly prominent around the lunula (the semicircular light area adjacent to the proximal nail fold). There is also evidence of onycholysis (separation of the nail from the nail bed). The vertical ridging is not abnormal.

Figure 2 shows a well-circumscribed brown discoloration in the proximal nail called an oil spot. These nail findings are classic for psoriasis.¹

Figure 1 also shows subtle swelling of the distal interphalangeal (DIP) joint. It is this area the patient said was painful, and she had joint tenderness to palpation over this DIP joint only.

Hypotheses

The 2 most likely diagnoses are:

• psoriasis causing nail changes while psoriatic arthritis is developing
• onychomycosis with incidental joint pain of the DIP joint.

Other causes of nail changes include lichen planus, chronic candida paronychia, and Reiter’s disease. Epidemiologically the most likely diagnosis is onychomycosis, which is far more prevalent than the other conditions. However, this patient has already failed a course of an oral antifungal agent, and her nail changes are more consistent with psoriasis.

Hypothesis testing

Questions and physical examination focus on collecting data to determine the more likely of the two diagnoses, psoriasis and fungal nail disease. The patient denied having any skin lesions and a history of psoriasis. She also said she had no athlete’s foot or problems with her toenails or other hand. Her knees ache from time to time, which she attributed to aging.

Physical exam revealed no evidence of psoriasis on the skin and no tinea pedis or onychomycosis of the toenails. She had no other skin findings suggestive of lichen planus or Reiter’s disease. Looking more closely at the fingernails, we saw no evidence of subungual keratoses, which are frequently found in onychomycosis.

A scraping and clipping of the fingernail was sent for fungal culture, and an x-ray film of that digit revealed no bony changes. The fungal culture results 2 weeks later were negative.

Patient follow-up

We made a presumptive diagnosis of psoriatic nail changes and psoriatic arthritis, and the patient was sent to a rheumatologist for consultation. The rheumatologist agreed with the diagnosis and placed the patient on nonsteroidal anti-inflammatory drugs to treat the early psoriatic arthritis.

The patient developed more areas of psoriatic arthritis involvement over the subsequent years and became less concerned about the appearance of her nails. Eventually the psoriatic arthritis progressed to the point where the patient was taking remititive agents for inflammatory arthropathy. She never did develop the skin lesions of psoriasis.

Nail changes of psoriasis

It has been reported that 30% of patients with psoriasis have nail changes, the most common being pitting. Onycholysis is the next most frequent change, and the oil spot is less frequent but not rare.

Not everyone with nail pitting has psoriasis; however, there is a high correlation between psoriatic arthritis and nail pitting.

Patients with psoriasis and psoriatic arthritis have a higher percentage of nail changes than patients with psoriasis of the skin only. In 1 study, nail changes were noted in 86.5% of patients affected by arthropathic psoriasis, and the most common fingernail change was pitting.²

This particular case shows it is possible to have psoriatic arthritis and psoriatic nail changes without psoriasis of the skin. Fortunately, the patient did not have an adverse reaction to the itraconazole prescribed for the incorrectly diagnosed onychomycosis.

It is debatable whether fungal cultures are needed before prescribing oral antifungal agents for onychomycosis. This was 1 case in which the nail findings may have steered the clinician toward getting a nail scraping for microscopic analysis using potassium hydroxide or a fungal culture. Negative findings would have spared the patient the treatment with an expensive agent with known liver toxicity.

The onset of pain, swelling, and tenderness of the DIP joint of the affected nail helped to make the diagnosis. It is the finger joint most commonly affected by psoriatic arthritis.

Treatment of psoriasis of the nails

There is no good treatment for psoriasis of the nails. Treatment regimens that have been studied include injection of steroids into the nail matrix and use of topical retinoids. Intralesional steroid injections are very painful, and the results are not adequate to recommend this treatment.

A study of topical retinoid tazorotene showed some promise.³ The study size was small, however, and the measured change was not great. But for patients desperately looking for help for psoriatic nail changes, the topical treatment may be worth a try.

Figure 3 shows a different patient with an interesting connection between involvement of psoriatic arthritis in the finger and accompanying nail changes. This man had psoriatic plaques over his fingers and a severely swollen DIP joint of the middle finger with significant accompanying nail changes. The inflammatory reaction in the DIP joint is accompanied by abnormal changes in the nail matrix, producing a psoriatic nail on the same finger.

FIGURE 3
Another patient’s hand, with psoriatic plaques and swollen distal interphalangeal joint.

