Practical Pearls

Clinical Challenge

An odontogenic cutaneous sinus tract (OCST) of dental origin is an uncommon occurrence and is most commonly caused by chronic periodontitis, specifically a periapical abscess due to chronic dental infection.^1,2 Odontogenic cutaneous sinus tract commonly is misdiagnosed due to a lack of symptoms on presentation, location, and variations in clinical appearance mimicking other lesions. Patients with OCSTs typically present with a fixed, erythematous, crusty, and nontender nodule with periodic drainage that easily can be mistaken for a pustule, furuncle, cyst, foreign-body lesion, squamous cell carcinoma (SCC), basal cell carcinoma, or granulomatous disorder.³ It becomes challenging for dermatologists to correctly diagnose these lesions and refer for proper evaluation and treatment.

Practice Gap

It is estimated that half of patients with an extraoral fistula are treated with multiple dermatologic surgical operations, radiotherapy, antibiotic therapy, and chemotherapy before the correct diagnosis is made.¹ Thus, proper identification of these lesions is crucial for prognosis and treatment. The most common locations for OCSTs are the mandibular, submandibular, and cervical skin.^1,2 Given these locations, patients with OCSTs commonly present to the dermatology office for evaluation. Education regarding the clinical presentation, histopathology, and proper evaluation and further referral for treatment is essential for dermatologists.

Tools and Technique for Diagnosis

We present 2 patients with OCSTs who were referred for cutaneous surgery for an SCC and epidermal cyst, but the proper diagnosis was rendered after an index of suspicion and clinicopathologic correlation led to additional testing and eventual referral for imaging.

Patient 1
A 68-year-old woman presented for Mohs micrographic surgery (MMS) of a biopsy-proven SCC on the chin. The tumor cleared after 2 MMS stages (Figure 1A). Due to notable inflammation in each stage, the slides were sent to a pathologist who confirmed clear margins. Within 2 weeks of MMS, the wound began to dehisce (Figure 1B). The patient presented 4 months later with a crusted ulcerated nodule at the MMS site (Figure 1C). A biopsy showed likely recurrence of SCC. Upon presentation to the Mohs surgeon, the nodule felt fixed to the underlying jaw, and the patient was noted to have poor dentition. The patient was sent for computed tomography (CT), which showed focal thinning of the mandible, likely postsurgical, and clear maxillary sinuses. Due to the clinical appearance and anatomic location of the lesion, a request was made for a second read of the CT, specifically looking for an OCST at the prior surgical site. With this information, the radiologist noted an OCST extending from the mandible to the lesion, reported as a periapical lucency (representing a periapical abscess) at a mandibular tooth with a dental sinus draining into the soft tissues. The patient was started on antibiotics and referred to an oral surgeon for OCST excision.

Practice Implications

Odontogenic cutaneous sinus tracts commonly are misdiagnosed due to variations in clinical presentations resembling more common cutaneous diagnoses, nonspecific histopathologic findings, and lack of dental symptoms or concerns about dentition. Clinically, an OCST presents as a fixed, red, crusty, nontender nodule with intermittent draining. With palpation of the involved area, the clinician may feel a cord of tissue connecting the skin lesion intraorally.^2,4 A clinician should have a high index of suspicion for an OCST when evaluating fixed lesions of the lower face, jawline, and neck due to the possibility of a dental origin,¹ which is important because an OCST can have similar clinical findings to lesions such as congenital fistulas, pustules, cysts, osteomyelitis, foreign-body granulomas, pyogenic granulomas, syphilis, metastatic carcinomas, basal cell carcinomas, and SCCs.^2,4 A PubMed search of articles indexed for MEDLINE using the terms Mohs, MMS, chemosurgery, odontogenic sinus, odontogenic cutaneous sinus tract, and dental sinus yielded only 2 OCSTs that were referred for MMS in the last 30 years, both of which were in the nasolabial fold/medial malar cheek.^2,4 Histopathologic findings of an OCST are nonspecific; a mixed or granulomatous inflammatory infiltrate, granulation tissue, and scarring can be seen.¹ Pseudocarcinomatous/pseudoepitheliomatous hyperplasia of the epidermis can be seen and cause histologic misinterpretation for an SCC.² Given that these findings are nonspecific without a clinical context, even with a histopathologic diagnosis of SCC or cyst, a clinical suspicion for an OCST should lead to an intraoral examination. Imaging can be ordered to look for an OCST in the area of interest. Although panoramic or periapical radiography with or without dental probes/radiopaque markers commonly have been used, more recent literature has suggested that CT may be superior to radiographs for making an OCST diagnosis.^1,3 If imaging is not consistent with the clinically suspected OCST, we recommend directly contacting the radiologist to explain the clinical history and even refresh his/her suspicion for this diagnosis.

If a diagnosis of an OCST is made, oral antibiotics can be prescribed, though the use of antibiotics has been controversial. For severe odontogenic infections, typically beta-lactam antibiotics, cephalosporins, metronidazole, clindamycin, moxifloxacin, or erythromycin can be given for 7 days or until 3 days after symptoms have resolved.⁵ Although antibiotics can bring temporary resolution, it is imperative to treat the source of infection to prevent recurrence. It is crucial for these patients to be referred to an oral surgeon for evaluation and treatment of OCST by either a root canal or tooth extraction.

Final Thoughts

We present this pearl on the diagnosis and management of an OCST, also known as a dental sinus, to better assist clinicians in making this diagnosis. With an index of suspicion as well as intraoral and radiologic evaluations, a proper diagnosis may be rendered, potentially avoiding unnecessary cutaneous surgery. In addition, we highlight the importance of communication between the clinician and the radiologist to directly look for OCST in the area of concern and consider a re-read of the images when clinical suspicion does not correlate with the radiology report.

Clinical Challenge

An odontogenic cutaneous sinus tract (OCST) of dental origin is an uncommon occurrence and is most commonly caused by chronic periodontitis, specifically a periapical abscess due to chronic dental infection.^1,2 Odontogenic cutaneous sinus tract commonly is misdiagnosed due to a lack of symptoms on presentation, location, and variations in clinical appearance mimicking other lesions. Patients with OCSTs typically present with a fixed, erythematous, crusty, and nontender nodule with periodic drainage that easily can be mistaken for a pustule, furuncle, cyst, foreign-body lesion, squamous cell carcinoma (SCC), basal cell carcinoma, or granulomatous disorder.³ It becomes challenging for dermatologists to correctly diagnose these lesions and refer for proper evaluation and treatment.

Practice Gap

It is estimated that half of patients with an extraoral fistula are treated with multiple dermatologic surgical operations, radiotherapy, antibiotic therapy, and chemotherapy before the correct diagnosis is made.¹ Thus, proper identification of these lesions is crucial for prognosis and treatment. The most common locations for OCSTs are the mandibular, submandibular, and cervical skin.^1,2 Given these locations, patients with OCSTs commonly present to the dermatology office for evaluation. Education regarding the clinical presentation, histopathology, and proper evaluation and further referral for treatment is essential for dermatologists.

Tools and Technique for Diagnosis

We present 2 patients with OCSTs who were referred for cutaneous surgery for an SCC and epidermal cyst, but the proper diagnosis was rendered after an index of suspicion and clinicopathologic correlation led to additional testing and eventual referral for imaging.

Patient 1
A 68-year-old woman presented for Mohs micrographic surgery (MMS) of a biopsy-proven SCC on the chin. The tumor cleared after 2 MMS stages (Figure 1A). Due to notable inflammation in each stage, the slides were sent to a pathologist who confirmed clear margins. Within 2 weeks of MMS, the wound began to dehisce (Figure 1B). The patient presented 4 months later with a crusted ulcerated nodule at the MMS site (Figure 1C). A biopsy showed likely recurrence of SCC. Upon presentation to the Mohs surgeon, the nodule felt fixed to the underlying jaw, and the patient was noted to have poor dentition. The patient was sent for computed tomography (CT), which showed focal thinning of the mandible, likely postsurgical, and clear maxillary sinuses. Due to the clinical appearance and anatomic location of the lesion, a request was made for a second read of the CT, specifically looking for an OCST at the prior surgical site. With this information, the radiologist noted an OCST extending from the mandible to the lesion, reported as a periapical lucency (representing a periapical abscess) at a mandibular tooth with a dental sinus draining into the soft tissues. The patient was started on antibiotics and referred to an oral surgeon for OCST excision.

Practice Implications

Odontogenic cutaneous sinus tracts commonly are misdiagnosed due to variations in clinical presentations resembling more common cutaneous diagnoses, nonspecific histopathologic findings, and lack of dental symptoms or concerns about dentition. Clinically, an OCST presents as a fixed, red, crusty, nontender nodule with intermittent draining. With palpation of the involved area, the clinician may feel a cord of tissue connecting the skin lesion intraorally.^2,4 A clinician should have a high index of suspicion for an OCST when evaluating fixed lesions of the lower face, jawline, and neck due to the possibility of a dental origin,¹ which is important because an OCST can have similar clinical findings to lesions such as congenital fistulas, pustules, cysts, osteomyelitis, foreign-body granulomas, pyogenic granulomas, syphilis, metastatic carcinomas, basal cell carcinomas, and SCCs.^2,4 A PubMed search of articles indexed for MEDLINE using the terms Mohs, MMS, chemosurgery, odontogenic sinus, odontogenic cutaneous sinus tract, and dental sinus yielded only 2 OCSTs that were referred for MMS in the last 30 years, both of which were in the nasolabial fold/medial malar cheek.^2,4 Histopathologic findings of an OCST are nonspecific; a mixed or granulomatous inflammatory infiltrate, granulation tissue, and scarring can be seen.¹ Pseudocarcinomatous/pseudoepitheliomatous hyperplasia of the epidermis can be seen and cause histologic misinterpretation for an SCC.² Given that these findings are nonspecific without a clinical context, even with a histopathologic diagnosis of SCC or cyst, a clinical suspicion for an OCST should lead to an intraoral examination. Imaging can be ordered to look for an OCST in the area of interest. Although panoramic or periapical radiography with or without dental probes/radiopaque markers commonly have been used, more recent literature has suggested that CT may be superior to radiographs for making an OCST diagnosis.^1,3 If imaging is not consistent with the clinically suspected OCST, we recommend directly contacting the radiologist to explain the clinical history and even refresh his/her suspicion for this diagnosis.

If a diagnosis of an OCST is made, oral antibiotics can be prescribed, though the use of antibiotics has been controversial. For severe odontogenic infections, typically beta-lactam antibiotics, cephalosporins, metronidazole, clindamycin, moxifloxacin, or erythromycin can be given for 7 days or until 3 days after symptoms have resolved.⁵ Although antibiotics can bring temporary resolution, it is imperative to treat the source of infection to prevent recurrence. It is crucial for these patients to be referred to an oral surgeon for evaluation and treatment of OCST by either a root canal or tooth extraction.

Final Thoughts

We present this pearl on the diagnosis and management of an OCST, also known as a dental sinus, to better assist clinicians in making this diagnosis. With an index of suspicion as well as intraoral and radiologic evaluations, a proper diagnosis may be rendered, potentially avoiding unnecessary cutaneous surgery. In addition, we highlight the importance of communication between the clinician and the radiologist to directly look for OCST in the area of concern and consider a re-read of the images when clinical suspicion does not correlate with the radiology report.

Clinical Challenge

An odontogenic cutaneous sinus tract (OCST) of dental origin is an uncommon occurrence and is most commonly caused by chronic periodontitis, specifically a periapical abscess due to chronic dental infection.^1,2 Odontogenic cutaneous sinus tract commonly is misdiagnosed due to a lack of symptoms on presentation, location, and variations in clinical appearance mimicking other lesions. Patients with OCSTs typically present with a fixed, erythematous, crusty, and nontender nodule with periodic drainage that easily can be mistaken for a pustule, furuncle, cyst, foreign-body lesion, squamous cell carcinoma (SCC), basal cell carcinoma, or granulomatous disorder.³ It becomes challenging for dermatologists to correctly diagnose these lesions and refer for proper evaluation and treatment.

Practice Gap

It is estimated that half of patients with an extraoral fistula are treated with multiple dermatologic surgical operations, radiotherapy, antibiotic therapy, and chemotherapy before the correct diagnosis is made.¹ Thus, proper identification of these lesions is crucial for prognosis and treatment. The most common locations for OCSTs are the mandibular, submandibular, and cervical skin.^1,2 Given these locations, patients with OCSTs commonly present to the dermatology office for evaluation. Education regarding the clinical presentation, histopathology, and proper evaluation and further referral for treatment is essential for dermatologists.

Tools and Technique for Diagnosis

We present 2 patients with OCSTs who were referred for cutaneous surgery for an SCC and epidermal cyst, but the proper diagnosis was rendered after an index of suspicion and clinicopathologic correlation led to additional testing and eventual referral for imaging.

Patient 1
A 68-year-old woman presented for Mohs micrographic surgery (MMS) of a biopsy-proven SCC on the chin. The tumor cleared after 2 MMS stages (Figure 1A). Due to notable inflammation in each stage, the slides were sent to a pathologist who confirmed clear margins. Within 2 weeks of MMS, the wound began to dehisce (Figure 1B). The patient presented 4 months later with a crusted ulcerated nodule at the MMS site (Figure 1C). A biopsy showed likely recurrence of SCC. Upon presentation to the Mohs surgeon, the nodule felt fixed to the underlying jaw, and the patient was noted to have poor dentition. The patient was sent for computed tomography (CT), which showed focal thinning of the mandible, likely postsurgical, and clear maxillary sinuses. Due to the clinical appearance and anatomic location of the lesion, a request was made for a second read of the CT, specifically looking for an OCST at the prior surgical site. With this information, the radiologist noted an OCST extending from the mandible to the lesion, reported as a periapical lucency (representing a periapical abscess) at a mandibular tooth with a dental sinus draining into the soft tissues. The patient was started on antibiotics and referred to an oral surgeon for OCST excision.

