Quiz

ANSWER
The correct interpretation includes atrial fibrillation with a rapid ventricular response and aberrantly conducted complexes, left axis deviation, and a left bundle branch block.

Atrial fibrillation is evidenced by the irregularly irregular heart rhythm without a measurable PR interval, and the rapid ventricular response is indicated by a ventricular rate > 100 beats/min.

Aberrant conduction, caused by conduction delay down the His-Purkinje system, is evidenced by the wide QRS complexes with a normally conducted beat (see first beat in leads V₁-V₃). Criteria for left axis deviation include an R axis between –30° and –90°, and left bundle branch block criteria include a QRS duration > 120 ms, a dominant S wave in V₁, and broad monophasic R waves in leads I, aVL, and V₅-V₆.

ANSWER
The correct interpretation includes atrial fibrillation with a rapid ventricular response and aberrantly conducted complexes, left axis deviation, and a left bundle branch block.

Atrial fibrillation is evidenced by the irregularly irregular heart rhythm without a measurable PR interval, and the rapid ventricular response is indicated by a ventricular rate > 100 beats/min.

Aberrant conduction, caused by conduction delay down the His-Purkinje system, is evidenced by the wide QRS complexes with a normally conducted beat (see first beat in leads V₁-V₃). Criteria for left axis deviation include an R axis between –30° and –90°, and left bundle branch block criteria include a QRS duration > 120 ms, a dominant S wave in V₁, and broad monophasic R waves in leads I, aVL, and V₅-V₆.

ANSWER
The correct interpretation includes atrial fibrillation with a rapid ventricular response and aberrantly conducted complexes, left axis deviation, and a left bundle branch block.

Atrial fibrillation is evidenced by the irregularly irregular heart rhythm without a measurable PR interval, and the rapid ventricular response is indicated by a ventricular rate > 100 beats/min.

Aberrant conduction, caused by conduction delay down the His-Purkinje system, is evidenced by the wide QRS complexes with a normally conducted beat (see first beat in leads V₁-V₃). Criteria for left axis deviation include an R axis between –30° and –90°, and left bundle branch block criteria include a QRS duration > 120 ms, a dominant S wave in V₁, and broad monophasic R waves in leads I, aVL, and V₅-V₆.

ANSWER
The correct answer is erythema nodosum (EN; choice “c”), a reactive form of septal panniculitis with many potential triggers.

Erythema induratum (choice “a”) is a manifestation of lobular panniculitis, which affects the fat lobules but not the septae. It too has numerous triggers, but it tends to manifest with more discrete nodules, which eventually open and drain. It is far less common than EN.

Urticaria (choice “b”), also known as hives, presents as itchy, stingy wheals that are typically evanescent (eg, they appear suddenly, within seconds, and disappear within hours). Despite the itching and stinging, urticaria rarely hurts when it presents on the skin.

Erysipelas (choice “d”) is a superficial form of skin infection. More superficial than cellulitis, it usually is caused by a member of the Streptococcus family. It has a bright red appearance and sharply demarcated margins, with a peau d’orange (dimpled, like an orange peel) effect on its surface. It is acute in origin and responds readily to most common anti­biotics.

DISCUSSION
Erythema nodosum, a reactive process involving fibrous septae that support and separate subcutaneous adipocytes, is notable for the complete lack of epidermal change (eg, scaling, broken skin, pointing, draining). The incidence is about 2 in 10,000 population, with women outnumbering men at a rate of 4:1 and the 18-to-34 age-group most affected. The anterior leg is involved in the vast majority of cases.

EN often starts with flulike symptoms, followed by the appearance of discrete, bright red nodules, measuring 2 to 4 cm, on the anterior legs; these darken and coalesce over a period of seven to 10 weeks. New lesions can continue to appear for up to six weeks. As they progress, the lesions often become ecchymotic. Idiopathic cases (at least 20%) can last months.

Notable triggers include Crohn disease flares and use of drugs such as sulfa, gold salts, and oral contraceptives. Several infections have been identified as triggers, including strep, mycoplasma, and campylobacter, as well as deep fungal infections (histoplasmosis, blastomycosis, coccidioidomycosis, and sporotrichosis). More unusual causes include pregnancy and diseases such as sarcoidosis, tuberculosis, Behçet disease, and leukemia/lymphoma.

The diagnostic workup for EN includes punch biopsy of deep adipose tissue and throat culture, and when indicated, ASO titer (if strep is suspected) and chest films (to rule out tuberculosis and sarcoid). In most cases, the diagnosis can be made on clinical grounds alone, although the triggering entity may be difficult to identify. The identification and elimination of the underlying trigger is nonetheless crucial for diagnosis and treatment.

That issue aside, most cases of EN resolve with minimal treatment; this can include the use of NSAIDs and elevation of the limbs when possible. In this particular case, the intense pain the patient was experiencing called for stronger therapy (ibuprofen 800 mg tid, plus a two-week taper of prednisone 40 mg). She responded quite well, and the problem was almost totally resolved at a follow-up visit several weeks later.

In the absence of findings to the contrary, it is likely that the trigger for this patient’s EN was strep, given the timing of its manifestation after a sore throat.

ANSWER
The correct answer is erythema nodosum (EN; choice “c”), a reactive form of septal panniculitis with many potential triggers.

Erythema induratum (choice “a”) is a manifestation of lobular panniculitis, which affects the fat lobules but not the septae. It too has numerous triggers, but it tends to manifest with more discrete nodules, which eventually open and drain. It is far less common than EN.

Urticaria (choice “b”), also known as hives, presents as itchy, stingy wheals that are typically evanescent (eg, they appear suddenly, within seconds, and disappear within hours). Despite the itching and stinging, urticaria rarely hurts when it presents on the skin.

Erysipelas (choice “d”) is a superficial form of skin infection. More superficial than cellulitis, it usually is caused by a member of the Streptococcus family. It has a bright red appearance and sharply demarcated margins, with a peau d’orange (dimpled, like an orange peel) effect on its surface. It is acute in origin and responds readily to most common anti­biotics.

DISCUSSION
Erythema nodosum, a reactive process involving fibrous septae that support and separate subcutaneous adipocytes, is notable for the complete lack of epidermal change (eg, scaling, broken skin, pointing, draining). The incidence is about 2 in 10,000 population, with women outnumbering men at a rate of 4:1 and the 18-to-34 age-group most affected. The anterior leg is involved in the vast majority of cases.

EN often starts with flulike symptoms, followed by the appearance of discrete, bright red nodules, measuring 2 to 4 cm, on the anterior legs; these darken and coalesce over a period of seven to 10 weeks. New lesions can continue to appear for up to six weeks. As they progress, the lesions often become ecchymotic. Idiopathic cases (at least 20%) can last months.

