Irritant contact dermatitis is the most common and occurs in response to a physical or chemical insult to the outer layer of the skin. In other words, it is a response to a direct toxic effect on the skin. Any person who would be exposed to such effect would develop a rash. The associated rash characteristically appears shortly after exposure. Strong irritants tend to cause evident skin damage within hours while weaker irritants may require multiple exposures to develop the dermatitis. Examples of irritants include acids, alkalis, solvents, adhesives and detergents.

Allergic contact dermatitis is known as a “delayed-type hypersensitivity” reaction. It is an immunologic response that causes tissue inflammation. It happens in some, but not all people exposed to a certain chemical. No history of eczema is needed, as allergic contact dermatitis can occur in patients with or without eczema. Sensitization or priming of the skin occurs 1 to 2 weeks after the first exposure. Subsequent exposure leads to rash hours to days after the re-exposure. Following is a list of common allergens causing allergic contact dermatitis:

Poison ivy, oak, and sumac: Poison ivy and oak are common culprits of allergic contact dermatitis during the summer time. The sensitizing allergens are pentadecylcatechol and heptadecylcatechol which are found in the sap of these plants. Sensitivity to poison ivy, oak and sumac results in sensitivity to the other plants in the same family which would include cashews, mango and lacquer trees.

Iodine: Iodine preparations are widely used in antiseptics. The degree of allergic contact dermatitis caused by iodine varies depending on the type of preparation. A study by Lee et al tested iodine in petrolatum, iodine in 70% isopropyl alcohol and povidone-iodine. It was found that when iodine was complexed with povidone, less subjects developed dermatitis.

Nickel: Nickel sensitivity is typically seen in women wearing nickel earrings. Nickel is also found in the buttons of jeans, costume jewelry and wrist watches. It is important to note that although stainless steel used in some jewelry has nickel, it is so tightly bound that it usually does not cause an allergic reaction.

Rubber: The most frequent rubber allergens are mercaptobenzothiazole and thiuram. Shoes and gloves are the most common causes of allergic contact dermatitis by rubber. The reaction will usually be limited to the hands or feet in a patchy distribution where there has been direct contact to the rubber.

Certain topical medications: Benzocaine 5% (cross reacts with Para-aminobenzoic acid (PABA)-containing sun screen), Neomycin Sulfate 20%, Ethylenediamine 1 % have all been documented as possible causes of allergic contact dermatitis.

Cosmetics: An allergy to a specific ingredient or ingredients in a product is usually present. Paraphenylenediamine is a dye found in permanent hair coloring. Sensitization to paraphenylenediamine occurs in hairdressers and in clients who have their hair colored. When completely oxidized, as the dye on a fur coat, paraphenylenediamine is no longer a source of allergic contact dermatitis.

Presentation:
The rash is often very itchy. The appearance of the rash depends on the stage. In the acute phase, one would expect to see red patches and fluid-filled bumps (vesicles) with oozing; swelling may also be present. In the chronic phase we would expect longer term changes such as crusting, thickening, and scaling.

Diagnosis:
The diagnosis is usually made clinically. A detailed history of occupation, hygienic habits, and hobbies is frequently necessary to find the culprit. The causative agent for allergic contact dermatitis may be identified by a patch test. In fact, patch testing is the only way to differentiate an irritant contact dermatitis and allergic contact dermatitis. Clinically and even under a microscope, they cannot be reliably distinguished. In patch testing, multiple different chemicals are applied to patches which are taped onto a the back of the patient. The patches are then removed after 48 hours and interpreted by a dermatologist at 48 and 96 hours. Patch testing is indicated in the following cases: 1) diagnosis is in doubt, 2) rash does not respond to treatment, 3) rash recurs.

Treatment:
Wearing protective clothing, and avoiding the contact allergen are the two most important ways to prevent further dermatitis. One should also avoid frequent water exposure as it will dry and chap the skin. Moisturizing plays a key role in aiding the skin’s natural healing.

For symptoms, astringent dressings or soothing baths reduce weeping and itching while oral histamines often help the itch. Cool tap water compresses are useful if vesicles are present. Topical steroids generally aid in diminishing the inflammatory reaction that causes all of the symptoms associated with contact dermatitis. Dermatologists will frequently use a topical steroid for therapy in mild to moderate rashes. Systemic steroids may also be used for severe cases.

References:
J. Bourke; I. Coulson; J. English: Guidelines for the Management of Contact Dermatitis: an Update. The British Journal of Dermatology. 2009; 160(5):946–954
S. K. Lee; H. Zhai; H. I. Maibach: Allergic contact dermatitis from iodine preparations: a conundrum. Exog Dermatol 2002;1:238-24

Marigdalia K. Ramirez-Fort
Ponce School of Medicine
Ponce, Puerto Rico

Alexander Doctoroff, D.O., F.A.O.C.D.
Assistant Chief of Dermatology, Veterans Administration Medical Center
East Orange, New Jersey
Assistant Clinical Professor of Medicine,
University of Medicine and Dentistry of New Jersey.
www.metropolitanderm.com

Hemangiomas are the most common benign growth in infancy, occurring in 10% of full term babies and up to 25% of premature babies.  They represent excessive blood vessel growth, most obviously in the dermis layer of the skin, but they can occur in the fatty layer of the skin, and also deeper within the body such as in the liver.  For unclear reasons they occur 3 times more frequently in girls. 60% of hemangiomas occur in the head and neck area, but they can occur anywhere on or inside the body.

