The Unfavorable Result in Plastic Surgery_ Avoidance and Treatment (2018, Thieme)

SECTION II LEGAL AND SAFETY ISSUES
66
Box 10.1
1.  Surgical or Invasive Procedure Events
•• Surgery or other invasive procedure performed
on the wrong site
•• Surgery or other invasive procedure performed
on the wrong patient
•• Wrong surgical or other invasive procedure
performed on a patient
•• Unintended retention of a foreign object in a
patient after surgery or other invasive procedure
•• Intraoperative or immediately postoperative or
postprocedure death in an ASA class 1 patient
2.  Product or Device Events
•• Patient death or serious injury associated with
the use of contaminated drugs, devices, or
biologics provided by the health care setting
•• Patient death or serious injury associated with
the use or function of a device in patient care, in
which the device is used or functions other than
as intended
•• Patient death or serious injury associated with
intravascular air embolism that occurs while
being cared for in a health care setting
3.  Patient Protection Events
•• Discharge or release of a patient or resident
of any age who is unable to make decisions to
other than an authorized person
•• Patient death or serious injury associated with
patient elopement (disappearance)
•• Patient suicide, attempted suicide, or self-harm
that results in serious injury, while being cared
for in a health care setting
4.  Care Management Events
•• Patient death or serious injury associated with
a medication error (e.g., errors involving the
wrong drug, wrong dose, wrong patient, wrong
time, wrong rate, wrong preparation, or wrong
route of administration)
•• Patient death or serious injury associated with
unsafe administration of blood products
•• Maternal death or serious injury associated with
labor or delivery in a low-risk pregnancy while
being cared for in a health care setting; updated:
applicable in hospitals, outpatient, and office-
based surgery centers
•• Death or serious injury of a neonate associated
with labor or delivery in a low-risk pregnancy
•• Patient death or serious injury associated with
a fall while being cared for in a health care
setting
•• Any stage 3, stage 4, or unstageable pressure
ulcers acquired after admission or presentation
to a health care setting
•• Artificial insemination with the wrong donor
sperm or wrong egg
•• Patient death or serious injury resulting from
the irretrievable loss of an irreplaceable
biological specimen
•• Patient death or serious injury resulting from
failure to follow up regarding or communicate
laboratory, pathology, or radiology test results
5.  Environmental Events
•• Patient or staff death or serious injury associated
with an electric shock in the course of a patient
care process in a health care setting
•• Any incident in which systems designated
for oxygen or other gas to be delivered to a
patient contains no gas or the wrong gas or are
contaminated by toxic substances
•• Patient or staff death or serious injury associated
with a burn incurred from any source in the
course of a patient care process in a health care
setting
•• Patient death or serious injury associated with
the use of physical restraints or bed rails while
being cared for in a health care setting
6.  Radiological Events
•• Death or serious injury of a patient or staff
member associated with the introduction of a
metallic object into the MRI area
7.  Potential Criminal Events
•• Any instance of care ordered by or provided by
someone impersonating a physician, nurse,
phar­macist, or other licensed health care
provider
•• Abduction of a patient or resident of any age
•• Sexual abuse or assault on a patient or staff
member within or on the grounds of a health
care setting
•• Death or serious injury of a patient or staff
member resulting from a physical assault (i.e.,
battery) that occurs within or on the grounds of
a health care setting
Never Events
Abbreviations: ASA, American Society of Anesthesiologists; MRI, magnetic resonance imaging.
Source: Reproduced from Never Events. AHRQ Patient Safety Network. 2014. Available at

67
Chapter 10 Safety in the Outpatient Setting
surgery4 in 2002. The program was designed to monitor
nine modules of outpatient surgery center management to
facilitate compliance with necessary standards. Physician
and staff credentialing; patient routing through the preop­
erative, intraoperative, and postoperative phases of care;
vendor agreements; and formulary, incident, and pathol­
ogy reports and reports to satisfy accrediting associations
and states were all covered using the checklist concept for
ensuring completion.
Expanding upon this idea, my colleagues and I devel­
oped a peer-review program9 that integrates the surgical
process with outcomes. Included in the program documen­
tation is a checklist for collection of data pertinent to patient
routing through preoperative, intraoperative, and postopera­
tive care; the American Society of Anesthesiologists (ASA)
Physical Status Classification System; the Caprini Risk As­
sessment Model checklist; and comorbidity fields. Through
analyzing the diagnosis, procedure, and perioperative man­
agement in concert with outcomes, there is an opportunity
to determine the efficacy of the entire care process and im­
prove its delivery. Use of this program at the time of surgery,
either through a printout of the checklists or on a computer
or tablet, documents compliance with accepted standards
for patient care and provides clinical data that may help bet­
ter define evidence-based medicine (EBM).9
Data Collection
Data collected on morbidity and mortality in the AAAASF
mandated peer-review system (IBQUA) has been previously
reported through 2008. An updated report was published
in 2013 and is the basis for the statistics in this review.9,10
Analysis of Sequelae
Overview
There were 5,525,225 plastic surgery procedures per­
formed on 3,918,599 patients, with the average number of
procedures per case being 1.41. Breast augmentation, ab­
dominoplasty, mastopexy and reduction mammoplasty, li­
posuction, and facelift and related procedures were the five
most commonly performed procedures2 (Fig. 10.1). The
lofacial surgery. With the advent of AB 995, the number of
accredited facilities by this organization increased dramati­
cally.
AAAASF has promoted mandatory accreditation or li­
censure for all surgery centers throughout the United States,
championing safe surgical care. Safety and improvement in
patient care is their mission.4
In 2001, recognizing the importance of accreditation, the
American Society of Plastic Surgeons (ASPS) and the Ameri­
can Society for Aesthetic Plastic Surgery (ASAPS) established
a mandate that all of the members from each society must
operate only in accredited facilities to maintain member­
ship, regardless of state requirements.4
A variety of surgical procedures, performed by all surgi­
cal specialties, are now performed on an outpatient basis.
The outpatient surgery setting offers convenience, patient
privacy and comfort, increased efficiency, and lower costs.
Facilities that are licensed or accredited must adhere to
standards established by both their state and accrediting as­
sociations. Although monitoring outpatient facility compli­
ance with these standards is necessary to confirm patient
safety, assessing the quality of care delivered is a difficult
task.
With this concept in mind, I created the first Internet-
based quality assurance program (IBQUA) for AAAASF in
1999. This was the first Internet-based outpatient surgery
data collection system that used the concept of checklists
for ensuring specific quality assurance processes were con­
ducted in a surgical case. This database has provided infor­
mation for previously published papers on outpatient sur­
gery outcomes.6,7
The aerospace industry has used checklists for safety
since 1935. Standardized procedures were developed after
the crash of the Boeing 299 Flying Fortress. Analysis of the
crash revealed the cause to most likely be failure to recog­
nize that the elevator locks were still engaged during the
takeoff. This would have been noticed if a checklist had been
used before takeoff. The complexity of preparation of a plane
for flight and this incident inspired the creation of checklists
to document compliance with vital functions necessary for
flight.8
Taking a lead from the aerospace industry, I developed
the first compliance management program for outpatient
Facelift and related procedures
Liposuction
Mastopexy and reduction
Abdominoplasty
Breast augmentation and related procedures
1,125,274
462,588
515,252
688,241
499,477
Fig. 10.1 The five most commonly
performed procedures in outpatient
plastic surgery. (Data from https://

is-AAAASF.)

SECTION II LEGAL AND SAFETY ISSUES
68
Sequelae Types
Fig. 10.4 demonstrates the five most common sequelae out
of 21,944 reported.2
Hematoma
Hematomas occurred almost twice as frequently as infec­
tions. Of the hematomas that occurred, 6.75% were hos­
total number of sequelae reported was 21,994. There was
an incidence of 0.40% sequelae, or 1 in 251 plastic surgery
procedures, and 0.56% sequelae, or 1 in 178 cases.2
Although breast augmentation was the most com­
monly performed procedure and had the largest number
of sequelae2 (Fig. 10.2), abdominoplasty was the procedure
most commonly associated with a sequela on a percentage
basis. The incidence of unanticipated sequelae with abdomi­
noplasty was 0.93%2 (Fig. 10.3).
Facelift and related procedures
Liposuction
Mastopexy and reduction
Abdominoplasty
Breast augmentation and related procedures
5,797
4,278
3,388
3,193
3,103
Fig. 10.2 The most common plas­
tic surgery procedures associated
with sequelae. (Data from https://

is-AAAASF.)
Facelift and related procedures
Liposuction
Mastopexy and reduction
Abdominoplasty
Breast augmentation and related procedures
0.52%
0.93%
0.66%
0.46%
0.62%
Fig. 10.3 The percentage of se­
quelae per commonly performed
plastic surgery procedures. (Data
from
we-are/who-is-AAAASF.)
Skin necrosis
Wound dehiscence
Seroma
Infection
Hematoma
7,931
3,062
1,713
1,387
628
Fig. 10.4 The five most common sequelae out of 21,944 re­
ported. (Data from
is-AAAASF.)

69
Chapter 10 Safety in the Outpatient Setting
state inspection and accreditation of all outpatient facili­
ties.4
The reality is that infections in outpatient surgery are
relatively rare. In the IBQUA collection system, 3,063 infec­
tions were reported for the 3,922,202 cases performed. Al­
though infection accounted for 14% of all sequelae, their in­
cidence was only 0.08% of all cases and 0.06% of procedures
reported.2,3
Infections were identified in 921 breast augmentations,
757 abdominoplasties, 582 mastopexies or related proce­
dures, 517 liposuctions, and 346 facelifts or related proce­
dures2 (Fig. 10.5). The incidence of infections as a percentage
by procedure is depicted in Fig. 10.6.2
The most common organisms cultured were Staphylo­
coccus aureus, both methicillin-sensitive and methicillin-
resistant, and Serratia marcescens.2,3
pitalized. There were 535 patients hospitalized with he­
matomas, accounting for 0.2% of all plastic surgery cases
performed. The increasing use of chemoprophylaxis for
the prevention of venous thromboembolism (VTE) may
have contributed to some of these cases of hematomas. No
deaths were reported as a result of a hematoma.2
Infection
An example of the effect of a serious infection issue in out­
patient surgery is the report that a number of patients were
exposed to hepatitis in Nevada gastroenterology facilities
in 2008.2 It was determined that insufficient infection con­
trol oversight and improper injection practices were re­
sponsible for these cases. The publicity associated with this
incident led to increased regulation, with requirements for
Facelift
Liposuction
Breast augmentation
Mastopexy
Abdominoplasty
757
582
921
517
346
Fig. 10.5 Top five plastic surgery procedures to result in infec­
tions. (Data from
is-AAAASF.)
Facelift
Liposuction
Breast augmentation
Mastopexy
Abdominoplasty
0.16%
0.11%
0.82%
0.08%
0.07%
Fig. 10.6 Infection rate by percentage of procedure. (Data
from )

SECTION II LEGAL AND SAFETY ISSUES
70
with one or two other procedures increased the risk for a
VTE and specifically for a PE. Interestingly, when abdomi­
noplasty was performed with three other procedures, the
risk did not increase. However, the number of cases with ab­
dominoplasty and three other procedures was far less than
those cases that only had one to two additional procedures.2
The incidence of VTE and PE occurring when an abdomi­
noplasty was performed alone or in combination with other
procedures is demonstrated in Figs. 10.7 and 10.8.2
The overall incidence of VTE when abdominoplasty is
the only procedure or is performed with one or more proce­
dures was 0.066%, or 1 in 1,502. The risk of a VTE occurring
in all plastic surgery procedures is of 0.012%, or 1 in 8,188.
Abdominoplasty is a procedure that has an increased risk of
VTE, including both DVT and PE.2
Venous Thromboembolism
VTE, used to describe either deep venous thrombosis (DVT)
or pulmonary embolism (PE), is a dreaded sequela of either
inpatient or outpatient surgery. From 2001 through 2012
the number of VTE entered into the IBQUA system num­
bered 479; this included 215 DVTs and 264 PEs.10 This rep­
resents an incidence of 0.012%, or 1 in 8,188 cases.
Forty of the 264 PEs were fatal, representing a 15% mor­
tality from the occurrence of an embolism.2 Of the 5,525,225
procedures analyzed, there were 462,564 abdominoplasties
performed either as the only procedure or in conjunction
with one to three other procedures.2
More than 60% of the cases in which an abdominoplasty
was performed included other procedures. Abdominoplasty
VTE abdominoplasty + 3 other procedures
VTE abdominoplasty + 2 other procedures
VTE abdominoplasty + 1 other procedure
VTE abdominoplasty alone
0.06%
0.73%
0.08%
0.06%
Fig. 10.7 Percentage of occurrence of
venous thromboembolism (VTE) per
number of procedures that included an
abdominoplasty. (Data from https://

AAAASF.)
PE abdominoplasty + 3 other procedures
PE abdominoplasty + 2 other procedures
PE abdominoplasty + 1 other procedure
PE abdominoplasty alone
0.03%
0.04%
0.05%
0.03%
Fig. 10.8 Percentage of occurrence of
pulmonary embolism (PE) per num­
ber of procedures performed with
abdominoplasty. (Data from https://

AAAASF.)

71
Chapter 10 Safety in the Outpatient Setting
causes of death within the study population are listed in
Fig. 10.10.10
Conclusion
Data collection through IBQUA has demonstrated a low in­
cidence of sequelae in the outpatient surgery setting. This
analysis is helpful, but true improvement in patient care
will evolve through the assessment of outcomes that include
data as to how the care was delivered. Following the patient
through each phase of the surgical process and document­
ing compliance with accepted surgical care delivery stan­
dards will lead to the practice of evidence-based medicine.
This can be demonstrated, for example, by noting
whether chemoprophylaxis was used in a procedure whose
outcome resulted in the development of a VTE. A data collec­
tion system will have the ability to digitize important care
delivery data points, enhancing its value.
Centralization of data collection through the Internet
from the multiple accrediting, licensing, and patient care
managing entities will provide the means for assessing
the surgical process to achieve this goal, which will evolve
through the development of a data hub.9
Pneumothorax
Pneumothorax occurred in 154 cases, for an incidence of
0.0031%. Seventy-seven, or one half of the reported pneu­
mothoraces, occurred with breast augmentations. The dis­
tribution of pneumothoraces by procedures is shown in
Fig. 10.9.2
Mortality
Death rarely occurs as a result of outpatient surgery. Never
events have already been reviewed, and their incidence is
significantly lower. In the data reported, 94 deaths occurred,
for an incidence of 0.0017% of all procedures or 0.0024% of
total cases. Plastic surgery carries a risk of approximately
1 in 41,726. The most common cause of death was a PE. Of
particular interest is that 26 of the 40 deaths caused by a PE
occurred in conjunction with an abdominoplasty.
Fatal PEs occurred in 20 cases in which abdominoplasty
was combined with other procedures. PE was reported as
the leading cause of death in outpatient surgery in prior
reports.10 Death was less common as the result of cardiac
arrhythmia, myocardial infarction, and drug overdose. The
Capsulectomy and capsulotomy
Abdominoplasty
Mastopexy and reduction
Liposuction
Breast augmentation
77
29
21
19
8
Fig. 10.9 Distribution of 120 pneumothoraces
by plastic surgery procedure. (Data from https://
)
Pneumonia
Drug overdose
Myocardial infarction
Cardiac arrhythmia
Pulmonary embolism
40
12
11
10
4
Fig. 10.10 The five most common causes of death for plastic
surgery patients. (Data from
we-are/who-is-AAAASF.)