A 48-year-old African American woman came to our office because the discoloration of one fingernail that began months earlier had spread to a second finger, and the first finger to become discolored had begun to hurt.

The patient had initially seen another physician, who prescribed itraconazole for presumptive onychomycosis. The patient received a pulse therapy course of itraconazole for 3 months and had no improvement. Therapy ended 4 months ago, and a month ago the end of her left index finger began to ache.

The patient works at a computer, and typing causes pain in the left index finger. A review of her chart reveals she is taking a diuretic for hypertension; there are no other health problems.

What is the diagnosis?

Before taking a more extensive history, it is appropriate to look at her fingers more closely to collect data that will inform questioning. By applying pattern recognition skills first, you can form hypotheses and use the remainder of the exam to test them.

How would you describe the abnormalities seen in Figure 1 and Figure 2 (pattern recognition), and what would be the differential diagnosis (hypotheses)?

What further history, physical exam, or laboratory tests should be completed (hypothesis testing)?

FIGURE 1
This patient’s fingernail had been discolored for months and the fingertip had recently begun to hurt.

Figure 1 shows a brownish discoloration of the fingernail, with small pits particularly prominent around the lunula (the semicircular light area adjacent to the proximal nail fold). There is also evidence of onycholysis (separation of the nail from the nail bed). The vertical ridging is not abnormal.

Figure 2 shows a well-circumscribed brown discoloration in the proximal nail called an oil spot. These nail findings are classic for psoriasis.¹

Figure 1 also shows subtle swelling of the distal interphalangeal (DIP) joint. It is this area the patient said was painful, and she had joint tenderness to palpation over this DIP joint only.

Hypotheses

The 2 most likely diagnoses are:

• psoriasis causing nail changes while psoriatic arthritis is developing
• onychomycosis with incidental joint pain of the DIP joint.

Other causes of nail changes include lichen planus, chronic candida paronychia, and Reiter’s disease. Epidemiologically the most likely diagnosis is onychomycosis, which is far more prevalent than the other conditions. However, this patient has already failed a course of an oral antifungal agent, and her nail changes are more consistent with psoriasis.

Hypothesis testing

Questions and physical examination focus on collecting data to determine the more likely of the two diagnoses, psoriasis and fungal nail disease. The patient denied having any skin lesions and a history of psoriasis. She also said she had no athlete’s foot or problems with her toenails or other hand. Her knees ache from time to time, which she attributed to aging.

Physical exam revealed no evidence of psoriasis on the skin and no tinea pedis or onychomycosis of the toenails. She had no other skin findings suggestive of lichen planus or Reiter’s disease. Looking more closely at the fingernails, we saw no evidence of subungual keratoses, which are frequently found in onychomycosis.

A scraping and clipping of the fingernail was sent for fungal culture, and an x-ray film of that digit revealed no bony changes. The fungal culture results 2 weeks later were negative.

Patient follow-up

We made a presumptive diagnosis of psoriatic nail changes and psoriatic arthritis, and the patient was sent to a rheumatologist for consultation. The rheumatologist agreed with the diagnosis and placed the patient on nonsteroidal anti-inflammatory drugs to treat the early psoriatic arthritis.

The patient developed more areas of psoriatic arthritis involvement over the subsequent years and became less concerned about the appearance of her nails. Eventually the psoriatic arthritis progressed to the point where the patient was taking remititive agents for inflammatory arthropathy. She never did develop the skin lesions of psoriasis.

Nail changes of psoriasis

It has been reported that 30% of patients with psoriasis have nail changes, the most common being pitting. Onycholysis is the next most frequent change, and the oil spot is less frequent but not rare.

Not everyone with nail pitting has psoriasis; however, there is a high correlation between psoriatic arthritis and nail pitting.

Patients with psoriasis and psoriatic arthritis have a higher percentage of nail changes than patients with psoriasis of the skin only. In 1 study, nail changes were noted in 86.5% of patients affected by arthropathic psoriasis, and the most common fingernail change was pitting.²

This particular case shows it is possible to have psoriatic arthritis and psoriatic nail changes without psoriasis of the skin. Fortunately, the patient did not have an adverse reaction to the itraconazole prescribed for the incorrectly diagnosed onychomycosis.

It is debatable whether fungal cultures are needed before prescribing oral antifungal agents for onychomycosis. This was 1 case in which the nail findings may have steered the clinician toward getting a nail scraping for microscopic analysis using potassium hydroxide or a fungal culture. Negative findings would have spared the patient the treatment with an expensive agent with known liver toxicity.