Diagnosis and work up

Most hemangiomas can be diagnosed by history and physical examination alone. In most cases the hemangioma is not present at birth but appears as a small red spot in the first couple weeks of life.  It then begins to grow faster than the child grows, often protruding above the surface of the skin.  Most hemangiomas will stop growing somewhere between 6-12 months of age and then begin to regress.  The bright red color becomes more pale, with grayish-white patches, and the hemangioma loses its engorged appearance (Fig 1).  Hemangiomas shrink very slowly, over an average of 5 years. Parents should realize that this means some hemangiomas will take longer than 5 years (even into the early teenage years) to fully shrink.

Hemangiomas in the fatty layer tend to appear more blue in pigmentation than red, and some hemangiomas will have both a central superficial red portion and a deeper bluer subcutaneous portion (Fig 2).

Hemangiomas that involve the eye region risk blockage of vision and possible permanent visual impairment, therefore these babies should be evaluated by a pediatric ophthalmologist. (Fig 3) Hemangiomas that occur below the vocal cords are potentially life-threatening because of airway blockage, and these should be immediately evaluated by a pediatric otolaryngologist.  Large facial hemangiomas warrant an MRI scan to rule possible related abnormalities of the brain, as well as a possible cardiac evaluation to rule out heart and great vessels abnormalities. Rarely, a sternal cleft can also occur. This constellation of findings as been given the name PHACES syndrome – Posterior cranial fossa abnormalities, Hemangioma, Arterial abnormalities, Cardiac abnormalities and coarctation of the aorta, Eye abnormalities, and Sternal cleft, but patients do not need to have every abnormality to be diagnosed with this syndrome.

Hemangiomas involving the central back and buttocks warrant an MRI scan to rule a possible spinal cord abnormality (lipomyelomeningocele with tethered cord), and other genital and urologic abnormalities should be checked.  There is another constellation of findings termed PELVIS syndrome – Perineal hemangioma, External genitalia deformities, Lipomyelomeningocele, Vesicorenal defects, Imperforate anus, and Skin tag, and again, patients need not have every abnormality to fulfill the diagnosis, but they should be ruled out.  (Fig 4)

Babies who have 6 or more external hemangiomas should have an ultrasound to rule out possible liver or spleen hemangiomas.  Large liver hemangiomas may inactivate thyroid hormone, resulting in symptomatic hypothyroidism. Additionally large liver hemangiomas and any very large hemangioma elsewhere may put additional stress on the heart resulting in high output heart failure.

Lastly, there are always some exceptions to the rule – some hemangiomas shrink extremely rapidly within a year (RICH – rapidly involuting congenital hemangioma) (Fig 5) and some seem to never shrink, maintaining a bluish pigmentation with small superficial red vessels and a very warm temperature due to the increased blood flow . (NICH – non-involuting congenital hemangioma) (fig 6)

Actual biopsy is rarely indicated unless the diagnosis remains unclear.  On rare occasions other tumors can mimic hemangiomas, in which case a biopsy may be warranted. Classic hemangiomas of infancy will stain positive for Glucose transporter protein 1 (Glut-1).  Interestingly, neither RICH nor NICH hemangiomas stain positive for Glut-1.

Medical treatment of hemangiomas

The vast majority of hemangiomas can be treated conservatively with serial observation and parental reassurance. Hemangiomas will typically grow for 6-12 months, then reach a plateau and shrink slowly over an average of 5 years.  It has been estimated that up to 70% of hemangiomas will adequately regress and require no additional treatment.

However, that still leaves 30% of hemangiomas that can sometimes leave significant deformity, and all treatment methods should be discussed with the parents to avoid medicolegal issues whereby parents may feel a treatment option was withheld from them that might have prevented a permanent deformity.

Hemangiomas that threaten the airway or vision of the child cannot be followed conservatively, and medical intervention is indicated, usually in the form of steroid therapy.  In the majority of cases, this is given orally in the form of prednisolone 2-4 mg/kg/day mixed with the morning feeding.  Liquid Zantac is often prescribed simultaneously.  Once a response is detected, the steroids can be tapered slowly.  Some practitioners will cycle on and off steroids while others will start at a high dose, then slowly taper down, occasionally bumping the dose slightly and tapering more slowly if rebound growth is detected –  the dosage graph resembling a roller coaster ride. Babies on steroid therapy cannot receive live-attentuated virus vaccinations (rotavirus, measles, mumps, rubella, chicken pox) until the steroids have been discontinued for at least a month.

Steroids can also be injected into hemangiomas every 4-6 weeks using slowly absorbed preparations such as triamcinolone (Kenalog), however in the eye region, this should only be done by an ophthalmologist because of the potential risk of steroid particles travelling through the blood stream to the eye, causing possible blindness.

Topical steroid cream ( clobetasol propionate – Temovate) can be applied to relatively indolent hemangiomas, but the amount of steroid absorption is unpredictable, and therefore the oral route is preferred for hemangiomas that threaten vision, breathing, or significant permanent deformity.  The topical cream can be applied once a day in cyclical fashion, two weeks on, two weeks off for as long as is deemed necessary.

Laser therapy

The most commonly used laser for hemangiomas is the pulsed yellow dye laser. The laser light is absorbed by the blood inside the vessels, causing them to heat up, swell, and burst.  The light penetrates only about 1-2 mm into the skin, therefore the laser works best on small flat hemangiomas.  The effect is unpredictable.  Some hemangiomas seem to shrink and disappear with a single treatment.  Most hemangiomas will exhibit some initial shrinkage but then show rebound growth within 2-3 weeks, warranting a series of laser treatments until no further growth is noticeable. Some hemangiomas will show little or no benefit to laser treatment.  Large thick hemangiomas do not respond well as the light cannot penetrate very deeply into the tissues. Parents should be aware that the laser treatments are painful, although pre-treatment with a topical anesthetic cream and a coolant spray attached to the laser can reduce the discomfort of the laser sessions.