SECTION II LEGAL AND SAFETY ISSUES
72
6. Nazarian Mobin SS, Keyes GR, Singer R, Yates J, Thomp­
son D. Infections in outpatient surgery. Clin Plast Surg
2013;40(3):439–446
7. Pearcy J, Terranova T. Mandate for accreditation in plas­
tic surgery ambulatory/outpatient clinics. Clin Plast Surg
2013;40(3):489–492
8. Newkirk JD. Preventing surgical mishaps: using surgical
checklists. Clin Plast Surg 2013;40(3):475–487
9. Keyes GR, Nahai F, Iverson RE, Singer R. Evidence-based
medicine and data sharing in outpatient plastic surgery.
Clin Plast Surg 2013;40(3):453–463
10. Iverson RE, Gomez JL. Deep venous thrombosis: pre­
vention and management. Clin Plast Surg 2013;40(3):
389–398
References
1. AHRQ Patient Safety Network. Never events. https://
psnet.ahrq.gov/primers/primer/3/never-events
2. American Association for Accreditation of Ambulatory
Surgery Facilities. Who we are.
who-we-are/who-is-AAAASF
3. Keyes GR, Singer R, Iverson RE, et al. Mortality in outpa­
tient surgery. Plast Reconstr Surg 2008;122(1):245–250,
discussion 251–253
4. Keyes GR, Singer R, Iverson RE, et al. Analysis of outpa­
tient surgery center safety using an internet-based qual­
ity improvement and peer review program. Plast Reconstr
Surg 2004;113(6):1760–1770
5. Soltani AM, Keyes GR, Singer R, Reed L, Fodor PB. Outpa­
tient surgery and sequelae: an analysis of the AAAASF In­
ternet-based quality assurance and peer review database.
Clin Plast Surg 2013;40(3):465–473

73
Chapter 11 Disclosure of Adverse Events: A Principled Approach to Doing the Right Thing
Human beings, no matter how well trained or well inten­
tioned, make mistakes. Although there is no debate regard­
ing the issue of human error, the medical community has
not agreed on how best to disclose these errors when they
occur. Plastic surgery is no exception. In fact, this specialty
brings its own set of challenges. Many of the performed
procedures are elective in nature. Many patients have very
unrealistic expectations. Even when plastic and reconstruc­
tive surgeons clearly communicate the potential positives
and negatives of a procedure before it occurs, patients may
be disappointed. When patients believe that they have been
harmed, the integrity of the individual practitioner is often
defined by how he or she responds, whether the harm is
real or perceived.
Across the spectrum of medical specialties, adverse out­
comes are an uncomfortable reality of medical care.1 When
an unanticipated outcome occurs, physicians may deny, min­
imize, rationalize, and blame others, including the patient.
On the other hand, some physicians may embrace a commit­
ment to an open inquiry and honest communication after a
bad outcome using a “principled approach.”2 This approach
is based on a theoretical framework that is optimally en­
acted immediately after any adverse event.3,4
A shift from the perception of error as a moral failure,
as well as fear of legal repercussions, is essential to counter­
balance the “shame and blame” culture and move to a new
paradigm of disclosure.3 In addition, disclosure is by nature
a time-sensitive event and to be successful must adhere to
a specific time frame.
Given the medical complexity of error and disclo­
sure, this chapter focuses on one systematic approach
to generate an understanding of the inherent value of
disclosure.
Creating a Culture That
Facilitates Disclosure
In an arena of extreme complexity, mistakes, whether a re­
sult of human error or system error, are inevitable. It has
been suggested that health care is unsafe.5 In a specialty
that performs elective procedures, plastic surgeons are
not immune. Often they are at even more at risk because
of variations in outcomes and expectations. The way that
many physicians typically address errors reflects the previ­
ously embraced “shame and blame” culture instead of one
that promotes sharing and learning. So how does the health
care profession in general, and surgery in particular, make
the shift from “deny and defend” to a “communicate and
respond” strategy?6
Before medical disclosure can become standard prac­
tice, a “just culture” must be established. This is true of all
specialties of medicine and in every hospital and health care
setting. In a just culture, a clear distinction exists between
blame-free and culpable actions. In this environment, lead­
ership does not seek to punish unintentional errors and un­
derstands that human beings are fallible. Furthermore, phy­
sicians and other providers are more likely to report errors,
Disclosure of Adverse Events:
A Principled Approach to
Doing the Right Thing
David J. Birnbach and Timothy B. McDonald
CHAPTER
11
73

SECTION II LEGAL AND SAFETY ISSUES
74
Understanding the Principled Approach
The principled approach to patient harm follows six spe­
cific steps, highlighted in the following sections:
1.  The immediate response
2.  Reporting of harm
3.  Investigation
4.  Communication: initially and in follow-up
5.  Identification of process and performance improvement
opportunities
6.  The necessary follow-up
The Immediate Response
Responding to patient safety events and appropriately re­
porting them are the first steps in any principled process
to patient harm. Reporting triggers the institutional re­
sponse process, while the health care team responds to the
immediate medical needs of the patient. Most hospitals
encourage health care professionals, especially physicians,
to report any patient safety incident to the Safety, Quality,
and/or Risk Management Department. Reports are gener­
ally made by telephone, handwritten letters, online, or in
person. Hospitals are mandated by the Centers for Medi­
care and Medicaid (CMS) and The Joint Commission (TJC)
to provide for a reporting process for patient harm events.
Furthermore, some studies have specific requirements for
error reporting.
It is incumbent upon physicians to understand and ap­
preciate the reporting process used in any hospital where
they work. Of importance, all physicians need to recognize
the importance of their role in taking care of the patient
when harm occurs and ensuring that neither the patient nor
the family is abandoned during this critical time.
Benefits of Reporting
Reporting is essential if, as a specialty, surgeons are to ul­
timately learn, improve, and regain the confidence of their
patients. The benefits of rapid institutional reporting of
patient safety events within the organization provide sub­
stantial incentive for all physicians to report and encourage
reporting harm events. These benefits include the follow­
ing:
•• Activation of the internal patient safety and risk
management processes, including a crisis management
plan, if indicated
•• Preservation of data and information
•• Opportunity to trigger immediate support for the
patient, family, and care professionals
•• Initiation of a “quality committee” investigation and the
“legal privilege” most states afford such investigations
•• Establishment of a communication link with the harmed
patient and his or her family
near misses, and error-likely situations, helping the entire
institution to learn and improve.
This does not mean that those who make preventable
errors are not accountable, but it focuses on improving the
systems that allow errors to occur. Moreover, even when an
error occurs that does not result in patient harm, physicians
have an ethical obligation to share the information to pre­
vent future harm to another patient. After all, an error that
occurs in one hospital or surgical center can easily occur at
a different location, and today’s “near miss” can be tomor­
row’s “hit” to a less lucky individual.
A just culture can be achieved by fostering and main­
taining a work environment that encourages disclosure
without fear of reprisal or retribution.7 According to the Ca­
nadian Medical Practice Association,8 in this environment
health care providers, patients, and those in leadership po­
sitions share a collective commitment to processes that are
anchored in fairness and trust. A just culture that encour­
ages learning from adverse events to strengthen the sys­
tem and protect patients is a prerequisite if the principled
approach, as discussed in the next section, is to be applied
and embraced.
The Principled Approach
Barriers to Honest Communication
Although apologizing to patients when something goes
wrong should be a simple matter, it is fraught with difficul­
ties and complications.9 In fact, many practitioners support
medical disclosure yet lack the education about how to do
so in an appropriate manner.4 Fear of litigation; humilia­
tion; perceived risk to income, hospital privileges, and li­
cense; and the uncertainty of outcome are all barriers to
medical disclosure. However, physician failure to disclose,
or delegating the management of harm to the legal com­
munity, has arguably not prevented any of those feared
outcomes and perhaps severely damaged the reputation of
the medical profession. Furthermore, the approach to man­
agement of bad outcomes in the past has often prevented
essential learning to improve patient safety.
In most cases, patients want and respond well to full dis­
closure. Moreover, patients often react unfavorably to what
they perceive as a lack of transparency or a “partial apology,”
one that is limited to an expression of sympathy without ac­
knowledging details or fault. In fact, it has been suggested
that full disclosure may tip the balance to give the physician
the benefit of the doubt.10
To advance the safety of patients and the reputation of
the medical profession, barriers to honest communication
need to be evaluated. To reduce the concerns regarding a
culture of “shame and blame” and to facilitate open dialogue
both with the patient and within the institution, health care
organizations are creating programs for guidance and educa­
tion about the specifics of disclosure. One such program is
the principled approach presented in this chapter.

75
Chapter 11 Disclosure of Adverse Events: A Principled Approach to Doing the Right Thing
transparency, abandonment, or “cover-up.”11 In that land­
mark study, Vincent and colleagues reported that “The de­
cision to take legal action was determined not only by the
original injury, but also by insensitive handling and poor
communication after the original incident.” A transparent
process with open lines of communication and disclosure
of all pertinent information can mitigate those patient and
family perceptions.2
In a study of physicians, nurses, resident physicians, pa­
tients, and hospital administrators at five academic medi­
cal centers within one university health system, researchers
found that all groups believed that errors should be dis­
closed.6 Important influences on whether disclosure would
occur include the outcome of the error and whether it would
become known to the patient and institution. In fact, the
errors that were most likely to be discussed with patients
were the ones with immediate or significant consequences.
Patients, on the other hand, sought information and rapport
with the provider.
Disclosure of any medical error is a multifaceted process
that requires careful planning, preparation, and coordina­
tion by physicians and hospital administrators. When done
well, it has many advantages (Box 11.1). Given its complex­
ity, physicians understandably fear that an inadequate or
poorly executed disclosure of medical errors will only serve
to frustrate frontline practitioners, ruin the reputation of the
organization and individual practitioners involved in the in­
cident, and encourage lawsuits. Researchers found that the
aftermath of a bad outcome is sometimes so devastating to
the physician that the term “the second victim” was cre­
ated.15 Others have suggested that a “second victim” support
program should be developed.16
Successful adverse event response programs that include
full disclosure rely heavily upon integration between clinical
departments and the hospital’s risk managers. This integra­
tion ensures that the various stakeholders are “on board” or
at least aware of the plan for communication after an ad­
verse event. The stakeholder list should optimally include
the medical malpractice insurance carriers for the various
parties who might be affected. To provide a consistent ap­
proach to adverse events for providers, patients, and fami­
lies, all of the steps involved in the response to harm should
As with documentation in the medical record, when re­
porting a patient safety event, physicians should optimally
provide the necessary factual information to commence an
investigation, while avoiding speculation with incomplete
facts. Most significantly, this document should not be an
exercise in “finger-pointing” or used to start what has been
characterized as a “chart war.”
Another benefit of disclosure relates to the issue of liti­
gation. Contrary to urban myth, reports indicate that only
a minority of patients who sue their physicians state that
obtaining financial compensation is their primary goal in
malpractice suits.11,12 Furthermore, it appears that the act of
disclosure reduces the incidence of malpractice lawsuits.13
Investigation
As advocates for quality medical care and patient safety,
some physicians with previous specialized training possess
unique skills for participating in the investigation of serious
adverse outcomes. Patients and families want and deserve
the “facts” after a harm event, but this is not an easy task.
An appropriate investigatory process is generally needed
to provide them with the necessary and adequate infor­
mation. The physician assigned to this role should commit
to participating in any institutional root cause analysis or
other investigatory process after a serious harm event. Such
investigations should try to avoid the traditional “shame
and blame” approach to adverse events and instead focus
on systems-based issues and identification of possible ar­
eas of improvement.
Nonetheless, before they know all the facts, patients and
families are still entitled to effective communication in the
early aftermath of a harm event. David Marx,14 in his im­
portant book Whack-a-Mole: The Price We Pay for Expecting
Perfection, advocates that we abandon the “no harm, no foul”
approach to liability and institute meaningful tort reform,
revise regulations that outlaw human error, and reconsider
society’s perception of both wrongdoers and injured victims.
Communication
Once harm occurs, honest and effective communication
is essential to maintain trust between the patient and the
physician. Every hospital should have a designated individ­
ual who is uniquely positioned to facilitate such communi­
cation. This is generally not the physician who performed
the surgery. In many hospitals, because of their immediate
availability on a 24-hour basis, this person is a hospitalist.
Although some conversations can wait, others cannot. For
the patient who has experienced an unexpected outcome,
every hour that goes by without effective communication
constitutes more harm, anger, and an adversarial stance.
Honest and effective communication after a harmful ad­
verse event is not just the right thing to do, but the smart
thing to do as well. It has been suggested that patients and
families sue, in large part, because they perceive a lack of
Box 11.1
•• Helps patient recover
•• Restores trust with patient and family
•• Enables physician to deal with situation in a
positive manner
•• Reduces antagonism and lawsuits
•• Allows for fast action, including settlement
discussions before a lawsuit is filed
Benefits of Apology

