Panniculectomy vs Abdominoplasty

Updated 3/2017-- photos and links removed as many no longer active.

You’ve had your gastric bypass and have lost over 100 lbs. Now you have "all this loose, saggy skin that just hangs" and you have "rashes under the fold all the time". Will your insurance pay for a tummy tuck? Probably not what you are thinking of as a tummy tuck. They may pay for a panniculectomy, but not an abdominoplasty. So let me try to tell you the difference between the two. Photo from article (see below).

Panniculectomy is the removal of the loose (excess) skin and fat tissue below the belly button (umbilicus). Nothing is done to the (possible/probable) loose skin above the belly button. It is strictly to help remove the overhanging skin that is trapping moisture and creating a hygiene and chronic rash problem. It is not meant to improve your overall body shape.

An abdominoplasty is the removal of the loose (excess) skin and fat tissue from the abdomen (stomach area) with transposition of the skin around the umbilicus (the belly button doesn’t usually get moved, the skin around it does) and often tightening (plication) of the abdominal muscles. This creates a more pleasing shape as it addresses the entire abdomen. It is not just a functional surgery, but a cosmetic one.

Look at the above photos. The one on the left with minimal upper body excess skin might get both the functional and improved body shape (cosmetic result) with the panniculectomy. The one on the right would still have the "upper" skin roll as this is from skin above the umbilicus. So by definition, the panniculectomy would not do anything to improve this. The insurance company (see the California BC restrictions) would probably not be persuaded to make an exception for a full abdominoplasty which is what she would need. Chances are this person gets skin irritation below the upper roll also. Frustrating, isn’t it?

Prior to this year (2007) when a surgeon coded the surgical procedure for a panniculectomy or an abdominoplasty the same code was used. This made it difficult (without reading the operative note) to truly tell what had been done.
CPT 15831 Excision, excessive skin and subcutaneous tissue (including lipectomy);abdomen (abdominoplasty)

As of this year the coding has changed which makes it more clear to an insurance company what has been done for the patient. Perhaps it will also help clarify for the patient that a "cosmetic tummy tuck" is not what they will get (unless they are willing to pay the difference) when a panniculectomy is done. The new codes are:
CPT 15830 Excision, excessive skin and subcutaneous tissue (includes lipectomy); abdomen, infraumbilical panniculectomy
CPT 15847 Excision, excessive skin and subcutaneous tissue (includes lipectomy), abdomen (eg abdominoplasty) (includes umbilical transposition and fascial plication) (List separately in addition to code for primary procedure)
Use 15847 in conjuction with 15830

To know whether your insurance policy will help you out with this issue, check your policy or call your insurance provider. Here is BC of California’s policy on the issue. Here is Cigna's. Many insurance companies have similar policies. Some consider it all cosmetic.

Photo--A Classification of Contour Deformities after Bariatric Weight Loss: The Pittsburgh Rating Scale; Plastic & Reconstructive Surgery. 116(5):1535-1544, October 2005; Song, Angela Y. M.D.; Jean, Raymond D. M.D.; Hurwitz, Dennis J. M.D.; Fernstrom, Madelyn H. Ph.D.; Scott, John A. M.S.; Rubin, J Peter M.D.

Community Acquired MRSA--Prevention Tips

Updated 3/2017-- photos and all links (except to my own posts) removed as many no longer active.

Staphylococcus aureus, or “staph” as it is sometimes called, is a common bacterium found on the skin or in the nose of ~25-30% of humans. Staph aureus is usually harmless, but in certain instances it may cause moderate to severe skin infections. Less commonly, it causes more serious systemic infections: bloodstream, surgical wound and pneumonia requiring hospitalization. One group of staph known as MRSA (methicillin-resistant Staphylococcus aureus) was first identified in the 1960’s. It is now prevalent in most hospitals. The organisms are resistant to multiple antibiotics (specifically, all antibiotics known as beta lactams, as well as other antibiotic families), and are therefore cause for considerable concern.

A newer form of staph infection, known as CA-MRSA (for community-acquired, or community-associated Staphylococcus aureus) has appeared with increasing frequency and is now epidemic within certain community populations. Whereas hospital MRSA is almost always found in persons with established risk factors associated with prior medical treatment, these are not present in CA-MRSA. Today, in the U.S. a little more than 10% of all MRSA infections are CA-MRSA. This form causes serious skin and soft tissue infections in otherwise healthy persons who have not been recently hospitalized or undergone invasive medical procedures. Hospitalization is required in approximately one out of five cases.

CA-MRSA has been identified most frequently among specific populations, including prisoners, athletes, children, men who have sex with men, military recruits, Pacific Islanders, Alaskan Natives and Native Americans.

Rather than getting into treatment, I want to highlight was that can help PREVENT getting or spreading CA-MRSA.

1. Clean your hands frequently with soap and warm water or an alcohol-based hand rub.
2. Keep your linens and clothes clean. Wash sports clothing and washable athletic gear with laundry detergent after each use (not after a week or two of use).
3. Do not share personal care items. At home this includes washcloths, towels, and razors. At the gym or school this includes sports towels, sports equipment (helmets, gym mats), uniforms/clothing. Equipment that can't be washed should be cleaned with an antibacterial solution after each use.
4. Take care of skin cuts or abrasions before they get infected. Wash them with soap and water, then cover with a dry, sterile bandage daily. Promptly throw away the old bandage. Wash your hands before and after changing the bandages.

If you are given antibiotics for an infection, it is important to take ALL of the doses. Don't quit "when you feel better" or the skin "looks better". Finish all the doses. The bacteria that don't get killed by the missed doses can morph into tomorrow's superbugs.

Staph Infections--e-Medicine article by Robert W Tolan Jr, MD

Community-Associated MRSA Information for the Public --Centers for Disease Control

Staphylococcus aureus Section--Minnesota Department of Health

An "Awe"-some Birthday!

Updated 3/2017-- photos and all links (except to my own posts) removed as many no longer active.

Today is my 50th birthday. I like Kim over at Emergiblog am a 1957 Classic Model. I have always been in awe that so many babies are born "perfect" with the correct number of fingers and toes, eyes and ears in the correct place, etc. My mother had 8 "perfect" babies (one stillborn). A few years ago she and I were on the phone talking about drugs and side effects (don't recall why). I happened to bring up Thalidomide as an example of how a "good" drug used for the wrong thing or at the wrong time (during pregnancy) could have horrible "side effects". She asked me what kind of problem thalidomide caused, as she remembered taking it for morning sickness when pregnant with me. I was stunned, but managed to gently (I hope) tell her about the horrible birth defects it could cause if taken during a narrow window early in pregnancy. Unfortunately this is when morning sickness is often a problem. I asked her how she had come to take thalidomide. Had a doctor prescribed it for her? She told me that she had bought it over the counter at the drug store in Tokyo. My dad was stationed in Tokyo, Japan. They had been there for a few years. My older brother was 3 yr and my older sister (born in Japan in April 1956) was only around 7 months old when she got pregnant with me. My mom told me that she had not seen one of the military doctors because she knew she would not be allowed to return to the States as they were due to be re-stationed in Ft Leonard Wood, Missouri. It was around Thanksgiving, early December 1956. In the 50's women were not allowed to travel such distances while pregnant. So if my mother is correct and she took Thalidomide while pregnant with me, then I am even more in awe that I was a "perfect" baby. Photo credit

The individual type of thalidomide malformation depends on the time of intake. Thalidomide does not produce malformations if only taken before the 34th day after the last menstruation and usually no malformation if taken only after the 50th day.

Within the sensitive period from day 35 to day 49 there is the following sequence:
1. Absence of ears and deafness: 35th - 37th day
2. Absence of arms: 39th - 41st day
3. Phocomelia with 3 fingers: 43rd - 44th day
4. Thumbs with 3 joints: 46th - 48th day.

If thalidomide has been taken throughout the sensitive period, the consequence may be severe defects of ears, arms and legs and of internal malformations, which often led to early death. About 40 per cent of thalidomide victims died before their first birthday.

Check out

Frances Oldham Kelsey: FDA Medical Reviewer Leaves Her Mark on History
By Linda Bren; FDA Consumer Magazine; March-April 2001

The Schizophrenic Career of a "Monster Drug" by William A. Silverman, MD; PEDIATRICS Vol. 110 No. 2 August 2002, pp. 404-406
The Current Status of Thalidomide in the Management of Multiple Myeloma; Glasmacher A, von Lilienfeld-Toal M; Acta Haematology 2005; 114 Suppliment 1:3-7

Tips for Finding a Good Bra Fit

Updated 3/2017-- photos and all links (except to my own posts) removed as many no longer active.

Tips for finding your proper bra size:

First put on the best fitting, unpadded bra you own. If necessary pin the straps up to bring the breasts to the correct level. Get a tape measure and either measure yourself or have a friend measure you. The general rule of thumb for all measuring is: less than ½”, round DOWN, more than a ½”, round UP. So if your measurement is 32 ¼”, call it 32.

1. The first measurement is taken under the bust. You want to hold the tape snugly, but not tight. You will add either 4" or 5" to this measurement to make it an even number. This is the "band size" for the bra size.
2. Next measure the circumference above the bust under the arms (upper bust).
3. Measure the full bust circumference (nipple level). Make sure the tape measure is straight. Do not let the tape droop in the back.
4. Subtract measurement 2 (upper bust) from measurement 3 (full bust). Each inch difference is a bra cup size. For example, 1" corresponds to an A cup, 2" to a B cup, 3" to a C cup.

Second, you must try on bras. As we women know, there are variance between different styles and manufactures, so now you take your measurements and go try on different styles. Find the bra style that feels and looks best on you. You want the area between the cups to touch or almost touch the chest wall (no big air gap). The bra is not a sling for the breasts. They should be supported by the whole bra, not hanging from the straps.