The pulsed yellow dye laser has two other uses in hemangiomas.  Hemangiomas that have ulcerated (the overlying skin breaks open) can be exquisitely sensitive, especially in the genital and buttock region.  The laser may help to decrease the pain significantly within 24-48 hours (probably by cauterizing sensitive nerve endings) and also speed the rate of healing (perhaps by causing temporary hemangioma suppression) in many patients.  Older hemangiomas that have shrunk but left residual spider vessels in the skin can be treated with the laser to reduce the size and number of vessels.  Often more than one treatment session is necessary for best results (Fig 7) .

Interferon and beta blockers

In the 1990’s interferon alfa-2a showed promising results in hemangioma suppression, however significant side effects have limited its use to life or vision-threatening hemangiomas that appear resistant to steroid therapy.

Very recently beta-blockers have been shown to significantly suppress large hemangiomas, although the exact mechanism remains unclear. The use of beta blockers currently requires initial ICU monitoring, and is generally restricted to significant steroid-resistant hemangiomas that are life or vision threatening, or likely to otherwise cause severe facial deformity. As more experience is gained with this therapy, therapeutic indications and protocols will evolve appropriately.

Surgery for hemangiomas

The role of surgery in the treatment of hemangiomas has evolved significantly.  Initially pediatricians were taught to follow the majority of hemangiomas conservatively, advise parents to wait at least 5 years, and then refer patients for surgical excision or revision if the hemangiomas failed to adequately involute. This strategy worked very well for the majority of families, as an estimated 70% of patients required no surgical treatment.

Unfortunately, 30% of hemangiomas will not shrink satisfactorily, leaving either thin, crệpey redundant skin, bulky fatty scar tissue, dermal scarring (which always occurs if a hemangiomas has ulcerated at some point), or distortion of facial features, including the nose, lips, eyelids, and ears, or distortion of the trunk and extremities.  Surgery is often indicated in these situations, and each patient must be individually evaluated to determine the appropriate timing and extent of surgery.

With the popularity of the internet, parents are well aware of the variety of treatment options, and the pendulum may have swung too far to the surgical side.  While early surgery is often a good option, surgical excision always leaves a scar, and impatient parents and overly aggressive surgeons may be doing some patients a disservice in the long run if they accept a permanent surgical scar for something nature might have completely erased.  Surgery is appropriate if one can be reasonably certain that natural involution will leave a worse result.

Timing of surgery

Hemangiomas can be excised during the early growth phase or after many years when there is residual deformity and no further perceived improvement, or anywhere in between.  It is a combination of clinical judgment and parental input that will help to determine when it is appropriate to proceed with surgery.

Early excision

Excision during the growth phase of a hemangioma can be considered for problematic hemangiomas such as those that have ulcerated and bled significantly.  These are fairly rare, but occasionally an ulcerated hemangioma erodes into an arterial vessel, causing spurting bleeding, or occasionally an ulcerated hemangiomas may ooze enough to cause anemia.  In such cases surgery may consists of suture placement around the bleeding area, or if the hemangioma is small enough, complete excision and suture closure of the wound.  In this situation, the creation of a permanent surgical scar is a worthwhile exchange for control of bleeding and parental peace of mind (Fig 8).

Excision during the regression phase

The majority of hemangiomas can be excised at some point during the shrinkage phase, prior to complete involution.  At this point there is no further growth, but there is still active circulation through the residual hemangioma vessels.  If it is determined that unsatisfactory shrinkage is likely to occur, and if the operation can be done safely with acceptable blood loss, then surgical excision can be considered.  In many cases, the boundaries of the hemangioma are well-defined, there is adequate adjacent skin laxity for closure, and the hemangioma can be excised with minimal blood loss by staying peripheral to it (Fig 9).  Pedunculated hemangiomas can often be excised with a reasonably short scar.  Hemangiomas with both a central dermal component and a peripheral subcutaneous component can usually be incised just peripheral to the central part, and then the entire hemangioma removed through the central opening.

Hemangiomas that infiltrate normal adjacent skin and are too big to be excised in their entirety are more challenging. Not only is there more intraoperative bleeding because one must cut through the hemangioma, but the surgeon must also decide how much hemangioma to intentionally leave behind to avoid a deficiency of soft tissue in the future.  This commonly occurs with lip and nasal tip hemangiomas, Aggressive debulking or complete excision may result in inadequate long term lip or nasal tip volume, especially if the residual hemangioma goes on to shrink more than anticipated.

It may be advisable to intentionally stage the procedure into at least 2 separate operations.  The first procedure removes the majority of the bulk, and then the second procedure can fine tune any residual asymmetries that persist after at least a year of follow up. Parents should be advised of what can reasonably be expected, that symmetry may be an impossible goal, and that multiple revisions may be necessary for best results.

Excision after complete regression

Many hemangiomas will leave behind a combination of redundant stretched skin and bulky subcutaneous fibrofatty tissue after the vessels have involuted. These patients are the safest candidates for surgical debulking because there are few if any residual vessels, and it is much easier to judge how much soft tissue to leave behind.  A smooth surgical scar is generally superior to a protruding mound or loose redundant skin.  In most cases, however, patients and their parents will be reluctant to wait until complete shrinkage because the waiting period will extend into the early school years.