SECTION II LEGAL AND SAFETY ISSUES
76
that follow suboptimal outcomes. Patients and families in­
volved in adverse events are interested in learning the ways
in which similar events are less likely to occur. Discussing
these quality improvement measures with them also helps
to maintain the trust and bond between patient and pro­
vider.
Follow-Up
It is important that the patient understands that the phy­
sician or liaison will remain in close contact while the is­
sues are being resolved. Any additional questions should
be addressed along with continued expressions of empa­
thy as warranted. Equally important is that the institution
engages in quality improvement and embraces necessary
changes from the lessons learned to ensure the safety of
all patients.
Conclusion
Ample evidence supports the idea that there are abundant
opportunities to improve patient care and prevent patient
harm. The concept of “no pay for low-quality performance”
is increasingly going to apply to a significant proportion
of episodes of care in the United States. To that end, well-
trained physicians are ideally situated to positively influ­
ence the quality of care outcomes through their perfor­
mance improvement efforts, their communication skills,
and their ability to lead multidisciplinary efforts.
In addition, all physicians can take a lead in providing
honest, open, and effective communication to patients and
families after unexpected adverse event outcomes. However,
this is not a skill that comes naturally and should optimally
be practiced before an event occurs. This is also true for resi­
dent physicians. Experienced physicians have an obligation
to trainees to make sure they understand the importance
of medical disclosure early on to ensure that this practice is
implemented going forward.17,18 This transparent approach
can be the catalyst for the transformation of an organiza­
tion’s culture for effectively responding to the needs of pa­
tients, providers, and the health care system.
Adopting a policy and practice of transparency related
to harm events represents a major shift in organizational
focus and will need the full support of hospitalists to fully
implement. This approach requires strong and persistent en­
dorsement by the kind of leadership that hospitalists can
provide their organizations. The added value of transparency
is found in the opportunity to rapidly learn from, respond
to, and modify practices based on harm investigation with
these now-transparent events.
Many physicians unfortunately continue to leave out
key information or “choose their words carefully” by fail­
ing to provide the necessary details. Steps are necessary to
increase the amount and quality of error disclosure in ev­
ery area of medicine, including plastic and reconstructive
surgery.19 Plastic surgery is potentially different from other
areas, because unrealistic patient expectations may factor
be preapproved by all appropriate stakeholders before im­
plementation. The time to develop such a program is not
after a bad outcome. It must be in place, with a designated
person on board, and ready to launch at a moment’s notice.
Risk mitigation in the real world is a function of both when
and how disclosure takes place.
The process of communication after harm in a plastic or
reconstructive surgery case generally falls in three phases
(1) immediate, (2) intermediate, and (3) final (also known
as the follow-up phase). The extent of the physician’s in­
volvement in this type of communication will depend on
his or her relationship with the patient and family. Long-
term close physician–patient relationships are conducive to
multiple meetings and fruitful discussions. Most physicians
who have had a frank conversation followed by informed
consent will quickly discover that disclosure is a process and
not an event.
It is important to identify a liaison for the family and
that appropriate empathy and assurance is expressed at each
visit. Equally important is for the patient and family to know
that they will have the ongoing support of both the physician
and institution. It is critical for the physician to understand
the difference between “empathy” and “apology.” Empathy is
the understanding or sharing of another person’s emotions
and feelings, whereas an apology is admitting that a mistake
has caused harm. In medicine, there is an ethical impera­
tive to express empathy when patients suffer harm. Apolo­
gies, however, should be reserved for situations in which it
is clear that mistakes or errors have caused the harm. Apolo­
gies, though nondiscoverable in some states, may carry real
legal implications and should be offered when the facts are
clear and agreed upon by the stakeholders with knowledge
of the event. Thus all the physicians must meet before any­
one speaks with the patient. An example of problematic be­
havior would be for a plastic surgeon in discussions with a
patient to blame the anesthesiologist (or vice versa) with­
out first having all the necessary information and talking to
that colleague.
An example of an expression of empathy is, “I am sorry
your pneumonia has progressed to the point where, despite
our best efforts, we now need to put a breathing tube in
your windpipe to help you breathe.” By way of comparison,
an example of an apology is, “I am sorry I did not check
your abnormally low blood sugar result this morning. If I
had seen the result I could have given you some extra sugar
to prevent your seizure this morning, and then you would
not have developed pneumonia because of aspiration dur­
ing the seizure.”
Process Improvements
The value in a principled, transparent approach to adverse
patient events lies in the ability to learn from mistakes
within a rigorous, reflective environment that promotes
performance improvement efforts designed to significantly
improve the delivery of care. To be effective, physicians
must play a role in the performance improvement efforts

77
Chapter 11 Disclosure of Adverse Events: A Principled Approach to Doing the Right Thing
help them understand what occurred and eventually heal.
Many physicians do not feel free to report errors.20 Physi­
cians must be compelled to strive for a better system that
allows for reform in the way they practice and in their ap­
proach to error. The American Medical Association Code of
Ethics clearly and unequivocally recommends disclosure of
medical errors by physicians to patients. This is our moral
imperative, and as physicians we must take this seriously.
into perceptions of failure or harm. Attention to presurgical
communication is essential for increasing understanding of
the procedure and moderating expectations.
Unfortunately, many victims of medical error never
learn the truth about what occurred. Lack of transparent
communication worsens the situation and the way the pa­
tient feels. Without transparency, patients and their families
are deprived of receiving the information that is essential to
References
1. Committee on Patient Safety and Quality Improvement;
Committee on Professional Liability. ACOG Committee
Opinion No. 520: Disclosure and discussion of adverse
events. Obstet Gynecol 2012;119(3):686–689
2. McDonald TB. Preventing and managing adverse patient
events: patient safety and the hospitalist. In: McKean SC,
et al, eds. Principles and Practice of Hospital Medicine.
New York: McGraw Hill; 2012:227–232
3. Liang BA. A system of medical error disclosure. Qual Saf
Health Care 2002;11(1):64–68
4. Allan A, McKillop D, Dooley J, Allan MM, Preece DA. Apol­
ogies following an adverse medical event: The impor­
tance of focusing on the consumer’s needs. Patient Educ
Couns 2015;98(9):1058–1062
5. Leape L, Berwick D, Clancy C, et al; Lucian Leape Institute
at the National Patient Safety Foundation. Transform­
ing healthcare: a safety imperative. Qual Saf Health Care
2009;18(6):424–428
6. Patient Safety Primer AHRQ. https:psnet.ahrq.gov/prim­
ers/primer/2. Accessed Feb 21, 2016
7. Birnbach DJ, Rosen LF, Williams L, Fitzpatrick M, Lubarsky
DA, Menna JD. A framework for patient safety: a defense
nuclear industry—based high-reliability model. Jt Comm J
Qual Patient Saf 2013;39(5):233–240
8. Learning from adverse events: Fostering a just culture of
safety in Canadian hospitals and health care institutions.
Ottowa, ON: Canadian Medical Practice Association;
2009
9. Godlee F. It’s time to apologise. BMJ 2015;351:h4695
10. Frenkel DN, Liebman CB. Words that heal. Ann Intern Med
2004;140(6):482–483
11. Vincent C, Young M, Phillips A. Why do people sue doc­
tors? A study of patients and relatives taking legal action.
Lancet 1994;343(8913):1609–1613
12. Friele RD, Sluijs EM. Patient expectations of fair complaint
handling in hospitals: empirical data. BMC Health Serv
Res 2006;6:106
13. Kachalia A, Kaufman SR, Boothman R, et al. Liability
claims and costs before and after implementation of a
medical error disclosure program. Ann Intern Med 2010;
153(4):213–221
14. Marx D. Whack-a-Mole: The Price We Pay for Expecting
Perfection. Eden Prairie, MN: By Your Side Studios; 2009
15. Wu AW. Medical error: the second victim. The doctor who
makes the mistake needs help too. BMJ 2000;320(7237):
726–727
16. Pratt S, Kennedy L, Scott SD, Wu AW. The Joint Commis­
sion on Quality and Patient Safety. 2012;26:235–240
17. Wu AW, Huang IC, Stokes S, Pronovost PJ. Disclosing med­
ical errors to patients: it’s not what you say, it’s what they
hear. J Gen Intern Med 2009;24(9):1012–1017
18. Raper SE, Resnick AS, Morris JB. Simulated disclosure
of a medical error by residents: development of a course
in specific communication skills. J Surg Educ 2014;71(6):
e116–e126
19. Gallagher TH, Garbutt JM, Waterman AD, et al. Choos­
ing your words carefully: how physicians would disclose
harmful medical errors to patients. Arch Intern Med
2006;166(15):1585–1593
20. Anderson B, Stumpf PG, Schulkin J. Medical error re­
porting, patient safety, and the physician. J Patient Saf
2009;5(3):176–179

(Trang không có chữ)

General
Problems
S E C T I O N I I I

Head of Goddess Hygeia (goddess of health), late classic period, 4th Century BC.
(National Archaeological Museum, Athens, Greece. Photo: Athanassios Meliarakis.
© Hellenic Ministry of Culture and Sports/Archeological Receipts Fund.)

81
CHAPTER
12

Scars and Scar Revisions
Warren Garner
Patients regularly come to a plastic surgeon because they
are unhappy with a scar. Many times this means that their
tissues have responded to an injury or surgery with a heal­
ing result that has not restored the skin to normal. Often
the tissue response results in little scarring but rather ex­
hibits abnormal contour or pigmentation. It is possible to
treat these problems, but not with the same techniques as
used for exaggerated scars.
Excessive (Proliferative) Scar
Hypertrophic Scar and Keloid Scar
Although wounds always heal with some scarring, exces­
sive scarring disturbs patients by limiting functional and
aesthetic outcomes. A surgeon with a mechanistic knowl­
edge of how wounds heal can limit these complications.
However, perfect healing seldom occurs. Correction of scar
deformities requires thoughtful application of the breadth
of reconstructive techniques. Even the most precise surgeon
will sometimes have patients who have unsightly postop­
erative scars.
Wound Healing
Understanding how to manage the consequences of dysreg­
ulated healing and exaggerated scar requires an understand­
ing of cutaneous wound healing. Very superficial epithelial
skin injuries regenerate normal anatomy. Deeper injuries,
including surgical incisions, do not regenerate normal struc­
ture but rather scar. The difference is in how much scarring
occurs. The restoration of dermal continuity achieved by su­
turing cut dermal edges occurs when disorganized collagen
fibers cross-link to the organized dermis that formed during
development. Recognizing the external influences on this
scar and managing them is an essential component of scar
treatment. Understanding how wound healing occurs is also
essential to managing the final result.
Wound healing is a highly organized, interrelated set
of biochemical and cellular responses. These events need
to proceed in a specific manner for the wound to heal opti­
mally. Release of platelet-derived growth factor (PDGF) and
transforming growth factor beta (TGF-β) from platelets dur­
ing hemostasis induces an inflammatory recruitment that
includes the macrophages, which then orchestrate the ma­
trix synthesis that becomes scar. Restoration of the epithelial
barrier decreases the inflammatory signals, matrix synthe­
sis, and scarring. Ongoing or persistent inflammation stimu­
lates continued production of the mediators, which induce
matrix protein synthesis. Wound remodeling occurs in re­
sponse to mechanical signals in the wound. Newly synthe­
sized matrix contracts as cells that were required for wound
healing migrate out of the wound. After attachment to newly
synthesized and uncross-linked collagen, they activate my­
osin and actin, pulling together the protein fibers. During
optimal healing, matrix synthesis wanes in a few weeks. Re­
modeling continues for months.
When wound healing becomes abnormal, the result is
either failed healing or excessive scar. Ongoing hemorrhage
or blood within the tissues induces ongoing inflammation,
resulting in scar contusions and nonhealing, as occurs dur­
ing the venous hypertension of venous disease. There is
also usually significant scar in such tissues. If the wound
inflammation does not wane, matrix synthesis continues,
and increased scar forms. This happens when wounds are
infected or are closed poorly or if the patient has an intrinsic

SECTION III GENERAL PROBLEMS
82
or extrinsic wound-healing abnormality that delays healing.
Many of these situations are under the control of the sur­
geon (Figs. 12.1 and 12.2, Box 12.1).
In addition to the biochemical events already discussed,
tension increases scar spreading and hypertrophy. Sites like
the sternum, where the skin is fixed and motion increases
tension, are well-recognized examples of this (Fig. 12.3).
The implication of these facts is that some scar is nor­
mal, but excessive scar is not. Robson1 described abnormal
scarring as proliferative, because unfavorable scars are usu­
ally the result of exaggerated scar formation. In addition,
scars can be of normal thickness but have spread or wid­
ened. I describe these as normal scar, spread scar, or hyper­
trophic scar.2 There is also a pathologic exaggerated healing
response, called a keloid. There is much misunderstanding
about the distinction between a keloid and a hypertrophic
scar. They are not the same disease. They have different
pathophysiologic mechanisms.3 A hypertrophic scar is ex­
aggerated normal healing, usually the result of large injuries
that heal slowly. The classic cause for hypertrophic scarring
is a burn injury, in which delayed wound closure and pro­
longed inflammation often result in hypertrophic scarring.
Hypertrophic scars get worse for 3 to 6 months, then im­
Box 12.1
Preventable
•• Wound infection
•• Poor nutrition
•• Tissue tension
•• Technical failure
Unpreventable
•• Preexisting healing derangement
•• Patient age
•• Comorbidities that affect healing:
○
○Diabetes
○
○Cancer
Causes of Poor Wound Healing
Fig. 12.1 Deep second-degree burn of the medial thigh. Healing
without grafting will predictably result in a hypertrophic scar. Graft­
ing the thigh will improve the scar but will create a donor site scar.
Fig. 12.2 (a) A skin graft donor site that healed poorly after 8 weeks because of patient scratching, poor nutrition, and inadequate wound
care. (b) The hypertrophic scar 1 year later, currently under treatment with compression and silicone.
a
b
Fig. 12.3 Twelve months after a second-degree burn of the chest
and upper arms that healed uneventfully. Significant scarring is pres­
ent at areas of stretch in the sternum and shoulders.

83
Chapter 12 Scars and Scar Revisions
whereas others have determined that these dermal nodules
are present, though less well defined in keloids as opposed
to hypertrophic scars.3,10 Still others believe that scars have
a dynamic morphology and differences in characterization
are a result of incomplete sampling.11 These data may result
from the asymmetrical nature of keloid scars, which tend
to have more quiescent centers and more active peripheral
edges.
Collagen imbalance is another dysregulated pathway
that has been studied. In normal scars, collagen 1 and 3 in­
crease with time, but the proportion of collagen 3 decreases
as scars mature. In hypertrophic scars and keloids, the rela­
tive amount of collagen 3 remains increased even in scars
that have been present for up to 20 years.12
Avoiding Unfavorable Results
and Complications in Scar
Revision Surgery
prove for 12 to 24 months. Patients with a hypertrophic scar
heal normally before and after the event that triggers the
scar (Fig. 12.4).
The Science of Scarring
When healing exceeds the restorative needs of tissue in­
tegrity, it should be considered excessive. The two types of
excessive (proliferative) scar are hypertrophic and keloid.
Most experienced clinicians and scar researchers consider
these two distinct entities. They have different clinical ex­
pressions, cell biology and biochemistry, and response to
treatment. Although there have been hundreds of scientific
studies on the pathogenesis of abnormal scarring, neither
type is fully characterized. The global summary of this re­
search is that changes in cell function, matrix composition
and organization, and tissue microenvironment all occur.4
Most investigators believe that hypertrophic scar is an
exaggerated version of normal wound-healing mechanisms
and keloid is a distinct physiologic response. There is general
agreement that hypertrophic scarring occurs after exces­
sive inflammatory states, likely mediated by dysregulated T
helper 2 responses. The result is excess local TGF-β and thus
an increase in matrix synthesis and contraction5,6: exagger­
ated participation by bone marrow–derived mesenchymal
cells, particularly fibrocytes, keratinocyte, and endothelial
hyperproliferation; and abnormal protease regulation.7 The
most common contributor to this process is delayed healing,
as often occurs in serious burn injuries.
Keloid pathophysiology is even less well understood.
Some researchers believe that TGF-β is also involved in ke­
loid pathogenesis, and that keloid fibroblasts are genetically
abnormal in their responses to stimulatory factors compared
with their hypertrophic and normal scar counterparts.8 This
suggests that keloid proliferation originates from one genetic
mutation and that the keloid fibroblasts should be mono­
clonal. However, clinical experiments show that keloid fi­
broblasts are polyclonal in nature.9 Attempts to classify ke­
loid histopathology have also led to conflicting reports, with
some describing an absence of dermal nodules in keloids,
Summary Box
Complications Associated with Scar Revision
Excessive scarring:
Hypertrophic scar
Keloid scar
Delayed healing because of infection
Fig. 12.4 Minimal shearing around this skin graft resulted in several
millimeters of ungrafted full-thickness wound. This healed slowly.
The surrounding “frame” of hypertrophic scar is the area that was
not successfully grafted and healed poorly.
Preventing Scarring
The best way to treat a problem is to prevent it. Preventing
scarring involves closing wounds as early as possible and
with no tension. I achieve these goals with a staged strat­
egy. Elective surgical incisions should be closed with preci­
sion, usually in layers. When there is tension, I use a bur­
ied polyglyconate or polydioxanone suture to anchor the
dermal edges together during the initial several months of
wound healing. Other absorbable sutures and removable
sutures lose this ability after a few weeks, resulting in scar
spreading and hypertrophy. Acute skin trauma cannot be
treated this way because of the general tissue damage and
presence of bacteria.
A common cause for delayed healing is infection. A topi­
cal antimicrobial is an easy and effective adjunct to wound
closure and can limit this problem. For simple incisions and
wounds I use 2% mupirocin, because it is highly effective
against Staphylococcus and Streptococcus spp., the usual
agents of infection. For larger wounds or burns, skin grafts,
and donor sites, the broad-spectrum benefits make silver
sulfadiazine or a silver-releasing dressing ideal choices. In
my practice all wounds are treated with an antimicrobial
dressing.