Women with augmented breasts (implants) may find it more difficult to find a good fit as the implant shape may alter the way the bra fits. Because of this two plastic surgeons developed a bra designed for the augmented breast. "Le Mystère No.9 is a collection of innovative, designer bras incorporating patented technology so as to compliment the unique changes in shape and size that occur after a breast augmentation. Le Mystère has created the only bra on the market designed specifically for augmented women that fits true to size. You will no longer have to go up one cup size to accommodate the increased depth of your breast, since the design of the No.9 garments has taken into account all of the anatomic changes that occur after your breast enhancement. Now it’s easy for you to find a superior fitting bra for your post augmentation breasts. Look no further, Le Mystère No.9 is here!"

Resources:
Teen Health--Finding the Right Bra
Sandra Saffle, Nordstrom's top bra fitter for Oprah's Bra Fitting Tips
Sew Sassy Fabrics (if you want to make your own)

Kidney Stones

Updated 3/2017-- photos and all links (except to my own posts) removed as many no longer active.

My brother-in-law has kidney stones and my sister is asking me "Do you know of anything that will dissolve stones? He has been in the hospital in Nashville, with 2 kidney stones. One passed the other is approx 1.5 cm. He is home right now." I am not an expert on kidney stones, but thought I might pass this on. The article referenced below is a very nice one. This is the e-mail I sent her:

Dear Sis,
There is a really nice article on Medscape [The Role of Diet in the Prevention of Common Kidney Stones by Christy Krieg]. Some of it depends on what type of stone he has (oxalate, etc). In case you can't access it, here are the main points:

Dietary Changes to help prevent kidney stones:
1. Increased fluid intact (to the point of pale urine).
Many patients ask what fluids are recommended, and which are prohibited. The simple answer is that water is best. For those with excessive urinary oxalates, black tea should be eliminated because black tea is a high-oxalate beverage. In summary, stone formers should drink more water and avoid excess caffeine, black tea, and grapefruit and apple juices. Lemonade is often recommended, as it supplies dietary citrate, a stone inhibitor and pH buffer when excreted later in the urine.

2. Consume adequate calcium.
Several recent studies have shown, in fact, that adequate calcium intake is associated with decreased stone formation. Why might increased dietary calcium reduce the risk of calcium stone formation? Calcium and oxalate bind in the gut and in the urine to form a nonabsorbable compound. Low dietary calcium permits greater free oxalate to be absorbed in the gut and excreted in the urine, which may be counterproductive for calcium oxalate stone formers. Restricted calcium intake results in increased urinary oxalates, a risk for stone formation. Low-fat dairy products, green leafy vegetables, broccoli, fortified foods, and almonds are excellent sources. Patients should consume enough dietary calcium to meet (but not exceed) the United States Recommended Daily Allowance (RDA) of calcium, which ranges from 1,000 to 1,200 milligrams daily for adults.

3. Limit dietary oxalates
Oxalate restriction should be attempted. The highest levels of oxalate are found in chocolate, nuts, beans (including soybeans), rhubarb, spinach, beets, and black tea. A thorough oxalate list can be found on the Web site of the Oxalosis and Hyperoxaluria Foundation (http://www.ohf.org/diet.html). This list is exhaustive and may be overwhelming to patients. Vitamin C is a precursor to endogenous production of oxalates, so some clinicians recommend avoiding mega-doses of vitamin C

For a simple list of high-oxalate foods, visit http://www.gicare.com/pated/edtgs29.htm.

4. Limit sodium (salt) intact.
Because calcium and sodium compete for reabsorption in the renal tubules, excess sodium intake and consequent excretion result in loss of calcium in the urine. High-sodium diets are associated with greater calcium excretion in the urine. The goal of therapy should be a "no added salt diet," or the equivalent of 2,000 mg per day or less of dietary sodium. Reduction of dietary sodium is difficult and disappointing to patients. They may believe they have made significant reductions and sacrifices, while their urine sodium remains high. Consultation with a registered dietician may help the patient achieve the specific goal of a sodium intake of 2,000 milligrams or less per day.

5. Limit animal protein
The effect of excess animal protein (purine) is most obvious for the uric acid stone former. Uric acid, a byproduct of purine metabolism, is excreted in large quantities in the urine. Excess protein creates urine with high total urine uric acid, potentially high supersaturation of urine uric acid, and a low pH, necessary for formation of uric acid stones. There is no inhibitor of uric acid crystal formation (Menon & Resnick, 2002), so dietary measures focus on reducing uric acid and increasing urine volume. Reduction of animal protein to 12 ounces per day for adults is recommended.


I hope this will help, though I know it will be tough to get him to make some of the dietary changes. Start small--first with the water intact, less caffeine, etc.

Love you,
rlb

Other sources of information:

Mayo Clinic article--Kidney Stones

Urology Channel--Kidney Stones

NIH.gov MedlinePlus--Kidney Stones

Bags and Purses

I finished this bag this past weekend. The fabric used to be a skirt. The elephants march around the purse and are "seamed" together such that each elephant is whole. You have to look very closely to see the seam. The fabric is quilted. The bag is fully lined with a cardboard reinforced bottom. It has a Straight Hex-Open Frame closure (18") and 1.5" nylon straps. The pattern and hardware are from Ghee's. I made it to donate to a Silent Auction that the Historic Arkansas Museum will have this fall during a quilt exhibit.

I am working on a "messenger bag". It has 2 zipper pockets and 1 magnetic-snap pocket. It will have a long strap that can be worn across the body from shoulder to hip for security. The finished size will be 12 in. by 11 1/2 in. The back of the pattern states "A make it in minutes bag, use double faced quilted fabric with belting or webbing strap. For added pizzazz, chevron strip piece." Since I am quilting my own double faced fabric it is taking me longer, but I can use prettier fabric this way. It also gives me a chance to try to improve my "free motion" machine quilting. I do better with a walking foot and the start-stop method.

Surgery and Birth Control Pills

Updated 3/2017-- photos and all links (except to my own posts) removed as many no longer active.

So you are having surgery and don't want to get pregnant in the postoperative period. What are the issues surrounding surgery that could interfere with your birth control pills (BCPs)? Photo credit

Antibiotics

You most likely will have at least one IV (intravenous) dose of an antibiotic and may be sent home on an antibiotic. Most references (PDR, pharmacy) that I have easy access to continue to say "yes, antibiotics may interfere with the efficacy of your BCP's". This is based on early data (20 yrs ago) which seemed to indicate that when antibiotics were taken along with BCP, more women got pregnant than you would normally expect. Drugs like ampicillin and tetracycline were suspected to interfere with BCPs. However, all the recent studies that have looked at this, have shown that antibiotics do not increase the pregnancy rate at all. These studies point out that the old data was not reliable enough to draw conclusions about pregnancy rates on any of the antibiotics. some antibiotic have been studied and shown not to affect the metabolism of BCPs. Ciporfloxcin is one that does not seem to alter metabolism. Fluconazole (used to treat vaginal yeast infections) does not decrease estrogen levels in pill users, and may actually raise estrogen levels. The safe thing to do is follow the "old rule" and use alternative methods (abstinence, condoms, spermicides) while taking the antibiotics and for an additional 2 weeks.

Postop Nausea and Vomiting

You may end up with postop nausea and vomiting and can't take (or simple forget to take) your birth control pills. If we compare this to when you have the flu, gastritis or a diarrhea condition, the issue becomes whether you are able to absorb the pill. There is little data to address this issue. Fortunately most of these illness (including postop nausea and vomiting) do not last long. It is known that missing up to 10 pills in a row (7 placebo pills and the 1st 3 pills of a pill pack) does not result in ovulation. So it may be unlikely that this would decrease the efficacy of your BCPs. Once again, the safe thing to do is use alternative methods (when feeling up to it)--abstinence, condoms, spermicides for an additional 2 weeks.

Drugs Affecting Birth Control Pills (web article) by Frederick R. Jelovsek MD
5 Reasons for Contraceptive Failure (web article)--About.com, Women's Health

Routine--Urine Pregnancy Tests Preop

Updated 3/2017-- all links (except to my own posts) removed as many no longer active.

At the surgery center and hospitals that I operate in, every woman with a uterus gets a urine pregnancy test. It is difficult to tell the woman who is scheculed for a tummy tuck or breast lift that she is pregnant. They have gone through the mental checks-and-balance sheet and decided they don't want any more children. And if they are younger (scheduled for an augmentation mammoplasty), may not be "ready" to start a family. So I find it difficult (and the nurses tell me even more stories--the woman who came to have a tubal only to find out she was pregnant............). I'm not sure what the "score" is. Some are happy instantly. Some are shocked, but went I check on them later (a day or so) are happy. Some are angry or scared. Some never find the news happy, even a week or so later. I have always been the one who goes and tells the woman, never leaving it to the nurses. I don't enjoy it. Though it can turn out to be a happy event. You just never know. And this happens to me or another surgery every month or so.

More Information:

Sensitivity of Over-the-Counter Pregnancy Tests: Comparison of Utility and Marketing Messages by Laurence A. Cole; Jaime M. Sutton-Riley; Sarah A. Khanlian; Marianna Borkovskaya; Brittany B. Rayburn; William F. Rayburn (MedScape Article)

Web MD--Home Pregnancy Tests

Breast Self-Exam (BSE)

 Updated 3/2017-- photos and all links (except to my own posts) removed as many no longer active.

Recently a small study at Leo Jenkins Cancer Center, North Carolina found that most women with breast cancer had found their own tumors through self examination. "Conclusions: Most breast cancers (75%) were found by self-examination, even among women who had regular mammography. We did not find any demographic factor that predicted mammography as the primary method of tumor identification. These findings suggest that self-examination remains an important method of breast cancer identification." Photo credit.

