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Preventing, Identifying, and Managing Cosmetic Procedure Complications, Part 1: Soft-Tissue Augmentation and Botulinum Toxin Injections

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Preventing, Identifying, and Managing Cosmetic Procedure Complications, Part 1: Soft-Tissue Augmentation and Botulinum Toxin Injections

The primary cosmetic procedures that dermatology residents will perform or assist in performing during their training are soft-tissue augmentation, botulinum toxin injections, chemical peels, and laser therapy. Because complications can occur from these procedures, it is important for residents to learn how to prevent, identify, and manage them for optimal patient outcomes. In part 1 of this 2-part series, soft-tissue augmentation and botulinum toxin injections are discussed. Chemical peels and laser therapy will be addressed in part 2.

Soft-Tissue Augmentation

Soft-tissue fillers include those that are made from collagen (bovine or human), hyaluronic acid (HA), poly-L-lactic acid, calcium hydroxylapatite, silicone, and polymethylmethacrylate. In general, acute complications of soft-tissue filler injections include erythema, swelling, and bruising.1-3 Patients who take blood thinners or supplements (eg, vitamin E, ginseng, garlic, ginger) should be asked to discontinue use 1 week prior to the procedure. Patients who take blood thinners also should be counseled to expect some bruising. Prior to injection, the skin should be thoroughly cleansed to avoid introducing skin bacteria into the injection site and to reduce infection risk. Postinjection erythema may be related to mast cell activation, which is temporary and should resolve after a few days.1-3

If you find yourself injecting the filler too superficially, you may notice that the skin begins to take on a blue-gray hue1-3 that is known as the Tyndall effect and can be prevented by injecting the filler at the proper level. For example, collagen-based fillers should be placed at the mid dermis, thicker HA fillers should be placed in the deep dermis, and calcium hydroxylapatite should be placed at the junction of the dermis and subcutaneous tissue. Polymethylmethacrylate and poly-L-lactic acid should both be placed subdermally.1-3

The gravest immediate complications associated with soft-tissue filler injections are occlusion of the central retinal artery and/or skin necrosis.1-4 Residents should never inject filler to the glabella or to the nose.1-3 Injections at these sites are sometimes performed but should only be performed by experienced dermatologists. The perioral and tear trough regions also are high-risk injection areas that require a high degree of experience and should only be injected with proper supervision by an experienced dermatologist.1-3 Residents generally can avoid these complications, though not with a 100% guarantee, by avoiding injections in high-risk areas, aspirating to check for blood, and slowly injecting a small amount of filler into the treatment area.1-3 A consensus statement on management of injection-induced necrosis advises to apply a nitropaste ointment 2% to the treatment site or administer an oral aspirin if the patient develops severe pain; vision loss; or acute skin discoloration, especially blanching.4 For HA-based fillers, at least 200 U of hyaluronidase should be injected. It has been suggested that saline can be injected to flush out calcium hydroxylapatite fillers.3 Warm compresses should be placed on the involved area. Following these interventions, any patient with vision loss or orbital pain should immediately undergo ophthalmologic evaluation.3 The most important intervention occurs in the first 24 hours.3,4 After 24 hours, careful wound care, oral anticoagulants, and hyperbaric oxygen therapy have been suggested as management options.3

There are 2 major chronic complications of soft-tissue filler injection, including delayed-onset infection, which occurs 2 weeks or more postinjection, and granuloma formation.1-3 Chronic low-grade infection at the injection site may be indicative of biofilm formation. If an HA filler was used, it should be dissolved with hyaluronidase to help break up the biofilm nidus.3 A course of oral antibiotics also may be indicated.1-3 Intralesional steroids may be used but only after antibiotics have been administered. A biofilm that develops from more permanent fillers may be more difficult to manage. Atypical mycobacterial infections have been known to develop at injection sites, which should be considered in refractory cases.1-3,5

Calcium hydroxylapatite, polymethylmethacrylate, and silicone can stimulate chronic immune system activation, which makes them more prone to granuloma formation.1-3 Once infection is ruled out, granulomas may be treated with intralesional steroids, surgical excision (if the results would be cosmetically acceptable), laser therapy, or potentially local injection of an immunosuppressant (eg, methotrexate, 5-fluorouracil).3

Botulinum Toxin Injections

Patients who are pregnant, lactating, or have neuromuscular disease are not candidates for botulinum toxin injections. There also is a risk that patients taking calcium channel blockers or aminoglycoside antibiotics may experience potentiated effects of the botulinum toxin.6

Patients should be informed that a postinjection headache may occur and should be treated with over-the-counter medications.6 Complication-free botulinum toxin procedures depend heavily on the physician’s knowledge of facial anatomy.1,6 The diagrams provided by Hirsch and Stier1 offer an excellent guide on where to place the injections. Brow droop, eyelid ptosis, and “Spock brow” (eyebrows that are overarched) largely can be avoided by proper injection point placement. A Spock brow may be corrected by injecting the lateral upper forehead with a few units to correct the exaggerated arch.6,7 For eyelid ptosis, apraclonidine 0.05% drops (1–2 drops 3 times daily) should be used until the ptosis resolves.6 Phenylephrine hydrochloride drops may be used should a patient have a documented sensitivity to apraclonidine but should not be used in a patient with acute angle-closure glaucoma or aneurysms.6

 

 

Final Thoughts

Learning to perform soft-tissue augmentation and botulinum toxin injections can be a satisfying and fun part of dermatology residency. Preventing, identifying, and managing any complications that may occur is an integral part of performing these procedures.

References
  1. Hirsch R, Stier M. Complications and their management in cosmetic dermatology. Dermatol Clin. 2009;27:507-520.
  2. Gladstone HB, Cohen JL. Adverse effects when injecting facial fillers. Semin Cutan Med Surg. 2007;26:34-39.
  3. Boulle K, Heydenrych I. Patient factors influencing dermal filler complications: prevention, assessment, and treatment. Clin Cosmet Investig Dermatol. 2015;8:205-214.
  4. Cohen JL, Biesman BS, Dayan SH, et al. Treatment of hyaluronic acid filler–induced impending necrosis with hyaluronidase: consensus recommendations [published online May 10, 2015]. Aesthet Surg J. 2015;35:844-849.
  5. Rodriguez JM, Xie YL, Winthrop KL, et al. Mycobacterium chelonae facial infections following injection of dermal filler. Aesthet Surg J. 2013;33:265-269.
  6. Nigam PK, Nigam A. Botulinum toxin. Indian J Dermatol. 2010;55:8-14.
  7. Carruthers A, Carruthers J. Update on the botulinum neurotoxins. Skin Therapy Lett. 2001;6:1-2.
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Dr. Brown is from the Department of Dermatology, University of California, San Diego.

The author reports no conflict of interest.

This article is the first of a 2-part series. The next part will appear online in August 2016.

Correspondence: Megan Brown, MD, 8899 University Center Ln, Ste 350, San Diego, CA 92122 ([email protected]).

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Dr. Brown is from the Department of Dermatology, University of California, San Diego.

The author reports no conflict of interest.

This article is the first of a 2-part series. The next part will appear online in August 2016.

Correspondence: Megan Brown, MD, 8899 University Center Ln, Ste 350, San Diego, CA 92122 ([email protected]).

Author and Disclosure Information

Dr. Brown is from the Department of Dermatology, University of California, San Diego.

The author reports no conflict of interest.

This article is the first of a 2-part series. The next part will appear online in August 2016.

Correspondence: Megan Brown, MD, 8899 University Center Ln, Ste 350, San Diego, CA 92122 ([email protected]).

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The primary cosmetic procedures that dermatology residents will perform or assist in performing during their training are soft-tissue augmentation, botulinum toxin injections, chemical peels, and laser therapy. Because complications can occur from these procedures, it is important for residents to learn how to prevent, identify, and manage them for optimal patient outcomes. In part 1 of this 2-part series, soft-tissue augmentation and botulinum toxin injections are discussed. Chemical peels and laser therapy will be addressed in part 2.

Soft-Tissue Augmentation

Soft-tissue fillers include those that are made from collagen (bovine or human), hyaluronic acid (HA), poly-L-lactic acid, calcium hydroxylapatite, silicone, and polymethylmethacrylate. In general, acute complications of soft-tissue filler injections include erythema, swelling, and bruising.1-3 Patients who take blood thinners or supplements (eg, vitamin E, ginseng, garlic, ginger) should be asked to discontinue use 1 week prior to the procedure. Patients who take blood thinners also should be counseled to expect some bruising. Prior to injection, the skin should be thoroughly cleansed to avoid introducing skin bacteria into the injection site and to reduce infection risk. Postinjection erythema may be related to mast cell activation, which is temporary and should resolve after a few days.1-3

If you find yourself injecting the filler too superficially, you may notice that the skin begins to take on a blue-gray hue1-3 that is known as the Tyndall effect and can be prevented by injecting the filler at the proper level. For example, collagen-based fillers should be placed at the mid dermis, thicker HA fillers should be placed in the deep dermis, and calcium hydroxylapatite should be placed at the junction of the dermis and subcutaneous tissue. Polymethylmethacrylate and poly-L-lactic acid should both be placed subdermally.1-3

The gravest immediate complications associated with soft-tissue filler injections are occlusion of the central retinal artery and/or skin necrosis.1-4 Residents should never inject filler to the glabella or to the nose.1-3 Injections at these sites are sometimes performed but should only be performed by experienced dermatologists. The perioral and tear trough regions also are high-risk injection areas that require a high degree of experience and should only be injected with proper supervision by an experienced dermatologist.1-3 Residents generally can avoid these complications, though not with a 100% guarantee, by avoiding injections in high-risk areas, aspirating to check for blood, and slowly injecting a small amount of filler into the treatment area.1-3 A consensus statement on management of injection-induced necrosis advises to apply a nitropaste ointment 2% to the treatment site or administer an oral aspirin if the patient develops severe pain; vision loss; or acute skin discoloration, especially blanching.4 For HA-based fillers, at least 200 U of hyaluronidase should be injected. It has been suggested that saline can be injected to flush out calcium hydroxylapatite fillers.3 Warm compresses should be placed on the involved area. Following these interventions, any patient with vision loss or orbital pain should immediately undergo ophthalmologic evaluation.3 The most important intervention occurs in the first 24 hours.3,4 After 24 hours, careful wound care, oral anticoagulants, and hyperbaric oxygen therapy have been suggested as management options.3

There are 2 major chronic complications of soft-tissue filler injection, including delayed-onset infection, which occurs 2 weeks or more postinjection, and granuloma formation.1-3 Chronic low-grade infection at the injection site may be indicative of biofilm formation. If an HA filler was used, it should be dissolved with hyaluronidase to help break up the biofilm nidus.3 A course of oral antibiotics also may be indicated.1-3 Intralesional steroids may be used but only after antibiotics have been administered. A biofilm that develops from more permanent fillers may be more difficult to manage. Atypical mycobacterial infections have been known to develop at injection sites, which should be considered in refractory cases.1-3,5

Calcium hydroxylapatite, polymethylmethacrylate, and silicone can stimulate chronic immune system activation, which makes them more prone to granuloma formation.1-3 Once infection is ruled out, granulomas may be treated with intralesional steroids, surgical excision (if the results would be cosmetically acceptable), laser therapy, or potentially local injection of an immunosuppressant (eg, methotrexate, 5-fluorouracil).3

Botulinum Toxin Injections

Patients who are pregnant, lactating, or have neuromuscular disease are not candidates for botulinum toxin injections. There also is a risk that patients taking calcium channel blockers or aminoglycoside antibiotics may experience potentiated effects of the botulinum toxin.6

Patients should be informed that a postinjection headache may occur and should be treated with over-the-counter medications.6 Complication-free botulinum toxin procedures depend heavily on the physician’s knowledge of facial anatomy.1,6 The diagrams provided by Hirsch and Stier1 offer an excellent guide on where to place the injections. Brow droop, eyelid ptosis, and “Spock brow” (eyebrows that are overarched) largely can be avoided by proper injection point placement. A Spock brow may be corrected by injecting the lateral upper forehead with a few units to correct the exaggerated arch.6,7 For eyelid ptosis, apraclonidine 0.05% drops (1–2 drops 3 times daily) should be used until the ptosis resolves.6 Phenylephrine hydrochloride drops may be used should a patient have a documented sensitivity to apraclonidine but should not be used in a patient with acute angle-closure glaucoma or aneurysms.6

 

 

Final Thoughts

Learning to perform soft-tissue augmentation and botulinum toxin injections can be a satisfying and fun part of dermatology residency. Preventing, identifying, and managing any complications that may occur is an integral part of performing these procedures.

The primary cosmetic procedures that dermatology residents will perform or assist in performing during their training are soft-tissue augmentation, botulinum toxin injections, chemical peels, and laser therapy. Because complications can occur from these procedures, it is important for residents to learn how to prevent, identify, and manage them for optimal patient outcomes. In part 1 of this 2-part series, soft-tissue augmentation and botulinum toxin injections are discussed. Chemical peels and laser therapy will be addressed in part 2.

Soft-Tissue Augmentation

Soft-tissue fillers include those that are made from collagen (bovine or human), hyaluronic acid (HA), poly-L-lactic acid, calcium hydroxylapatite, silicone, and polymethylmethacrylate. In general, acute complications of soft-tissue filler injections include erythema, swelling, and bruising.1-3 Patients who take blood thinners or supplements (eg, vitamin E, ginseng, garlic, ginger) should be asked to discontinue use 1 week prior to the procedure. Patients who take blood thinners also should be counseled to expect some bruising. Prior to injection, the skin should be thoroughly cleansed to avoid introducing skin bacteria into the injection site and to reduce infection risk. Postinjection erythema may be related to mast cell activation, which is temporary and should resolve after a few days.1-3

If you find yourself injecting the filler too superficially, you may notice that the skin begins to take on a blue-gray hue1-3 that is known as the Tyndall effect and can be prevented by injecting the filler at the proper level. For example, collagen-based fillers should be placed at the mid dermis, thicker HA fillers should be placed in the deep dermis, and calcium hydroxylapatite should be placed at the junction of the dermis and subcutaneous tissue. Polymethylmethacrylate and poly-L-lactic acid should both be placed subdermally.1-3

The gravest immediate complications associated with soft-tissue filler injections are occlusion of the central retinal artery and/or skin necrosis.1-4 Residents should never inject filler to the glabella or to the nose.1-3 Injections at these sites are sometimes performed but should only be performed by experienced dermatologists. The perioral and tear trough regions also are high-risk injection areas that require a high degree of experience and should only be injected with proper supervision by an experienced dermatologist.1-3 Residents generally can avoid these complications, though not with a 100% guarantee, by avoiding injections in high-risk areas, aspirating to check for blood, and slowly injecting a small amount of filler into the treatment area.1-3 A consensus statement on management of injection-induced necrosis advises to apply a nitropaste ointment 2% to the treatment site or administer an oral aspirin if the patient develops severe pain; vision loss; or acute skin discoloration, especially blanching.4 For HA-based fillers, at least 200 U of hyaluronidase should be injected. It has been suggested that saline can be injected to flush out calcium hydroxylapatite fillers.3 Warm compresses should be placed on the involved area. Following these interventions, any patient with vision loss or orbital pain should immediately undergo ophthalmologic evaluation.3 The most important intervention occurs in the first 24 hours.3,4 After 24 hours, careful wound care, oral anticoagulants, and hyperbaric oxygen therapy have been suggested as management options.3

There are 2 major chronic complications of soft-tissue filler injection, including delayed-onset infection, which occurs 2 weeks or more postinjection, and granuloma formation.1-3 Chronic low-grade infection at the injection site may be indicative of biofilm formation. If an HA filler was used, it should be dissolved with hyaluronidase to help break up the biofilm nidus.3 A course of oral antibiotics also may be indicated.1-3 Intralesional steroids may be used but only after antibiotics have been administered. A biofilm that develops from more permanent fillers may be more difficult to manage. Atypical mycobacterial infections have been known to develop at injection sites, which should be considered in refractory cases.1-3,5

Calcium hydroxylapatite, polymethylmethacrylate, and silicone can stimulate chronic immune system activation, which makes them more prone to granuloma formation.1-3 Once infection is ruled out, granulomas may be treated with intralesional steroids, surgical excision (if the results would be cosmetically acceptable), laser therapy, or potentially local injection of an immunosuppressant (eg, methotrexate, 5-fluorouracil).3

Botulinum Toxin Injections

Patients who are pregnant, lactating, or have neuromuscular disease are not candidates for botulinum toxin injections. There also is a risk that patients taking calcium channel blockers or aminoglycoside antibiotics may experience potentiated effects of the botulinum toxin.6

Patients should be informed that a postinjection headache may occur and should be treated with over-the-counter medications.6 Complication-free botulinum toxin procedures depend heavily on the physician’s knowledge of facial anatomy.1,6 The diagrams provided by Hirsch and Stier1 offer an excellent guide on where to place the injections. Brow droop, eyelid ptosis, and “Spock brow” (eyebrows that are overarched) largely can be avoided by proper injection point placement. A Spock brow may be corrected by injecting the lateral upper forehead with a few units to correct the exaggerated arch.6,7 For eyelid ptosis, apraclonidine 0.05% drops (1–2 drops 3 times daily) should be used until the ptosis resolves.6 Phenylephrine hydrochloride drops may be used should a patient have a documented sensitivity to apraclonidine but should not be used in a patient with acute angle-closure glaucoma or aneurysms.6

 

 

Final Thoughts

Learning to perform soft-tissue augmentation and botulinum toxin injections can be a satisfying and fun part of dermatology residency. Preventing, identifying, and managing any complications that may occur is an integral part of performing these procedures.

References
  1. Hirsch R, Stier M. Complications and their management in cosmetic dermatology. Dermatol Clin. 2009;27:507-520.
  2. Gladstone HB, Cohen JL. Adverse effects when injecting facial fillers. Semin Cutan Med Surg. 2007;26:34-39.
  3. Boulle K, Heydenrych I. Patient factors influencing dermal filler complications: prevention, assessment, and treatment. Clin Cosmet Investig Dermatol. 2015;8:205-214.
  4. Cohen JL, Biesman BS, Dayan SH, et al. Treatment of hyaluronic acid filler–induced impending necrosis with hyaluronidase: consensus recommendations [published online May 10, 2015]. Aesthet Surg J. 2015;35:844-849.
  5. Rodriguez JM, Xie YL, Winthrop KL, et al. Mycobacterium chelonae facial infections following injection of dermal filler. Aesthet Surg J. 2013;33:265-269.
  6. Nigam PK, Nigam A. Botulinum toxin. Indian J Dermatol. 2010;55:8-14.
  7. Carruthers A, Carruthers J. Update on the botulinum neurotoxins. Skin Therapy Lett. 2001;6:1-2.
References
  1. Hirsch R, Stier M. Complications and their management in cosmetic dermatology. Dermatol Clin. 2009;27:507-520.
  2. Gladstone HB, Cohen JL. Adverse effects when injecting facial fillers. Semin Cutan Med Surg. 2007;26:34-39.
  3. Boulle K, Heydenrych I. Patient factors influencing dermal filler complications: prevention, assessment, and treatment. Clin Cosmet Investig Dermatol. 2015;8:205-214.
  4. Cohen JL, Biesman BS, Dayan SH, et al. Treatment of hyaluronic acid filler–induced impending necrosis with hyaluronidase: consensus recommendations [published online May 10, 2015]. Aesthet Surg J. 2015;35:844-849.
  5. Rodriguez JM, Xie YL, Winthrop KL, et al. Mycobacterium chelonae facial infections following injection of dermal filler. Aesthet Surg J. 2013;33:265-269.
  6. Nigam PK, Nigam A. Botulinum toxin. Indian J Dermatol. 2010;55:8-14.
  7. Carruthers A, Carruthers J. Update on the botulinum neurotoxins. Skin Therapy Lett. 2001;6:1-2.
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Racing against burnout

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Racing against burnout

At 6 a.m., after eight admissions back to back, I feel like I can’t stay awake any longer. I desperately need a nap. I have 30 minutes before my next admission, but I know I’m not going to rest. I close my eyes, and I only see charts. I’m trying not to collapse, but I still have three more patients to admit before I go home. And I can’t rest.

I’m scared that I’ll make a mistake. While I write my history of presenting illness, I imagine the day team reading my notes and hoping they don’t notice that I was about to crash on the desk. I check my documentation multiple times to make sure I don’t miss anything, and I know that won’t relieve my anxiety. When I leave, I will still feel the failure of not being able to give my best for my patient or for my night team, because I’m too tired. I know this frustration is going to give room to the emptiness – that indifference of being so beaten up that you can’t feel anymore.