Surgical treatment of hemangiomas in special cases

Some hemangiomas seem to have a great propensity for leaving residual deformity, particularly those in the facial area.  Suppression with steroids is a judgment call, but the temporary side effects of steroids are often well worth it if one can prevent or at least minimize the potential lifetime deformity caused by an enlarging or ulcerated hemangioma

Nasal tip hemangiomas

Nasal tip hemangiomas often create a bulbous tip (Cyrano deformity, named after Cyrano de Bergerac) as they leave behind bulky fibrofatty tissue, redundant skin, and splayed nasal tip cartilages. Surgical correction often requires excision of redundant skin, centralization of the two pieces of cartilage that make up the nasal tip that have been separated by the hemangioma, and debulking of the excess soft tissue (Fig 10).  Overly aggressive soft tissue removal, however, can leave very thin skin over the tip cartilage, therefore it is advisable to intentionally leave residual hemangioma or fatty tissue to soften the nasal tip and improve the long term result.   Steroid suppression during the growth phase of the hemangioma may avoid the need for any surgery, or at least prevent over-expansion of the skin envelope. In such cases, debulking can be done through an intranasal approach, avoiding any external scars.

Lip hemangiomas

The vast majority of lip hemangiomas will leave excess soft tissue despite years of slow regression, and commonly hemangiomas can ulcerate because of feeding trauma to the thin fragile vermilion. Large hemangiomas may also affect the ability to suck.  Steroid suppression is often advisable to limit the degree of distortion.  Early first-stage debulking may assist with feeding issues and also help parents cope with the stress of dealing with a child with an oral hemangioma deformity.  Depending upon the location of the hemangioma, the scars can often be at least partially hidden just inside the lip vermilion.  However hemangiomas that extend onto the skin portion of the upper or lower lip usually require partial skin excision and therefore leave permanent external lip scars.  Upper lip hemangioma debulking can often take advantage of techniques learned through cleft lip reconstruction, placing the scars along natural boundaries to make them as subtle as possible (Fig 11).  Scar revisions are often desirable to optimize the final outcome, and therefore parents should understand that more than one operation is often necessary to improve the final result.

Eyelid (periorbital) hemangiomas

The thin eyelid skin is subject to significant distortion and expansion by the growing hemangioma.  If the eyebrow is involved, this can result in excess skin, low hair density, and distortion of the eyebrow shape. Steroids are usually indicated to avoid obstruction of vision, and this will also help to decrease the amount of skin distortion.   In cases where visual impairment is still a concern, ophthalmologists and pediatric oculoplastic surgeons may institute a patching regiment for the opposite eye, to encourage the child to use the obstructed eye, or they may elect early debulking to facilitate eyelid opening.

Late debulking of excess skin and subcutaneous tissue is often desirable, at the expense of a permanent surgical scar (Fig 12). Reconstruction of a missing or distorted eyebrow can be very difficult. Micrografting from the scalp results in hairs that require frequent trimming because they will continue to grow like scalp hair.  Micropigmentation (tattoo) is sometimes a good option, particularly if the patient can achieve good results initially with an eyebrow pencil.

Cheek and parotid hemangiomas

The salivary gland in front of the ear is the parotid gland, and sometimes intraparotid hemangioma growth can cause massive cheek enlargement. This can also cause partial obstruction of the external auditory canal, and if bilateral involvement is noted, steroid suppression is indicated to maintain auditory stimulation. In addition to parotid gland involvement, often the skin around the ear and cheek is involved.  This will usually regress very well over time, although there may be some residual cheek skin redundancy that may benefit from a facelift type reduction.  Overly aggressive debulking, however, risks injury to the facial nerve that runs through the parotid gland.  Early debulking when vessels are still active can increase the risk of inadvertent nerve injury because of the increased risk of blood in the field that may obscure anatomic landmarks.

Hemangiomas involving the skin of the cheek and often the underlying subcutaneous tissue can be problematic.  The surgeon and parents must decide whether a linear surgical scar is preferable to a circular or oval patch of scarred dermis or redundant skin left by the hemangioma.  Some surgeons have advocated excision of the hemangioma using a purse-string type closure, but the vast majority of hemangiomas are excised in a football shaped pattern, which results in a long linear scar because of the need to taper the corners (Fig 13). Sometimes if the skin is in relatively good shape but there is underlying subcutaneous bulk, liposuction may provide a significant contour improvement using an intraoral puncture site to avoid any external scars.

Subcutaneous hemangiomas

Subcutaneous hemangiomas often grow without causing overlying skin expansion and loss of skin tone.  In these cases, conservative observation is the best initial course to see if the hemangioma will spontaneously shrink completely, leaving totally intact normal skin.  Aggressive early surgical removal is contraindicated, as this will leave an unnecessary surgical scar.  If the hemangioma regresses but leaves behind bulky fatty tissue, at this point liposuction can provide excellent contour reduction through 1 or 2 small puncture sites.

Breast mound hemangiomas

Particularly in female infants, breast mound hemangiomas (Fig 14) should be left alone to avoid potential injury to the breast bud that can result in failure of breast development during puberty.  In many cases, as the hemangioma regresses and the breast develops, surgical correction will become unnecessary.  Nipple distortion or redundant skin can be addressed after normal breast development, and fortunately the deformity can usually be easily camouflaged with clothing until that time. 

Since breast bud preservation is not necessary in male patients, any nipple or chest wall deformity can be addressed at a much earlier age, usually at some point during the shrinkage phase, or after complete regression.