Notable triggers include Crohn disease flares and use of drugs such as sulfa, gold salts, and oral contraceptives. Several infections have been identified as triggers, including strep, mycoplasma, and campylobacter, as well as deep fungal infections (histoplasmosis, blastomycosis, coccidioidomycosis, and sporotrichosis). More unusual causes include pregnancy and diseases such as sarcoidosis, tuberculosis, Behçet disease, and leukemia/lymphoma.

The diagnostic workup for EN includes punch biopsy of deep adipose tissue and throat culture, and when indicated, ASO titer (if strep is suspected) and chest films (to rule out tuberculosis and sarcoid). In most cases, the diagnosis can be made on clinical grounds alone, although the triggering entity may be difficult to identify. The identification and elimination of the underlying trigger is nonetheless crucial for diagnosis and treatment.

That issue aside, most cases of EN resolve with minimal treatment; this can include the use of NSAIDs and elevation of the limbs when possible. In this particular case, the intense pain the patient was experiencing called for stronger therapy (ibuprofen 800 mg tid, plus a two-week taper of prednisone 40 mg). She responded quite well, and the problem was almost totally resolved at a follow-up visit several weeks later.

In the absence of findings to the contrary, it is likely that the trigger for this patient’s EN was strep, given the timing of its manifestation after a sore throat.

ANSWER
The correct answer is erythema nodosum (EN; choice “c”), a reactive form of septal panniculitis with many potential triggers.

Erythema induratum (choice “a”) is a manifestation of lobular panniculitis, which affects the fat lobules but not the septae. It too has numerous triggers, but it tends to manifest with more discrete nodules, which eventually open and drain. It is far less common than EN.

Urticaria (choice “b”), also known as hives, presents as itchy, stingy wheals that are typically evanescent (eg, they appear suddenly, within seconds, and disappear within hours). Despite the itching and stinging, urticaria rarely hurts when it presents on the skin.

Erysipelas (choice “d”) is a superficial form of skin infection. More superficial than cellulitis, it usually is caused by a member of the Streptococcus family. It has a bright red appearance and sharply demarcated margins, with a peau d’orange (dimpled, like an orange peel) effect on its surface. It is acute in origin and responds readily to most common anti­biotics.

DISCUSSION
Erythema nodosum, a reactive process involving fibrous septae that support and separate subcutaneous adipocytes, is notable for the complete lack of epidermal change (eg, scaling, broken skin, pointing, draining). The incidence is about 2 in 10,000 population, with women outnumbering men at a rate of 4:1 and the 18-to-34 age-group most affected. The anterior leg is involved in the vast majority of cases.

EN often starts with flulike symptoms, followed by the appearance of discrete, bright red nodules, measuring 2 to 4 cm, on the anterior legs; these darken and coalesce over a period of seven to 10 weeks. New lesions can continue to appear for up to six weeks. As they progress, the lesions often become ecchymotic. Idiopathic cases (at least 20%) can last months.

Notable triggers include Crohn disease flares and use of drugs such as sulfa, gold salts, and oral contraceptives. Several infections have been identified as triggers, including strep, mycoplasma, and campylobacter, as well as deep fungal infections (histoplasmosis, blastomycosis, coccidioidomycosis, and sporotrichosis). More unusual causes include pregnancy and diseases such as sarcoidosis, tuberculosis, Behçet disease, and leukemia/lymphoma.

The diagnostic workup for EN includes punch biopsy of deep adipose tissue and throat culture, and when indicated, ASO titer (if strep is suspected) and chest films (to rule out tuberculosis and sarcoid). In most cases, the diagnosis can be made on clinical grounds alone, although the triggering entity may be difficult to identify. The identification and elimination of the underlying trigger is nonetheless crucial for diagnosis and treatment.

That issue aside, most cases of EN resolve with minimal treatment; this can include the use of NSAIDs and elevation of the limbs when possible. In this particular case, the intense pain the patient was experiencing called for stronger therapy (ibuprofen 800 mg tid, plus a two-week taper of prednisone 40 mg). She responded quite well, and the problem was almost totally resolved at a follow-up visit several weeks later.

In the absence of findings to the contrary, it is likely that the trigger for this patient’s EN was strep, given the timing of its manifestation after a sore throat.

The Diagnosis: Porokeratosis of Mibelli

There are 5 variants of porokeratosis: disseminated superficial actinic porokeratosis (DSAP), linear porokeratosis, porokeratosis of Mibelli, porokeratosis palmaris et plantaris disseminata, and punctate porokeratosis. The most common type is DSAP,¹ which is characterized by multiple lesions on the body, particularly in sun-exposed areas. The distinguishing feature of porokeratosis is the cornoid lamella, which is made up of parakeratotic cells extending through the stratum corneum. There also is a thin or absent granular layer beneath it (Figure).²

Patients generally present in the third and fourth decades of life.¹ Risk factors for porokeratosis include sun exposure, immunosuppression, and genetics.^2-4 Overexpression of the protein p53 in porokeratosis lesions has been demonstrated in studies investigating the genetics of porokeratosis.^5,6 A study of Chinese families with DSAP identified 3 different loci associated with DSAP: DSAP1, DSAP2, and DSAP3.² The progression to cancer has been noted in all types of porokeratosis lesions. Malignancies include squamous cell carcinoma, Bowen disease, and basal cell carcinoma.^7,8

Many treatments have been tried for DSAP including cryotherapy, topical 5-fluorouracil, photodynamic therapy, and topical imiquimod with varying success.¹ Our patient was treated with 
cryotherapy but had side effects from treatment including cellulitis and local infections with ulceration before finally healing.

Interestingly, our patient had a single lesion with pathology findings most consistent with DSAP at a later age. Although the pathology suggested DSAP, the size and solitary lesion was more consistent with porokeratosis of Mibelli. Porokeratosis of Mibelli can occur concurrently with DSAP,⁹ but we have not seen other lesions in this patient. We have educated our patient to be aware of other lesions that may occur in the future. Due to risk for malignant conversion, it is generally viewed as beneficial to treat patients who present with porokeratosis lesions. Our patient’s lesion ultimately cleared and he has not developed new lesions at 1-year follow-up.

Although DSAP generally presents in the third and fourth decades of life and porokeratosis of Mibelli during childhood, it is important to educate both dermatologists and primary care physicians to be aware of the possibility of both diagnoses in the elderly population.