The onset of pain, swelling, and tenderness of the DIP joint of the affected nail helped to make the diagnosis. It is the finger joint most commonly affected by psoriatic arthritis.

Treatment of psoriasis of the nails

There is no good treatment for psoriasis of the nails. Treatment regimens that have been studied include injection of steroids into the nail matrix and use of topical retinoids. Intralesional steroid injections are very painful, and the results are not adequate to recommend this treatment.

A study of topical retinoid tazorotene showed some promise.³ The study size was small, however, and the measured change was not great. But for patients desperately looking for help for psoriatic nail changes, the topical treatment may be worth a try.

Figure 3 shows a different patient with an interesting connection between involvement of psoriatic arthritis in the finger and accompanying nail changes. This man had psoriatic plaques over his fingers and a severely swollen DIP joint of the middle finger with significant accompanying nail changes. The inflammatory reaction in the DIP joint is accompanied by abnormal changes in the nail matrix, producing a psoriatic nail on the same finger.

FIGURE 3
Another patient’s hand, with psoriatic plaques and swollen distal interphalangeal joint.

A 52-year-old African American homeless man visited a clinic at the local shelter, complaining of pain in his left knee for the past 2 days. He denied trauma or any history of knee injuries. He also denied any recent sexual activity. The patient was limping from significant pain. The patient’s clothes and hygiene were in poor condition. He worked in the fish market and had taken on the odor of his workplace. He admitted to a history of alcohol and substance abuse and was unwilling to discuss his psychiatric history. His chart indicated he had been diagnosed with schizophrenia.

The patient was afebrile and had a swollen warm left knee (Figure 1). A crusty skin lesion with a small amount of purulence was seen over his patella. There was evidence of a joint effusion and the skin appeared red around the whole knee region. The patient could not fully flex his knee. The physical exam demonstrated normal ligamentous stability.

We offered to take the patient to the county hospital to obtain the appropriate diagnostic procedure and to initiate inpatient care. He adamantly refused treatment in a hospital, stating he was “too busy” to go the hospital and he only wanted “some pills.”

What else could you now do to care for this patient?

The differential diagnosis includes septic arthritis (such as staphylococcal and gonococcal infections of the knee joint), inflammatory types of arthritis, septic bursitis, cellulitis, and impetigo. Joint aspiration was performed in the clinic because the patient refused to go to the emergency room for diagnosis and treatment.

As seen in Figure 2, 10 mL of clear viscous yellow fluid was aspirated from the affected joint. Nine mL of aspirate was sent to a clinical laboratory for cell count, Gram stain, culture and sensitivity, crystal analysis, and microscopic examination. A drop of aspirate was placed on a wet mount and examined with plain light microscopy (Figure 3).

FIGURE 2
10 mL of clear viscous yellow fluid was aspirated from the joint.

Epidemiology of acute gout

Acute gout is predominantly a disease of the lower extremity, but any joint of any extremity may be involved. Ninety percent of patients experience acute attacks in the great toe at some time during the course of their disease. Next in order of frequency are the insteps, ankles, heels, knees, wrists, fingers, and elbows. The incidence of gout varies in populations from 0.20 to 0.35 per thousand per year, with an overall prevalence of 1.6 to 13.6 per thousand. The prevalence seems to increase substantially with age and increasing serum urate concentration.¹ Prevalence is 3/100,000 for those 18 to 44 years of age; 21/100,000 for those 45 to 64, and 35/100,000 for those over 65. Men are 20 times more likely to have gout than women.²

Diagnosis

Most cases of gout are characterized by rapid onset of monoarticular arthritis resulting from deposition of urate crystals and a subsequent inflammatory response. The joint most commonly affected by gout is the first metatarsal phalangeal joint; the knee is the second most commonly involved joint. The diagnosis of acute gout was made based on the presence of the characteristic clinical history with urate crystals in the joint fluid.³

Management

Three treatments are available for patients suffering from acute gouty arthritis.

Colchicine inhibits microtubule formation and thus interferes with phagocytosis of the crystals, attenuating the inflammatory response. It also inhibits the release of chemotactic factors reducing the migration of neutrophils into the joint. In a randomized controlled trial, two thirds of patients treated with colchicine improved after 48 hours, but only one third of the patients receiving placebo demonstrated similar improvement. Improvement occurred earlier in the colchicine-treated patients. There were significant differences compared with placebo after 18–30 hours. All patients given colchicine (mean dose of 6.7 mg) developed diarrhea after a median time of 24 hours. Diarrhea occurred before relief of pain in most patients.⁴

The principal side effects of colchicine are gastrointestinal symptoms including abdominal pain and diarrhea. The dose associated with these symptoms is very close to the therapeutic dose.