And eventually, shame comes in. I’m ashamed of how I feel, because somehow, it means I am weak. All these feelings threaten to cripple me. Then I get home and cry till I fall asleep.

Recently, I read an article about a young physician contemplating suicide in her first year of practice. She described the dread of going into work and the emptiness left at the end of the day. Halfway through my second year of residency, I could relate to those feelings. I dealt with the anxiety of wondering what type of shift I was going to walk into, and experienced the stress of not wanting to disappoint the team, my peers, the patient, or myself.

 

Dr. Patricia Serrano

Being constantly afraid of making a mistake is tiring. Sometimes, I get the pat on the back from senior physicians, saying I will survive. But it’s not enough. I can’t blame them. It’s human nature to forget how bad it hurt and just remember being strong enough to bear it. I count the days til I have a day off or the weeks til my next vacation. I try not to complain as much because nobody wants to hear it, and nothing is going to change. I feel deeply alone, like nobody cares.

And in the end I put myself onto this path. I knew what I was getting myself into. And I get myself out of it. I hold on to the smiles my staff give me when I walk in. I experience that 10-minute interview with someone whose thought process was so disorganized, and I realize that it took some skill to connect with that patient.

I am heartened by my ability to deescalate a patient who was about to become violent because I know Spanish. I notice that I am able to work faster than I did just a year ago. So I hold on. The trick was to find what made me want to hold on and what motivates me.

I’m not going to write about socializing or finding a hobby outside of medicine. But I must acknowledge that I have a wonderful book club, supportive boyfriend, and family. I lose myself in books, TV shows, cooking. I even started reading comic books. Plenty of articles are out there about how to beat physician burnout. They all help. I tried knitting, coloring, you name it, but for me, those activities were just not enough. I had to try to find meaning behind the work I do. I had to grab all those small moments during a shift and knit them together to build a bridge to where my passion lies. Then I started by reminding myself why I wanted to practice medicine and why psychiatry.

What inspires me is learning how to decipher what hides behind a symptom – why patient A’s anxiety is different from patient B’s. I find psychodynamics fascinating, so I read. I read literature, articles, and books with subjects around my interests. So when I see a patient at 4 a.m. for 5 minutes, I can knit it together with what I read. So it has meaning. And then it’s easier to hold on. Because the 12-hour overnight shift becomes hours of learning about my passion. Because I feel a step closer. And even though last night’s shift was so hard, I’m happy to be back at work today. When I read about the psychopathology of depression and then admit five patients with suicidal ideation, it stops being the same story over and over. It turns into an exploration, and it becomes fascinating. I won’t hear the same story again. So many times, attendings told me to read, and I had to be at my breaking point to understand why it was so essential. Now I’m motivated, and I plan to keep pushing myself to the limit to find a new challenge and to surprise myself in the middle of my beat-up tiredness when I see something in my patient that so many have written about. The adrenaline rush comes on the path of becoming that psychiatrist I aim to be, not in the diploma I will get 2 years from now.

 

 

I am racing against burnout, but I’m winning. And I wanted to share my experience to remind others that we are not alone on this path, and we should not have higher suicide rates than other professional groups.

If you are a resident or more experienced physician, know that you are not alone. Many others just like you are stretching themselves thin. Follow the tips of how to beat burnout that you’ve seen around. Find what works for you and dig into yourself, into what drove you in this direction, into where your passion lies. Find the meaning behind this hard work, and connect it to the passion that motivates you. Think of what made you want to become a doctor! I’m not sure it works 100% of the time.

Ask me again in 6 months.

Dr. Serrano is a PGY2 psychiatry resident at the Einstein Medical Center in Philadelphia.

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At 6 a.m., after eight admissions back to back, I feel like I can’t stay awake any longer. I desperately need a nap. I have 30 minutes before my next admission, but I know I’m not going to rest. I close my eyes, and I only see charts. I’m trying not to collapse, but I still have three more patients to admit before I go home. And I can’t rest.

I’m scared that I’ll make a mistake. While I write my history of presenting illness, I imagine the day team reading my notes and hoping they don’t notice that I was about to crash on the desk. I check my documentation multiple times to make sure I don’t miss anything, and I know that won’t relieve my anxiety. When I leave, I will still feel the failure of not being able to give my best for my patient or for my night team, because I’m too tired. I know this frustration is going to give room to the emptiness – that indifference of being so beaten up that you can’t feel anymore.

And eventually, shame comes in. I’m ashamed of how I feel, because somehow, it means I am weak. All these feelings threaten to cripple me. Then I get home and cry till I fall asleep.

Recently, I read an article about a young physician contemplating suicide in her first year of practice. She described the dread of going into work and the emptiness left at the end of the day. Halfway through my second year of residency, I could relate to those feelings. I dealt with the anxiety of wondering what type of shift I was going to walk into, and experienced the stress of not wanting to disappoint the team, my peers, the patient, or myself.

 

Dr. Patricia Serrano

Being constantly afraid of making a mistake is tiring. Sometimes, I get the pat on the back from senior physicians, saying I will survive. But it’s not enough. I can’t blame them. It’s human nature to forget how bad it hurt and just remember being strong enough to bear it. I count the days til I have a day off or the weeks til my next vacation. I try not to complain as much because nobody wants to hear it, and nothing is going to change. I feel deeply alone, like nobody cares.

And in the end I put myself onto this path. I knew what I was getting myself into. And I get myself out of it. I hold on to the smiles my staff give me when I walk in. I experience that 10-minute interview with someone whose thought process was so disorganized, and I realize that it took some skill to connect with that patient.

I am heartened by my ability to deescalate a patient who was about to become violent because I know Spanish. I notice that I am able to work faster than I did just a year ago. So I hold on. The trick was to find what made me want to hold on and what motivates me.

I’m not going to write about socializing or finding a hobby outside of medicine. But I must acknowledge that I have a wonderful book club, supportive boyfriend, and family. I lose myself in books, TV shows, cooking. I even started reading comic books. Plenty of articles are out there about how to beat physician burnout. They all help. I tried knitting, coloring, you name it, but for me, those activities were just not enough. I had to try to find meaning behind the work I do. I had to grab all those small moments during a shift and knit them together to build a bridge to where my passion lies. Then I started by reminding myself why I wanted to practice medicine and why psychiatry.

What inspires me is learning how to decipher what hides behind a symptom – why patient A’s anxiety is different from patient B’s. I find psychodynamics fascinating, so I read. I read literature, articles, and books with subjects around my interests. So when I see a patient at 4 a.m. for 5 minutes, I can knit it together with what I read. So it has meaning. And then it’s easier to hold on. Because the 12-hour overnight shift becomes hours of learning about my passion. Because I feel a step closer. And even though last night’s shift was so hard, I’m happy to be back at work today. When I read about the psychopathology of depression and then admit five patients with suicidal ideation, it stops being the same story over and over. It turns into an exploration, and it becomes fascinating. I won’t hear the same story again. So many times, attendings told me to read, and I had to be at my breaking point to understand why it was so essential. Now I’m motivated, and I plan to keep pushing myself to the limit to find a new challenge and to surprise myself in the middle of my beat-up tiredness when I see something in my patient that so many have written about. The adrenaline rush comes on the path of becoming that psychiatrist I aim to be, not in the diploma I will get 2 years from now.

 

 

I am racing against burnout, but I’m winning. And I wanted to share my experience to remind others that we are not alone on this path, and we should not have higher suicide rates than other professional groups.

If you are a resident or more experienced physician, know that you are not alone. Many others just like you are stretching themselves thin. Follow the tips of how to beat burnout that you’ve seen around. Find what works for you and dig into yourself, into what drove you in this direction, into where your passion lies. Find the meaning behind this hard work, and connect it to the passion that motivates you. Think of what made you want to become a doctor! I’m not sure it works 100% of the time.

Ask me again in 6 months.

Dr. Serrano is a PGY2 psychiatry resident at the Einstein Medical Center in Philadelphia.

At 6 a.m., after eight admissions back to back, I feel like I can’t stay awake any longer. I desperately need a nap. I have 30 minutes before my next admission, but I know I’m not going to rest. I close my eyes, and I only see charts. I’m trying not to collapse, but I still have three more patients to admit before I go home. And I can’t rest.

I’m scared that I’ll make a mistake. While I write my history of presenting illness, I imagine the day team reading my notes and hoping they don’t notice that I was about to crash on the desk. I check my documentation multiple times to make sure I don’t miss anything, and I know that won’t relieve my anxiety. When I leave, I will still feel the failure of not being able to give my best for my patient or for my night team, because I’m too tired. I know this frustration is going to give room to the emptiness – that indifference of being so beaten up that you can’t feel anymore.

And eventually, shame comes in. I’m ashamed of how I feel, because somehow, it means I am weak. All these feelings threaten to cripple me. Then I get home and cry till I fall asleep.

Recently, I read an article about a young physician contemplating suicide in her first year of practice. She described the dread of going into work and the emptiness left at the end of the day. Halfway through my second year of residency, I could relate to those feelings. I dealt with the anxiety of wondering what type of shift I was going to walk into, and experienced the stress of not wanting to disappoint the team, my peers, the patient, or myself.

 

Dr. Patricia Serrano

Being constantly afraid of making a mistake is tiring. Sometimes, I get the pat on the back from senior physicians, saying I will survive. But it’s not enough. I can’t blame them. It’s human nature to forget how bad it hurt and just remember being strong enough to bear it. I count the days til I have a day off or the weeks til my next vacation. I try not to complain as much because nobody wants to hear it, and nothing is going to change. I feel deeply alone, like nobody cares.

And in the end I put myself onto this path. I knew what I was getting myself into. And I get myself out of it. I hold on to the smiles my staff give me when I walk in. I experience that 10-minute interview with someone whose thought process was so disorganized, and I realize that it took some skill to connect with that patient.

I am heartened by my ability to deescalate a patient who was about to become violent because I know Spanish. I notice that I am able to work faster than I did just a year ago. So I hold on. The trick was to find what made me want to hold on and what motivates me.

I’m not going to write about socializing or finding a hobby outside of medicine. But I must acknowledge that I have a wonderful book club, supportive boyfriend, and family. I lose myself in books, TV shows, cooking. I even started reading comic books. Plenty of articles are out there about how to beat physician burnout. They all help. I tried knitting, coloring, you name it, but for me, those activities were just not enough. I had to try to find meaning behind the work I do. I had to grab all those small moments during a shift and knit them together to build a bridge to where my passion lies. Then I started by reminding myself why I wanted to practice medicine and why psychiatry.

What inspires me is learning how to decipher what hides behind a symptom – why patient A’s anxiety is different from patient B’s. I find psychodynamics fascinating, so I read. I read literature, articles, and books with subjects around my interests. So when I see a patient at 4 a.m. for 5 minutes, I can knit it together with what I read. So it has meaning. And then it’s easier to hold on. Because the 12-hour overnight shift becomes hours of learning about my passion. Because I feel a step closer. And even though last night’s shift was so hard, I’m happy to be back at work today. When I read about the psychopathology of depression and then admit five patients with suicidal ideation, it stops being the same story over and over. It turns into an exploration, and it becomes fascinating. I won’t hear the same story again. So many times, attendings told me to read, and I had to be at my breaking point to understand why it was so essential. Now I’m motivated, and I plan to keep pushing myself to the limit to find a new challenge and to surprise myself in the middle of my beat-up tiredness when I see something in my patient that so many have written about. The adrenaline rush comes on the path of becoming that psychiatrist I aim to be, not in the diploma I will get 2 years from now.

 

 

I am racing against burnout, but I’m winning. And I wanted to share my experience to remind others that we are not alone on this path, and we should not have higher suicide rates than other professional groups.

If you are a resident or more experienced physician, know that you are not alone. Many others just like you are stretching themselves thin. Follow the tips of how to beat burnout that you’ve seen around. Find what works for you and dig into yourself, into what drove you in this direction, into where your passion lies. Find the meaning behind this hard work, and connect it to the passion that motivates you. Think of what made you want to become a doctor! I’m not sure it works 100% of the time.

Ask me again in 6 months.

Dr. Serrano is a PGY2 psychiatry resident at the Einstein Medical Center in Philadelphia.

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Management of Vitiligo Patients With Surgical Interventions

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Management of Vitiligo Patients With Surgical Interventions

Vitiligo is a common, asymptomatic, acquired depigmentation disorder that is caused by an unknown etiology. Lesions appear as sharply demarcated, depigmented macules and patches that are scattered symmetrically or unsymmetrically over the body. The presentation can be delineated based on the segmental or nonsegmental nature of the disease. According to the revised classification/nomenclature of vitiligo,1 the disorder can be classified as nonsegmental, segmental, mixed, or unclassified. The pathogenesis of the vitiligo disease process is due to multiple modalities that contribute to melanocyte loss. Theories for melanocyte destruction include but are not limited to autoimmunity, biochemicals, epidermal cytokines, increased hydrogen peroxide and free radicals, and humoral and cellular immune alteration.2,3

Despite its long history, the most frustrating aspect of the vitiligo disease process remains its treatment due to limited efficacy, frequent application of topicals, and the need for high-potency steroids. Medical therapies usually are the first line of treatment and are most effective with few side effects for bilateral nonsegmental or evolving vitiligo.2 Some of the primary therapies with the highest efficacies appear to be calcipotriene and psoralen plus UVA, psoralen plus UVA as monotherapy, excimer laser, narrowband UVB, oral steroids, 8-methoxypsoralen, tacrolimus, and topical steroids.4 The theory is that these treatments would be successful if the patient had active melanocytes in the external root sheath that would be able to repigment a patch of vitiligo.5 Hence, it would be more difficult to treat areas such as the dorsal aspect of the fingers and toes because they lack hair-bearing areas with melanocytes.6 The alternative approach to treating vitiligo patches would be surgical intervention techniques, as they provide melanocytic cells to a previously depigmented area.3,5 The focus of this article is to evaluate the efficacy and appropriate use of some of the surgical procedures that can be used in the treatment of vitiligo patients.

Candidate Selection

First, vitiligo patients for whom first-line treatment with medical therapies has failed are candidates for surgical techniques. The second vital component is to clinically confirm the diagnosis of vitiligo as opposed to other genetic, infectious, or autoimmune causes of pigment loss. Lastly, the vitiligo patch should be stable. A stable vitiligo patch does not continue to progress and is no longer responsive to topical medications that are meant to repigment for a discernible period of time.7

Classification of Disease Stage

To classify the stage of vitiligo prior to surgical intervention, Gauthier8 created a basic grading system: grade I, with partial depletion of epidermal melanocytes in a vitiligo patch that responds to repigmentation in a follicular pattern evenly such as on the face and neck; grade II, with complete depletion of epidermal melanocytes with a usual follicular pattern of repigmentation; and grade III, indicating complete depletion of follicular melanocytes with no hope of response to medical therapy. According to Rusfianti and Wirohadidjodjo,2 the surgical techniques that have developed over the years for treatment of grade III vitiligo patients include split-thickness skin grafting, suction blister grafting, miniature punch grafting, and cultured melanocyte transplantation.

Surgical Techniques

Split-thickness skin grafting is an older procedure that entails the use of a harvesting graft site with no pigment loss and dermabrasion of the recipient area to allow interaction with the wound bed.9 With proper care and minimal movement or wrinkling of the graft site, patients can have repigmentation without skip areas.

Suction blister grafting is another tried and tested surgical intervention. Hasegawa et al10 conducted a study of 15 patients (13 males, 2 females; age range, 16–38 years) diagnosed with segmental vitiligo who were treated using the suction blister grafting technique with CO2 laser resurfacing. Patients were recruited 1 month prior to initiating therapy and no other treatments were used during the month or in conjunction with the surgical intervention. Suction blisters were harvested from the left thigh and transferred in saline to the recipient site, which was abraded with 1 pass of the short-pulse CO2 laser system. The recipient sites were then closed with 7-0 nylon sutures and covered tightly with tie-over dressings for at least 1 week. Within 6 months of the procedure, a treatment response of 100% was seen in 15 patients, making it an effective method for treatment-resistant vitiligo patients.10

Miniature punch grafting is another possible treatment option for resistant cases of vitiligo. Mapar et al11 conducted a study in 25 patients (21 women, 4 men; age range, 20–47 years) who had been diagnosed with stable vitiligo (ie, no progression in the last 2 years) and were treated with single hair follicle transplant versus miniature punch grafting. The theory behind the study was to use the melanocytic reservoir noted in the normal hair follicle to repigment the vitiligo patch. With follow-up of both methods of treatment, there was no statistical difference in treatment results.11 A similar study was conducted by Malakar and Lahiri12 in patients with lip leukoderma (a variant of vitiligo). One hundred eight patients (41 males, 67 females; age range, 14–62 years) who had been diagnosed with stable lip leukoderma (ie, stable vitiligo for at least 6 months) underwent treatment via autologous miniature punch grafting. Punch biopsies were performed in donor sites of the buttocks and upper thighs with 72% of patients noting complete repigmentation. Complications noted were herpes labialis–induced lip leukoderma, which ultimately led to rejection of the graft site.12 Overall, however, miniature punch grafting is a viable surgical option in stable vitiligo patients.

 

 

Cultured melanocyte transplantation, or a noncultured epidermal suspension, was first initiated in 1992.13 Silpa-Archa et al14 conducted an open, split-comparison study of 6 vitiligo patients (5 women, 1 man; age range, 20–65 years) with stable lesions. Fifty percent of patients received autologous pigmented skin cellular suspension, which was applied to vitiligo-affected skin that was treated with a fractionated CO2 laser, and 50% received dermabrasion. Composite dressing was placed overlying the site with dressing removal in 1 week. The degree of repigmentation was based on a modified vitiligo area scoring index scale of poor (0%–25%), fair (26%–50%), good (51%–75%), very good (76%–90%), or excellent (91%–100%). Overall repigmentation was very good to excellent in all 6 patients.14 Potentially, this method can far improve the surgical treatment options for future vitiligo patients.

Final Thoughts

Overall, when evaluating surgical interventions for the treatment of vitiligo, careful consideration of the patient’s disease progression, failed therapies, outcome expectations, and repigmentation is warranted prior to initiating any procedure. For appropriate candidates, a range of surgical methodologies has proven to be effective in treatment of stable vitiligo patients.

References
  1. Taïeb A, Picardo M; VETF members. The definition and assessment of vitiligo: a consensus report of the Vitiligo European Task Force. Pigment Cell Res. 2007;20:27-35. Cited by: Ezzedine K, Lim HW, Suzuki T, et al; Vitiligo Global Issue Consensus Conference Panelists. Revised classification/nomenclature of vitiligo and related issues: the Vitiligo Global Issues Consensus Conference. Pigment Cell Melanoma Res. 2012;25:E1-E13.
  2. Rusfianti M, Wirohadidjodjo YW. Dermatosurgical techniques for repigmentation of vitiligo. Int J Dermatol. 2006;45:411-417.
  3. Falabella R. Surgical therapies for vitiligo. Clin Dermatol. 1997;15:927-939.
  4. Whitton ME, Pinart M, Batchelor J, et al. Interventions for vitiligo. Cochrane Database Syst Rev. 2015;2:CD003263.
  5. Mulekar SV, Isedeh P. Surgical interventions for vitiligo: an evidence-based review. Br J Dermatol. 2013;169(suppl 3):57-66.
  6. Dutta AK, Mandal SB. A clinical study of 650 vitiligo cases and their classification. Indian J Dermatol. 1969;14:103-111.
  7. Falabella R, Arrunategui A, Barona MI, et al. The minigrafting test for vitiligo: detection of stable lesions for melanocyte transplantation. J Am Acad Dermatol. 1995;32:228-232.
  8. Gauthier Y. Le vitiligo. Gaz Med. 1994;101:8-12.
  9. Malakar S, Malakar RS. Surgical pearl: composite film and graft unit for the recipient area dressing after split-thickness skin grafting in vitiligo. J Am Acad Dermatol. 2001;44:856-858.
  10. Hasegawa T, Suga Y, Ikejima A, et al. Suction blister grafting with CO2 laser resurfacing of the graft recipient site for vitiligo. J Dermatol. 2007;34:490-492.
  11. Mapar MA, Safarpour M, Mapar M, et al. A comparative study of the mini-punch grafting and hair follicle transplantation in the treatment of refractory and stable vitiligo. J Am Acad Dermatol. 2014;70:743-747.
  12. Malakar S, Lahiri K. Punch grafting for lip leukoderma. Dermatology. 2004;208:125-128.
  13. Gauthier Y, Surleve-Bazeille JE. Autologous grafting with noncultured melanocytes: a simplified method for treatment of depigmented lesions. J Am Acad Dermatol. 1992;26(2, pt 1):191-194.
  14. Silpa-Archa N, Griffith JL, Williams MS, et al. Prospective comparison of recipient-site preparation with fractional carbon dioxide laser versus dermabrasion and recipient-site dressing composition in melanocyte-keratinocyte transplantation procedure in vitiligo: a preliminary study [published online January 24, 2016]. Br J Dermatol. 2016;174:895-897.
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From the Department of Dermatology, University of Florida, Gainesville.