The Five Steps of a Breast Self Exam:

1. Begin by looking at your breasts in the mirror with your shoulders straight and your arms on your hips. Look for any changes in the size, shape, and color. Look for any dimpling, puckering, or bulging of the skin. Has the nipple changed position or become inverted? Is there redness, soreness, a rash, or swelling?
2. Now, raise your arms and look for the same changes.


3. While you're at the mirror, gently squeeze each nipple between your finger and thumb and check for nipple discharge (this could be a milky or yellow fluid or blood).


4. Next, feel your breasts while lying down, using your right hand to feel your left breast and then your left hand to feel your right breast. Use a firm, smooth touch with the first few fingers of your hand, keeping the fingers flat and together. Cover the entire breast from top to bottom, side to side—from your collarbone to the top of your abdomen, and from your armpit to your cleavage. Follow a regular grid pattern, so that no areas are missed.Begin examining each area with a very soft touch, and then increase pressure so that you can feel the deeper tissue, down to your ribcage.


5. Finally, feel your breasts while you are standing or sitting. Many women find that the easiest way to feel their breasts is when their skin is wet and slippery, so they like to do this step in the shower. Cover your entire breast, using the same hand movements described in Step 4.

If you find any changes, lumps, or nipple discharge, then call your physician. Schedule an exam and mammogram. Breast cancer is the most common cancer in women, but it can be successfully treated. The key? Early detection.

Bell's Palsy

Updated 3/2017-- photos and all links (except to my own posts) removed as many no longer active.

The picture to the right features the characteristic asymmetric smile of Bell's Palsy caused by paralysis of one side of the face. (photo credit)

Five years ago I experience such a smile (and when really tired still do to a small extent). I woke up that Saturday morning and noticed that my tongue felt "thick" and my head ached, especially on the right side and mostly in my ear. Over the course of the day, I went on to loose the muscle function of my mouth on the right side, then the check, then the eyelid function, and last the forehead. I knew what it was. I had ruled out a stroke early on--no vision problems, no weakness in either arm or leg. The ascending facial paralysis cinched the diagnosis for me. Bell's Palsy.

I didn't bother any of my colleagues that weekend, but waited until Monday morning to call an ENT friend. He put me on a Decadron dose pkg and Acyclovair. The steroids decreased the swelling around my facial nerve and the ear pain subsided within 24 hours. I didn't appreciate any return of my facial nerve until 5-6 weeks later. I had a "mild" case. I didn't drool, but could not use a straw nor could I whistle (both actions need a good seal of the lips). Food tasted different on one side than the other. The teeth on the right side of my mouth were (and to a degree remain) very sensitive to cold/heat. I found myself chewing (these muscles aren't involved as they are CN V not VII) more on the left side for multiple reasons--fear of drool, taste buds off, teeth sensitivity. My right eye closed at night, but needed Lacrilube to keep it closed. I was fortunate that I did not have to patch it for more than a few weeks. With my blink reflex gone, it seemed that dust particles and gnats found there way into my right eye. I wore my sun glasses on the walks with the dogs to help protect my eye (don't usually do this). I also found I needed plain lens glasses indoors where fans or air condition drafts would irritate my eye. The glasses helped to prevent this. I kept artificial tears at home, in my purse, and at my office.

Most of my facial function returned--98-99%. There are some very minor things that didn't. There is a difference (I can feel and see) in the muscles around my eye (obicularis oculi) and the mouth (slightly uneven). And the tongue and teeth still off some. Nothing anyone would be able to measure. Also, the right ear canal is more sensitive to breezes, so on fall/winter days that are windy I am more likely to wear 180 degree ear muffs.

I did not miss a day of work. My hands still functioned, so did my brain. I admit I was very self-conscious (the plain lens glasses gave me something to "hide" behind as well as helped protect my eye) around people. With poor control over the right side of my mouth, some words were not easy to pronounce (plosive constant's need a good lip seal). If patient's noticed, I would tell them what was going on. If not, I tried to be as "normal" as possible. I did more "closed-lip" smiles than previous. Oh, yeah, it's weird kissing when only one half of your mouth works (smile).

Bell's palsy is a form of temporary facial paralysis characterized by facial drooping on the affected half. It is due to malfunction of the facial nerve (CN VII) which controls most of the muscles of the face. Named after Scottish anatomist Charles Bell, who first described it, Bell's palsy is the most common acute mononeuropathy (disease involving only one nerve), and is the most common cause of acute facial nerve paralysis. Bell’s palsy affects about 40,000 people in the United States every year. It affects men and women equally and can occur at any age, but is most common between 15 and 60 yrs of age. It affects approximately 1 person in 65 during a lifetime. Most scientists believe that a viral infection such as viral meningitis or the common cold sore virus -- herpes simplex-- causes the disorder when the facial nerve swells and becomes inflamed in reaction to the infection.

The prognosis for individuals with Bell's palsy is generally very good. The extent of nerve damage determines the extent of recovery. Improvement is gradual and recovery times vary. With or without treatment, most individuals begin to get better within 2 weeks after the initial onset of symptoms and most recover completely, returning to normal function within 3 to 6 months. For some, however, the symptoms may last longer. In a few cases, the symptoms may never completely disappear. In rare cases, the disorder may recur, either on the same or the opposite side of the face.

REFERENCES

Mayo Clinic--Bell's Palsy

National Institute for Neurologic Disorders & Stroke--Bell's Palsy Fact Sheet

Bell's Palsy Information Site & Forum

HOW CRUEL TO CALL IT 'BELL'S PALSY!' By Graeme Garden

e-Medicine article--Bell's Palsy by Michael Lambert, MD

Skin Cancer--Melanoma

Updated 3/2017-- photos and all links (except to my own posts) removed as many no longer active.

Melanoma is a malignancy of pigment-producing cells (melanocytes) located predominantly in the skin, but also found in the eyes, ears, GI tract, leptomeninges, and oral and genital mucous membranes. Melanoma accounts for only 4% of all skin cancers; however, is responsible for more than 77% of skin cancer deaths worldwide. Early detection of thin cutaneous melanoma is the best means of reducing mortality. In the United States, one person each hour dies from metastatic melanoma.

The development of melanoma appears to be related to multiple risk factors, including fair complexion, excessive childhood sun exposure and blistering childhood sunburns, an increased number of common and dysplastic moles, a family history of melanoma, the presence of a changing mole or evolving lesion on the skin, and, importantly, older age. Melanoma occurs most commonly on the trunk in white males and the lower legs and back in white females. In African American, Hispanic, and Asian person, the most common site is the plantar foot (sole), followed by subungual, palmar, or mucosal sites.  

A new or changing mole or blemish is the most common warning sign for melanoma. ABCDE criteria (Friedman, 1985, Abassi 2004) for a changing mole is very useful. They have the greatest diagnostic accuracy when used in combination. More recent use of the "ugly duckling" warning sign, wherein skin examination is focused on recognition of a pigmented or clinically amelanotic lesion that simply looks different from the rest, may assist with detection of lesions that lack the classic ABCDE criteria (Grob, 1998; Gachon, 2005).

Asymmetry: Half the lesion does not match the other half.
Border irregularity: The edges are ragged, notched, or blurred.
Color variegation: Pigmentation is not uniform and may display shades of tan, brown, or black. White, reddish, or blue discoloration is of particular concern.
Diameter: A diameter greater than 6 mm (the size of a pencil eraser) is characteristic, although some may have smaller diameters. Any growth in a nevus warrants an evaluation.
Evolving: Changes in the lesion over time are characteristic. This factor is critical for nodular or amelanotic (no color or pigment) melanoma, which may not exhibit the classic criteria above.

Four major subtypes of primary cutaneous melanoma have been identified:
Superficial spreading melanoma is most common on the trunk in men and women, and on the legs in women. It is most commonly seen in individuals aged 30-50 years. It manifests as a flat or slightly elevated brown lesion with variegate pigmentation (ie black, blud, pink, or white discoloration). It is generally greater than 6 mm in diameter, irregular, and with asymmetric borders.

Nodular melanoma occurs in 15-30% of patients. It is most commonly seen on the legs and trunk. Rapid growth may occur over weeks to months. This subtype is responsible for the most thick melanomas. It manifests as a dark brown-to-black papule or dome-shaped nodule, which may ulcerate and bleed with minor trauma. It may also be amelanotic. It tends to lack the typical ABCDE melanoma warning signs and may elude early detection.

Lentigo maligna melanoma is typically located on the head, neck, and arms (chronically sun-damaged skin) of fair-skinned older individuals (average age 65 yrs). It grows slowly over 5-20 years. The in-situ precursor lesion is usually large (1-3 cm or more in diameter), present for a minimum of 10-15 years, and demonstrates macular pigmentation ranging from dark brown to black, although hypopigmented (white) areas are common within lentigo maligna. Dermal invasion (progression to lentigo maligna melanoma) is characterized by the development of raised blue-black nodules within the in-situ lesion.

Acral lentiginous melanoma is the least common subtype (2-8% of melanoma cases in white persons). It accounts for 29-72% of melanoma cases in dark-skinned individuals (African American, Asian, and Hispanic persons) and because of delays in diagnosis, may be associated with a worse prognosis. Acral lentiginous melanoma occurs on the palms, on the soles, and beneath the nail plate (subungual variant). Subungual melanoma may manifest as diffuse nail discoloration or a longitudinal pigmented band within the nail plate. It must be differentiated from a benign junctional melanocytic nevus of the nail bed which has a similar appearance. Pigment spread to the proximal or lateral nail folds is termed the Hutchinson sign and is a hallmark for acral lentiginous melanoma.

Rare melanoma variants (less than 5%) include desmoplastic/neurotropic melanoma, mucosal (lentiginous) melanoma, malignant blue nevus, melanoma arising in a giant congenital nevus, and melanoma of soft parts (clear cell sarcoma).

Amelanotic melanoma (less than 5% of melanomas) is non-pigmented. It appears, clinically, pink or flesh-colored, often mimicking basal cell or squamous cell carcinoma or a ruptured hair follicle. It occurs most commonly in the setting of the nodular melanoma subtype or melanoma metastasis to the skin.