Practice Implications

Odontogenic cutaneous sinus tracts commonly are misdiagnosed due to variations in clinical presentations resembling more common cutaneous diagnoses, nonspecific histopathologic findings, and lack of dental symptoms or concerns about dentition. Clinically, an OCST presents as a fixed, red, crusty, nontender nodule with intermittent draining. With palpation of the involved area, the clinician may feel a cord of tissue connecting the skin lesion intraorally.^2,4 A clinician should have a high index of suspicion for an OCST when evaluating fixed lesions of the lower face, jawline, and neck due to the possibility of a dental origin,¹ which is important because an OCST can have similar clinical findings to lesions such as congenital fistulas, pustules, cysts, osteomyelitis, foreign-body granulomas, pyogenic granulomas, syphilis, metastatic carcinomas, basal cell carcinomas, and SCCs.^2,4 A PubMed search of articles indexed for MEDLINE using the terms Mohs, MMS, chemosurgery, odontogenic sinus, odontogenic cutaneous sinus tract, and dental sinus yielded only 2 OCSTs that were referred for MMS in the last 30 years, both of which were in the nasolabial fold/medial malar cheek.^2,4 Histopathologic findings of an OCST are nonspecific; a mixed or granulomatous inflammatory infiltrate, granulation tissue, and scarring can be seen.¹ Pseudocarcinomatous/pseudoepitheliomatous hyperplasia of the epidermis can be seen and cause histologic misinterpretation for an SCC.² Given that these findings are nonspecific without a clinical context, even with a histopathologic diagnosis of SCC or cyst, a clinical suspicion for an OCST should lead to an intraoral examination. Imaging can be ordered to look for an OCST in the area of interest. Although panoramic or periapical radiography with or without dental probes/radiopaque markers commonly have been used, more recent literature has suggested that CT may be superior to radiographs for making an OCST diagnosis.^1,3 If imaging is not consistent with the clinically suspected OCST, we recommend directly contacting the radiologist to explain the clinical history and even refresh his/her suspicion for this diagnosis.

If a diagnosis of an OCST is made, oral antibiotics can be prescribed, though the use of antibiotics has been controversial. For severe odontogenic infections, typically beta-lactam antibiotics, cephalosporins, metronidazole, clindamycin, moxifloxacin, or erythromycin can be given for 7 days or until 3 days after symptoms have resolved.⁵ Although antibiotics can bring temporary resolution, it is imperative to treat the source of infection to prevent recurrence. It is crucial for these patients to be referred to an oral surgeon for evaluation and treatment of OCST by either a root canal or tooth extraction.

Final Thoughts

We present this pearl on the diagnosis and management of an OCST, also known as a dental sinus, to better assist clinicians in making this diagnosis. With an index of suspicion as well as intraoral and radiologic evaluations, a proper diagnosis may be rendered, potentially avoiding unnecessary cutaneous surgery. In addition, we highlight the importance of communication between the clinician and the radiologist to directly look for OCST in the area of concern and consider a re-read of the images when clinical suspicion does not correlate with the radiology report.

Practice Gap

Invasive fungal infections are a leading cause of morbidity and mortality among neutropenic, immunocompromised, and critically ill patients. Candida species are the most common cause of fungemia, with portals of entry into the bloodstream including the gastrointestinal tract, contaminated intravascular catheters, and localized foci of infection.¹ Diagnosis of invasive candidiasis remains challenging due to an absence of specific clinical signs and symptoms, varying from a mild fever that is unresponsive to antibiotics to florid sepsis. When present, clinical clues may include chorioretinitis; muscle abscesses; and skin eruptions, characteristically with Candida tropicalis. Cutaneous manifestations of disseminated Candida infections appear in only 13% of affected patients.¹ The lesions typically present as 5- to 10-mm pink dermal papules or painless pustules on an erythematous base and may be singular, localized, or diffuse in distribution. Body regions normally involved are the trunk, arms, and legs, rarely the head and neck.¹ Cutaneous lesions often develop at a time when patients are febrile, are not responding to antibiotics, and are clinically deteriorating.

A 15-year-old adolescent boy with pre–B-cell acute lymphoblastic leukemia was admitted with febrile neutropenia for presumed septic shock secondary to an unknown infectious etiology. The patient was started on broad-spectrum intravenous antibiotics, and blood cultures were obtained. On the second day of hospitalization, he developed approximately 10 to 15 discrete, 3- to 6-mm, pink to violaceous papules scattered on the chest and arms (Figure 1). Over several hours, the number of lesions increased to more than 50 with involvement of the legs (Figure 2). A punch biopsy of lesional skin from the left dorsal wrist demonstrated a circumscribed abscess of yeast in the papillary dermis, which was highlighted by periodic acid–Schiff staining with minimal associated inflammation (Figure 3). Blood and tissue cultures persistently grew C tropicalis. The patient was started on intravenous liposomal amphotericin B but died on day 5 of hospitalization after developing endocarditis.

Early and reliable diagnosis of Candida species fungemia is of critical importance to successful treatment, particularly with the emergence of multidrug-resistant strains such as Candida auris.² In patients with apparent cutaneous manifestations, a lesional punch biopsy for culture and histopathologic evaluation is recommended in addition to blood culture; however, organisms may or may not be present in large numbers, and they may be difficult to identify on routine hematoxylin and eosin–stained tissue sections. To enhance the likelihood of highlighting the fungus within the sample, the pathologist must be made aware of the presumptive diagnosis of disseminated candidiasis so that special techniques can be utilized, such as periodic acid–Schiff stain.

Although positive blood culture is the gold standard for candidemia diagnosis, only 30% to 50% of patients with disseminated candidiasis had positive blood cultures at autopsy.¹ Another study showed the sensitivity of blood culture for the detection of invasive fungal infection to be as low as 8.3%.³ In cases with positive blood cultures, the median time to positivity is 2 to 3 days, but it can take as long as 8 days, thus limiting its clinical utility in acutely ill patients.⁴ Given the low sensitivity and prolonged time required for culture growth of most fungal organisms, novel assays for rapid, non–culture-based diagnosis of systemic fungal infections hold substantial clinical promise moving forward.

The Technique

One of the more promising non–culture-based fungal diagnostic methodologies is an antigen assay based on the detection of serum (1,3)-β-D-glucan (BDG), a major cell wall constituent of most pathogenic fungi. This assay is not specific for Candida species and can be positive for Aspergillosis species, Fusarium species, Coccidioides immitis, Histoplasma capsulatum, and Pneumocystis jirovecii pneumonia, among others; therefore, it functions as a general biomarker for fungi in the bloodstream.^4,5 (1,3)-β-D-glucan assay can be useful as an adjunct for blood cultures and punch biopsy, especially when cultures are negative or the results remain outstanding. The results of the BDG assay are available in less than 24 hours at minimal cost, and the test is approved by the US Food and Drug Administration for use as an aid in invasive fungal disease diagnosis. In a meta-analysis of 11 studies, BDG sensitivity was 75%.⁴ In a study based on autopsy cases from 6 years, BDG specificity was 98.4% with positive and negative predictive values of 86.7% and 97.1%, respectively.³ Optimal results were achieved when 2 consecutive tests were positive.⁴ The serum assay output is based on spectrophotometer readings, which are converted to BDG concentrations (negative, <60 pg/mL; indeterminate, 60–79 pg/mL; positive ≥80 pg/mL).⁵ Although we cannot be certain, utilizing the BDG assay in our patient may have led to earlier treatment and a better outcome.

A disadvantage of the BDG assay is the potential for false-positive results, which have been reported in lung transplant recipients with respiratory mold colonization and patients with other systemic bacterial infections.⁴ False-positive results also have been associated with use of ampicillin-clavulanate and piperacillin-tazobactam antibiotics and human blood products, hemodialysis, and severe mucositis, thus reaffirming the importance of judicious interpretation of BDG assay results by the clinician.^4,6 There also is a potential for false-negative results, as the BDG assay does not detect certain fungal species such as Cryptococcus species and Blastomyces dermatitidis, which produce very low levels of BDG, or zygomycetes (Absidia, Mucor, and Rizopus species), which are not known to produce BDG.⁶

Practice Implications

In the setting of invasive fungal infections, a high degree of clinical suspicion is paramount due to the often subtle nature of cutaneous manifestations. A positive BDG assay can be used to identify high-risk patients for empiric antifungal therapy, prompting early intervention and improved outcomes in these acutely ill patients. The BDG assay’s excellent negative predictive value is useful in ruling out invasive Candida infections and may justify stopping unnecessary empiric antifungal therapy.⁴ For the dermatology hospitalist, incorporation of the BDG assay as a noninvasive screening tool may allow for more rapid initiation of appropriate antifungal therapy while awaiting confirmatory skin biopsy or culture results in disseminated candidemia and other invasive fungal infections.

Practice Gap

Invasive fungal infections are a leading cause of morbidity and mortality among neutropenic, immunocompromised, and critically ill patients. Candida species are the most common cause of fungemia, with portals of entry into the bloodstream including the gastrointestinal tract, contaminated intravascular catheters, and localized foci of infection.¹ Diagnosis of invasive candidiasis remains challenging due to an absence of specific clinical signs and symptoms, varying from a mild fever that is unresponsive to antibiotics to florid sepsis. When present, clinical clues may include chorioretinitis; muscle abscesses; and skin eruptions, characteristically with Candida tropicalis. Cutaneous manifestations of disseminated Candida infections appear in only 13% of affected patients.¹ The lesions typically present as 5- to 10-mm pink dermal papules or painless pustules on an erythematous base and may be singular, localized, or diffuse in distribution. Body regions normally involved are the trunk, arms, and legs, rarely the head and neck.¹ Cutaneous lesions often develop at a time when patients are febrile, are not responding to antibiotics, and are clinically deteriorating.

A 15-year-old adolescent boy with pre–B-cell acute lymphoblastic leukemia was admitted with febrile neutropenia for presumed septic shock secondary to an unknown infectious etiology. The patient was started on broad-spectrum intravenous antibiotics, and blood cultures were obtained. On the second day of hospitalization, he developed approximately 10 to 15 discrete, 3- to 6-mm, pink to violaceous papules scattered on the chest and arms (Figure 1). Over several hours, the number of lesions increased to more than 50 with involvement of the legs (Figure 2). A punch biopsy of lesional skin from the left dorsal wrist demonstrated a circumscribed abscess of yeast in the papillary dermis, which was highlighted by periodic acid–Schiff staining with minimal associated inflammation (Figure 3). Blood and tissue cultures persistently grew C tropicalis. The patient was started on intravenous liposomal amphotericin B but died on day 5 of hospitalization after developing endocarditis.

Early and reliable diagnosis of Candida species fungemia is of critical importance to successful treatment, particularly with the emergence of multidrug-resistant strains such as Candida auris.² In patients with apparent cutaneous manifestations, a lesional punch biopsy for culture and histopathologic evaluation is recommended in addition to blood culture; however, organisms may or may not be present in large numbers, and they may be difficult to identify on routine hematoxylin and eosin–stained tissue sections. To enhance the likelihood of highlighting the fungus within the sample, the pathologist must be made aware of the presumptive diagnosis of disseminated candidiasis so that special techniques can be utilized, such as periodic acid–Schiff stain.

Although positive blood culture is the gold standard for candidemia diagnosis, only 30% to 50% of patients with disseminated candidiasis had positive blood cultures at autopsy.¹ Another study showed the sensitivity of blood culture for the detection of invasive fungal infection to be as low as 8.3%.³ In cases with positive blood cultures, the median time to positivity is 2 to 3 days, but it can take as long as 8 days, thus limiting its clinical utility in acutely ill patients.⁴ Given the low sensitivity and prolonged time required for culture growth of most fungal organisms, novel assays for rapid, non–culture-based diagnosis of systemic fungal infections hold substantial clinical promise moving forward.

The Technique

One of the more promising non–culture-based fungal diagnostic methodologies is an antigen assay based on the detection of serum (1,3)-β-D-glucan (BDG), a major cell wall constituent of most pathogenic fungi. This assay is not specific for Candida species and can be positive for Aspergillosis species, Fusarium species, Coccidioides immitis, Histoplasma capsulatum, and Pneumocystis jirovecii pneumonia, among others; therefore, it functions as a general biomarker for fungi in the bloodstream.^4,5 (1,3)-β-D-glucan assay can be useful as an adjunct for blood cultures and punch biopsy, especially when cultures are negative or the results remain outstanding. The results of the BDG assay are available in less than 24 hours at minimal cost, and the test is approved by the US Food and Drug Administration for use as an aid in invasive fungal disease diagnosis. In a meta-analysis of 11 studies, BDG sensitivity was 75%.⁴ In a study based on autopsy cases from 6 years, BDG specificity was 98.4% with positive and negative predictive values of 86.7% and 97.1%, respectively.³ Optimal results were achieved when 2 consecutive tests were positive.⁴ The serum assay output is based on spectrophotometer readings, which are converted to BDG concentrations (negative, <60 pg/mL; indeterminate, 60–79 pg/mL; positive ≥80 pg/mL).⁵ Although we cannot be certain, utilizing the BDG assay in our patient may have led to earlier treatment and a better outcome.