The Diagnosis: Porokeratosis of Mibelli

There are 5 variants of porokeratosis: disseminated superficial actinic porokeratosis (DSAP), linear porokeratosis, porokeratosis of Mibelli, porokeratosis palmaris et plantaris disseminata, and punctate porokeratosis. The most common type is DSAP,¹ which is characterized by multiple lesions on the body, particularly in sun-exposed areas. The distinguishing feature of porokeratosis is the cornoid lamella, which is made up of parakeratotic cells extending through the stratum corneum. There also is a thin or absent granular layer beneath it (Figure).²

Patients generally present in the third and fourth decades of life.¹ Risk factors for porokeratosis include sun exposure, immunosuppression, and genetics.^2-4 Overexpression of the protein p53 in porokeratosis lesions has been demonstrated in studies investigating the genetics of porokeratosis.^5,6 A study of Chinese families with DSAP identified 3 different loci associated with DSAP: DSAP1, DSAP2, and DSAP3.² The progression to cancer has been noted in all types of porokeratosis lesions. Malignancies include squamous cell carcinoma, Bowen disease, and basal cell carcinoma.^7,8

Many treatments have been tried for DSAP including cryotherapy, topical 5-fluorouracil, photodynamic therapy, and topical imiquimod with varying success.¹ Our patient was treated with 
cryotherapy but had side effects from treatment including cellulitis and local infections with ulceration before finally healing.

Interestingly, our patient had a single lesion with pathology findings most consistent with DSAP at a later age. Although the pathology suggested DSAP, the size and solitary lesion was more consistent with porokeratosis of Mibelli. Porokeratosis of Mibelli can occur concurrently with DSAP,⁹ but we have not seen other lesions in this patient. We have educated our patient to be aware of other lesions that may occur in the future. Due to risk for malignant conversion, it is generally viewed as beneficial to treat patients who present with porokeratosis lesions. Our patient’s lesion ultimately cleared and he has not developed new lesions at 1-year follow-up.

Although DSAP generally presents in the third and fourth decades of life and porokeratosis of Mibelli during childhood, it is important to educate both dermatologists and primary care physicians to be aware of the possibility of both diagnoses in the elderly population.

The Diagnosis: Porokeratosis of Mibelli

There are 5 variants of porokeratosis: disseminated superficial actinic porokeratosis (DSAP), linear porokeratosis, porokeratosis of Mibelli, porokeratosis palmaris et plantaris disseminata, and punctate porokeratosis. The most common type is DSAP,¹ which is characterized by multiple lesions on the body, particularly in sun-exposed areas. The distinguishing feature of porokeratosis is the cornoid lamella, which is made up of parakeratotic cells extending through the stratum corneum. There also is a thin or absent granular layer beneath it (Figure).²

Patients generally present in the third and fourth decades of life.¹ Risk factors for porokeratosis include sun exposure, immunosuppression, and genetics.^2-4 Overexpression of the protein p53 in porokeratosis lesions has been demonstrated in studies investigating the genetics of porokeratosis.^5,6 A study of Chinese families with DSAP identified 3 different loci associated with DSAP: DSAP1, DSAP2, and DSAP3.² The progression to cancer has been noted in all types of porokeratosis lesions. Malignancies include squamous cell carcinoma, Bowen disease, and basal cell carcinoma.^7,8

Many treatments have been tried for DSAP including cryotherapy, topical 5-fluorouracil, photodynamic therapy, and topical imiquimod with varying success.¹ Our patient was treated with 
cryotherapy but had side effects from treatment including cellulitis and local infections with ulceration before finally healing.

Interestingly, our patient had a single lesion with pathology findings most consistent with DSAP at a later age. Although the pathology suggested DSAP, the size and solitary lesion was more consistent with porokeratosis of Mibelli. Porokeratosis of Mibelli can occur concurrently with DSAP,⁹ but we have not seen other lesions in this patient. We have educated our patient to be aware of other lesions that may occur in the future. Due to risk for malignant conversion, it is generally viewed as beneficial to treat patients who present with porokeratosis lesions. Our patient’s lesion ultimately cleared and he has not developed new lesions at 1-year follow-up.

Although DSAP generally presents in the third and fourth decades of life and porokeratosis of Mibelli during childhood, it is important to educate both dermatologists and primary care physicians to be aware of the possibility of both diagnoses in the elderly population.

The Diagnosis: Amelanotic Melanoma In Situ

Histopathology revealed a broad asymmetric melanocytic proliferation at the dermoepidermal junction, consisting both of singly dispersed cells as well as randomly positioned nests (Figure 1). The single cells demonstrated junctional confluence and extension along adnexal structures highlighted by melan-A stain 
(Figure 2). The melanocytes were markedly atypical with enlarged and hyperchromatic nuclei containing multiple nucleoli. No dermal involvement was seen. There was papillary dermal fibrosis and an active host lymphocytic response. Based on these findings, a diagnosis of amelanotic melanoma in situ was made.

Figure 1. Histopathology revealed confluence of atypical melanocytes at the dermoepidermal junction and pagetoid scatter of melanocytes to the spinous layer (A)(H&E, original magnification ×4). Higher-power magnification highlighted the atypia of the individual melanocytes (B)(H&E, original magnification ×10).

Subsequent scouting punch biopsies at the superior, anterior, and posterior aspects of the lesion were performed (Figure 3). All 3 revealed a similar nested and single cell proliferation at the dermoepidermal junction, confirming residual amelanotic melanoma in situ. The patient was referred to the otolaryngology department and underwent wide local excision with 5-mm margins and reconstructive repair.

Amelanotic melanoma comprises 2% to 8% of cutaneous melanomas. It is more common in fair-skinned elderly women with an average age of diagnosis of 61.8 years. Because features typically associated with melanoma such as asymmetry, border irregularity, and color variegation often are absent, amelanotic melanoma represents a notable diagnostic challenge for clinicians. Lesions can present nonspecifically as erythematous macules, papules, patches, or plaques and can have associated pruritus and scale.^1,2

Clinical misdiagnoses for amelanotic melanoma include Bowen disease, basal cell carcinoma, actinic keratosis, lichenoid keratosis, intradermal nevus, dermatofibroma, inflamed seborrheic keratosis, nummular dermatitis, pyogenic granuloma, and granuloma annulare.^1-6 There have been few case reports of amelanotic melanoma in situ, with most being the lentigo maligna variant that were initially clinically diagnosed as superficial basal cell carcinoma, 
Bowen disease, or dermatitis.^7,8 In one case report, an amelanotic lentigo maligna was incidentally discovered after performing a mapping shave biopsy on what was normal-appearing skin.⁹

Dermoscopic evidence of vascular structures in lesions, including the presence of dotted vessels, milky red areas, and/or serpentine (linear irregular) vessels, may be the only clues to suggest amelanotic melanoma before biopsy. However, these findings are nonspecific and can be seen in other benign and malignant skin conditions.²

Complete surgical excision is the standard treatment of amelanotic melanoma in situ given its potential for invasion. However, the lack of pigment can make margins difficult to define. Because of its ability to detect disease beyond visual margins, Mohs micrographic surgery may have better cure rates than conventional excision.⁴ Prognosis for amelanotic melanoma is the same as other melanomas of equal thickness and location, though delay in diagnosis can adversely affect outcomes. Furthermore, amelanotic melanoma in situ can rapidly progress to invasive melanoma.^3,5 Thus it is important to maintain clinical suspicion for amelanotic melanoma in fair-skinned elderly women presenting with a persistent or recurring erythematous scaly lesion on sun-exposed skin.