Scalp hemangiomas

Many scalp hemangiomas will obliterate the hair roots, leaving patches of redundant, non-hairbearing scalp (Fig 15).  These can be easily excised either during the shrinkage phase or later, with minimal blood loss since one can compress the surround scalp during the excision to control bleeding.  A surgical scar always results, but usually there is adequate adjacent hair density to help camouflage this.  With short hair, the scar may be more obvious. With advancing age and a history of male-pattern baldness, some scalp scars may become evident later in life.

Buttock and perineal/genital hemangiomas

While these often cause significant problems during the growth period because of their propensity to ulcerate, causing

significant pain with urination or stooling, these rarely need any surgical revision later on (Fig 16).  Sometimes a hemangioma in the labial area can result in some excessive skin, but this is a

rarity.  Laser can be useful during the ulcerated phase, as described in the laser treatment section above.  Topical lidocaine jelly (2%) followed by antibiotic ointment is a common temporizing strategy until the skin has healed.

David W. Low, MD
Associate Professor of Surgery, Division of Plastic Surgery
University of Pennsylvania School of Medicine
Clinical Associate, The Children’s Hospital of Philadelphia

Figures

Fig 1 – typical bright red dermal hemangioma with signs of early regression

Fig 2 – hemangioma with both a superficial dermal and a deeper subcutaneous component

Fig 3 – periorbital hemangioma that is causing partial visual obstruction, which can cause permanent amblyopia

Fig 4 – PELVIS syndrome patient with extensive ulcerated hemangioma.  MRI scan confirmed the presence of a lipomyelomeningocele and a tethered cord

Fig 5 – Rapidly involuting congenital hemangioma (RICH). The photos are taken 3 months apart

Fig 6 – Non-involuting congential hemangioma (NICH) which was later surgically excised

Fig 7 – laser treatment for residual vessels after hemangioma involution

Fig 8 – early excision of an ulcerated, bleeding hemangioma

Fig 9 – typical complete hemangioma excision using a football-shaped pattern

Fig 10 – nasal tip hemangioma debulking utilizing a cosmetically favorable incision that permits skin excision, cartilage adjustment, and soft tissue debulking.

Fig 11 – lip hemangioma debulking, utilizing cleft lip techniques to maximize symmetry

Fig 12 – periorbital hemangioma debulking of the lower eyelid. Complete excision would have resulted in lower lid retraction (ectropion)

Fig 13 – cheek hemangioma excision with subsequent hypertrophic scar.  The contour improvement is an acceptable trade off for the less than optimal scar

Fig 14 – chest hemangioma involving the nipple and underlying breast bud

Fig 15 – scalp hemangioma, with destruction of involved hair follicles

Fig 16 – ulcerated buttock hemangioma, with complete healing within 2 months

Mohs surgery (MS) is a specialized and very effective method of removing skin cancers.  Developed by Frederic Mohs, M.D. at the University of Wisconsin, MS is now practiced throughout the world.  MS permits the surgeon to ensure that all the “roots” of a skin cancer have been removed.  Mohs surgery has the highest reported cure rates of any form of skin cancer.

Most skin cancers do not require MS.  It is reserved for skin cancers that have re-grown after previous treatment, are at greater risk for growing back, or are located in areas where preservation of normal skin is important.  MS is practiced by surgeons who have received specialized education, either during or after their residency training.

WHEN IS MOHS SURGERY RECOMMENDED?

Some skin cancers are much larger under the skin than they appear on the surface.  These may grow into and below the skin and along blood vessels, nerves, or cartilage.  Cancers that have come back again after treatment may also grow deeply and under scar tissue.  MS is specifically designed to track and remove the “roots” of these cancers.

HOW IS MOHS SURGERY PERFORMED?

Mohs surgery requires three steps:

1)  The skin is first made completely numb using a local anesthetic.  The visible cancer is removed along with a thin layer of additional tissue.  This takes only a few minutes and patients may then return to the waiting room.  A diagram (called a Mohs map) of the surgery site is drawn.

2)  The specimen is carefully oriented and processed.  A technician freezes the tissue and removes very thin slices from the entire undersurface.  These slices are placed on microscope slides and prepared for the surgeon to exam under the microscope.  This step is the most time consuming, often requiring 20 to 60 minutes.

The surgeon then examines the slides to determine whether any cancer remains.  The size and location of any cancer roots are pinpointed on the Mohs map.  The surgeon then uses the Mohs map as a guide to remove additional tissue only where cancer roots are present.  This is why the Mohs surgery technique leaves the smallest possible surgical wound, because there is no guess work involved in deciding where to remove additional tissue.  Only tissue around the roots and extensions of cancer is removed.

HOW LONG DOES MOHS SURGERY TAKE?

Most cases are completed in less than four hours, while larger or more complex cases may take longer.  No one can predict in advance how extensive a given cancer will be.  You should reserve the entire day for your surgery.

WILL THE SURGERY LEAVE A SCAR?

Yes, any form of surgery leaves a scar.  The scar will usually be smaller than those from other forms of skin cancer surgery.

WHAT HAPPENS AFTER THE MOHS SURGERY IS COMPLETED?

After the cancer is removed, the surgeon will discuss with you whether 1) to allow the wound to heal naturally, without additional surgery, 2) to repair the wound that day, or 3) to have a different surgeon repair the wound.

WILL I HAVE PAIN, BRUISING, OR SWELLING AFTER SURGERY?

Most patients do not have significant pain, and over-the-counter pain medications often control it.  Stronger prescription pain medications are prescribed, when needed.  Discuss any concerns you have about pain control with your surgeon.  You will almost certainly have some bruising and swelling, especially if surgery is being done close to the eyes.