Generally the initial dose is 1 mg, with 0.5 mg added every 2 hours until a total dose of up to 8 mg has been reached, or abdominal symptoms develop³ (Level of evidence, 1b; single RCT).⁴

Another option for treatment of acute gout is nonsteroidal anti-inflammatory agents. Indomethacin has been the standard for years but there is no proof that it is better than other NSAIDs^5-8 (Level of evidence, 1b; a set of RCTs). The starting dose is 50 mg tid, tapered over approximately 1 week as symptoms subside. NSAIDs are also limited by their gastrointestinal and renal side effects.

Intra-articular injection of corticosteroids is an additional treatment for acute gout. The dose given depends on the size of the affected joint. The appropriate dose of methylprednisolone would be 5–10 mg for a small joint and 20–60 mg for a large joint such as the knee¹ (Level of evidence, 5; expert opinion).

The patient’s treatment and outcome

The patient had a history of gastric ulcers and intolerance to NSAIDs. Therefore, he was started on oral colchicine for the probable gout. He was also given 500 mg of cephalexin po, qid, for the cellulitis and impetigo. He refused any blood tests, but accepted a follow-up appointment for the next day.

When we thought the patient had a septic joint, the optimal treatment would have involved hospitalization. The patient’s fear of hospitalization and losing his job made the choice of hospitalization a nonoption for this mentally ill homeless man. Instead of doing nothing, we began the diagnostic process in the outpatient setting.

If we had obtained purulent joint fluid it would have been incumbent upon us to press once again for hospitalization for septic arthritis. The appearance of yellow fluid and joint crystals gave us the option of attempting outpatient care.

Unfortunately, the patient never returned. Joint fluid Gram stain and culture results were negative, and the cell counts were consistent with inflammation. The hospital lab read the crystal analysis as negative even though our photograph documents the presence of crystals consistent with urate crystals.

Health care delivery must be flexible and creative in the setting of a shelter clinic. We can only hope that the oral medications he received allowed him full recovery from his acute illnesses.

A 52-year-old African American homeless man visited a clinic at the local shelter, complaining of pain in his left knee for the past 2 days. He denied trauma or any history of knee injuries. He also denied any recent sexual activity. The patient was limping from significant pain. The patient’s clothes and hygiene were in poor condition. He worked in the fish market and had taken on the odor of his workplace. He admitted to a history of alcohol and substance abuse and was unwilling to discuss his psychiatric history. His chart indicated he had been diagnosed with schizophrenia.

The patient was afebrile and had a swollen warm left knee (Figure 1). A crusty skin lesion with a small amount of purulence was seen over his patella. There was evidence of a joint effusion and the skin appeared red around the whole knee region. The patient could not fully flex his knee. The physical exam demonstrated normal ligamentous stability.

We offered to take the patient to the county hospital to obtain the appropriate diagnostic procedure and to initiate inpatient care. He adamantly refused treatment in a hospital, stating he was “too busy” to go the hospital and he only wanted “some pills.”

What else could you now do to care for this patient?

The differential diagnosis includes septic arthritis (such as staphylococcal and gonococcal infections of the knee joint), inflammatory types of arthritis, septic bursitis, cellulitis, and impetigo. Joint aspiration was performed in the clinic because the patient refused to go to the emergency room for diagnosis and treatment.

As seen in Figure 2, 10 mL of clear viscous yellow fluid was aspirated from the affected joint. Nine mL of aspirate was sent to a clinical laboratory for cell count, Gram stain, culture and sensitivity, crystal analysis, and microscopic examination. A drop of aspirate was placed on a wet mount and examined with plain light microscopy (Figure 3).

FIGURE 2
10 mL of clear viscous yellow fluid was aspirated from the joint.

