Reoperative Aesthetic & Reconstructive Plastic Surgery

7. During the initial consultation, a patient starts crying when talking about her
dissatisfaction with the results of her face-lift procedure performed by a differ-
ent surgeon 9 months ago. She reports that she is currently taking an antidepres-
sant, 20 mg/day, as prescribed by her primary care physician. The current sur-
geon should:
a. Go ahead and schedule her for surgery,since she is taking an antidepressant.
b. Contact the primary care physician to further assess the patient’s depressive
symptoms
c. Inquire about current or past psychotherapy.
d. Not schedule her for surgery.
8. During the initial consultation, a patient reports signi cant dissatisfaction with
a previous rhinoplasty procedure. She reports that she is now “dis gured” and
cannot date because of her nose. In the surgeon’s opinion, the initial result is
very good, although some slight revisions could be made. The patient denies
any current or past psychiatric treatment.The current surgeon should:
a. Go ahead and schedule her for surgery, since it is only a slight revision
b. Contact the primary care physician to further assess the patient’s functioning
c. Consider a psychiatric evaluation before scheduling surgery
d. Not schedule her for surgery
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77
The Surgeon
Robert M. Goldwyn
C ha pter 4
Few events are as demanding on the surgeon and the patient as when another
operation is necessary because something went wrong. The surgeon who is reop-
erating or considering doing so will be treating his or her patient, or someone
else’s, with differing circumstances and consequences.1-3
WHEN THE PATIENT IS YOUR OWN
IF,W HEN, AND HOW TO R EOPERATE: ESTABLISHING
THE PROBLEM
In most instances, the problem is evident to both the patient and the surgeon as, for
example, with an expanding hematoma, or a uctuant, infected wound.These in-
escapable realities require immediate, unequivocal attention and action. However,
with a slightly asymmetrical nipple after breast reduction or a persistent unilateral
fullness following rhytidectomy, the patient may be quicker to recognize the prob-
lem than the surgeon is. It is axiomatic that anything that concerns the patient
should concern the surgeon, who should not deceptively minimize its existence
or cavalierly dismiss it.
Mistakes, no less bene ts, witness to the
existence of the art;for what bene ted did so because
correctly administered. Now where correctness and incorrectness
each have a de ned limit, surely there must be an art. For absence
of art I take to be absence of correctness and incorrectness;
but where both are present, art cannot be absent.
Hippocrates

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Not every patient in whom something has gone wrong should have
another operation.
Not doing anything further is frequently the best treatment, but the decision is
harder when the patient is our own, because we may be less objective. If the deci-
sion is made not to operate, the patient may believe that the surgeon’s unwilling-
ness is a way of minimizing his or her dissatisfaction and think the surgeon is try-
ing to dodge the problem. In that situation, the surgeon must carefully and
unhurriedly explain the bene ts of waiting. If the patient does not accept the ad-
vice or mistrusts the surgeon’s motives after a thorough discussion, the surgeon
would be wise to refer that patient for another opinion.
A referral serves not only to obtain advice but also to gain time, avoiding a rush into
an ill-advised procedure because of the patient’s anxiety and the desire of the pa-
tient and surgeon to rectify the problem quickly. Patients are seldom patient—and
surgeons are frequently impatient. If the patient has been told to wait, you must
provide structure and not leave that person suspended with ambiguous responses.
Saying “We’ll see how it does” carries no reassurance and spawns anxiety. A better
alternative would be something like the following:“Your incision has opened, as
you already know. It looks as if it is infected, and I will give you antibiotics for 10
days. Every day you should change your dressing at least twice; I will show you
how to do it. But I want to see you at least three times a week, and certainly as of-
ten as necessary and you desire. I know that with time everything will get better [if
true].We’ll see this through together.”That statement lets the patient know that you
are not abandoning him or her, that you care, that you also are concerned about the
problem. By assuring the patient that you are committed, you have lessened anxi-
ety and increased con dence. A few of my patients who needed additional surgery
because of a complication later became my most devoted and enthusiastic patients.
Adversity, if managed properly, can be a uniting experience.
The worst mistakes a surgeon can make with a patient who has had
a complication or an unfavorable result are to trivialize or deny its ex-
istence, to become angry at the patient, to be unavailable or shunt the
patient to an assistant—a nurse, a secretary, or a resident.1
The primary responsibility belongs to the surgeon who did the operation, with
whom the patient has had an implicit if not explicit contract. In the words of Pres-
ident Truman,“The buck stops here.”
In this regard, I remember a patient describing her surgeon:“He was always there
to get the money, and before the operation his of ce treated me like royalty. But
when I had this happen (separation of the wound after reduction mammaplasty), he
was never around. Even the FBI would have had trouble nding him.”

To emphasize to patients that I am available, I ask them to call me at my of ce or
at home (I give them my number, even though it is listed in the telephone book)
whenever they wish. It is surprising how few phone calls I receive. Just the realiza-
tion that the surgeon truly cares and is ready to help may be suf cient for the pa-
tient if this is combined with frequent, scheduled visits to the of ce.
With a patient who is either dissatis ed with the result and/or requires reoperation,
the surgeon should be empathetic. He or she should be willing to say,“I am sorry
this happened. I too am frustrated and distressed, but I know that both of us to-
gether can bring this to a successful conclusion [if true].”
This openness comforts the patient, who realizes you share his or her discomfort,
but at the same time that you are in charge, and con dent and competent to solve
the problem.
GATHERING SUPPORT
After having admitted the existence of the problem and after having outlined a
plan, the surgeon must marshal support among those close to the patient:members
of the family, perhaps a friend, and de nitely the referring physician and/or the
family physician.You and the patient need every ally possible. It is not easy to call
the physician who has referred the patient and report an unfortunate outcome, but
it must be done as quickly as possible before the physician has heard it from the
angry patient or an irate family member.
USING A CONSULTANT
The proper use of a consultant requires tact and skill. Most patients want to re-
main with the original physician, but it can comfort the patient as well as the sur-
geon to have another opinion when warranted. If you are attuned to sense when
the patient wishes a consultation, do not make the patient jump through hurdles to
obtain one. At the same time, however, the patient should not feel discarded but di-
rected to the other physician. I usually dictate a letter in the patient’s presence de-
scribing the problem and asking the other physician for advice, which, I state,
should be discussed freely with the patient. An occasional patient may declare
that he or she does not want to pay for “your mistake.” You must address that
statement and try to explain that you did your best, but no physician, no surgeon
can control every aspect of treatment. That is why informed consent exists, and
it serves as a gentle reminder to the patient that he or she understood that com-
plications could occur and that this was so stated in the informed consent.
Ideally, a surgeon will see an aggrieved patient for a colleague at no charge to help
the unhappy individual and the hard-pressed physician. If you believe, however,
that the patient should not be charged for the consultation and that the physician
to whom you have referred the patient will likely not forgo a fee, you should in-
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form the patient and the surgeon that you would be willing to pay for the consul-
tation. This does not signify culpability per se; it acknowledges the reality of your
having an unhappy patient.Your volunteering to defray the consultation fee shows
your empathy, especially with a patient who is nancially stressed. As mentioned, if
the patient does not want to see a consultant of your choice, make it clear to the pa-
tient that he or she is certainly free to select a physician and that you would be
happy to forward records and confer with the other surgeon, but only with the pa-
tient’s signed permission.
R EOPERATING ON YOUR OW N PATIENT
When you must perform another procedure because the original operation did
not accomplish its goal, the patient is likely to be disappointed, even hostile, but has
suf cient con dence in you to let you try again. If you conclude that correcting the
problem requires not just your efforts but those of another surgeon, you should
not hesitate to inform the patient and urge him or her to see the other surgeon.You
both should make the arrangements, with the patient’s knowledge, to combine sur-
gical efforts, if required.
The following story illustrates how not to behave. A colleague once called me to
help with a secondary procedure on his patient. I agreed, but then refused when he
said,“She’ll never know you’re there, because she’ll be asleep.” I did not want to
participate in something that was unfair and unethical. Fortunately, the other plas-
tic surgeon reversed eld, sent the patient to me, and with full disclosure we both
operated on her successfully (a redo reduction mammaplasty).
The surgeon who reoperates on a patient already has one strike against him or her.
Another strike and the surgeon may be out, since it is a rare patient and a persis-
tent surgeon who would make a third attempt, at least on his or her own.
In this situation, it is not a question of courage but of common sense. I am not al-
luding to a staged procedure about which the patient should have been informed
initially as with a dif cult breast reconstruction. I am not referring to minor revi-
sions.
Much different, for example, is the male rhinoplasty patient on whom you have
already tried to rectify the problem twice. He should probably not have you as a
surgeon a third, or worse, a fourth or fth time. Better for each of you that an-
other surgeon enter the scene.
LISTEN TO THE PATIENT
This instruction is so elemental that it is often neglected.The following case is apt:
Ms. B. came because of pain behind her right ear after having had a face lift 3 years
previously.When I had last seen her, 11⁄2 years earlier, she had no complaints about
her result, which we both thought was completely satisfactory. In taking her history

on this occasion, I elicited the fact that the pain behind her ear began when her
lover, a married man, was diagnosed and hospitalized because of colon cancer. Not
surprisingly, as his treatment progressed and he became better, her pain disappeared.
Throughout those months, I did see her periodically, more for her psyche than her
scar, which was minimal and without evidence of a neuroma.
W HEN PSYCHOTHERAPY IS NEEDED
Some patients may complain about a problem that neither you nor an objective ob-
server can detect, as in the patient just cited. However, unlike that patient, some may
become extremely depressed, hostile, and threaten to sue if you do not “do some-
thing.” With this level of anxiety and acrimony, and even if the problem would
eventually bene t by an operation, the help of a therapist, psychologist, or psychi-
atrist may be necessary. The challenge is then how to get that patient to go for a
consultation. Sometimes the patient adamantly refuses. If so, speaking with the fam-
ily or the patient’s physician to get their help is successful. It is often effective to tell
the patient that you know he or she is intelligent enough to realize that medicine
and surgery have made many advances and that one would be foolish to ignore
anything that could improve the patient’s well-being. For example, you can say that
if she or he were having a heart problem during the course of treatment with you,
you would need the help of a cardiologist and you know he or she would willingly
go. Now you believe that a psychologist or psychiatrist could be bene cial, at least
for a consultation. It does not mean that you should tell the patient that years of
psychotherapy will be necessary, but certainly a consultation is in order and perhaps
some help for a few weeks to “get over the hump.”You can add, if it is true, that you
have had other patients who have been helped immeasurably and rather quickly by
a psychotherapist.You know one or two therapists with whom you have worked [if
true] and with whom you can arrange a consultation. At the same time, you must
tell the patient that you still consider yourself his or her plastic surgeon and will
want to see him or her regularly until “things get better.” Again, it is impossible to
overemphasize that no patient, indeed no human being, wants to feel abandoned,
and certainly not after a failed operation by the surgeon he or she has chosen and
whom that person still considers to be his or her physician.
The plastic surgeon would do well to remember that unlike a family physician, he
or she has likely been consulted only once or twice and has had limited interaction
with the patient. In an urban area, the paths of the patient and the surgeon may
cross only in the of ce, operating room, or hospital.This relationship is very differ-
ent from that between the patient and his or her family physician, whose interac-
tion has been longer and deeper.
The usual reasons that bring adults to consult a plastic surgeon result in short-term
contact and brief treatment, unlike what transpires between patients and their in-
ternist. When something goes wrong between a patient and a plastic surgeon, the
basis on which to continue what could be a strained relationship is less solid—all
the more reason for the surgeon to make himself or herself easily accessible. A tele-
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phone call to the patient at home, for example, in between scheduled visits and
not in response to the patient’s call, can do much to ameliorate a dif cult situa-
tion.
FINANCIAL ASPECTS
If the failed operation and the condition that prompted it were of a reconstructive
nature, insurance will generally cover the cost of reoperating, including the cost of
the hospital stay. An astute and understanding surgeon will not charge the patient
more than what the insurance pays.
Aside from the question of the surgeon’s fee, the patient with an unsuccessful out-
come from an aesthetic operation might have to confront additional hospital costs
unless the surgeon has his or her own operating facility and does not charge for its
use.
I never billed a patient for a revision, but since I operated in a hospital, the patient
had to pay those associated costs. Every patient undergoing aesthetic surgery signed
a form saying that he or she would be financially responsible for the hospital charges
relating to the “improvement” of a result. However, the act of signing the form
does not mean that the patient acquiesces calmly to these additional charges. Usu-
ally patients resent them, because they believe that the surgeon “should have done
it right the rst time.” The surgeon is then in the uncomfortable situation of fear-
ing that the patient will sue, particularly if reoperation fails. On a few occasions I
asked the hospital to reduce or write off the charges, and once, at the patient’s re-
quest, I paid those costs when I was convinced that the patient would not sue. Be-
fore doing that, it is well to obtain advice from the malpractice insurance carrier
and an attorney to avoid the possible allegation that your willingness to pay those
expenses was an admission of negligence.
The problem of nances becomes more dif cult when the patient is another sur-
geon’s.
WHEN THE PATIENT IS SOMEONE ELSE’S
One would hope that the surgeon seeing a colleague’s patient with a problem
would not use the situation to denigrate the other surgeon or to plump his or her
own ego. Because all of us who operate are destined to have some failures, rejoic-
ing openly or secretly in a colleague’s poor result is puerile and myopic. At the
time that this patient is in your of ce, one of yours may be in his or hers.
IF AND W HEN TO O PERATE
As with a patient of your own, the medical-surgical problem should determine the
decision of whether to operate. The alternative of not operating may be the best
treatment. You should not unconsciously undertake an operation to bolster your