The author reports no conflict of interest.

Correspondence: Divya Shokeen, MD ([email protected]).

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Correspondence: Divya Shokeen, MD ([email protected]).

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The author reports no conflict of interest.

Correspondence: Divya Shokeen, MD ([email protected]).

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Related Articles

Vitiligo is a common, asymptomatic, acquired depigmentation disorder that is caused by an unknown etiology. Lesions appear as sharply demarcated, depigmented macules and patches that are scattered symmetrically or unsymmetrically over the body. The presentation can be delineated based on the segmental or nonsegmental nature of the disease. According to the revised classification/nomenclature of vitiligo,1 the disorder can be classified as nonsegmental, segmental, mixed, or unclassified. The pathogenesis of the vitiligo disease process is due to multiple modalities that contribute to melanocyte loss. Theories for melanocyte destruction include but are not limited to autoimmunity, biochemicals, epidermal cytokines, increased hydrogen peroxide and free radicals, and humoral and cellular immune alteration.2,3

Despite its long history, the most frustrating aspect of the vitiligo disease process remains its treatment due to limited efficacy, frequent application of topicals, and the need for high-potency steroids. Medical therapies usually are the first line of treatment and are most effective with few side effects for bilateral nonsegmental or evolving vitiligo.2 Some of the primary therapies with the highest efficacies appear to be calcipotriene and psoralen plus UVA, psoralen plus UVA as monotherapy, excimer laser, narrowband UVB, oral steroids, 8-methoxypsoralen, tacrolimus, and topical steroids.4 The theory is that these treatments would be successful if the patient had active melanocytes in the external root sheath that would be able to repigment a patch of vitiligo.5 Hence, it would be more difficult to treat areas such as the dorsal aspect of the fingers and toes because they lack hair-bearing areas with melanocytes.6 The alternative approach to treating vitiligo patches would be surgical intervention techniques, as they provide melanocytic cells to a previously depigmented area.3,5 The focus of this article is to evaluate the efficacy and appropriate use of some of the surgical procedures that can be used in the treatment of vitiligo patients.

Candidate Selection

First, vitiligo patients for whom first-line treatment with medical therapies has failed are candidates for surgical techniques. The second vital component is to clinically confirm the diagnosis of vitiligo as opposed to other genetic, infectious, or autoimmune causes of pigment loss. Lastly, the vitiligo patch should be stable. A stable vitiligo patch does not continue to progress and is no longer responsive to topical medications that are meant to repigment for a discernible period of time.7

Classification of Disease Stage

To classify the stage of vitiligo prior to surgical intervention, Gauthier8 created a basic grading system: grade I, with partial depletion of epidermal melanocytes in a vitiligo patch that responds to repigmentation in a follicular pattern evenly such as on the face and neck; grade II, with complete depletion of epidermal melanocytes with a usual follicular pattern of repigmentation; and grade III, indicating complete depletion of follicular melanocytes with no hope of response to medical therapy. According to Rusfianti and Wirohadidjodjo,2 the surgical techniques that have developed over the years for treatment of grade III vitiligo patients include split-thickness skin grafting, suction blister grafting, miniature punch grafting, and cultured melanocyte transplantation.

Surgical Techniques

Split-thickness skin grafting is an older procedure that entails the use of a harvesting graft site with no pigment loss and dermabrasion of the recipient area to allow interaction with the wound bed.9 With proper care and minimal movement or wrinkling of the graft site, patients can have repigmentation without skip areas.

Suction blister grafting is another tried and tested surgical intervention. Hasegawa et al10 conducted a study of 15 patients (13 males, 2 females; age range, 16–38 years) diagnosed with segmental vitiligo who were treated using the suction blister grafting technique with CO2 laser resurfacing. Patients were recruited 1 month prior to initiating therapy and no other treatments were used during the month or in conjunction with the surgical intervention. Suction blisters were harvested from the left thigh and transferred in saline to the recipient site, which was abraded with 1 pass of the short-pulse CO2 laser system. The recipient sites were then closed with 7-0 nylon sutures and covered tightly with tie-over dressings for at least 1 week. Within 6 months of the procedure, a treatment response of 100% was seen in 15 patients, making it an effective method for treatment-resistant vitiligo patients.10

Miniature punch grafting is another possible treatment option for resistant cases of vitiligo. Mapar et al11 conducted a study in 25 patients (21 women, 4 men; age range, 20–47 years) who had been diagnosed with stable vitiligo (ie, no progression in the last 2 years) and were treated with single hair follicle transplant versus miniature punch grafting. The theory behind the study was to use the melanocytic reservoir noted in the normal hair follicle to repigment the vitiligo patch. With follow-up of both methods of treatment, there was no statistical difference in treatment results.11 A similar study was conducted by Malakar and Lahiri12 in patients with lip leukoderma (a variant of vitiligo). One hundred eight patients (41 males, 67 females; age range, 14–62 years) who had been diagnosed with stable lip leukoderma (ie, stable vitiligo for at least 6 months) underwent treatment via autologous miniature punch grafting. Punch biopsies were performed in donor sites of the buttocks and upper thighs with 72% of patients noting complete repigmentation. Complications noted were herpes labialis–induced lip leukoderma, which ultimately led to rejection of the graft site.12 Overall, however, miniature punch grafting is a viable surgical option in stable vitiligo patients.

 

 

Cultured melanocyte transplantation, or a noncultured epidermal suspension, was first initiated in 1992.13 Silpa-Archa et al14 conducted an open, split-comparison study of 6 vitiligo patients (5 women, 1 man; age range, 20–65 years) with stable lesions. Fifty percent of patients received autologous pigmented skin cellular suspension, which was applied to vitiligo-affected skin that was treated with a fractionated CO2 laser, and 50% received dermabrasion. Composite dressing was placed overlying the site with dressing removal in 1 week. The degree of repigmentation was based on a modified vitiligo area scoring index scale of poor (0%–25%), fair (26%–50%), good (51%–75%), very good (76%–90%), or excellent (91%–100%). Overall repigmentation was very good to excellent in all 6 patients.14 Potentially, this method can far improve the surgical treatment options for future vitiligo patients.

Final Thoughts

Overall, when evaluating surgical interventions for the treatment of vitiligo, careful consideration of the patient’s disease progression, failed therapies, outcome expectations, and repigmentation is warranted prior to initiating any procedure. For appropriate candidates, a range of surgical methodologies has proven to be effective in treatment of stable vitiligo patients.

Vitiligo is a common, asymptomatic, acquired depigmentation disorder that is caused by an unknown etiology. Lesions appear as sharply demarcated, depigmented macules and patches that are scattered symmetrically or unsymmetrically over the body. The presentation can be delineated based on the segmental or nonsegmental nature of the disease. According to the revised classification/nomenclature of vitiligo,1 the disorder can be classified as nonsegmental, segmental, mixed, or unclassified. The pathogenesis of the vitiligo disease process is due to multiple modalities that contribute to melanocyte loss. Theories for melanocyte destruction include but are not limited to autoimmunity, biochemicals, epidermal cytokines, increased hydrogen peroxide and free radicals, and humoral and cellular immune alteration.2,3

Despite its long history, the most frustrating aspect of the vitiligo disease process remains its treatment due to limited efficacy, frequent application of topicals, and the need for high-potency steroids. Medical therapies usually are the first line of treatment and are most effective with few side effects for bilateral nonsegmental or evolving vitiligo.2 Some of the primary therapies with the highest efficacies appear to be calcipotriene and psoralen plus UVA, psoralen plus UVA as monotherapy, excimer laser, narrowband UVB, oral steroids, 8-methoxypsoralen, tacrolimus, and topical steroids.4 The theory is that these treatments would be successful if the patient had active melanocytes in the external root sheath that would be able to repigment a patch of vitiligo.5 Hence, it would be more difficult to treat areas such as the dorsal aspect of the fingers and toes because they lack hair-bearing areas with melanocytes.6 The alternative approach to treating vitiligo patches would be surgical intervention techniques, as they provide melanocytic cells to a previously depigmented area.3,5 The focus of this article is to evaluate the efficacy and appropriate use of some of the surgical procedures that can be used in the treatment of vitiligo patients.

Candidate Selection

First, vitiligo patients for whom first-line treatment with medical therapies has failed are candidates for surgical techniques. The second vital component is to clinically confirm the diagnosis of vitiligo as opposed to other genetic, infectious, or autoimmune causes of pigment loss. Lastly, the vitiligo patch should be stable. A stable vitiligo patch does not continue to progress and is no longer responsive to topical medications that are meant to repigment for a discernible period of time.7

Classification of Disease Stage

To classify the stage of vitiligo prior to surgical intervention, Gauthier8 created a basic grading system: grade I, with partial depletion of epidermal melanocytes in a vitiligo patch that responds to repigmentation in a follicular pattern evenly such as on the face and neck; grade II, with complete depletion of epidermal melanocytes with a usual follicular pattern of repigmentation; and grade III, indicating complete depletion of follicular melanocytes with no hope of response to medical therapy. According to Rusfianti and Wirohadidjodjo,2 the surgical techniques that have developed over the years for treatment of grade III vitiligo patients include split-thickness skin grafting, suction blister grafting, miniature punch grafting, and cultured melanocyte transplantation.

Surgical Techniques

Split-thickness skin grafting is an older procedure that entails the use of a harvesting graft site with no pigment loss and dermabrasion of the recipient area to allow interaction with the wound bed.9 With proper care and minimal movement or wrinkling of the graft site, patients can have repigmentation without skip areas.

Suction blister grafting is another tried and tested surgical intervention. Hasegawa et al10 conducted a study of 15 patients (13 males, 2 females; age range, 16–38 years) diagnosed with segmental vitiligo who were treated using the suction blister grafting technique with CO2 laser resurfacing. Patients were recruited 1 month prior to initiating therapy and no other treatments were used during the month or in conjunction with the surgical intervention. Suction blisters were harvested from the left thigh and transferred in saline to the recipient site, which was abraded with 1 pass of the short-pulse CO2 laser system. The recipient sites were then closed with 7-0 nylon sutures and covered tightly with tie-over dressings for at least 1 week. Within 6 months of the procedure, a treatment response of 100% was seen in 15 patients, making it an effective method for treatment-resistant vitiligo patients.10

Miniature punch grafting is another possible treatment option for resistant cases of vitiligo. Mapar et al11 conducted a study in 25 patients (21 women, 4 men; age range, 20–47 years) who had been diagnosed with stable vitiligo (ie, no progression in the last 2 years) and were treated with single hair follicle transplant versus miniature punch grafting. The theory behind the study was to use the melanocytic reservoir noted in the normal hair follicle to repigment the vitiligo patch. With follow-up of both methods of treatment, there was no statistical difference in treatment results.11 A similar study was conducted by Malakar and Lahiri12 in patients with lip leukoderma (a variant of vitiligo). One hundred eight patients (41 males, 67 females; age range, 14–62 years) who had been diagnosed with stable lip leukoderma (ie, stable vitiligo for at least 6 months) underwent treatment via autologous miniature punch grafting. Punch biopsies were performed in donor sites of the buttocks and upper thighs with 72% of patients noting complete repigmentation. Complications noted were herpes labialis–induced lip leukoderma, which ultimately led to rejection of the graft site.12 Overall, however, miniature punch grafting is a viable surgical option in stable vitiligo patients.

 

 

Cultured melanocyte transplantation, or a noncultured epidermal suspension, was first initiated in 1992.13 Silpa-Archa et al14 conducted an open, split-comparison study of 6 vitiligo patients (5 women, 1 man; age range, 20–65 years) with stable lesions. Fifty percent of patients received autologous pigmented skin cellular suspension, which was applied to vitiligo-affected skin that was treated with a fractionated CO2 laser, and 50% received dermabrasion. Composite dressing was placed overlying the site with dressing removal in 1 week. The degree of repigmentation was based on a modified vitiligo area scoring index scale of poor (0%–25%), fair (26%–50%), good (51%–75%), very good (76%–90%), or excellent (91%–100%). Overall repigmentation was very good to excellent in all 6 patients.14 Potentially, this method can far improve the surgical treatment options for future vitiligo patients.

Final Thoughts

Overall, when evaluating surgical interventions for the treatment of vitiligo, careful consideration of the patient’s disease progression, failed therapies, outcome expectations, and repigmentation is warranted prior to initiating any procedure. For appropriate candidates, a range of surgical methodologies has proven to be effective in treatment of stable vitiligo patients.

References
  1. Taïeb A, Picardo M; VETF members. The definition and assessment of vitiligo: a consensus report of the Vitiligo European Task Force. Pigment Cell Res. 2007;20:27-35. Cited by: Ezzedine K, Lim HW, Suzuki T, et al; Vitiligo Global Issue Consensus Conference Panelists. Revised classification/nomenclature of vitiligo and related issues: the Vitiligo Global Issues Consensus Conference. Pigment Cell Melanoma Res. 2012;25:E1-E13.
  2. Rusfianti M, Wirohadidjodjo YW. Dermatosurgical techniques for repigmentation of vitiligo. Int J Dermatol. 2006;45:411-417.
  3. Falabella R. Surgical therapies for vitiligo. Clin Dermatol. 1997;15:927-939.
  4. Whitton ME, Pinart M, Batchelor J, et al. Interventions for vitiligo. Cochrane Database Syst Rev. 2015;2:CD003263.
  5. Mulekar SV, Isedeh P. Surgical interventions for vitiligo: an evidence-based review. Br J Dermatol. 2013;169(suppl 3):57-66.
  6. Dutta AK, Mandal SB. A clinical study of 650 vitiligo cases and their classification. Indian J Dermatol. 1969;14:103-111.
  7. Falabella R, Arrunategui A, Barona MI, et al. The minigrafting test for vitiligo: detection of stable lesions for melanocyte transplantation. J Am Acad Dermatol. 1995;32:228-232.
  8. Gauthier Y. Le vitiligo. Gaz Med. 1994;101:8-12.
  9. Malakar S, Malakar RS. Surgical pearl: composite film and graft unit for the recipient area dressing after split-thickness skin grafting in vitiligo. J Am Acad Dermatol. 2001;44:856-858.
  10. Hasegawa T, Suga Y, Ikejima A, et al. Suction blister grafting with CO2 laser resurfacing of the graft recipient site for vitiligo. J Dermatol. 2007;34:490-492.
  11. Mapar MA, Safarpour M, Mapar M, et al. A comparative study of the mini-punch grafting and hair follicle transplantation in the treatment of refractory and stable vitiligo. J Am Acad Dermatol. 2014;70:743-747.
  12. Malakar S, Lahiri K. Punch grafting for lip leukoderma. Dermatology. 2004;208:125-128.
  13. Gauthier Y, Surleve-Bazeille JE. Autologous grafting with noncultured melanocytes: a simplified method for treatment of depigmented lesions. J Am Acad Dermatol. 1992;26(2, pt 1):191-194.
  14. Silpa-Archa N, Griffith JL, Williams MS, et al. Prospective comparison of recipient-site preparation with fractional carbon dioxide laser versus dermabrasion and recipient-site dressing composition in melanocyte-keratinocyte transplantation procedure in vitiligo: a preliminary study [published online January 24, 2016]. Br J Dermatol. 2016;174:895-897.
References
  1. Taïeb A, Picardo M; VETF members. The definition and assessment of vitiligo: a consensus report of the Vitiligo European Task Force. Pigment Cell Res. 2007;20:27-35. Cited by: Ezzedine K, Lim HW, Suzuki T, et al; Vitiligo Global Issue Consensus Conference Panelists. Revised classification/nomenclature of vitiligo and related issues: the Vitiligo Global Issues Consensus Conference. Pigment Cell Melanoma Res. 2012;25:E1-E13.
  2. Rusfianti M, Wirohadidjodjo YW. Dermatosurgical techniques for repigmentation of vitiligo. Int J Dermatol. 2006;45:411-417.
  3. Falabella R. Surgical therapies for vitiligo. Clin Dermatol. 1997;15:927-939.
  4. Whitton ME, Pinart M, Batchelor J, et al. Interventions for vitiligo. Cochrane Database Syst Rev. 2015;2:CD003263.
  5. Mulekar SV, Isedeh P. Surgical interventions for vitiligo: an evidence-based review. Br J Dermatol. 2013;169(suppl 3):57-66.
  6. Dutta AK, Mandal SB. A clinical study of 650 vitiligo cases and their classification. Indian J Dermatol. 1969;14:103-111.
  7. Falabella R, Arrunategui A, Barona MI, et al. The minigrafting test for vitiligo: detection of stable lesions for melanocyte transplantation. J Am Acad Dermatol. 1995;32:228-232.
  8. Gauthier Y. Le vitiligo. Gaz Med. 1994;101:8-12.
  9. Malakar S, Malakar RS. Surgical pearl: composite film and graft unit for the recipient area dressing after split-thickness skin grafting in vitiligo. J Am Acad Dermatol. 2001;44:856-858.
  10. Hasegawa T, Suga Y, Ikejima A, et al. Suction blister grafting with CO2 laser resurfacing of the graft recipient site for vitiligo. J Dermatol. 2007;34:490-492.
  11. Mapar MA, Safarpour M, Mapar M, et al. A comparative study of the mini-punch grafting and hair follicle transplantation in the treatment of refractory and stable vitiligo. J Am Acad Dermatol. 2014;70:743-747.
  12. Malakar S, Lahiri K. Punch grafting for lip leukoderma. Dermatology. 2004;208:125-128.
  13. Gauthier Y, Surleve-Bazeille JE. Autologous grafting with noncultured melanocytes: a simplified method for treatment of depigmented lesions. J Am Acad Dermatol. 1992;26(2, pt 1):191-194.
  14. Silpa-Archa N, Griffith JL, Williams MS, et al. Prospective comparison of recipient-site preparation with fractional carbon dioxide laser versus dermabrasion and recipient-site dressing composition in melanocyte-keratinocyte transplantation procedure in vitiligo: a preliminary study [published online January 24, 2016]. Br J Dermatol. 2016;174:895-897.
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Boards Review Resources

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Books

There are a number of classic textbooks that serve as primary resources for dermatology training1-4; however, there also are other options if memorizing these books seems a little daunting. The “first aid” books of dermatology are the Derm In-Review binder and Jain’s5 Dermatology: Illustrated Study Guide and Comprehensive Board Review. Mariwalla and Leffell’s6Primer in Dermatologic Surgery: A Study Companion is helpful for surgical review and is available at a discounted price for members of the American Society for Dermatologic Surgery (https://www.asds.net/store/product.aspx?id=3914&terms=primer%20in%20Dermatologic%20surgery). The American Academy of Dermatology (AAD) provides a list of additional textbooks that dermatology residents may find useful for board review.7

Guided Study

The AAD offers board review courses for dermatology residents (cost varies).7 The Florida Dermatology and Dermatopathology Board Review Course (http://dermatology.med.ufl.edu/education/florida-dermatology-and-dermatopathology-board-review-course/) is an annual review course held in Tampa (early registration fee, $800 [does not include travel costs]). The Oakstone Institute also offers its Dermatology Board Review Course, which is a self-study program that can be completed online for approximately $1195 (http://www.oakstone.com/dermatology-board-review-course). Be sure to take advantage of free didactics lectures, society meetings with board review courses, and study groups, as these resources can be just as helpful and more budget friendly.

Digital Resources

The Derm In-Review question bank (http://dermatologyinreview.com/Merz) is probably one of the most popular board review resources and is free to US dermatology residents; however, be cautious when using this resource, as a fair number of the answers to questions may actually be outdated or based on older studies. A group study session can help tease out why certain answers are erroneous and provide a forum for discussing what would be a more correct answer. Take advantage of the opportunity to provide feedback on this website, as your comments will improve this resource for future dermatology residents.