Primary risk factor for or clinical warning signs of melanoma include:
Changing mole (most important clinical warning sign)
Clinical atypical/dysplastic nevi (particulary more than 5-10)
Large number of common nevi (more than 100)
Large (giant) congenital nevi (more than 20 cm in diameter in an adult)
Personal history of melanoma or First-degree relative with melanoma
Sun sensitivity/history of excessive sun exposure
Prior nonmelanoma skin cancer (BCC or SCC)
Male
Age older than 50 years
Presence of xeroderma pigmentosum or familial atypical mole melanoma syndrome (Both of these genodermatoses confer a 500-1000 fold greater relative risk of developing melanoma)
A fair-skin phenotype (blue/green eyes, blond or red hair, light complexion, sun sensitivity) and the occurrence of blistering sunburn(s) in childhood and adolescence are universal risk factors for melanoma.

Surgery is the primary mode of therapy for localized cutaneous melanoma. The narrowest efficacious margins for cutaneous melanoma have yet to be determined. Surgical margins of 5 mm are currently recommended for melanoma-in-situ, and margins of 1 cm are recommended for melanomas up to 1 mm in depth (low-risk primaries). In some settings, tissue sparing may be critical and Mohs margin-controlled excision may be appropriate. Prophylactic lymph node dissection for primary cutaneous melanoma of intermediate thickness initially was believed to confer a survival advantage on patients with tumors of 1-4 mm in depth. Lymphatic mapping and sentinel node biopsy have effectively solved the dilemma of whether to perform regional lymphadenectomy (in the absence of clinically palpable nodes) in patients with thicker melanomas (>1 mm in depth).

Surgical oncologist will usually do the surgical excision, lymph node excision, etc. Medical oncologist are needed to discuss adjuvant therapy with IFN alfa, experimental melanoma vaccines, or other clinical trials. They may also discuss (and initiate) treatment of metastatic melanoma (stage IV) with chemotherapy, high-dose IL-2, biochemotherapy, or clinical trials, as indicated. Radiation oncologist may be needed for adjuvant treatment of resected regional nodal metastasis with extracapsular extension or for palliative treatment fo distant metastatic disease (particularly bone metastasis or brain involvement).

Skin Cancer--Squamous Cell Carcinaoma

Updated 3/2017-- photos and all links (except to my own posts) removed as many no longer active.

Squamous cell carcinoma (SCC) is the second most common form of skin cancer, with over 250,000 new cases per year estimated in the United States. Most (96-97%) are localized and if identified early and treated promptly will not be serious. The other 3-4% can be very invasive in nature, can spread to distant organs (metastasize) and become life-threatening. SCC on the lip or ear appear to be the sites most likely to metastasize. These should be taken seriously. 

SCC is a malignant tumor that arises in the squamous cells of the upper layer of skin (of epidermal keratinocytes). Most arise from sun-induced precancerous lesions known as actinic keratoses (AKs) and patients with multiple AKs are at increased risk for developing SCC. SCC is capable of locally infiltrative growth, spread to regional lymph nodes, and distant metastasis, most often to the lungs. Once lung metastasis occurs, the disease is incurable.

General risk factors include :
Age 50 yrs or older, Male, Fair Skin (burns easily, very or rarely tans)
Geography–lives closer to the equator (Florida, Australia)
History of prior non-melanoma skin cancer
Exposure to UV light--natural or tanning bed or treatment (psoralen plus UVA (PUVA) for psoriasis
Exposure to chemical carcinogens (arsenic, tar)
Radiation exposure–treatment for other cancers (lymphomas, etc)
Chronic immunosuppression–a history of solid-organ transplantation, hematologic malignancy (CLL), HIV infection or long-term use of immunosuppressive medications for an autoimmune condition
Chronic scarring condition–Marjolin ulcer refers to an SCC that arises from chronically scarred or inflamed skin. Patients may report a change in the skin (induration, ulceration, weeping) at the site of a preexisting scar or ulcer. The latency period is often 20-30 years. Major burn scars. Chronic venous ulcers. Not scars from simple lacerations.
Genodermatoses
Human Papilloma Virus (HPV) infections–Virally induced SCC most commonly manifests as a new or enlarging warty growth on the penis, vulva, perianal area, or periungual region. Patients often present with a history of "warts" that have been refractory to various treatment modalities in the past.

Warning signs:
A wart-like growth that crusts and occasionally bleeds.
A persistent, scaly red patch with irregular borders that sometimes crusts or bleeds
An open sore that bleeds and crusts and persists for weeks.
An elevated growth with a central depression that occasionally bleeds. A growth of this type may rapidly increase in size.

Treatment Modalities are similar to those of BCC (see yesterday's post).

Prognosis:
Most SCCs are readily treated with an expectation of cure. The 3-year disease-specific survival rate has recently been estimated to be 85%; this rate approaches 100% for lesions with no high-risk factors (see below), but it decreases to 70% for patients with at least 1 risk factor. Local recurrence following definitive treatment is not uncommon, and metastasis and death may ensue. Most series in the literature quote an across-the-board prevalence rate of metastasis for primary cutaneous SCC of 2-6%.

When SCC does metastasize, it is usually occurs within several years from the time of diagnosis and involves the primary draining lymph nodes. In general, metastasis from SCC of the forehead, the temples, the eyelids, the cheeks, and the ears is to the parotid nodes; metastasis from SCC of the lips and the perioral region is primarily to the submental and submaxillary (upper cervical) nodes. Once nodal metastasis of cutaneous SCC has occurred, the overall 5-year survival rate has historically been in the range of 25-35%. Prognosis is extremely poor for patients who have 1) a compromised immune system, 2) metastasis to multiple lymph nodes, or 3) cervical lymph nodes greater than 3 cm in diameter. Metastasis to distant organs remains incurable. Thus, close surveillance and early detection of nodal metastasis can be life saving and is extremely important.

There is a subset of SCC that is considered high risk because of its aggressive behavior. These SCC have a tendency for rapid local growth, higher rates of recurrence and regional metastasis, and a poor prognosis. SCC can be characterized as high-risk by virtue of tumor-related factors (intrinsic factors), patient-related factors (extrinsic factors), or a combination of both.

Risk factors associated with higher rates of recurrence and metastasis
Tumor-related factors in high-risk SCC:
Tumor location (ie, lips,ears, scar)--The historical rates of metastases for SCC of the external ear and the lip are approximately 11% and 10-14%, respectively. Marjolin ulcer subtype of SCC behaves aggressively, with a metastatic rate of approximately 18-38%.
Tumor size greater than 2 cm –These may have a metastatic rate of up to 30.3%.
Invasion to subcutaneous fat (or deeper) --SCC with a depth of less than 2 mm rarely metastasizes. SCC with a depth of invasion less than 4 mm has a historical recurrence rate of 5.3% and a metastasis rate of 6.7%; these rates increase to 17.2% and 45.7%, respectively, for tumors invading greater than 4 mm.
Poorly differentiated tumor – are generally accepted to behave more aggressively.
Recurrent tumor-- has a site-dependent rate of metastasis of 25-45%.
Perineural involvement --has been estimated to occur in 2.4-14% of persons with cutaneous SCC, most commonly in elderly men with tumors of the head and neck. The prognosis in such cases is extremely poor, with historical rates of local recurrence and metastasis reported to be as high as 47%.

Patient-related factors in high-risk SCC
Organ transplant recipient --SCC in OTRs occurs more frequently, appears at an earlier age, is often multicentric, and may be clinically aggressive. The rate of local recurrence has been reported to be as high as 13.4%, while metastasis occurs in 5-8% of patients. Metastatic SCC in OTRs has a dismal prognosis, with a 3-year disease-specific survival of only 56%.
Hematologic malignancy (eg, CLL) --in patients with CLL, the recurrence rate of SCC treated with MMS was 7-fold higher at 5 years compared with patients without CLL. In addition, a small case-control study found the 5-year cumulative incidence of SCC metastasis to be 17.7% for patients with CLL.
Chronic immunosuppressive therapy or disease state: HIV infection or AIDS--In one small case series, 5 of 10 patients with HIV and aggressive SCC died of metastasis within 7 years of the initial diagnosis.

Patients should be counseled to avoid excessive UV radiation by limiting outdoor activity to early morning and late afternoon, using protective clothing, and wearing a broad-brimmed hat to shade the head and the neck area. Counseling patients regarding treatment of areas of chronic skin inflammation or trauma is important in preventing the future development of SCC at those sites.

Skin Cancer--Basal Cell Carcinoma

 Updated 3/2017-- photos and all links (except to my own posts) removed as many no longer active.

Basal Cell Carcinoma (BCC) is the most common skin cancer. It typically occurs in areas of chronic sun exposure. BCC is usually slow growing and rarely metastasizes, but it can cause significant local destruction and disfigurement if neglected or treated inadequately. BCC are most commonly seen in the head and neck. Therefore, disfigurement is not uncommon. Loss of vision or the eye may occur with orbital involvement. This skin cancer likes to spread along nerves (perineural spread) and this can result in loss of nerve function, as well as deep invasion of the tumor. BCC are prone to ulceration and this provides a nidus for infection. Death from BCC is extremely rare. Prognosis is excellent with proper therapy. Early treatment is necessary to avoid disfigurement.

Many believe that BCCs arise from pluripotential cells in the basal layer of the epidermis or follicular structures. These cells form continuously during life and can form hair, sebaceous glands, and apocrine glands. Tumors usually arise from the epidermis and occasionally arise from the outer root sheath of a hair follicle, specifically from hair follicle stem cells residing just below the sebaceous gland duct in an area called the bulge. Causes include UV radiation, other radiation (X-ray, grenz-ray exposure), arsenic exposure, immunosuppression, Xeroderma pigmentosum, Nevoid BCC syndrome (basal cell nevus syndrome, Gorlin syndrome), Bazex syndrome, and a history of nonmelanoma skin cancer. Person with 1 nonmelanoma skin cancer are at increased risk of developing others in the future. The rate of new nonmelanoma skin cancer is 35% at 3 years and 50% at 5 years after an initial diagnosis of skin cancer.