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stature or placate an overwrought patient. The fact that we can operate does not
mean that we should.
THE R EOPERATING SURGEON AND THE O RIGINAL SURGEON
The surgeon who may be reoperating on another plastic surgeon’s patient should
focus on the problem without directly or indirectly attacking the original surgeon
by an explicit statement or innuendo or by body language such as a raised eye-
brow, a sigh, or an “oh, my” shake of the head.
W hen you are not the original surgeon, you should act as does a good
relief pitcher in baseball called to do a dif cult task; he does not chas-
tise the other pitcher for having loaded the bases.
Unfortunately, some plastic surgeons take pleasure in verbally assassinating a col-
league.The patient should not be the victim of a personal vendetta.
A patient once related that a surgeon whom she had seen in consultation said to
her,“I never knew he performed this kind of operation.” It was a rhinoplasty, a sta-
ple in his practice and in that of most plastic surgeons. Other wounding remarks
that patients have shared with me are:“He is getting too old to operate, I would
think,” or “He just opened his practice. I know eventually he will be excellent, but
now he’s just learning the ropes.” Another gem was:“He’s a wonderful guy, but in
the operating room, he can really be unpredictable.”
Those comments make patients feel stupid and exploited, believing that they went
to the wrong surgeon. Plastic surgery demands enough of our energy without wast-
ing it in slander.
As you obtain the patient’s history, remember that you are hearing the patient’s
version, not the surgeon’s.The two might differ markedly. It is to be hoped that the
patient will allow you to communicate with the other surgeon; if not, you should
tell the patient that it is in his or her best interests for you to have as much infor-
mation as possible.
If a patient still refuses, you must decide whether to terminate the relationship or
continue it. Since our primary commitment is to the patient, it is dif cult, occasion-
ally impossible, or wrong to refuse to be the patient’s next surgeon. For the patient’s
well-being and perhaps for the other surgeon’s professional well-being, treating the
patient may be advisable,even though the patient has restricted your communication.
At no time should the second surgeon write or speak with the original surgeon,
even if a close friend, unless the patient has given permission. One has no legal or
ethical right to breach con dentiality without speci c consent. Aside from the le-
gal implications, you lose credibility and effectiveness if the patient discovers that
communication has occurred without his or her knowledge.

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Although the ideal may be to convince the patient to return to this original sur-
geon, who may have referred the patient to you, I do not believe it is wise medically
or correct ethically to force a patient to return to a physician whom he or she no
longer trusts or likes, even though the patient’s reasons might be unjust and un-
founded.
Furthermore, you might be the logical person to correct the problem.
If the patient does allow communication with the original surgeon, the patient
may be suspicious about what you will say. To allay doubt, you can telephone the
other physician in the patient’s presence. To obtain a thorough report and a
thoughtful opinion from the other physician and to have documentation for the
record, I prefer a letter or email, with a copy to the patient. This open approach
does much to reduce the patient’s suspicions, anxiety, and hostility and makes your
task easier.
Patient Example
A 20-year-old student had a reduction mammaplasty in another state a month be-
fore she consulted me. Some of her wounds had dehisced. Every time I saw the pa-
tient, I not only dictated a report to her surgeon but on several occasions also called
him so that they could speak to each other. She healed without dif culty and told
me that as much as she liked me, she wanted to have her breasts “made better” by
her rst surgeon.Thus an ideal outcome was reached for all concerned. She had no
insurance for her visits, and I did not charge her.
FINANCIAL ASPECTS
As mentioned, the nancial aspects of reoperating on another surgeon’s patient can
be extremely trying. If the original procedure was reconstructive, in most instances,
the patient would fortunately be covered by insurance for hospital charges and,
hopefully, for the surgeon’s bill. Again, if the procedure had been aesthetic, the pa-
tient will have had to pay the entire cost. If you are the reoperating surgeon, you
can theoretically charge whatever you wish, but I would hope that colleagues
would be kind to each other and the patient by charging fairly or not at all if, for
example, only a minor revision were needed.
It is not unusual for a patient to tell you, the reoperating surgeon, that the original
surgeon should pay for your charges or the hospital’s.“After all,” they may say,“I
went to him (or her) and he (she) messed up. Now I have to have another opera-
tion, and why should I pay for it?” The patient incorrectly views a surgical opera-
tion as a commodity, an item to be purchased, repaired, or replaced if necessary.
The patient considers his relationship with the surgeon like that of a consumer.
No matter how eloquently you, the second surgeon, may dispute that viewpoint,
the patient may remain unconvinced and angry.

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On occasion I have called the rst surgeon and said that I would reduce my fee
considerably and that it might be advisable for him or her to speak with the patient
to come to some agreement, perhaps even returning the patient’s money or a por-
tion of it but this would be entirely between the surgeon and the patient, depend-
ing on the legal advice the other surgeon receives.
The decision about charging for reoperation can be tempered by a collegial and
humanitarian view of medicine and plastic surgery, an attitude not always possible
to maintain in today’s turbulent environment. However, if the surgeon considers the
medical world a jungle or a marketplace and feels a high level of entitlement, the
patient as well as the rst surgeon will likely not receive compassion. It is possible,
furthermore, that reoperation also will fail; the patient then will hold both sur-
geons accountable, not only medically but scally and legally.
THE PROBLEM SURGEON
The “problem surgeon” is not, as one might think, a surgeon who manages prob-
lems, but a surgeon who creates them. Unfortunately, a few physicians, among them
plastic surgeons, fail to learn from mistakes; they are incapable of introspection.
They may undertake a procedure for which they are ill trained. For reasons of
money or ego they may subject a patient to an operation that he or she should not
have had and the surgeon should never have attempted.
All surgeons should keep a list of their complications and attempt to detect a pos-
sible pattern.4 If you do this, you have the choice of improving your performance
by attending courses or consulting colleagues, or visiting them in their operating
room. If you are unwilling or incapable of doing better, for whatever reason, you
should drop that procedure from your repertoire. I have yet to meet a surgeon,
plastic or otherwise, who does all things equally well.
Every surgeon should have enough self-awareness to know whether he or she is in
good physical and mental health. A surgeon who is continually overstressed would
do well to consult an internist or a therapist, or both. The Biblical advice,“Physi-
cian, heal thyself,” is not only relevant but mandatory—if not for yourself, then for
your patients.
CONCLUSION
Few situations in the professional life of plastic surgeons are as dif cult as the cir-
cumstances under which they must reoperate, either on their own patient or on
someone else’s. In the process, reoperating surgeons, either with their own patient
or a colleague’s, may paradoxically forge a relationship stronger than what might
have been if the initial procedure had gone well.

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References—With Key Annotated Reference
1. Goldwyn RM. The Patient and the Plastic Surgeon, 2nd ed. Boston: Little Brown, 1991, pp
247-259.
2. Goldwyn, RM. The dissatis ed patient. In Goldwyn RM, Cohen MN, eds. The Unfavorable
Result in Plastic Surgery:Avoidance and Treatment, 3rd ed. Philadelphia:Lippincott Williams &
Wilkins, 2001, pp 9-13.
A collection of more than 26 years of clinical research on the complications that can result from var-
ious cosmetic surgeries.The text highlights advances in plastic surgery, in areas like bone, skin and nerve
grafts, facial reconstruction, and breast augmentation. Legal issues are also covered.
3. Goldwyn RM. Psychological aspects of plastic surgery: Observations and re ections. In Sarwer
DB, Prozinsky T, Cash TF, et al, eds. Psychological Aspects of Reconstructive and Cosmetic Plas-
tic Surgery: Clinical, Empirical, and Ethical Perspectives. Philadelphia: Lippincott Williams &
Wilkins, 2006, pp 13-22.
4. Goldwyn RM. Why we fail. In Goldwyn RM, Cohen MN, eds. The Unfavorable Result in
Plastic Surgery:Avoidance and Treatment, 3rd ed. Philadelphia:Lippincott Williams & Wilkins,
2001, pp 1-8.

SCARS,TISSUE MOVEMENT,
AND TRANSPLANTATION
P a r t II

(Trang không có chữ)

89
Common Secondary Complications
James C. Grotting
C ha pter 5
Reoperative Problems
Hematoma
Coagulation abnormalities
Seroma
Wound-healing problems
One thorn of experience is worth
A whole wilderness of warning.
James Russell Lowell
A number of complications are common to all plastic surgery procedures. Al-
though most are not serious, a small percentage of these can have major aesthetic
and functional repercussions. In rare instances, life-threatening complications can
occur.To be able to anticipate and prevent such problems, surgeons must be aware
of the factors predisposing to these complications. When such complications do
occur, prompt and de nitive management is imperative.
Common complications can be divided into four categories: hematoma, seroma,
coagulation abnormalities, and wound-healing problems.