SECTION III GENERAL PROBLEMS
84
Patients and physicians need to discuss whether limiting
scarring with a graft, adding a modest donor site scar, is a
better strategy for improved appearance.
Wounds that are closed incompletely often form hy­
pertrophic scars. This includes imprecisely closed incisions
that heal over days rather than hours. Incompletely grafted
wounds or widely meshed donor sites similarly heal with
more scarring and often become hypertrophic (Fig 12.6).
Scars spread when the mechanical forces on the un­
cross-linked matrix are sufficient to pull matrix fibers
apart. Avoiding excessive tension prevents this. The ben­
efits of deep buried sutures were mentioned previously.
Reorientation of tension with z-plasties or other local tis­
sue rearrangements also helps. There are many strategies
to decrease tension with taping, external appliances, and
massage. The best method to prevent scar spreading and
the only one of proven effectiveness is the Embrace device
(Neodyne Biosciences; Fig. 12.7). This is externally applied
up to 2 weeks after surgery to a closed, dry incision and lim­
An important consideration is that successfully clos­
ing larger wounds has other priorities than creating the
best scar. In many cases the plastic surgeon must develop
a plan with the patient that balances faster, more simple
wound closure and best long-term results. An example of
this conflict is the choice of meshed versus sheet grafts.
A more sophisticated example is the decision of whether
to use Integra regenerative dermal template (Integra Life­
Sciences) to improve the appearance of widely meshed skin
grafts (Fig. 12.5). By providing a template for dermal regen­
eration, the product creates a thicker graft with the predict­
able improvement in appearance. This improved appearance
does come with increased cost, however.
Finally, although some large wounds might heal over a
period of 4 to 6 weeks, the resulting scar will be significant.
Fig. 12.6 This patient demonstrates many of the deformities of an
untreated scar: scar contraction on the flexor surfaces of the digits
and the extensor surface of the dorsum, hypertrophic scar at the
shear planes between grafted and ungrafted skin (note the ulnar
side of the thumb), hypertrophic meshed patterning at the forearm,
and linear scar bands at proximal wrist where dorsiflexion occurs.
These would have been significantly more normal in function and
appearance with monitored use of silicone and pressure garments.
Fig. 12.7 Embrace device used to minimize scar hypertrophy and
spreading. (These images are provided courtesy of Neodyne Bio­
sciences, Inc.)
Treated
Untreated
Fig. 12.5 A distal foreleg that has been grafted with Integra dermal
template. The Integra was lost in the area noted. The entire leg was
regrafted with thin meshed autograft. The appearance of the area
with successful Integra engraftment is improved.
Area of Integra loss

85
Chapter 12 Scars and Scar Revisions
realistic. There are three accepted ways to nonoperatively
treat scars (Fig. 12.8):
1. External pressure
2. Silicone sheeting
3. Pharmacologic treatment with steroids
External Pressure
Pressure garments have been shown to produce scars that
are thinner, softer, and lighter in color than scars from the
same injury that healed without pressure garments at up
to 1 year of follow-up.13 For these external pressure mo­
dalities to work, they must be monitored and adjusted at
regular intervals. Although the scars may remain thick, the
pressure garments typically cause flattening of contour ir­
regularities. If not, they should be adjusted.
Silicone Sheeting
Silicone sheeting can be used to line pressure garments or
used alone. When used alone, silicone sheeting can be ap­
plied for only 12 hours a day.14 This treatment increases pa­
tient compliance, because the scars can be treated at home,
outside the workplace. Scars show improvement after
treatment for 2 to 3 months without further follow-up.15
Steroid Treatment
Corticosteroid injections are one of the oldest and most ac­
cepted treatments for abnormal scarring, with the greatest
and most lasting benefit occurring in those who receive the
injection earlier in the scar healing process16 (Fig. 12.9).
There is general agreement that triamcinolone injections
induce short- to long-term improvement in both keloids
and hypertrophic scars (Table 12.1). Steroid treatments for
abnormal scars have not been completely investigated at
its tension being transmitted to the uncross-linked, newly
synthesized matrix of the incision.
Limiting Unsightly Healing
Strategies that cause the wound to heal quickly are the best
tools for prevention of unattractive healing. Prevention of
infection, stretch, and shear were discussed previously. The
most common cause for unsightly healing in my practice is
hyperpigmentation.
Wound healing activates melanocytes, which make
more melanin in response to ultraviolet light. The result is
noticeable and disturbing. Hyperpigmentation is most no­
ticeable in patients with Fitzpatrick type 3 or 4 skin color
but can result in a noticeable difference in anyone except
patients with the lightest or darkest skin color. Prevention
with sunscreen is the best treatment, although tretinoin and
quinolones are effective when hyperpigmentation develops.
I ask patients to routinely use sunscreen with a sun protec­
tive factor of 30 or greater until the wound is not red.
Managing Unfavorable Results
and Complications in Scar
Revision Surgery
Treating Scarring
Although most plastic surgeons practice nonoperative scar
management, there is little objective data about the vari­
ous treatment options. (There is data about the treatment
of keloids, which are discussed later.) Most surgeons are
very willing to attribute scar improvement to their treat­
ment algorithms. However, the natural history of normal
and hypertrophic scars is to spontaneously improve 3 to 12
months after injury. I use available treatments but try to be
Fig. 12.9 A patient with a presternal keloid treated by steroid injec­
tion every 3 to 12 months for 15 years with excellent control of scar
progression. The inferior new lesion was being treated with its first
injection at this visit.
Fig. 12.8 Five years after treatment of a burn injury with a sheet
graft, compression garments, silicone sheeting, surgical scar revi­
sion, and dermabrasion. The result is excellent, but not normal.

SECTION III GENERAL PROBLEMS
86
However, these techniques result in different scars, not an
absence of scar.
Scars can cause abnormal motion by mass effect, from
fibrous attachments between the scarred skin and the un­
derlying muscle fascia, or by tissue remodeling that has re­
sulted in the formation of a contracture. Masses of scar have
abnormal biomechanical properties. They do not stretch,
bend, or move like unscarred skin. To restore normal mo­
tion, the scar must be resected and replaced with normally
flexible, unscarred tissue. Flaps are always more effective,
because they contract less. The traditional technique to ad­
vance tissue into the release is to use z-plasties (Fig. 12.11).
Adjacent tissue flaps are better when available because
they have a better skin match. However, any normal tissue
will move better than a mass of scar. Skin grafts are accept­
able alternatives but are never as successful as flaps. Full-
thickness grafts provide more contraction-preventing der­
mis and a more normal appearance but with a risk of worse
graft take.21 Split-thickness grafts have a more predictable
take and allow resection and coverage of large areas of scar­
ring but predictably contract and always look abnormal. The
choice to use any of these techniques must be individualized
to satisfy the patient.
When the skin is reasonably normal, but motion is lim­
ited by fasciocutaneous attachments, massage is often useful
more long-term follow-up periods, but keloids have been
known to recur more than a year after initial treatment. This
means that despite being universally used, corticosteroid
injections provide an unproven long-term benefit. In my ex­
perience, they improve symptoms of pain and itch in keloids
but provide only temporary benefit to keloid scar mass.
Because steroid injections do not predictably improve
keloid scars, other novel intralesional treatments have been
proposed and studied. Most practitioners consider these as
second-line treatments. These include imiquimod cream, in­
tralesional 5-fluorouracil (5-FU) injections, bleomycin, and
interferon-α2β.17–20
Surgery for Scars
The surgical treatment of scars can correct the sequelae of
scar, limitation of motion, contracture, and unsightly ap­
pearance. Excision of scars removes unsightly lesions and is
the obvious simple solution (Fig. 12.10).
Unfortunately, if the scar is the result of tension at the
time of injury or healing, the persistence of that condition
induces recurrent scar. Tissue rearrangements can alter ten­
sion and add tissue to the deficiency caused by wound con­
traction. In this situation, addition of tissue by graft or flap
is often the best technique to prevent recurrent hypertrophy.
Table 12.1 Injection algorithm for scars*
First injection
Subsequent injections
Keloid
2:1:1 mix of 40 mg/mL triamcinolone/
1% lidocaine with 1:100,000 epinephrine
2:1:1 mix of 40 mg/mL triamcinolone/
0.5% bupivacaine/1% lidocaine with 1:100,000
epinephrine
Hypertrophic scar
2:1:1 mix of 40 mg/mL
triamcinolone/0.5% bupivacaine/
1% lidocaine with 1:100,000 epinephrine
2:1:1 mix of 20 mg/mL triamcinolone/
0.5% bupivacaine/1% lidocaine with 1:100,000
epinephrine
*Small areas of scarring in adults can be injected in the clinic; large areas of scarring in adults or any scarring in children should be injected with the
patient sedated.
Fig. 12.10 Staged excision of a hypertrophic scar mass. (a) Preoperatively. (b) Four months postoperatively.
a
b

87
Chapter 12 Scars and Scar Revisions
wound healing has removed tissue, and the remaining tissue
does not have the mechanical properties that will allow it
to stretch. Although nonoperative therapies can be helpful,
most contractures require the addition of tissue. The same
surgical hierarchy applies as for excision of scar masses: Lo­
cal flaps are better than distant flaps, and flaps are better
than full-thickness grafts, which are better than split grafts.
The determination of the best procedure to use for a particu­
lar patient results from a balance of the patient’s needs and
preferences, the available tissues, and the surgeon’s skill and
experience (Fig. 12.13).
in stretching these attachments. Having the patient massage
and slowly stretch the tissue at risk for scarring is something
most experienced plastic surgeons recommend, is probably
helpful, but is of unproven efficacy. Physical therapists can
often be helpful in correcting established immobilities with
deep tissue massage. When nonoperative interventions are
not successful, I most often use a double-opposing V-Y plasty
(diamond flap).22 This technique releases the fasciocutane­
ous scar limiting motion (Fig. 12.12).
When motion is limited by contracted scar the result is
a contracture. In these situations, the remodeling phase of
Fig. 12.11 (a) A hypertrophic neck scar with adjacent scar contracture of the neck. (b) After treatment by excision of the scar and serial
z-plasties.
a
b
Fig. 12.12 Preoperative and postoperative images after multiple serial z-plasties to release scar contracture. Some of the scar at the base
of the neck was also resected. Opposing V-Y plasties (diamond flap) were used to release the area of contracture that had developed in the
hypertrophic skin graft.

SECTION III GENERAL PROBLEMS
88
scars by stimulating collagen production and encouraging
scar remodeling.29–32
Fat Grafting
There is some anecdotal evidence that fat grafting improves
the appearance and feel of hypertrophic scars, minimizing
scar volume and increasing scar elasticity. The theory be­
hind this is that the harvested fat includes adipose-derived
stem cells in the vascular portions that have multipotent
abilities and contribute to scar remodeling. Murine studies
suggest there is increased vascularity, wound remodeling,
and improvement of neuropathic pain with fat injections
early in the scar formation process, and these results have
been corroborated by human case series.33 In addition,
histologic studies of human scar before and after fat injec­
tion showed increased elastin fibers in fat-injected scars,
further substantiating anecdotal evidence of increased
scar pliability.34 With this evidence, it appears that treating
hypertrophic scars or wounds in a person predisposed to
hypertrophic scarring with fat injections could be a viable
method in decreasing scar volume and maximizing nor­
mal healing. The appropriate patient for such a treatment
method is one who has a sufficient supply of fat from which
to harvest, because the methods described are often serial
treatments that optimize the final appearance of scar.
Laser Treatment for Subacute and
Hypertrophic Scars
There is increasing clinical experience and published sup­
port for the use of laser therapy to improve scar appear­
ance.23–32 The pulsed dye laser (PDL) is used in the early,
subacute recovery period, and fractional ablative lasers are
effective for the treatment of more mature scars.
A PDL set at 585 or 595 nm selectively targets hemoglo­
bin and coagulates microvasculature in the papillary and
reticular dermis, up to a depth of 1.2 mm. All result from or
are related to pathologic neovascularization. The PDL causes
selective photothermolysis that induces coagulation necrosis
of the capillaries. When applied to burn scars, the PDL serves
to extinguish this hypervascular response. The evidence sup­
porting the use of PDL in the treatment of hypertrophic scar
is plentiful.23–25
Fractional ablative lasers (specifically CO2 and erbium-
doped: yttrium aluminum garnet [Er:YAG]) target intracellu­
lar water, leading to vaporization of tissue and denaturation
of surrounding extracellular proteins. By fractionating the
laser, microscopic columns of abnormal dermis are vapor­
ized or coagulated, leaving a significant amount of epidermis
and dermis intact. This leads to rapid and controlled wound
healing. In burn scars, fractional ablative lasers have been
shown to improve mature hypertrophic and atrophic burn
a
b
c
Fig. 12.13 (a) Dense posterior axillary contracture. (b) The contracture is released and the perforator flap on the upper arm marked.
(c) Postoperative view of the grafted donor site on the arm.