Histologically, BCC is divided into 2 categories: undifferentiated and differentiated. Undifferentiated BCC has little or no differentiation and is referred to as a solid BCC. The subtypes of Undifferentiated (BCC with little or no differentiation is referred to as solid BCC) include Pigmented BCC, Superficial BCC, Morpheaform or Sclerosing BCC, and Infiltrative BCC. Differentiated BCC often has slight differentiation toward cutaneous appendages, including hair (keratotic BCC), sebaceous glands (BCC with sebaceous differentiation), or tubular glands (adenoid BCC). Noduloulcerative (nodular) BCC usually is differentiated.

The 5 most typical characteristics of BCC can be seen in pictures here. They are:
An Open Sore that bleeds, oozes, or crusts and remains open for a few weeks. This persistent, non-healing sore is a very common sign of an early BCC..
A Reddish Patch or irritated area. It may itch or hurt. Often these occur on the chest, shoulders, arms, or legs.
A Shiny Bump or nodule that is pearly or translucent and is often pink, red, or white. This bump may also be tan, black, or brown, especially in dark-haired people, and can be confused with a mole (moles aren’t shiny).
A Pink Growth with a slightly elevated, rolled border and a crusted indentation in the center. As the growth slowly enlarges, tiny blood vessels may develop on the surface.
A Scar-Like Area which is white, yellow, or waxy, and often has poorly defined borders. The skin may appear shiny and taut. This warning sign can indicate the presence of small roots, which make the tumor larger than it appears on the surface.

TREATMENT:
Medication:
Imiquimod 5% cream has been used to treat superficial BCC’s. Duration of treatment varies from 6-16 weeks. Cure rates of 70-100% should be expected after a 6 week course of 5 times-per-week application.
Topical 5-FU 5% cream is sometimes used to treat small, superficial BCC’s. In thin tumors, cure rates of approximately 80% have been obtained using a twice daily application for at least 6 weeks. Percutaneous absorption of 5-FU is its major limiting factor, as it penetrates only 1 mm into the skin.
Interferon alfa-2b has shown some success in treating small (less than 1 cm), nodular, and superficial BCC’s. It is administered intralesionally, 3 times-per-week for 3 weeks. In appropriate tumors, cure rates of up to 80% have been obtained. Interferon has not become a mainstay in treatment fo BCC’s because of its cost, the inconvenience of multiple visits, the discomfort of administration, and its adverse effects.

Surgery–
Curettage may be used. It is a blind technique in which the specimen cannot be examined for margin control. This limits the usefulness of curettage in high-risk areas, such as the face and ears. Furthermore, the aggressive subtypes, such as morpheaform, infiltrating, micronodular, and recurrent tumors, are usually not friable and therefore difficult to remove by using the curette.

Surgical excision may be used to excise the clinically apparent tumor and a margin of clinically normal-appearing skin. This can be done in an ambulatory setting and provides the pathologist with a specimen to examine the tissue margins. It is more time-consuming and costly than curettage, but the margin can be examined. Margin of up to 4 mm may be needed to achieve a 95% cure rate. This margin can be difficult to obtain near the canthus of the eye/eyelid.

Mohs surgery involves removal of the clinically apparent tumor and a thin rim of normal appearing skin. The margin specimen is sectioned and marked so that the entirety of the undersurface and outer edges of the tumor are examined microscopically to minimize sampling error. Use of the frozen-section technique allows for an examination of tissue while the patient is in the office. Tissue is mapped microscopically so if any foci of tumor persist, further excision can be directed to only those areas to spare the normal tissue. With the Mohs technique, almost 100% of the tissue margins are examined. Excision and repair can usually be done on the same day. Of most impartance, Mohs micrographic surgical excision has the best long-term cure rates of any treatment modality for BCC. Cure rates for primary BCC are 98-99% with Mohs excision and 94-96% for recurrent BCC. The chief disadvantages of Mohs surgery are its increased expense and time required.

Radiation therapy can be an effective primary treatment for a variety of BCC’s. For most, cure rates approach 90%. It is especially useful for patients who cannot easily tolerate surgery. Radiation is also an excellent option in patients who refuse surgery because of the size of the lesion or its proximity to vital structures.

Cryotherapy is an effective treatment for nonaggressive BCC’s, with cure rates near 90%, in the hands of an experienced cryosurgeon. Patients must be willing to endure the immediate post-treatment swelling, resultant necrosis of treated areas, and unpredictable scarring that can occur with this approach.

Suggested Reading:

Rubin AI, Chen EH, Ratner D, "Basal-cell carcinoma." N Engl J Med. 2005 Nov 24;353(21):2262-9. Rubin AI, Chen EH, Ratner D, "Basal-cell carcinoma." N Engl J Med. 2005 Nov 24;353(21):2262-9.

Blue Nude 1952

Updated 3/2017-- all links (except to my own posts) removed as many no longer active.

Let me share something lovely with you. Give you a break from the "not-so-pretty" skin changes. This is one of the first quilts I did for my office. It is a close "replica" of Henri Matisse's Blue Nude 1952. My husband helped my "draft" the pattern. It is made of silk noire, appliqued, and then echo quilted by hand. I think that Mattisse would have made a wonderful quilt artist during his paper cutouts phase at the end of his life. Many of those remind me of quilts.

Henri-Émile-Benoît Matisse was born on December 31, 1869, in Le Cateau-Cambrésis, France. While recuperating from two major operations in 1941 and 1942, Matisse concentrated on a technique he had devised earlier: papiers découpés (paper cutouts). Jazz, written and illustrated by Matisse, was published in 1947; the plates are stencil reproductions of paper cutouts. In 1948 he began the design for the decoration of Chapelle du Rosaire in Vence, which was completed and consecrated in 1951. In 1952 the Musée Matisse was inaugurated at the artist’s birthplace of Le Cateau–Cambrésis. Matisse continued to make large paper cutouts, the last of which was a design for the rose window at Union Church of Pocantico Hills, New York. He died on November 3, 1954, in Nice.

Seborrheic Keratosis, Solar Lentigines, and Actinic Keratosis

 Updated 3/2017-- photos and all links (except to my own posts) removed as many no longer active.

Seborrheic keratoses are raised growths on the skin. Seborrheic means greasy and keratosis means thickening of the skin. They may occur as just one or clusters of many. They usually start off light tan and may darken to dark brown or nearly black. The most consistent feature of seborrheic keratoses is their waxy, "pasted-on" or "stuck-on" look. The look is often compared to brown candle wax that has been dropped onto the skin. They may be unsightly, but are not contagious and do not spread. They do not have any relationship to skin cancer, and never turn into melanom. They do not pose a health risk.

As people age they may develop more. Sometimes they seem to erupt during pregnancy, following hormone replacement therapy or as a result of other medical problems. They are most likely hereditary and not caused by sun exposure. They often are found on the trunk and on the face where the facial skin meets the scalp. They may be oval spots less than a fraction of an inch across, or may form long Christmas tree like patterns on the torso.

Clothing rubbing against them may irritate and make them grow larger. Alpha-hydroxy lotions and mild steriod creams may help this. If they get very itchy, irritated, or bleed easily they should be removed. When a seborrheic keratosis turns black, it may be difficult to distinguish it from a skin cancer without a biopsy.

Removal is often done using liquid nitrogen (cryosurgery). Another treatment done (as they are superifical–"pasted-on") consist of scraping off the lesion with a curette (ED&C). This is more useful when only a few need to be done or when one spot needs a biopsy (as the scrapings can be sent to the lab). Sometimes they are burnt off with an electric needle or laser.

Liver or age spots are solar lentigines. They are benign lesion that occur on sun-exposed areas of the body. The backs of the hands and face are the most common areas. They tend to increase in number with age. They can vary in size from 0.2 to 2 cm. Lenigines are flat, dark lesions that usually have discrete borders and may have an irregular shape. They are are caused by a marked increase in the number of pigment cells (melanocytes) located in the superficial layers of the skin. Lentigines are benign and no treatment is necessary. For cosmetic purposes, some are treated with cryotherapy, hydroquinone preparations (bleaching creams), retinoids, chemical peels or lasers. Preventive measures include avoidance of excessive sunlight. If a lesion develops a highly irregular border, changes in pigmentation, or changes in the thickness, then a biopsy should be done to rule out cancer.

Actinic keratosis, unlike seborrheic keratoses (AK’s), are from sun damage. They are also called solar keratosis, sun spots, or precancerous spots. They appear as a scaly or crusty bump on the skin surface. They range in size from as small as a pinhead to over an inch in diameter. AK’s may be light or dark, tan, pink, red, a combination of these, or the same color as the skin. They may be flat or raised in appearance. They may disappear only to reappear later. Half of all keratosis will go away on their own if one avoids all sun for a few years (difficult to do). AK’s appear on sun exposed areas: face, ears, bald scalp, neck, backs of hands and forearms, and lips.
Actinic keratosis can be the first step in the development of skin cancer. They are pre-cancer. It is estimated that 10-15 % of active lesions will progress to squamous cell carcinoma (SCC). The presence of AK’s indicates that sun damage has occurred. This increases the likelihood of any kind of skin cancer, not just SCC, can develop. People with AK’s are more likely to develop melanoma also. Sun exposure is the cause of almost all actinic keratoses. So use your sunscreen. Don’t forget the lip balm with sunscreen. Wear your hats, preferably wide brimmed.