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HEMATOMA
A hematoma is a localized mass of extravasated blood that is relatively or com-
pletely con ned within an organ, tissue, space, or potential space.The blood is usu-
ally clotted and may demonstrate various degrees of organization. Other forms of
extravasated blood include petechiae, purpura, and ecchymoses. Petechiae are
minute hemorrhagic spots usually measuring 2 to 3 mm in diameter. A purpura is
a larger extravasation of blood, measuring up to 1 cm. Ecchymoses, purplish patches
caused by extravasation of blood into the skin, tend to be blotchy and larger than
purpura.
Technical Reason
Failure to recognize and ligate arterial or venous bleeder
Predisposition to Perioperative Bleeding
Preexisting hemostatic defect
Platelet function disorder
Coagulopathy
Preoperative aspirin or anticoagulant therapy
Transfusion-related
Hemodilution
Hemolytic transfusion reaction; disseminated intravascular coagulation (DIC)
Sepsis
Endotoxin-induced thrombocytopenia
Acute postoperative increase in systemic or local pressure
Hypertension on extubation (for example, struggling or coughing that raises intra-
abdominal, retrobulbar pressures)
Causes of Hematoma Following Surgical Procedure
Blunt trauma
Hemostatic defect
Platelet function disorder
Coagulopathy
Medication
Tumors
Hemorrhage into necrotic tumor
Tumor-induced brinolysis
Thrombocytopenia resulting from bone
marrow involvement
Causes of Hematoma Unrelated to Surgical Procedure
Infection
Disseminated intravascular coagulation
Thrombocytopenia
Systemic disease
Hypertension
Liver disease
Atherosclerotic vascular disease
Metabolic disorder
Malnutrition/scurvy

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Hematomas can be categorized by etiologic factors as those resulting from surgi-
cal procedures and those unrelated to surgical procedures (see the boxes on p. 90).
PATHOPHYSIOLOGY
The ultimate fate of a hematoma, left to follow its natural course, depends largely
on its size and location and the presence or absence of infection. It may liquefy
and be completely absorbed, or it may undergo organization, with replacement by
a brous scar. After extravasated blood has accumulated, an anaerobic environment
gradually forms. Lactate production results, with red and white blood cell lysis oc-
curring because of the increased acidity.The reticuloendothelial system is respon-
sible for the uptake of iron, pigment, and cellular dermis released as a result of the
blood cell lysis. An in ammatory reaction ensues, with involvement of white blood
cells, macrophages, and broblasts.
The outcome of a hematoma at this juncture is determined by competition be-
tween the processes of absorption and organization. Many small hematomas may be
completely absorbed.Thus uptake and transport of the extravasated blood are facil-
itated by the reticuloendothelial system, with concomitant lymphatic drainage of
edematous fluid. This transport is hindered by infection or recurrent bleeding.
Hematomas that are not completely absorbed progress to organization, the process
wherein a hematoma is replaced by brous scar. Platelets and macrophages nor-
mally present in the in ammatory reaction stimulate broblast proliferation, with
subsequent ingrowth of granulation tissue and brous scar formation.
The most signi cant recent advance in the understanding of hema-
toma pathophysiology has been the identi cation of free radicals.
It was formerly presumed that overlying ap necrosis was caused by a pressure ef-
fect, resulting in obstruction of dermal ow. However, studies have shown that pres-
sure has a limited role; the most in uential mechanism is the direct toxic effect of
blood on skin aps.1 Free radicals tend to form in the anaerobic environment of the
hematoma.2 These ions are quite damaging to overlying tissues. Both iron and he-
moglobin, vital blood components, are involved in this process. Iron is a catalyst in
the reaction of superoxide to hydroxyl, a major step in the formation of free radi-
cals. It also interferes with host defenses. Hemoglobin inhibits polymorphonuclear
chemotaxis.3
COMPLICATIONS
Complications of hematomas are as varied as the tissues involved.They range from
the minor “blip” in the otherwise normal process of wound healing to the major
life-threatening compression of vital structures (see the box on p. 92).

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CLINICAL SIGNIFICANCE
The clinical signi cance of hematoma formation extends to all aspects of plastic
surgery practice.These areas are considered individually with particular emphasis on
prevention and treatment.
Skin Grafts
Any uid collection that separates a skin graft from its underlying bed impedes dif-
fusion and prevents vascularization. Prevention includes proper patient selection,
with particular attention to patients who are taking aspirin or anticoagulant med-
ications and patients with a history of bleeding disorders. Ensuring proper hemo-
stasis, use of drainage, and application of compressive dressings is vital.
Treatment requires early recognition, drainage, and reapplication of the skin graft af-
ter the predisposing factors are addressed.
Flaps
Surgical closures in plastic surgery often involve some type of ap. Hematomas,
which are known to cause dehiscence and overlying necrosis, can signi cantly jeop-
ardize ap survival.1 Prevention requires early detection, evacuation, and irrigation
of the hematoma cavity and subsequent arrest of any bleeding points. Drains placed
under aps may be helpful in the prevention of hematoma formation, but they cer-
tainly cannot be relied on in every circumstance.
Fibrosis
Aesthetic importance
Capsule formation around implants
Infection
Area of cellular debris
Interference of host defenses by iron
Inhibition of chemotaxis by hemoglobin
Wound dehiscence
Secondary to tissue necrosis and pressure
effect on wound edges
Toxic effect caused by free radicals
Overlying tissue necrosis
Pressure effect on dermal ow (old theory)
Toxic effect caused by free radicals
Complications of Hematoma in Plastic Surgery
Compression of vital structures
Airway
Visual axis
Nerves
Ossi cation
Results from mixing of periosteal cells
from locally traumatized bone
Most common near long bones and
skull
Seen with neonatal scalp and pelvic
hematomas caused by forceps
injury
Residual pigmentation
Hemosiderin

93
Chapter 5
Common Secondary Complications
Face
Hematoma is the foremost complication of a face lift (occurring in approximately
2% of cases).4-6 It usually takes one of two forms: a small collection of extravasated
blood that is rst noticed several days postoperatively, when swelling subsides, or an
expanding hematoma presenting during the rst few postoperative hours. However,
expanding face-lift hematomas caused by bleeding from the super cial temporal ar-
tery or vein have been reported to occur as late as 8 to 10 days postoperatively.7 We
monitor our patients carefully overnight for this complication and use compression
dressings only for the rst 2 to 3 hours until vital signs are stabilized. A small por-
tion of the postauricular incision may be left open to roll out any collected blood
on the rst postoperative morning.
Prevention calls for consideration of several factors, which helps to keep the inci-
dence of this complication to a minimum (see the box below).8
Patient selection (warning signs: bleeding diathesis, hypertension)
Laboratory test results: preoperative platelet count, prothrombin time, partial thrombo-
plastin time, bleeding time, platelet aggregation
Institution of hypotensive anesthesia
Avoidance of postoperative hypertension: 0.1 to 0.3 mg clonidine (Catapres) PO morning
of surgery has been recommended3
Use of local anesthesia versus general anesthesia (to avoid postoperative coughing)
Maintenance of meticulous hemostasis
Postoperative care: head elevation, application of cool packs
Insertion of drains
Application of compressive dressing
Avoidance of strenuous physical activity for several weeks postoperatively
Factors in Prevention of Face-Lift Hematoma

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Treatment of a face-lift hematoma is based on the size and speed of formation.The
expanding hematoma is best treated by surgical evacuation and inspection of the
entire wound. The bleeding vessel is rarely found. Small hematomas often liquefy
7 to 10 days postoperatively and may be aspirated or drained through small stab in-
cisions. Because of the deleterious effect of hematomas on all tissues, prompt diag-
nosis and treatment of all hematomas is warranted.
Nasal Septum
Nasal septal hematomas occur most frequently as a result of fracture-dislocation or
bending of septal cartilage with intact overlying mucosa. These hematomas may
be unilateral or bilateral. Postoperative septal hematomas may occur as adrenalin
effect wears off postoperatively.They must be drained urgently to prevent second-
ary complications. The septal hematoma may organize, causing septal thickening
and subsequent nasal obstruction.With large hematomas, pressure necrosis of car-
tilage with absorption may occur, resulting in septal perforation. Loss of the nasal
septum can cause collapse of the nasal dorsum, leading to saddle nose deformity.
The risk of septal hematomas in nasal surgery can be reduced by the use of Silas-
tic splints and by mattress suturing of the septal mucoperichondral aps to each
other.Treatment involves evacuation via horizontal incisions along the oor of the
nose with or without the use of concomitant packing, splint, or mattress sutures.
Ear
Auricular hematomas may be secondary to a single blow or repeated blows to the
anterior ear. Similar to the nasal septum, postoperative hematomas in the ear may
occur as the adrenaline effect subsides. These hematomas may develop in a sub-
perichondral or subcutaneous plane.Treatment of the subcutaneous hematoma in-
volves evacuation and the application of a form- tting compression dressing.
If the hematoma occurs in the deeper subperichondral plane, the avulsed perichon-
drium over time forms new cartilage, which is held in place by the tight perichon-
dreal envelope. A bulky, disorganized surface results, obliterating the normal con-
volutions of the ear and causing the so-called cauli ower ear.9 Treatment requires
evacuation of the hematomas and the use of a compressive dressing with or with-
out bolster sutures. Late treatment is more dif cult and involves the surgical carv-
ing of the delicate convolutions of the cartilaginous framework from the ill-
de ned cauli ower ear.

95
Chapter 5
Common Secondary Complications
Breast
Breast Augmentation
The incidence of hematomas following breast augmen-
tation is 1% to 2%.10 These hematomas usually present clinically with pain, swelling,
and occasionally fever. It should be kept in mind that breast hematomas often are
not palpable, especially when tense, thereby making diagnosis easier to miss. Breast
hematomas following augmentation have been implicated as an etiologic factor in
capsule formation. Prevention includes ensuring meticulous hemostasis, use of
drains, and application of a compression dressing. The classic treatment involves
evacuation of the hematoma, hemostasis, and drainage. Aspiration is not recom-
mended (see Chapter 34). We prefer to manage these in the operating room, al-
though sometimes local anesthetic with sedation is adequate. Failure to drain these
hematomas may lead to eventual capsular contracture.
Breast Reduction
Hematomas following breast-reduction surgery may lead to
necrosis of either the overlying skin aps or the nipple-areola complex.Treatment,
as with breast augmentation hematomas, requires evacuation, hemostasis, and drain
placement.
Eyelid
Subcutaneous Hematoma
Subcutaneous hematomas following blepharoplasty
are essentially an aesthetic problem only and are usually detected after postopera-
tive swelling subsides. Evacuation by aspiration or stab incision is required to avoid
the prolonged appearance of a “hump.” Diagnosis in the rst several hours after
surgery should be managed by teasing open the incision and rolling out the blood
collection.
Retrobulbar Hematoma
With a retrobulbar hematoma there is bleeding poste-
rior to the orbital septum, which could potentially result in blindness. The bleed-
ing is usually caused by vessel injury from a needle or by a transected fat pad. A

96
PART II
SCARS,TISSUE MOVEMENT, AND TRANSPLANTATION
retrobulbar hematoma causes a rm, protruding, and often painful eyeball. Deteri-
oration of vision may occur. Factors important in prevention include proper patient
selection, with special attention to the patient’s preoperative medication regimen
and preoperative hypertension, use of the bipolar cautery to cauterize fat pads,
avoidance of deep injections, and postoperative use of cool compresses with head
elevation.There continues to be a debate as to whether local anesthesia offers any
advantage over general anesthesia in the prevention of retrobulbar hematomas.
The most important factor in the management of retrobulbar hema-
tomas is early recognition.
Once a retrobulbar hematoma is diagnosed, all sutures should be removed promptly.
The surgeon must open the orbital septum widely and attempt to locate any bleed-
ing points. Performing a lateral canthotomy and administering mannitol intra-
venously should be considered. Prompt consultation with an ophthalmologist to as-
sist in evaluation and management is prudent and advisable.
Neonatal Pelvis or Scalp
Neonatal hematomas are most often caused by the application of forceps at deliv-
ery.They occur in the scalp and pelvis, usually secondary to shear stress and/or pro-
longed pressure.Treatment is conservative;the hematoma is allowed to be absorbed
and incorporated into the growing cranium.
SEROMA
There appear to be no clear disposing factors to seroma formation. Some re-
searchers have speculated that hypoproteinemia leads to an increased risk. Dissec-
tion of large areas with wide undermining is believed to increase the risk of seroma
formation.11 Seromas usually develop in wounds with large potential dead space.
PATHOPHYSIOLOGY
The pathophysiology of a seroma may be divided into a development phase, in am-
matory phase, and organization or resorption phase.The development of a seroma
usually begins with the formation of a transudate. Because there are few cellular el-
ements and little cellular debris in the transudate, no true liquefaction phase takes
place, like that in the development of hematomas. However, a local in ammatory
response often occurs in which protein levels rise, which may lead to further in-
creases in the volume of the transudate. Most seromas resolve by complete resorp-
tion, probably because there are few cellular components and thus a low risk of
infection. A pseudocapsule occasionally may develop; in this case there is an in-
creased likelihood of brosis and scarring.