Beyond traditional dermatopathology textbooks, there also are some excellent mobile applications (apps) available. The Clearpath app is a user-friendly dermatopathology study tool that is free for download in the iTunes store (https://itunes.apple.com/us/app/clearpath/id540260769?mt=8). However, the app is only compatible with iPads. The Clearpath website also offers virtual study slide sets that are easier to access (http://dermpathlab.com/slide-study-set-program). Your institution’s glass slide sets also are useful for building pattern recognition skills and practicing for the actual board examination. The DermOID website (http://www.derm-oid.com), which is powered by the David Geffen School of Medicine at the University of California, Los Angeles, is another online dermatopathology study database with free registration for access to the site. Another fun way to test your dermatopathology skills is in the exhibition hall at the AAD annual meeting where some vendors may offer daily dermatopathology quizzes and prizes for the residents with the most correct answers. Also, it is worth reviewing the Cutis® Fast Facts for Board Review (http://www.cutis.com/articles/fast-facts-for-board-review/), as this section offers many outstanding fact sheets that are an easy read and an efficient way to gain board knowledge. Some recent topics include fillers, paraneoplastic skin conditions, and medications in dermatology.

Many residents enjoy using the Anki flashcard app (http://ankisrs.net) for reviewing kodachromes. The AAD website also includes a Boards’ Fodder archive that is worth reviewing (https://www.aad.org/members/residents-fellows/boards-study-tools/boards-fodder/boards-fodder). New board review resources are constantly being posted on the AAD website, so definitely check this out. You may be able to access this resource through your residency program; it is also available for purchase ($425 for AAD members; $850 for nonmembers).

Journals

All the major dermatology journals are helpful in preparing for the board examination. Your resident journal club will likely review many of the most clinically relevant dermatology articles published over the course of your residency. Some other helpful journal resources that are recommended for board review include the Journal of the American Medical Association’s Clinical Challenge, which has many dermatologic cases (http://jama.jamanetwork.com/public/QuizzesAndPolls.aspx), and the New England Journal of Medicine’s Journal Watch (http://www.jwatch.org) and Image Challenge (http://www.nejm.org/image-challenge).

Practice Examinations

The American Board of Dermatology’s In-Training Examination is the most well-known practice examination among dermatology residents.8 A link to an additional practice examination usually is provided a few weeks prior to the examination. The Derm In-Review website also offers diagnostic practice examinations with some ability to custom select questions for your studying needs.

Conclusion

There are many board review resources out there. Find the ones that work for you, and be encouraged that your studying and hard work will pay off!

References

 

1. Bolognia JL, Jorizzo JL, Schaffer JV. Dermatology. 3rd ed. Philadelphia, PA: Elsevier Saunders; 2012.

2. James WD, Berger TG, Elston DM. Andrews’ Diseases of the Skin: Clinical Dermatology. 11th ed. Philadelphia, PA: Elsevier Saunders; 2011.

3. Spitz JL. Genodermatoses: A Clinical Guide to Genetic Skin Diseases. 2nd ed. Baltimore, MD: Lippincott Williams & Wilkins; 2004.

4. Weedon D. Weedon’s Skin Pathology. 3rd ed. London, England: Churchill Livingstone; 2010.

5. Jain S. Dermatology: Illustrated Study Guide and Comprehensive Board Review. New York, NY; Springer: 2012.

6. Mariwalla K, Leffell DJ. Primer in Dermatologic Surgery: A Study Companion. 2nd ed. Rolling Meadows, IL: American Society for Dermatologic Surgery; 2011.

7. Additional boards resources. American Academy of Dermatology website. https://www.aad.org/members/residents-fellows/boards-study-tools/more-boards-resources. Accessed March 31, 2016.

8. In-training examination (ITE). American Board of Dermatology website. https://www.abderm.org/residents-and-fellows/in-training-and-primary-certification-examinations/in-training-examination-ite.aspx. Accessed March 22, 2016.

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Megan Brown, MD

Dr. Brown is from the Department of Dermatology, University of California, San Diego.

The author reports no conflict of interest.

Correspondence: Megan Brown, MD, 8899 University Center Ln, Ste 350, San Diego, CA 92122 ([email protected]).

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Related Articles

Books

There are a number of classic textbooks that serve as primary resources for dermatology training1-4; however, there also are other options if memorizing these books seems a little daunting. The “first aid” books of dermatology are the Derm In-Review binder and Jain’s5 Dermatology: Illustrated Study Guide and Comprehensive Board Review. Mariwalla and Leffell’s6Primer in Dermatologic Surgery: A Study Companion is helpful for surgical review and is available at a discounted price for members of the American Society for Dermatologic Surgery (https://www.asds.net/store/product.aspx?id=3914&terms=primer%20in%20Dermatologic%20surgery). The American Academy of Dermatology (AAD) provides a list of additional textbooks that dermatology residents may find useful for board review.7

Guided Study

The AAD offers board review courses for dermatology residents (cost varies).7 The Florida Dermatology and Dermatopathology Board Review Course (http://dermatology.med.ufl.edu/education/florida-dermatology-and-dermatopathology-board-review-course/) is an annual review course held in Tampa (early registration fee, $800 [does not include travel costs]). The Oakstone Institute also offers its Dermatology Board Review Course, which is a self-study program that can be completed online for approximately $1195 (http://www.oakstone.com/dermatology-board-review-course). Be sure to take advantage of free didactics lectures, society meetings with board review courses, and study groups, as these resources can be just as helpful and more budget friendly.

Digital Resources

The Derm In-Review question bank (http://dermatologyinreview.com/Merz) is probably one of the most popular board review resources and is free to US dermatology residents; however, be cautious when using this resource, as a fair number of the answers to questions may actually be outdated or based on older studies. A group study session can help tease out why certain answers are erroneous and provide a forum for discussing what would be a more correct answer. Take advantage of the opportunity to provide feedback on this website, as your comments will improve this resource for future dermatology residents.

Beyond traditional dermatopathology textbooks, there also are some excellent mobile applications (apps) available. The Clearpath app is a user-friendly dermatopathology study tool that is free for download in the iTunes store (https://itunes.apple.com/us/app/clearpath/id540260769?mt=8). However, the app is only compatible with iPads. The Clearpath website also offers virtual study slide sets that are easier to access (http://dermpathlab.com/slide-study-set-program). Your institution’s glass slide sets also are useful for building pattern recognition skills and practicing for the actual board examination. The DermOID website (http://www.derm-oid.com), which is powered by the David Geffen School of Medicine at the University of California, Los Angeles, is another online dermatopathology study database with free registration for access to the site. Another fun way to test your dermatopathology skills is in the exhibition hall at the AAD annual meeting where some vendors may offer daily dermatopathology quizzes and prizes for the residents with the most correct answers. Also, it is worth reviewing the Cutis® Fast Facts for Board Review (http://www.cutis.com/articles/fast-facts-for-board-review/), as this section offers many outstanding fact sheets that are an easy read and an efficient way to gain board knowledge. Some recent topics include fillers, paraneoplastic skin conditions, and medications in dermatology.

Many residents enjoy using the Anki flashcard app (http://ankisrs.net) for reviewing kodachromes. The AAD website also includes a Boards’ Fodder archive that is worth reviewing (https://www.aad.org/members/residents-fellows/boards-study-tools/boards-fodder/boards-fodder). New board review resources are constantly being posted on the AAD website, so definitely check this out. You may be able to access this resource through your residency program; it is also available for purchase ($425 for AAD members; $850 for nonmembers).

Journals

All the major dermatology journals are helpful in preparing for the board examination. Your resident journal club will likely review many of the most clinically relevant dermatology articles published over the course of your residency. Some other helpful journal resources that are recommended for board review include the Journal of the American Medical Association’s Clinical Challenge, which has many dermatologic cases (http://jama.jamanetwork.com/public/QuizzesAndPolls.aspx), and the New England Journal of Medicine’s Journal Watch (http://www.jwatch.org) and Image Challenge (http://www.nejm.org/image-challenge).

Practice Examinations

The American Board of Dermatology’s In-Training Examination is the most well-known practice examination among dermatology residents.8 A link to an additional practice examination usually is provided a few weeks prior to the examination. The Derm In-Review website also offers diagnostic practice examinations with some ability to custom select questions for your studying needs.

Conclusion

There are many board review resources out there. Find the ones that work for you, and be encouraged that your studying and hard work will pay off!

Books

There are a number of classic textbooks that serve as primary resources for dermatology training1-4; however, there also are other options if memorizing these books seems a little daunting. The “first aid” books of dermatology are the Derm In-Review binder and Jain’s5 Dermatology: Illustrated Study Guide and Comprehensive Board Review. Mariwalla and Leffell’s6Primer in Dermatologic Surgery: A Study Companion is helpful for surgical review and is available at a discounted price for members of the American Society for Dermatologic Surgery (https://www.asds.net/store/product.aspx?id=3914&terms=primer%20in%20Dermatologic%20surgery). The American Academy of Dermatology (AAD) provides a list of additional textbooks that dermatology residents may find useful for board review.7

Guided Study

The AAD offers board review courses for dermatology residents (cost varies).7 The Florida Dermatology and Dermatopathology Board Review Course (http://dermatology.med.ufl.edu/education/florida-dermatology-and-dermatopathology-board-review-course/) is an annual review course held in Tampa (early registration fee, $800 [does not include travel costs]). The Oakstone Institute also offers its Dermatology Board Review Course, which is a self-study program that can be completed online for approximately $1195 (http://www.oakstone.com/dermatology-board-review-course). Be sure to take advantage of free didactics lectures, society meetings with board review courses, and study groups, as these resources can be just as helpful and more budget friendly.

Digital Resources

The Derm In-Review question bank (http://dermatologyinreview.com/Merz) is probably one of the most popular board review resources and is free to US dermatology residents; however, be cautious when using this resource, as a fair number of the answers to questions may actually be outdated or based on older studies. A group study session can help tease out why certain answers are erroneous and provide a forum for discussing what would be a more correct answer. Take advantage of the opportunity to provide feedback on this website, as your comments will improve this resource for future dermatology residents.

Beyond traditional dermatopathology textbooks, there also are some excellent mobile applications (apps) available. The Clearpath app is a user-friendly dermatopathology study tool that is free for download in the iTunes store (https://itunes.apple.com/us/app/clearpath/id540260769?mt=8). However, the app is only compatible with iPads. The Clearpath website also offers virtual study slide sets that are easier to access (http://dermpathlab.com/slide-study-set-program). Your institution’s glass slide sets also are useful for building pattern recognition skills and practicing for the actual board examination. The DermOID website (http://www.derm-oid.com), which is powered by the David Geffen School of Medicine at the University of California, Los Angeles, is another online dermatopathology study database with free registration for access to the site. Another fun way to test your dermatopathology skills is in the exhibition hall at the AAD annual meeting where some vendors may offer daily dermatopathology quizzes and prizes for the residents with the most correct answers. Also, it is worth reviewing the Cutis® Fast Facts for Board Review (http://www.cutis.com/articles/fast-facts-for-board-review/), as this section offers many outstanding fact sheets that are an easy read and an efficient way to gain board knowledge. Some recent topics include fillers, paraneoplastic skin conditions, and medications in dermatology.

Many residents enjoy using the Anki flashcard app (http://ankisrs.net) for reviewing kodachromes. The AAD website also includes a Boards’ Fodder archive that is worth reviewing (https://www.aad.org/members/residents-fellows/boards-study-tools/boards-fodder/boards-fodder). New board review resources are constantly being posted on the AAD website, so definitely check this out. You may be able to access this resource through your residency program; it is also available for purchase ($425 for AAD members; $850 for nonmembers).

Journals

All the major dermatology journals are helpful in preparing for the board examination. Your resident journal club will likely review many of the most clinically relevant dermatology articles published over the course of your residency. Some other helpful journal resources that are recommended for board review include the Journal of the American Medical Association’s Clinical Challenge, which has many dermatologic cases (http://jama.jamanetwork.com/public/QuizzesAndPolls.aspx), and the New England Journal of Medicine’s Journal Watch (http://www.jwatch.org) and Image Challenge (http://www.nejm.org/image-challenge).

Practice Examinations

The American Board of Dermatology’s In-Training Examination is the most well-known practice examination among dermatology residents.8 A link to an additional practice examination usually is provided a few weeks prior to the examination. The Derm In-Review website also offers diagnostic practice examinations with some ability to custom select questions for your studying needs.

Conclusion

There are many board review resources out there. Find the ones that work for you, and be encouraged that your studying and hard work will pay off!

References

 

1. Bolognia JL, Jorizzo JL, Schaffer JV. Dermatology. 3rd ed. Philadelphia, PA: Elsevier Saunders; 2012.

2. James WD, Berger TG, Elston DM. Andrews’ Diseases of the Skin: Clinical Dermatology. 11th ed. Philadelphia, PA: Elsevier Saunders; 2011.

3. Spitz JL. Genodermatoses: A Clinical Guide to Genetic Skin Diseases. 2nd ed. Baltimore, MD: Lippincott Williams & Wilkins; 2004.

4. Weedon D. Weedon’s Skin Pathology. 3rd ed. London, England: Churchill Livingstone; 2010.

5. Jain S. Dermatology: Illustrated Study Guide and Comprehensive Board Review. New York, NY; Springer: 2012.

6. Mariwalla K, Leffell DJ. Primer in Dermatologic Surgery: A Study Companion. 2nd ed. Rolling Meadows, IL: American Society for Dermatologic Surgery; 2011.

7. Additional boards resources. American Academy of Dermatology website. https://www.aad.org/members/residents-fellows/boards-study-tools/more-boards-resources. Accessed March 31, 2016.

8. In-training examination (ITE). American Board of Dermatology website. https://www.abderm.org/residents-and-fellows/in-training-and-primary-certification-examinations/in-training-examination-ite.aspx. Accessed March 22, 2016.

References

 

1. Bolognia JL, Jorizzo JL, Schaffer JV. Dermatology. 3rd ed. Philadelphia, PA: Elsevier Saunders; 2012.

2. James WD, Berger TG, Elston DM. Andrews’ Diseases of the Skin: Clinical Dermatology. 11th ed. Philadelphia, PA: Elsevier Saunders; 2011.

3. Spitz JL. Genodermatoses: A Clinical Guide to Genetic Skin Diseases. 2nd ed. Baltimore, MD: Lippincott Williams & Wilkins; 2004.

4. Weedon D. Weedon’s Skin Pathology. 3rd ed. London, England: Churchill Livingstone; 2010.

5. Jain S. Dermatology: Illustrated Study Guide and Comprehensive Board Review. New York, NY; Springer: 2012.

6. Mariwalla K, Leffell DJ. Primer in Dermatologic Surgery: A Study Companion. 2nd ed. Rolling Meadows, IL: American Society for Dermatologic Surgery; 2011.

7. Additional boards resources. American Academy of Dermatology website. https://www.aad.org/members/residents-fellows/boards-study-tools/more-boards-resources. Accessed March 31, 2016.

8. In-training examination (ITE). American Board of Dermatology website. https://www.abderm.org/residents-and-fellows/in-training-and-primary-certification-examinations/in-training-examination-ite.aspx. Accessed March 22, 2016.

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Cyclosporine in SJS/TEN Management: A Brief Review

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As dermatology residents, the telephone calls we get at 2 am usually are the toughest for 2 reasons: (1) we rarely get calls at 2 am, and (2) it usually means there is a case to rule out Stevens-Johnson syndrome (SJS) and toxic epidermal necrolysis (TEN). Stevens-Johnson syndrome and TEN are severe mucocutaneous eruptions that usually develop due to drug reactions and involve a continuum of conjunctivitis, mucocutaneous sloughing, keratinocyte death, and bullae development. Body surface area (BSA) coverage determines the distinction between SJS and TEN; less than 10% BSA affected indicates SJS, 10% to 30% BSA affected indicates overlap between SJS and TEN, and greater than 30% BSA affected indicates TEN.1 The mortality rates for these conditions range from 1% to 5% in SJS versus 25% to 30% in TEN.2

Being driven and dedicated residents, we rise to the challenge by arranging appropriate consultations, obtaining frozen section biopsies, providing recommendations to remove unnecessary medications, and offering skin care management. However, what comes next? Intravenous immunoglobulin (IVIG)? Cyclosporine? Or is it appropriate to allow the reaction to continue its course? Dermatology programs have a varying standard of care due to the limited number of studies conducted on SJS/TEN patients. Few studies have relayed the efficacy of cyclosporine; however, published results have shown that cyclosporine can decrease the overall mortality risk and minimize disease progression.2-5 In this article, I will review some of the key studies conducted in the last 5 years regarding the use of cyclosporine in the therapeutic plan for SJS/TEN.

In one retrospective analysis conducted by Kirchhof et al1 in 2014, 35 patients with SJS/TEN who were treated with IVIG and 15 who were treated with cyclosporine were evaluated for mortality benefit. Two patients were treated with both cyclosporine and IVIG and were included in both arms of the study. Overall, the evaluation indicated that cyclosporine can potentially have a better overall advantage in treatment of SJS/TEN over IVIG.1 Although this study had an uneven number of patients treated with IVIG versus cyclosporine, a nonstandardized way of comparing patients with early SJS to TEN patients, and no double-blind randomized trial, cyclosporine may still show benefit over IVIG.

Singh et al6 conducted an uncontrolled open study in a tertiary care center (July 2011–June 2012) that showed a similar result of benefit with cyclosporine in SJS, SJS/TEN, and TEN patients. Eleven participants were included in the study based on SCORTEN (Score of Toxic Epidermal Necrosis) criteria (age, >40 years; heart rate, >120 BPM; serum blood urea nitrogen level, >28 mg/dL; body surface area affected, >10%; serum bicarbonate, >20 mEq/L; serum glucose, >252 mg/dL). They were treated with cyclosporine 3 mg/kg for 7 days and then tapered over another 7 days. Six participants were treated with corticosteroids. Participants treated with cyclosporine reepithelialized in 16.7 days compared to 23 days with corticosteroids. The hospital stay was 18.09 days in participants treated with cyclosporine versus 26 days in those treated with corticosteroids. Lastly, 2 participants who were treated with corticosteroids died as opposed to none with cyclosporine.6 Although the power of this study also was limited and it was not a randomized, double-blind, controlled trial, it provides more evidence that cyclosporine can be efficacious in SJS/TEN patients.

A phase 2 open trial conducted by Valeyrie-Allanore et al7 evaluated the benefit and efficacy of cyclosporine in SJS/TEN patients. There were 29 participants at the start of the study (SJS, n=10; SJS/TEN, n=12; TEN, n=7) and 26 completed treatment. Cyclosporine was administered orally at 3 mg/kg for 10 days and tapered over the following month. This study noted 3 basic principles: First, patients tolerated cyclosporine well; second, limited disease progression was noted in 62% (18/29) of participants around day 3 and in only about 35% (11/29) of IVIG patients; and third, no deaths were noted in all participants.7

Final Thoughts

Case reports have indicated that cyclosporine may be effective in limiting progression of SJS/TEN; however, a double-blind study has not validated this finding. Hence, patients should be evaluated on a case-by-case basis to determine if they should be treated with cyclosporine or IVIG or simply complete the course of the disease process with supportive care.

References

 

1. Kirchhof MG, Miliszewski MA, Sikora S, et al. Retrospective review of Stevens-Johnson syndrome/toxic epidermal necrolysis treatment comparing intravenous immunoglobulin with cyclosporine. J Am Acad Dermatol. 2014;71:941-947.

2. Schwartz RA, McDonough PH, Lee BW. Toxic epidermal necrolysis, part I: introduction, history, classification, clinical features, systemic manifestations, etiology, and immunopathogenesis. J Am Acad Dermatol. 2013;69:173.e1-173.e13, quiz 185-186.

3. Arévalo JM, Lorente JA, González-Herrada C, et al. Treatment of toxic epidermal necrolysis with cyclosporin A. J Trauma. 2000;48:473-478.

4. Aihara Y, Ito R, Ito S, et al. Toxic epidermal necrolysis in a child successfully treated with cyclosporine A and methylprednisolone. Pediatr Int. 2007;49:659-662.

5. Hewitt J, Ormerod AD. Toxic epidermal necrolysis treated with cyclosporin. Clin Exp Dermatol. 1992;17:264-265.

6. Singh GK, Chatterjee M, Verma R. Cyclosporine in Stevens Johnson syndrome and toxic epidermal necrolysis and retrospective comparison with systemic corticosteroid. Indian J Dermatol Venereol Leprol. 2013;79:686-692.

7. Valeyrie-Allanore P, Wolkenstein L, Brochard N, et al. Open trial of ciclosporin treatment for Stevens-Johnson syndrome and toxic epidermal necrolysis. Br J Dermatol. 2010;163:847-853.

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Correspondence: Divya Shokeen, MD ([email protected]).