89
Chapter 12 Scars and Scar Revisions
19. Atiyeh BS. Nonsurgical management of hypertrophic
scars: evidence-based therapies, standard practices, and
emerging methods. Aesthetic Plast Surg 2007;31(5):468–
492, discussion 493–494
20. Granstein RD, Rook A, Flotte TJ, et al. A controlled trial of
intralesional recombinant interferon-gamma in the treat­
ment of keloidal scarring. Clinical and histologic findings.
Arch Dermatol 1990;126(10):1295–1302
21. Brown D, Garner W, Young VL. Skin grafting: dermal com­
ponents in inhibition of wound contraction. South Med J
1990;83(7):789–795
22. Geh JL, Niranjan NS. Perforator-based fasciocutaneous
island flaps for the reconstruction of axillary defects fol­
lowing excision of hidradenitis suppurativa. Br J Plast
Surg 2002;55(2):124–128
23. Alster TS, Nanni CA. Pulsed dye laser treatment of hy­
pertrophic burn scars. Plast Reconstr Surg 1998;102(6):
2190–2195
24. Liew SH, Murison M, Dickson WA. Prophylactic treatment
of deep dermal burn scar to prevent hypertrophic scar­
ring using the pulsed dye laser: a preliminary study. Ann
Plast Surg 2002;49(5):472–475
25. Donelan MB, Parrett BM, Sheridan RL. Pulsed dye laser
therapy and z-plasty for facial burn scars: the alternative
to excision. Ann Plast Surg 2008;60(5):480–486
26. Hultman CS, Edkins RE, Lee CN, Calvert CT, Cairns BA.
Shine on: review of laser- and light-based therapies for
the treatment of burn scars. Dermatol Res Pract 2012;
2012:243651
27. Hultman CS, Edkins RE, Wu C, Calvert CT, Cairns BA. Pro­
spective, before-after cohort study to assess the efficacy
of laser therapy on hypertrophic burn scars. Ann Plast
Surg 2013;70(5):521–526
28. Hultman CS, Friedstat JS, Edkins RE, Cairns BA, Meyer
AA. Laser resurfacing and remodeling of hypertrophic
burn scars: the results of a large, prospective, before-
after cohort study, with long-term follow-up. Ann Surg
2014;260(3):519–529, discussion 529–532
29. Waibel J, Beer K. Ablative fractional laser resurfacing for
the treatment of a third-degree burn. J Drugs Dermatol
2009;8(3):294–297
30. Haedersdal M, Moreau KE, Beyer DM, Nymann P, Alsbjørn
B. Fractional nonablative 1540 nm laser resurfacing for
thermal burn scars: a randomized controlled trial. Lasers
Surg Med 2009;41(3):189–195
31. Taudorf EH, Danielsen PL, Paulsen IF, et al. Non-ablative
fractional laser provides long-term improvement of ma­
ture burn scars—a randomized controlled trial with histo­
logical assessment. Lasers Surg Med 2015;47(2):141–147
32. Levi B, Ibrahim A, Mathews K, et al. The Use of CO2 Frac­
tional Photothermolysis for the Treatment of Burn Scars.
J Burn Care Res 2016;37(2):106–114
33. Condé-Green A, Marano AA, Lee ES, et al. Fat grafting and
adipose-derived regenerative cells in burn wound healing
and scarring: a systematic review of the literature. Plast
Reconstr Surg 2016;137(1):302–312
34. Piccolo NS, Piccolo MS, Piccolo MT. Fat grafting for treat­
ment of burns, burn scars, and other difficult wounds.
Clin Plast Surg 2015;42(2):263–283
References
1. Robson MC. Proliferative scarring. Surg Clin North Am
2003;83(3):557–569
2. Garner WL, Smith DJ Jr. Reconstruction of burn deformi­
ties of the extremities and trunk. In: Cohen M, ed. Mas­
ter of Surgery: Plastic and Reconstructive Surgery. Little
Brown and Company; 1994
3. Ehrlich HP, Desmoulière A, Diegelmann RF, et al. Morpho­
logical and immunochemical differences between keloid
and hypertrophic scar. Am J Pathol 1994;145(1):105–113
4. Engrav LH, Garner WL, Tredget EE. Hypertrophic scar,
wound contraction and hyper-hypopigmentation. J Burn
Care Res 2007;28(4):593–597
5. Garner WL, Karmiol S, Rodriguez JL, Smith DJ Jr, Phan SH.
Phenotypic differences in cytokine responsiveness of hy­
pertrophic scar versus normal dermal fibroblasts. J Invest
Dermatol 1993;101(6):875–879
6. Garner WL, Rittenberg T, Ehrlich HP, et al. Hypertro­
phic scar fibroblasts accelerate collagen gel contraction.
Wound Repair Regen 1995;3(2):185–191
7. Yang L, Scott PG, Dodd C, et al. Identification of fibro­
cytes in postburn hypertrophic scar. Wound Repair Regen
2005;13(4):398–404
8. Tuan TL, Nichter LS. The molecular basis of keloid and
hypertrophic scar formation. Mol Med Today 1998;4(1):
19–24
9. Chevray PM, Manson PN. Keloid scars are formed by poly­
clonal fibroblasts. Ann Plast Surg 2004;52(6):605–608
10. Clark JA, Turner ML, Howard L, et al. Description of fa­
milial keloids in five pedigrees: evidence for autosomal
dominant inheritance and phenotypic heterogeneity. BMC
Dermatol 2009;9:8
11. Burd A, Huang L. Hypertrophic response and keloid dia­
thesis: two very different forms of scar. Plast Reconstr
Surg 2005;116(7):150e–157e
12. Di Cesare PE, Cheung DT, Perelman N, Libaw E, Peng L,
Nimni ME. Alteration of collagen composition and cross-
linking in keloid tissues. Matrix 1990;10(3):172–178
13. Engrav LH, Heimbach DM, Rivara FP, et al. 12-Year within-
wound study of the effectiveness of custom pressure gar­
ment therapy. Burns 2010;36(7):975–983
14. Ahn ST, Monafo WW, Mustoe TA. Topical silicone gel: a new
treatment for hypertrophic scars. Surgery 1989;106(4):
781–786, discussion 786–787
15. Berman B, Perez OA, Konda S, et al. A review of the biolog­
ic effects, clinical efficacy, and safety of silicone elastomer
sheeting for hypertrophic and keloid scar treatment and
management. Dermatol Surg 2007;33(11):1291–1302,
discussion 1302–1303
16. Ketchum LD, Smith J, Robinson DW, Masters FW. The treat­
ment of hypertrophic scar, keloid and scar contracture by
triamcinolone acetonide. Plast Reconstr Surg 1966;38(3):
209–218
17. Atiyeh BS. Nonsurgical management of hypertrophic
scars: evidence-based therapies, standard practices, and
emerging methods. Aesthetic Plast Surg 2007;31(5):468–
492, discussion 493–494
18. Fitzpatrick RE. Treatment of inflamed hypertrophic scars
using intralesional 5-FU. Dermatol Surg 1999;25(3):
224–232

SECTION III GENERAL PROBLEMS
90
Discussion by Tulsi Roy and Raphael C. Lee
Scar formation is a natural tissue wound-healing mech­
anism in most terrestrial vertebrates; the scar serves
as a connective tissue “patch” rather than a true re­
placement of the damaged tissue. Scarring is a survival
mechanism that, in the setting of modern medical fa­
cilities, often limits the quality of the clinical outcome.
Scars can be problematic if they are too abundant or
lead to excessive contraction. Achieving the aestheti­
cally optimal result from surgical procedures may re­
quire a multipronged approach to scar management.
Wound healing is a complex, highly-regulated, mul­
tiphase tissue repair process involving inflammation,
transitional repair, and remodeling after tissue injury.
Normal wound healing results in a functional connec­
tive interface. Fundamentally, any factor that prolongs or
amplifies wound inflammation, increases dynamic ten­
sion on the healing wound, or metabolically stimulates
tissue growth will lead to excessive scarring. Therefore
basic strategies necessary to achieve acceptable scarring
are removal of foreign or devitalized material from the
wound, gentle handling of tissues, establishment of pri­
mary closure as soon as possible, reduction of mechani­
cal tension by alignment of the incision in the skin ten­
sion lines, and performing elective procedures between
rapid body growth phases.
Scar Terminology
Confusing and outdated terminology is often used to
describe wound healing, and scarring. This is a factor
that limits both research and clinical care related to
excessive scarring. Skin melanin content is generally
believed to correlate with extent of scar formation.
People with darker skin manifest a greater incidence of
hypertrophic scarring. Hypertrophic scars are mostly
related to epigenetic factors such as mechanical ten­
sion, chronic folliculitis, prolonged inflammation, and
adolescence, among others. Keloid scars, on the other
hand, are essentially benign, neoplastic scar tumors
associated with a strong family history of this pheno­
type. This difference suggests that keloid scarring has a
significant genetic component. True keloids, therefore,
are rare. Of course, keloid scar behavior is also influ­
enced by the same epigenetic factors as hypertrophic
scarring. It is important to distinguish keloids from hy­
pertrophic scars to stratify operative risk and initiate
appropriate treatment.
Prevention
Although it may be difficult to predict the extent of
scarring from any particular wound, several general
surgical principles are important to keep in mind to re­
duce the incidence of hypertrophic and unsightly scars.
The persistence of chronic inflammation in wounds
is a major and often controllable factor deterministic of
scar magnitude. Operative technique should be guided
toward reducing duration and magnitude of wound in­
flammation: early wound closure, gentle and careful tis­
sue handling that minimizes tissue trauma, evacuation
of blood and reduction of bacteria load with sterile tech­
nique and adequate débridement, ideal suture choice,
and minimization of foreign suture material are all good
basic surgical practices to develop. Absorbable monofila­
ment biopolymer sutures tend to be more biologically in­
ert and have a less robust inflammatory reaction, which
make them more ideal for superficial layer closure.
Skin is a highly specialized mechanoresponsive in­
terface that models along imposed mechanical demands.
For this reason, a key component of surgical scar preven­
tion (and intervention) is limiting mechanical tension on
surgical incisions. Orienting incisions parallel to relaxed
lines of skin tension corresponding to the orientation of
collagen fibers in the dermis is an easy way to minimize
postsurgical hypertrophic scarring. Likewise, meticu­
lous wound edge approximation and suture placement
permits faster wound closure and reestablishment of an
epithelium and sterile wound bed. Thicker skin grafting,
skin flaps, static splinting, and even paper tape are all
effective options to minimize scar tension. Joint contrac­
ture is best avoided by midaxial placement of incisions
and crossing the deformable skin parallel to the joint
creases. Several novel approaches to reduce mechani­
cal tension on surgical incisions have been developed,
including stress shields with polymer backing materi­
als and pressure-sensitive adhesives that decrease tissue
deformation and subsequently reduce scar hypertrophy,
matrix deposition, and epithelial thickening.
The higher incidence of hypertrophic scar formation
and vitamin D insufficiency in populations with darker
skin suggests that vitamin D may also be key in the de­
velopment of keloids and hypertrophic scars.1 In in vitro
studies by Zhang et al,2 not only were keloid fibroblasts
shown to have increased vitamin D receptor expression,
but also 1,25(OH)2D3 was shown to inhibit proliferation
of keloid fibroblasts and extracellular matrix (ECM) pro­
duction by decreasing TGF-β expression and increasing
matrix metalloprotease activity to promote ECM degra­
dation. Vitamin D3 can exert its effects through inhibit­
ing nuclear factor–κB (NF-κB)–mediated interleukin 6
(IL-6) gene activation, implicated in a wide array of fi­
brotic processes including scar deposition and adhesion
formation through the upregulation of proinflammatory
cytokines and growth factors.3,4 Though more studies are

91
Chapter 12 Scars and Scar Revisions
warranted to validate this relationship, the direct role
of vitamin D as a regulator of inflammation and wound
healing provides a good basis for normalizing vitamin
D3 levels in trauma patients.
Scar massage is commonly recommended to pa­
tients as a simple and cost-effective strategy to improve
scar cosmesis through mechanical disruption of fibrotic
tissue. Deep massage around stiff joints or tendons
seems to help. However, massaging scars is antitheti­
cal to demonstrated benefits of preventing mechanical
stimulation of wounds. Dynamic mechanical stress is a
well-established upregulator of fibroplasias and fibrosis.
A review of the clinical literature on the benefits of scar
massage concluded that there are no clear evidence-
based guidelines regarding when to initiate treatment,
massage technique, frequency, or duration of therapy
in the literature.
Along similar lines, pressure garment therapy (PGT)
has long been popularized as a noninvasive method for
management of hypertrophic scars, particularly in burn
scars. Although the ideal pressure required for optimum
results is unknown, the recommended level is greater
than 25 mm Hg, although good clinical results have been
reported with pressure as low as 5 to 15 mm Hg. All
theories of accelerated scar remodeling with PGT, how­
ever, are incomplete because the compression pressure
is actually not maintained throughout the duration of
therapy. Clinical studies on the efficacy of pressure gar­
ments fail to show a significant benefit.
Interventions
Again, interventions for hypertrophic and keloid scar­
ring should be guided by well-founded and straightfor­
ward principles of minimizing inflammation, decreas­
ing mechanical tension, and promoting collagenase
production through alterations in cell signaling. This
section discusses several treatment options for hyper­
trophic scarring.
Occlusive Barriers: Gel Sheeting
Silicone sheeting is a well-established mainstay of non­
invasive scar management, believed to affect scarring
by increasing heat and hydration of the stratum cor­
neum with subsequent cytokine-mediated signaling
from keratinocytes to dermal fibroblasts to increase
collagenase production.5 Silicone gel sheeting is a soft,
self-adhesive sheet that is applied to intact skin as an
occlusive barrier. General recommendations for sili­
cone therapy are at least 12 hours continuous appli­
cation per day for 12 to 24 weeks. Of the noninvasive
methods outlined in this chapter, it is also one of the
few that can be used both prophylactically and thera­
peutically, and it serves as a useful adjunct with other
topical agents. The use of silicone sheeting has several
functional limitations, particularly over joints, the face,
large areas, and highly contoured areas where achieving
occlusion is particularly difficult.6 However, several new
formulations of topical silicone gel that dry into water-
impermeable membranes have shown similar effects to
silicone sheeting and are much more pliable and better
tolerated in contoured areas such as the face and ears.
Interferon Therapy
In vitro, interferon-α (IFN-α) and IFN-γ have been
shown to reduce the synthesis of collagen by normal
and hypertrophic scar fibroblasts.7 The mechanism of
action of IFN may be partially accounted for by a de­
crease in messenger ribonucleic acid (mRNA) stability,
downregulation of procollagen gene-activating tran­
scription factors, and promotion of intracellular degra­
dation of collagen molecules.8
McCauley et al9 have suggested that keloid patients
have deficient production of systemic IFN-α and IFN-γ,
which may provide a theoretical basis for the provision
of exogenous IFN. Although the use of interferon therapy
is scientifically sound, clinically speaking the benefits
should be balanced against the severe side effects, in­
cluding fever, chills, night sweats, fatigue, myalgia, and
headache, which may limit its broad usage.
Nonsteroidal Antiinflammatory Drugs
Antiinflammatory drugs such as cyclo-oxygenase in­
hibitors, in particular aspirin, ibuprofen, and naproxen,
have been shown to decrease fibrosis in autoimmune
disease. These drugs are commonly used in medicine to
inhibit IL-1 and prostaglandin production—key stimu­
lators of inflammation and subsequent fibrosis—and
their safety is widely understood. In our own practice,
we have achieved significant improvement in postop­
erative scarring with topical applications of nonsteroi­
dal antiinflammatory drugs.
Histamine has been found in increased quantities in
keloid fibroblasts in in vitro studies and demonstrates
subsequent growth suppression with the application
of antihistamine pharmacotherapy. Topical diphen-
hydramine and calamine both have antipruritic prop­
erties and thus can be used to prevent scratch irritation,
reducing a potential prolonged inflammatory phase,
thereby limiting stimulators of excessive scarring.
Intralesional Corticosteroids
Intralesional and topical steroid therapy has long been
considered a first line approach to pathologic hyper­
trophic and keloid scarring. As previously mentioned,
inflammation is a critical mediator of hypertrophic