97
Chapter 5
Common Secondary Complications
COMPLICATIONS
Complications occur less frequently with seromas than with hematomas. Compli-
cations include organization (with formation of scar tissue), infection, wound de-
hiscence, and pseudocapsule formation with chronic drainage. Seromas do not
cause necrosis of overlying tissues.
TREATMENT
Treatment of seromas is more varied than that for hematomas, because no one
modality will succeed in all cases. Some surgeons advocate benign neglect: they
believe that with the natural history of seroma resorption, the problem will spon-
taneously resolve. Aspiration followed by application of a compressive dressing is the
most frequently administered treatment. If the seroma fails to resolve after two at-
tempts at treatment by aspiration alone, we prefer to insert a dependent passive or
active drain after aspiration. If a pseudocapsule forms, excision or curettage of the
capsule with or without fibrin glue administration has been advocated. If the
seroma becomes infected, administering an antibiotic is useful, because these have
been shown to penetrate serous uid.
CLINICAL SIGNIFICANCE
In plastic surgery, seromas are associated most often with latissimus dorsi ap trans-
fer, abdominoplasty, and skin grafting.There is a high incidence of seroma in latis-
simus dorsi donor sites; patients undergoing the transfer of this ap should be in-
formed of this risk preoperatively. Prevention includes the use of drains and
compression dressings. Some surgeons advocate deep tissue closure with mattress
sutures in vertical layers to subcompartmentalize the dissected area. If a seroma is as-
pirated, the needle should be inserted in a dependent location (for example, for a
seroma at a right-sided latissimus dorsi ap site, a drain should be placed in the left
lateral decubitus position).
Seroma following abdominoplasty is common. Again, patients should be informed
of the risk of this complication preoperatively. Prevention is effected by insertion of
drains and the application of compressive dressings. Persistent seromas are aspirated
as needed. Like hematomas, seromas are capable of elevating skin grafts off the un-
derlying bed. Interestingly enough, case reports in the literature describe skin grafts
vascularizing directly over a seroma.
COAGULATION ABNORMALITIES
Coagulation problems lead to unexpected and potentially dangerous complica-
tions. Bleeding disorders may be categorized as platelet function disorders and clot-
ting factor disorders. These abnormalities may be inherited, acquired, or drug in-
duced. To understand coagulation abnormalities, one must be familiar with the
various stages of hemostasis and the steps in the coagulation pathway.12,13

98
PART II
SCARS,TISSUE MOVEMENT, AND TRANSPLANTATION
Hemostasis is commonly initiated by blood vessel or tissue injury. Subendothelial
exposure results in platelet adhesion at the injured blood vessel. Platelet membrane
lipases are activated, causing the release of thromboxane A2, which potentiates the
release of the platelet-aggregating agent adenosine diphosphate (ADP).This release
leads to platelet aggregation and formation of a platelet plug at the injury site.
The extrinsic pathway of coagulation can be activated by the interaction of tissue
factor (TF) and factor VII.The complex factor VIIa/ TF activates factor X and sub-
sequently leads to the generation of thrombin (T) from prothrombin (PT). It is
now known that the VIIa/ TF complex also activates factors IX to IXa, thereby
serving as the link between the extrinsic and classic intrinsic pathways.
The intrinsic pathway of coagulation can be initiated by the activation of factor XII
by negatively charged surfaces (the contact phase of coagulation). In vivo, this step
is not essential, since the intrinsic pathway can be activated via the VIIa/ TF com-
plex, as noted previously, or via thrombin-mediated activation of factor XI to XIa.
IXa/VIIIa
T
T
T
T
TF
VIIa/TF
PT
VIIa
VII
VIII
VIIIa
Fibrin
Fibrinogen
CLOT
FORMATION
XIa
XI
IX
IXa
Xa
X
Xa/Va
V
Va

99
Chapter 5
Common Secondary Complications
Both pathways lead to the conversion of prothrombin to thrombin, which con-
verts brinogen to brin.The hemostatic clot consisting of brin polymers is fur-
ther stabilized by factor XIIIa.
Antithrombin III (AT III) is a naturally occurring inhibitor of thrombin and other
serine proteases, which act at different stages of the coagulation cascade. It is pro-
duced by endothelial cells and helps to regulate clot formation. Heparin is a cofac-
tor for AT III and exerts its anticoagulant effect via AT III.Therefore patients who
do not respond to heparin therapy need to be examined for AT III de ciency.
PLATELET DISORDERS
Platelet disorders tend to present with bruising and petechiae.They can be divided
into quantitative and qualitative defects (see the box below). At preoperative con-
sultation the patient should be queried about bruising and bleeding problems and
medication regimens.14 The patient should be asked about any family history of
bleeding problems in addition to the patient’s own history of bleeding problems (or
lack thereof) during serious surgical procedures. Obtaining a thorough history is
crucial to guiding further diagnostic workup. Physical signs of platelet function dis-
orders are the presence of petechiae and ecchymosis. Laboratory investigations
should include a complete blood cell count, bleeding time, and liver function tests.
In general, bleeding complications are uncommon at platelet counts above
50,000/mm3, and even lower platelet counts can be tolerated in patients with im-
mune thrombocytopenic purpura (ITP). In an otherwise healthy individual, platelet
Thrombocytopenic Purpura (Quantitative)
Decreased production
Hereditary (for example, amegacaryocytosis)
Bone marrow suppression (for example, drugs, radiation, chemotherapy)
Bone marrow in ltration (for example, leukemia, lymphoma, metastatic carcinoma)
Aplastic anemia
Decreased survival
Immune thrombocytopenic purpura
Hypersplenism
Disseminated intravascular coagulation
Thrombotic thrombocytopenic purpura
Nonthrombocytopenic Purpura (Qualitative)
Defective platelet function
Hereditary (for example, von Willebrand disorder)
Acquired (for example, aspirin, NSAIDs, uremia)
Vascular disorders
Immunologic (for example, vasculitis, Henoch-Schonlein purpura)
Nonimmunologic (for example, vitamin C de ciency, steroid)
Platelet Disorders

100
PART II
SCARS,TISSUE MOVEMENT, AND TRANSPLANTATION
counts below 20,000/mm3 are frequently associated with spontaneous bleeding.
This condition can be signi cantly exacerbated by administration of nonsteroidal
antiin ammatory drugs (NSAIDs). It is important to recall that aspirin (but not
other NSAIDs) interferes with platelet function for the entire lifespan of the platelet
(7 days).
Platelet transfusions may be indicated in patients with thrombocytopenia or platelet
dysfunction.
DISORDERS OF CLOTTING FACTORS
Unlike platelet abnormalities, which tend to present with bruising, coagulopathies
tend to present with bleeding. A detailed patient history and preoperative labora-
tory tests may be helpful in de ning speci c areas of concern regarding factor de-
ciency. In general, prothrombin time is a measure of the extrinsic clotting path-
way’s integrity. Partial thromboplastin time measures the function of the intrinsic
clotting pathway.Thrombin time measures the conversion of brinogen to brin;
it is prolonged with brinogen de ciency, dys brinogenemia, and/or circulating
antithrombin. De ciency of speci c clotting factors requires replacement therapy
using fresh frozen plasma, cryoprecipitate, or speci c factor concentrates.The level
and frequency of factor replacement therapy are determined by the type of de -
ciency and the planned surgical procedure.15,16 This treatment should be coordi-
nated in conjunction with a hematologist.
Hemophilia A is an X-linked recessive disorder associated with factor VIII de -
ciency. Symptomatology ranges from mild to severe bleeding tendency, depending
on the level of residual factor VIII.Treatment involves administration of factor VIII
concentrate and/or cryoprecipitate. Mild cases can be treated with desmopressin
acetate (DDAVP). Hemophilia B (Christmas disease) is an X-linked recessive dis-
order associated with factor IX de ciency. Treatment includes administration of
fresh frozen plasma, cryoprecipitate, or factor IX concentrate.
Von Willebrand disease is an autosomal dominant disorder resulting in mild factor
VIII de ciency and platelet dysfunction.Treatment requires administration of cryo-
precipitate, which provides factor VIII and von Willebrand factor.
The vitamin K–dependent factors are factors II,VII, IX, and X. Causes of vitamin
K de ciency include dietary de ciency (usually in chronically ill individuals re-
ceiving long-term antibiotic therapy, which kills intestinal bacterial ora), malab-
sorption, chronic biliary tract obstruction, and oral anticoagulant administration.
Treatment requires parenteral administration of vitamin K (5 to 15 mg intrave-
nously), which corrects the de ciency within 4 to 6 hours. If active bleeding is oc-
curring, fresh frozen plasma or cryoprecipitate should be administered to relieve the
factor de ciency.

101
Chapter 5
Common Secondary Complications
Liver disease may result in gross malfunction of the coagulation cascade, because all
factors except factor VIII are produced in the liver.The platelet count may be con-
comitantly reduced as a result of hypersplenism. Treatment involves correction of
the underlying cause of liver failure and factor replacement therapy.
Disseminated intravascular coagulation (DIC) refers to the generalized and uncon-
trolled activation of the coagulation cascade. Coagulation factors and platelets are
consumed and secondary stimulation of brinolysis occurs, resulting in prolonged
prothrombin time, partial thromboplastin time, and thrombin time, with increased
levels of brin degradation products and decreased brinogen levels. Causes in-
clude sepsis, transfusion reactions, metastatic cancer (for example, mucin-producing
adenocarcinoma), placental abruption, and eclampsia.The underlying cause must be
treated, and adjunctive infusion of fresh frozen plasma and platelets must be per-
formed. Some hematologists advocate administration of heparin.
Aggressive replacement of blood loss by red blood cell units without concomitant
plasma and platelet transfusion can lead to dilution of clotting factors.The under-
lying cause must be treated and plasma, cryoprecipitate, and platelets administered.
Medications can also interfere with the coagulation process.16 The most common
clinically significant drugs that can affect coagulation are heparin, warfarin (Couma-
din), and aspirin. Heparin is a potent organic acid with a strong negative charge. It
accelerates the inhibiting action of antithrombin III on thrombin. Its half-life is ap-
proximately 60 minutes, and it is degraded in the liver and excreted by the kidney.
Its anticoagulant ef cacy is monitored by evaluation of the partial thromboplastin
time. Heparin may be administered intravenously or subcutaneously but not intra-
muscularly. Its antidote is protamine sulfate administered intravenously (10 mg of
protamine sulfate/ 1000 U heparin).
Warfarin, an oral anticoagulant, inhibits the y-carboxylation of vitamin K–depend-
ent factors. Its full therapeutic effect may take 3 to 5 days. Degradation of warfarin
occurs in the liver and excretion is achieved via the kidney. Its anticoagulant ef -
cacy is monitored by the evaluation of the prothrombin time.Vitamin K and fresh
frozen plasma are effective antidotes.
Aspirin inhibits platelet granule release and platelet aggregation by blocking throm-
boxane A2 production.This effect lasts through the life cycle of the affected platelet;
there is no effective antidote except for platelet transfusions.
Plastic surgeons commonly encounter patients who are self-treating with over-the-
counter herbal medications, vitamins, and plant extracts. Many of these agents have
measurable effects on clotting and should be discontinued before any additional
surgical procedures are undertaken.17 Some of the more commonly used substances
are outlined in the table on pp. 102-104.