Epidemiology of acute gout

Acute gout is predominantly a disease of the lower extremity, but any joint of any extremity may be involved. Ninety percent of patients experience acute attacks in the great toe at some time during the course of their disease. Next in order of frequency are the insteps, ankles, heels, knees, wrists, fingers, and elbows. The incidence of gout varies in populations from 0.20 to 0.35 per thousand per year, with an overall prevalence of 1.6 to 13.6 per thousand. The prevalence seems to increase substantially with age and increasing serum urate concentration.¹ Prevalence is 3/100,000 for those 18 to 44 years of age; 21/100,000 for those 45 to 64, and 35/100,000 for those over 65. Men are 20 times more likely to have gout than women.²

Diagnosis

Most cases of gout are characterized by rapid onset of monoarticular arthritis resulting from deposition of urate crystals and a subsequent inflammatory response. The joint most commonly affected by gout is the first metatarsal phalangeal joint; the knee is the second most commonly involved joint. The diagnosis of acute gout was made based on the presence of the characteristic clinical history with urate crystals in the joint fluid.³

Management

Three treatments are available for patients suffering from acute gouty arthritis.

Colchicine inhibits microtubule formation and thus interferes with phagocytosis of the crystals, attenuating the inflammatory response. It also inhibits the release of chemotactic factors reducing the migration of neutrophils into the joint. In a randomized controlled trial, two thirds of patients treated with colchicine improved after 48 hours, but only one third of the patients receiving placebo demonstrated similar improvement. Improvement occurred earlier in the colchicine-treated patients. There were significant differences compared with placebo after 18–30 hours. All patients given colchicine (mean dose of 6.7 mg) developed diarrhea after a median time of 24 hours. Diarrhea occurred before relief of pain in most patients.⁴

The principal side effects of colchicine are gastrointestinal symptoms including abdominal pain and diarrhea. The dose associated with these symptoms is very close to the therapeutic dose.

Generally the initial dose is 1 mg, with 0.5 mg added every 2 hours until a total dose of up to 8 mg has been reached, or abdominal symptoms develop³ (Level of evidence, 1b; single RCT).⁴

Another option for treatment of acute gout is nonsteroidal anti-inflammatory agents. Indomethacin has been the standard for years but there is no proof that it is better than other NSAIDs^5-8 (Level of evidence, 1b; a set of RCTs). The starting dose is 50 mg tid, tapered over approximately 1 week as symptoms subside. NSAIDs are also limited by their gastrointestinal and renal side effects.

Intra-articular injection of corticosteroids is an additional treatment for acute gout. The dose given depends on the size of the affected joint. The appropriate dose of methylprednisolone would be 5–10 mg for a small joint and 20–60 mg for a large joint such as the knee¹ (Level of evidence, 5; expert opinion).

The patient’s treatment and outcome

The patient had a history of gastric ulcers and intolerance to NSAIDs. Therefore, he was started on oral colchicine for the probable gout. He was also given 500 mg of cephalexin po, qid, for the cellulitis and impetigo. He refused any blood tests, but accepted a follow-up appointment for the next day.

When we thought the patient had a septic joint, the optimal treatment would have involved hospitalization. The patient’s fear of hospitalization and losing his job made the choice of hospitalization a nonoption for this mentally ill homeless man. Instead of doing nothing, we began the diagnostic process in the outpatient setting.

If we had obtained purulent joint fluid it would have been incumbent upon us to press once again for hospitalization for septic arthritis. The appearance of yellow fluid and joint crystals gave us the option of attempting outpatient care.

Unfortunately, the patient never returned. Joint fluid Gram stain and culture results were negative, and the cell counts were consistent with inflammation. The hospital lab read the crystal analysis as negative even though our photograph documents the presence of crystals consistent with urate crystals.

Health care delivery must be flexible and creative in the setting of a shelter clinic. We can only hope that the oral medications he received allowed him full recovery from his acute illnesses.

A 52-year-old African American homeless man visited a clinic at the local shelter, complaining of pain in his left knee for the past 2 days. He denied trauma or any history of knee injuries. He also denied any recent sexual activity. The patient was limping from significant pain. The patient’s clothes and hygiene were in poor condition. He worked in the fish market and had taken on the odor of his workplace. He admitted to a history of alcohol and substance abuse and was unwilling to discuss his psychiatric history. His chart indicated he had been diagnosed with schizophrenia.

The patient was afebrile and had a swollen warm left knee (Figure 1). A crusty skin lesion with a small amount of purulence was seen over his patella. There was evidence of a joint effusion and the skin appeared red around the whole knee region. The patient could not fully flex his knee. The physical exam demonstrated normal ligamentous stability.

We offered to take the patient to the county hospital to obtain the appropriate diagnostic procedure and to initiate inpatient care. He adamantly refused treatment in a hospital, stating he was “too busy” to go the hospital and he only wanted “some pills.”

What else could you now do to care for this patient?