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As dermatology residents, the telephone calls we get at 2 am usually are the toughest for 2 reasons: (1) we rarely get calls at 2 am, and (2) it usually means there is a case to rule out Stevens-Johnson syndrome (SJS) and toxic epidermal necrolysis (TEN). Stevens-Johnson syndrome and TEN are severe mucocutaneous eruptions that usually develop due to drug reactions and involve a continuum of conjunctivitis, mucocutaneous sloughing, keratinocyte death, and bullae development. Body surface area (BSA) coverage determines the distinction between SJS and TEN; less than 10% BSA affected indicates SJS, 10% to 30% BSA affected indicates overlap between SJS and TEN, and greater than 30% BSA affected indicates TEN.1 The mortality rates for these conditions range from 1% to 5% in SJS versus 25% to 30% in TEN.2

Being driven and dedicated residents, we rise to the challenge by arranging appropriate consultations, obtaining frozen section biopsies, providing recommendations to remove unnecessary medications, and offering skin care management. However, what comes next? Intravenous immunoglobulin (IVIG)? Cyclosporine? Or is it appropriate to allow the reaction to continue its course? Dermatology programs have a varying standard of care due to the limited number of studies conducted on SJS/TEN patients. Few studies have relayed the efficacy of cyclosporine; however, published results have shown that cyclosporine can decrease the overall mortality risk and minimize disease progression.2-5 In this article, I will review some of the key studies conducted in the last 5 years regarding the use of cyclosporine in the therapeutic plan for SJS/TEN.

In one retrospective analysis conducted by Kirchhof et al1 in 2014, 35 patients with SJS/TEN who were treated with IVIG and 15 who were treated with cyclosporine were evaluated for mortality benefit. Two patients were treated with both cyclosporine and IVIG and were included in both arms of the study. Overall, the evaluation indicated that cyclosporine can potentially have a better overall advantage in treatment of SJS/TEN over IVIG.1 Although this study had an uneven number of patients treated with IVIG versus cyclosporine, a nonstandardized way of comparing patients with early SJS to TEN patients, and no double-blind randomized trial, cyclosporine may still show benefit over IVIG.

Singh et al6 conducted an uncontrolled open study in a tertiary care center (July 2011–June 2012) that showed a similar result of benefit with cyclosporine in SJS, SJS/TEN, and TEN patients. Eleven participants were included in the study based on SCORTEN (Score of Toxic Epidermal Necrosis) criteria (age, >40 years; heart rate, >120 BPM; serum blood urea nitrogen level, >28 mg/dL; body surface area affected, >10%; serum bicarbonate, >20 mEq/L; serum glucose, >252 mg/dL). They were treated with cyclosporine 3 mg/kg for 7 days and then tapered over another 7 days. Six participants were treated with corticosteroids. Participants treated with cyclosporine reepithelialized in 16.7 days compared to 23 days with corticosteroids. The hospital stay was 18.09 days in participants treated with cyclosporine versus 26 days in those treated with corticosteroids. Lastly, 2 participants who were treated with corticosteroids died as opposed to none with cyclosporine.6 Although the power of this study also was limited and it was not a randomized, double-blind, controlled trial, it provides more evidence that cyclosporine can be efficacious in SJS/TEN patients.

A phase 2 open trial conducted by Valeyrie-Allanore et al7 evaluated the benefit and efficacy of cyclosporine in SJS/TEN patients. There were 29 participants at the start of the study (SJS, n=10; SJS/TEN, n=12; TEN, n=7) and 26 completed treatment. Cyclosporine was administered orally at 3 mg/kg for 10 days and tapered over the following month. This study noted 3 basic principles: First, patients tolerated cyclosporine well; second, limited disease progression was noted in 62% (18/29) of participants around day 3 and in only about 35% (11/29) of IVIG patients; and third, no deaths were noted in all participants.7

Final Thoughts

Case reports have indicated that cyclosporine may be effective in limiting progression of SJS/TEN; however, a double-blind study has not validated this finding. Hence, patients should be evaluated on a case-by-case basis to determine if they should be treated with cyclosporine or IVIG or simply complete the course of the disease process with supportive care.

As dermatology residents, the telephone calls we get at 2 am usually are the toughest for 2 reasons: (1) we rarely get calls at 2 am, and (2) it usually means there is a case to rule out Stevens-Johnson syndrome (SJS) and toxic epidermal necrolysis (TEN). Stevens-Johnson syndrome and TEN are severe mucocutaneous eruptions that usually develop due to drug reactions and involve a continuum of conjunctivitis, mucocutaneous sloughing, keratinocyte death, and bullae development. Body surface area (BSA) coverage determines the distinction between SJS and TEN; less than 10% BSA affected indicates SJS, 10% to 30% BSA affected indicates overlap between SJS and TEN, and greater than 30% BSA affected indicates TEN.1 The mortality rates for these conditions range from 1% to 5% in SJS versus 25% to 30% in TEN.2

Being driven and dedicated residents, we rise to the challenge by arranging appropriate consultations, obtaining frozen section biopsies, providing recommendations to remove unnecessary medications, and offering skin care management. However, what comes next? Intravenous immunoglobulin (IVIG)? Cyclosporine? Or is it appropriate to allow the reaction to continue its course? Dermatology programs have a varying standard of care due to the limited number of studies conducted on SJS/TEN patients. Few studies have relayed the efficacy of cyclosporine; however, published results have shown that cyclosporine can decrease the overall mortality risk and minimize disease progression.2-5 In this article, I will review some of the key studies conducted in the last 5 years regarding the use of cyclosporine in the therapeutic plan for SJS/TEN.

In one retrospective analysis conducted by Kirchhof et al1 in 2014, 35 patients with SJS/TEN who were treated with IVIG and 15 who were treated with cyclosporine were evaluated for mortality benefit. Two patients were treated with both cyclosporine and IVIG and were included in both arms of the study. Overall, the evaluation indicated that cyclosporine can potentially have a better overall advantage in treatment of SJS/TEN over IVIG.1 Although this study had an uneven number of patients treated with IVIG versus cyclosporine, a nonstandardized way of comparing patients with early SJS to TEN patients, and no double-blind randomized trial, cyclosporine may still show benefit over IVIG.

Singh et al6 conducted an uncontrolled open study in a tertiary care center (July 2011–June 2012) that showed a similar result of benefit with cyclosporine in SJS, SJS/TEN, and TEN patients. Eleven participants were included in the study based on SCORTEN (Score of Toxic Epidermal Necrosis) criteria (age, >40 years; heart rate, >120 BPM; serum blood urea nitrogen level, >28 mg/dL; body surface area affected, >10%; serum bicarbonate, >20 mEq/L; serum glucose, >252 mg/dL). They were treated with cyclosporine 3 mg/kg for 7 days and then tapered over another 7 days. Six participants were treated with corticosteroids. Participants treated with cyclosporine reepithelialized in 16.7 days compared to 23 days with corticosteroids. The hospital stay was 18.09 days in participants treated with cyclosporine versus 26 days in those treated with corticosteroids. Lastly, 2 participants who were treated with corticosteroids died as opposed to none with cyclosporine.6 Although the power of this study also was limited and it was not a randomized, double-blind, controlled trial, it provides more evidence that cyclosporine can be efficacious in SJS/TEN patients.

A phase 2 open trial conducted by Valeyrie-Allanore et al7 evaluated the benefit and efficacy of cyclosporine in SJS/TEN patients. There were 29 participants at the start of the study (SJS, n=10; SJS/TEN, n=12; TEN, n=7) and 26 completed treatment. Cyclosporine was administered orally at 3 mg/kg for 10 days and tapered over the following month. This study noted 3 basic principles: First, patients tolerated cyclosporine well; second, limited disease progression was noted in 62% (18/29) of participants around day 3 and in only about 35% (11/29) of IVIG patients; and third, no deaths were noted in all participants.7

Final Thoughts

Case reports have indicated that cyclosporine may be effective in limiting progression of SJS/TEN; however, a double-blind study has not validated this finding. Hence, patients should be evaluated on a case-by-case basis to determine if they should be treated with cyclosporine or IVIG or simply complete the course of the disease process with supportive care.

References

 

1. Kirchhof MG, Miliszewski MA, Sikora S, et al. Retrospective review of Stevens-Johnson syndrome/toxic epidermal necrolysis treatment comparing intravenous immunoglobulin with cyclosporine. J Am Acad Dermatol. 2014;71:941-947.

2. Schwartz RA, McDonough PH, Lee BW. Toxic epidermal necrolysis, part I: introduction, history, classification, clinical features, systemic manifestations, etiology, and immunopathogenesis. J Am Acad Dermatol. 2013;69:173.e1-173.e13, quiz 185-186.

3. Arévalo JM, Lorente JA, González-Herrada C, et al. Treatment of toxic epidermal necrolysis with cyclosporin A. J Trauma. 2000;48:473-478.

4. Aihara Y, Ito R, Ito S, et al. Toxic epidermal necrolysis in a child successfully treated with cyclosporine A and methylprednisolone. Pediatr Int. 2007;49:659-662.

5. Hewitt J, Ormerod AD. Toxic epidermal necrolysis treated with cyclosporin. Clin Exp Dermatol. 1992;17:264-265.

6. Singh GK, Chatterjee M, Verma R. Cyclosporine in Stevens Johnson syndrome and toxic epidermal necrolysis and retrospective comparison with systemic corticosteroid. Indian J Dermatol Venereol Leprol. 2013;79:686-692.

7. Valeyrie-Allanore P, Wolkenstein L, Brochard N, et al. Open trial of ciclosporin treatment for Stevens-Johnson syndrome and toxic epidermal necrolysis. Br J Dermatol. 2010;163:847-853.

References

 

1. Kirchhof MG, Miliszewski MA, Sikora S, et al. Retrospective review of Stevens-Johnson syndrome/toxic epidermal necrolysis treatment comparing intravenous immunoglobulin with cyclosporine. J Am Acad Dermatol. 2014;71:941-947.

2. Schwartz RA, McDonough PH, Lee BW. Toxic epidermal necrolysis, part I: introduction, history, classification, clinical features, systemic manifestations, etiology, and immunopathogenesis. J Am Acad Dermatol. 2013;69:173.e1-173.e13, quiz 185-186.

3. Arévalo JM, Lorente JA, González-Herrada C, et al. Treatment of toxic epidermal necrolysis with cyclosporin A. J Trauma. 2000;48:473-478.

4. Aihara Y, Ito R, Ito S, et al. Toxic epidermal necrolysis in a child successfully treated with cyclosporine A and methylprednisolone. Pediatr Int. 2007;49:659-662.

5. Hewitt J, Ormerod AD. Toxic epidermal necrolysis treated with cyclosporin. Clin Exp Dermatol. 1992;17:264-265.

6. Singh GK, Chatterjee M, Verma R. Cyclosporine in Stevens Johnson syndrome and toxic epidermal necrolysis and retrospective comparison with systemic corticosteroid. Indian J Dermatol Venereol Leprol. 2013;79:686-692.

7. Valeyrie-Allanore P, Wolkenstein L, Brochard N, et al. Open trial of ciclosporin treatment for Stevens-Johnson syndrome and toxic epidermal necrolysis. Br J Dermatol. 2010;163:847-853.

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Disability Insurance: What Dermatology Residents Need to Know

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Several older physicians have emphasized to me the importance of choosing an excellent disability insurance policy during residency. However, choosing the right policy can be a difficult task. The policy definitions are complicated, and there is a lot of fine print. To understand this confusing topic, start with answers to these 3 questions: What is my most valuable asset? When is the best point in my career to purchase disability insurance? What would I do if I were no longer able to perform the material and substantial duties of my occupation as a dermatologist?

A Resident’s Assets

In the world of disability insurance, your most valuable assets are your education and your ability to earn an income in the future.1,2 A resident’s ability to earn an income in the future reflects a massive investment of time, cost of education, and postponed accruement of wealth due to time spent in training. Any negative impact on your health (eg, back injury, vision loss, hand injury) can jeopardize these assets. Purchasing disability insurance while still in dermatology residency will protect this investment; it also will ensure that you obtain a policy while you are still healthy.1,2

Choosing a Policy

Disability insurance comes in 2 main forms: individual or group. Individual insurance may be slightly more expensive but may offer better coverage than group insurance. Group insurance often is offered through a large medical association such as the American Academy of Dermatology. Group insurance may be less expensive but often has more limits to coverage. A definite must-have in a disability insurance policy is one that has guaranteed renewal and is noncancellable.1-3

Interestingly, women are considered a higher risk for disability, and many insurance policies will charge a higher monthly rate for women than men because women are slightly more likely than men to develop a disability, and women are more likely to develop a disability that prevents them from being able to work.4 Some insurance companies do offer a unisex policy, which does not discriminate.

When choosing a policy, you want to carefully read the vendor’s definition of disability. The best definition of the term disability is going to be one that includes phrases such as “unable to perform the material and substantial duties of your [own] occupation . . . even if you are gainfully employed in another occupation.”1-3,5,6 This definition of disability is the least restrictive and would allow you to receive full benefits even if you are able to work in another capacity or occupation.1-3,5,6 The benefit period of the policy also is something to choose carefully. It is recommended to choose a benefit period that extends to at least 65 years of age.1-3,5 It is important to remember that the devil is in the details; for example, some disability insurance policies with more restrictive definitions will not pay you benefits if you are working in another capacity (eg, a physician who develops an injury that prohibits working with patients and then chooses to work in another capacity).

Some policies will only pay benefits if you become totally disabled. Shy away from these more restrictive policies; instead, look for a policy that has a liberal definition of what constitutes disability and allows you the option to add in a future purchase option rider. It is important that your policy includes a future purchase option rider, which means that as your income increases you have the option to purchase an increase in your disability coverage.1-3,5 Look for a policy that allows you to be insured without penalizing you for preexisting conditions; during residency is one of the few times some policy vendors will do it, as they assume residents are generally young and healthy.1-3,5,7

Final Thoughts

When you choose your policy, read the details carefully. Finally, remember that other physicians in the community are available as resources; they can be a wealth of information on different policies. There are many websites available to read more on this topic. Often, your training institution will offer a disability policy for the duration of your residency. Many residents choose to purchase their postresidency policies while in their third or fourth year of training. Take the time to choose a good policy now; you will be glad you did.

References
  1. Relvas M. Must-know disability insurance policy features. MR Insurance Consultants website. https://www.mr-disability-insurance.com/Policy-Information.php. Accessed January 25, 2016.
  2. Keller L. Disability insurance: what you need to know before you buy. Dermatology Resident Roundup. 2003:4-5.
  3. Dahle JM, Relvas MR. 4 critical steps in purchasing resident disability insurance. Physician’s Money Digest website. http://www.hcplive.com/physicians-money-digest/personal-finance/dahle-4-critical-steps-in-purchasing-resident-disability-insurance. Published March 22, 2014. Accessed January 25, 2016.
  4. Schneider L, Quist-Newens M. Women and the risk of disability. insights from a landmark study by the State Farm Center for women and financial services at The American College. The American College of Financial Services web site. http://womenscenter.theamericancollege.edu/uploads/documents/Women-and-the-Risk-of-Disability-Study-5-4-12-v1a.pdf. Published May 7, 2012. Accessed February 16, 2016.
  5. Hill J. Consider buying disability insurance during residency.” Medical Economics website. http://medicaleconomics.modernmedicine.com/medical-economics/news/modernmedicine/modern-medicine-now/consider-buying-disability-insurance-durin. Published August 10, 2011. Accessed January 25, 2016.
  6. Walters C. What is own occupation disability insurance? Policy Genius. https://www.policygenius.com/blog/own-occupation-disability-insurance/. Published October 20, 2014. Accessed February 12, 2016.
  7. The five big money items you should do as a resident. The White Coat Investor website. http://whitecoatinvestor.com/the-five-big-money-items-you-should-do-as-a-resident/. Published July 7, 2011. Accessed January 25, 2016.
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Dr. Brown is from the Department of Dermatology, University of California, San Diego.

The author reports no conflict of interest.

Correspondence: Megan Brown, MD, 8899 University Center Ln, Ste 350, San Diego, CA 92122 ([email protected]).

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Dr. Brown is from the Department of Dermatology, University of California, San Diego.

The author reports no conflict of interest.

Correspondence: Megan Brown, MD, 8899 University Center Ln, Ste 350, San Diego, CA 92122 ([email protected]).

Author and Disclosure Information

Dr. Brown is from the Department of Dermatology, University of California, San Diego.

The author reports no conflict of interest.

Correspondence: Megan Brown, MD, 8899 University Center Ln, Ste 350, San Diego, CA 92122 ([email protected]).

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Several older physicians have emphasized to me the importance of choosing an excellent disability insurance policy during residency. However, choosing the right policy can be a difficult task. The policy definitions are complicated, and there is a lot of fine print. To understand this confusing topic, start with answers to these 3 questions: What is my most valuable asset? When is the best point in my career to purchase disability insurance? What would I do if I were no longer able to perform the material and substantial duties of my occupation as a dermatologist?

A Resident’s Assets

In the world of disability insurance, your most valuable assets are your education and your ability to earn an income in the future.1,2 A resident’s ability to earn an income in the future reflects a massive investment of time, cost of education, and postponed accruement of wealth due to time spent in training. Any negative impact on your health (eg, back injury, vision loss, hand injury) can jeopardize these assets. Purchasing disability insurance while still in dermatology residency will protect this investment; it also will ensure that you obtain a policy while you are still healthy.1,2

Choosing a Policy

Disability insurance comes in 2 main forms: individual or group. Individual insurance may be slightly more expensive but may offer better coverage than group insurance. Group insurance often is offered through a large medical association such as the American Academy of Dermatology. Group insurance may be less expensive but often has more limits to coverage. A definite must-have in a disability insurance policy is one that has guaranteed renewal and is noncancellable.1-3

Interestingly, women are considered a higher risk for disability, and many insurance policies will charge a higher monthly rate for women than men because women are slightly more likely than men to develop a disability, and women are more likely to develop a disability that prevents them from being able to work.4 Some insurance companies do offer a unisex policy, which does not discriminate.

When choosing a policy, you want to carefully read the vendor’s definition of disability. The best definition of the term disability is going to be one that includes phrases such as “unable to perform the material and substantial duties of your [own] occupation . . . even if you are gainfully employed in another occupation.”1-3,5,6 This definition of disability is the least restrictive and would allow you to receive full benefits even if you are able to work in another capacity or occupation.1-3,5,6 The benefit period of the policy also is something to choose carefully. It is recommended to choose a benefit period that extends to at least 65 years of age.1-3,5 It is important to remember that the devil is in the details; for example, some disability insurance policies with more restrictive definitions will not pay you benefits if you are working in another capacity (eg, a physician who develops an injury that prohibits working with patients and then chooses to work in another capacity).

Some policies will only pay benefits if you become totally disabled. Shy away from these more restrictive policies; instead, look for a policy that has a liberal definition of what constitutes disability and allows you the option to add in a future purchase option rider. It is important that your policy includes a future purchase option rider, which means that as your income increases you have the option to purchase an increase in your disability coverage.1-3,5 Look for a policy that allows you to be insured without penalizing you for preexisting conditions; during residency is one of the few times some policy vendors will do it, as they assume residents are generally young and healthy.1-3,5,7

Final Thoughts

When you choose your policy, read the details carefully. Finally, remember that other physicians in the community are available as resources; they can be a wealth of information on different policies. There are many websites available to read more on this topic. Often, your training institution will offer a disability policy for the duration of your residency. Many residents choose to purchase their postresidency policies while in their third or fourth year of training. Take the time to choose a good policy now; you will be glad you did.

Several older physicians have emphasized to me the importance of choosing an excellent disability insurance policy during residency. However, choosing the right policy can be a difficult task. The policy definitions are complicated, and there is a lot of fine print. To understand this confusing topic, start with answers to these 3 questions: What is my most valuable asset? When is the best point in my career to purchase disability insurance? What would I do if I were no longer able to perform the material and substantial duties of my occupation as a dermatologist?

A Resident’s Assets

In the world of disability insurance, your most valuable assets are your education and your ability to earn an income in the future.1,2 A resident’s ability to earn an income in the future reflects a massive investment of time, cost of education, and postponed accruement of wealth due to time spent in training. Any negative impact on your health (eg, back injury, vision loss, hand injury) can jeopardize these assets. Purchasing disability insurance while still in dermatology residency will protect this investment; it also will ensure that you obtain a policy while you are still healthy.1,2

Choosing a Policy

Disability insurance comes in 2 main forms: individual or group. Individual insurance may be slightly more expensive but may offer better coverage than group insurance. Group insurance often is offered through a large medical association such as the American Academy of Dermatology. Group insurance may be less expensive but often has more limits to coverage. A definite must-have in a disability insurance policy is one that has guaranteed renewal and is noncancellable.1-3

Interestingly, women are considered a higher risk for disability, and many insurance policies will charge a higher monthly rate for women than men because women are slightly more likely than men to develop a disability, and women are more likely to develop a disability that prevents them from being able to work.4 Some insurance companies do offer a unisex policy, which does not discriminate.

