Five years have elapsed since the publication of the first edition of Plastic Surgery: Facts, a text that essentially consolidated my preparation for the FRCS(Plast) examination in 1999. Since then I have been gratified and encouraged by the feedback that I have received from many trainees in plastic surgery who have found the book useful as part of their own structured revision for examinations or simply as a source of information in their training.

The second edition of Plastic Surgery: Facts updates much of the plastic surgery and related literature over the past 5 years. Some areas have developed rapidly, while others have changed little. Plastic surgery encompasses many different disciplines under one umbrella and at times it would seem that future disintegration into a number of factions allied to other surgical specialties is inevitable. However, it is precisely this broad spectrum of principles and techniques that is fundamental to our cohesion and versatility as plastic surgeons and this remains our greatest strength.

In each chapter there are new citations that have been selected either for their educational value or scientific importance but, perhaps predictably, my own sub-specialty interests have received particular attention. Consequently, the sections on malignant melanoma and soft tissue sarcoma have expanded to reflect my own greater understanding of these areas.

Future editions of the book are likely to increasingly rely upon contributions from other authors and my intention is that Plastic Surgery: Facts will propagate as a text written by trainees for trainees.

Aesthetic breast surgery (see Chapter 7)

Laser surgery

Grabb and Smith, Lasers in Plastic Surgery; Achauer. PRS 1997

1. 1916 – Einsteins's theory of stimulated emission of radiation

2. 1950s – Schawlow and Townes: microwave amplification by stimulation emission of radiation (MASER)

3. 1957 – Maiman: light amplification by stimulated emission of radiation (LASER) using a synthetic ruby crystal

4. Helium neon laser, Nd:YAG, CO2 and argon lasers all developed in the early 1960s

5. Components of a laser:

• energy source

• electricity (argon laser)

• flashlamp (pulsed dye laser)

• another laser (CO2 laser)

1. laser medium – solid or gas

2. laser cavity (resonator)

• Laser medium is energized to excite electrons into a higher energy state (unstable orbit around the nucleus, ‘singlet state’)

• As electrons move back into a stable orbit (via a ‘metastable state’) a photon of light is emitted, i.e. spontaneous emission

• Generation of photons then perpetuates the movement of electrons of other atoms back into a stable orbit → more photons, i.e. stimulated emission

• Photons move randomly in the resonator but emerge through a pair of mirrors (one partially reflective) to become a parallel or collimated laser beam with all the same wavelength

• Longer wavelength → better penetration

• Energy (J) ∝ number of photons

• Power = energy s− 1, i.e. rate of delivery of energy (W)

• 1 W = 1 J s− 1

• rate of input of energy to create the laser beam

• Irradiance = power per unit area (W/cm2)

• Fluence = energy cm− 2 (J cm− 2)

• Gaussian distribution of heat within the spot – 10% overlap is not harmful

• Absorption coefficient of tissues also determines penetration

• Continuous wave lasers may be broken intermittently by a mechanical shutter to form a pulsed wave (pulsed-dye laser)

• […]

Chilling the skin of this five-year-old boy was like sticking a dagger into him. Contact with any cold object brought him unbearable pain. Even a moderately cool drink would make him vomit. It had been that way ever since birth, his parents told us. Our patient treated a cold object as the rest of us would treat an open flame. There was no family history of such a condition.

On examination this little boy was a happy healthy individual with perfectly normal skin. But when he was held down, his trust betrayed, to test his skin reaction to a tiny ice chip, he became a pathetic screaming child covered with tears and muscle spasms. The test site with the ice chip flared out four inches with bright red skin and local sweating. The edges of the erythema were irregular, as seen with blood vessel dilatation induced by local nerve paths. There was no hive. The redness and screaming remained for a full hour. Later, the skin was perfectly normal again.

Testing with tubes of water at varying temperatures showed that his reaction developed whenever the temperature was below 68°F. Hot water was tolerated normally, but being put in a cool room was tragic torture. His skin sensory system seemed normal with touch and pain responses being unremarkable.

We had never seen such a reaction to cold. As we reviewed our experience with cold as a cause of disease we remembered that we had seen hives develop in chilled skin.

It seemed to be an ordinary case of acne. A nineteen-year-old boy had numerous blackheads and pimples, as well as small scars, evidence of former battles fought in his skin down through the adolescent years. We knew it was the H & H disease, due to hormones and heredity. The androgens were pumping up oil production in the sebaceous glands of the face, while at the same time blocking its flow to the surface. The blockage was produced by plugs of dead horny cells, seen as blackheads but known scientifically as comedones. The name derives from the Spanish word for worms and, indeed, as we press them out, they look like little black worms. The black color is not due to dirt, but simply comes from a darkening of the plug due to oxidation. Scrubbing won't remove them any more than sanding a board will remove a nail. Each comedo is deep in the pore of an oil gland. At the time we prescribed vitamin A in large doses to promote shedding of these stagnant cells. Now, we would have prescribed the vitamin A derivative, Accutane®.