The differential diagnosis includes septic arthritis (such as staphylococcal and gonococcal infections of the knee joint), inflammatory types of arthritis, septic bursitis, cellulitis, and impetigo. Joint aspiration was performed in the clinic because the patient refused to go to the emergency room for diagnosis and treatment.

As seen in Figure 2, 10 mL of clear viscous yellow fluid was aspirated from the affected joint. Nine mL of aspirate was sent to a clinical laboratory for cell count, Gram stain, culture and sensitivity, crystal analysis, and microscopic examination. A drop of aspirate was placed on a wet mount and examined with plain light microscopy (Figure 3).

FIGURE 2
10 mL of clear viscous yellow fluid was aspirated from the joint.

Epidemiology of acute gout

Acute gout is predominantly a disease of the lower extremity, but any joint of any extremity may be involved. Ninety percent of patients experience acute attacks in the great toe at some time during the course of their disease. Next in order of frequency are the insteps, ankles, heels, knees, wrists, fingers, and elbows. The incidence of gout varies in populations from 0.20 to 0.35 per thousand per year, with an overall prevalence of 1.6 to 13.6 per thousand. The prevalence seems to increase substantially with age and increasing serum urate concentration.¹ Prevalence is 3/100,000 for those 18 to 44 years of age; 21/100,000 for those 45 to 64, and 35/100,000 for those over 65. Men are 20 times more likely to have gout than women.²

Diagnosis

Most cases of gout are characterized by rapid onset of monoarticular arthritis resulting from deposition of urate crystals and a subsequent inflammatory response. The joint most commonly affected by gout is the first metatarsal phalangeal joint; the knee is the second most commonly involved joint. The diagnosis of acute gout was made based on the presence of the characteristic clinical history with urate crystals in the joint fluid.³

Management

Three treatments are available for patients suffering from acute gouty arthritis.

Colchicine inhibits microtubule formation and thus interferes with phagocytosis of the crystals, attenuating the inflammatory response. It also inhibits the release of chemotactic factors reducing the migration of neutrophils into the joint. In a randomized controlled trial, two thirds of patients treated with colchicine improved after 48 hours, but only one third of the patients receiving placebo demonstrated similar improvement. Improvement occurred earlier in the colchicine-treated patients. There were significant differences compared with placebo after 18–30 hours. All patients given colchicine (mean dose of 6.7 mg) developed diarrhea after a median time of 24 hours. Diarrhea occurred before relief of pain in most patients.⁴

The principal side effects of colchicine are gastrointestinal symptoms including abdominal pain and diarrhea. The dose associated with these symptoms is very close to the therapeutic dose.

Generally the initial dose is 1 mg, with 0.5 mg added every 2 hours until a total dose of up to 8 mg has been reached, or abdominal symptoms develop³ (Level of evidence, 1b; single RCT).⁴

Another option for treatment of acute gout is nonsteroidal anti-inflammatory agents. Indomethacin has been the standard for years but there is no proof that it is better than other NSAIDs^5-8 (Level of evidence, 1b; a set of RCTs). The starting dose is 50 mg tid, tapered over approximately 1 week as symptoms subside. NSAIDs are also limited by their gastrointestinal and renal side effects.

Intra-articular injection of corticosteroids is an additional treatment for acute gout. The dose given depends on the size of the affected joint. The appropriate dose of methylprednisolone would be 5–10 mg for a small joint and 20–60 mg for a large joint such as the knee¹ (Level of evidence, 5; expert opinion).

The patient’s treatment and outcome

The patient had a history of gastric ulcers and intolerance to NSAIDs. Therefore, he was started on oral colchicine for the probable gout. He was also given 500 mg of cephalexin po, qid, for the cellulitis and impetigo. He refused any blood tests, but accepted a follow-up appointment for the next day.

When we thought the patient had a septic joint, the optimal treatment would have involved hospitalization. The patient’s fear of hospitalization and losing his job made the choice of hospitalization a nonoption for this mentally ill homeless man. Instead of doing nothing, we began the diagnostic process in the outpatient setting.

If we had obtained purulent joint fluid it would have been incumbent upon us to press once again for hospitalization for septic arthritis. The appearance of yellow fluid and joint crystals gave us the option of attempting outpatient care.

Unfortunately, the patient never returned. Joint fluid Gram stain and culture results were negative, and the cell counts were consistent with inflammation. The hospital lab read the crystal analysis as negative even though our photograph documents the presence of crystals consistent with urate crystals.

Health care delivery must be flexible and creative in the setting of a shelter clinic. We can only hope that the oral medications he received allowed him full recovery from his acute illnesses.