When choosing a policy, you want to carefully read the vendor’s definition of disability. The best definition of the term disability is going to be one that includes phrases such as “unable to perform the material and substantial duties of your [own] occupation . . . even if you are gainfully employed in another occupation.”1-3,5,6 This definition of disability is the least restrictive and would allow you to receive full benefits even if you are able to work in another capacity or occupation.1-3,5,6 The benefit period of the policy also is something to choose carefully. It is recommended to choose a benefit period that extends to at least 65 years of age.1-3,5 It is important to remember that the devil is in the details; for example, some disability insurance policies with more restrictive definitions will not pay you benefits if you are working in another capacity (eg, a physician who develops an injury that prohibits working with patients and then chooses to work in another capacity).

Some policies will only pay benefits if you become totally disabled. Shy away from these more restrictive policies; instead, look for a policy that has a liberal definition of what constitutes disability and allows you the option to add in a future purchase option rider. It is important that your policy includes a future purchase option rider, which means that as your income increases you have the option to purchase an increase in your disability coverage.1-3,5 Look for a policy that allows you to be insured without penalizing you for preexisting conditions; during residency is one of the few times some policy vendors will do it, as they assume residents are generally young and healthy.1-3,5,7

Final Thoughts

When you choose your policy, read the details carefully. Finally, remember that other physicians in the community are available as resources; they can be a wealth of information on different policies. There are many websites available to read more on this topic. Often, your training institution will offer a disability policy for the duration of your residency. Many residents choose to purchase their postresidency policies while in their third or fourth year of training. Take the time to choose a good policy now; you will be glad you did.

References
  1. Relvas M. Must-know disability insurance policy features. MR Insurance Consultants website. https://www.mr-disability-insurance.com/Policy-Information.php. Accessed January 25, 2016.
  2. Keller L. Disability insurance: what you need to know before you buy. Dermatology Resident Roundup. 2003:4-5.
  3. Dahle JM, Relvas MR. 4 critical steps in purchasing resident disability insurance. Physician’s Money Digest website. http://www.hcplive.com/physicians-money-digest/personal-finance/dahle-4-critical-steps-in-purchasing-resident-disability-insurance. Published March 22, 2014. Accessed January 25, 2016.
  4. Schneider L, Quist-Newens M. Women and the risk of disability. insights from a landmark study by the State Farm Center for women and financial services at The American College. The American College of Financial Services web site. http://womenscenter.theamericancollege.edu/uploads/documents/Women-and-the-Risk-of-Disability-Study-5-4-12-v1a.pdf. Published May 7, 2012. Accessed February 16, 2016.
  5. Hill J. Consider buying disability insurance during residency.” Medical Economics website. http://medicaleconomics.modernmedicine.com/medical-economics/news/modernmedicine/modern-medicine-now/consider-buying-disability-insurance-durin. Published August 10, 2011. Accessed January 25, 2016.
  6. Walters C. What is own occupation disability insurance? Policy Genius. https://www.policygenius.com/blog/own-occupation-disability-insurance/. Published October 20, 2014. Accessed February 12, 2016.
  7. The five big money items you should do as a resident. The White Coat Investor website. http://whitecoatinvestor.com/the-five-big-money-items-you-should-do-as-a-resident/. Published July 7, 2011. Accessed January 25, 2016.
References
  1. Relvas M. Must-know disability insurance policy features. MR Insurance Consultants website. https://www.mr-disability-insurance.com/Policy-Information.php. Accessed January 25, 2016.
  2. Keller L. Disability insurance: what you need to know before you buy. Dermatology Resident Roundup. 2003:4-5.
  3. Dahle JM, Relvas MR. 4 critical steps in purchasing resident disability insurance. Physician’s Money Digest website. http://www.hcplive.com/physicians-money-digest/personal-finance/dahle-4-critical-steps-in-purchasing-resident-disability-insurance. Published March 22, 2014. Accessed January 25, 2016.
  4. Schneider L, Quist-Newens M. Women and the risk of disability. insights from a landmark study by the State Farm Center for women and financial services at The American College. The American College of Financial Services web site. http://womenscenter.theamericancollege.edu/uploads/documents/Women-and-the-Risk-of-Disability-Study-5-4-12-v1a.pdf. Published May 7, 2012. Accessed February 16, 2016.
  5. Hill J. Consider buying disability insurance during residency.” Medical Economics website. http://medicaleconomics.modernmedicine.com/medical-economics/news/modernmedicine/modern-medicine-now/consider-buying-disability-insurance-durin. Published August 10, 2011. Accessed January 25, 2016.
  6. Walters C. What is own occupation disability insurance? Policy Genius. https://www.policygenius.com/blog/own-occupation-disability-insurance/. Published October 20, 2014. Accessed February 12, 2016.
  7. The five big money items you should do as a resident. The White Coat Investor website. http://whitecoatinvestor.com/the-five-big-money-items-you-should-do-as-a-resident/. Published July 7, 2011. Accessed January 25, 2016.
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Postinflammatory Hyperpigmentation in Patients With Skin of Color

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Postinflammatory hyperpigmentation (PIH) develops as darkly pigmented macules that occur after an inflammatory process of the skin such as acne, folliculitis, eczema, or shaving irritation. Patients with Fitzpatrick skin types III to VI usually are most commonly affected, and for many, the remnant pigmentation can be an even greater concern than the original inflammatory process.1,2 Reported treatments of PIH include tretinoin, hydroquinone, azelaic acid, and chemical peels. The ideal combination of therapy has yet to be delineated.

Tretinoin (Vitamin A Derivative)

Bulengo-Ransby et al3 performed one of the first clinical trials testing tretinoin cream 0.1% for PIH in patients with Fitzpatrick skin types IV to VI . The study included 54 patients (24 applied tretinoin and 30 applied a vehicle) with moderate to severe PIH on the face and arms. The patients were divided into therapy and placebo groups and were evaluated for 40 weeks. Changes were evaluated through colorimetry, light microscopy, histology, and photography, with significant clinical improvement in the tretinoin-treated group (P<.001).3 A double-blind, randomized study of 45 photoaged Chinese and Japanese patients using tretinoin cream 0.1% also was conducted for treatment of photoaging-associated hyperpigmented lesions of the face and hands. Assessment was done with clinical, colorimetric, and histological evaluation, with an overall statistical improvement noted in hyperpigmentation.4 Both of the above studies showed mild irritation (ie, retinoid dermatitis) with application of tretinoin, which creates a compliance issue in patients who are recommended to continue therapy with higher-strength tretinoin. This side-effect profile can be circumvented through gradual elevation in the strength of tretinoin.5

Combination Therapies

Combination therapies with tretinoin also have been used to improve PIH. Callender et al6 conducted a study evaluating the efficacy of clindamycin phosphate 1.2%–tretinoin 0.025% gel for the treatment of PIH secondary to mild to moderate acne in patients with Fitzpatrick skin types IV to VI. Thirty patients participated in the randomized, double-blinded, placebo-controlled study, with 15 patients in the clindamycin-tretinoin gel group and 15 in the placebo control group. Based on objective assessment using a chromameter and evaluator global acne severity scale score, clinical efficacy was demonstrated for treating acne and PIH as well as preventing further PIH.6

Hydroquinone Formulation (Tyrosine Inhibitor)

Hydroquinone bleaching cream has been the standard therapy for hyperpigmentation. It works by blocking the conversion of dihydroxyphenylalanine to melanin by inhibiting tyrosinase.7 Topical steroids directly inhibit the synthesis of melanin, and when combined with hydroquinone and tretinoin, they can be effective for short periods of time and may decrease the irritation of application.7,8 The most widely accepted formula consists of a topical steroid (triamcinolone cream 0.1%) in combination with hydroquinone 4% and tretinoin cream 0.05%.8 In a similar 12-week open-label study of 25 patients with darker skin types, Grimes9 used an alternative combination formula of hydroquinone 4% and retinol 0.15%. Overall improvement and tolerance was demonstrated through the use of colorimetry measurement. A combination of hydroquinone 4%, tretinoin 0.05%, and fluocinolone acetonide 0.01% also has been used effectively for the treatment of melasma.10 This formulation has been used more anecdotally for the treatment of PIH and has yet to have a randomized-controlled trial. The concern with repeated long-term use of hydroquinone remains. Permanent leukoderma, exogenous ochronosis, and hyperpigmentation of the surrounding normal skin (halo effect) can occur.

Azelaic Acid (Tyrosinase Inhibitor)

Azelaic acid is a dicarboxylic acid isolated from pityriasis versicolor that acts similar to a tyrosine inhibitor and has an antiproliferative effect toward abnormal melanocytes. Lowe et al11 conducted a randomized, double-blind, vehicle-controlled trial in patients with Fitzpatrick skin types IV through VI with facial hyperpigmentation using azelaic acid cream 20%. Over the course of 24 weeks, patients noted a decrease in overall pigment using both an investigator subjective scale and chromometer analysis.11

Kojic Acid (Tyrosinase Inhibitor)

Kojic acid is a tyrosinase inhibitor found in fungal metabolite species such as Acetobacter, Aspergillus, and Penicillium. It is commonly combined with other skin lightening agents such as hydroquinone or vitamin C to further enhance its efficacy. A randomized, 12-week, split-face study of Chinese women with melasma compared treatment with a glycolic acid 10%–hydroquinone 2% gel versus the combination plus kojic acid 2%. The results showed that 60% (24/40) of patients improved with the use of kojic acid as compared to those using the medication without kojic acid.12 Anecdotal data suggest kojic acid may be effective for PIH13; however, no studies specifically for PIH have been conducted.

 

 

Chemical Peels

Chemical peels have been used for a number of years, though their benefits in patients with skin of color is still being elucidated. The ideal chemical peels for Fitzpatrick skin types IV through VI are superficial to medium-depth peeling agents and techniques.14 Glycolic acid is a naturally occurring α-hydroxy acid that causes an increase in collagen synthesis, stimulates epidermolysis, and disperses basal layer melanin. Neutralization of glycolic acid peels can be done with the use of water, sodium bicarbonate, or sodium hydroxide to avoid unnecessary epidermal damage. Multiple clinical trials have been conducted to determine the response of glycolic acid peels in clearing PIH in patients with skin of color. Kessler et al15 compared glycolic acid 30% to salicylic acid 30% in 20 patients with mild to moderate acne and associated PIH. Chemical peels were performed every 2 weeks for 12 weeks. The study showed that salicylic acid was better tolerated than glycolic acid and both were equally effective after the second application (P<.05) for PIH.15 Finally, another study conducted for PIH in patients with Fitzpatrick skin types III and IV utilized glycolic acid peels with 20%, 35%, and 70% concentrations. The results showed overall improvement of PIH and acne from the use of all concentrations of glycolic peels, though faster efficacy was noted at higher concentrations.16

Other self-neutralizing peeling agents include salicylic acid and Jessner solution. Salicylic acid is a β-hydroxy acid that works through keratolysis and disrupting intercellular linkages. Jessner solution is a combination of resorcinol 14%, lactic acid 14%, and salicylic acid 14% in an alcohol base. Salicylic acid is well-tolerated in patients with Fitzpatrick skin types I through VI and has been helpful in treating acne, rosacea, melasma, hyperpigmentation, texturally rough skin, and mild photoaging. Jessner peeling solution has been used for a number of years and works as a keratolytic agent causing intercellular and intracellular edema, and due to its self-neutralizing agent, it is fairly superficial.17 Overall, superficial peeling agents should be used on patients with darker skin types to avoid the risk for worsening dyspigmentation, keloid formation, or deep scarring.18

Conclusion

These treatments are only some of the topical and chemical modalities for PIH in patients with skin of color. The patient history, evaluation, skin type, and underlying medical problems should be considered prior to using any topical or peeling agent. Lastly, photoprotection should be heavily emphasized with both sun protective gear and use of broad-spectrum sunscreens with a high sun protection factor, as UV radiation can cause darkening of PIH areas regardless of skin type and can reverse the progress made by a given therapy.18

References
  1. Savory SA, Agim NG, Mao R, et al. Reliability assessment and validation of the postacne hyperpigmentation index (PAHPI), a new instrument to measure postinflammatory hyperpigmentation from acne vulgaris. J Am Acad Dermatol. 2014;70:108-114.
  2. Halder RM. The role of retinoids in the management of cutaneous conditions in blacks. J Am Acad Dermatol. 1998;39(2, pt 3):S98-S103.
  3. Bulengo-Ransby SM, Griffiths CE, Kimbrough-Green CK, et al. Topical tretinoin (retinoid acid) therapy for hyperpigmented lesions caused by inflammation of the skin in black patients. N Engl J Med. 1993;328:1438-1443.
  4. Griffiths CE, Goldfarb MT, Finkel LJ, et al. Topical tretinoin (retinoic acid) treatment of hyperpigmented lesions associated with photoaging in Chinese and Japanese patients: a vehicle-controlled trial. J Am Acad Dermatol. 1994;30:76-84.
  5. Callendar VD. Acne in ethnic skin: special considerations for therapy. Dermatol Ther. 2004;17:184-195.
  6. Callender VD, Young CM, Kindred C, et al. Efficacy and safety of clindamycin phosphate 1.2% and tretinoin 0.025% gel for the treatment of acne and acne-induced post-inflammatory hyperpigmentation in patients with skin of color. J Clin Aesthet Dermatol. 2012;5:25-32.
  7. Badreshia-Bansal S, Draelos ZD. Insight into skin lightening cosmeceuticals for women of color. J Drugs Dermatol. 2007;6:32-39.
  8. Kligman AM, Willis I. A new formula for depigmenting human skin. Arch Dermatol. 1975;111:40-48.
  9. Grimes PE. A microsponge formulation of hydroquinone 4% and retinol 0.15% in the treatment of melasma and postinflammatory hyperpigmentation. Cutis. 2004;74:326-328.
  10. Chan R, Park KC, Lee MH, et al. A randomized controlled trial of the efficacy and safety of a fixed triple combination (fluocinolone acetonide 0.01%, hydroquinone 4%, tretinoin 0.05%) compared with hydroquinone 4% cream in Asian patients with moderate to severe melasma. Br J Dermatol. 2008;159:697-703.
  11. Lowe NJ, Rizk D, Grimes P. Azelaic acid 20% cream in the treatment of facial hyperpigmentation in darker-skinned patients. Clin Ther. 1998;20:945-959.
  12. Lim JT. Treatment of melasma using kojic acid in a gel containing hydroquinone and glycolic acid. Dermatol Surg. 1999;25:282-284.
  13. Alexis AF, Blackcloud P. Natural ingredients for darker skin types: growing options for hyperpigmentation. J Drugs Dermatol. 2013;12:123-127.
  14. Roberts WE. Chemical peeling in ethnic/dark skin. Dermatol Ther. 2004;17:196-205.
  15. Kessler E, Flanagan K, Chia C, et al. Comparison of alpha- and beta-hydroxy acid chemical peels in the treatment of mild to moderately severe facial acne vulgaris [published online December 5, 2007]. Dermatol Surg. 2008;34:45-50, discussion 51.
  16. Erbağci Z, Akçali C. Biweekly serial glycolic acid peels vs. long-term daily use of topical low-strength glycolic acid in the treatment of atrophic acne scars. Int J Dermatol. 2000;39:789-794.
  17. Jackson A. Chemical peels [published online January 31, 2014]. Facial Plast Surg. 2014;30:26-34.
  18. Davis EC, Callender VD. Postinflammatory hyperpigmentation: a review of the epidemiology, clinical features, and treatment options in skin of color. J Clin Aesthet Dermatol. 2010;3:20-31.
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From the Department of Dermatology, University of Florida, Gainesville.

The author reports no conflict of interest.

Correspondence: Divya Shokeen, MD ([email protected]).

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From the Department of Dermatology, University of Florida, Gainesville.

The author reports no conflict of interest.

Correspondence: Divya Shokeen, MD ([email protected]).

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From the Department of Dermatology, University of Florida, Gainesville.

The author reports no conflict of interest.

Correspondence: Divya Shokeen, MD ([email protected]).

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Related Articles

Postinflammatory hyperpigmentation (PIH) develops as darkly pigmented macules that occur after an inflammatory process of the skin such as acne, folliculitis, eczema, or shaving irritation. Patients with Fitzpatrick skin types III to VI usually are most commonly affected, and for many, the remnant pigmentation can be an even greater concern than the original inflammatory process.1,2 Reported treatments of PIH include tretinoin, hydroquinone, azelaic acid, and chemical peels. The ideal combination of therapy has yet to be delineated.

Tretinoin (Vitamin A Derivative)

Bulengo-Ransby et al3 performed one of the first clinical trials testing tretinoin cream 0.1% for PIH in patients with Fitzpatrick skin types IV to VI . The study included 54 patients (24 applied tretinoin and 30 applied a vehicle) with moderate to severe PIH on the face and arms. The patients were divided into therapy and placebo groups and were evaluated for 40 weeks. Changes were evaluated through colorimetry, light microscopy, histology, and photography, with significant clinical improvement in the tretinoin-treated group (P<.001).3 A double-blind, randomized study of 45 photoaged Chinese and Japanese patients using tretinoin cream 0.1% also was conducted for treatment of photoaging-associated hyperpigmented lesions of the face and hands. Assessment was done with clinical, colorimetric, and histological evaluation, with an overall statistical improvement noted in hyperpigmentation.4 Both of the above studies showed mild irritation (ie, retinoid dermatitis) with application of tretinoin, which creates a compliance issue in patients who are recommended to continue therapy with higher-strength tretinoin. This side-effect profile can be circumvented through gradual elevation in the strength of tretinoin.5

Combination Therapies

Combination therapies with tretinoin also have been used to improve PIH. Callender et al6 conducted a study evaluating the efficacy of clindamycin phosphate 1.2%–tretinoin 0.025% gel for the treatment of PIH secondary to mild to moderate acne in patients with Fitzpatrick skin types IV to VI. Thirty patients participated in the randomized, double-blinded, placebo-controlled study, with 15 patients in the clindamycin-tretinoin gel group and 15 in the placebo control group. Based on objective assessment using a chromameter and evaluator global acne severity scale score, clinical efficacy was demonstrated for treating acne and PIH as well as preventing further PIH.6

Hydroquinone Formulation (Tyrosine Inhibitor)

Hydroquinone bleaching cream has been the standard therapy for hyperpigmentation. It works by blocking the conversion of dihydroxyphenylalanine to melanin by inhibiting tyrosinase.7 Topical steroids directly inhibit the synthesis of melanin, and when combined with hydroquinone and tretinoin, they can be effective for short periods of time and may decrease the irritation of application.7,8 The most widely accepted formula consists of a topical steroid (triamcinolone cream 0.1%) in combination with hydroquinone 4% and tretinoin cream 0.05%.8 In a similar 12-week open-label study of 25 patients with darker skin types, Grimes9 used an alternative combination formula of hydroquinone 4% and retinol 0.15%. Overall improvement and tolerance was demonstrated through the use of colorimetry measurement. A combination of hydroquinone 4%, tretinoin 0.05%, and fluocinolone acetonide 0.01% also has been used effectively for the treatment of melasma.10 This formulation has been used more anecdotally for the treatment of PIH and has yet to have a randomized-controlled trial. The concern with repeated long-term use of hydroquinone remains. Permanent leukoderma, exogenous ochronosis, and hyperpigmentation of the surrounding normal skin (halo effect) can occur.

Azelaic Acid (Tyrosinase Inhibitor)

Azelaic acid is a dicarboxylic acid isolated from pityriasis versicolor that acts similar to a tyrosine inhibitor and has an antiproliferative effect toward abnormal melanocytes. Lowe et al11 conducted a randomized, double-blind, vehicle-controlled trial in patients with Fitzpatrick skin types IV through VI with facial hyperpigmentation using azelaic acid cream 20%. Over the course of 24 weeks, patients noted a decrease in overall pigment using both an investigator subjective scale and chromometer analysis.11

Kojic Acid (Tyrosinase Inhibitor)

Kojic acid is a tyrosinase inhibitor found in fungal metabolite species such as Acetobacter, Aspergillus, and Penicillium. It is commonly combined with other skin lightening agents such as hydroquinone or vitamin C to further enhance its efficacy. A randomized, 12-week, split-face study of Chinese women with melasma compared treatment with a glycolic acid 10%–hydroquinone 2% gel versus the combination plus kojic acid 2%. The results showed that 60% (24/40) of patients improved with the use of kojic acid as compared to those using the medication without kojic acid.12 Anecdotal data suggest kojic acid may be effective for PIH13; however, no studies specifically for PIH have been conducted.