SECTION III GENERAL PROBLEMS
92
scarring. By suppressing the migration of inflamma­
tory cells and decreasing the activation of fibroblasts
by downregulating TGF-β and VEGF, triamcinolone
acetonide can reduce collagen production and promote
scar tissue atrophy. Clinical guidelines for intralesional
administration vary from 10 to 40 mg/mL at intervals
of 3 to 6 weeks for several months or until the scar is
flattened. Injections can be painful and may be poorly
tolerated by pediatric patients, so local or regional an­
esthesia may be helpful in this patient population to
alleviate injection discomfort. Adverse effects of cor­
ticosteroid injection also include skin atrophy, telan­
giectasias, and hypopigmentation. Confining the injec­
tions to the dermal region and maintaining the steroid
concentration below 5 mg/mL can minimize local hy­
popigmentation and atrophy. Although intralesional
steroid monotherapy has demonstrated some efficacy,
response and recurrence rates are variable. That being
said, steroid therapy in conjunction with antimitotic
agents, pulsed-dye laser treatments, cryotherapy, or
surgical excision have been shown to have improved
and more reliable outcomes.10
Stimulation of Proteolytic Enzyme
Synthesis
A balance of ECM synthesis and breakdown governs
scar homeostasis. One effective therapeutic strategy to
limit scar formation is based on acceleration of matrix
degradation. This approach may involve the use of topi­
cal or intralesional application of calmodulin or protein
kinase C (PKC) inhibitors. These agents appear to trig­
ger similar phenotypic and cytomorphologic changes
in fibroblasts.
In our own work, we have reported that verapamil
and nifedipine, clinically used safely as calcium channel
blockers (CCBs), inhibit the incorporation of proline into
ECM protein and increase ECM degradation by upregu­
lating collagenase production.11 In our clinical practice,
treated patients report significant improvement in scar
color and texture with 0.1 to 0.5 mmol/L of verapamil
hydrochloride therapy. CCBs have fewer complications
than intralesional steroid injection, are readily available,
and have been shown to be safe for systemic use. In ad­
dition, topically applied CCBs are too rapidly metabo­
lized intradermally to have systemic effects. For this rea­
son, larger controlled trials are necessary to fully explore
the use of topical calcium channel blockers in effectively
treating hypertrophic and keloid scars.
Radiotherapy
In a 2015 study, postoperative administration of elec­
tron beam radiotherapy after keloid excision demon­
strated a more than 80% reduction in recurrent dis­
ease.12 Radiation therapy has showed greatest benefit
when initiated 72 hours postoperatively and adminis­
tered every other day at 3 or 4 Gy for a total dose of 12
to 18 Gy.12 Preoperative radiation, on the other hand,
has not shown any benefit. Generally, there are con­
cerns of neoplasia related to applying ionizing radia­
tion to benign tumors, particularly in children. Though
ionizing radiation has shown promise, this mode of
therapy should be considered primarily for older indi­
viduals who have keloids with surrounding normal tis­
sues that are well shielded and when other modalities
have been exhausted. Although radiation is helpful to
target rapidly dividing cells, care must be taken to limit
inflammation, including radiation-induced dermatitis.
A Note on Laser Therapy
Alster and Williams13 have described the use of a 585-
nm flash lamp pulse-dye laser for the selective pho­
tothermolysis of vascular endothelial cells in hyper­
trophic scars. They found a 57 to 83% improvement
in the surface texture measurements and in clinical
criteria after one or two treatments. Others, however,
have reported conflicting results. Laser therapy (and
cryotherapy) are both modeled on the imposition of
small bursts of unregulated cell death and downstream
release of inflammatory mediators that contribute to
prolonged inflammation and eventual fibrosis. There­
fore we would caution against its large-scale use in the
general population of individuals with hypertrophic
scarring.
Surgery
Clinical judgment and timing are essential in decision-
making for surgical intervention. If the hypertrophic
scar resulted from a complex skin injury or delayed
closure, surgical excision and closure will likely result
in improvement. Surgery may also be indicated for hy­
pertrophic scars oriented unfavorably if it is feasible to
reorient the wound in relaxed skin tension lines or to
bring new tissue to reduce abnormal tension. For ex­
ample, z-plasty, flap closure, and serial excision should
be considered after hypertrophic scar excision to pre­
vent tension.
Care must be taken during the surgical excision of
keloid and hypertrophic scars to remove all residual
sources of inflammation that may be trapped in hair fol­
licles, epithelial cysts, sinus tracts, and pilosebaceous
units that could be the source of fibrogenic growth fac­
tors. Again, it is paramount to minimize tissue trauma
and wound tension during surgical reconstruction while
avoiding foreign material, infection, or seroma and he­
matoma that would prevent fibrin clot formation. Intra­
marginal excision of hypertrophic scars and keloids has

93
Chapter 12 Scars and Scar Revisions
been proposed as a useful surgical technique to mini­
mize the recurrence of lesions that have failed nonop­
erative therapy. Similar approaches that maintain rem­
nants of keloid epithelium have been proposed, but
objective trials of this approach are lacking.
Conclusion
Keloids and hypertrophic scarring can largely be
thought of as a fibroproliferative disorder influenced
by local, systemic, and genetic factors. Through deeper
understanding of the physiology of wound healing and
physicochemical principles of scarring, biomedical sci­
ence facilitates the development of new strategies in
treatment and prevention. It is important for practic­
ing physicians and surgeons to be better aware of the
full range of available techniques to control scar forma­
tion and for any medical intervention to be planned in
such a way that potential problems are anticipated and
minimized.
References
1. Lee DE, Trowbridge RM, Ayoub NT, Agrawal DK. High-
mobility Group Box Protein-1, Matrix Metallopro­
teinases, and Vitamin D in Keloids and Hypertrophic
Scars. Plast Reconstr Surg Glob Open 2015;3(6):e425
2. Zhang GY, Cheng T, Luan Q, et al. Vitamin D: a novel
therapeutic approach for keloid, an in vitro analysis.
Br J Dermatol 2011;164(4):729–737
3. Sahbaz A, Aynioglu O, Isik H, Gulle K, Akpolat Fe­
rah M, Cicekler Sahbaz H. Cholecalciferol (vitamin
D3) prevents postoperative adhesion formation
by inactivating the nuclear factor kappa B path­
way: a randomized experimental study. J Surg Res
2015;198(1):252–259
4. Cooke GL, Chien A, Brodsky A, Lee RC. Incidence
of hypertrophic scars among African Americans
linked to vitamin D-3 metabolism? J Natl Med Assoc
2005;97(7):1004–1009
5. Gilman TH. Silicone sheet for treatment and pre­
vention of hypertrophic scar: a new proposal for
the mechanism of efficacy. Wound Repair Regen
2003;11(3):235–236
6. Mustoe TA. Evolution of silicone therapy and mecha­
nism of action in scar management. Aesthetic Plast
Surg 2008;32(1):82–92
7. Harrop AR, Ghahary A, Scott PG, Forsyth N, Uji-Fried­
land A, Tredget EE. Regulation of collagen synthesis
and mRNA expression in normal and hypertrophic
scar fibroblasts in vitro by interferon-gamma. J Surg
Res 1995;58(5):471–477
8. Ghahary A, Shen YJ, Nedelec B, Scott PG, Tredget EE.
Interferons gamma and alpha-2b differentially regu­
late the expression of collagenase and tissue inhibi­
tor of metalloproteinase-1 messenger RNA in human
hypertrophic and normal dermal fibroblasts. Wound
Repair Regen 1995b;3(2):176–184
9. McCauley RL, Chopra V, Li YY, Herndon DN, Robson
MC. Altered cytokine production in black patients
with keloids. J Clin Immunol 1992;12(4):300–308
10. Asilian A, Darougheh A, Shariati F. New combination
of triamcinolone, 5-Fluorouracil, and pulsed-dye la­
ser for treatment of keloid and hypertrophic scars.
Dermatol Surg 2006;32(7):907–915
11. Lee RC, Ping JA. Calcium antagonists retard extracel­
lular matrix production in connective tissue equiva­
lent. J Surg Res 1990;49(5):463–466
12. Lee SY, Park J. Postoperative electron beam radio­
therapy for keloids: treatment outcome and factors
associated with occurrence and recurrence. Ann Der­
matol 2015;27(1):53–58
13. Alster TS, Williams CM. Treatment of keloid ster-
notomy scars with 585 nm flashlamp-pumped
pulsed-dye laser. Lancet 1995;345(8959):1198–1200

CHAPTER
13

Surgical Infections
Jillian M. McLaughlin, Ali Shirafkan, and Linda G. Phillips
For centuries knowledge of infectious diseases rested on
theories, which only recently have been replaced by the
discoveries of science and the advances of technology. Until
the development of bacteriology in the mid-19th century,
the comprehension of infection in Western civilization was
based on theoretical doctrines, and few preventive and
therapeutic approaches had validity. Finally, near the end
of the 20th century, scientific investigation augmented the
understanding of infectious diseases by identifying hun­
dreds of microorganisms and producing a diverse spectrum
of antimicrobial agents for use in prophylactic and thera­
peutic regimens.
Risk Factors for Infection
Risk Factors for Surgical Infections
Infection is defined as the product of the entrance, growth,
metabolic activities, and pathophysiologic effect of micro­
organisms in the tissues of a patient. The normal biologic
state of humans is not germ-free. Both transient and per­
manent flora resides on all skin and mucosal surfaces, all
with the potential to cause infection.
The absence of infection represents equilibrium be­
tween the factors of host resistance and the actions of bac­
teria. Clinical infection may result when this equilibrium is
upset, by either an increase in bacterial inoculums or im­
pairment in the host defense system. Surgical infections can
be divided into two basic categories: infections requiring
surgery and infections following surgery. Recognizing and
minimizing the risk of surgical infection is crucial in mini­
mizing patient morbidity and mortality.
Multiple host factors have been shown to increase the
risk of surgical infection (Box 13.1). Older age is a risk factor
for surgical infection. Studies show that the risk of surgical
infection increases by 1.1% every year between the ages of
17 and 65.1 Immune system senescence, among other fac­
tors, plays a role in increased infection risk.
Hyperglycemia impairs the host immune system. Dia­
betic patients have an overall combined relative risk of 2.2
for surgical infection compared with nondiabetic patients.2
Obesity reflects overall poor health and is often associated
with other factors that cause surgical infection, including
Box 13.1
•• Older age
•• Malnutrition
•• Obesity
•• Diabetes mellitus/hyperglycemia
•• Prior site irradiation
•• Hypothermia
•• Hypoxia (at times secondary to hypoxemia)
•• Coexisting infection remote to surgical site
•• Immunosuppression (genetic, acquired
[infection, malignancy, immunosuppressant
medication, hypothermia, severe nutritional
deficiency, hyperglycemia])
•• Recent operation, especially of the chest or
abdomen
•• Chronic inflammation
•• Nicotine use
Host Factors Known to Increase
Surgical Infection Risk
94

95
Chapter 13 Surgical Infections
hyperglycemia, malnutrition, and tissue ischemia. Studies
have shown a stepwise increase in infection risk with in­
creasing body mass index (BMI) (overweight BMI odds ratio
[OR]: 1.6; obese BMI OR: 2.1; morbidly obese BMI OR: 2.5).3
Malnutrition is the lack of appropriate nutrients necessary
to allow for appropriate synthetic function. This can be in
the form of vitamin deficiency or caloric or protein defi­
ciency. Low albumin (chronic malnutrition) and low pre­
albumin (acute malnutrition) is associated with a higher
risk of wound infection after surgery. Vitamin deficiency,
if suspected, should be treated to decrease the risk of infec­
tion. Early enteral feeding leading to improved nutrition in
the first 48 hours has been shown to be clearly beneficial
in reducing surgical infection risk (55% reduction in risk of
surgical infection).
Nicotine causes direct microvascular vasoconstric­
tion, and indirect pathways of vasoconstriction include the
enhancement of thromboxane A2 and stimulation of cat­
echolamine release. It also causes hypoxemia by decreas­
ing oxygen carrying capacity (because of increased levels
of carboxyhemoglobin) and is found to induce a prothrom­
botic state through multiple different pathways. Smoking
was found to increase the risk of any type of surgical-site
infection by an OR of 1.21.4
Patients with genetic alterations in their immune sys­
tem or acquired alterations in their immune system (as a
result of malignancy, infection, immunosuppressant agents,
older age, malnutrition, or hypothermia, for example) are at
increased risk for surgical infection.
Tissue hypoxia predisposes to surgical infection. Tis­
sue hypoxia can arise from hypoxemia caused by ane­
mia, environmental toxins (i.e., carbon monoxide, meth-
emoglobinemia), or pulmonary shunting (i.e., acute
respiratory distress syndrome), among other causes. Tissue
hypoxia can also arise from poor arterial inflow, as is the case
in peripheral arterial disease, and can arise from direct tissue
compression, or from compression of soft tissue impairing
lymphatic or venous drainage, leading to edema, ischemia,
and other conditions favorable to colonization and infection
by microorganisms. Krizek et al5 quantified the effect of pres­
sure on bacterial count, showing that incisions created in ar­
eas of applied pressure and inoculated with known concen­
trations of organisms allowed for a 100-fold greater bacterial
growth than in areas not subjected to pressure.
Risk Factors Specific to Surgical-Site
Infections
Numerous factors are involved in determining a patient’s
risk for surgical-site infections. These are typically catego­
rized as patient, environment, or treatment factors.
All patient risk factors for infection are risk factors for
surgical-site infection (see Box 13.1). In addition to those
risk factors listed previously, an active remote infection at
the time of an elective operation increases the risk for post­
operative wound infection. These infections typically arise
from the urinary tract, skin, or respiratory tract. Also, stud­
ies show that methicillin-resistant Staphylococcus aureus
(MRSA) carriers are 4.5 times more likely to develop surgi­
cal infections with MRSA than noncarriers. Carriers were
divided into a control group and treatment group with mu­
pirocin. Carriers treated with mupirocin had a significant re­
duction in the rate of surgical-site infection (3.7%) compared
with the control group (5.9%).6
Environmental factors can increase the risk of surgical-
site infection. Inadequate skin antisepsis has been shown
to increase surgical-site infection. Studies comparing skin
antiseptic agents have previously shown chlorhexidine-alco­
hol to be superior to all other skin antiseptics in preventing
both superficial and deep surgical-site infections. However,
subsequent studies have shown no statistically significant
difference in skin antiseptic agents as long as one of the fol­
lowing is used: chlorhexidine, chlorhexidine in isopropyl al­
cohol, povidone-iodine, or iodine-povacrylex in isopropyl
alcohol. Inadequate disinfection and sterilization techniques
have also been implicated in causing increased risk of surgi­
cal-site infection. However, no convincing evidence has been
found to prove that other environmental factors, including
preoperative scrub technique, surgical glove damage, and
barrier materials (e.g., caps, masks, shoe covers) correlate
with postoperative rates of wound infections.
Treatment risk factors have been associated with in­
creased risk of surgical-site infections and can be divided
into those that occur in the preoperative, intraoperative, or
postoperative setting.
Preoperative Infections
In regards to preoperative hair removal, hair shaving dou­
bles the risk of surgical-site infection when compared with
hair clipping. The surgical site is an important factor in
the assessment of surgical infection risk. Surgical sites are
classified as clean, clean-contaminated, contaminated, or
dirty-infected wounds according to the bacterial load of the
wound7,8 (Table 13.1). The American College of Surgeons
National Surgical Quality Improvement Program (ACS-
NSQIP) performed a study on the rates and OR of wound
infection based on the wound classification9 (Table 13.2).
Preoperative antibiotic prophylaxis can reduce the inci­
dence of wound infection in selected cases. To be at an ap­
propriate concentration at the operative site, a prophylactic
antibiotic must be administered before an incision is made—
preferably at least 1 hour before the procedure has begun.
Several clinical trials and cohort studies have evaluated
the efficacy of prophylactic antibiotics in plastic surgery. The
decision to administer prophylactic preoperative antibiot­
ics is not always obvious and requires that the risk factors
for infection (i.e., dirty wound, devastating consequence to
infection, prolonged operative time, implant use) be con­
sidered. The recommendations for antibiotic coverage are
listed in Table 13.3.10