The most aggressive form of keratosis, actinic cheilitis, appears on the lips and can evolve into squamous cell carcinoma. When this happens, roughly one-fifth of these carcinomas metastasize. It occurs primarily in men and does not present until after 50 years of age, but the cause is often extreme sun exposure during the teen years and young adult life. Life-time occupational sun exposure increases the risk. The lip becomes puffy and blotchy red and pale pink, with occasional white plaques (leukoplakia) and chronic ulcers. This is a precancer, with an estimated 6% risk of cancer development. Treatment is close follow-up and removal of thick white or white/red patches or nonhealing ulcers. Extensive lesions require complete removal of the lip mucosa and replacement with mucosa inside the mouth.

Treatment:
Cryosurgery freezes off the lesions through application of liquid nitrogen. This is done with a special spray device or cotton-tipped applicator. It does not require anesthesia and produces no bleeding. The longer the spot is frozen the better the chance it will never come back. Longer freezes can result in hypopigmented areas.
Curettage scrapes the lesion off and may be used as a biopsy specimen. Bleeding is controlled by cautery (application of an acid or heat produced by an electric needle).
Shave Removal utilizes a scalpel to shave the keratosis (provides a specimen). As with curettage, the base of the lesion is destroyed and the bleeding stopped by cauterization.
Chemical Peels make use of acids (Jessners solution and /or trichloroacetic acid) applied over the area. The top layers of the skin are "peeled" off by controlled burning (done by the acid strength used and time left on the skin). It may take up to seven days for the area to heal. Redness and soreness associated with the peel usually disappear after a few days.
Topical creams used to treat keratoses is an effective solution when there are numerous lesions. Aldara works by stimulating the body’s immune system to "recognize" these precancerous lesions and treat them. This ointment is applied to the affected areas twice weekly for 6-12 weeks. 5-fluorouracil (Efudex, Carac) cream works by directly attacking the precancerous cell. This ointment is applied once or twice daily for 2-4 weeks. Treatment leaves the affected area temporarily reddened and raw. The more raw and inflamed the skin becomes, the better the end result. Solaraze gel is a non-steroidal medication that also works fairly well on AK’s. This ointment is applied twice daily for 90 days.

Regular follow-up visits with your dermatologist is recommended to "catch" these pre-cancerous lesions and treat them before they evolve into skin cancer (SCC or melanoma).

Vascular Birthmarks

Updated 3/2017-- photos and all links (except to my own posts) removed as many no longer active.

Macular stains. Also called salmon patches, angel kisses, or stork bites, these faint red marks are the most common type of vascular birthmark. They're often on the forehead or eyelids, the back of the neck, or on the nose, upper lip, or on the back of the head. They may be more noticeable when the baby cries. Most often they fade on their own by the time a child is 1 to 2 years old, although some last into adulthood.

Hemangiomas. Hemangiomas are classified as superficial when they appear on the surface of the skin ("strawberry marks") and cavernous when found deeper below the skin's surface. They can be slightly raised and bright red and sometimes aren't visible until a few days or weeks after a baby is born. Cavernous, deep hemangiomas may be bluish because they involve blood vessels in deeper layers of the skin. Hemangiomas grow rapidly during the first 6 months or so of life, but usually shrink back and disappear by the time a child is 5 to 9 years old. Some, particularly larger ones, may leave a scar as they regress that can be corrected by minor plastic surgery. Most are on the head or neck, although they can be anywhere on the body, and can cause complications if their location interferes with sight, feeding, breathing, or other body functions.

Approximately thirty percent of all hemangiomas are visible at birth. The remaining seventy percent become visible within one to four weeks after birth. They affect approximately one in 10 to 20 Caucasian children, with a 3:1 predilection for the female sex. The incidence in non-Caucasian infants is lower. Hemangiomas are endothelial neoplasms. To date, there is no universally accepted model for the etiology of hemangiomas. There is general consensus on the importance of endothelial cells, but the source of the endothelial cells is speculative and there is no consensus on the possible mechanisms by which the hemangioma endothelium interacts with surrounding cells. There is a scientific debate on whether they are of mutational or placental origin or fit in a developmental field disruption. In the past hemangiomas were once thought to be due to maternal behavior or thoughts during pregnancy. The term vascular birthmark itself implies a connection between birth and a vascular lesion. The term strawberry nevus indicates that the mother's intake of red fruits (strawberries) was once thought to cause birthmarks. It is important for the family to remember that the cause of hemangiomas has not been determined, and neither parent should bear guilt over the occurrence or appearance of one of these birthmarks. Approximately 83% percent occur on the head and neck area. The remaining 17% appear throughout the rest of the body (both externally and internally).

At birth, a precursor lesion may be present as an erythematous patch or a telangiectasia. Within weeks the lesion expands rapidly. Hemangiomas can grow for up to 18 months and then begin a long slow regression known as involution. This involution can last from 3- 10 years. This dramatic/fast growth of a hemangioma may seem alarming, but usually no treatment is indicated. This is because this rapid growth phase is followed by a gradual involution (regression) in the following years. At the age of 5 years, 50 percent of the hemangiomas have involuted, and at the age of 9 years 90 percent have. The ones that do need treatment are the ones that ulcerate, obstruct the airway, or cause visual deficits or cardiovascular symptoms. Current treatment may include intralesional or systemic corticosteroid treatment, systemic interferon treatment, local bleomycin treatment, and surgery. A hemangioma usually occurs as a solitary, superficial lesion in the head and neck area, but it can be present anywhere in or on the body. Size can vary greatly, from nodular lesions several millimeters in diameter to plaque-like tumors covering the entire face or a quadrant of the body. In selected cases, however, prompt intervention is needed. These cases involve hemangiomas that ulcerate, obstruct the airway, or cause visual deficits or cardiovascular symptoms. Early intervention has been shown to reduce the need for corrective surgery after "involution" has occurred; or to, at least, minimize extensive corrective surgeries in the future. Psycho-social scarring which occurs when a child has been forced to live with a facial deformity until "involution" has been completed can be avoided by early, aggressive intervention.

Vascular Malformations differ from hemangiomas in several crucial ways. Most distinctively, vascular malformations are present at birth, grow commensurately with the body, and never show signs of spontaneous involution. Photo credit.

Port wine stains are Venual Malformations. They are always present at birth and can range from pale pink to dark purple in color. These are discolorations that look like wine was spilled on an area of the body, most often on the face, neck, arms, or legs. Port wine stains can be any size, but grow only as the child grows. They tend to darken over time and can thicken and feel like pebbles in midlife adulthood unless treated. They never go away on their own. Ones near the eye must be assessed for possible complications involving the eye. In the past these lesions were erroneously called "capillary hemangiomas." Port Wine Stains occur in 0.3% of births and occur equally among males and females. The cause has been associated with a deficiency or absence in the nerve supply to the blood vessels of the affected area. These nerves control the diameter of the blood vessels. If the nerves are absent or defective, the vessels will continue to dilate and blood will pool or collect in the affected area. The result will be a visible birth mark. This is important to know because laser therapy which is used to remove a port wine stain will only be temporary. Since the deficiency is in the nervous system, in time the blood will repool in the affected area and the birthmark will once again appear. Once a Port Wine Stain is lasered, it is important at the first sign of reoccurence to have one or two treatments to keep it faded. The individual will have to have maintenance laser treatments for life. Because Port Wine Stains can be progressive, treatment should be done early to prevent cobbling of the skin and thickening and darkening of the stain. These lesions vary from low-grade to high-grade, pale to dark. Low-grade progress at a slower rate than high-grade. Rarely capillary malformations are clues to the presence of other defects such as Sturge-Weber Syndrome or Klippel-Trenaunay Syndrome.

Venous Malformation is an abnormality of the larger, deep veins and is often mistakenly called a "hemangioma." A good history will reveal whether or not the lesion is a hemangioma or vascular malformation. A venous malformation can be deep or superficial, localized or diffused. The closer the vessels are to the surface, the deeper the color to the eye. A very deep lesion will have no color but will show a protruding mass. The jaw, cheek, tongue and lips are common sites for a venous malformation. These lesions are soft to the touch, the color disappears and empties as the lesion is compressed. When the child cries or is lying down, the lesion expand, the vessels fill and the color becomes more intense. The natural history is a slow-steady enlargement. Regardless of how small it is upon detection, it will grow. Certain things can cause them to grow more rapidly such as serious sickness, trauma, infection, hormone changes (puberty, pregnancy, menopause). Partial removal is not recommended since these lesions will just grow back.

Arteriovenous Malformations are always present at birth but are usually not noticed until later in life. Sometimes they do not appear until adulthood. Defective blood flow has been associated with these lesions. As the lesion ages, the vessels enlarge and thicken to compensate for the increased blood supply. There are two grades: low and high. Low grade grow slowly with the child and high grade expand rapidly, growing faster than the child until the lesion may eventually become life threatening. An AV malformation is a firm mass. Common sites are the lips and other head and neck areas. Mixed malformations include a combination of two or more vascular lesions.

Lymphatic Malformations used to be called cystic hygroma, hemangiolymphangioma, or lymphangiomas. Lymphatic malformations are composed of dilated lymphatic channels. The lymphatics serve as a collection and transfer system for tiisue fluids. When something disturbs this system, a lymphatic malformation is formed. The excess fluid accumulates and the affected lymphatic vessels enlarge and you see a mass. If the lymph vessels in the face are affected, the face swells because the normal active transport mechanism has been disturbed. These lesions can occur anywhere but are common in the head and neck area. These lesions may be superficial or deep (superficial ones are seen in the mouth area and look like frogs eggs) . These lesions increase or grow with the individual. They may enlarge following an upper respiratory infection.