WILL MY INSURANCE COVER THE COST?

Most insurance policies cover the cost of both MS and the surgical reconstruction of the wound.  Please check with your insurance carrier for exact information relating to your surgery.

HOW DO I PREPARE MYSELF FOR SURGERY?

Get a good night’s rest and eat normally the day of surgery.  Bring reading material to occupy your time while waiting for your slides to be processed and examined.  Also, you should consider arrange for someone to drive you home after surgery is completed.

If you are taking prescription medications, continue to take them unless otherwise directed by your surgeon.  You must inform your surgeon, in advance, if you are taking any medications or supplements that can thin the blood.  These include Coumadin, Plavix, baby aspirin, ibuprofen, Advil, Motrin, Naprosyn, etc.  Many supplements, including ginseng, garlic, gecko, ginko belloba, vitamin E, and niacin will thin your blood.  You may be asked to stop taking some or all of your supplements before your surgery.

Howard K. Steinman, M.D.

Associate Professor of Dermatology
Director, Dermatologic and Skin Cancer Surgery                                                                                        Department of Dermatology                                                                                                                       Texas A&M University Health Sciences Center College of Medicine

Camouflage makeup provides immediate appearance normalization.  It is easy to apply and safely and effectively masks bruising, redness, and brown discoloration.  Use of CM allows patients to confidently go out in public much sooner after surgery and trauma and appear normal immediately while treating other skin conditions.

Camouflage makeup cannot correct the appearance of swelling, raised or depressed scars, deep furrows, smooth texture changes from scars, and very dark bruising.

Camouflage makeups are very different from store-bought concealers or color-tinted “correctors.” Camouflage makeups cover imperfections completely, using opaque colors, precisely matched to each patient’s normal skin color.  Single-color concealers cannot correct discolorations on the many different natural skin tones of human skin.  Most patients, untrained in color matching and makeup end up with less-than-desirable results using these products.  Although their imperfections may be diminished, they are not completely masked.

There are two main forms of CM:  Specialized foundations and mineral makeups.

Specialized CM foundations are often offered by formally trained camouflage makeup artists, who work closely with dermatologists, often in their offices.   This is because they require more detailed instruction for proper use.  These foundations can camouflage most forms of skin discoloration.  They can adhere to smooth, pore-less areas (such as burn scars), are heat, movement, water and sweat resistant, long lasting, will not cause acne, and contain potent sun blocks.

Mineral makeups have greatly improved the availability and ease of application of CM.  They are crushed inert minerals in powder form very useful for less intense post-surgical and post-traumatic skin changes and nearly all other causes of skin discoloration.  They are hypoallergenic, water-resistant and will not cause acne.  Mineral makeups can be applied with a brush for a light finish or with a sponge for heavier concentrations of color.  They can also be mixed with water to make a highly concentrated concealer and with sunscreens to make a tinted sunscreen.

Your doctor can help you find a properly trained camouflage makeup artist or esthetician experienced in the use of camouflage makeup.

References:

1) Steinman, D.A. and Steinman, H.K:  Skin camouflage, pg 107 – 115 in Atlas of Cosmetic Surgery, 2nd Edition  Saunders Elsevier, Inc., 2009

2) Steinman, H.K: Cosmetic Camouflage. American Academy of Dermatology Dialogues in Dermatology 61(5), February 2008.

3) Aydogdu E, et. Al., Postoperative camouflage therapy in facial aesthetic surgery. Aesthetic Plast Surg 2005; 29(3):190-4.

4) Holme SA, Beattie PE, Fleming CJ. Cosmetic camouflage advice improves quality of life. Br J Dermatol 2002; 147(5):946-9.

Diedre A. Steinman
Paramedical Camouflage Makeup Artist

Howard K. Steinman, M.D.

Associate Professor of Dermatology
Director, Dermatologic and Skin Cancer Surgery                                                                                        Department of Dermatology                                                                                                                       Texas A&M University Health Sciences Center College of Medicine

Do not touch or wet the dressing the day of procedure. If bleeding or oozing occurs, hold steady pressure with gauze for 10 to 15 minutes. If bleeding does not stop, call your doctor.

The next day after procedure, remove dressing covering the wound. Gently apply hydrogen peroxide with gauze or cotton to the surgical area. Apply topical antibiotic ointment (such as Bacitracin, Neomycin, Polysporin, etc.) to the area twice daily followed by a band-aid. Topical antibiotics are available in pharmacies without a prescription. You should clean and cover the wound and use antibiotic ointment untill wound heals completely. One may shower as usual the day after the procedure. Avoid direct water pressure on the wound from the shower stream.
If you observe any reactions that are unusual, or concerning to you, please call your doctor or go to the nearest emergency room.

These instructions should only serve as guidelines, and not medical advice. They should not be relied upon for treatment of your wounds. Your doctor is responsible for providing you with detailed instuctions on wound care.

Alexander Doctoroff, D.O., F.A.O.C.D.
Assistant Chief of Dermatology,
Veterans Administration Medical Center
East Orange, New Jersey

Assistant Clinical Professor of Medicine,
University of Medicine and Dentistry of New Jersey
www.metropolitanderm.com

Common warts are caused by the human papilloma virus (HPV). The virus replicates inside the cells of the top layer of the skin. HPV “hijacks” the skin cells and tells them to divide. Rapidly dividing cells form protruding growths on the skin. These growths are not cancerous.

The HPV virus is transmitted from person to person, usually by skin to skin contact. The risk of catching common warts from another person is small. Warts are more common where skin has been broken, for example where fingernails are bitten.