A disadvantage of the BDG assay is the potential for false-positive results, which have been reported in lung transplant recipients with respiratory mold colonization and patients with other systemic bacterial infections.⁴ False-positive results also have been associated with use of ampicillin-clavulanate and piperacillin-tazobactam antibiotics and human blood products, hemodialysis, and severe mucositis, thus reaffirming the importance of judicious interpretation of BDG assay results by the clinician.^4,6 There also is a potential for false-negative results, as the BDG assay does not detect certain fungal species such as Cryptococcus species and Blastomyces dermatitidis, which produce very low levels of BDG, or zygomycetes (Absidia, Mucor, and Rizopus species), which are not known to produce BDG.⁶

Practice Implications

In the setting of invasive fungal infections, a high degree of clinical suspicion is paramount due to the often subtle nature of cutaneous manifestations. A positive BDG assay can be used to identify high-risk patients for empiric antifungal therapy, prompting early intervention and improved outcomes in these acutely ill patients. The BDG assay’s excellent negative predictive value is useful in ruling out invasive Candida infections and may justify stopping unnecessary empiric antifungal therapy.⁴ For the dermatology hospitalist, incorporation of the BDG assay as a noninvasive screening tool may allow for more rapid initiation of appropriate antifungal therapy while awaiting confirmatory skin biopsy or culture results in disseminated candidemia and other invasive fungal infections.

Practice Gap

Invasive fungal infections are a leading cause of morbidity and mortality among neutropenic, immunocompromised, and critically ill patients. Candida species are the most common cause of fungemia, with portals of entry into the bloodstream including the gastrointestinal tract, contaminated intravascular catheters, and localized foci of infection.¹ Diagnosis of invasive candidiasis remains challenging due to an absence of specific clinical signs and symptoms, varying from a mild fever that is unresponsive to antibiotics to florid sepsis. When present, clinical clues may include chorioretinitis; muscle abscesses; and skin eruptions, characteristically with Candida tropicalis. Cutaneous manifestations of disseminated Candida infections appear in only 13% of affected patients.¹ The lesions typically present as 5- to 10-mm pink dermal papules or painless pustules on an erythematous base and may be singular, localized, or diffuse in distribution. Body regions normally involved are the trunk, arms, and legs, rarely the head and neck.¹ Cutaneous lesions often develop at a time when patients are febrile, are not responding to antibiotics, and are clinically deteriorating.

A 15-year-old adolescent boy with pre–B-cell acute lymphoblastic leukemia was admitted with febrile neutropenia for presumed septic shock secondary to an unknown infectious etiology. The patient was started on broad-spectrum intravenous antibiotics, and blood cultures were obtained. On the second day of hospitalization, he developed approximately 10 to 15 discrete, 3- to 6-mm, pink to violaceous papules scattered on the chest and arms (Figure 1). Over several hours, the number of lesions increased to more than 50 with involvement of the legs (Figure 2). A punch biopsy of lesional skin from the left dorsal wrist demonstrated a circumscribed abscess of yeast in the papillary dermis, which was highlighted by periodic acid–Schiff staining with minimal associated inflammation (Figure 3). Blood and tissue cultures persistently grew C tropicalis. The patient was started on intravenous liposomal amphotericin B but died on day 5 of hospitalization after developing endocarditis.

Early and reliable diagnosis of Candida species fungemia is of critical importance to successful treatment, particularly with the emergence of multidrug-resistant strains such as Candida auris.² In patients with apparent cutaneous manifestations, a lesional punch biopsy for culture and histopathologic evaluation is recommended in addition to blood culture; however, organisms may or may not be present in large numbers, and they may be difficult to identify on routine hematoxylin and eosin–stained tissue sections. To enhance the likelihood of highlighting the fungus within the sample, the pathologist must be made aware of the presumptive diagnosis of disseminated candidiasis so that special techniques can be utilized, such as periodic acid–Schiff stain.

Although positive blood culture is the gold standard for candidemia diagnosis, only 30% to 50% of patients with disseminated candidiasis had positive blood cultures at autopsy.¹ Another study showed the sensitivity of blood culture for the detection of invasive fungal infection to be as low as 8.3%.³ In cases with positive blood cultures, the median time to positivity is 2 to 3 days, but it can take as long as 8 days, thus limiting its clinical utility in acutely ill patients.⁴ Given the low sensitivity and prolonged time required for culture growth of most fungal organisms, novel assays for rapid, non–culture-based diagnosis of systemic fungal infections hold substantial clinical promise moving forward.

The Technique

One of the more promising non–culture-based fungal diagnostic methodologies is an antigen assay based on the detection of serum (1,3)-β-D-glucan (BDG), a major cell wall constituent of most pathogenic fungi. This assay is not specific for Candida species and can be positive for Aspergillosis species, Fusarium species, Coccidioides immitis, Histoplasma capsulatum, and Pneumocystis jirovecii pneumonia, among others; therefore, it functions as a general biomarker for fungi in the bloodstream.^4,5 (1,3)-β-D-glucan assay can be useful as an adjunct for blood cultures and punch biopsy, especially when cultures are negative or the results remain outstanding. The results of the BDG assay are available in less than 24 hours at minimal cost, and the test is approved by the US Food and Drug Administration for use as an aid in invasive fungal disease diagnosis. In a meta-analysis of 11 studies, BDG sensitivity was 75%.⁴ In a study based on autopsy cases from 6 years, BDG specificity was 98.4% with positive and negative predictive values of 86.7% and 97.1%, respectively.³ Optimal results were achieved when 2 consecutive tests were positive.⁴ The serum assay output is based on spectrophotometer readings, which are converted to BDG concentrations (negative, <60 pg/mL; indeterminate, 60–79 pg/mL; positive ≥80 pg/mL).⁵ Although we cannot be certain, utilizing the BDG assay in our patient may have led to earlier treatment and a better outcome.

A disadvantage of the BDG assay is the potential for false-positive results, which have been reported in lung transplant recipients with respiratory mold colonization and patients with other systemic bacterial infections.⁴ False-positive results also have been associated with use of ampicillin-clavulanate and piperacillin-tazobactam antibiotics and human blood products, hemodialysis, and severe mucositis, thus reaffirming the importance of judicious interpretation of BDG assay results by the clinician.^4,6 There also is a potential for false-negative results, as the BDG assay does not detect certain fungal species such as Cryptococcus species and Blastomyces dermatitidis, which produce very low levels of BDG, or zygomycetes (Absidia, Mucor, and Rizopus species), which are not known to produce BDG.⁶

Practice Implications

In the setting of invasive fungal infections, a high degree of clinical suspicion is paramount due to the often subtle nature of cutaneous manifestations. A positive BDG assay can be used to identify high-risk patients for empiric antifungal therapy, prompting early intervention and improved outcomes in these acutely ill patients. The BDG assay’s excellent negative predictive value is useful in ruling out invasive Candida infections and may justify stopping unnecessary empiric antifungal therapy.⁴ For the dermatology hospitalist, incorporation of the BDG assay as a noninvasive screening tool may allow for more rapid initiation of appropriate antifungal therapy while awaiting confirmatory skin biopsy or culture results in disseminated candidemia and other invasive fungal infections.

Practice Gap

Anxiety is common in patients undergoing surgery with general anesthesia and may be exacerbated in patients undergoing dermatologic surgery with local anesthesia. Apprehension might be worse for nail surgery patients because the nail unit is highly innervated and vascular. Many patients fear the anesthetic injections, and there often is pain postoperatively. Perioperative anxiety correlates with increased postoperative pain,¹ analgesic use,² and delayed recovery.³ Several alternatives have been proposed to decrease perioperative anxiety, including nonpharmacologic interventions such as using educational videos, personalized music, hand holding, art activities, and virtual reality, as well as pharmacologic interventions such as benzodiazepines. However, these techniques have not been well studied for nail surgery.

The Technique

Patients generally are anxious about nail surgery secondary to the pain associated with the local anesthetic infiltration; hence, it is crucial to decrease anxiety during this initial step. In our practice, we provide patients with a palm-sized stress ball made of closed-cell polyurethane foam rubber before surgery. Patients are then instructed to hold the stress ball with the free hand and squeeze it whenever they feel anxious or when they feel any discomfort related to the procedure (Figure). A variety of balls can be bought for less than $1 each, thus making it a cost-effective option.

Practice Implications

Holding a stress ball has been found to reduce both pain and anxiety in patients undergoing conscious surgery.⁴ Furthermore, squeezing a stress ball perioperatively may increase feelings of empowerment, given that patients have direct control over the object, which in turn may have a positive effect on anxiety and patient satisfaction without interfering with the surgical procedure.⁵ Holding a stress ball is a safe, widely accessible, and inexpensive technique that may aid in decreasing patients’ anxiety related to nail surgery. Nonetheless, controlled clinical trials assessing the efficacy of this method in reducing anxiety related to nail surgery are needed to determine its benefit compared to other methods.

Practice Gap

Anxiety is common in patients undergoing surgery with general anesthesia and may be exacerbated in patients undergoing dermatologic surgery with local anesthesia. Apprehension might be worse for nail surgery patients because the nail unit is highly innervated and vascular. Many patients fear the anesthetic injections, and there often is pain postoperatively. Perioperative anxiety correlates with increased postoperative pain,¹ analgesic use,² and delayed recovery.³ Several alternatives have been proposed to decrease perioperative anxiety, including nonpharmacologic interventions such as using educational videos, personalized music, hand holding, art activities, and virtual reality, as well as pharmacologic interventions such as benzodiazepines. However, these techniques have not been well studied for nail surgery.

The Technique

Patients generally are anxious about nail surgery secondary to the pain associated with the local anesthetic infiltration; hence, it is crucial to decrease anxiety during this initial step. In our practice, we provide patients with a palm-sized stress ball made of closed-cell polyurethane foam rubber before surgery. Patients are then instructed to hold the stress ball with the free hand and squeeze it whenever they feel anxious or when they feel any discomfort related to the procedure (Figure). A variety of balls can be bought for less than $1 each, thus making it a cost-effective option.

Practice Implications

Holding a stress ball has been found to reduce both pain and anxiety in patients undergoing conscious surgery.⁴ Furthermore, squeezing a stress ball perioperatively may increase feelings of empowerment, given that patients have direct control over the object, which in turn may have a positive effect on anxiety and patient satisfaction without interfering with the surgical procedure.⁵ Holding a stress ball is a safe, widely accessible, and inexpensive technique that may aid in decreasing patients’ anxiety related to nail surgery. Nonetheless, controlled clinical trials assessing the efficacy of this method in reducing anxiety related to nail surgery are needed to determine its benefit compared to other methods.

Practice Gap

Anxiety is common in patients undergoing surgery with general anesthesia and may be exacerbated in patients undergoing dermatologic surgery with local anesthesia. Apprehension might be worse for nail surgery patients because the nail unit is highly innervated and vascular. Many patients fear the anesthetic injections, and there often is pain postoperatively. Perioperative anxiety correlates with increased postoperative pain,¹ analgesic use,² and delayed recovery.³ Several alternatives have been proposed to decrease perioperative anxiety, including nonpharmacologic interventions such as using educational videos, personalized music, hand holding, art activities, and virtual reality, as well as pharmacologic interventions such as benzodiazepines. However, these techniques have not been well studied for nail surgery.

The Technique

Patients generally are anxious about nail surgery secondary to the pain associated with the local anesthetic infiltration; hence, it is crucial to decrease anxiety during this initial step. In our practice, we provide patients with a palm-sized stress ball made of closed-cell polyurethane foam rubber before surgery. Patients are then instructed to hold the stress ball with the free hand and squeeze it whenever they feel anxious or when they feel any discomfort related to the procedure (Figure). A variety of balls can be bought for less than $1 each, thus making it a cost-effective option.

Practice Implications

Holding a stress ball has been found to reduce both pain and anxiety in patients undergoing conscious surgery.⁴ Furthermore, squeezing a stress ball perioperatively may increase feelings of empowerment, given that patients have direct control over the object, which in turn may have a positive effect on anxiety and patient satisfaction without interfering with the surgical procedure.⁵ Holding a stress ball is a safe, widely accessible, and inexpensive technique that may aid in decreasing patients’ anxiety related to nail surgery. Nonetheless, controlled clinical trials assessing the efficacy of this method in reducing anxiety related to nail surgery are needed to determine its benefit compared to other methods.

Practice Gap

A 69-year-old man underwent staged excision for an invasive melanoma (0.4-mm Breslow depth; stage Ia) of the right dorsal nose. Two stages were required to achieve clear margins, leaving a 3.0×2.5-cm defect involving the nasal dorsum, right nasal sidewall, and nasal supratip (Figure 1). He declined any multistage repair and preferred a full-thickness skin graft (FTSG) over any interpolation flap.

Given the size of our patient’s defect, primary repair was not possible and second intention healing may have resulted in a suboptimal cosmetic outcome, potential alar distortion, and prolonged healing. No single local flap, such as the dorsal nasal rotation flap, crescentic advancement flap, bilobed flap, and Rintala flap, would have provided adequate coverage. A FTSG of the entire defect would not have been an ideal tissue match, and given the limited surrounding laxity, a Burow FTSG would have required the linear repair to extend well into the forehead with a questionable cosmetic outcome.

The Technique

We opted to repair the defect using a combination of local flaps for a single-stage repair. Using the right cheek reservoir, a crescentic advancement flap was performed to restore the right nasal sidewall as best as possible with a standing cone taken superiorly. To execute this flap, an incision was made extending from the alar sulcus into the nasolabial fold while preserving the apical triangle of the upper cutaneous lip. The flap was elevated submuscularly on the nose, and broad undermining was performed in the subcutaneous plane of the medial cheek. A crescentic redundancy above the alar sulcus was excised, and periosteal tacking sutures were placed to both help advance the flap and to recreate the nasofacial sulcus.¹

Next, a nasal tip spiral/rotation flap was designed to restore the remaining nasal defect.² An incision was made at the right inferiormost aspect of the defect and extended along the inferior border of the nasal tip as it crossed the midline to the left side of the nose. After incising and elevating the flap in the submuscular plane, there was not enough of a tissue reservoir to cover the entire remaining nasal defect.