Of particular note was a tender inflamed acne cyst on his left upper cheek. These cysts develop when bacteria, trapped by the closed pore, produce inflammatory changes with the accumulation of pus. When the plugged oil gland is unable to dump its product, it finally swells like a balloon until becoming so large that it bursts.

“Funny hair” was the only diagnosis that had been made on a two-year-old boy. His mother said she had never been able to comb it. Indeed, the little lad's straw-colored hair stood straight out from his scalp and was totally noncompliant with the wishes of any comb. It was right out of the old German fairy-tale featuring “Struwel Peter.” Here was a boy whose hair was a mess (Strüwel), never once combed, looking as if electrostatic forces were in complete control. Indeed they were.

But why? Not only was the hair noncombable, but it came out in clumps on gentle pulling. It grew very slowly and was the same length as it was six months ago despite never having been cut. The hairs were fragile and thin, and broke when they were twisted. Reflected light gave the hairs a spangled appearance. The eyelashes, eyebrows, fingernails, toenails, and teeth were all normal. His parents and brother, as well as other relatives, had normal hair. He had always been in good health, except for two attacks of ear infection (otitis media).

Under the microscope the hairs appeared to be normal, showing no nodes, knots, rings, twists, or fractures. Ultraviolet light examination revealed no evidence of ringworm infection.

It was not the physical examination, nor the blood and urine studies, that made the diagnosis. It was the scanning electron microscope.

A sixty-six-year-old woman came fully frightened. She had been told that her rash could be mycosis fungoides, a rare form of malignant lymphoma. The diagnosis had been made on the basis of skin biopsy findings.

She related to us her eighteen-month history of a scaly, mildly itchy eruption. It had begun on her breasts, spreading later to her back, abdomen, and thighs. At first her condition had been called parapsoriasis, but a second skin biopsy suggested that the problem had become malignant, converting the diagnosis to mycosis fungoides.

Treatments had included cortisone preparations, both internally and externally, antihistamines, and the avoidance of bathing (which magnifies itch). Nothing had helped. She still had large red scaly patches on her trunk and thighs. We felt she had the benign parapsoriasis, and not the dreaded mycosis fungoides, which insidiously leads to skin tumors and eventually spreads internally.

Since there is no known cause of parapsoriasis, it is labeled “idiopathic.” A century of looking for causes of parapsoriasis had yielded no answers. It would have remained that way in our patient, but for our detective work. Actually, nothing blunts a doctor's zest for studying a patient more than a dermatosis known to be idiopathic.

But nothing occurs without cause, and elimination of the cause spells cure for disease. We, therefore, always zestfully hunt for a cause. Our most successful maneuver has been to look for foods, bugs, and drugs that might be incriminated.

“His scalp is showing” was the delicate phrasing of a ten-year-old boy's mother. We learned that three months ago he had developed three perfectly round areas of perfectly bald skin on the right side of his scalp. They were totally symptomless, and not inflamed, looking like totally normal skin. Around the edges we could see tiny short hairs that looked like exclamation points. These helped confirm the diagnosis of alopecia areata.

The hair had simply suddenly fallen out without a trace. This was not the hair loss of lupus erythematosus, which is inflammatory, or the hair loss of ringworm with its broken hairs. This was not the hair loss of trichotillomania where the child plucks out his own hairs in frustration, leaving a tell-tale stubble of very short hairs (too short to pull).

No, this was an autoimmune condition known as alopecia areata. Somehow, the body rejects the hairs without any sign of obvious inflammation. As the hair follicles stumble to recovery around the edges, short atrophic exclamation point hairs are produced, constricted at the base in a sputtering regeneration.

We did not need a skin biopsy for diagnosis, but we needed to study him for a cause. Although alopecia areata is classified as an autoimmune disease, and thus a rejection phenomenon, we know from experience that a focus of infection may trigger such hair loss. What was this boy's source of infection? We did not have to look far.

“I don't have a skin problem … but I was told you might help. A few months ago I woke up smelling smoke. But there was no smoke and ever since then everything has smelled like burnt toast,” was our introduction to a seventy-one-year-old woman. She went on to explain that this perception of the aroma of burnt toast was continuous, twenty-four hours a day, week in and week out. It seriously depressed her appetite. She no longer enjoyed food, although her sense of taste was perfectly normal. She had already lost 10 pounds in weight.

It wasn't that she had lost the sense of smell, but instead was a case of misidentification of odors. Even as people are color blind, she was odor blind. All stimuli of smell evoked only the smell of burnt toast, including coffee, onions and cantaloupe. The more powerful the stimulus the more intense the odor of burnt toast. Her medical diagnosis was dysosmia, or as some prefer to call it, parosmia.