How many kinds of warts are there?
The most common types of warts are common warts (verruca vulgaris), foot warts (verruca plantaris), and flat warts (verruca plana). The type of wart you get depends on a kind (or serotype) of HPV that caused it. There are more than 100 subtypes of HPV virus, and they all cause different types of warts. New types of HPV are discovered every year. All of the subtypes of HPV virus are similar to each other and share about 90% similarity in structure. The differences in structure of different HPV types produce differences in types of warts that can occur.

In addition to common warts, HPV is implicated in multiple diseases of the skin and mucous membranes, such as epidermodysplasia verruciformis, condyloma accuminata (genital warts), cervical dysplasia and carcinoma, and laryngeal papillomatosis.. Various serotypes cause specific types of warts, and favor certain anatomic locations. HPV type 1 is known to cause deep warts on hands and feet, types 2,4,27,29 are the culprits in common warts, types 3,10,28,49 cause flat warts, types 5,8,9,12,14 cause epidermodysplasia verruciformis. Most of the warts are harmless and never turn into cancer.

Treatment:
Currently there is no antiviral therapy available to eradicate the wart virus. HPV is resistant to freezing, drying, and solvents. The warts will go away when patient’s own immune system suppresses the HPV virus. While you wait for this suppression to occur, your doctor may use multiple types of treatment to speed up the process of recovery.

Destructive modalities include surgical removal, cryotherapy, surgery, electrocautery, cantharidin, and topical application of salicylic acid. None of these methods is 100% effective. The majority of therapies require multiple treatment sessions. The purpose of these treatments is not to kill the HPV virus. As pointed out above, this is not possible. Destructive treatments simply destroy or remove cells in which HPV virus accumulates. These modalities reduce viral load on the body, and allow the patient’s immune system to finish the job of destroying warts.

Immunotherapy attempts to use the body’s own immune system to get rid of warts. In this method, the patient is made allergic to a certain chemical which is then applied to the wart. Redness and irritation occur around the treated warts, and may result in their disappearance. Imiquimod is a cream used to boost the immune reaction of the body and clear the warts.

Since warts differ depending on their type and location on your body, only your doctor can choose the best method to treat your warts.

References:
Silverberg NB. Human papillomavirus infections in children. Current Opinion in Pediatrics. 16(4):402-9, 2004 Aug.

Alexander Doctoroff, D.O., F.A.O.C.D.
Assistant Chief of Dermatology,
Veterans Administration Medical Center
East Orange, New Jersey

Assistant Clinical Professor of Medicine,
University of Medicine and Dentistry of New Jersey
www.metropolitanderm.com

Presentation:
Half of patients develop vitiligo before the age of 20. The disorder presents with white patches surrounded by normal or darkened border. Both sides of the body usually have similarly distributed light patches (symmetrical involvement). Hairs in diseased areas also become white. Stress or trauma to the skin may provoke appearance of new patches.

Additional associations:
Since the immune system of patients with vitiligo is not working properly, it sometimes attacks tissues outside skin. If hair is attacked, patients present with patches of hair loss (alopecia areata). If thyroid gland is targeted, thyroiditis or Grave’s disease occurs. Additionally, pancreas, red blood cells, and adrenal glands can be rarely affected. That results in diabetes, anemia, and Addison’s disease respectively.

Treatment:
Treatment of vitiligo is difficult and sometimes frustrating. The course of vitiligo is chronic. Many areas successfully regaining color may become depigmented again. New white patches may appear during therapy. Yet, many patients get better with treatment, and regain their color.

If vitiligo involves a small area of the skin, topical corticosteroid preparations, tacrolimus ointment, or pimecrolimus cream may be tried first. The treatment is prolonged. First signs of success usually are not seen until after 3 months of use of a topical medicine. Corticosteroid creams have significant risk of glaucoma if used around the eyes. Additionally, they should not be used in the areas of thinner skin (e.g. genitals, groin). If these areas are involved, tacrolimus or pimecrolimus are safer. Your dermatologist should monitor skin for side effects (stretch marks, thinning, or appearance of blood vessels) if topical corticosteroids are used.

Phototherapy or light therapy (UVB and PUVA) is beneficial for many patients with vitiligo. This treatment is usually conducted in physician’s offices and therefore requires multiple visits per week. UVB therapy involves exposure to UVB light emitted by an artificial light source. Narrow band UVB (UVB with wavelengths 310-315 nm) is preferred to a broad band UVB (multiple wavelengths of UVB spectrum). PUVA first involves ingestion of a medication (psoralen) or topical application of psoralen solution. Psoralen prepares skin for a second phase of treatment – exposure to UVA light from the light box.

Surgical treatments, such as grafting or melanocyte transplantation can be tried on patches of stable vitiligo. In grafting, tiny pieces of person’s own normal skin are transplanted onto areas without pigment. Melanocyte transplantation involves cells cultured from the person’s unaffected skin and injected into blisters on the depigmented areas or directly into dermabraded skin. These treatment modalities are not widely available. Large dermatology departments in medical schools are more likely to be involved in surgical treatment of vitiligo then individual practicing dermatologists.

Cosmetic camouflage with various cosmetics is helpful if disease is not responding to treatment. If the disease involves large areas of the body, some patients choose to completely depigment (get rid of pigment) their whole skin.

Since areas with vitiligo lack pigmented cells, they also lack natural protection from sunlight. Therefore, broad-spectrum sunscreens should be used on affected areas at all times to protect from solar radiation.