102
PART II
SCARS,TISSUE MOVEMENT, AND TRANSPLANTATION
Herbs, Foods, and Spices to be Avoided for at Least Two Weeks Before Any Surgery
Substance
Also Known As
Effect
Agrimony
Agrimonia eupatoria, agrimonia, cocklebur
Coagulant effect from vitamin K constituent
Alfalfa
Medicago saliva, Lucerne, purple medick
Anticoagulant effect from coumarin constituents
and coagulant effect from vitamin K
Aloe vera gel
May enhance wound healing
Angelica
Angelica archangelica, root of the Holy
Anticoagulant and antiplatelet effect from cou-
Ghost
marin constituents
Anise
Pimpinella anisum, aniseed, sweet cumin
Anticoagulant effect from excessive doses from
coumarin constituents
Arnica
Arnica montana, leopard’s bane, wolf’s
Anticoagulant effect from coumarin constituents
bane, mountain tobacco
Asafoetida
Ferula assafoetida, assant, fum, giant fennel,
Anticoagulant effect from coumarin constituents
devil’s drug
Aspen
Populi cortex, Populi folium
Antiplatelet effect from salicin constituent
Black cohosh
Cimicifuga racemosa, bugwort, black
Antiplatelet effect from salicylate constituent
snakeroot, baneberry
Bogbean
Menyanthes trifoliata, water shamrock,
Bleeding risk from unknown constituent
buckbean, marsh trefoil
Boldo
Peumus boldus, boldine
Anticoagulant effect from coumarin constituents
Borage seed oil
Borago of cinalis, star ower, bee plant,
Anticoagulant effect from gamma linolenic acid
burage
and antiplatelet effect
Bromelain
Ananas comosus, bromelin
Anticoagulant effect from enzyme constituents
Capsicum
Capsicum frutescen, African pepper,
Antiplatelet effect from capsaicinoid constituents
cayenne pepper, chili pepper
Celery
Apium graveolens, smallage, Apii fructus
Antiplatelet effect from apiogenin (coumarin)
constituent
Clove
Syzygium aromaticum, caryophyllus
Antiplatelet effect from eugenol constituent
Danshen
Salvia miltiorrhiza, red sage, salvia root
Anticoagulant effect from protocatechualdehyde
3,4-dihydroxyphenyl-lactic acid constituent
Dong quai
Angelica sinensis, Danggui, Chinese
Anticoagulant and antiplatelet from coumarin
angelica
constituents
European mistletoe
Viscum album, devil’s fuge, drudenfuss,
Coagulant effect from lectin constituent
all-heal
Fenugreek
Trigonella foenum-graecum, bird’s foot,
Anticoagulant effect from coumarin constituents
Greek hay
Feverfew
Tanacetum parthenium, bachelor’s button,
Antiplatelet effect from the crude extracts
featherfew, midsummer daisy
Fish oils
Omega-3 fatty acids
Antiplatelet effect with prostacyclin synthesis,
vasodilation, reduced platelets and adhesiveness,
and prolonged bleeding time
Fucus
Fucus vesiculosis, kelp, black tang, bladder-
Anticoagulant effect which can increase the risk
wrack, cutweed
of bleeding

103
Chapter 5
Common Secondary Complications
Substance
Also Known As
Effect
Garlic
Allium sativum, nectar of the gods, stink-
Inhibition of platelet aggregation and can increase
ing rose
risk of bleeding in excessive doses
Ginger
Zingiber of cinale
Anticoagulant effect with increased risk of
bleeding
Ginkgo
Ginkgo biloba, maidenhair
Inhibits platelet aggregation and decreases blood
viscosity
Ginseng
Panax ginseng, Asian ginseng, Korean red,
Anticoagulant and antiplatelet effects
jintsam
Goldenseal
Hydrastis canadensis, eye balm, yellow
Coagulant effect from berberine constituent
puccoon
Horsechestnut
Aesculus hippocastanum, escine,Venostat
Anticoagulant effect from aesculin (coumarin)
constituent
Horseradish
Armoracia rusticana, pepperroot, mountain
Anticoagulant effect from coumarin constituents
radish
Licorice
Glycyrrhiza glabra, sweet root
Antiplatelet effect from coumarin constituent
Meadowsweet
Filipendula ulmaria, bridewort, dropwort
Anticoagulant effect from salicylate constituents
Northern prickly ash
Xanthoxylum americanum, pepper wood,
Anticoagulant effect from coumarin constituents
toothache bark
Onion
Allium cepa
Antiplatelet effect from unknown constituents
Papain
Carica papaya
Bleeding risk from unknown constituent
Passion ower
Passi ora incarnate, apricot vine, Maypop
Anticoagulant effect from coumarin constituents
Pau d’Arco
Tabebuia impetiginosa, ipes, taheebo tea,
Anticoagulant effect from lapachol constituent
lapacho
Plantain
Plantago major, common plantain, greater
Coagulant effect from vitamin K constituent
plantain
Poplar
Populus tacamahacca, balm of Gilead
Antiplatelet effect from salicin constituent
Quassia
Quassia amara, bitterwood
Anticoagulant effect from coumarin constituents
Red clover
Trifolium praetense, trefoil, cow clover,
Anticoagulant effect from coumarin constituents
beebread
Roman chamomile
Chamaemelum nobile, English chamomile,
Anticoagulant effect from coumarin constituents
whig plant, garden chamomile
Saf ower
Carthamus tinctorium, saffron, zaffer
Anticoagulant effect from saf ower yellow
constituent
Southern prickly ash
Zanthoxylum clava-herculis, sea ash,
Anticoagulant effect from coumarin constituents
yellow wood
St. John’s wort
Hypericum perforatum, Klamath weed,
Photosensitivity, especially when used with
goat weed
Retin-A
Stinging nettle
Urtica dioica, nettle
Anticoagulant effect from vitamin K constituent
Sweet clover
Melilotus of cinalis, hay ower, common
Anticoagulant effect from dicumarol constituent
melilot, sweet Lucerne
Sweet vernal grass
Anthoxanthum odoratum, spring grass
Anticoagulant effect from coumarin constituent
Continued

104
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Herbs, Foods, and Spices to be Avoided for at Least Two Weeks Before Any Surgery—cont’d
Substance
Also Known As
Effect
Tonka bean
Dipteryx odorata, coumarouna, torquin bean
Anticoagulant effect from coumarin constituent
Turmeric
Curcuma longa, Indian saffron, turmeric
Anticoagulant effect from coumarin constituent
Vitamin E
Alpha-tocopherol
Inhibits platelet aggregation and adhesion and
interferes with vitamin K–dependent clotting
factor in large doses
Wild carrot
Daucus carota, Queen Anne’s lace,
Anticoagulant effect from coumarin constituents
beesnest plant
W ild lettuce
Lactuca virosa, green endive, lettuce opium
Anticoagulant effect from coumarin constituents
Willow bark
Salix alba, white willow, silbereide
Antiplatelet effects from salicylate constituents
Yarrow
Achillea millefolium, wound wort,
Anticoagulant effect from achilleine constituent
thousand-leaf
WOUND-HEALING PROBLEMS
Wound healing is necessary for survival. Classic wound healing involves, at its most
simplistic level, three phases: (1) in ammation (lag phase), (2) repair ( broprolifer-
ation phase:collagen production and broplasia occur), and (3) maturation (consol-
idation phase).The arrest of healing can occur at any phase (see Chapter 1). For ex-
ample, the repair phase cannot begin until acute in ammation begins to subside.
Many individual factors adversely affect wound healing, and they often present
concomitantly18 (see the box on p. 105).
DRUGS
Of all interventional drugs used in plastic surgery, steroids have the greatest effect
on wound healing. Steroids decrease and in some cases even arrest in ammatory re-
sponse.This action is secondary to macrophage inhibition, with delay in brogen-
esis and angiogenesis.The macrophage is considered to be the principal cell in the
modulation of wound repair.3 In addition, lysosomal membranes are stabilized, fur-
ther contributing to an antiin ammatory effect. Collagen production may be de-
creased, because steroids have an inhibitory effect on propyl and lysyl hydroxylase,
two important enzymes in collagen production. The most important effect of
steroids on collagen is in collagenolysis stimulation. Secondary wound contraction
is also inhibited.The clinical effects of steroids on wound healing include atrophy,
depigmentation, and an increased tendency toward wound dehiscence.
Vitamin A is known to reverse the stabilizing effects of steroids on lysosomal mem-
branes. It counteracts steroid-retarded monocytic in ammation and theoretically
may reactivate the disease for which the steroids were originally administered.The
Everyday foods and spices are listed in bold letters.

105
Chapter 5
Common Secondary Complications
exact mechanism is unknown.Vitamin A is also a necessary cofactor for collagen
synthesis and cross-linkage. In the absence of steroids, vitamin A offers no bene t
to healing.
Vitamin C is a cofactor necessary for collagen synthesis in the intracellular hydrox-
ylation of proline and lysine. Scurvy (vitamin C de ciency) results when broblasts
remain immature.With a lack of ascorbic acid, broblasts revert to inactivated bro-
cytes. A buildup of free ribosomes, a decrease in endoplasmic reticulum, and an in-
crease in stored fat occur, which lead to an overall decrease in protein synthesis and
a halting in wound repair. In addition, immature granulation tissue forms. New
capillaries are defective, leading to hemorrhage in the wound area.Tensile strength
in a healed scar will decrease in the absence of vitamin C secondary to decreased
collagen synthesis in the face of active ongoing physiologic collagenolysis. The
presence of an excessive concentration of vitamin C does not promote supernor-
mal healing.
Vitamin E inhibits wound healing, decreasing tensile strength in the collagen pro-
duced.This effect may be related to the membrane-stabilizing properties of vitamin
E; hence its attractiveness for the treatment of bromatoses such as those that oc-
cur with Peyronie’s disease. It does not reverse the retardation of wound healing
caused by steroids.The effects of vitamin E are reversed by vitamin A.The mech-
anism is unclear. Vitamin E has been found to increase the breaking strength of
wounds exposed to preoperative irradiation. Its antioxidant effect neutralizes the
lipid peroxidation caused by ionizing radiation, thereby decreasing the production
of free radical products via lipid peroxidation known to cause cellular damage.Vi-
tamin E’s therapeutic ef cacy and indications remain to be de ned.The conviction
among the lay public regarding vitamin E is so strong that many apply topical
preparations of vitamin E to their scars without consulting their physicians.There
seems to be no evidence that this practice improves the quality or the aesthetic ap-
pearance of the surgical scars. Patients should be advised of the high incidence of
minor adverse reactions (rash or itching) when vitamin E is applied to the skin.
Drugs: Steroids, vitamin A, vitamin C, vitamin E,
trace metals, beta-aminopropionitrile (BAPN),
colchicine, chemotherapeutic agents, peni-
cillamine, antiin ammatory medications,
nicotine
Edema
Anemia
Local oxygen tension
Nutrition
Factors Affecting Wound Healing
Surgical technique
Infection
Denervation
Hydration
Diabetes mellitus
Radiation
Uremia
Inheritable disorders of collagen
metabolism