The diagnosis was easy, but what caused this sudden malfunction of an organ which, in its own way, is as exquisitely specialized as the eye? The organ of olfaction is located in a patch of specialized mucosa high in each nostril. It is truly remarkable, for there, totally hidden from view, are over 10 million separate bare nerve endings. They are actually outside the body, unlike any other nerve.

“My skin is turning hard and I've been told that nothing can be done,” said a seventy-four-year-old woman who had just moved to our area from the South. She had recently been carefully studied by a number of doctors during a five-day stay in a university hospital. They told her she had generalized morphea, a condition for which no treatment was known. Unlike them, we greeted her with great optimism. Surely, we could do something to stop the inexorable progress of the hardening of her skin. She did not have to be Lot's wife.

She had first noted the indurated firm areas on her chest, but they had extended in eight months to also involve her back and abdomen. Her skin felt tight and itchy. Last week her right calf also started to become involved with the firm slightly darkened patches, which now we could also detect on her right forearm and both elbows. The breasts were the worst areas, with very shiny hard skin. Her hands, feet and face were unaffected.

Her past history revealed she took no medications, had no allergies, neither smoked cigarettes nor drank alcohol, and had never had any prior skin disease. She had worked in a poultry plant dressing chickens for twenty years, but was now retired. We could elicit no history of skin trauma at her work or of any tick bite preceding the hardening of the skin.

His mother brought him in for light therapy. He was eight years old and for the past year had been going to a distant skin clinic for ultraviolet light treatments for his psoriasis. The trip demanded three hours of driving three times a week. His mother finally asked, “Isn't there somewhere nearer to my home I could go to for these light treatments?” And so, he had been brought to us requesting a series of late after school appointments on Monday, Wednesday, and Friday.

We examined her son. He had extensive psoriasis on his trunk, arms, and legs, which was responding well to the ultraviolet light treatments. But, as parents, we thought of the drain of three visits each week to the doctor, even if close by. We knew there could be another way. Our research had shed a new light on psoriasis.

We explained to the mother that psoriasis has a hereditary background, which we could not alter. We explained that the silvery white scales her son shed everyday were dead flakes of his outermost skin, the epidermis. Normally, our skin sheds this dead stratum corneum invisibly because the particles are so small. They rub off in the bath or on the clothing without notice. But, in psoriasis, the epidermis is growing 10 times faster than normal, resulting in big thick white scales. The secret of treatment is to slow down the rapid division of the cells.

“I've been having hot flashes for three years and no one knows why,” stated a thirty-one-year-old secretary. It soon developed that not only did she get sudden flushes, but they were accompanied by both hives and headaches during severe attacks. She had noted that both the flushing and hives began about an hour after arising, and continued to develop throughout the day and evening, vanishing while she slept. The flushing then began again the next morning as a gradual wave of warmth spreading over her head, neck, and shoulders. The hives were small and scattered over the trunk.

Complete gynecologic and endocrinologic workups were to no avail. She was taking no medications and denied chemical exposures at work. Furthermore, the flushing, hives and headaches did not remit during vacations. It was not occupational.

Examination at her first visit found our patient to be healthy, but her face, neck and shoulders were flushed and warm. There were isolated small wheals, less than a half inch in diameter, scattered over these areas as well as her trunk. Individual hives faded in one to two hours, even as new ones developed. Firm stroking of her skin produced a linear hive, the cardinal sign of dermographism, a condition known as “skin writing.” More importantly, it told us that the cause was something circulating in her blood. It could be a food or something she was inhaling.

“What can I do? What can I do?” came the sobbing voice over the telephone. It was a former patient of ours. “What can I do?” she continued, “My mother has pemphigus with blisters all over her body. Her doctors tell her she will die if she doesn't have treatment.” “So?” we replied. “But, my mother won't accept any treatment, since it's against her religious beliefs. Last year she had a blood clot and lost her leg because she would not allow any treatment. What can I do?” We tried to calm the daughter, telling her we would see what we could do. “Tell your mother I would like to see her as a friend, not as a patient. Just bring her over for a chat.”

The next day in came the daughter with her mother. As we sat in the consultation room, the tears were rolling down the daughter's cheeks. And clear fluid was dripping down the mother's leg from large open blisters. Indeed, the dye from her purple shoes was being leached out onto our carpet.

The mystery was, how to treat this little old lady so she could hold onto life and her religious beliefs. The epiphany came in a flash as we began talking about the dye on our carpet. It was then that we saw a magic carpet of therapy. We said to the mother, “We see that your daughter is very sick. May we help her?” The mother gave a wan assent.