References:
Whitton ME. Ashcroft DM. Barrett CW. Gonzalez U. Interventions for vitiligo. Cochrane Database of Systematic Reviews. (1):CD003263, 2006.
UI: 16437451.

Support organizations:
www.vitiligosupport.org
www.avrf.org
www.nvfi.org
www.vitiligoforum.com

Alexander Doctoroff, D.O., F.A.O.C.D.
Assistant Chief of Dermatology,
Veterans Administration Medical Center
East Orange, New Jersey

Assistant Clinical Professor of Medicine,
University of Medicine and Dentistry of New Jersey
www.metropolitanderm.com

Presentation:
Tinea versicolor is characterized by scaly, pink to tan, or white patches which occur most commonly on the neck, shoulders, chest, and back. The lesions of tinea versicolor do not tan normally and often become more noticeable when the surrounding skin is tan.

Treatment:
Tinea versicolor is caused by a yeast that normally occurs on the skin and is therefore not contagious. It is often successfully treated with various topical antifungal agents. In more diffuse cases, oral antifungal therapy may be necessary. Tinea versicolor often has a high rate of recurrence after treatment and may require prophylactic treatment with antifungal creams and dandruff shampoos a few times a week.

References:
Faergemann J, Gupta AK, Al Mofadi A, Abanami A, Shareaah AA, Marynissen G. Efficacy of itraconazole in the prophylactic treatment of pityriasis (tinea) versicolor. Arch Dermatol. Jan 2002;138(1):69-73.
Mellen LA, Vallee J, Feldman SR, Fleischer AB Jr. Treatment of pityriasis versicolor in the United States. J Dermatolog Treat. Jun 2004;15(3):189-92.
Karakas M, Durdu M, Memisoglu HR. Oral fluconazole in the treatment of tinea versicolor. J Dermatol. Jan 2005;32(1):19-21.

Mollie Jan, D.O.
Department of Dermatology
Philadelphia College of Osteopathic Medicine/Frankford Hospital
Philadelphia, Pennsylvannia.

In telogen effluvium, a certain precipitating event (some of which are listed below) shifts hairs into telogen. As a result, more than 10% (e.g. 20 or 30%) of scalp hair start their resting phase and get lost from scalp surface. Such hair loss is not permanent, since hairs only stay in a telogen phase for a limited amount of time. Once telogen phase is completed, hairs usually regrow.

Telogen effluvium usually occurs two to three months following various precipitating events. The most common causes include high fevers, severe emotional and physical traumas, surgical operations, crash diets, child birth, and certain medications. Hair re-growth can usually be seen by six months. To make the diagnosis of telogen effluvium, the physician may ask the patient to do a two-week hair count and may perform a hair pull test (where strands of hair are pulled from the scalp).

Daily hair counts of greater than 100 hairs and more than four easily pulled hairs (hair pull test) are suggestive of the diagnosis of telogen effluvium. The most important issue in telogen effluvium is finding a precipitating event or underlying cause. Often times, blood tests may be needed to find underlying causes.

Presentation:
Telogen effluvium presents with an acute onset of diffuse uniform hair loss involving the entire scalp. There is no redness or scarring of the scalp. The degree of shedding is usually much less than 50% of the total scalp hair. Telogen effluvium almost never results in total baldness.

Treatment:
Telogen effluvium does not require treatment and is usually self-limited. If a medication is found as the causative agent, discontinuation of the medication will result in resolution of the telogen effluvium.
In rare cases, a chronic type of telogen effluvium may occur. It usually lasts longer than six months, is found mostly in middle-age women, and may require a biopsy of the scalp to make the diagnosis. As is the case with acute telogen effluvium, it will not result in complete hair loss and will tend to resolve on its own.

References:
Camacho F: Alopecias due to telogen effluvium. In: Camacho F, Montagna W, eds. Trichology: Diseases of the Pilosebaceous Follicle. Madrid, Spain: Aula Medica Group; 1993: 403-10.
Goette DK, Odom RB: Alopecia in crash dieters. JAMA 1976 Jun 14; 235(24): 2622-3.
Kligman AM: Pathologic dynamics of human hair loss. I. Telogen effuvium. Arch Dermatol 1961 Feb; 83: 175-98.
Sinclair R: Chronic telogen effluvium: A study of 5 patients over 7 years. J Amer Acad Dermatol 2005; 52 (2 Suppl 1): S12-S16.

Mollie Jan, D.O.
Department of Dermatology
Philadelphia College of Osteopathic Medicine/Frankford Hospital
Philadelphia, Pennsylvania.

Presentation:
Telangiectasias present as blue, purple or red lines on the surface of the skin. They may also appear as a central red dot with red lines emerging radially from the central area, a so-called “spider” telangiectasia. Telangiectasias occur anywhere on the body but are most commonly observed on the face, especially around the nose.

Treatment:
Telangiectasias not associated with an underlying skin cancer are benign and do not need to be treated. If the telangiectasias are cosmetically disturbing, they may be treated with an electric needle, intense pulse light or lasers. Multiple treatments are sometimes needed to obtain the best results.

Reference:
James WD, Berger TG, Elston DM. Andrews’ Diseases of the Skin Clinical Dermatology 10th edition. Elsevier 2006.

Anita Osmundson, D.O.
Department of Dermatology
Philadelphia College of Osteopathic Medicine/Frankford Hospital
Philadelphia, Pennsylvannia.

Stephen M. Purcell, D.O., F.A.O.C.D.
Professor and Chairman of the Department of Dermatology
Philadelphia College of Osteopathic Medicine
Philadelphia, Pennsylvannia
www.adaltd.com