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Trace metals play an important role in wound healing. Zinc is a normal component
of many enzyme systems and serves as a cofactor for both collagen production and
the enzyme systems responsible for cellular proliferation. However, administration
of zinc in the absence of a de ciency has no bene cial effect. Zinc de ciency re-
sults in a reduction in the rate of epithelialization, rate of gain of wound strength,
and diminution of collagen strength.
Copper is a cofactor that acts extracellularly. It is involved in deamination of lysyl
oxidase and the formation of aldehyde groups for intramolecular collagen cross-
linking.
Magnesium is a cofactor involved in glycosylation when glucosyl or glucosylgalac-
tosyl residues are attached to hydroxylysine. Other vitamins such as ribo avin and
thiamine also serve as cofactors in collagen cross-linking.
Lathyrogens prevent the formation of aldehyde intermediates in a cross-linking
process of collagen formation. The result is reduced strength of collagen bundles.
Lathyrism occurs as a result of ingestion of certain varieties of peas (Lathyrus odor-
atus), commonly known as sweet peas. The active agent of the pea that causes the
effect on collagen is beta-aminopropionitrile (BAPN). BAPN inhibits the enzyme
systems necessary for intramolecular and intermolecular bonding outside the cell by
preventing deamination of lysyl oxidase.
Colchicine interferes with the extracellular secretion of collagen precursors, thereby
causing a form of “cellular constipation.”
Penicillamine inhibits chelation of copper, thereby producing copper de ciency in
a concomitant inhibitory effect in collagen cross-linking.
Cancer chemotherapeutic agents have been shown to affect almost all phases of
wound-healing. Neutropenia prolongs the in ammatory phase. Agents such as cy-
clophosphamide inhibit the early vasodilatory phase of in ammation. In addition,
chemotherapeutic agents are known to interfere with DNA replication, RNA pro-
duction, and protein synthesis.With chemotherapy, proliferation of broblasts and
secondary wound contraction are decreased. When chemotherapy is begun 10 to
14 days postoperatively, little effect is noted on wound-healing over the long term
despite a demonstrable early decrease in wound strength.
Nonsteroidal antiin ammatory drugs (for example, aspirin, ibuprofen) have been
shown to decrease collagen synthesis even at ordinary therapeutic doses.The effect
is dose dependent and mediated through prostaglandins.
Nicotine is the principal vasoactive component in the gas phase of cigarette smoke.
It is an odorless, colorless, poisonous alkaloid that, when ingested or inhaled, can
liberate adrenal catecholamines. In addition, nicotine has a direct cutaneous vaso-

constrictive effect. Nicotine impairs wound contraction in animal models from the
fourth to the tenth day of wound-healing. From the twelfth to the twentieth days,
wounds contract at essentially a normal rate.Therefore cigarette smoking, with its
associated nicotine ingestion, is adverse to the early stages of wound healing.
OTHER FACTORS IN W OUND HEALING
Mild anemia has little effect on collagen synthesis. Normal physiologic adjustments
such as an increased blood circulation rate are able to compensate. However, a
hematocrit level of 20% or less will begin to seriously affect oxygen delivery.
With edema, the expansion of tissue uid increases the distance between capillar-
ies and the collagen-synthesizing broblasts. This effect may result from increased
venous pressure with secondary reduced capillary blood ow.Venous stasis is a pri-
mary example.
Fibroblasts are known to be oxygen sensitive. Fibroblast replication is potentiated by
a PO2 of 30 to 40 mm Hg, but collagen synthesis requires higher levels. Collagen
production and tensile strength are stimulated by hyperoxia. In patients on a nor-
mal diet with an adequate vitamin C intake, the rate-limiting cofactor in collagen
production is the availability of oxygen to the broblasts.
Tissue oxygen de ciency is the most common cause of qualitatively inadequate
healing. Proper tissue oxygenation requires suf cient inspired PO2 transfer of oxy-
gen by suf cient hemoglobin for transport and adequate tissue vascularity. Problems
in maintaining local oxygen tension accounts for healing problems in such diverse
conditions as radiation diabetes, peripheral vascular disease, chronic infection, and
pressure sores.
There has been a resurgence in the use of hyperbaric oxygen therapy, especially
for enhancing healing and treatment of selected problem wounds.19 The most im-
portant effects of hyperbaric oxygen therapy for the plastic surgeon are the stimu-
lation of leukocyte microbial killing, improvement of broblast replication, and in-
creased collagen formation and neovascularization in ischemic tissue. Preoperative
hyperbaric oxygen therapy induces neovascularization in radionecrotic tissue. Re-
fractory osteomyelitis and necrotizing fasciitis appear to respond to adjunctive hy-
perbaric oxygen. Crush injury and compartmental syndrome appear to bene t from
hyperbaric oxygen therapy through presentation of adenosine 5 -triphosphate in
cell membranes, which limits edema. Hyperbaric oxygen therapy for burn injury
permits shorter hospital stays, reduced number of surgeries, and less uid replace-
ment.When hyperbaric oxygen therapy is instituted postoperatively, skin grafts are
reported to take more completely and more rapidly. The same mechanisms may
apply to ischemic problem wounds, such as infected extremities in diabetic pa-
tients. Hyperbaric oxygen therapy will not cause normal wounds to heal more rap-
idly but may under certain circumstances cause problem wounds to heal at a more
normal rate.
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Wound infection occurs when the number of pathogenic organisms exceeds the
ability of local tissue defenses to combat them. Infection has a detrimental effect on
wound healing by decreasing tissue PO2, increasing collagen lysis, and perpetuating
the continued presence of an in ammatory reaction.
Good nutrition is essential for the effective repair of wounds. Since all wound re-
pair requires a certain amount of regeneration, the raw biologic materials must be
present at the correct place and time to allow proper tissue synthesis. Lack of pro-
tein (kwashiorkor) causes a marked decrease in the tensile strength of the wound as
a result of a shortage of both broblasts and collagen. Protein depletion also pro-
longs the in ammatory phase. Although methionine represents only 1% of all of the
essential amino acids required in the synthesis of collagen, methionine is an espe-
cially critical factor, because it cannot be synthesized by humans. Methionine is
the most important source of cysteine. Cysteine, a sulfated amino acid, is not di-
rectly involved in collagen synthesis, but since formation of disul de bonds is crit-
ical to the proper alignment and attachment of peptide chains in the triple-helix
structure of tropocollagen, sulfur-containing amino acids (cysteine, arginine, histi-
dine) have an important support role.
Much less is known about the role of carbohydrates and fats in the wound-healing
process. Glucose is required as an energy source by white blood cells during the in-
ammatory phase. Fats are essential constituents of cell membranes, but there ap-
pears to be no impairment of wound healing associated with fatty acid de ciency.
Wound contraction and epithelialization are not affected by denervation. How-
ever, denervated skin is prone to ulcerate because of high rates of collagenase activ-
ity. Paralyzed patients tend to develop large, progressive skin ulcerations over anes-
thetic areas that are often worse than the pressure sores experienced by debilitated
patients with intact nervous systems.
Poor surgical technique is detrimental to wound healing. The degree of tissue
necrosis increases with the severity of the trauma induced by the surgical procedure.
Tight sutures cause tension on the incision, resulting in local ischemia. Excessive
cauterization and the use of irritative sutures (for example, plain catgut, silk) all
prolong the in ammatory phase.These factors, depending on their extent, may re-
sult in subsequent wound breakdown in a patient with an otherwise normal intrin-
sic repair mechanism.
A well-hydrated wound will epithelialize faster than a dry wound. Biologic dress-
ings, grafts, and synthetic occlusive wound coverings hasten epithelial repair and
control the proliferation of granulation tissue.
Diabetes mellitus has both metabolic and mechanical effects on wound-healing
outcome. Metabolic effects include a decrease in collagen synthesis. In addition,
there is a defect in leukocyte function, with decreased chemotaxis and phagocyto-
sis, resulting in an increased risk of infection and impaired healing. Mechanical im-

pairments include microangiopathy and major arterial occlusion. Diabetic neu-
ropathy, a separate category, may also have a deleterious in uence on wound heal-
ing. Instituting insulin therapy soon after a skin wound occurs in a diabetic patient
restores an adequate in ammatory response and enhances collagen synthesis.
Uremia has a detrimental effect on wound healing and a particularly negative in-
uence on broblast proliferation.
Radiation is especially deleterious to wound healing. The effects of radiation at a
molecular level result in the death or partial injury of the cell directly or indirectly
secondary to the ionization of cell water with liberation of free radicals. Free rad-
icals interact with DNA molecules, which are then damaged. The exact lesion of
ionizing radiation remains unde ned, but once alterations in nucleotide sequences
occur, a change in transcription or defective repair sets the stage for interference
with wound healing.The degree of cell damage is determined by the relative im-
portance of the destroyed molecule to the function of the cell, dose of radiation, and
ability of the tissue involved to repair itself.The net effect of radiation on wounds
includes loss of the ability of cells to replicate. Fibroblasts are particularly sensitive,
leading to decreased collagen production and delayed wound contraction. Fibrosis
constricts lymphatic vessels and small capillaries, causing increased edema. Obliter-
ative endarteritis/endothelial cell swelling leads to luminal narrowing and gradual
obliteration of small arterial vessels, resulting in late fibrosis, necrosis, and poor
wound healing; and depletion of parenchymal stem cells.
Therapy for tissue breakdown secondary to radiation essentially consists of debride-
ment of the necrotic area and the introduction of fresh, well-vascularized tissue
with or without adjunctive hyperbaric oxygen therapy.
Numerous genetic disorders are known to affect wound healing. Some of the more
signi cant syndromes relevant to plastic surgery include pseudoxanthoma elasticum,
cutis hyperelastica (Ehlers-Danlos syndrome), cutis laxa, Werner’s syndrome, and
progeria. Detailed descriptions of these individual syndromes are beyond the scope
of this chapter.
CONCLUSION
The cellular mechanisms in the biochemical events discussed are the processes by
which common complications occur in plastic surgery as well as in surgery in gen-
eral. As we learn more about the complex interactions between the patient host,
surgical alteration of tissues, and pharmacologic manipulation of cellular events, we
can begin to in uence outcome on a cellular level and hopefully decrease morbid-
ity. A surgeon aware of pharmacologic and cellular events that predispose to coag-
ulation and wound-healing complications is one who is best prepared to prevent
these problems. Although the incidence of these complications may never be re-
duced to zero, awareness of the contributing etiologic factors is the rst step toward
minimizing their incidence and severity.
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SCARS,TISSUE MOVEMENT, AND TRANSPLANTATION
References—With Key Annotated References
1. Mulliken J. Pathogenesis of skin ap necrosis from an underlying hematoma. Plast Reconstr
Surg 63:540-545, 1979.
2. Angel MF, Narayanan K, Swartz WM, et al. The etiologic role of free radicals in hematoma-
induced ap necrosis. Plast Reconstr Surg 77:795-801, 1986.
3. Diegelmann RF, Cohen IK, Kopler AM.The role of macrophages in wound repair:A review.
Plast Reconstr Surg 68:107-113, 1981.
4. Straith R. The study of hematomas in 500 consecutive face lifts. Plast Reconstr Surg 59:694-
698, 1977.
5. Thompson DP, Ashley FL. Face lift complications:A study of 922 cases performed in a 6-year
period. Plast Reconstr Surg 61:40, 1978.
6. Rees T. Expanding hematoma after rhytidectomy. Plast Reconstr Surg 51:149-153, 1973.
7. Baker DC. Complications of cervicofacial rhytidectomy. Clin Plast Surg 10:543, 1983.
8. Baker TM, Baker TJ, Stuzin JM. Browlift and facelift. In Goldwyn RM, Cotten MN, eds.The
Unfavorable Result in Plastic Surgery. Philadelphia: JB Lippincott, 2001.
9. Skoog T.The pathogenesis of cauli ower ear. Scand J Plast Surg 9:34-39, 1975.
10. Madden JW, Peacock EE Jr. Studies on the biology of collagen during wound healing:III. Dy-
namic metabolism of scar collagen and remodeling of clinical wounds. Ann Surg 174:511-
520, 1971.
11. Coons MS, Folliquet T, Rodriquez C. Prevention of seroma after dissection of musculocuta-
neous aps. Am Surg 59:215-218, 1993.
12. Furie B, Furie BC. Molecular and cellular biology of blood coagulation. N Engl J Med 326:
800-806, 1992.
13. Roberts HR, Lozier JN. New perspectives on the coagulation cascade. Hosp Pract 15:97-112,
1992.
14. Goldsmith SM, Leshin B, Owen J. Management of patients taking anticoagulants and platelet
inhibitors prior to dermatologic surgery. J Dermatol Surg Oncol 19:578-581, 1993.
15. Todd D, Galbraith D. Management of an orthognathic surgery patient with factor XI de -
ciency. J Oral Maxillofac Surg 51:417-420, 1993.
16. Weaver DW. Differential diagnosis and management of unexplained bleeding. Surg Clin North
Am 73:353-361, 1993.
17. Pribitkin ED, Boger F. Herbal therapy: What every facial plastic surgeon must know. Arch
Facial Plast Surg 3:127-132, 2001.
18. Hunt TK. Disorder of wound healing.World J Surg 4:271-277, 1980.
19. Kindwall EP, Gottlieb LJ, Larson DL. Hyperbaric oxygen therapy in plastic surgery: A review
article. Plast Reconstr Surg 88:898-906, 1991.
The most important effects of hyperbaric oxygen (HBO), for the surgeon, are the stimulation of leuko-
cyte microbial killing, the enhancement of broblast replication, and increased collagen formation and
neovascularization of ischemic tissue. Preoperative hyperbaric oxygen induces neovascularization in tis-
sue with radionecrosis. Refractory osteomyelitis and necrotizing fasciitis appear to respond to adjunc-
tive hyperbaric oxygen. Crush injury and compartment syndrome appear to bene t through preser-
vation of ATP in cell membranes, which limits edema.The use of hyperbaric oxygen in the treatment
of burn injury permits shorter hospital stays, a reduced number of surgeries, and less uid replacement.
Skin grafts and aps are reported to take more completely and more rapidly.The same mechanisms
may apply in ischemic problem wounds such as infected diabetic extremities. Contraindications and
side effects are described. Hyperbaric oxygen will not heal normal wounds more rapidly but may, un-
der certain circumstances, induce problem wounds to heal more like normal ones.