The Diagnosis: Amelanotic Melanoma In Situ

Histopathology revealed a broad asymmetric melanocytic proliferation at the dermoepidermal junction, consisting both of singly dispersed cells as well as randomly positioned nests (Figure 1). The single cells demonstrated junctional confluence and extension along adnexal structures highlighted by melan-A stain 
(Figure 2). The melanocytes were markedly atypical with enlarged and hyperchromatic nuclei containing multiple nucleoli. No dermal involvement was seen. There was papillary dermal fibrosis and an active host lymphocytic response. Based on these findings, a diagnosis of amelanotic melanoma in situ was made.

Figure 1. Histopathology revealed confluence of atypical melanocytes at the dermoepidermal junction and pagetoid scatter of melanocytes to the spinous layer (A)(H&E, original magnification ×4). Higher-power magnification highlighted the atypia of the individual melanocytes (B)(H&E, original magnification ×10).

Subsequent scouting punch biopsies at the superior, anterior, and posterior aspects of the lesion were performed (Figure 3). All 3 revealed a similar nested and single cell proliferation at the dermoepidermal junction, confirming residual amelanotic melanoma in situ. The patient was referred to the otolaryngology department and underwent wide local excision with 5-mm margins and reconstructive repair.

Amelanotic melanoma comprises 2% to 8% of cutaneous melanomas. It is more common in fair-skinned elderly women with an average age of diagnosis of 61.8 years. Because features typically associated with melanoma such as asymmetry, border irregularity, and color variegation often are absent, amelanotic melanoma represents a notable diagnostic challenge for clinicians. Lesions can present nonspecifically as erythematous macules, papules, patches, or plaques and can have associated pruritus and scale.^1,2

Clinical misdiagnoses for amelanotic melanoma include Bowen disease, basal cell carcinoma, actinic keratosis, lichenoid keratosis, intradermal nevus, dermatofibroma, inflamed seborrheic keratosis, nummular dermatitis, pyogenic granuloma, and granuloma annulare.^1-6 There have been few case reports of amelanotic melanoma in situ, with most being the lentigo maligna variant that were initially clinically diagnosed as superficial basal cell carcinoma, 
Bowen disease, or dermatitis.^7,8 In one case report, an amelanotic lentigo maligna was incidentally discovered after performing a mapping shave biopsy on what was normal-appearing skin.⁹

Dermoscopic evidence of vascular structures in lesions, including the presence of dotted vessels, milky red areas, and/or serpentine (linear irregular) vessels, may be the only clues to suggest amelanotic melanoma before biopsy. However, these findings are nonspecific and can be seen in other benign and malignant skin conditions.²

Complete surgical excision is the standard treatment of amelanotic melanoma in situ given its potential for invasion. However, the lack of pigment can make margins difficult to define. Because of its ability to detect disease beyond visual margins, Mohs micrographic surgery may have better cure rates than conventional excision.⁴ Prognosis for amelanotic melanoma is the same as other melanomas of equal thickness and location, though delay in diagnosis can adversely affect outcomes. Furthermore, amelanotic melanoma in situ can rapidly progress to invasive melanoma.^3,5 Thus it is important to maintain clinical suspicion for amelanotic melanoma in fair-skinned elderly women presenting with a persistent or recurring erythematous scaly lesion on sun-exposed skin.

The Diagnosis: Amelanotic Melanoma In Situ

Histopathology revealed a broad asymmetric melanocytic proliferation at the dermoepidermal junction, consisting both of singly dispersed cells as well as randomly positioned nests (Figure 1). The single cells demonstrated junctional confluence and extension along adnexal structures highlighted by melan-A stain 
(Figure 2). The melanocytes were markedly atypical with enlarged and hyperchromatic nuclei containing multiple nucleoli. No dermal involvement was seen. There was papillary dermal fibrosis and an active host lymphocytic response. Based on these findings, a diagnosis of amelanotic melanoma in situ was made.

Figure 1. Histopathology revealed confluence of atypical melanocytes at the dermoepidermal junction and pagetoid scatter of melanocytes to the spinous layer (A)(H&E, original magnification ×4). Higher-power magnification highlighted the atypia of the individual melanocytes (B)(H&E, original magnification ×10).

Subsequent scouting punch biopsies at the superior, anterior, and posterior aspects of the lesion were performed (Figure 3). All 3 revealed a similar nested and single cell proliferation at the dermoepidermal junction, confirming residual amelanotic melanoma in situ. The patient was referred to the otolaryngology department and underwent wide local excision with 5-mm margins and reconstructive repair.

Amelanotic melanoma comprises 2% to 8% of cutaneous melanomas. It is more common in fair-skinned elderly women with an average age of diagnosis of 61.8 years. Because features typically associated with melanoma such as asymmetry, border irregularity, and color variegation often are absent, amelanotic melanoma represents a notable diagnostic challenge for clinicians. Lesions can present nonspecifically as erythematous macules, papules, patches, or plaques and can have associated pruritus and scale.^1,2

Clinical misdiagnoses for amelanotic melanoma include Bowen disease, basal cell carcinoma, actinic keratosis, lichenoid keratosis, intradermal nevus, dermatofibroma, inflamed seborrheic keratosis, nummular dermatitis, pyogenic granuloma, and granuloma annulare.^1-6 There have been few case reports of amelanotic melanoma in situ, with most being the lentigo maligna variant that were initially clinically diagnosed as superficial basal cell carcinoma, 
Bowen disease, or dermatitis.^7,8 In one case report, an amelanotic lentigo maligna was incidentally discovered after performing a mapping shave biopsy on what was normal-appearing skin.⁹

Dermoscopic evidence of vascular structures in lesions, including the presence of dotted vessels, milky red areas, and/or serpentine (linear irregular) vessels, may be the only clues to suggest amelanotic melanoma before biopsy. However, these findings are nonspecific and can be seen in other benign and malignant skin conditions.²

Complete surgical excision is the standard treatment of amelanotic melanoma in situ given its potential for invasion. However, the lack of pigment can make margins difficult to define. Because of its ability to detect disease beyond visual margins, Mohs micrographic surgery may have better cure rates than conventional excision.⁴ Prognosis for amelanotic melanoma is the same as other melanomas of equal thickness and location, though delay in diagnosis can adversely affect outcomes. Furthermore, amelanotic melanoma in situ can rapidly progress to invasive melanoma.^3,5 Thus it is important to maintain clinical suspicion for amelanotic melanoma in fair-skinned elderly women presenting with a persistent or recurring erythematous scaly lesion on sun-exposed skin.