 

 

Chemical Peels

Chemical peels have been used for a number of years, though their benefits in patients with skin of color is still being elucidated. The ideal chemical peels for Fitzpatrick skin types IV through VI are superficial to medium-depth peeling agents and techniques.14 Glycolic acid is a naturally occurring α-hydroxy acid that causes an increase in collagen synthesis, stimulates epidermolysis, and disperses basal layer melanin. Neutralization of glycolic acid peels can be done with the use of water, sodium bicarbonate, or sodium hydroxide to avoid unnecessary epidermal damage. Multiple clinical trials have been conducted to determine the response of glycolic acid peels in clearing PIH in patients with skin of color. Kessler et al15 compared glycolic acid 30% to salicylic acid 30% in 20 patients with mild to moderate acne and associated PIH. Chemical peels were performed every 2 weeks for 12 weeks. The study showed that salicylic acid was better tolerated than glycolic acid and both were equally effective after the second application (P<.05) for PIH.15 Finally, another study conducted for PIH in patients with Fitzpatrick skin types III and IV utilized glycolic acid peels with 20%, 35%, and 70% concentrations. The results showed overall improvement of PIH and acne from the use of all concentrations of glycolic peels, though faster efficacy was noted at higher concentrations.16

Other self-neutralizing peeling agents include salicylic acid and Jessner solution. Salicylic acid is a β-hydroxy acid that works through keratolysis and disrupting intercellular linkages. Jessner solution is a combination of resorcinol 14%, lactic acid 14%, and salicylic acid 14% in an alcohol base. Salicylic acid is well-tolerated in patients with Fitzpatrick skin types I through VI and has been helpful in treating acne, rosacea, melasma, hyperpigmentation, texturally rough skin, and mild photoaging. Jessner peeling solution has been used for a number of years and works as a keratolytic agent causing intercellular and intracellular edema, and due to its self-neutralizing agent, it is fairly superficial.17 Overall, superficial peeling agents should be used on patients with darker skin types to avoid the risk for worsening dyspigmentation, keloid formation, or deep scarring.18

Conclusion

These treatments are only some of the topical and chemical modalities for PIH in patients with skin of color. The patient history, evaluation, skin type, and underlying medical problems should be considered prior to using any topical or peeling agent. Lastly, photoprotection should be heavily emphasized with both sun protective gear and use of broad-spectrum sunscreens with a high sun protection factor, as UV radiation can cause darkening of PIH areas regardless of skin type and can reverse the progress made by a given therapy.18

Postinflammatory hyperpigmentation (PIH) develops as darkly pigmented macules that occur after an inflammatory process of the skin such as acne, folliculitis, eczema, or shaving irritation. Patients with Fitzpatrick skin types III to VI usually are most commonly affected, and for many, the remnant pigmentation can be an even greater concern than the original inflammatory process.1,2 Reported treatments of PIH include tretinoin, hydroquinone, azelaic acid, and chemical peels. The ideal combination of therapy has yet to be delineated.

Tretinoin (Vitamin A Derivative)

Bulengo-Ransby et al3 performed one of the first clinical trials testing tretinoin cream 0.1% for PIH in patients with Fitzpatrick skin types IV to VI . The study included 54 patients (24 applied tretinoin and 30 applied a vehicle) with moderate to severe PIH on the face and arms. The patients were divided into therapy and placebo groups and were evaluated for 40 weeks. Changes were evaluated through colorimetry, light microscopy, histology, and photography, with significant clinical improvement in the tretinoin-treated group (P<.001).3 A double-blind, randomized study of 45 photoaged Chinese and Japanese patients using tretinoin cream 0.1% also was conducted for treatment of photoaging-associated hyperpigmented lesions of the face and hands. Assessment was done with clinical, colorimetric, and histological evaluation, with an overall statistical improvement noted in hyperpigmentation.4 Both of the above studies showed mild irritation (ie, retinoid dermatitis) with application of tretinoin, which creates a compliance issue in patients who are recommended to continue therapy with higher-strength tretinoin. This side-effect profile can be circumvented through gradual elevation in the strength of tretinoin.5

Combination Therapies

Combination therapies with tretinoin also have been used to improve PIH. Callender et al6 conducted a study evaluating the efficacy of clindamycin phosphate 1.2%–tretinoin 0.025% gel for the treatment of PIH secondary to mild to moderate acne in patients with Fitzpatrick skin types IV to VI. Thirty patients participated in the randomized, double-blinded, placebo-controlled study, with 15 patients in the clindamycin-tretinoin gel group and 15 in the placebo control group. Based on objective assessment using a chromameter and evaluator global acne severity scale score, clinical efficacy was demonstrated for treating acne and PIH as well as preventing further PIH.6

Hydroquinone Formulation (Tyrosine Inhibitor)

Hydroquinone bleaching cream has been the standard therapy for hyperpigmentation. It works by blocking the conversion of dihydroxyphenylalanine to melanin by inhibiting tyrosinase.7 Topical steroids directly inhibit the synthesis of melanin, and when combined with hydroquinone and tretinoin, they can be effective for short periods of time and may decrease the irritation of application.7,8 The most widely accepted formula consists of a topical steroid (triamcinolone cream 0.1%) in combination with hydroquinone 4% and tretinoin cream 0.05%.8 In a similar 12-week open-label study of 25 patients with darker skin types, Grimes9 used an alternative combination formula of hydroquinone 4% and retinol 0.15%. Overall improvement and tolerance was demonstrated through the use of colorimetry measurement. A combination of hydroquinone 4%, tretinoin 0.05%, and fluocinolone acetonide 0.01% also has been used effectively for the treatment of melasma.10 This formulation has been used more anecdotally for the treatment of PIH and has yet to have a randomized-controlled trial. The concern with repeated long-term use of hydroquinone remains. Permanent leukoderma, exogenous ochronosis, and hyperpigmentation of the surrounding normal skin (halo effect) can occur.

Azelaic Acid (Tyrosinase Inhibitor)

Azelaic acid is a dicarboxylic acid isolated from pityriasis versicolor that acts similar to a tyrosine inhibitor and has an antiproliferative effect toward abnormal melanocytes. Lowe et al11 conducted a randomized, double-blind, vehicle-controlled trial in patients with Fitzpatrick skin types IV through VI with facial hyperpigmentation using azelaic acid cream 20%. Over the course of 24 weeks, patients noted a decrease in overall pigment using both an investigator subjective scale and chromometer analysis.11

Kojic Acid (Tyrosinase Inhibitor)

Kojic acid is a tyrosinase inhibitor found in fungal metabolite species such as Acetobacter, Aspergillus, and Penicillium. It is commonly combined with other skin lightening agents such as hydroquinone or vitamin C to further enhance its efficacy. A randomized, 12-week, split-face study of Chinese women with melasma compared treatment with a glycolic acid 10%–hydroquinone 2% gel versus the combination plus kojic acid 2%. The results showed that 60% (24/40) of patients improved with the use of kojic acid as compared to those using the medication without kojic acid.12 Anecdotal data suggest kojic acid may be effective for PIH13; however, no studies specifically for PIH have been conducted.

 

 

Chemical Peels

Chemical peels have been used for a number of years, though their benefits in patients with skin of color is still being elucidated. The ideal chemical peels for Fitzpatrick skin types IV through VI are superficial to medium-depth peeling agents and techniques.14 Glycolic acid is a naturally occurring α-hydroxy acid that causes an increase in collagen synthesis, stimulates epidermolysis, and disperses basal layer melanin. Neutralization of glycolic acid peels can be done with the use of water, sodium bicarbonate, or sodium hydroxide to avoid unnecessary epidermal damage. Multiple clinical trials have been conducted to determine the response of glycolic acid peels in clearing PIH in patients with skin of color. Kessler et al15 compared glycolic acid 30% to salicylic acid 30% in 20 patients with mild to moderate acne and associated PIH. Chemical peels were performed every 2 weeks for 12 weeks. The study showed that salicylic acid was better tolerated than glycolic acid and both were equally effective after the second application (P<.05) for PIH.15 Finally, another study conducted for PIH in patients with Fitzpatrick skin types III and IV utilized glycolic acid peels with 20%, 35%, and 70% concentrations. The results showed overall improvement of PIH and acne from the use of all concentrations of glycolic peels, though faster efficacy was noted at higher concentrations.16

Other self-neutralizing peeling agents include salicylic acid and Jessner solution. Salicylic acid is a β-hydroxy acid that works through keratolysis and disrupting intercellular linkages. Jessner solution is a combination of resorcinol 14%, lactic acid 14%, and salicylic acid 14% in an alcohol base. Salicylic acid is well-tolerated in patients with Fitzpatrick skin types I through VI and has been helpful in treating acne, rosacea, melasma, hyperpigmentation, texturally rough skin, and mild photoaging. Jessner peeling solution has been used for a number of years and works as a keratolytic agent causing intercellular and intracellular edema, and due to its self-neutralizing agent, it is fairly superficial.17 Overall, superficial peeling agents should be used on patients with darker skin types to avoid the risk for worsening dyspigmentation, keloid formation, or deep scarring.18

Conclusion

These treatments are only some of the topical and chemical modalities for PIH in patients with skin of color. The patient history, evaluation, skin type, and underlying medical problems should be considered prior to using any topical or peeling agent. Lastly, photoprotection should be heavily emphasized with both sun protective gear and use of broad-spectrum sunscreens with a high sun protection factor, as UV radiation can cause darkening of PIH areas regardless of skin type and can reverse the progress made by a given therapy.18

References
  1. Savory SA, Agim NG, Mao R, et al. Reliability assessment and validation of the postacne hyperpigmentation index (PAHPI), a new instrument to measure postinflammatory hyperpigmentation from acne vulgaris. J Am Acad Dermatol. 2014;70:108-114.
  2. Halder RM. The role of retinoids in the management of cutaneous conditions in blacks. J Am Acad Dermatol. 1998;39(2, pt 3):S98-S103.
  3. Bulengo-Ransby SM, Griffiths CE, Kimbrough-Green CK, et al. Topical tretinoin (retinoid acid) therapy for hyperpigmented lesions caused by inflammation of the skin in black patients. N Engl J Med. 1993;328:1438-1443.
  4. Griffiths CE, Goldfarb MT, Finkel LJ, et al. Topical tretinoin (retinoic acid) treatment of hyperpigmented lesions associated with photoaging in Chinese and Japanese patients: a vehicle-controlled trial. J Am Acad Dermatol. 1994;30:76-84.
  5. Callendar VD. Acne in ethnic skin: special considerations for therapy. Dermatol Ther. 2004;17:184-195.
  6. Callender VD, Young CM, Kindred C, et al. Efficacy and safety of clindamycin phosphate 1.2% and tretinoin 0.025% gel for the treatment of acne and acne-induced post-inflammatory hyperpigmentation in patients with skin of color. J Clin Aesthet Dermatol. 2012;5:25-32.
  7. Badreshia-Bansal S, Draelos ZD. Insight into skin lightening cosmeceuticals for women of color. J Drugs Dermatol. 2007;6:32-39.
  8. Kligman AM, Willis I. A new formula for depigmenting human skin. Arch Dermatol. 1975;111:40-48.
  9. Grimes PE. A microsponge formulation of hydroquinone 4% and retinol 0.15% in the treatment of melasma and postinflammatory hyperpigmentation. Cutis. 2004;74:326-328.
  10. Chan R, Park KC, Lee MH, et al. A randomized controlled trial of the efficacy and safety of a fixed triple combination (fluocinolone acetonide 0.01%, hydroquinone 4%, tretinoin 0.05%) compared with hydroquinone 4% cream in Asian patients with moderate to severe melasma. Br J Dermatol. 2008;159:697-703.
  11. Lowe NJ, Rizk D, Grimes P. Azelaic acid 20% cream in the treatment of facial hyperpigmentation in darker-skinned patients. Clin Ther. 1998;20:945-959.
  12. Lim JT. Treatment of melasma using kojic acid in a gel containing hydroquinone and glycolic acid. Dermatol Surg. 1999;25:282-284.
  13. Alexis AF, Blackcloud P. Natural ingredients for darker skin types: growing options for hyperpigmentation. J Drugs Dermatol. 2013;12:123-127.
  14. Roberts WE. Chemical peeling in ethnic/dark skin. Dermatol Ther. 2004;17:196-205.
  15. Kessler E, Flanagan K, Chia C, et al. Comparison of alpha- and beta-hydroxy acid chemical peels in the treatment of mild to moderately severe facial acne vulgaris [published online December 5, 2007]. Dermatol Surg. 2008;34:45-50, discussion 51.
  16. Erbağci Z, Akçali C. Biweekly serial glycolic acid peels vs. long-term daily use of topical low-strength glycolic acid in the treatment of atrophic acne scars. Int J Dermatol. 2000;39:789-794.
  17. Jackson A. Chemical peels [published online January 31, 2014]. Facial Plast Surg. 2014;30:26-34.
  18. Davis EC, Callender VD. Postinflammatory hyperpigmentation: a review of the epidemiology, clinical features, and treatment options in skin of color. J Clin Aesthet Dermatol. 2010;3:20-31.
References
  1. Savory SA, Agim NG, Mao R, et al. Reliability assessment and validation of the postacne hyperpigmentation index (PAHPI), a new instrument to measure postinflammatory hyperpigmentation from acne vulgaris. J Am Acad Dermatol. 2014;70:108-114.
  2. Halder RM. The role of retinoids in the management of cutaneous conditions in blacks. J Am Acad Dermatol. 1998;39(2, pt 3):S98-S103.
  3. Bulengo-Ransby SM, Griffiths CE, Kimbrough-Green CK, et al. Topical tretinoin (retinoid acid) therapy for hyperpigmented lesions caused by inflammation of the skin in black patients. N Engl J Med. 1993;328:1438-1443.
  4. Griffiths CE, Goldfarb MT, Finkel LJ, et al. Topical tretinoin (retinoic acid) treatment of hyperpigmented lesions associated with photoaging in Chinese and Japanese patients: a vehicle-controlled trial. J Am Acad Dermatol. 1994;30:76-84.
  5. Callendar VD. Acne in ethnic skin: special considerations for therapy. Dermatol Ther. 2004;17:184-195.
  6. Callender VD, Young CM, Kindred C, et al. Efficacy and safety of clindamycin phosphate 1.2% and tretinoin 0.025% gel for the treatment of acne and acne-induced post-inflammatory hyperpigmentation in patients with skin of color. J Clin Aesthet Dermatol. 2012;5:25-32.
  7. Badreshia-Bansal S, Draelos ZD. Insight into skin lightening cosmeceuticals for women of color. J Drugs Dermatol. 2007;6:32-39.
  8. Kligman AM, Willis I. A new formula for depigmenting human skin. Arch Dermatol. 1975;111:40-48.
  9. Grimes PE. A microsponge formulation of hydroquinone 4% and retinol 0.15% in the treatment of melasma and postinflammatory hyperpigmentation. Cutis. 2004;74:326-328.
  10. Chan R, Park KC, Lee MH, et al. A randomized controlled trial of the efficacy and safety of a fixed triple combination (fluocinolone acetonide 0.01%, hydroquinone 4%, tretinoin 0.05%) compared with hydroquinone 4% cream in Asian patients with moderate to severe melasma. Br J Dermatol. 2008;159:697-703.
  11. Lowe NJ, Rizk D, Grimes P. Azelaic acid 20% cream in the treatment of facial hyperpigmentation in darker-skinned patients. Clin Ther. 1998;20:945-959.
  12. Lim JT. Treatment of melasma using kojic acid in a gel containing hydroquinone and glycolic acid. Dermatol Surg. 1999;25:282-284.
  13. Alexis AF, Blackcloud P. Natural ingredients for darker skin types: growing options for hyperpigmentation. J Drugs Dermatol. 2013;12:123-127.
  14. Roberts WE. Chemical peeling in ethnic/dark skin. Dermatol Ther. 2004;17:196-205.
  15. Kessler E, Flanagan K, Chia C, et al. Comparison of alpha- and beta-hydroxy acid chemical peels in the treatment of mild to moderately severe facial acne vulgaris [published online December 5, 2007]. Dermatol Surg. 2008;34:45-50, discussion 51.
  16. Erbağci Z, Akçali C. Biweekly serial glycolic acid peels vs. long-term daily use of topical low-strength glycolic acid in the treatment of atrophic acne scars. Int J Dermatol. 2000;39:789-794.
  17. Jackson A. Chemical peels [published online January 31, 2014]. Facial Plast Surg. 2014;30:26-34.
  18. Davis EC, Callender VD. Postinflammatory hyperpigmentation: a review of the epidemiology, clinical features, and treatment options in skin of color. J Clin Aesthet Dermatol. 2010;3:20-31.
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Good medical care for psychiatric patients is imperative

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The first year of residency came faster than I had expected and concluded just as quickly. At times, it felt like medical school, with different rotations, adjusting to newly formed teams, dealing with the pressures of getting the right diagnosis and treatment, managing the unrelenting speed of rounds, and trying to make a difference for the better. I must be honest – there were times when I was counting down the days for the rotation to end so that I could begin focusing and working directly in the mental health field.

Now, in my second year, the pace has improved, and the rotations resemble the work and patient population that I chose during the match process. Nonetheless, I am thankful for the time spent and the knowledge gained during my intern year, because it is only now that I understand the true value of my first-year experiences and the need to continue getting a well-rounded medical education for the benefit of my patients.

During my second year of residency, I have come across multiple instances of health disparities for people with mental illness. While working in several inpatient units, I have witnessed delayed time of visit from medical/surgical or ob.gyn. consults, shorter evaluation times from visiting consulting personnel, and postponed follow-up appointments for general medical conditions. I remember one occasion when a patient with urinary incontinence waited 3 days until internal medicine completed its consult. These experiences remind me of the conversations I had in medical school. Some of my colleagues would say, “Psychiatric patients are difficult.” Others were honest in admitting that they were scared to even enter a psychiatric inpatient unit.

Medical comorbidities common

During one 24-hour shift, I was paged to the inpatient unit. A new admission from that afternoon was complaining of “toe pain.”

The patient had been admitted for suicidal ideation and alcohol withdrawal. He reported tripping over a concrete step 2 weeks prior to admission. Under examination, he had an open laceration with purulent, foul-smelling discharge, erythema, and edema around the wound. The patient had signs of cellulitis, had a possible fracture of the phalanx, and was at risk for osteomyelitis.

He had been medically cleared at another facility prior to his admission, where he also had complained of toe pain. At that time, however, he was told, “You are not here for that,” and the extremity was not examined during the medical clearance. I ordered a referral, imaging was completed, and antibiotic treatment was started for his infection. Unfortunately, this is not an incidental or isolated case; situations similar to this one have become more frequent than we would like for those with mental illness.

Often, psychiatric patients are overlooked and undertreated. We frequently are the only physicians who evaluate the patient and help improve their quality of life. After reviewing the literature, I found countless studies concluding that patients who have a psychiatric diagnosis often have increased medical comorbidity and even increased mortality. A review and meta-analysis published earlier this year suggested that “people with mental disorders often do not receive preventive services, such as immunizations, cancer screenings, and tobacco counseling, and often receive a lower quality of care for medical conditions” (JAMA Psychiatry 2015;72:334-41). The researchers also found that “mortality was significantly higher among people with mental disorders than among the comparison population.”

Focusing on mind, body

I knew I wanted to be a psychiatrist since my early years in training. Initially, I was drawn toward psychology, in which I completed a bachelor’s degree, but my world turned around after a conversation with the father of a high school classmate. He told me: “I commend you on your decision to want to help people; however, I would like to give you food for thought. If your goal is to be of service to your patients and provide care, it would be to their benefit to address not only the mind but also the body” (which, coincidentally, is the theme of this year’s American Psychiatric Association meeting in Toronto.)

At that time, I was weighing becoming a clinician versus a physician; after all, both have instrumental roles in treatment. Yet, those words resonate now in my life for a new reason, namely, that my duty as an advocate for mental health is not only to treat psychiatric disorders but also to work toward treating general medical conditions.

I have been fortunate to cross paths with mentors who helped strengthen my commitment to well-rounded care and a multidisciplinary approach for the mentally ill. I am thankful to have worked with Dr. Jill Williams, who stressed the need to treat tobacco dependence, and Dr. Anthony Tobia, who emphasized the need to rule out substance- and medication-induced disorders prior to treatment. I have had the pleasure of working with many other attending psychiatrists who not only focused on psychiatric symptoms and diagnosis but stressed the need to address the medical care of our patients.