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Common Secondary Complications
1. A 47-year-old man develops a hematoma following a face lift. The most likely
technical reason for this complication is:
a. A platelet function disorder
b. Uncontrolled hypertension
c. Failure to recognize and control an arterial or venous bleeder
d. Preoperative aspirin therapy
e. Hemolytic transfusion reaction
2. The single most important factor causing ap necrosis from hematoma occurs
as a result of:
a. Pressure from obstruction of dermal ow
b. Tight suture line closure
c. No re ow phenomenon
d. Direct toxic effect of free radical formation on skin ap
e. Hemoglobin
3. Factors to consider in the prevention of face-lift hematoma include:
a. Hypotensive anesthesia
b. Meticulous hemostasis
c. Avoidance of postoperative hypertension
d. Head elevation and application of cool packs
e. All of the above
4. The treatment for retrobulbar hematoma is:
a. Observation
b. Diamox
c. Suture removal, opening of orbital septum, and lateral canthotomy
d. Ice
e. Needle aspiration
5. All of the following medications can affect bleeding except:
a. Aspirin
b. Warfarin
c. Torodol
d. Vitamin C
e. Vitamin E
R EVIEW QUESTIONS

(Trang không có chữ)

113
Scars are the inevitable result of any surgical procedure.The plastic surgeon’s goal
is to generate a scar that does not impair form or function to any signi cant degree.
Attention to detail and precision in wound creation and closure maximize the oppor-
tunity for producing an excellent scar as the primary result.
Sometimes, however, a surgeon must close unfavorable wounds resulting from
burns, trauma, or oncologic ablations.The resulting scar may be imperfect because
of limitations created by the wound itself. In other cases, patient characteristics can
contribute to less-satisfactory scarring. Severely injured or very ill patients are of-
ten incapable of healing wounds in a precise manner. Chronic problems such as
diabetes can also contribute to less-satisfactory healing and scarring. Some patients
have a predisposition to hypertrophic scars or keloids that can affect surgical re-
sults. When a plastic surgeon is facing a reoperative problem related to scarring,
Scars and Scar Revision
Kenneth B. Hughes and W. Thomas Lawrence
C ha pter 6
Reoperative Problems
Impaired wound healing
Nonsurgical scar modi cations
Scar realignment
Abnormal scarring conditions
More complex tissue rearrangements
Though the wound be healed,
yet the scar remains.
English proverb

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the goal is to overcome the limitations in form or function created by the healing
of the original wound. He or she must be aware that not all factors that contributed
to undesirable scarring can be overcome, and this needs to be considered in any
plans for scar revision. Patients must also understand that surgeons are not magicians
and cannot make scars disappear. All that can be hoped for is a minimally apparent
scar that does not impair function in any way. The scar should be at and narrow
and should match the surrounding skin in color and texture to the best degree
possible. It should not generate any tightness or bow-stringing, even with move-
ment. Imperfect scars may have excessive width, prominence, thickness, tightness,
or abnormal pigmentation. They may also be atrophic and depressed or have an
undesirable orientation. An individual scar may have one or more unfavorable char-
acteristics;both the surgeon and the patient must be aware that not all problems can
be corrected.
The goal of any revision procedure is to correct the speci c characteristics of the
individual scar that are less than ideal and amenable to correction. Only a portion
of a scar may harbor these characteristics, and in such cases, any intervention should
be targeted to only the unsatisfactory portion of the scar.
As with many surgical enterprises, the key to improving a surgical result starts with
diagnosis of the problem and an understanding of what caused the problem to oc-
cur. This requires some knowledge of what is involved in normal wound healing
and what problems result from aberrations in the normal process.
WOUND HEALING
Ideally, wound healing is a carefully orchestrated process that involves distinct yet
intimately related processes:hemostasis, in ammation, cellular proliferation, matrix
production, wound contraction, and remodeling. Deviations from the ideal pro-
gression of wound-healing events can contribute to less-satisfactory scars. One must
ensure that the environment that contributed to less desirable scarring has been
modi ed to the best degree possible before attempting to revise the scar.
HEMOSTASIS
Hemostasis occurs as the rst response to skin penetration and is initially mediated
by the vasoconstriction of blood vessels at the point of injury.The coagulation cas-
cades are subsequently activated, resulting in the formation of brin. Factors pro-
duced by damaged cells activate platelets that aggregate at the site of injury as well.
The combination of brin and aggregated platelets along with erythrocytes and
other trapped cellular elements make up the clot that plugs damaged blood vessels.
The brin lattice resulting from this process also serves as the early wound matrix
that facilitates progression of wound healing. Platelets release multiple cytokines as

they aggregate, including platelet-derived growth factor (PDGF) and transforming
growth factor beta (TGF-beta), and these cytokines also play active roles in orches-
trating later cellular processes involved in healing.
Derangements in hemostasis or severe trauma that overtax the hemostatic mecha-
nism can lead to an excessive accumulation of blood in wounded tissues. Such col-
lections of blood provide a mechanical barrier to healing and can predispose to in-
fection. They can prolong the in ammatory process, which contributes to edema
and imprecise healing. Precise hemostasis is required during any revision surgery to
maximize the opportunities for optimal scarring.
INFLAMMATION
The in ammatory process is initiated within hours after the wound occurs, result-
ing in erythema, edema, and heat. Inflammatory mediators such as histamine,
prostacyclins, and leukotrienes contribute to vasodilation and the migration of in-
ammatory cells such as polymorphonuclear (PMN) cells and monocytes to the in-
jury site.These in ammatory cells produce a wide variety of proteinases and reac-
tive oxygen species that aid in the breakdown and phagocytosis of damaged matrix
and cells. Macrophages and lymphocytes, in addition, produce cytokines, which,
along with the platelet-derived cytokines, have a major in uence on the orchestra-
tion of the overall healing mechanism.1,2
Derangements in wound healing that lead to undesirable scarring may result from
inadequate or excessive in ammation. Inadequate in ammation may be a conse-
quence of poor nutrition, systemic steroid administration, or a multitude of other
problems and can generate an inadequate stimulus to scar formation. This can re-
sult in an atrophic, excessively wide scar. Prolonged in ammation can result in an
excess of in ammatory mediators and cytokines in the wound environment. This
can contribute to excessive scar formation, resulting in scar prominence or tightness
or prolonged scar erythema.
Edema is a signi cant aspect of the in ammatory response, and signi cant edema
limits skin perfusion and oxygenation. All aspects of healing are impaired in a hyp-
oxic environment, and this can also contribute to a wide and/or depressed scar.
CELLULAR PROLIFERATION
After the in ammatory reaction to injury begins to diminish, keratinocytes and
mesenchymal cells begin to actively migrate into the wound environment and pro-
liferate. Endothelial cells also migrate and proliferate in the wound environment
resulting in new blood vessels that revascularize the damaged area.These processes
predominate between 2 and 5 days after injury.
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Signi cant trauma can damage cells over a large area, limiting the ability of kera-
tinocytes, broblasts, and endothelial cells to contribute optimally to the healing
process. Limitations in cellular function can also be produced by ischemia resulting
either from vascular damage or simply, prolonged edema.This impairment can lead
to inadequate scar formation and excessive scar width.
MATRIX PRODUCTION AND SCAR CONTRACTION
Beginning about 5 days after injury, the synthesis of collagen and other matrix
components, and active wound contraction, result in an increase in wound strength
and diminished scar size.These processes are all mediated by cytokines produced by
macrophages and other cell types during the earlier healing phases.
Cellular damage and vascular impairment limit matrix proliferation and scar con-
traction, similar to the way in which they limit cellular proliferation. The end re-
sult of these limitations is weaker scars that will widen and possibly be atrophic.
Excessive wound contraction can produce scars that limit movement, especially
when they occur in the vicinity of joints. Semicircular scars are particularly predis-
posed to problems related to wound contraction.The tissue within the curve is of-
ten elevated upward by contractile forces, producing a pincushion effect.The semi-
circular nature of the wound must be altered in any revision procedure to minimize
this problem.
R EMODELING
During this last phase of tissue repair, which begins approximately 3 weeks after in-
jury, wound remodeling results in increased cross-linking of collagen and improved
collagen alignment resulting in greater wound strength.3,4 The greatest percentage
of ultimate wound strength is generated during this phase of healing. In addition to
active collagen synthesis, appropriate metalloproteinase function is required to mod-
ulate the quantity and alignment of scar in a wound. Any derangement in the
wound environment that alters cytokine or metalloproteinase function can limit
the process of scar remodeling. Depending on the nature of the derangement, col-
lagen and matrix synthesis and wound contraction can be impaired or excessive.
Impaired cross-linking and collagen realignment can result in a widened, possibly
depressed scar. Alternatively, an imbalance resulting in excessive collagen synthesis
can produce an excess of scar.