ANSWER 
The correct answer is oral terbinafine or griseofulvin, plus a two-week taper of prednisone (choice “d”); further discussion follows. Most authorities recommend the use of oral steroids with terbinafine (choice “a”) or griseofulvin (choice “b”), to dampen the acute inflammatory reaction to the fungal antigen. Some sources advise the use of itraconazole (choice “c”) but not as a single agent.

DISCUSSION
This case is a classic representation of kerion, a type of tinea capitis. This distinctive presentation results from not only active localized fungal infection with one of the dermatophytes, but also an allergic response to the fungal antigen. (This antigen can also trigger a widespread eczematous rash called an id reaction.) The resulting boggy, tender mass often oozes pus and usually provokes significant localized adenopathy.

A more common type of tinea capitis is uncomplicated dermatophytic infection of the scalp, presenting as mild localized scaling and modest hair loss, with no edema or redness to speak of. Kerion, by contrast, is far more acute and involves an impressive amount of localized redness and edema, along with modest hair loss, purulence, bloody drainage, and marked tenderness. Untreated, kerion can result in permanent scarring alopecia.

Several different dermatophytes have been isolated from kerions, including Trichophyton tonsurans, T violaceum, and various members of the Microsporum family. These zoophilic or geophilic organisms affect children far more than adults. Distinguishing the causative type is significant, because different drugs are required to effectively treat each. This is why a fungal culture is done at the outset.

When the diagnosis is in doubt, a punch biopsy may be necessary, with the sample divided for processing of default H&E stains and for fungal culture. Other information can be obtained by plucking a few hairs from the mass and examining them under 10x power to see if fungal hyphae are confined to the insides of the hair shafts (endothrix) or the outside of the shafts (ectothrix).

This is one situation in which KOH is not helpful for diagnosis: The organisms are too deep to obtain with a superficial scrape.

A number of scalp conditions can mimic a kerion, including lichen planopilaris and folliculitis decalvans. Several years ago, I had a patient who presented with a similar lesion that turned out to be squamous cell carcinoma—which eventually metastasized and led to his death.

TREATMENT
Treatment of more severe types of tinea capitis can be trying, even when the diagnosis is nailed down. The challenge becomes treating the problem long and strong enough to produce a cure.

In this case, I started the patient (who, at age 8, weighed 110 pounds) on a month-long course of terbinafine (250 mg/d) with a two-week taper of prednisone (40 mg). The expectation was that this would rapidly diminish the edema and pain while we waited for the culture results.

If the results showed the expected T tonsurans, treatment would continue as planned. If the cause turned out to be one of the Microsporum species, a switch to griseofulvin, at relatively high doses, would be considered. 

ANSWER 
The correct answer is oral terbinafine or griseofulvin, plus a two-week taper of prednisone (choice “d”); further discussion follows. Most authorities recommend the use of oral steroids with terbinafine (choice “a”) or griseofulvin (choice “b”), to dampen the acute inflammatory reaction to the fungal antigen. Some sources advise the use of itraconazole (choice “c”) but not as a single agent.

DISCUSSION
This case is a classic representation of kerion, a type of tinea capitis. This distinctive presentation results from not only active localized fungal infection with one of the dermatophytes, but also an allergic response to the fungal antigen. (This antigen can also trigger a widespread eczematous rash called an id reaction.) The resulting boggy, tender mass often oozes pus and usually provokes significant localized adenopathy.

A more common type of tinea capitis is uncomplicated dermatophytic infection of the scalp, presenting as mild localized scaling and modest hair loss, with no edema or redness to speak of. Kerion, by contrast, is far more acute and involves an impressive amount of localized redness and edema, along with modest hair loss, purulence, bloody drainage, and marked tenderness. Untreated, kerion can result in permanent scarring alopecia.

Several different dermatophytes have been isolated from kerions, including Trichophyton tonsurans, T violaceum, and various members of the Microsporum family. These zoophilic or geophilic organisms affect children far more than adults. Distinguishing the causative type is significant, because different drugs are required to effectively treat each. This is why a fungal culture is done at the outset.

When the diagnosis is in doubt, a punch biopsy may be necessary, with the sample divided for processing of default H&E stains and for fungal culture. Other information can be obtained by plucking a few hairs from the mass and examining them under 10x power to see if fungal hyphae are confined to the insides of the hair shafts (endothrix) or the outside of the shafts (ectothrix).

This is one situation in which KOH is not helpful for diagnosis: The organisms are too deep to obtain with a superficial scrape.

A number of scalp conditions can mimic a kerion, including lichen planopilaris and folliculitis decalvans. Several years ago, I had a patient who presented with a similar lesion that turned out to be squamous cell carcinoma—which eventually metastasized and led to his death.

TREATMENT
Treatment of more severe types of tinea capitis can be trying, even when the diagnosis is nailed down. The challenge becomes treating the problem long and strong enough to produce a cure.

In this case, I started the patient (who, at age 8, weighed 110 pounds) on a month-long course of terbinafine (250 mg/d) with a two-week taper of prednisone (40 mg). The expectation was that this would rapidly diminish the edema and pain while we waited for the culture results.

If the results showed the expected T tonsurans, treatment would continue as planned. If the cause turned out to be one of the Microsporum species, a switch to griseofulvin, at relatively high doses, would be considered. 

ANSWER 
The correct answer is oral terbinafine or griseofulvin, plus a two-week taper of prednisone (choice “d”); further discussion follows. Most authorities recommend the use of oral steroids with terbinafine (choice “a”) or griseofulvin (choice “b”), to dampen the acute inflammatory reaction to the fungal antigen. Some sources advise the use of itraconazole (choice “c”) but not as a single agent.

DISCUSSION
This case is a classic representation of kerion, a type of tinea capitis. This distinctive presentation results from not only active localized fungal infection with one of the dermatophytes, but also an allergic response to the fungal antigen. (This antigen can also trigger a widespread eczematous rash called an id reaction.) The resulting boggy, tender mass often oozes pus and usually provokes significant localized adenopathy.