To resolve this intraoperative conundrum, simple interrupted sutures were placed into the nasal cartilage at midline to narrow the structure of the nose (Figure 2). Three 4-0 polyglactin 910 sutures were placed beginning with the upper lateral cartilages and extending inferiorly to the lower lateral cartilages. Narrowing the nasal cartilages allowed for a smaller residual defect. The nasal tip rotation flap was then spiraled into place with adequate coverage. Some of the flap tip was trimmed after the superior aspect of the rotation flap was sutured to the inferior edge of the crescentic advancement flap. The immediate postoperative appearance is shown in Figure 3.

Practice Implications

Cartilage sutures highlight an underutilized technique in nasal reconstruction, with few cases reported in the dermatologic surgery literature.^3,4 The interdomal suture is placed through the left and right lower lateral cartilages to help narrow and redefine the nasal tip.⁵ Reported techniques include simple interrupted suture or horizontal mattress suture. Suture material for nasal cartilage may be permanent (nylon or polypropylene) or long-lasting (polydioxanone or polyglactin 910).⁵ The use of interdomal sutures has been reported to narrow and decrease the volume of nasal tip defects prior to repair with local flaps and FTSG.^3,4 In addition to the interdomal suture of the lower lateral nasal cartilage, simple interrupted sutures were placed in the upper lateral cartilages that created an even smaller residual defect. Sutures of the nasal cartilage may be a good option for select patients in dermatologic reconstruction, allowing for a simple repair with the added benefit of improved cosmetic result.

A combination of local flaps may be used to repair large nasal defects involving multiple subunits, especially in patients who decline multistage reconstruction. A nasal tip rotation/spiral flap can be considered for the appropriate nasal tip defect. Suturing the nasal cartilage with either permanent or long-lasting suture can narrow the cartilage and facilitate flap coverage for nasal defects while also improving the appearance of patients with wide prominent lower noses.

Practice Gap

A 69-year-old man underwent staged excision for an invasive melanoma (0.4-mm Breslow depth; stage Ia) of the right dorsal nose. Two stages were required to achieve clear margins, leaving a 3.0×2.5-cm defect involving the nasal dorsum, right nasal sidewall, and nasal supratip (Figure 1). He declined any multistage repair and preferred a full-thickness skin graft (FTSG) over any interpolation flap.

Given the size of our patient’s defect, primary repair was not possible and second intention healing may have resulted in a suboptimal cosmetic outcome, potential alar distortion, and prolonged healing. No single local flap, such as the dorsal nasal rotation flap, crescentic advancement flap, bilobed flap, and Rintala flap, would have provided adequate coverage. A FTSG of the entire defect would not have been an ideal tissue match, and given the limited surrounding laxity, a Burow FTSG would have required the linear repair to extend well into the forehead with a questionable cosmetic outcome.

The Technique

We opted to repair the defect using a combination of local flaps for a single-stage repair. Using the right cheek reservoir, a crescentic advancement flap was performed to restore the right nasal sidewall as best as possible with a standing cone taken superiorly. To execute this flap, an incision was made extending from the alar sulcus into the nasolabial fold while preserving the apical triangle of the upper cutaneous lip. The flap was elevated submuscularly on the nose, and broad undermining was performed in the subcutaneous plane of the medial cheek. A crescentic redundancy above the alar sulcus was excised, and periosteal tacking sutures were placed to both help advance the flap and to recreate the nasofacial sulcus.¹

Next, a nasal tip spiral/rotation flap was designed to restore the remaining nasal defect.² An incision was made at the right inferiormost aspect of the defect and extended along the inferior border of the nasal tip as it crossed the midline to the left side of the nose. After incising and elevating the flap in the submuscular plane, there was not enough of a tissue reservoir to cover the entire remaining nasal defect.

To resolve this intraoperative conundrum, simple interrupted sutures were placed into the nasal cartilage at midline to narrow the structure of the nose (Figure 2). Three 4-0 polyglactin 910 sutures were placed beginning with the upper lateral cartilages and extending inferiorly to the lower lateral cartilages. Narrowing the nasal cartilages allowed for a smaller residual defect. The nasal tip rotation flap was then spiraled into place with adequate coverage. Some of the flap tip was trimmed after the superior aspect of the rotation flap was sutured to the inferior edge of the crescentic advancement flap. The immediate postoperative appearance is shown in Figure 3.

Practice Implications

Cartilage sutures highlight an underutilized technique in nasal reconstruction, with few cases reported in the dermatologic surgery literature.^3,4 The interdomal suture is placed through the left and right lower lateral cartilages to help narrow and redefine the nasal tip.⁵ Reported techniques include simple interrupted suture or horizontal mattress suture. Suture material for nasal cartilage may be permanent (nylon or polypropylene) or long-lasting (polydioxanone or polyglactin 910).⁵ The use of interdomal sutures has been reported to narrow and decrease the volume of nasal tip defects prior to repair with local flaps and FTSG.^3,4 In addition to the interdomal suture of the lower lateral nasal cartilage, simple interrupted sutures were placed in the upper lateral cartilages that created an even smaller residual defect. Sutures of the nasal cartilage may be a good option for select patients in dermatologic reconstruction, allowing for a simple repair with the added benefit of improved cosmetic result.

A combination of local flaps may be used to repair large nasal defects involving multiple subunits, especially in patients who decline multistage reconstruction. A nasal tip rotation/spiral flap can be considered for the appropriate nasal tip defect. Suturing the nasal cartilage with either permanent or long-lasting suture can narrow the cartilage and facilitate flap coverage for nasal defects while also improving the appearance of patients with wide prominent lower noses.

Practice Gap

A 69-year-old man underwent staged excision for an invasive melanoma (0.4-mm Breslow depth; stage Ia) of the right dorsal nose. Two stages were required to achieve clear margins, leaving a 3.0×2.5-cm defect involving the nasal dorsum, right nasal sidewall, and nasal supratip (Figure 1). He declined any multistage repair and preferred a full-thickness skin graft (FTSG) over any interpolation flap.

Given the size of our patient’s defect, primary repair was not possible and second intention healing may have resulted in a suboptimal cosmetic outcome, potential alar distortion, and prolonged healing. No single local flap, such as the dorsal nasal rotation flap, crescentic advancement flap, bilobed flap, and Rintala flap, would have provided adequate coverage. A FTSG of the entire defect would not have been an ideal tissue match, and given the limited surrounding laxity, a Burow FTSG would have required the linear repair to extend well into the forehead with a questionable cosmetic outcome.

The Technique

We opted to repair the defect using a combination of local flaps for a single-stage repair. Using the right cheek reservoir, a crescentic advancement flap was performed to restore the right nasal sidewall as best as possible with a standing cone taken superiorly. To execute this flap, an incision was made extending from the alar sulcus into the nasolabial fold while preserving the apical triangle of the upper cutaneous lip. The flap was elevated submuscularly on the nose, and broad undermining was performed in the subcutaneous plane of the medial cheek. A crescentic redundancy above the alar sulcus was excised, and periosteal tacking sutures were placed to both help advance the flap and to recreate the nasofacial sulcus.¹

Next, a nasal tip spiral/rotation flap was designed to restore the remaining nasal defect.² An incision was made at the right inferiormost aspect of the defect and extended along the inferior border of the nasal tip as it crossed the midline to the left side of the nose. After incising and elevating the flap in the submuscular plane, there was not enough of a tissue reservoir to cover the entire remaining nasal defect.

To resolve this intraoperative conundrum, simple interrupted sutures were placed into the nasal cartilage at midline to narrow the structure of the nose (Figure 2). Three 4-0 polyglactin 910 sutures were placed beginning with the upper lateral cartilages and extending inferiorly to the lower lateral cartilages. Narrowing the nasal cartilages allowed for a smaller residual defect. The nasal tip rotation flap was then spiraled into place with adequate coverage. Some of the flap tip was trimmed after the superior aspect of the rotation flap was sutured to the inferior edge of the crescentic advancement flap. The immediate postoperative appearance is shown in Figure 3.

Practice Implications

Cartilage sutures highlight an underutilized technique in nasal reconstruction, with few cases reported in the dermatologic surgery literature.^3,4 The interdomal suture is placed through the left and right lower lateral cartilages to help narrow and redefine the nasal tip.⁵ Reported techniques include simple interrupted suture or horizontal mattress suture. Suture material for nasal cartilage may be permanent (nylon or polypropylene) or long-lasting (polydioxanone or polyglactin 910).⁵ The use of interdomal sutures has been reported to narrow and decrease the volume of nasal tip defects prior to repair with local flaps and FTSG.^3,4 In addition to the interdomal suture of the lower lateral nasal cartilage, simple interrupted sutures were placed in the upper lateral cartilages that created an even smaller residual defect. Sutures of the nasal cartilage may be a good option for select patients in dermatologic reconstruction, allowing for a simple repair with the added benefit of improved cosmetic result.

A combination of local flaps may be used to repair large nasal defects involving multiple subunits, especially in patients who decline multistage reconstruction. A nasal tip rotation/spiral flap can be considered for the appropriate nasal tip defect. Suturing the nasal cartilage with either permanent or long-lasting suture can narrow the cartilage and facilitate flap coverage for nasal defects while also improving the appearance of patients with wide prominent lower noses.

The number of skin cancer surgeries continues to rise, especially in the older population, many of whom are on blood thinners. The sequela of bleeding, even in minor cases, is one of the most frequently encountered complications of cutaneous surgery. Surgical site bleeding can increase the risk for infection, skin graft failure, wound dehiscence, and hematoma formation, which may lead to disrupted wound healing and eventual poor scar outcome. Although achieving hemostasis is important, it is recommended to limit certain alternative modalities such as electrosurgery due to the accompanied thermal tissue damage that in turn can prolong healing time, worsen scarring, and increase the risk for infection.¹

Practice Gap

Hydrogen peroxide (H₂O₂) is a common topical antiseptic used to clean wounds by killing pathogens through oxidation burst and local oxygen production.² It is generally affordable, nonallergenic, and easy to obtain. We describe our positive experience using H₂O₂ as a hemostatic agent during dermatologic surgery, highlighting the agent’s underutilization as well as the recent literature negating traditional viewpoints that it probably causes tissue necrosis and impaired wound healing through its high oxidative property.

The Technique

Before surgery, the site is prepared with chlorhexidine gluconate. A stack of 4×4-in gauze on the surgical tray is saturated with 3% H₂O₂ and used by the surgeon and surgical assistant throughout the procedure. We currently use this technique during standard excisions, Mohs micrographic surgery stages, repairs, and dermabrasion. Additionally, as a first measure of hemostasis, we recommend H₂O₂ soaks immediately postoperatively in patients with active bleeding.

We have been utilizing this technique since H₂O₂ was described as an intraprocedural hemostatic agent during manual dermabrasion.³ Hydrogen peroxide is known to facilitate hemostasis with several accepted mechanisms that include regulating the contractility and barrier function of endothelial cells, activating latent cell surface tissue factor and platelet aggregation, and stimulating platelet-derived growth factor activation.⁴ It has been reported that increasing H₂O₂ levels leads to a dose-response increase in aggregation in the presence of subaggregating amounts of collagen.⁵ This concept was described in an article that utilizes H₂O₂ as a way to obtain hemostasis before skin grafting burn patients.⁶ A PubMed search of articles indexed for MEDLINE using the terms h202, hydrogen peroxide, hemostasis, wound healing, surgery, and wound produced several surgical specialties—neurosurgery, orthopedics, gastroenterology, and maxillofacial surgery—that also utilize H₂O₂ as a hemostatic agent.^7,8 One article described a dual-enzyme H₂O₂ generation machinery in hydrogels as a novel antimicrobial wound treatment.⁹

Practice Implications

The use of H₂O₂ as a topical hemostatic agent during surgery was described in 1984.² The use of H₂O₂ is not suggested as a substitute for other strong and well-known hemostatic agents, such as aluminum chloride and ferric subsulfate, but rather as a technique that can be used in conjunction with standard methods of hemostasis and antisepsis. For surgical sites that are intended to be closed, we do not suggest these hemostatic agents, as they are known to be caustic, irritating, and pigmenting. In addition to H₂O₂’s known hemostatic and antiseptic properties, more recent literature invalidates wound impairment concerns and describes its possible role in signaling effector cells to respond downstream, contributing to tissue formation and remodeling.⁴ The use of H₂O₂ in wound and incision care has been controversial and avoided due to described skin irritation and possible premature removal of suture¹⁰; however, positive biochemical effects of H₂O₂ on acute wounds have been reported and dispel arguments that this agent causes tissue damage.⁴ Contrary to the traditional viewpoint that H₂O₂ probably impairs tissue through its high oxidative property, a proper level of H₂O₂ is considered an important requirement for normal wound healing. The report published in 1985 that raised concerns of H₂O₂ causing impaired wound healing through its effect on fibroblasts has been challenged given that the killed cultured fibroblasts were in an in vitro model and not likely representative of the complexities of a healing wound.¹⁰ In our experience, the use of H₂O₂ has not demonstrated any impairments or delays in wound healing, and we postulate that the exposure to H₂O₂ as described in our technique is not sufficient to cause notable impairment in fibroblast function in vivo. In addition, the role of H₂O₂ promoting oxidative stress as well as resolving inflammation may suggest it serves as a bidirectional regulator.

Future Directions

Additional studies are needed to assess this precise balance of H₂O₂ forming a favorable microenvironment in wounds. Similarly, although we discuss minimal and brief use of H₂O₂ during a procedure, the lack of data on the role of H₂O₂ as a prophylactic anti-infective agent for postoperative wound care also may be an area of future exploration.