SECTION III GENERAL PROBLEMS
96
Table 13.1 Classification of surgical wounds
Clean
An uninfected operative wound in which no inflammation is encountered and the
respiratory, alimentary, genital, or uninfected urinary tract is not entered. In addition, clean
wounds are primarily closed and, if necessary, drained with closed drainage. Operative
incisional wounds that follow nonpenetrating (blunt) trauma should be included in this
category if they meet the criteria.
Clean-contaminated
An operative wound in which the respiratory, alimentary, genital, or urinary tracts are
entered under controlled conditions and without unusual contamination. Specifically,
operations involving the biliary tract, appendix, vagina, and oropharynx are included in this
category, provided no evidence of infection or major break in technique is encountered.
Contaminated
Open, fresh, accidental wounds. In addition, operations with major breaks in sterile
technique (e.g., open cardiac massage) or gross spillage from the gastrointestinal tract and
incisions in which acute, nonpurulent inflammation is encountered are included in this
category.
Dirty-infected
Old traumatic wounds with retained devitalized tissue and those that involve existing
clinical infection or perforated viscera. This definition suggests that the organisms causing
postoperative infection were present in the operative field before the operation.
Source: Reproduced from Simmons BP. CDC Guidelines on Infection Control. Infect Control 1982;3(2 suppl):187–196.
Table 13.2 Rates and odds ratio of wound infection based on the wound
classification
Clean
Clean-
contaminated
Contaminated
Dirty-infected
Superficial SSI
Rate
Adjusted OR
1.76
Reference
3.94
2.31 (2.23–2.39)
4.75
2.91 (2.77–3.06)
5.16
2.56 (2.42–2.70)
Deep incisional SSI
Rate
Adjusted OR
0.54
Reference
0.86
1.58 (1.48–1.70)
1.31
2.35 (2.14–2.58)
2.1
2.66 (2.42–2.91)
Organ or space SSI
Rate
Adjusted OR
0.28
Reference
1.87
6.66 (6.19–7.18)
2.55
8.47 (7.76–9.25)
4.54
11.81 (10.82–12.88)
Abbreviations: OR, odds ratio; SSI, surgical-site infection.
Source: Reproduced from Ortega G, Rhee DS, Papandria DJ, et al. An evaluation of surgical site infections by wound classification system using the
ACS-NSQIP. J Surg Res 2012;174(1):33–38.
Note: ORs of SSIs are adjusted for patient age category, ethnicity, gender, preoperative comorbidities, and risk factors, sepsis, and emergent proce­
dures.
In clean, elective hand surgery, prophylactic antibiotic
administration does not reduce the incidence of surgical-site
infection in the outpatient population.11 However, antibi­
otic prophylaxis is recommended for patients who undergo
elective surgery using K-wires or implants or who have a
surgery that lasts longer than 2 hours. Also, those patients
undergoing emergency hand surgery are recommended to
receive antibiotic prophylaxis.12
Infections rarely complicate plastic surgical procedures
to correct congenital anomalies. Postoperative wound infec­
tion or dehiscence after cleft lip and palate repair is reported
to be as low as 1.3 to 4.3%. A prospective, randomized, dou­
ble-blind study demonstrated no increased risk when cleft
lip and palate repairs were performed without antibiotic
prophylaxis.13 However, when performing ear reconstruc­
tions, studies support the use of prophylactic antibiotics,

97
Chapter 13 Surgical Infections
studies have demonstrated lower infection rates in groups
treated with prophylactic antibiotics. Fractures within dirty
skin wounds require prophylaxis for S. aureus and other cu­
taneous flora. Fractures communicating with the oral mu­
cosa require prophylaxis for streptococci and the anaerobes
Peptostreptococcus and Clostridium, which are common or­
ganisms of the oral flora.
Studies on septoplasty and rhinoplasty surgery showed
an overall significant reduction in risk of surgical-site infec­
tion with antibiotic prophylaxis versus control (4.9% versus
whether the support construct is formed of cartilage or allo­
plast, because of statistically higher rates of wound infection
for auricular procedures than for procedures involving the
rest of the face.13 If the surgical site involves the ear, an anti-
Pseudomonas fluoroquinolone may be considered to cover
Pseudomonas species.
The treatment of maxillofacial injuries, including facial
fractures and laceration, incurs a moderate risk for infection,
because the placement of hardware within dirty wounds
is often required. In the treatment of open facial fractures,
Table 13.3 Prophylactic antibiotic recommendations for plastic surgery
Type of procedure
Recommended antibiotics
Alternative antibiotics
Hand
Clean
Hardware placement
Open reduction internal fixation
None
Cefazolin
Cefazolin
None
Vancomycin
Clindamycin or vancomycin
Craniofacial
Orthognathic (including cleft lip
and palate) and mandibular,
clean
Orthognathic and mandibular,
contaminated
Hardware placement
Septoplasty or rhinoplasty
Ear reconstruction
Ophthalmic
Cancer-related surgery
None
Cefazolin
Cefazolin or cefuroxime
Cefazolin
Cefazolin + consider fluoroquinolone
Topical neomycin–polymyxin B–
gramicidin
Cefazolin or cefuroxime + metronidazole
or ampicillin–sulbactam
None
Clindamycin
Clindamycin
Clindamycin
Clindamycin + consider
fluoroquinolone
Fourth-generation topical
fluoroquinolones (gatifloxacin or
moxifloxacin): 1 drop every 5–15
min for 5 doses
Clindamycin
Aesthetic surgery
Abdominoplasty, clean
Skin, clean
Skin, clean-contaminated
None
None
Cefazolin
None
None
Clindamycin
Breast surgery
Clean (augmentation, reduction,
reconstruction)
Implant placement
Cancer-related surgery
Cefazolin
Cefazolin
Cefazolin
Clindamycin or vancomycin
Clindamycin or vancomycin
Clindamycin or vancomycin
Microsurgery
All flaps
Cefazolin
Clindamycin or vancomycin
Source: Reproduced from Ariyan S, Martin J, Lal A, et al. Antibiotic prophylaxis for preventing surgical-site infection in plastic surgery: an evidence-
based consensus conference statement from the American Association of Plastic Surgeons. Plast Reconstr Surg 2015;135:1723–1739.

SECTION III GENERAL PROBLEMS
98
Maintenance of intraoperative normothermia has a signifi­
cant effect on the rates of wound infection. Patients with
total intraoperative time (49 minutes) spent below 36°C de­
veloped more surgical-site infections (p = 0.04). One study
showed a relative risk reduction of 57.7% in surgical-site
infection when using systemic warming versus none.22
Glycemic control plays an important role in surgical
patients’ outcome. Hyperglycemia interferes with heal­
ing and increases the infection rates and mortality in pa­
tients undergoing surgery. The risk of postoperative infec­
tions increases by 30% with every 40-point increase from
normoglycemia (less than 110 mg/dL). Studies have shown
chronic (Hgb A1C above 6.5%) and perioperative glucose lev­
els (blood glucose levels higher than 200 mg/dL) were associ­
ated with an increased rate of dehiscence and infection.23 A
statistically significant reduction in surgical-site infections
has been seen with the use of higher intraoperative FiO2
levels. However, a subsequent Cochrane database system­
atic review of 28 randomized clinical trials including 7,597
participants compared a higher intraoperative FiO2 to a rou­
tine FiO2 and found it was not associated with a significant
reduction in surgical-site infections and did not support the
routine use of a high fraction of inspired oxygen during an­
esthesia and surgery.24
Studies have shown that surgical-site infections can be
reduced by 20% with pulsatile lavage.25 High-pressure pulsa­
tile lavage has been evaluated extensively in soft tissue con­
tamination and shown to be seven times more effective in
reducing bacterial load than bulb syringe lavage. The inher­
ent elastic recoil of the soft tissues allows particulate matter
to escape between pulses of fluid. The optimal pressure and
pulse frequency seems to be 50 to 70 lb/in2 and 800 pulses/
min. Adding antibiotics to lavage solutions, although com­
monly practiced, has not been shown to definitively improve
outcomes.
Vacuum-assisted wound closure (VAC) optimizes blood
flow, decreases edema, and aspirates accumulated fluid,
thereby facilitating bacterial clearance. Therefore placement
of a VAC device in the appropriate setting can be helpful in
preventing surgical-site infection.
Postoperative Infections
Appropriate postoperative treatment can also decrease the
risk of surgical-site infection. Despite good evidence for
the use of antibiotic prophylaxis, antibiotic prophylaxis
for more than 24 hours provides no advantage unless there
is definite evidence of a wound infection. In some studies,
use of antibiotics for longer than 24 to 48 hours has been
shown to be harmful.26
The use of drains is controversial. Several studies have
shown that drains placed in clean or clean-contaminated in­
cisions have not shown a reduction in surgical-site infection.
Prolonged drain use may pose an even higher risk; therefore
they should be removed as soon as possible.27
11.3%; OR 0.45; 95% CI 0.24 to 0.86; p = 0.02). Antibiotic
prophylaxis significantly reduces the risk of surgical-site in­
fection in patients undergoing contaminated septoplasty or
rhinoplasty.10
In surgery for head and neck cancer, violation of the oro­
pharynx appears to be a major risk factor for infection. Stud­
ies have demonstrated that infection rates are lower with
the administration of antibiotic prophylaxis (5.8–38%) to
patients undergoing tumor resection that violates the oro­
pharynx versus placebo (24–78%) using a variety of regi­
mens, including cefazolin, third-generation cephalosporins,
and ampicillin plus cloxacillin.14–16 Antibiotics selected for
prophylaxis or treatment in this patient population should
provide coverage for S. aureus, Streptococcus, Peptostrepto­
coccus, and gram-negative organisms.
Infections are relatively common after breast opera­
tions (1–30% of cases), because breast tissue has its own
endogenous flora.17 As a consequence of communication
with the external skin through lactiferous ducts, deep
breast tissue contains a flora similar to that of normal
breast skin.18 The organisms most commonly cultured from
breast tissue include coagulase-negative Staphylococcus
(53%), Propionibacterium acnes (30%), and diphtheroids or
lactobacilli (9%).18 Antibiotic prophylaxis was found to pre­
vent 38% of predicted infections in a prospective, random­
ized, multicenter study of 2,587 cases of reduction mam­
moplasties, lumpectomies, and mastectomies.19 A recent
Cochrane review found prophylactic antibiotics beneficial
in all procedures related to breast cancer.20 Also, antibi­
otic prophylaxis was found to significantly reduce the risk
of surgical-site infection in patients undergoing cosmetic
breast surgery.10
There are few studies evaluating antibiotic prophylaxis
for aesthetic surgery. Studies have shown that for clean sur­
gery of the skin, antibiotic prophylaxis did not significantly
reduce surgical-site infection. Findings were similar for pa­
tients who underwent clean abdominoplasty. Therefore an­
tibiotic prophylaxis is not recommended for patients who
undergo clean abdominoplasty.10 At this time, it is unknown
whether patients who undergo clean-contaminated skin op­
erations need antibiotic prophylaxis.
There is a paucity of data addressing the use of preop­
erative antibiotics in free-flap reconstruction. Studies per­
formed on patients undergoing oncologic head and neck re­
constructive surgery and lower extremity reconstruction
after traumatic injury show that preoperative antibiotics are
effective in reducing surgical-site infections. Microsurgeons
generally agree that this data should be extrapolated to all
free-flap reconstructions and recommend preoperative an­
tibiotic prophylaxis.21
Intraoperative Infections
Prolonged surgical time increases surgical-site infection
risk, the rate of which doubles with each hour of surgery.

99
Chapter 13 Surgical Infections
treatment by opening the infected portion of the wound
usually suffices, antibiotic therapy may be necessary when
the infection is not well localized. A penicillinase-resistant
penicillin or cephalosporin provides reliable S. aureus cover­
age. Given the higher incidence of MRSA, coverage for this
must be considered, particularly in patients with a history
of MRSA infection.
The number of wound infections caused by Staphylo­
coccus epidermidis, which is a normal component of the
skin flora, is increasing. The presence of this organism in
wounds containing a foreign body (prostheses) is a reason
for concern. A penicillinase-resistant penicillin or cephalo­
sporin is required for adequate coverage of this organism,
because strains resistant to penicillin are becoming increas­
ingly common. If the infection involves a wound that con­
tains a prosthesis, successful treatment may require removal
of the prosthetic device. This is well described by the case
presented in Fig. 13.1. The patient was managed accord­
ing to the algorithm in Fig. 13.2 with appropriate antibiotic
therapy and wound care before reconstruction.
Wound infections caused by gram-negative bacilli are
increasing in frequency. Because the incubation period is
7 to 14 days, many patients are at home when the infec­
tion becomes evident. Infections caused by gram-negative
organisms are associated with less erythema, edema, and
pain than are staphylococcal infections. Instead of local in­
flammation, systemic signs, including fever or tachycardia,
develop. Aminoglycosides and third-generation cephalospo­
rins provide consistent gram-negative coverage, and quino­
lones are an acceptable alternative when oral administra­
tion is desired.
Infections with group A streptococci can run a fulmi­
nant course after initial presentation and diffuse cellulitis,
lymphangitis, or lymphadenopathy. An area of rapidly ad­
vancing erythema with a raised, delineated border char­
acterizes the cellulitis. Large, blood-filled blebs may form
around the primary focus of infection, with the potential
for local breakdown and progression to gangrene or necro­
tizing fasciitis if untreated (see discussion later in chapter).
Streptococcal cellulitis usually responds to high doses of
parenteral penicillin.
Infections caused by enterococci, S. faecalis, or other
group D streptococci are less invasive than those caused by
group A streptococci. Enterococcal infections are usually
mixed, with enteric gram-negative organisms present. Thus
enterococcal infections should be treated with ampicillin
and aminoglycoside.
Soft Tissue Infections
Organisms that cause surgical-site infections are often the
cause of surgical soft tissue infections. The two gram-pos­
itive cocci, S. aureus and Streptococcus pyogenes (group A),
account for most skin and soft tissue infections. S. aureus
invades skin and causes impetigo, folliculitis, cellulitis, and
furuncles. Elaboration of toxins by S. aureus causes the le­
sions of bullous impetigo and staphylococcal scalded skin
syndrome. The streptococci are secondary invaders of trau­
matic skin lesions and cause impetigo, erysipelas, cellulitis,
Diagnosing and Managing
Specific Infections
Summary Box
Common Surgical Infections
•• Surgical wound infection
•• Soft tissue infection
•• Necrotizing fasciitis and gas gangrene
•• Marine exposure
•• Diabetic foot infections
•• Osteomyelitis and septic arthritis
•• Animal bites
•• Snake, scorpion, and spider bites
Surgical Wound Infection
Although the risk of surgical-site infections is low, they
comprise the largest portion (38%) of nosocomial infections.
Anatomically, infections can be categorized as superficial,
deep, or organ or space infection28 (Box 13.2). Depending
on the location, they can present differently. Superficial in­
fections present with the four signs of inflammation:
1. Calor
2. Dolor
3. Rubor
4. Tumor
or
1. Heat
2. Pain
3. Redness
4. Swelling
Deep infections have pus or an abscess with wound tender­
ness and fever. Deep infections can dehisce incision edges,
exposing deeper tissues. Organ or space surgical-site infec­
tions occur within a body cavity and are directly related to
the surgical procedure but may occur at the surgical site
(mimicking incisional surgical-site infections) or at distant
sites. Diagnosis of organ or space surgical-site infections re­
quires postoperative imaging to confirm the site and extent
of infection.
S. aureus causes many wound infections. The incubation
period for S. aureus infection is 4 to 6 days. These infections
tend to be localized with initial erythema, edema, pain,
and eventual abscess formation. The pus is usually thick,
creamy, white or yellow, and odorless. Spread to lymph
nodes is unusual, but bacteremia is common. Fever and leu­
kocytosis may be present. Furthermore, exotoxin release
in S. aureus infection can lead to toxic shock syndrome,
characterized by fever, rash, desquamation, involvement of
three or more organ systems, and hypotension. Although