A more common type of tinea capitis is uncomplicated dermatophytic infection of the scalp, presenting as mild localized scaling and modest hair loss, with no edema or redness to speak of. Kerion, by contrast, is far more acute and involves an impressive amount of localized redness and edema, along with modest hair loss, purulence, bloody drainage, and marked tenderness. Untreated, kerion can result in permanent scarring alopecia.

Several different dermatophytes have been isolated from kerions, including Trichophyton tonsurans, T violaceum, and various members of the Microsporum family. These zoophilic or geophilic organisms affect children far more than adults. Distinguishing the causative type is significant, because different drugs are required to effectively treat each. This is why a fungal culture is done at the outset.

When the diagnosis is in doubt, a punch biopsy may be necessary, with the sample divided for processing of default H&E stains and for fungal culture. Other information can be obtained by plucking a few hairs from the mass and examining them under 10x power to see if fungal hyphae are confined to the insides of the hair shafts (endothrix) or the outside of the shafts (ectothrix).

This is one situation in which KOH is not helpful for diagnosis: The organisms are too deep to obtain with a superficial scrape.

A number of scalp conditions can mimic a kerion, including lichen planopilaris and folliculitis decalvans. Several years ago, I had a patient who presented with a similar lesion that turned out to be squamous cell carcinoma—which eventually metastasized and led to his death.

TREATMENT
Treatment of more severe types of tinea capitis can be trying, even when the diagnosis is nailed down. The challenge becomes treating the problem long and strong enough to produce a cure.

In this case, I started the patient (who, at age 8, weighed 110 pounds) on a month-long course of terbinafine (250 mg/d) with a two-week taper of prednisone (40 mg). The expectation was that this would rapidly diminish the edema and pain while we waited for the culture results.

If the results showed the expected T tonsurans, treatment would continue as planned. If the cause turned out to be one of the Microsporum species, a switch to griseofulvin, at relatively high doses, would be considered. 

ANSWER
The radiograph shows an enteric tube passing through the gastrointestinal tract. However, it extends low into the left lower quadrant, loops around the right lower quadrant, and then heads up toward the left upper quadrant. Such a course is atypical and concerning for displaced position.

The radiologists concurred, and it was decided to instill some water-soluble contrast and repeat the KUB for further evaluation. That image is shown here. Note that the contrast does not appear to be in the stomach, as no gastric folds are visible. It accumulates in the left upper quadrant, under the diaphragm. Such a finding is concerning for possible gastric perforation.

The tube was promptly withdrawn, and urgent surgical consultation was obtained.

ANSWER
The radiograph shows an enteric tube passing through the gastrointestinal tract. However, it extends low into the left lower quadrant, loops around the right lower quadrant, and then heads up toward the left upper quadrant. Such a course is atypical and concerning for displaced position.

The radiologists concurred, and it was decided to instill some water-soluble contrast and repeat the KUB for further evaluation. That image is shown here. Note that the contrast does not appear to be in the stomach, as no gastric folds are visible. It accumulates in the left upper quadrant, under the diaphragm. Such a finding is concerning for possible gastric perforation.

The tube was promptly withdrawn, and urgent surgical consultation was obtained.

ANSWER
The radiograph shows an enteric tube passing through the gastrointestinal tract. However, it extends low into the left lower quadrant, loops around the right lower quadrant, and then heads up toward the left upper quadrant. Such a course is atypical and concerning for displaced position.

The radiologists concurred, and it was decided to instill some water-soluble contrast and repeat the KUB for further evaluation. That image is shown here. Note that the contrast does not appear to be in the stomach, as no gastric folds are visible. It accumulates in the left upper quadrant, under the diaphragm. Such a finding is concerning for possible gastric perforation.

The tube was promptly withdrawn, and urgent surgical consultation was obtained.

ANSWER
The correct interpretation is normal sinus rhythm with an acute anterior MI (STEMI) and inferolateral injury. In the absence of left ventricular hypertrophy and left bundle-branch block, an acute anterior MI manifests with new ST elevations ≥ 0.1 mV, measured at the J point in leads V₂-V₃. Inferolateral injury is indicated by ST elevations in leads II, III, and aVF, as well as ST elevations in leads V₄-V₆.

Laboratory findings confirmed the diagnosis of a new infarction, and cardiac catheterization revealed significant blockage in the proximal left anterior descending and circumflex coronary arteries. These were treated percutaneously, and the patient recovered without sequelae.

ANSWER
The correct interpretation is normal sinus rhythm with an acute anterior MI (STEMI) and inferolateral injury. In the absence of left ventricular hypertrophy and left bundle-branch block, an acute anterior MI manifests with new ST elevations ≥ 0.1 mV, measured at the J point in leads V₂-V₃. Inferolateral injury is indicated by ST elevations in leads II, III, and aVF, as well as ST elevations in leads V₄-V₆.

Laboratory findings confirmed the diagnosis of a new infarction, and cardiac catheterization revealed significant blockage in the proximal left anterior descending and circumflex coronary arteries. These were treated percutaneously, and the patient recovered without sequelae.

ANSWER
The correct interpretation is normal sinus rhythm with an acute anterior MI (STEMI) and inferolateral injury. In the absence of left ventricular hypertrophy and left bundle-branch block, an acute anterior MI manifests with new ST elevations ≥ 0.1 mV, measured at the J point in leads V₂-V₃. Inferolateral injury is indicated by ST elevations in leads II, III, and aVF, as well as ST elevations in leads V₄-V₆.

Laboratory findings confirmed the diagnosis of a new infarction, and cardiac catheterization revealed significant blockage in the proximal left anterior descending and circumflex coronary arteries. These were treated percutaneously, and the patient recovered without sequelae.

The Diagnosis: Herpes Simplex Vegetans

Histopathologic examination using hematoxylin and eosin stain demonstrated marked pseudoepitheliomatous hyperplasia with granulation tissue, ulceration, and abundant exudate joined by a dense mixed inflammatory cell infiltrate that included a myriad of eosinophils (Figure, A). At higher power (Figure, B), many single and multinucleate acantholytic keratinocytes showed ground-glass nuclei and peripheral margination of chromatin within zones of ulceration and crust. Viral culture and direct fluorescent antibody assay identified herpes simplex virus (HSV) type 2. Based on the clinical and histopathologic findings, the patient was diagnosed with herpes simplex vegetans. He was initially treated with oral acyclovir and then oral famciclovir but showed minimal improvement. Eventually, he was referred to surgery and the mass was totally excised with clear margins and no evidence of underlying malignancy.

Histopathology revealed marked pseudoepitheliomatous hyperplasia, ulceration, and a dense mixed inflammatory cell infiltrate (A)(H&E, original magnification ×20). Many multinucleate acantholytic keratinocytes with ground-glass nuclei and peripheral margination of chromatin were shown (B)(H&E, original magnification ×400).