The number of skin cancer surgeries continues to rise, especially in the older population, many of whom are on blood thinners. The sequela of bleeding, even in minor cases, is one of the most frequently encountered complications of cutaneous surgery. Surgical site bleeding can increase the risk for infection, skin graft failure, wound dehiscence, and hematoma formation, which may lead to disrupted wound healing and eventual poor scar outcome. Although achieving hemostasis is important, it is recommended to limit certain alternative modalities such as electrosurgery due to the accompanied thermal tissue damage that in turn can prolong healing time, worsen scarring, and increase the risk for infection.¹

Practice Gap

Hydrogen peroxide (H₂O₂) is a common topical antiseptic used to clean wounds by killing pathogens through oxidation burst and local oxygen production.² It is generally affordable, nonallergenic, and easy to obtain. We describe our positive experience using H₂O₂ as a hemostatic agent during dermatologic surgery, highlighting the agent’s underutilization as well as the recent literature negating traditional viewpoints that it probably causes tissue necrosis and impaired wound healing through its high oxidative property.

The Technique

Before surgery, the site is prepared with chlorhexidine gluconate. A stack of 4×4-in gauze on the surgical tray is saturated with 3% H₂O₂ and used by the surgeon and surgical assistant throughout the procedure. We currently use this technique during standard excisions, Mohs micrographic surgery stages, repairs, and dermabrasion. Additionally, as a first measure of hemostasis, we recommend H₂O₂ soaks immediately postoperatively in patients with active bleeding.

We have been utilizing this technique since H₂O₂ was described as an intraprocedural hemostatic agent during manual dermabrasion.³ Hydrogen peroxide is known to facilitate hemostasis with several accepted mechanisms that include regulating the contractility and barrier function of endothelial cells, activating latent cell surface tissue factor and platelet aggregation, and stimulating platelet-derived growth factor activation.⁴ It has been reported that increasing H₂O₂ levels leads to a dose-response increase in aggregation in the presence of subaggregating amounts of collagen.⁵ This concept was described in an article that utilizes H₂O₂ as a way to obtain hemostasis before skin grafting burn patients.⁶ A PubMed search of articles indexed for MEDLINE using the terms h202, hydrogen peroxide, hemostasis, wound healing, surgery, and wound produced several surgical specialties—neurosurgery, orthopedics, gastroenterology, and maxillofacial surgery—that also utilize H₂O₂ as a hemostatic agent.^7,8 One article described a dual-enzyme H₂O₂ generation machinery in hydrogels as a novel antimicrobial wound treatment.⁹

Practice Implications

The use of H₂O₂ as a topical hemostatic agent during surgery was described in 1984.² The use of H₂O₂ is not suggested as a substitute for other strong and well-known hemostatic agents, such as aluminum chloride and ferric subsulfate, but rather as a technique that can be used in conjunction with standard methods of hemostasis and antisepsis. For surgical sites that are intended to be closed, we do not suggest these hemostatic agents, as they are known to be caustic, irritating, and pigmenting. In addition to H₂O₂’s known hemostatic and antiseptic properties, more recent literature invalidates wound impairment concerns and describes its possible role in signaling effector cells to respond downstream, contributing to tissue formation and remodeling.⁴ The use of H₂O₂ in wound and incision care has been controversial and avoided due to described skin irritation and possible premature removal of suture¹⁰; however, positive biochemical effects of H₂O₂ on acute wounds have been reported and dispel arguments that this agent causes tissue damage.⁴ Contrary to the traditional viewpoint that H₂O₂ probably impairs tissue through its high oxidative property, a proper level of H₂O₂ is considered an important requirement for normal wound healing. The report published in 1985 that raised concerns of H₂O₂ causing impaired wound healing through its effect on fibroblasts has been challenged given that the killed cultured fibroblasts were in an in vitro model and not likely representative of the complexities of a healing wound.¹⁰ In our experience, the use of H₂O₂ has not demonstrated any impairments or delays in wound healing, and we postulate that the exposure to H₂O₂ as described in our technique is not sufficient to cause notable impairment in fibroblast function in vivo. In addition, the role of H₂O₂ promoting oxidative stress as well as resolving inflammation may suggest it serves as a bidirectional regulator.

Future Directions

Additional studies are needed to assess this precise balance of H₂O₂ forming a favorable microenvironment in wounds. Similarly, although we discuss minimal and brief use of H₂O₂ during a procedure, the lack of data on the role of H₂O₂ as a prophylactic anti-infective agent for postoperative wound care also may be an area of future exploration.

The number of skin cancer surgeries continues to rise, especially in the older population, many of whom are on blood thinners. The sequela of bleeding, even in minor cases, is one of the most frequently encountered complications of cutaneous surgery. Surgical site bleeding can increase the risk for infection, skin graft failure, wound dehiscence, and hematoma formation, which may lead to disrupted wound healing and eventual poor scar outcome. Although achieving hemostasis is important, it is recommended to limit certain alternative modalities such as electrosurgery due to the accompanied thermal tissue damage that in turn can prolong healing time, worsen scarring, and increase the risk for infection.¹

Practice Gap

Hydrogen peroxide (H₂O₂) is a common topical antiseptic used to clean wounds by killing pathogens through oxidation burst and local oxygen production.² It is generally affordable, nonallergenic, and easy to obtain. We describe our positive experience using H₂O₂ as a hemostatic agent during dermatologic surgery, highlighting the agent’s underutilization as well as the recent literature negating traditional viewpoints that it probably causes tissue necrosis and impaired wound healing through its high oxidative property.

The Technique

Before surgery, the site is prepared with chlorhexidine gluconate. A stack of 4×4-in gauze on the surgical tray is saturated with 3% H₂O₂ and used by the surgeon and surgical assistant throughout the procedure. We currently use this technique during standard excisions, Mohs micrographic surgery stages, repairs, and dermabrasion. Additionally, as a first measure of hemostasis, we recommend H₂O₂ soaks immediately postoperatively in patients with active bleeding.

We have been utilizing this technique since H₂O₂ was described as an intraprocedural hemostatic agent during manual dermabrasion.³ Hydrogen peroxide is known to facilitate hemostasis with several accepted mechanisms that include regulating the contractility and barrier function of endothelial cells, activating latent cell surface tissue factor and platelet aggregation, and stimulating platelet-derived growth factor activation.⁴ It has been reported that increasing H₂O₂ levels leads to a dose-response increase in aggregation in the presence of subaggregating amounts of collagen.⁵ This concept was described in an article that utilizes H₂O₂ as a way to obtain hemostasis before skin grafting burn patients.⁶ A PubMed search of articles indexed for MEDLINE using the terms h202, hydrogen peroxide, hemostasis, wound healing, surgery, and wound produced several surgical specialties—neurosurgery, orthopedics, gastroenterology, and maxillofacial surgery—that also utilize H₂O₂ as a hemostatic agent.^7,8 One article described a dual-enzyme H₂O₂ generation machinery in hydrogels as a novel antimicrobial wound treatment.⁹

Practice Implications

The use of H₂O₂ as a topical hemostatic agent during surgery was described in 1984.² The use of H₂O₂ is not suggested as a substitute for other strong and well-known hemostatic agents, such as aluminum chloride and ferric subsulfate, but rather as a technique that can be used in conjunction with standard methods of hemostasis and antisepsis. For surgical sites that are intended to be closed, we do not suggest these hemostatic agents, as they are known to be caustic, irritating, and pigmenting. In addition to H₂O₂’s known hemostatic and antiseptic properties, more recent literature invalidates wound impairment concerns and describes its possible role in signaling effector cells to respond downstream, contributing to tissue formation and remodeling.⁴ The use of H₂O₂ in wound and incision care has been controversial and avoided due to described skin irritation and possible premature removal of suture¹⁰; however, positive biochemical effects of H₂O₂ on acute wounds have been reported and dispel arguments that this agent causes tissue damage.⁴ Contrary to the traditional viewpoint that H₂O₂ probably impairs tissue through its high oxidative property, a proper level of H₂O₂ is considered an important requirement for normal wound healing. The report published in 1985 that raised concerns of H₂O₂ causing impaired wound healing through its effect on fibroblasts has been challenged given that the killed cultured fibroblasts were in an in vitro model and not likely representative of the complexities of a healing wound.¹⁰ In our experience, the use of H₂O₂ has not demonstrated any impairments or delays in wound healing, and we postulate that the exposure to H₂O₂ as described in our technique is not sufficient to cause notable impairment in fibroblast function in vivo. In addition, the role of H₂O₂ promoting oxidative stress as well as resolving inflammation may suggest it serves as a bidirectional regulator.

Future Directions

Additional studies are needed to assess this precise balance of H₂O₂ forming a favorable microenvironment in wounds. Similarly, although we discuss minimal and brief use of H₂O₂ during a procedure, the lack of data on the role of H₂O₂ as a prophylactic anti-infective agent for postoperative wound care also may be an area of future exploration.

Practice Gap

Management of nonmelanoma skin cancer (NMSC) in elderly patients can cause morbidity because these patients frequently struggle to care for their biopsy sites and experience biopsy- and surgery-related complications. To minimize this treatment-related morbidity, we designed a knifeless treatment approach that employs reflectance confocal microscopy (RCM) in lieu of skin biopsy to establish the diagnosis of NMSC, then uses either intralesional or topical chemotherapy or immunotherapy (as appropriate, depending on depth of invasion) to cure the NMSC. With this approach, the patient is spared both biopsy- and surgery-related difficulties, though both intralesional and topical chemotherapy are accompanied by their own risks for adverse effects.

The Technique

Elderly patients, diabetic patients, and patients with lesions suspicious for NMSC on areas prone to poor wound healing or to notable treatment-related morbidity (eg, lower legs, genitals, the face of younger patients) are offered skin biopsy or RCM; the latter is performed during the appointment by an RCM-trained medical assistant. Patients who elect to undergo RCM and who have a diagnosis of superficial basal cell carcinoma (BCC) or squamous cell carcinoma (SCC) in situ are then treated with topical imiquimod or 5-fluorouracil. Patients with an invasive subtype of either BCC, SCC, or keratoacanthoma receive intralesional 5-fluorouracil injected at a concentration of 50 mg/cc at weekly intervals until the lesion blanches, with ongoing follow-up until the lesion is observed to have resolved under dermoscopic inspection.

When resolution is uncertain, RCM is repeated to assess for tumor clearance. Repeat RCM is performed at least 4 weeks after termination of treatment to avoid misinterpretation caused by treatment-related tissue inflammation. Patients who are not cured using this management approach are offered appropriate surgical management.

Practice Implications

Reflectance confocal microscopy has emerged as an effective modality for confirming the diagnosis of NMSC with high sensitivity and specificity.^1,2 Emergence of this technology presents an opportunity for improving the way the NMSC is managed because RCM allows dermatologists to confirm the diagnosis of BCC and SCC by interpretation of RCM mosaics rather than by histopathologic examination of biopsied tissue. Our knifeless approach to skin cancer management is especially beneficial when biopsy and dermatologic surgery are likely to confer notable morbidity, such as managing NMSC on the face of a young adult, in the frail elderly population, or in diabetic patients, and when treating sites on the lower extremity prone to poor wound healing.

Practice Gap

Management of nonmelanoma skin cancer (NMSC) in elderly patients can cause morbidity because these patients frequently struggle to care for their biopsy sites and experience biopsy- and surgery-related complications. To minimize this treatment-related morbidity, we designed a knifeless treatment approach that employs reflectance confocal microscopy (RCM) in lieu of skin biopsy to establish the diagnosis of NMSC, then uses either intralesional or topical chemotherapy or immunotherapy (as appropriate, depending on depth of invasion) to cure the NMSC. With this approach, the patient is spared both biopsy- and surgery-related difficulties, though both intralesional and topical chemotherapy are accompanied by their own risks for adverse effects.

The Technique

Elderly patients, diabetic patients, and patients with lesions suspicious for NMSC on areas prone to poor wound healing or to notable treatment-related morbidity (eg, lower legs, genitals, the face of younger patients) are offered skin biopsy or RCM; the latter is performed during the appointment by an RCM-trained medical assistant. Patients who elect to undergo RCM and who have a diagnosis of superficial basal cell carcinoma (BCC) or squamous cell carcinoma (SCC) in situ are then treated with topical imiquimod or 5-fluorouracil. Patients with an invasive subtype of either BCC, SCC, or keratoacanthoma receive intralesional 5-fluorouracil injected at a concentration of 50 mg/cc at weekly intervals until the lesion blanches, with ongoing follow-up until the lesion is observed to have resolved under dermoscopic inspection.

When resolution is uncertain, RCM is repeated to assess for tumor clearance. Repeat RCM is performed at least 4 weeks after termination of treatment to avoid misinterpretation caused by treatment-related tissue inflammation. Patients who are not cured using this management approach are offered appropriate surgical management.

Practice Implications

Reflectance confocal microscopy has emerged as an effective modality for confirming the diagnosis of NMSC with high sensitivity and specificity.^1,2 Emergence of this technology presents an opportunity for improving the way the NMSC is managed because RCM allows dermatologists to confirm the diagnosis of BCC and SCC by interpretation of RCM mosaics rather than by histopathologic examination of biopsied tissue. Our knifeless approach to skin cancer management is especially beneficial when biopsy and dermatologic surgery are likely to confer notable morbidity, such as managing NMSC on the face of a young adult, in the frail elderly population, or in diabetic patients, and when treating sites on the lower extremity prone to poor wound healing.