References:
Hemangiomas and Vascular Malformations in Infants and Children: A Classification Based on Endothelial Characteristics; The Pathogenesis of Hemangiomas: A Review; Bauland, Constantijn G. M.D.; van Steensel, Maurice A. M. M.D., Ph.D.; Steijlen, Peter M. M.D., Ph.D.; Rieu, Paul N. M. A. M.D., Ph.D.; Spauwen, Paul H. M. M.D., Ph.D.; Plastic and Reconstructive Surgery:Volume 117(2)February 2006
Progress to ward Understanding Vascular Malformations [Special Topic]; Breugem, Corstiaan C. M.B.Ch.B.; van der Horst, Chantal M. A. M. M.D., Ph.D., and; Hennekam, Raoul C. M. M.D., Ph.D.; Plastic and Reconstructive Surgery:Volume 107(6)May 2001
Vascular Birthmarks: Hemangioma and Malformations. by Mulliken, John B. MD; Young, Anthony E. MD; Textbook--W.B. Saunder, Philadelphia, PA, 1988.
Hemangiomas and Vascular Malformations of the Head and Neck edited by Milton Waner, MD and James Suen, MD--Wiley-Liss, NY 1999

Pigmented Birthmarks

Updated 3/2017-- photos and all links (except to my own posts) removed as many no longer active.

Birthmarks fall into two categories: pigmented or vascular (I'll deal with those in the future). Birthmarks (both types) are present at birth or develop shortly after birth. Pigmented birthmarks can be brown, tan, black, or bluish/bluish-gray. The cause of pigmented birthmarks is unknown. Most birthmarks are not inherited. There is no known way to prevent birthmarks. People with birthmarks, just like everyone else, should use a good quality sunscreen with a high SPF when outdoors in order to help prevent skin cancer. In most cases, health care professionals can diagnose birthmarks based on the appearance of the skin. Many folk tales and myths exist about the causes of birthmarks, but none of these stories have been proven to explain the true causes of birthmarks. Photo credit

Types of Pigmented Birthmarks

• Cafe-au-lait spots are light tan or light brown spots that are usually oval in shape. They usually appear at birth but may develop in the first few years of a child's life. Cafe-au-lait spots may be a normal type of birthmark, but the presence of several cafe-au-lait spots larger than a quarter may occur in neurofibromatosis (a genetic disorder that causes abnormal cell growth of nerve tissues).


• Congenital nevi are moles that are present at birth. These birthmarks have a slightly increased risk of becoming skin cancer depending on their size. Larger (covers an area larger than the size of a fist) congenital nevi have a greater risk of developing skin cancer than do smaller congenital nevi. All congenital nevi should be examined by a health care provider and any change in the birthmark should be reported.


• Pigmented nevi (moles) are growths on the skin that usually are flesh-colored, brown or black. Moles can appear anywhere on the skin, alone or in groups. Moles occur when cells in the skin grow in a cluster instead of being spread throughout the skin. Moles may darken after exposure to the sun, during the teen years and during pregnancy.


• Mongolian spots usually are bluish and appear as bruises. They often appear on the buttocks and/or lower back, but they sometimes also appear on the trunk or arms. The spots are seen most often in people who have darker skin. They usually fade (often completely) by school age without treatment.

Treatment of Pigmented Birthmarks
Pigmented birthmarks are usually left alone, with the exception of moles and, occasionally, café-au-lait spots. Moles, particularly large or giant congenital nevi, often are surgically removed, though larger ones may be more difficult to remove. Café-au-lait spots can be removed with lasers (highly concentrated light energy) but often return. If a mole exhibits potentially cancerous changes, a biopsy may be performed. Large or prominent moles that affect appearance and self-esteem may be covered with special cosmetics.

Warning Signs Since there is an increased risk of skin cancer in congenital nevi, see a doctor if you notice a change in color, size, or texture of a mole or other skin lesion. Also, see a doctor right away if there is any pain, bleeding, itching, inflammation, or ulceration of a congenital mole or other skin lesion.

Skin Tags

Updated 3/2017-- photos and all links (except to my own posts) removed as many no longer active.

Acrochordons, aka skin tags, are small benign skin tumors that form primarily in areas where the skin forms creases, such as the neck, armpits, and groin. They also occur on the face, usually on the eyelids. They range in size from rice to golf ball size. The surface of skin tags may be smooth or irregular in appearance. Most often they are raised from the surface of the skin on a fleshy stalk called a peduncle. This stalk is why skin tags are also called pedunculated papillomas. Microscopically, a skin tag consists of a fibrovascular core (a small artery and vein in the stalk of skin) and sometimes some fat cells covered by an unremarkable epidermis.

Skin tags are harmless. Sometimes they are irritated by clothing or jewelry and can interfere with shaving and other routine grooming. It is not entirely known as to why or how skin tags form, but there are correlations with age and obesity. They are more common in people with diabetes and in pregnant women. It is estimated that by age 70, up to 59 percent of people have them. A genetic component (causation) is thought to exist.

Your doctor can remove a skin tag by cutting it off with a scalpel or scissors, with cryotherapy (freezing it off), or with electrosurgery (burning it off with an electric current). If the skin tag is small and has a thin (think thread) stalk (and the patient is not on a blood thinner--coumadin, etc), then the simplest thing to do is to use small curved scissors and snip (no local necessary--a needle or a quick snip) next to the skin. If the stalk is thick (think twine or yarn), then it will have more of a blood supply and will need to be cauterized (electrosurgery) or excised and closed with a stitch. These need local anesthesia. A simple band-aid or antibiotic ointment is all that is usually needed for a dressing. Then simple good hygiene for care, as you would a bug bite or scratch at home.

Mud Pies and Geophagia

Updated 3/2017-- photos and all links (except to my own posts) removed as many no longer active.

Recently I read a newspaper article in on geophagia. This phenomenon has fascinated me since medical school. I recall making mud pies as a child, decorating them with Queen’s Anne Lace and Black-eyed Susans. We never thought to eat them.

Geophagia is a type or subgroup of pica. Pica (from the Latin name for magpie, a bird known for its unusual and indiscriminate eating habits) is the persistent craving and compulsive eating of nonfood substances. It is classified in the Diagnostic and Statistical Manual of Mental Disorders, fourth edition, as a feeding and eating disorder of childhood. It may begin in childhood, but does not always get left there.

Pica has been recognized and described since ancient times. It has been observed in ethnic groups worldwide, in both primitive and modern cultures, in both sexes, and in all age groups. Pica has also been observed in other animals, including the chimpanzee. There is a higher incidence of pica in pregnant women, iron deficient individuals, early childhood, and certain cultural and religious groups.

Pica in humans has many different subgroups, defined by the substance that is ingested. Some of the most commonly described types of pica are eating earth, soil or clay (geophagia), ice (pagophagia) and starch (amylophagia). However, pica involving dozens of other substances, including cigarette butts and ashes, hair, paint chips, and paper have also been reported.

Evidence suggests that there may be several causes of pica. One widely held theory points to iron deficiency as a major cause of pica. Several reports have described pica in individuals with documented iron deficiency. It remains uncertain as to whether the iron deficiency caused the pica or is a result of the pica (chicken and egg problem). Because some substances, such as clay, are believed to block the absorption of iron into the bloodstream, it was thought that low blood levels of iron could be the direct result of pica.

Other reports suggest that pica may have a psychological basis and may even fall into the spectrum of obsessive-compulsive disorder. Pica has a higher incidence in populations with an underlying diagnosis involving mental functioning. These diagnoses include psychiatric conditions like schizophrenia, developmental disorders including autism, and conditions with mental retardation. These conditions are not characterized by iron deficiency, which supports a psychological component in the cause of pica.

Cultural and religious traditions may also play a role in pica behavior. It seems that the tradition may be dying out, as the more recent generations are not picking up the habit of geophagia here in the south (US). In some cultures, nonfood substances are believed to have positive health or spiritual effects. Among some African Americans in the south, ingesting a particular kind of white clay is believed to promote health and reduce morning sickness during pregnancy. Other cultures practice pica out of belief that eating a particular substance may promote fertility or bring good luck.

Because the eating behaviors of pica are not usually detected or reported, it is the complications of the behavior that bring it to attention. Complications vary, depending on the type of pica. Geophagia has potential side effects that most commonly affect the intestine and bowel. Complications can include constipation, cramping, pain, obstruction caused by formation of an indigestible mass, perforation from sharp objects like rocks or gravel and contamination and infection from soil-dwelling parasites.

Other Sources:

Geophagia: the history of earth-eating by Alexander Woywodt MD, Akos Kiss FCS (SA)

Clinical Vignette--A Case of Geophagia by Patrick Yao, M.D.

The Soil Eaters by Magnus Bärtås & Fredrik Ekman

A Bear Hug

Updated 3/2017-- all links (except to my own posts) removed as many no longer active.

I named this quilt "A Bear Hug" because of the fabric and the sentiment. It is being given to a young man who has bone cancer, osteosarcoma. He has gone through most of his treatments for the cancer (surgery, chemotherapy, etc) and recently has been dealing with the after effects (an infection in his new knee joint, scar tissue in the joint, etc). He is not one of my patients, nor do I know him personally. I know of him. Still I hope this quilt (54" X 72") helps "warm" him and in some small measure helps him get through it all.

For more information on osteosarcoma see:

E-Medicine Article on osteosarcoma

Trigger Finger

Updated 3/2017-- photos and all links (except to my own posts) removed as many no longer active.

Stenosing tenosynovitis is more commonly known as trigger finger or trigger thumb. It involves the pulleys and tendons in the hand. These tendons and pulley work together to bend the fingers. The tendons work like long ropes going from the muscles in the forearm to connect to the bones of the fingers and thumb. In the finger, the pulleys are a series of rings (made of connective tissue) that form a tunnel that the tendons must pass through. This is very much like the guides on a fishing rod through which the line (or tendon) passes. These pulleys hold the tendons close against the bone. The tendons and the pulley (tunnel) have a slick lining that allows easy gliding.