Herpes simplex virus is one of the most common sexually transmitted infections, with a notably increased incidence and prevalence among individuals with human immunodeficiency virus (HIV) infection.¹ Although typical HSV manifestation in immunocompetent patients includes clustered vesicles and/or ulcerations, immunocompromised patients may have unusual presentations, such as persistent and extensive ulcerations or nodular hyperkeratotic lesions.^2,3 Herpes vegetans, a term used to describe these atypical exophytic lesions, rarely has been reported in literature, but its presence should raise suspicion for possible underlying immunocompromise. The pathogenesis behind the hypertrophic nature of these lesions is not well understood, but it is postulated that the immune dysregulation from concomitant HIV and HSV infection plays a role.² Overproduction of tumor necrosis factor and IL-6 by HIV-infected dermal dendritic cells causes an increase in antiapoptotic factors within the epidermis, resulting in enhanced keratinocyte proliferation and clinical hyperkeratosis.^2,4

The differential diagnosis for herpes vegetans is somewhat broad, owing to the verrucous and often eroded appearance of the lesions. Biopsy and cultures can be obtained to differentiate from condyloma acuminatum, condyloma latum (secondary syphilis), pyoderma vegetans, pemphigus vegetans, granuloma inguinale, extraintestinal Crohn disease, deep fungal infections, cutaneous tuberculosis, and malignancy.^2-4 Histopathology shows epithelial hyperplasia and ulceration with scattered multinucleate keratinocytes, usually at the periphery of the ulcer, and intranuclear inclusions typical of HSV. In addition, a dense dermal infiltrate of lymphocytes, histiocytes, plasma cells, and eosinophils is usually present beneath the base of the ulcer.^2,4

Treatment options for herpes vegetans are limited due to the high prevalence of acyclovir-resistant (ACV-R) HSV-2 strains in HIV patients. Valacyclovir and penciclovir have been largely ineffective against ACV-R HSV due to their dependence on the same enzyme—thymidine kinase—involved in the mechanism of acyclovir resistance. Intravenous foscarnet and cidofovir have shown efficacy against ACV-R virus, but concerns of nephrotoxicity have limited their use over prolonged intervals.⁵ Castelo-Soccio et al⁶ reported promising results with intralesional cidofovir. This route of administration provides the advantage of increased bioavailability with reduced risk for nephrotoxicity.⁶ Finally, surgical resection may be considered for refractory lesions to circumvent the toxicity from systemically administered drugs.³

The Diagnosis: Herpes Simplex Vegetans

Histopathologic examination using hematoxylin and eosin stain demonstrated marked pseudoepitheliomatous hyperplasia with granulation tissue, ulceration, and abundant exudate joined by a dense mixed inflammatory cell infiltrate that included a myriad of eosinophils (Figure, A). At higher power (Figure, B), many single and multinucleate acantholytic keratinocytes showed ground-glass nuclei and peripheral margination of chromatin within zones of ulceration and crust. Viral culture and direct fluorescent antibody assay identified herpes simplex virus (HSV) type 2. Based on the clinical and histopathologic findings, the patient was diagnosed with herpes simplex vegetans. He was initially treated with oral acyclovir and then oral famciclovir but showed minimal improvement. Eventually, he was referred to surgery and the mass was totally excised with clear margins and no evidence of underlying malignancy.

Histopathology revealed marked pseudoepitheliomatous hyperplasia, ulceration, and a dense mixed inflammatory cell infiltrate (A)(H&E, original magnification ×20). Many multinucleate acantholytic keratinocytes with ground-glass nuclei and peripheral margination of chromatin were shown (B)(H&E, original magnification ×400).

Herpes simplex virus is one of the most common sexually transmitted infections, with a notably increased incidence and prevalence among individuals with human immunodeficiency virus (HIV) infection.¹ Although typical HSV manifestation in immunocompetent patients includes clustered vesicles and/or ulcerations, immunocompromised patients may have unusual presentations, such as persistent and extensive ulcerations or nodular hyperkeratotic lesions.^2,3 Herpes vegetans, a term used to describe these atypical exophytic lesions, rarely has been reported in literature, but its presence should raise suspicion for possible underlying immunocompromise. The pathogenesis behind the hypertrophic nature of these lesions is not well understood, but it is postulated that the immune dysregulation from concomitant HIV and HSV infection plays a role.² Overproduction of tumor necrosis factor and IL-6 by HIV-infected dermal dendritic cells causes an increase in antiapoptotic factors within the epidermis, resulting in enhanced keratinocyte proliferation and clinical hyperkeratosis.^2,4

The differential diagnosis for herpes vegetans is somewhat broad, owing to the verrucous and often eroded appearance of the lesions. Biopsy and cultures can be obtained to differentiate from condyloma acuminatum, condyloma latum (secondary syphilis), pyoderma vegetans, pemphigus vegetans, granuloma inguinale, extraintestinal Crohn disease, deep fungal infections, cutaneous tuberculosis, and malignancy.^2-4 Histopathology shows epithelial hyperplasia and ulceration with scattered multinucleate keratinocytes, usually at the periphery of the ulcer, and intranuclear inclusions typical of HSV. In addition, a dense dermal infiltrate of lymphocytes, histiocytes, plasma cells, and eosinophils is usually present beneath the base of the ulcer.^2,4

Treatment options for herpes vegetans are limited due to the high prevalence of acyclovir-resistant (ACV-R) HSV-2 strains in HIV patients. Valacyclovir and penciclovir have been largely ineffective against ACV-R HSV due to their dependence on the same enzyme—thymidine kinase—involved in the mechanism of acyclovir resistance. Intravenous foscarnet and cidofovir have shown efficacy against ACV-R virus, but concerns of nephrotoxicity have limited their use over prolonged intervals.⁵ Castelo-Soccio et al⁶ reported promising results with intralesional cidofovir. This route of administration provides the advantage of increased bioavailability with reduced risk for nephrotoxicity.⁶ Finally, surgical resection may be considered for refractory lesions to circumvent the toxicity from systemically administered drugs.³

The Diagnosis: Herpes Simplex Vegetans

Histopathologic examination using hematoxylin and eosin stain demonstrated marked pseudoepitheliomatous hyperplasia with granulation tissue, ulceration, and abundant exudate joined by a dense mixed inflammatory cell infiltrate that included a myriad of eosinophils (Figure, A). At higher power (Figure, B), many single and multinucleate acantholytic keratinocytes showed ground-glass nuclei and peripheral margination of chromatin within zones of ulceration and crust. Viral culture and direct fluorescent antibody assay identified herpes simplex virus (HSV) type 2. Based on the clinical and histopathologic findings, the patient was diagnosed with herpes simplex vegetans. He was initially treated with oral acyclovir and then oral famciclovir but showed minimal improvement. Eventually, he was referred to surgery and the mass was totally excised with clear margins and no evidence of underlying malignancy.