Practice Gap

Management of nonmelanoma skin cancer (NMSC) in elderly patients can cause morbidity because these patients frequently struggle to care for their biopsy sites and experience biopsy- and surgery-related complications. To minimize this treatment-related morbidity, we designed a knifeless treatment approach that employs reflectance confocal microscopy (RCM) in lieu of skin biopsy to establish the diagnosis of NMSC, then uses either intralesional or topical chemotherapy or immunotherapy (as appropriate, depending on depth of invasion) to cure the NMSC. With this approach, the patient is spared both biopsy- and surgery-related difficulties, though both intralesional and topical chemotherapy are accompanied by their own risks for adverse effects.

The Technique

Elderly patients, diabetic patients, and patients with lesions suspicious for NMSC on areas prone to poor wound healing or to notable treatment-related morbidity (eg, lower legs, genitals, the face of younger patients) are offered skin biopsy or RCM; the latter is performed during the appointment by an RCM-trained medical assistant. Patients who elect to undergo RCM and who have a diagnosis of superficial basal cell carcinoma (BCC) or squamous cell carcinoma (SCC) in situ are then treated with topical imiquimod or 5-fluorouracil. Patients with an invasive subtype of either BCC, SCC, or keratoacanthoma receive intralesional 5-fluorouracil injected at a concentration of 50 mg/cc at weekly intervals until the lesion blanches, with ongoing follow-up until the lesion is observed to have resolved under dermoscopic inspection.

When resolution is uncertain, RCM is repeated to assess for tumor clearance. Repeat RCM is performed at least 4 weeks after termination of treatment to avoid misinterpretation caused by treatment-related tissue inflammation. Patients who are not cured using this management approach are offered appropriate surgical management.

Practice Implications

Reflectance confocal microscopy has emerged as an effective modality for confirming the diagnosis of NMSC with high sensitivity and specificity.^1,2 Emergence of this technology presents an opportunity for improving the way the NMSC is managed because RCM allows dermatologists to confirm the diagnosis of BCC and SCC by interpretation of RCM mosaics rather than by histopathologic examination of biopsied tissue. Our knifeless approach to skin cancer management is especially beneficial when biopsy and dermatologic surgery are likely to confer notable morbidity, such as managing NMSC on the face of a young adult, in the frail elderly population, or in diabetic patients, and when treating sites on the lower extremity prone to poor wound healing.

Practice Gap

Hypergranulation is a frequent complication of dermatologic surgery, especially when surgical defects are left to heal by secondary intention (eg, after electrodesiccation and curettage). Although management of postoperative hypergranulation with routine wound care, superpotent topical corticosteroids, and/or topical silver nitrate often is effective, refractory cases pose a difficult challenge given the paucity of treatment options. Effective management of these cases is important because hypergranulation can delay wound healing, cause patient discomfort, and lead to poor wound cosmesis.

The Technique

If refractory hypergranulation fails to respond to treatment with routine wound care and topical silver nitrate, we prescribe twice-daily application of timolol maleate ophthalmic gel forming solution 0.5% for up to 14 days or until complete resolution of the hypergranulation is achieved. We counsel patients to continue routine wound care with daily dressing changes in conjunction with topical timolol application.

We initiated treatment with topical timolol in a patient who developed hypergranulation at 2 separate electrodesiccation and curettage sites that was refractory to 6 weeks of routine wound care with white petrolatum under nonadherent sterile gauze dressings and 2 subsequent topical silver nitrate applications (Figure 1). After 2 weeks of treatment with topical timolol, resolution of the hypergranulation and re-epithelialization of the surgical sites was observed (Figure 2). Another patient presented with hypergranulation that developed following a traumatic injury on the left upper arm and had been treated unsuccessfully for several months at a wound care clinic with daily nonadherent sterile gauze dressings and both topical and oral antibiotics (Figure 3A). After treatment for 9 days with topical timolol, resolution of the hypergranulation and re-epithelialization of the surgical sites was observed (Figure 3B).

Practice Implications

Beta-blockers are increasingly being used for management of chronic nonhealing wounds since the 1990s when oral administration of propranolol initially was reported to be an effective adjuvant therapy for managing severe burns.¹ Since then, topical beta-blockers have been reported to be effective for management of ulcerated hemangiomas, venous stasis ulcers, chronic diabetic ulcers, and chronic nonhealing surgical wounds; however, there are no known reports of using topical beta-blockers for management of hypergranulation.^2-5 We found timolol ophthalmic gel to be an excellent second-line therapy for management of postoperative hypergranulation if prior treatment with routine wound care and superpotent topical corticosteroids has failed. To date, we have found no reported adverse effects from the use of topical timolol for this indication that have required discontinuation of the medication. Use of this simple and safe intervention can be effective as a solution to a common postoperative condition.

Practice Gap

Hypergranulation is a frequent complication of dermatologic surgery, especially when surgical defects are left to heal by secondary intention (eg, after electrodesiccation and curettage). Although management of postoperative hypergranulation with routine wound care, superpotent topical corticosteroids, and/or topical silver nitrate often is effective, refractory cases pose a difficult challenge given the paucity of treatment options. Effective management of these cases is important because hypergranulation can delay wound healing, cause patient discomfort, and lead to poor wound cosmesis.

The Technique

If refractory hypergranulation fails to respond to treatment with routine wound care and topical silver nitrate, we prescribe twice-daily application of timolol maleate ophthalmic gel forming solution 0.5% for up to 14 days or until complete resolution of the hypergranulation is achieved. We counsel patients to continue routine wound care with daily dressing changes in conjunction with topical timolol application.

We initiated treatment with topical timolol in a patient who developed hypergranulation at 2 separate electrodesiccation and curettage sites that was refractory to 6 weeks of routine wound care with white petrolatum under nonadherent sterile gauze dressings and 2 subsequent topical silver nitrate applications (Figure 1). After 2 weeks of treatment with topical timolol, resolution of the hypergranulation and re-epithelialization of the surgical sites was observed (Figure 2). Another patient presented with hypergranulation that developed following a traumatic injury on the left upper arm and had been treated unsuccessfully for several months at a wound care clinic with daily nonadherent sterile gauze dressings and both topical and oral antibiotics (Figure 3A). After treatment for 9 days with topical timolol, resolution of the hypergranulation and re-epithelialization of the surgical sites was observed (Figure 3B).

Practice Implications

Beta-blockers are increasingly being used for management of chronic nonhealing wounds since the 1990s when oral administration of propranolol initially was reported to be an effective adjuvant therapy for managing severe burns.¹ Since then, topical beta-blockers have been reported to be effective for management of ulcerated hemangiomas, venous stasis ulcers, chronic diabetic ulcers, and chronic nonhealing surgical wounds; however, there are no known reports of using topical beta-blockers for management of hypergranulation.^2-5 We found timolol ophthalmic gel to be an excellent second-line therapy for management of postoperative hypergranulation if prior treatment with routine wound care and superpotent topical corticosteroids has failed. To date, we have found no reported adverse effects from the use of topical timolol for this indication that have required discontinuation of the medication. Use of this simple and safe intervention can be effective as a solution to a common postoperative condition.

Practice Gap

Hypergranulation is a frequent complication of dermatologic surgery, especially when surgical defects are left to heal by secondary intention (eg, after electrodesiccation and curettage). Although management of postoperative hypergranulation with routine wound care, superpotent topical corticosteroids, and/or topical silver nitrate often is effective, refractory cases pose a difficult challenge given the paucity of treatment options. Effective management of these cases is important because hypergranulation can delay wound healing, cause patient discomfort, and lead to poor wound cosmesis.

The Technique

If refractory hypergranulation fails to respond to treatment with routine wound care and topical silver nitrate, we prescribe twice-daily application of timolol maleate ophthalmic gel forming solution 0.5% for up to 14 days or until complete resolution of the hypergranulation is achieved. We counsel patients to continue routine wound care with daily dressing changes in conjunction with topical timolol application.

We initiated treatment with topical timolol in a patient who developed hypergranulation at 2 separate electrodesiccation and curettage sites that was refractory to 6 weeks of routine wound care with white petrolatum under nonadherent sterile gauze dressings and 2 subsequent topical silver nitrate applications (Figure 1). After 2 weeks of treatment with topical timolol, resolution of the hypergranulation and re-epithelialization of the surgical sites was observed (Figure 2). Another patient presented with hypergranulation that developed following a traumatic injury on the left upper arm and had been treated unsuccessfully for several months at a wound care clinic with daily nonadherent sterile gauze dressings and both topical and oral antibiotics (Figure 3A). After treatment for 9 days with topical timolol, resolution of the hypergranulation and re-epithelialization of the surgical sites was observed (Figure 3B).

Practice Implications

Beta-blockers are increasingly being used for management of chronic nonhealing wounds since the 1990s when oral administration of propranolol initially was reported to be an effective adjuvant therapy for managing severe burns.¹ Since then, topical beta-blockers have been reported to be effective for management of ulcerated hemangiomas, venous stasis ulcers, chronic diabetic ulcers, and chronic nonhealing surgical wounds; however, there are no known reports of using topical beta-blockers for management of hypergranulation.^2-5 We found timolol ophthalmic gel to be an excellent second-line therapy for management of postoperative hypergranulation if prior treatment with routine wound care and superpotent topical corticosteroids has failed. To date, we have found no reported adverse effects from the use of topical timolol for this indication that have required discontinuation of the medication. Use of this simple and safe intervention can be effective as a solution to a common postoperative condition.

Practice Gap

Habit-tic nail deformity results from repetitive manipulation of the cuticle and/or proximal nail fold. It most commonly affects one or both thumbnails and presents with a characteristic longitudinal midline furrow with parallel transverse ridges in the nail plate. Complications may include permanent onychodystrophy, frictional melanonychia, and infections. Treatment is challenging, as diagnosis first requires patient insight to the cause of symptoms. Therapeutic options include nonpharmacologic techniques (eg, occlusion of the nails to prevent trauma, cyanoacrylate adhesives, cognitive behavioral therapy) and pharmacologic techniques (eg, N-acetyl cysteine, selective serotonin reuptake inhibitors, tricyclic antidepressants, antipsychotics), with limited supporting data and potential adverse effects.¹

The Technique

Benzethonium chloride solution 0.2% is an antiseptic that creates a polymeric layer that binds to the skin. It normally is used to treat small skin erosions and prevent blisters. In patients with habit-tic nail deformity, we recommend once-daily application of benzethonium chloride to the proximal nail fold, thereby artificially recreating the cuticle and forming a sustainable barrier from trauma (Figure, A). Patients should be reminded not to manipulate the cuticle and/or nail fold during treatment. In one 36-year-old man with habit tic nail deformity, we saw clear nail growth after 4 months of treatment (Figure, B).

Practice Implications

Successful treatment of habit-tic nail deformity requires patients to have some insight into their behavior. The benzethonium chloride serves as a reminder for patients to stop picking as an unfamiliar artificial barrier and reminds them to substitute the picking behavior for another more positive behavior. Therefore, benzethonium chloride may be offered to patients as a novel therapy to both protect the cuticle and alter behavior in patients with habit-tic nail deformity, as it can be difficult to treat with few available therapies.

Allergic contact dermatitis to benzethonium chloride is a potential side effect and patients should be cautioned prior to treatment; however, it is extremely rare with 6 cases reported to date based on a PubMed search of articles indexed for MEDLINE using the terms allergic contact dermatitis and benzethonium chloride,² and much rarer than contact allergy to cyanoacrylates.

Practice Gap

Habit-tic nail deformity results from repetitive manipulation of the cuticle and/or proximal nail fold. It most commonly affects one or both thumbnails and presents with a characteristic longitudinal midline furrow with parallel transverse ridges in the nail plate. Complications may include permanent onychodystrophy, frictional melanonychia, and infections. Treatment is challenging, as diagnosis first requires patient insight to the cause of symptoms. Therapeutic options include nonpharmacologic techniques (eg, occlusion of the nails to prevent trauma, cyanoacrylate adhesives, cognitive behavioral therapy) and pharmacologic techniques (eg, N-acetyl cysteine, selective serotonin reuptake inhibitors, tricyclic antidepressants, antipsychotics), with limited supporting data and potential adverse effects.¹

The Technique

Benzethonium chloride solution 0.2% is an antiseptic that creates a polymeric layer that binds to the skin. It normally is used to treat small skin erosions and prevent blisters. In patients with habit-tic nail deformity, we recommend once-daily application of benzethonium chloride to the proximal nail fold, thereby artificially recreating the cuticle and forming a sustainable barrier from trauma (Figure, A). Patients should be reminded not to manipulate the cuticle and/or nail fold during treatment. In one 36-year-old man with habit tic nail deformity, we saw clear nail growth after 4 months of treatment (Figure, B).

Practice Implications

Successful treatment of habit-tic nail deformity requires patients to have some insight into their behavior. The benzethonium chloride serves as a reminder for patients to stop picking as an unfamiliar artificial barrier and reminds them to substitute the picking behavior for another more positive behavior. Therefore, benzethonium chloride may be offered to patients as a novel therapy to both protect the cuticle and alter behavior in patients with habit-tic nail deformity, as it can be difficult to treat with few available therapies.

Allergic contact dermatitis to benzethonium chloride is a potential side effect and patients should be cautioned prior to treatment; however, it is extremely rare with 6 cases reported to date based on a PubMed search of articles indexed for MEDLINE using the terms allergic contact dermatitis and benzethonium chloride,² and much rarer than contact allergy to cyanoacrylates.