When the tendon develops a nodule or swelling of its lining, it has difficulty passing through the pulley (which is not elastic, but fixed in diameter). The "popping" or "catching" feeling in the finger or thumb comes from the tendon "squeezing" through and giving as it makes it past the pulley. The swollen tendon is irritated more as it has to be squeezed through the pulley, producing more swelling. A vicious cycle of triggering, inflammation, and swelling. Sometimes the finger will become stuck (locked) and it may be hard to straighten or bend the finger. This is like having a finger swell and not being able to get your ring off.

So what causes this condition. Repetitive grasping of objects or an injury to the palm may irritate the flexor tendons. Medical conditions such as rheumatoid arthritis, gout, and diabetes may create swelling around the tendons which then lead to the "vicious" cycle of irritation/inflammation/swelling. Sometimes the cause is not clear.

So the goal of treatment is to eliminate the catching or locking and allow movement without discomfort. To do this the swelling around the tendon must be reduced to allow smooth gliding of the tendon. Wearing a splint or taking anti-inflammatory medication by mouth or injection into the area around the tendon (a corticosteroid shot) are ways to reduce the swelling. Changing how the hand is used, better body mechanics to reduce the impact or repetitive motions helps. If nonsurgical forms of treatment do not improve symptoms, then surgery may be recommended. This surgery is usually performed on an outpatient basis. Most often it is done using local anesthesia, but a regional (where only the arm is numbed) or a general may be used. The surgery cuts the pulley (only one and the finger still has other pulleys to keep it near the bone) which gives the tendon more room to glide, removing the restriction (cutting the ring off the swollen finger). Active motion of the finger is generally begun immediately after surgery. Normal use of the hand can be resumed once comfort permits.

Ganglion Cyst of the Hand

Updated 3/2017-- photos and all links (except to my own posts) removed as many no longer active.

Ganglion cysts are very common. The cyst are generally found on the top (dorsum) of the wrist (60-70%), the end joint of a finger (distal phalangeal joint), and at the base of a finger (palm-side). Ganglion cyst usually come up from nearby joint linings or tendon sheaths. These cysts can be painful, especially when they first appear and with constant or strenuous use of the hand or wrist. Ganglions often change in size and may disappear completely. These cyst are benign. There is no known specific cause for ganglions, but often there has been an injury before the appearance of the cyst. A ganglion cyst contains a thick, clear, mucus-like fluid similar to the fluid found in the joint. Women are more likely to be affected than men. Ganglia are common among gymnasts, who repeatedly apply stress to the wrist.

A ganglion grows out of a joint, like a balloon on a stalk. It rises out of the connective tissues between bones and muscles. Inside the balloon is a thick, slippery fluid similar to the fluid in your joints. Usually, the more active the wrist, the larger the cyst becomes. With rest, the lump generally decreases in size.

The diagnosis of a ganglion cyst is based on where the cyst is an d what it looks like. Your doctor may ask you how long you've had the ganglion, whether it changes in size, and whether it is painful. Pressure may be applied to identify any tenderness. A penlight may be held up to the cyst to see whether light shines through. X-rays may be taken to rule out other conditions, such as arthritis or a bone tumor. Sometimes, an MRI or ultrasound is needed to find a ganglion cyst that is not visible.

Treatment of ganglion cysts may consist of

• Doing nothing. The cysts are benign and if yours is not painful, does not limit activity, and its appearance is acceptable to you, then there is no reason for further treatment. Just watch it for changes.
• If it is painful, does limit activity, or you dislike its appearance, then treatment may include removing fluid from the cyst (putting a needle into the cyst and aspirating) and /or wearing a splint to keep the hand or wrist from moving.
• If these non-surgical treatments fail, surgery to remove the cyst can be done. This surgery is performed on an outpatient basis. Anesthesia may be local, regional (where only the arm is numbed), or general. The goal of surgery is to remove the source of the cyst. This may require removal of a portion of the joint capsule or tendon sheath next to the ganglion. If the ganglion is removed from the wrist, a splint may be recommended following surgery for a few weeks. Some patients may feel tenderness, discomfort, and swelling at the site, but full activity can be resumed once comfort permits. While surgery offers the best success in removing ganglions, these cyst can and do return.

Ganglion Cysts, Mayo Clinic

Sunday Morning Walk

 Updated 3/2017-- photos and all links (except to my own posts) removed as many no longer active.

I had a nice Sunday morning walk with my dogs. We saw two box turtles. The Arkansas Natural Heritage Department is conducting a "citizen survey" of box turtles. There is concern that these turtles are quietly disappearing from the landscapes across the country. Results from studies across the US suggest that box turtles are becoming less common. They want to develop conservation strategies for the turtles before they become rare. So they have asked the citizen of Arkansas (and any visiting tourist) to help them "gather empirical data will we be able to understand the true status and trends of these endearing species".

Baby Quilts and Books

Updated 3/2017-- photos and all links (except to my own posts) removed as many no longer active.

This is a baby quilt I just finished for a great-niece (and her mother is 21 yo, tells you how old I am getting to be). I like to make baby quilts. I like for them to be colorful and interactive in some way. For this one I found a panel for a fabric book and made a quilt out of it. So the squares are the pages of the book. There are the primary colors--red, yellow, green, and blue. There are animals to count. There are the words of the book which are actually a song (Old friend Noah had an ark, eieio and on his ark he had ...). I like for my baby quilts to get used, so hopefully this one will encourage the mother (or aunts, etc) to get down on the floor with the baby/toddler and teach (while playing) the colors, animals, basic counting, etc

I love books. I love reading. I enjoyed reading to my younger brothers. I hope I can pass it along to at least a few people. I agree with Sean Connery who said when he won the AFI 34th Annual Life Achievement Award that "My big break was when I was 5 years old. You see at 5, I learned to read." Being literate is a wonderful gift.

First Book is an organization that puts new books into the hands of children in need.

Laura Bush Foundation provides schools with grants of up to $5,000 to expand, update and diversify their library book collections.

Lullalee Productions has donated books, services and other accessories to the following organizations such as I AM Foundation and Shriners Hospital.

Praise for John Hopkins Facial Plastic Surgeons

Updated 3/2017-- all links (except to my own posts) removed as many no longer active.

Rebuilding--restoring--repairing. That is what drew me to Plastic Surgery. Recently John Hopkins Facial Plastic Surgeons rebuilt a young soldier's nose. You need to check out this article. Photo credit-reference #1.

In the history of plastic surgery, facial injuries have done much to move us forward. The first surgical attempts at nasal reconstruction were recorded in India (1500 b.c.), where nasal mutilation was prevalent. Nasal reconstruction was at that time performed by brickmakers or potters. It is known that forehead flap reconstructions were being carried out in Kangra (near Delhi) from 1000 a.d. onward by the Kanghiara family. The operative technique was a family secret, such that a daughter-in-law would be allowed to watch and assist but not a daughter, who might subsequently marry and take the secret outside the family. The surgical technique practiced in India arrived in England via a circuitous route in the eighteenth century. From 1769 to 1799, wars were fought between Tipu Sultan and the British. A bullock cart driver named Kawasjee and four Indian soldiers of the British army fell into the hands of the Sultan. Their noses and right arms were cut off as punishment, and the men were sent back to their English command. When faced with the amputees, an English officer recalled the case of a merchant’s nose that had been cut off and subsequently reconstructed by a potter named Maratha Vaidya. The commanding officer sent for Vaidya and asked him to reconstruct the nose of Kawasjee. The operation was performed in the presence of two English doctors, Thomas Cruso and James Findlay. Subsequently, the article was reproduced in the Gentleman’s Magazine of London in October of 1794 and signed with the initials “B. L.,” the English author being a surgeon named Cully Lyon Lucas. Thereafter, the forehead flap method became known as the “Indian method.”

Alessandro Benedetti (about 1445-1525) was Professor of Anatomy and Surgery at Padua University. He published articles on many subjects, first of all on anatomy. His work Anatomice, sive Historia Corporis Humani (Anatomy, or the History of the Human Body), first printed in Venice in 1502, was very popular and influential at that time. Of the many topics treated in the book, one is of special interest to plastic surgeons, i.e., the description of nasal reconstruction by means of a skin flap taken from the arm. The procedure is the same as the one the Branca family practiced in Sicily in the middle of fifteenth century. It is well known that the Brancas kept secret the operation and never published it. Hence, Alessandro Benedetti played an important role in the history of plastic surgery because he first reported in the Western surgical literature the procedure of nasal repair, later called the "Italian" method, almost 100 years before Tagliacozzi's publication in 1597.

Dr. Tagliacozzi’s procedure was not, however, for the faint-hearted. First, a flap of skin was partially cut from the upper arm. When enough healing had taken place to ensure that the tissue remained living, a second operation was performed, in which the flap was shaped into a rudimentary nose and attached to the face. After about two weeks (and presumably a lot of arm ache) the new nose was finally severed from the arm. Then the doctor operated yet again, this time to refine the contours and general appearance. The entire procedure took from 3 to 5 months. Presumably it was accompanied by considerable pain, as anesthetics were virtually unknown in those days.

The John Hopkins surgeons have built on all this history and more. Their results are wonderful!

References:

1. ORIGINS OF THE "INDIAN METHOD" OF NASAL RECONSTRUCTION; Plastic & Reconstructive Surgery; Vol 116(4):1177-1179, September 15, 2005. Singh, Gurminder B.Sc., M.B.B.S.; Kelly, Martin F.R.C.S.(Plast.)
2. Nasal Reconstruction: Forehead Flap; Plastic & Reconstructive Surgery; Vol 113(6):100e-111e, May 2004; Menick, Frederick J. M.D.
3. Alessandro Benedetti, a Fifteenth Century Anatomist and Surgeon: His Role in the History of Nasal Reconstruction; Plastic & Reconstructive Surgery; Vol 96(3):739-743, September 1995; Furlan, Silvano; Mazzola, Riccardo F.
4. Nasal reconstruction: the state of the art; Jin Soon Chang, Samuel S. Becker and Stephen S. Park