 

 

If I can understand my patients by learning about human behavior, conditioning, defense mechanisms, and interpersonal relationships and also focus on pathophysiology, comorbid conditions, differential diagnosis, and exacerbating medical conditions, I will be able to give them the best medical care possible.

Dr. Poulsen, a second-year psychiatry resident at the Robert Wood Johnson Medical School, Piscataway, N.J., is interested in cultural psychiatry and advocacy, and in pursuing a fellowship in child and adolescent psychiatry. After obtaining a bachelor of science degree at the University of Florida, Gainesville, he earned a medical degree at the University of Puerto Rico. He is currently serving in multiple leadership positions, including vice president of the New Jersey Psychiatric Association (NJPA) Residents Chapter and NJPA chapter advocacy coordinator. In addition, he has been selected as resident-fellow representative of the APA’s Area 3.

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The first year of residency came faster than I had expected and concluded just as quickly. At times, it felt like medical school, with different rotations, adjusting to newly formed teams, dealing with the pressures of getting the right diagnosis and treatment, managing the unrelenting speed of rounds, and trying to make a difference for the better. I must be honest – there were times when I was counting down the days for the rotation to end so that I could begin focusing and working directly in the mental health field.

Now, in my second year, the pace has improved, and the rotations resemble the work and patient population that I chose during the match process. Nonetheless, I am thankful for the time spent and the knowledge gained during my intern year, because it is only now that I understand the true value of my first-year experiences and the need to continue getting a well-rounded medical education for the benefit of my patients.

During my second year of residency, I have come across multiple instances of health disparities for people with mental illness. While working in several inpatient units, I have witnessed delayed time of visit from medical/surgical or ob.gyn. consults, shorter evaluation times from visiting consulting personnel, and postponed follow-up appointments for general medical conditions. I remember one occasion when a patient with urinary incontinence waited 3 days until internal medicine completed its consult. These experiences remind me of the conversations I had in medical school. Some of my colleagues would say, “Psychiatric patients are difficult.” Others were honest in admitting that they were scared to even enter a psychiatric inpatient unit.

Medical comorbidities common

During one 24-hour shift, I was paged to the inpatient unit. A new admission from that afternoon was complaining of “toe pain.”

The patient had been admitted for suicidal ideation and alcohol withdrawal. He reported tripping over a concrete step 2 weeks prior to admission. Under examination, he had an open laceration with purulent, foul-smelling discharge, erythema, and edema around the wound. The patient had signs of cellulitis, had a possible fracture of the phalanx, and was at risk for osteomyelitis.

He had been medically cleared at another facility prior to his admission, where he also had complained of toe pain. At that time, however, he was told, “You are not here for that,” and the extremity was not examined during the medical clearance. I ordered a referral, imaging was completed, and antibiotic treatment was started for his infection. Unfortunately, this is not an incidental or isolated case; situations similar to this one have become more frequent than we would like for those with mental illness.

Often, psychiatric patients are overlooked and undertreated. We frequently are the only physicians who evaluate the patient and help improve their quality of life. After reviewing the literature, I found countless studies concluding that patients who have a psychiatric diagnosis often have increased medical comorbidity and even increased mortality. A review and meta-analysis published earlier this year suggested that “people with mental disorders often do not receive preventive services, such as immunizations, cancer screenings, and tobacco counseling, and often receive a lower quality of care for medical conditions” (JAMA Psychiatry 2015;72:334-41). The researchers also found that “mortality was significantly higher among people with mental disorders than among the comparison population.”

Focusing on mind, body

I knew I wanted to be a psychiatrist since my early years in training. Initially, I was drawn toward psychology, in which I completed a bachelor’s degree, but my world turned around after a conversation with the father of a high school classmate. He told me: “I commend you on your decision to want to help people; however, I would like to give you food for thought. If your goal is to be of service to your patients and provide care, it would be to their benefit to address not only the mind but also the body” (which, coincidentally, is the theme of this year’s American Psychiatric Association meeting in Toronto.)

At that time, I was weighing becoming a clinician versus a physician; after all, both have instrumental roles in treatment. Yet, those words resonate now in my life for a new reason, namely, that my duty as an advocate for mental health is not only to treat psychiatric disorders but also to work toward treating general medical conditions.

I have been fortunate to cross paths with mentors who helped strengthen my commitment to well-rounded care and a multidisciplinary approach for the mentally ill. I am thankful to have worked with Dr. Jill Williams, who stressed the need to treat tobacco dependence, and Dr. Anthony Tobia, who emphasized the need to rule out substance- and medication-induced disorders prior to treatment. I have had the pleasure of working with many other attending psychiatrists who not only focused on psychiatric symptoms and diagnosis but stressed the need to address the medical care of our patients.

 

 

If I can understand my patients by learning about human behavior, conditioning, defense mechanisms, and interpersonal relationships and also focus on pathophysiology, comorbid conditions, differential diagnosis, and exacerbating medical conditions, I will be able to give them the best medical care possible.

Dr. Poulsen, a second-year psychiatry resident at the Robert Wood Johnson Medical School, Piscataway, N.J., is interested in cultural psychiatry and advocacy, and in pursuing a fellowship in child and adolescent psychiatry. After obtaining a bachelor of science degree at the University of Florida, Gainesville, he earned a medical degree at the University of Puerto Rico. He is currently serving in multiple leadership positions, including vice president of the New Jersey Psychiatric Association (NJPA) Residents Chapter and NJPA chapter advocacy coordinator. In addition, he has been selected as resident-fellow representative of the APA’s Area 3.

The first year of residency came faster than I had expected and concluded just as quickly. At times, it felt like medical school, with different rotations, adjusting to newly formed teams, dealing with the pressures of getting the right diagnosis and treatment, managing the unrelenting speed of rounds, and trying to make a difference for the better. I must be honest – there were times when I was counting down the days for the rotation to end so that I could begin focusing and working directly in the mental health field.

Now, in my second year, the pace has improved, and the rotations resemble the work and patient population that I chose during the match process. Nonetheless, I am thankful for the time spent and the knowledge gained during my intern year, because it is only now that I understand the true value of my first-year experiences and the need to continue getting a well-rounded medical education for the benefit of my patients.

During my second year of residency, I have come across multiple instances of health disparities for people with mental illness. While working in several inpatient units, I have witnessed delayed time of visit from medical/surgical or ob.gyn. consults, shorter evaluation times from visiting consulting personnel, and postponed follow-up appointments for general medical conditions. I remember one occasion when a patient with urinary incontinence waited 3 days until internal medicine completed its consult. These experiences remind me of the conversations I had in medical school. Some of my colleagues would say, “Psychiatric patients are difficult.” Others were honest in admitting that they were scared to even enter a psychiatric inpatient unit.

Medical comorbidities common

During one 24-hour shift, I was paged to the inpatient unit. A new admission from that afternoon was complaining of “toe pain.”

The patient had been admitted for suicidal ideation and alcohol withdrawal. He reported tripping over a concrete step 2 weeks prior to admission. Under examination, he had an open laceration with purulent, foul-smelling discharge, erythema, and edema around the wound. The patient had signs of cellulitis, had a possible fracture of the phalanx, and was at risk for osteomyelitis.

He had been medically cleared at another facility prior to his admission, where he also had complained of toe pain. At that time, however, he was told, “You are not here for that,” and the extremity was not examined during the medical clearance. I ordered a referral, imaging was completed, and antibiotic treatment was started for his infection. Unfortunately, this is not an incidental or isolated case; situations similar to this one have become more frequent than we would like for those with mental illness.

Often, psychiatric patients are overlooked and undertreated. We frequently are the only physicians who evaluate the patient and help improve their quality of life. After reviewing the literature, I found countless studies concluding that patients who have a psychiatric diagnosis often have increased medical comorbidity and even increased mortality. A review and meta-analysis published earlier this year suggested that “people with mental disorders often do not receive preventive services, such as immunizations, cancer screenings, and tobacco counseling, and often receive a lower quality of care for medical conditions” (JAMA Psychiatry 2015;72:334-41). The researchers also found that “mortality was significantly higher among people with mental disorders than among the comparison population.”

Focusing on mind, body

I knew I wanted to be a psychiatrist since my early years in training. Initially, I was drawn toward psychology, in which I completed a bachelor’s degree, but my world turned around after a conversation with the father of a high school classmate. He told me: “I commend you on your decision to want to help people; however, I would like to give you food for thought. If your goal is to be of service to your patients and provide care, it would be to their benefit to address not only the mind but also the body” (which, coincidentally, is the theme of this year’s American Psychiatric Association meeting in Toronto.)

At that time, I was weighing becoming a clinician versus a physician; after all, both have instrumental roles in treatment. Yet, those words resonate now in my life for a new reason, namely, that my duty as an advocate for mental health is not only to treat psychiatric disorders but also to work toward treating general medical conditions.

I have been fortunate to cross paths with mentors who helped strengthen my commitment to well-rounded care and a multidisciplinary approach for the mentally ill. I am thankful to have worked with Dr. Jill Williams, who stressed the need to treat tobacco dependence, and Dr. Anthony Tobia, who emphasized the need to rule out substance- and medication-induced disorders prior to treatment. I have had the pleasure of working with many other attending psychiatrists who not only focused on psychiatric symptoms and diagnosis but stressed the need to address the medical care of our patients.

 

 

If I can understand my patients by learning about human behavior, conditioning, defense mechanisms, and interpersonal relationships and also focus on pathophysiology, comorbid conditions, differential diagnosis, and exacerbating medical conditions, I will be able to give them the best medical care possible.

Dr. Poulsen, a second-year psychiatry resident at the Robert Wood Johnson Medical School, Piscataway, N.J., is interested in cultural psychiatry and advocacy, and in pursuing a fellowship in child and adolescent psychiatry. After obtaining a bachelor of science degree at the University of Florida, Gainesville, he earned a medical degree at the University of Puerto Rico. He is currently serving in multiple leadership positions, including vice president of the New Jersey Psychiatric Association (NJPA) Residents Chapter and NJPA chapter advocacy coordinator. In addition, he has been selected as resident-fellow representative of the APA’s Area 3.

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Trading in work-life balance for a well-balanced life

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My residency supervisor candidly asked me today – Isn’t stressing out about writing an article on work-life balance kind of missing the point? Well, yeah, that’s why she’s my supervisor. This brings me to one of the lesser advertised tips to avoiding burnout, which is: Get yourself a great mensch. But I’m getting ahead of myself here. The plan was to have 10 perfectly delineated rules, because if it worked for Letterman and Moses, it should work for residency. More to come on that.

 

Dr. Kristen A. Schmidt

Another part of the plan was to have this article finished by last weekend, but long call was Saturday. This was followed by long call recovery consisting of sleeping in so late my dad texted and left a voicemail asking, what happened? I haven’t heard from you all weekend. Then there was the obligatory run on the treadmill so the gooey cinnamon rolls the nurses baked and generously invited me to on Thursday would not stick around long enough for my husband to wonder if this was the beginning of me letting myself go. Isn’t that a lovely phrase?

Monday was Monday. How does anyone get anything done on Mondays? I had a new team, two new patients to learn and discharge. Plus, it was the first day that cracked 50 degrees in 5 months. I had to meet up with a friend, grab some coffee, and gossip walk around the lake. This was before we found out another friend was being slammed with consults in the emergency room. So there I was right back at the hospital Monday night with a cream cheese cherry pastry to cheer up my compatriot in the struggle.

This brings me to Tuesday. I had planned to be at the editing stage of this article on Tuesday. But didactics ran long due to everyone being so engaged in our formulations lecture, I didn’t have a shot at looking at this thing until lunchtime. Lunchtime came, and as I opened Microsoft Word among my dollar turkey sandwich and mini Purell bottles stationed around me like glorious little sergeants, I heard the gingerly utterings of a medical student: Um, if you have a moment, could you tell me the difference between the side-effect profile of first-generation and second-generation antipsychotics?

An hour later, I was informed that an admit was on the way and was traveling from out of state, set to arrive a half-hour before shift’s end. Did I mention he arrived with two family members in tow who wanted to talk about how things went wrong starting 20 years ago? Then there was the patient to see who I knew would pout if I didn’t spend at least a half-hour checking in. You know, the one the nurses always try to save me from even though I secretly never wanted to be saved.

I finally drove home 2 hours later than anticipated with a smile on my face. I should repeat that, WITH A SMILE ON MY FACE. I felt good because I’d done good. After all, there’s even a little sunlight left. When I walk in the front door, I kiss my husband and then immediately delve into a new story from the day. We laugh. We warm up leftovers, sit on the couch with our bare feet on the table, and catch an hour of American Idol (talent never gets old). Then it’s time to meet this maker.

The strange thing is, the person who began this column with all of her well-intentioned plans feels very different from the person who has made it to the deadline. There is a whole life lived in between. All of the readings I had done, notations I had made, seem kind of beside the point. I could pepper you with statistics and evidence-based outcomes warning of divorce, substance abuse, physician suicide, patient errors, and the like, which are all very real outcomes of poorly balanced lives. But I think we know all of that. It’s the in between space, the living part where so many of us lose our way. So instead of referenced journals, I offer you my journey. Because I can truly say that for the last 3 months of the most difficult year of residency, I have been happy. May this piece be also with you.

Dr. Schmidt, a second-year psychiatry resident at the Mayo Clinic in Rochester, Minn., is interested in psychodynamic therapy and in pursuing a fellowship in addictions. After obtaining a bachelor of arts at the University of California, Berkeley, she earned a master of arts degree in philosophy and humanities at the University of Chicago. She attended medical school at the University of Illinois College of Medicine at Peoria.

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My residency supervisor candidly asked me today – Isn’t stressing out about writing an article on work-life balance kind of missing the point? Well, yeah, that’s why she’s my supervisor. This brings me to one of the lesser advertised tips to avoiding burnout, which is: Get yourself a great mensch. But I’m getting ahead of myself here. The plan was to have 10 perfectly delineated rules, because if it worked for Letterman and Moses, it should work for residency. More to come on that.

 

Dr. Kristen A. Schmidt

Another part of the plan was to have this article finished by last weekend, but long call was Saturday. This was followed by long call recovery consisting of sleeping in so late my dad texted and left a voicemail asking, what happened? I haven’t heard from you all weekend. Then there was the obligatory run on the treadmill so the gooey cinnamon rolls the nurses baked and generously invited me to on Thursday would not stick around long enough for my husband to wonder if this was the beginning of me letting myself go. Isn’t that a lovely phrase?

Monday was Monday. How does anyone get anything done on Mondays? I had a new team, two new patients to learn and discharge. Plus, it was the first day that cracked 50 degrees in 5 months. I had to meet up with a friend, grab some coffee, and gossip walk around the lake. This was before we found out another friend was being slammed with consults in the emergency room. So there I was right back at the hospital Monday night with a cream cheese cherry pastry to cheer up my compatriot in the struggle.

This brings me to Tuesday. I had planned to be at the editing stage of this article on Tuesday. But didactics ran long due to everyone being so engaged in our formulations lecture, I didn’t have a shot at looking at this thing until lunchtime. Lunchtime came, and as I opened Microsoft Word among my dollar turkey sandwich and mini Purell bottles stationed around me like glorious little sergeants, I heard the gingerly utterings of a medical student: Um, if you have a moment, could you tell me the difference between the side-effect profile of first-generation and second-generation antipsychotics?

An hour later, I was informed that an admit was on the way and was traveling from out of state, set to arrive a half-hour before shift’s end. Did I mention he arrived with two family members in tow who wanted to talk about how things went wrong starting 20 years ago? Then there was the patient to see who I knew would pout if I didn’t spend at least a half-hour checking in. You know, the one the nurses always try to save me from even though I secretly never wanted to be saved.

I finally drove home 2 hours later than anticipated with a smile on my face. I should repeat that, WITH A SMILE ON MY FACE. I felt good because I’d done good. After all, there’s even a little sunlight left. When I walk in the front door, I kiss my husband and then immediately delve into a new story from the day. We laugh. We warm up leftovers, sit on the couch with our bare feet on the table, and catch an hour of American Idol (talent never gets old). Then it’s time to meet this maker.

The strange thing is, the person who began this column with all of her well-intentioned plans feels very different from the person who has made it to the deadline. There is a whole life lived in between. All of the readings I had done, notations I had made, seem kind of beside the point. I could pepper you with statistics and evidence-based outcomes warning of divorce, substance abuse, physician suicide, patient errors, and the like, which are all very real outcomes of poorly balanced lives. But I think we know all of that. It’s the in between space, the living part where so many of us lose our way. So instead of referenced journals, I offer you my journey. Because I can truly say that for the last 3 months of the most difficult year of residency, I have been happy. May this piece be also with you.

Dr. Schmidt, a second-year psychiatry resident at the Mayo Clinic in Rochester, Minn., is interested in psychodynamic therapy and in pursuing a fellowship in addictions. After obtaining a bachelor of arts at the University of California, Berkeley, she earned a master of arts degree in philosophy and humanities at the University of Chicago. She attended medical school at the University of Illinois College of Medicine at Peoria.

My residency supervisor candidly asked me today – Isn’t stressing out about writing an article on work-life balance kind of missing the point? Well, yeah, that’s why she’s my supervisor. This brings me to one of the lesser advertised tips to avoiding burnout, which is: Get yourself a great mensch. But I’m getting ahead of myself here. The plan was to have 10 perfectly delineated rules, because if it worked for Letterman and Moses, it should work for residency. More to come on that.

 

Dr. Kristen A. Schmidt

Another part of the plan was to have this article finished by last weekend, but long call was Saturday. This was followed by long call recovery consisting of sleeping in so late my dad texted and left a voicemail asking, what happened? I haven’t heard from you all weekend. Then there was the obligatory run on the treadmill so the gooey cinnamon rolls the nurses baked and generously invited me to on Thursday would not stick around long enough for my husband to wonder if this was the beginning of me letting myself go. Isn’t that a lovely phrase?

Monday was Monday. How does anyone get anything done on Mondays? I had a new team, two new patients to learn and discharge. Plus, it was the first day that cracked 50 degrees in 5 months. I had to meet up with a friend, grab some coffee, and gossip walk around the lake. This was before we found out another friend was being slammed with consults in the emergency room. So there I was right back at the hospital Monday night with a cream cheese cherry pastry to cheer up my compatriot in the struggle.

This brings me to Tuesday. I had planned to be at the editing stage of this article on Tuesday. But didactics ran long due to everyone being so engaged in our formulations lecture, I didn’t have a shot at looking at this thing until lunchtime. Lunchtime came, and as I opened Microsoft Word among my dollar turkey sandwich and mini Purell bottles stationed around me like glorious little sergeants, I heard the gingerly utterings of a medical student: Um, if you have a moment, could you tell me the difference between the side-effect profile of first-generation and second-generation antipsychotics?

An hour later, I was informed that an admit was on the way and was traveling from out of state, set to arrive a half-hour before shift’s end. Did I mention he arrived with two family members in tow who wanted to talk about how things went wrong starting 20 years ago? Then there was the patient to see who I knew would pout if I didn’t spend at least a half-hour checking in. You know, the one the nurses always try to save me from even though I secretly never wanted to be saved.

I finally drove home 2 hours later than anticipated with a smile on my face. I should repeat that, WITH A SMILE ON MY FACE. I felt good because I’d done good. After all, there’s even a little sunlight left. When I walk in the front door, I kiss my husband and then immediately delve into a new story from the day. We laugh. We warm up leftovers, sit on the couch with our bare feet on the table, and catch an hour of American Idol (talent never gets old). Then it’s time to meet this maker.

The strange thing is, the person who began this column with all of her well-intentioned plans feels very different from the person who has made it to the deadline. There is a whole life lived in between. All of the readings I had done, notations I had made, seem kind of beside the point. I could pepper you with statistics and evidence-based outcomes warning of divorce, substance abuse, physician suicide, patient errors, and the like, which are all very real outcomes of poorly balanced lives. But I think we know all of that. It’s the in between space, the living part where so many of us lose our way. So instead of referenced journals, I offer you my journey. Because I can truly say that for the last 3 months of the most difficult year of residency, I have been happy. May this piece be also with you.

Dr. Schmidt, a second-year psychiatry resident at the Mayo Clinic in Rochester, Minn., is interested in psychodynamic therapy and in pursuing a fellowship in addictions. After obtaining a bachelor of arts at the University of California, Berkeley, she earned a master of arts degree in philosophy and humanities at the University of Chicago. She attended medical school at the University of Illinois College of Medicine at Peoria.

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