Practice Gap

Habit-tic nail deformity results from repetitive manipulation of the cuticle and/or proximal nail fold. It most commonly affects one or both thumbnails and presents with a characteristic longitudinal midline furrow with parallel transverse ridges in the nail plate. Complications may include permanent onychodystrophy, frictional melanonychia, and infections. Treatment is challenging, as diagnosis first requires patient insight to the cause of symptoms. Therapeutic options include nonpharmacologic techniques (eg, occlusion of the nails to prevent trauma, cyanoacrylate adhesives, cognitive behavioral therapy) and pharmacologic techniques (eg, N-acetyl cysteine, selective serotonin reuptake inhibitors, tricyclic antidepressants, antipsychotics), with limited supporting data and potential adverse effects.¹

The Technique

Benzethonium chloride solution 0.2% is an antiseptic that creates a polymeric layer that binds to the skin. It normally is used to treat small skin erosions and prevent blisters. In patients with habit-tic nail deformity, we recommend once-daily application of benzethonium chloride to the proximal nail fold, thereby artificially recreating the cuticle and forming a sustainable barrier from trauma (Figure, A). Patients should be reminded not to manipulate the cuticle and/or nail fold during treatment. In one 36-year-old man with habit tic nail deformity, we saw clear nail growth after 4 months of treatment (Figure, B).

Practice Implications

Successful treatment of habit-tic nail deformity requires patients to have some insight into their behavior. The benzethonium chloride serves as a reminder for patients to stop picking as an unfamiliar artificial barrier and reminds them to substitute the picking behavior for another more positive behavior. Therefore, benzethonium chloride may be offered to patients as a novel therapy to both protect the cuticle and alter behavior in patients with habit-tic nail deformity, as it can be difficult to treat with few available therapies.

Allergic contact dermatitis to benzethonium chloride is a potential side effect and patients should be cautioned prior to treatment; however, it is extremely rare with 6 cases reported to date based on a PubMed search of articles indexed for MEDLINE using the terms allergic contact dermatitis and benzethonium chloride,² and much rarer than contact allergy to cyanoacrylates.

Practice Gap

Common donor sites for split-thickness skin grafts (STSGs) include the abdomen, buttocks, inner upper arms and forearms, and thighs. Challenges associated with donor site wounds in these areas include slow healing times and poor scar cosmesis. Although the scalp is not commonly considered when selecting a STSG donor site, harvesting from this area yields optimal results to improve these shortcomings.

Tools

A Weck knife facilitates STSG harvesting in an operationally timely, convenient fashion from larger donor sites up to 5.5 cm in width, such as the scalp, using adjustable thickness control guards.

The Technique

The donor site is lubricated with a sterile mineral oil. An assistant provides tension, leading the trajectory of the Weck knife with a guard. Small, gentle, back-and-forth strokes are made with the Weck knife to harvest the graft, which is then meshed with a No. 15 blade by placing the belly of the blade on the tissue and rolling it to-and-fro. The recipient site cartilage is fenestrated with a 2-mm punch biopsy.

A 48-year-old man underwent Mohs micrographic surgery for treatment of a primary basal cell carcinoma of the left helix, resulting in a 2.5×1.3-cm defect after 2 stages. A Weck knife with a 0.012-in guard was used to harvest an STSG from the postauricular scalp (Figure, A), and the graft was inset to the recipient wound bed. Hemostasis at the scalp donor site was achieved through application of pressure and sterile gauze that was saturated with local 1% lidocaine anesthesia containing 1:400,000 epinephrine. Both recipient and donor sites were dressed with tie-over bolsters that were sutured into place. At 2-week follow-up, the donor site was fully reepithelialized and hair regrowth obscured the defect (Figure, B).

Practice Implications

Our case demonstrates the advantages of the scalp as an STSG donor site with prompt healing time and excellent cosmesis. Because grafts are harvested at a depth superficial to the hair follicle, the hair regrows to conceal the donor site scar. Additionally, the robust blood supply of the scalp and hair follicle density optimize healing time. The location of the donor site at the postauricular scalp facilitates accessibility for wound care by the patient. Electrocautery or chemical styptics used for hemostasis may traumatize the hair follicles and risk causing alopecia; therefore, as demonstrated in our case, the preferred method to achieve hemostasis is the use of pressure or application of sterile gauze that has been saturated with local 1% lidocaine anesthesia containing 1:400,000 epinephrine, followed by a pressure dressing provided by a sutured bolster.

Our case also demonstrates the utility of the Weck knife, which was introduced in 1968 as a modification of existing instruments to improve the ease of harvesting STSGs by appending a fixed handle and interchangeable depth gauges to a straight razor.^1,2 The Weck knife can obtain grafts up to 5.5 cm in width (length may be as long as anatomically available), often circumventing the need to overlap grafts of smaller widths for repair of larger defects. Furthermore, grafts are harvested at a depth superficial to the hair follicle, averting donor site alopecia. These characteristics make the technique an ideal option for harvesting grafts from the scalp and other large donor sites.

Limitations of the Weck knife technique include the inability to harvest grafts from small donor sites in difficult-to-access anatomic regions or from areas with notable 3-dimensional structure. For harvesting such grafts, we prefer the DermaBlade (AccuTec Blades). Furthermore, assistance for providing tension along the trajectory of the Weck blade with a guard is optimal when performing the procedure. For practices not already utilizing a Weck knife, the technique necessitates additional training and cost. Nonetheless, for STSGs in which large donor site surface area, adjustable thickness, and convenient and timely operational technique are desired, the Weck knife should be considered as part of the dermatologic surgeon’s armamentarium.

Practice Gap

Common donor sites for split-thickness skin grafts (STSGs) include the abdomen, buttocks, inner upper arms and forearms, and thighs. Challenges associated with donor site wounds in these areas include slow healing times and poor scar cosmesis. Although the scalp is not commonly considered when selecting a STSG donor site, harvesting from this area yields optimal results to improve these shortcomings.

Tools

A Weck knife facilitates STSG harvesting in an operationally timely, convenient fashion from larger donor sites up to 5.5 cm in width, such as the scalp, using adjustable thickness control guards.

The Technique

The donor site is lubricated with a sterile mineral oil. An assistant provides tension, leading the trajectory of the Weck knife with a guard. Small, gentle, back-and-forth strokes are made with the Weck knife to harvest the graft, which is then meshed with a No. 15 blade by placing the belly of the blade on the tissue and rolling it to-and-fro. The recipient site cartilage is fenestrated with a 2-mm punch biopsy.

A 48-year-old man underwent Mohs micrographic surgery for treatment of a primary basal cell carcinoma of the left helix, resulting in a 2.5×1.3-cm defect after 2 stages. A Weck knife with a 0.012-in guard was used to harvest an STSG from the postauricular scalp (Figure, A), and the graft was inset to the recipient wound bed. Hemostasis at the scalp donor site was achieved through application of pressure and sterile gauze that was saturated with local 1% lidocaine anesthesia containing 1:400,000 epinephrine. Both recipient and donor sites were dressed with tie-over bolsters that were sutured into place. At 2-week follow-up, the donor site was fully reepithelialized and hair regrowth obscured the defect (Figure, B).

Practice Implications

Our case demonstrates the advantages of the scalp as an STSG donor site with prompt healing time and excellent cosmesis. Because grafts are harvested at a depth superficial to the hair follicle, the hair regrows to conceal the donor site scar. Additionally, the robust blood supply of the scalp and hair follicle density optimize healing time. The location of the donor site at the postauricular scalp facilitates accessibility for wound care by the patient. Electrocautery or chemical styptics used for hemostasis may traumatize the hair follicles and risk causing alopecia; therefore, as demonstrated in our case, the preferred method to achieve hemostasis is the use of pressure or application of sterile gauze that has been saturated with local 1% lidocaine anesthesia containing 1:400,000 epinephrine, followed by a pressure dressing provided by a sutured bolster.

Our case also demonstrates the utility of the Weck knife, which was introduced in 1968 as a modification of existing instruments to improve the ease of harvesting STSGs by appending a fixed handle and interchangeable depth gauges to a straight razor.^1,2 The Weck knife can obtain grafts up to 5.5 cm in width (length may be as long as anatomically available), often circumventing the need to overlap grafts of smaller widths for repair of larger defects. Furthermore, grafts are harvested at a depth superficial to the hair follicle, averting donor site alopecia. These characteristics make the technique an ideal option for harvesting grafts from the scalp and other large donor sites.

Limitations of the Weck knife technique include the inability to harvest grafts from small donor sites in difficult-to-access anatomic regions or from areas with notable 3-dimensional structure. For harvesting such grafts, we prefer the DermaBlade (AccuTec Blades). Furthermore, assistance for providing tension along the trajectory of the Weck blade with a guard is optimal when performing the procedure. For practices not already utilizing a Weck knife, the technique necessitates additional training and cost. Nonetheless, for STSGs in which large donor site surface area, adjustable thickness, and convenient and timely operational technique are desired, the Weck knife should be considered as part of the dermatologic surgeon’s armamentarium.

Practice Gap

Common donor sites for split-thickness skin grafts (STSGs) include the abdomen, buttocks, inner upper arms and forearms, and thighs. Challenges associated with donor site wounds in these areas include slow healing times and poor scar cosmesis. Although the scalp is not commonly considered when selecting a STSG donor site, harvesting from this area yields optimal results to improve these shortcomings.

Tools

A Weck knife facilitates STSG harvesting in an operationally timely, convenient fashion from larger donor sites up to 5.5 cm in width, such as the scalp, using adjustable thickness control guards.

The Technique

The donor site is lubricated with a sterile mineral oil. An assistant provides tension, leading the trajectory of the Weck knife with a guard. Small, gentle, back-and-forth strokes are made with the Weck knife to harvest the graft, which is then meshed with a No. 15 blade by placing the belly of the blade on the tissue and rolling it to-and-fro. The recipient site cartilage is fenestrated with a 2-mm punch biopsy.

A 48-year-old man underwent Mohs micrographic surgery for treatment of a primary basal cell carcinoma of the left helix, resulting in a 2.5×1.3-cm defect after 2 stages. A Weck knife with a 0.012-in guard was used to harvest an STSG from the postauricular scalp (Figure, A), and the graft was inset to the recipient wound bed. Hemostasis at the scalp donor site was achieved through application of pressure and sterile gauze that was saturated with local 1% lidocaine anesthesia containing 1:400,000 epinephrine. Both recipient and donor sites were dressed with tie-over bolsters that were sutured into place. At 2-week follow-up, the donor site was fully reepithelialized and hair regrowth obscured the defect (Figure, B).

Practice Implications

Our case demonstrates the advantages of the scalp as an STSG donor site with prompt healing time and excellent cosmesis. Because grafts are harvested at a depth superficial to the hair follicle, the hair regrows to conceal the donor site scar. Additionally, the robust blood supply of the scalp and hair follicle density optimize healing time. The location of the donor site at the postauricular scalp facilitates accessibility for wound care by the patient. Electrocautery or chemical styptics used for hemostasis may traumatize the hair follicles and risk causing alopecia; therefore, as demonstrated in our case, the preferred method to achieve hemostasis is the use of pressure or application of sterile gauze that has been saturated with local 1% lidocaine anesthesia containing 1:400,000 epinephrine, followed by a pressure dressing provided by a sutured bolster.

Our case also demonstrates the utility of the Weck knife, which was introduced in 1968 as a modification of existing instruments to improve the ease of harvesting STSGs by appending a fixed handle and interchangeable depth gauges to a straight razor.^1,2 The Weck knife can obtain grafts up to 5.5 cm in width (length may be as long as anatomically available), often circumventing the need to overlap grafts of smaller widths for repair of larger defects. Furthermore, grafts are harvested at a depth superficial to the hair follicle, averting donor site alopecia. These characteristics make the technique an ideal option for harvesting grafts from the scalp and other large donor sites.

Limitations of the Weck knife technique include the inability to harvest grafts from small donor sites in difficult-to-access anatomic regions or from areas with notable 3-dimensional structure. For harvesting such grafts, we prefer the DermaBlade (AccuTec Blades). Furthermore, assistance for providing tension along the trajectory of the Weck blade with a guard is optimal when performing the procedure. For practices not already utilizing a Weck knife, the technique necessitates additional training and cost. Nonetheless, for STSGs in which large donor site surface area, adjustable thickness, and convenient and timely operational technique are desired, the Weck knife should be considered as part of the dermatologic surgeon’s armamentarium.

What does your patient need to know at the first visit?  

A patient may be scheduled for a total-body skin examination (TBSE) through several routes: primary care referral, continued cancer screening for an at-risk patient or patient transfer, or patient-directed scheduling for general screening regardless of risk factors. At the patient's first visit, it is imperative that the course of the appointment is smooth and predictable for patient comfort and for a thorough and effective examination. The nurse initially solicits salient medical history, particularly personal and family history of skin cancer, current medications, and any acute concerns. The nurse then prepares the patient for the logistics of the TBSE, namely to undress, don a gown that ties and opens in the back, and be seated on the examination table. When I enter the room, the conversation commences with me seated across from the patient, reviewing specifics about his/her history and risk factors. Then the TBSE is executed from head to toe.  

Do you broadly recommend TBSE? 

Firstly, TBSE is a safe clinical tool, supported by data outlining a lack of notable patient morbidity during the examination, including psychosocial factors, and it is generally well-received by patients (Risica et al). In 2016, the US Preventative Services Task Force (USPSTF) outlined its recommendations regarding screening for skin cancer, concluding that there is insufficient evidence to broadly recommend TBSE. Unfortunately, USPSTF findings amassed data from all types of screenings, including those by nondermatologists, and did not extract specialty-specific benefits and risks to patients. The recommendation also did not outline the influence of TBSE on morbidity and mortality for at-risk groups. The guidelines target primary care practice trends; therefore, specialty societies such as the American Academy of Dermatology issued statements following the USPSTF recommendation outlining these salient clarifications, namely that TBSE detects melanoma and keratinocyte carcinomas earlier than in patients who are not screened. Randomized controlled trials to prove this observation are lacking, particularly because of the ethics of withholding screening from a prospective study group. However, in 2017, Johnson et al outlined the best available survival data in concert with the USPSTF statement to arrive at the most beneficial screening recommendations for patients, specifically targeting risk groups--those with a history of skin cancer, immunosuppression, indoor tanning and/or many blistering sunburns, and several other genetic parameters--for at least annual TBSE. 