IMPAIRED WOUND HEALING
As suggested, some derangements in healing result from characteristics of the
wound environment; other problems derive from characteristics of the patient
themselves.There are a variety of conditions, which negatively in uence scar for-
mation. Some of these conditions can be eliminated and some cannot.
A number of nutritional derangements can negatively impact healing. Protein de-
ciency results in impairments in capillary formation, broblast proliferation, and
collagen synthesis. It also contributes to an impairment in immune function, which
can increase infection risk.5-8 Vitamin de ciencies can also impair healing. A de -
ciency in vitamin A impairs epithelialization.Vitamin C de ciency prevents hydrox-
ylation of prolene and lysine and thereby limits collagen cross-link formation.9 A
de ciency of zinc, magnesium, or copper can also decrease the tensile strength of
the ultimate scar.10 If malnutrition of any sort has contributed to less-satisfactory
scarring, correction of the nutritional impairment must precede any surgical inter-
vention if the ultimate quality of the scar is to be improved.
Steroids impair almost all aspects of healing and can contribute to the formation of
widened, atrophic scars. Chemotherapeutic agents and immunosuppressive drugs
also inhibit wound healing and lead to the production of weaker scars.11 If these
agents are only required for a limited period, scar revision should be postponed
until use of the agents has been discontinued. If steroids cannot be discontinued be-
cause of the chronicity of the problem for which they are being used, their in-
hibitory effects on the healing process can be modulated by the concomitant ad-
ministration of vitamin A, either topically or systemically.
Diabetes is another patient characteristic that can impair healing. Although dia-
betes cannot be eliminated, its inhibitory effects on the healing process can be min-
imized through precise blood sugar control.12
Smoking causes local tissue ischemia by stimulating acute vasoconstriction and by
contributing to carboxyhemoglobin production, which limits the oxygen-carrying
capacity of the blood. In addition, it contributes to deleterious long-term effects on
the peripheral vasculature and lungs that limit tissue perfusion. Smoking should be
eliminated before scars are revised to maximize the opportunities for optimal heal-
ing and limit the likelihood of widened, atrophic scars.
In addition to patient characteristics that impair healing, impairments in the quality
of tissues locally can lead to impaired healing.The healing process is signi cantly im-
paired in radiated tissues as a result of impaired cellular function and relative tissue
hypoxia. Impaired circulation resulting from traumatic scarring can also slow heal-
ing and contribute to unsatisfactory scars. Hyperbaric oxygen treatment can some-
times improve local circulation and lead to improved healing and scarring.
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SURGICAL PRINCIPLES IN SCAR REVISION
Any surgical procedure used for scar revision must incorporate several basic surgi-
cal principles that contribute to optimal healing:
1. Gentle handling of tissues to minimally traumatize the structures involved in
the revision procedure
2. A tension-free wound closure to minimize stress on healing tissues
3. Incisions made perpendicular to the skin edge to allow for precise tissue
reapproximation
4. Incisions ideally oriented within the relaxed skin tension lines (RSTLs) to
the degree possible13; note the RSTLs in the illustrations below

119
Chapter 6
Scars and Scar Revision
Borges13 heightened awareness of the importance of placing scars in the RSTLs.
These relaxed skin tension lines are intrinsic to the skin itself and do not correspond
fully to wrinkle lines or Langer lines. In cases in which the RSTLs cannot be de-
termined, a circular incision can be made, and the surgeon can look for the forma-
tion of an ellipse to determine proper orientation. Antitension lines (ATLs) corre-
spond to lines perpendicular to RSTLs and should be avoided whenever possible.
Scars in ATLs are more apparent in that they do not mimic normal skin folds, and
they are also more prone to scar hypertrophy.
FUSIFORM EXCISION
The simplest procedure used for scar revision is fusiform excision. Fusiform exci-
sion typically requires only minimal lengthening of the scar and is best suited to
scars that already correspond to RSTLs. Fusiform excision can often be used to
modify scars that are excessively wide, depressed, or thick. However, the area excised
needs to adhere to a length-to-width ratio of 4:1 to avoid dog-ears.
A key to a satisfactory result after fusiform excision is prolonged support of the
closure to minimize scar spread. It has been suggested that support for up to 6
months with a permanent buried suture may be necessary to maximally limit scar
spread.14
For depressed scars, a modi cation of the simple fusiform excision can be used.
The skin is incised in a fusiform fashion around the scar to the subcutaneous level.
The central scar is then deepithelialized, and the peripheral skin edges are advanced
over the deepithelialized scar. The deepithelialized scar provides support to the
wound edges and prevents recurrent scar depression.
SCAR REALIGNMENT
For larger scars that do not correspond to RSTLs, scar realignment may lead to a
more aesthetic scar with fewer tendencies to hypertrophy or contraction. Some-
times this can be accomplished by excising a scar and reapproximating tissues in a
manner that either approximates the RSTLs or is more curvilinear and less prone
to contraction. Borges promoted the use of Z-plasties or W-plasties to improve scar
alignment for scars that deviate more severely from the ideal orientation. These
techniques are particularly useful at breaking up contracted scars and scars with
“pincushioning.”The choice of technique depends on whether scar lengthening is
desired.15,16 Alternative methods of realigning scars include geometric scar realign-
ment and YV-plasties.

Limb
Limb
Central limb
2
60°
1
1

2
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PART II
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Z-PLASTY
A Z-plasty both lengthens and breaks up a linear scar.17 It requires tissue laxity in
the plane perpendicular to the scar to allow advancement of the Z-plasty aps.
The Z-plasty is particularly useful in situations where the scar has be-
come somewhat contracted. It is often employed in the following sit-
uations18:
ATL scars of eyelids, lips, nasolabial folds, and nonfacial areas
that limit tissue mobility
Scars on forehead, temples, cheeks, nose, and chin running at
less than 35 degrees to inclination to RSTLs
Semicircular trapdoor scars
Several principles apply to Z-plasty design.The central limb of the Z-plasty should
always fall over the scar. The aps should be oriented so that, after transposition,
they are oriented close to RSTLs.19 The length of all limbs must be reasonably
equal.The inherent elasticity of skin allows for slight discrepancies in limb length,
though the discrepancy cannot be signi cant. The two lateral limb–central limb
angles can differ, though similar, if not identical, angles are generally used.20 The de-
gree of scar lengthening increases with the size of the central limb–lateral limb an-
gles, though ap transposition is often dif cult when angles exceed 60 degrees. For
that reason, a 60-degree angle is often used in that it provides reasonable central
limb lengthening needed while avoiding prohibitive tension at closure. A Z-plasty
with 60-degree angles produces a 75% lengthening of the scar as compared with a
30-degree angle that produces only 25% lengthening.20 In multiple Z-plasties, seg-
ments should not generally be smaller than 1 cm to provide aps of reasonable size
for transposition.
The scar length increase provided by a given Z-plasty or multiple Z-plasties in se-
ries can be readily calculated. The original central limb increases in length by a
factor of 3.21 The total gain in length increases with the size of the Z-plasty limbs

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Chapter 6
Scars and Scar Revision
and is generally greater with one large Z-plasty as opposed to multiple small
Z-plasties.17
However, Furnas demonstrated that geometric calculations for gain in length of a
Z-plasty on a two-dimensional surface do not precisely predict the gain in scar
length in vivo on a three-dimensional surface. The key element in this loss of pre-
dicted length was skin tension. Lengthening was always less than that predicted
mathematically, ranging from 55% to 84% of the predicted value based on regions
of the body and the individuals on which the Z-plasty was performed.
W-PLASTY
The W-plasty technique for scar revision is similar to Z-plasty in that it breaks up
a straight-line scar into a pattern that is less conspicuous. Unlike the Z-plasty, there
is no length gained;therefore there is no release of any contracture. Because the re-
sulting scar is irregular, however, it does provide some increase in scar elasticity and
provides fewer tendencies to contract secondarily than with a linear incision. It is
most useful when the original scar deviates more severely from the RSTLs. Simi-
lar to a fusiform excision, a W-plasty involves the removal of skin. For this reason
the method should be avoided if signi cant tension is present across the wound
edges.
W-plasty scar revision has been promoted for the following conditions22:
ATL scars of the forehead, eyebrows, temples, cheeks, nose, and chin
Small but broad, depressed scars
There are several principles involved in designing a W-plasty. The base of the tri-
angle at each end should be at right angles to the scar.The angles of the aps should
be 55 to 60 degrees. The length of individual segments should practically be be-
tween 5 and 7 mm. Limbs should be shorter toward the ends of the W-plasty to
prevent formation of dog-ears and limit the length of scars within ATLs.16

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PART II
SCARS,TISSUE MOVEMENT, AND TRANSPLANTATION
GEOMETRIC BROKEN-LINE R EVISION
Geometric broken-line revision can be used in all of the same situations as a W-plasty
to break up the zigzag pattern and presumably make the scar less conspicuous to the
eye. It differs from a Z-plasty in that the interdigitated shapes are not all angular. It
can be dif cult to execute and is not commonly used.
YV-PLASTY
2
1
2
1
2
1
2
1
Incision made

Flaps advanced
Multiple YV-plasties
A YV-plasty, like a Z-plasty, lengthens the scar to some degree and is useful for the
release of contracted scars. The orientation of the resulting scars is different from
those after a Z-plasty, which may provide advantages in some clinical situations. In
YV-plasties the skin for transposition is not detached from its substratum (in con-
trast to the Z-plasty) but is displaced by sliding it on its substratum.The tongues of
the upper part slide into the stem of the Y and form a V. 23 Tension along a scar can
be limited by several transverse Y-shaped incisions situated in parallel.
MORE COMPLEX TISSUE REARRANGEMENTS
As mentioned, a basic surgical requirement for ideal scar creation is tension-free
wound closure. In most cases, the resolution of edema and some skin stretching al-
lows for minimal tension in secondary revision procedures. In cases in which ten-
sion persists, additional tissue needs to be recruited to the area.This can often be ac-

complished through tissue expansion, which increases the volume of skin with sim-
ilar color and texture characteristics in the area of injury.This will provide the most
aesthetic reconstructive result. Alternatively, flaps can be rotated from adjacent
areas into the injured area to augment the volume of local tissue.
NONSURGICAL SCAR MODIFICATION
For scars that are not exceptionally wide or irregular, nonincisional modalities such
as dermabrasion, various laser treatments, and chemical peels can be useful. They
generally smooth the contour of the injured area so that fewer shadows are pro-
duced by changes in skin or scar contour.The resurfacing stimulated by these pro-
cedures often blurs the juncture of scarred and unscarred areas. The primary risks
are scarring and skin pigmentation changes:
Pigmentation issues are of particular concern in dark-skinned individuals.
Pigmentation changes and scarring are much more likely when resurfacing is
taken into the reticular dermis and are rare, especially in white individuals,
when treatment is limited to a more super cial level.
Pigmentation changes may also be more likely in pregnant women and those
taking oral contraceptives.
DERMABRASION AND MICRODERMABRASION
With dermabrasion, a high-speed abrasive device removes the super cial skin lay-
ers like a sander. Skin is generally removed down to the papillary dermis where
pinpoint bleeding is encountered to allow for prompt and reliable skin reepithelial-
ization. Harmon et al24 demonstrated an increase in collagen bundle density and
size, with a reorientation of collagen bers parallel to the epidermal surface in scars
treated with dermabrasion.These changes may contribute to the bene cial effects
noted with treatment.
Some have used refrigerants such as uoroethyl to make the skin rmer before
treatment, but these agents may be associated with more pain and increased risks of
scarring and pigmentation changes. Alternatively, a tumescent technique can be
used to rm tissues in lax areas before treatment.
Dermabrasion is a particularly useful technique for modifying acne scars. It does not
eliminate the pits entirely but smooths their margins, resulting in less shadowing
and scar prominence. Dermabrasion is also a useful technique for smoothing promi-
nent scars. Collins and Farber25 reported favorable results with dermabrasion for
postsurgical nasal scars in 1984. Robinson later demonstrated smoother contours af-
ter postoperative dermabrasion to full-thickness skin grafts.26,27 Rohrich et al28 have
used primary dermabrasion to wounds created during nasal reconstructions, and it
is their feeling that this has improved scarring.
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Chapter 6
Scars and Scar Revision

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PART II
SCARS,TISSUE MOVEMENT, AND TRANSPLANTATION
A W-plasty failed to conceal the scar adequately over its lateral portion;therefore derm-
abrasion was performed over the area outlined. A rotating dermabrasion wire brush
or wheel is used to plane down the area, going deeper where the ridges are most
prominent. It is important to feather the borders into the surrounding normal skin.
The immediate result shows punctate bleeding and the whitish scar is less visible.
This 32-year-old woman demonstrates a depressed linear scar of the left cheek after
excision of a basal cell carcinoma. Secondary correction via multiple Z-plasties was
attempted.Scars of this nature are prominent because they tend to re ect light along
their edges; they are dif cult to conceal with cosmetics.