Histopathology revealed marked pseudoepitheliomatous hyperplasia, ulceration, and a dense mixed inflammatory cell infiltrate (A)(H&E, original magnification ×20). Many multinucleate acantholytic keratinocytes with ground-glass nuclei and peripheral margination of chromatin were shown (B)(H&E, original magnification ×400).

Herpes simplex virus is one of the most common sexually transmitted infections, with a notably increased incidence and prevalence among individuals with human immunodeficiency virus (HIV) infection.¹ Although typical HSV manifestation in immunocompetent patients includes clustered vesicles and/or ulcerations, immunocompromised patients may have unusual presentations, such as persistent and extensive ulcerations or nodular hyperkeratotic lesions.^2,3 Herpes vegetans, a term used to describe these atypical exophytic lesions, rarely has been reported in literature, but its presence should raise suspicion for possible underlying immunocompromise. The pathogenesis behind the hypertrophic nature of these lesions is not well understood, but it is postulated that the immune dysregulation from concomitant HIV and HSV infection plays a role.² Overproduction of tumor necrosis factor and IL-6 by HIV-infected dermal dendritic cells causes an increase in antiapoptotic factors within the epidermis, resulting in enhanced keratinocyte proliferation and clinical hyperkeratosis.^2,4

The differential diagnosis for herpes vegetans is somewhat broad, owing to the verrucous and often eroded appearance of the lesions. Biopsy and cultures can be obtained to differentiate from condyloma acuminatum, condyloma latum (secondary syphilis), pyoderma vegetans, pemphigus vegetans, granuloma inguinale, extraintestinal Crohn disease, deep fungal infections, cutaneous tuberculosis, and malignancy.^2-4 Histopathology shows epithelial hyperplasia and ulceration with scattered multinucleate keratinocytes, usually at the periphery of the ulcer, and intranuclear inclusions typical of HSV. In addition, a dense dermal infiltrate of lymphocytes, histiocytes, plasma cells, and eosinophils is usually present beneath the base of the ulcer.^2,4

Treatment options for herpes vegetans are limited due to the high prevalence of acyclovir-resistant (ACV-R) HSV-2 strains in HIV patients. Valacyclovir and penciclovir have been largely ineffective against ACV-R HSV due to their dependence on the same enzyme—thymidine kinase—involved in the mechanism of acyclovir resistance. Intravenous foscarnet and cidofovir have shown efficacy against ACV-R virus, but concerns of nephrotoxicity have limited their use over prolonged intervals.⁵ Castelo-Soccio et al⁶ reported promising results with intralesional cidofovir. This route of administration provides the advantage of increased bioavailability with reduced risk for nephrotoxicity.⁶ Finally, surgical resection may be considered for refractory lesions to circumvent the toxicity from systemically administered drugs.³

ANSWER
The correct interpretation includes normal sinus rhythm, right atrial enlargement, left ventricular hypertrophy, and a prolonged QT interval. Normal sinus rhythm is indicated by a P for every QRS and a QRS for every P, with a constant PR interval (see rhythm strip of lead I).

Right atrial enlargement is evidenced by the tall P waves in leads II, III, aVF, and V₁. Note that there is no biphasic P wave in lead V₁, so there is no evidence of accompanying left atrial enlargement.

High-voltage limb leads (sum of R in lead I and S in lead III ≥ 25 mm) or precordial leads (sum of S in V1 and R in V₅ or V₆ ≥ 35 mm) are indicative of left ventricular hypertrophy.

The QTc interval of 653 ms with a normal sinus rate is worrisome for prolonged QT syndrome. A review of the history shows the patient to be taking two drugs (lithium, azithromycin) known to prolong the QT interval. Although it is not known whether this patient has inherent QT prolongation, use of these types of agents should be avoided.  

ANSWER
The correct interpretation includes normal sinus rhythm, right atrial enlargement, left ventricular hypertrophy, and a prolonged QT interval. Normal sinus rhythm is indicated by a P for every QRS and a QRS for every P, with a constant PR interval (see rhythm strip of lead I).

Right atrial enlargement is evidenced by the tall P waves in leads II, III, aVF, and V₁. Note that there is no biphasic P wave in lead V₁, so there is no evidence of accompanying left atrial enlargement.

High-voltage limb leads (sum of R in lead I and S in lead III ≥ 25 mm) or precordial leads (sum of S in V1 and R in V₅ or V₆ ≥ 35 mm) are indicative of left ventricular hypertrophy.

The QTc interval of 653 ms with a normal sinus rate is worrisome for prolonged QT syndrome. A review of the history shows the patient to be taking two drugs (lithium, azithromycin) known to prolong the QT interval. Although it is not known whether this patient has inherent QT prolongation, use of these types of agents should be avoided.  

ANSWER
The correct interpretation includes normal sinus rhythm, right atrial enlargement, left ventricular hypertrophy, and a prolonged QT interval. Normal sinus rhythm is indicated by a P for every QRS and a QRS for every P, with a constant PR interval (see rhythm strip of lead I).

Right atrial enlargement is evidenced by the tall P waves in leads II, III, aVF, and V₁. Note that there is no biphasic P wave in lead V₁, so there is no evidence of accompanying left atrial enlargement.

High-voltage limb leads (sum of R in lead I and S in lead III ≥ 25 mm) or precordial leads (sum of S in V1 and R in V₅ or V₆ ≥ 35 mm) are indicative of left ventricular hypertrophy.

The QTc interval of 653 ms with a normal sinus rate is worrisome for prolonged QT syndrome. A review of the history shows the patient to be taking two drugs (lithium, azithromycin) known to prolong the QT interval. Although it is not known whether this patient has inherent QT prolongation, use of these types of agents should be avoided.  

ANSWER
The radiograph shows a nondisplaced fracture of the proximal fibular head. No other fractures are evident. There is some evidence of soft-tissue injury and edema over the tibia.

An orthopedics consultation was obtained, with the presumption that the fracture would be nonsurgically managed.         

ANSWER
The radiograph shows a nondisplaced fracture of the proximal fibular head. No other fractures are evident. There is some evidence of soft-tissue injury and edema over the tibia.

An orthopedics consultation was obtained, with the presumption that the fracture would be nonsurgically managed.         

ANSWER
The radiograph shows a nondisplaced fracture of the proximal fibular head. No other fractures are evident. There is some evidence of soft-tissue injury and edema over the tibia.

An orthopedics consultation was obtained, with the presumption that the fracture would be nonsurgically managed.