The technique and reproducibility of TBSE also are not standardized, though they seem to have been endearingly apprenticed but variably implemented through generations of dermatology residents going forward into practice. As it is, depending on patient body surface area, mobility, willingness to disrobe, and adornments (eg, tattoos, hair appliances), multiple factors can restrict full view of a patient's skin. Recently, Helm et al proposed standardizing the TBSE sequence to minimize omitted areas of the body, which may become an imperative tool for streamlined resident teaching and optimal screening encounters.  

How do you keep patients compliant with TBSE? 

During and following TBSE, I typically outline any lesions of concern and plan for further testing, screening, and behavioral prevention strategies. Frequency of TBSE and importance of compliance are discussed during the visit and reinforced at checkout where the appointment templates are established a year in advance for those with skin cancer. Further, for those with melanoma, their appointment slots are given priority status so that any cancellations or delays are rescheduled preferentially. Particularly during the discussion about TBSE frequency, I emphasize the comparison and importance of this visit akin to other recommended screenings, such as mammograms and colonoscopies, and that we, as dermatologists, are part of their cancer surveillance team. 

What do you do if patients refuse your recommendations? 

Some patients refuse a gown or removal of certain clothing items (eg, undergarments, socks, wigs). Some patients defer a yearly TBSE upon checkout and schedule an appointment only when a lesion of concern arises. My advice is not to shame patients and to take advantage of as much as the patient is able and comfortable to show us and be present for, welcoming that we have the opportunity to take care of them and screen for cancer in any capacity. In underserved or limited budget practice regions, lesion-directed examination vs TBSE may be the only screening method utilized and may even attract more patients to a screening facility (Hoorens et al). 

In the opposite corner are those patients who deem the recommended TBSE interval as too infrequent, which poses a delicate dilemma. In my opinion, these situations present another cohort of risks. Namely, the patient may become (or continue to be) overly fixated on the small details of every skin lesion, and in my experience, they tend to develop the habit of expecting at least 1 biopsy at each visit, typically of a lesion of their choosing. Depending on the validity of this expectation vs my clinical examination, it can lead to a difficult discussion with the patient about oversampling lesions and the potential for many scars, copious reexcisions for ambiguous lesion pathology, and a trend away from prudent clinical care. In addition, multiple visits incur more patient co-pays and time away from school, work, or home. To ease the patient's mind, I advise to call our office for a more acute visit if there is a lesion of concern; I additionally recommend taking a smartphone photograph of a concerning lesion and monitoring it for changes or sending the photograph to our patient portal messaging system so we can evaluate its acuity. 

What take-home advice do you give to patients? 

As the visit ends, I further explain that home self-examination or examination by a partner between visits is intuitively a valuable screening adjunct for skin cancer. In 2018, the USPSTF recommended behavioral skin cancer prevention counseling and self-examination only for younger-age cohorts with fair skin (6 months to 24 years), but its utility in specialty practice must be qualified. The American Academy of Dermatology Association subsequently issued a statement to support safe sun-protective practices and diligent self-screening for changing lesions, as earlier detection and management of skin cancer can lead to decreased morbidity and mortality from these neoplasms.  

Resources for Patients

American Academy of Dermatology's SPOT Skin Cancer

Centers for Disease Control and Prevention: What Screening Tests Are There?
 

What does your patient need to know at the first visit?  

A patient may be scheduled for a total-body skin examination (TBSE) through several routes: primary care referral, continued cancer screening for an at-risk patient or patient transfer, or patient-directed scheduling for general screening regardless of risk factors. At the patient's first visit, it is imperative that the course of the appointment is smooth and predictable for patient comfort and for a thorough and effective examination. The nurse initially solicits salient medical history, particularly personal and family history of skin cancer, current medications, and any acute concerns. The nurse then prepares the patient for the logistics of the TBSE, namely to undress, don a gown that ties and opens in the back, and be seated on the examination table. When I enter the room, the conversation commences with me seated across from the patient, reviewing specifics about his/her history and risk factors. Then the TBSE is executed from head to toe.  

Do you broadly recommend TBSE? 

Firstly, TBSE is a safe clinical tool, supported by data outlining a lack of notable patient morbidity during the examination, including psychosocial factors, and it is generally well-received by patients (Risica et al). In 2016, the US Preventative Services Task Force (USPSTF) outlined its recommendations regarding screening for skin cancer, concluding that there is insufficient evidence to broadly recommend TBSE. Unfortunately, USPSTF findings amassed data from all types of screenings, including those by nondermatologists, and did not extract specialty-specific benefits and risks to patients. The recommendation also did not outline the influence of TBSE on morbidity and mortality for at-risk groups. The guidelines target primary care practice trends; therefore, specialty societies such as the American Academy of Dermatology issued statements following the USPSTF recommendation outlining these salient clarifications, namely that TBSE detects melanoma and keratinocyte carcinomas earlier than in patients who are not screened. Randomized controlled trials to prove this observation are lacking, particularly because of the ethics of withholding screening from a prospective study group. However, in 2017, Johnson et al outlined the best available survival data in concert with the USPSTF statement to arrive at the most beneficial screening recommendations for patients, specifically targeting risk groups--those with a history of skin cancer, immunosuppression, indoor tanning and/or many blistering sunburns, and several other genetic parameters--for at least annual TBSE. 

The technique and reproducibility of TBSE also are not standardized, though they seem to have been endearingly apprenticed but variably implemented through generations of dermatology residents going forward into practice. As it is, depending on patient body surface area, mobility, willingness to disrobe, and adornments (eg, tattoos, hair appliances), multiple factors can restrict full view of a patient's skin. Recently, Helm et al proposed standardizing the TBSE sequence to minimize omitted areas of the body, which may become an imperative tool for streamlined resident teaching and optimal screening encounters.  

How do you keep patients compliant with TBSE? 

During and following TBSE, I typically outline any lesions of concern and plan for further testing, screening, and behavioral prevention strategies. Frequency of TBSE and importance of compliance are discussed during the visit and reinforced at checkout where the appointment templates are established a year in advance for those with skin cancer. Further, for those with melanoma, their appointment slots are given priority status so that any cancellations or delays are rescheduled preferentially. Particularly during the discussion about TBSE frequency, I emphasize the comparison and importance of this visit akin to other recommended screenings, such as mammograms and colonoscopies, and that we, as dermatologists, are part of their cancer surveillance team. 

What do you do if patients refuse your recommendations? 

Some patients refuse a gown or removal of certain clothing items (eg, undergarments, socks, wigs). Some patients defer a yearly TBSE upon checkout and schedule an appointment only when a lesion of concern arises. My advice is not to shame patients and to take advantage of as much as the patient is able and comfortable to show us and be present for, welcoming that we have the opportunity to take care of them and screen for cancer in any capacity. In underserved or limited budget practice regions, lesion-directed examination vs TBSE may be the only screening method utilized and may even attract more patients to a screening facility (Hoorens et al). 

In the opposite corner are those patients who deem the recommended TBSE interval as too infrequent, which poses a delicate dilemma. In my opinion, these situations present another cohort of risks. Namely, the patient may become (or continue to be) overly fixated on the small details of every skin lesion, and in my experience, they tend to develop the habit of expecting at least 1 biopsy at each visit, typically of a lesion of their choosing. Depending on the validity of this expectation vs my clinical examination, it can lead to a difficult discussion with the patient about oversampling lesions and the potential for many scars, copious reexcisions for ambiguous lesion pathology, and a trend away from prudent clinical care. In addition, multiple visits incur more patient co-pays and time away from school, work, or home. To ease the patient's mind, I advise to call our office for a more acute visit if there is a lesion of concern; I additionally recommend taking a smartphone photograph of a concerning lesion and monitoring it for changes or sending the photograph to our patient portal messaging system so we can evaluate its acuity. 

What take-home advice do you give to patients? 

As the visit ends, I further explain that home self-examination or examination by a partner between visits is intuitively a valuable screening adjunct for skin cancer. In 2018, the USPSTF recommended behavioral skin cancer prevention counseling and self-examination only for younger-age cohorts with fair skin (6 months to 24 years), but its utility in specialty practice must be qualified. The American Academy of Dermatology Association subsequently issued a statement to support safe sun-protective practices and diligent self-screening for changing lesions, as earlier detection and management of skin cancer can lead to decreased morbidity and mortality from these neoplasms.  

Resources for Patients

American Academy of Dermatology's SPOT Skin Cancer

Centers for Disease Control and Prevention: What Screening Tests Are There?
 

What does your patient need to know at the first visit?  

A patient may be scheduled for a total-body skin examination (TBSE) through several routes: primary care referral, continued cancer screening for an at-risk patient or patient transfer, or patient-directed scheduling for general screening regardless of risk factors. At the patient's first visit, it is imperative that the course of the appointment is smooth and predictable for patient comfort and for a thorough and effective examination. The nurse initially solicits salient medical history, particularly personal and family history of skin cancer, current medications, and any acute concerns. The nurse then prepares the patient for the logistics of the TBSE, namely to undress, don a gown that ties and opens in the back, and be seated on the examination table. When I enter the room, the conversation commences with me seated across from the patient, reviewing specifics about his/her history and risk factors. Then the TBSE is executed from head to toe.  

Do you broadly recommend TBSE? 

Firstly, TBSE is a safe clinical tool, supported by data outlining a lack of notable patient morbidity during the examination, including psychosocial factors, and it is generally well-received by patients (Risica et al). In 2016, the US Preventative Services Task Force (USPSTF) outlined its recommendations regarding screening for skin cancer, concluding that there is insufficient evidence to broadly recommend TBSE. Unfortunately, USPSTF findings amassed data from all types of screenings, including those by nondermatologists, and did not extract specialty-specific benefits and risks to patients. The recommendation also did not outline the influence of TBSE on morbidity and mortality for at-risk groups. The guidelines target primary care practice trends; therefore, specialty societies such as the American Academy of Dermatology issued statements following the USPSTF recommendation outlining these salient clarifications, namely that TBSE detects melanoma and keratinocyte carcinomas earlier than in patients who are not screened. Randomized controlled trials to prove this observation are lacking, particularly because of the ethics of withholding screening from a prospective study group. However, in 2017, Johnson et al outlined the best available survival data in concert with the USPSTF statement to arrive at the most beneficial screening recommendations for patients, specifically targeting risk groups--those with a history of skin cancer, immunosuppression, indoor tanning and/or many blistering sunburns, and several other genetic parameters--for at least annual TBSE. 

The technique and reproducibility of TBSE also are not standardized, though they seem to have been endearingly apprenticed but variably implemented through generations of dermatology residents going forward into practice. As it is, depending on patient body surface area, mobility, willingness to disrobe, and adornments (eg, tattoos, hair appliances), multiple factors can restrict full view of a patient's skin. Recently, Helm et al proposed standardizing the TBSE sequence to minimize omitted areas of the body, which may become an imperative tool for streamlined resident teaching and optimal screening encounters.  

How do you keep patients compliant with TBSE? 

During and following TBSE, I typically outline any lesions of concern and plan for further testing, screening, and behavioral prevention strategies. Frequency of TBSE and importance of compliance are discussed during the visit and reinforced at checkout where the appointment templates are established a year in advance for those with skin cancer. Further, for those with melanoma, their appointment slots are given priority status so that any cancellations or delays are rescheduled preferentially. Particularly during the discussion about TBSE frequency, I emphasize the comparison and importance of this visit akin to other recommended screenings, such as mammograms and colonoscopies, and that we, as dermatologists, are part of their cancer surveillance team. 

What do you do if patients refuse your recommendations? 

Some patients refuse a gown or removal of certain clothing items (eg, undergarments, socks, wigs). Some patients defer a yearly TBSE upon checkout and schedule an appointment only when a lesion of concern arises. My advice is not to shame patients and to take advantage of as much as the patient is able and comfortable to show us and be present for, welcoming that we have the opportunity to take care of them and screen for cancer in any capacity. In underserved or limited budget practice regions, lesion-directed examination vs TBSE may be the only screening method utilized and may even attract more patients to a screening facility (Hoorens et al). 

In the opposite corner are those patients who deem the recommended TBSE interval as too infrequent, which poses a delicate dilemma. In my opinion, these situations present another cohort of risks. Namely, the patient may become (or continue to be) overly fixated on the small details of every skin lesion, and in my experience, they tend to develop the habit of expecting at least 1 biopsy at each visit, typically of a lesion of their choosing. Depending on the validity of this expectation vs my clinical examination, it can lead to a difficult discussion with the patient about oversampling lesions and the potential for many scars, copious reexcisions for ambiguous lesion pathology, and a trend away from prudent clinical care. In addition, multiple visits incur more patient co-pays and time away from school, work, or home. To ease the patient's mind, I advise to call our office for a more acute visit if there is a lesion of concern; I additionally recommend taking a smartphone photograph of a concerning lesion and monitoring it for changes or sending the photograph to our patient portal messaging system so we can evaluate its acuity. 

What take-home advice do you give to patients? 

As the visit ends, I further explain that home self-examination or examination by a partner between visits is intuitively a valuable screening adjunct for skin cancer. In 2018, the USPSTF recommended behavioral skin cancer prevention counseling and self-examination only for younger-age cohorts with fair skin (6 months to 24 years), but its utility in specialty practice must be qualified. The American Academy of Dermatology Association subsequently issued a statement to support safe sun-protective practices and diligent self-screening for changing lesions, as earlier detection and management of skin cancer can lead to decreased morbidity and mortality from these neoplasms.  

Resources for Patients

American Academy of Dermatology's SPOT Skin Cancer

Centers for Disease Control and Prevention: What Screening Tests Are There?