SECTION III GENERAL PROBLEMS
100
prevalence of MRSA. If clinically appropriate, oral antibiotics
(typically sulfamethoxazole/trimethoprim, clindamycin, or
doxycycline) are prescribed for a total of 5 to 7 days.
Hidradenitis suppurativa is a relapsing, inflammatory,
suppurative disease believed to result from chronic super­
infection of the apocrine sweat glands. It is most commonly
seen in the axillary region, but the groin and perineum may
also be affected. The most common isolated organisms for
hidradenitis suppurativa are S. aureus and viridans strepto­
coccus. Medical treatment is typically in the form of topical
antiseptics, topical antibiotics, and systemic antibiotic treat­
ment with agents effective against S. aureus and viridans
streptococcus. Typically, a macrolide or tetracycline can be
prescribed, but in areas with a high rate of MRSA, clindamy­
cin can also be considered.
Surgical treatment can offer long-term resolution of this
disease but requires complete excision of the hair-bearing
and lymphangitis.
Acute soft tissue infections of the hand are diagnosed
based on anatomic location but are also caused by these two
organisms. Hand cellulitis is acute inflammation of the skin
and subcutaneous tissues. A paronychia is an abscess of the
soft tissues surrounding the nail. A felon is an abscess of the
pulp of the thumb or fingertip. A volar or deep space ab­
scess is an abscess formed within one of the potential deep
spaces of the hand. Potential deep spaces in the hand in­
clude the midpalmar space, the thenar space, the hypothe­
nar space, the web space (known as a collar-button abscess),
and Parona’s space. Flexor tenosynovitis is an abscess within
the flexor tendon sheath. Emergency incision and drainage
in the operating room are required for most cases of soft tis­
sue infection of the hand. Antibiotic treatment with intrave­
nous antibiotics is typically recommended, and vancomycin
is typically used as the first-line treatment, given the high
Box 13.2
Superficial Incisional
Infection occurs within 30 days after the operation
and involves only the skin or subcutaneous tissue of
the incision and at least one of the following:
1. Purulent drainage, with or without laboratory con­
firmation, from the superficial incision.
2. Organisms isolated from an aseptically obtained
culture of fluid or tissue from the superficial inci­
sion.
3. At least one of the following signs or symptoms of
infection: pain or tenderness, localized swelling,
redness, or heat; superficial incision is deliberately
opened by surgeon, unless incision is culture-
negative.
4. Diagnosis of superficial incisional surgical-site in­
fection (SSI) by the surgeon or attending physician.
Deep Incisional
Infection occurs within 30 days after the operation if
no implanta is left in place or within 1 year if implant
is in place and the infection appears to be related to
the operation and involves deep soft tissues (e.g., fascial
and muscle layers) of the incision and at least one of the
following:
1. Purulent drainage from the deep incision but not
from the organ or space component of the surgical
site.
2. A deep incision spontaneously dehisces or is delib­
erately opened by a surgeon when the patient has
at least one of the following signs or symptoms:
fever (higher than 38°C), localized pain, or tender­
ness, unless the site is culture-negative.
3. An abscess or other evidence of infection involving
the deep incision is found on direct examination,
during reoperation, or by histopathologic or radio­
graphic examination.
4. Diagnosis of a deep incisional SSI by a surgeon or
attending physician.
Organ or Space
Infection occurs within 30 days after the operation if no
implanta is left in place or within 1 year if implant is in
place and the infection appears to be related to the op­
eration and infection involves any part of the anatomy
(e.g., organs or spaces) other than the incision, that was
opened or manipulated during an operation, and at
least one of the following:
1. Purulent drainage from a drain that is placed
through a stab woundb into the organ or space.
2. Organisms isolated from an aseptically obtained
culture of fluid or tissue in the organ or space.
3. An abscess or other evidence of infection involving
the organ or space that is found on direct examina­
tion, during reoperation, or by histopathologic or
radiographic examination.
4. Diagnosis of an organ or space SSI by a surgeon or
attending physician.
Types of Surgical-Site Infection
Source: Adapted from Mangram AJ, Horan TC, Pearson ML, et al; Centers for Disease Control and Prevention (CDC) Hospital Infection Control Practices
Advisory Committee. Guideline for prevention of surgical site infections, 1999. Am J Infect Control 1999;27(2):97–132; quiz 133–134; discussion 96.
aNational Nosocomial Infection Surveillance definition: a nonhuman-derived implantable foreign body (e.g., prosthetic heart valve, nonhuman vascu­
lar graft, mechanical heart, or hip prosthesis) that is permanently placed in a patient during surgery.
bIf the area around a stab wound becomes infected, it is not an SSI. It is considered a skin or soft tissue infection, depending on its depth.

101
Chapter 13 Surgical Infections
Fig. 13.1 Augmentation mammoplasty surgical-site infection (SSI). (a) This 59-year-old woman with a history of augmentation mammo­
plasty developed implant rupture 10 years after placement and later developed an infection with implant extrusion (20 years after place­
ment). Her only risk factor for developing an SSI was being a cigarette smoker. (b) The wound infection shows evidence of implant extru­
sion. (c) Left breast implant removal; the implant is grossly purulent. (d) Wound débridement. (e) One week postoperative follow-up. (f)
Evidence of continued purulence requiring additional débridement and antibiotic treatment before reconstruction.
a
b
c
d
e
f
Wound
Quantitative culture
Multiple core biopsy
≤105 organisms
Reconstruction with muscle,
flap primary closure,
split thickness skin graft,
random flap
Débridement,
continued wound care,
repeat quantitiative cultures,
intravenous antibotics,
cellulitis or systemic symptoms
Primary closure
or reconstruction
Single core biopsy
Rapid slide analysis
>105 organisms
Acute setting before primary
closure or reconstruction
Any
organism
No
organism
Uncomplicated wound
Large or
chronic wound
Fig. 13.2 Algorithm for the evaluation of a suspected wound infection

SECTION III GENERAL PROBLEMS
102
Similar to necrotizing fasciitis, this can rapidly progress.
The mortality rate of V. vulnificus infections is as high as
18%, but fatality can be prevented with early diagnosis
and treatment.29 Alcoholism, liver disease, hereditary he­
mochromatosis, and immunosuppression place patients
at a higher risk for development of V. vulnificus infection.30
Treatment of V. vulnificus includes initiation of appropriate
antibiotic therapy (tetracycline or fluoroquinolone in com­
bination with a third generation cephalosporin)31 along
with urgent surgical débridement of devitalized tissue.
Mycobacterium marinum is the most common atypical
mycobacterium seen in hand infections. It usually presents
as a chronic draining skin lesion. It is also a common cause
for chronic tenosynovitis. It can mimic flexor tenosynovitis,
causing symmetrical swelling of the finger and semiflexed
positioning of the involved digit but differs from suppurative
flexor tenosynovitis by the absence of pain. It can also cause
symptoms of carpal tunnel if infection is present within
the carpal canal. Granuloma formation with negative fun­
gal staining and rice bodies can be helpful diagnostic clues.
Culture in Lowenstein-Jensen medium at 31°C takes up to 8
weeks for positive identification. Antibiotic therapy should
be initiated with minocycline, clarithromycin, and etham­
butol when this infection is suspected. At times, adjunctive
surgical intervention is necessary.
Diabetic Foot Infections
It is estimated that 12% of adults in United States have dia­
betes.32 Hyperglycemia impairs humoral immunity (e.g.,
impaired neutrophil chemotaxis, phagocytosis, intracel­
lular killing) and monocyte-macrophage function and
favors bacterial proliferation. Hyperglycemia also leads
to peripheral neuropathy because of the destruction of
Schwann cells in peripheral nerves. Patients with diabetes
mellitus are particularly prone to diabetic foot infections
(DFIs). These infections usually occur as a consequence of
skin ulceration from ischemia or trauma to a neuropathic
foot. The compartmentalized anatomy of the foot, with its
various spaces, tendon sheaths, and neurovascular bundles,
allows ischemic necrosis to affect tissues within a compart­
ment or spread along anatomic tissue planes (Fig. 13.3).
skin of the affected area and use of skin grafts or local tissue
flaps for reconstruction. Even after complete resection and
reconstruction, this disease can still recur.
Necrotizing Fasciitis and Gas Gangrene
Necrotizing soft tissue infections (NSTIs) are severe surgi­
cal-site infections and true emergencies. The incidence of
NSTIs is estimated to be 1,000 cases annually in the United
States.28 Necrotizing fasciitis is classified into two types.
Type 1 is polymicrobial, and type 2 is caused by β-hemolytic
streptococcus alone or in combination with other bacte­
ria. Although this can occur after any surgical procedure,
in plastic and reconstructive surgery, cases of necrotizing
fasciitis are commonly reported after liposuction. Accord­
ing to data reported in the literature, the overall incidence
of necrotizing fasciitis after liposuction is equal to 0.4 per
100,000 patients.
They typically present early in the postoperative period,
usually within 1 to 3 days postoperatively. Signs are similar
to cellulitis or abscess. Cutaneous vesicles or bullae may be
present. In many cases, pain is present beyond the border of
erythema. Infection that initially arises from the upper levels
in the skin rapidly propagates deeper into the adipose, fascia,
and muscle. Chills, fever, tachycardia, sweats, prostration,
and other signs of toxemia are common.
Differential diagnosis of necrotizing fasciitis includes
Fournier’s gangrene or gas gangrene. Fournier’s gangrene
is necrotizing fasciitis that originated from the perineum.
Gas gangrene is typically only differentiated by how rapidly
fatal it is (death can occur within 12 hours). Organisms of
the Clostridium species cause gas gangrene; Clostridium per­
fringens is the most common.
Early diagnosis and treatment are critical steps in man­
agement. Because the cutaneous manifestations are not il­
lustrative of the severity of the disease in the deep tissues,
the diagnosis is often delayed. The gold standard for diag­
nosis is a small incision with operative exploration to evalu­
ate the adherence of the fascia to the surrounding tissues.
The surgeon will be able to effortlessly slide a finger along
the fascial plane. If an exudate is present, the characteristic
exudate is thin and watery.
When in doubt, surgical exploration with débridement
is indicated. The mortality rates are high and range from
20 to 70% but decrease to 4.2% after immediate surgical in­
tervention.28 Medical therapy with intravenous vancomy­
cin, piperacillin/tazobactam, high-dose penicillin G, and
clindamycin (antitoxin against Clostridium) should be initi­
ated any time necrotizing fasciitis is suspected.
Marine Exposure
Patients with a history of recent exposure to marine envi­
ronments can present with a unique set of infections. Vib­
rio vulnificus is a species of gram-negative, motile, curved
bacterium found in the coastal waters of the United States.
Infections caused by V. vulnificus result in painful cellulitis.
Fig. 13.3 Diabetic foot infection.

103
Chapter 13 Surgical Infections
also be used; the sensitivity and specificity are 81% and 93%,
respectively. Plain-film X-ray is not very specific for osteo­
myelitis and has a sensitivity and specificity of 88% and 32%,
respectively (Fig. 13.4).
To treat and prevent the recurrence of osteomyelitis, ag­
gressive débridement of overlying soft tissue and devitalized
bone must be performed in addition to long-term antibiotic
treatment (typically 4–6 weeks) of organisms isolated from
bone biopsy. The most common pathogens include Staphy­
lococcus species and Streptococcus species, but gram-neg­
ative, anaerobic, and polymicrobial infections are possible
(patients with decubitus ulcers, patients with diabetes mel­
litus, other immunocompromised states). When appropriate,
flap reconstruction should be considered.
Animal Bites
Animal bites are a common problem in the United States,
with 2 to 5 million occurring each year. Dog bites account for
80 to 95% of animal bites and occur more often in men and
children (median age 7 years). Cat bites account for 5 to 15%
of animal bites and occur more often in women and adults
(median age is 20 years).35 Cat and dog bite infections have
a complex microbiologic mix, with Pasteurella as the most
common isolate. Common aerobes isolated include strep­
tococci, staphylococci, Moraxella, and Neisseria; common
anaerobes include Fusobacterium, Bacteroides, Porphyromo­
nas, and Prevotella. Patients are most often treated with a
combination of a β-lactam antibiotic and a β-lactamase in­
hibitor, such as amoxicillin and clavulanic acid.
Infection rates after cat bites range from 50 to 75%.35
This is typically attributed to the fine, sharp teeth of cats,
which produce puncture wounds and penetrate deeply into
the soft tissues and joint capsules of the hand. These wounds
can seal almost immediately. Therefore wounds should be
sufficiently opened and washed out. If rabies is a concern,
washing the wound with povidone iodine will significantly
lesson the likelihood of rabies infection. Although rabies is
uncommon in cats and dogs in the United States, the ani­
mal should be quarantined to ensure it does not show signs
Acute infections are usually caused by gram-positive
cocci. S. aureus is the most important pathogen in DFIs. It is
often present as a monomicrobial infection, but it can also
be caused by polymicrobial infections. Chronic wounds, re­
current infections, and infections in hospitalized patients
are more likely to harbor complex flora, including aerobic
and anaerobic flora. Among gram-negative bacilli, bacteria of
the family Enterobacteriaceae are common, and Pseudomo­
nas aeruginosa may be isolated from wounds that have been
treated with hydrotherapy or wet dressings. Enterococci may
be recovered from patients treated previously with a cepha­
losporin. Anaerobic bacteria seldom cause DFIs as the sole
pathogen but may be isolated from deep infections or ne­
crotic tissue. Antibiotic-resistant bacteria, especially MRSA,
may be isolated from patients who have received antibiotics
previously or who have been hospitalized or reside in long-
term care facilities. Recurrent infections are common, and
15 to 27% of affected patients require resection of infected
bone and, at times, amputation.33
Osteomyelitis and Septic Arthritis
Infections of the joint and bone typically occur from direct
extension of soft tissue infection, penetrating injury with
direct bacterial inoculation, or open fracture. In pediatric
patients in particular, hematogenous spread from infection
elsewhere can cause septic arthritis and osteomyelitis.
Septic arthritis is infection of the joint space. Synovial
fluid analysis with evidence of a white blood cell count
(WBC) above 50,0000/mm3 with 75% neutrophils strongly
suggests septic arthritis. Patients will typically present with
a swollen, erythematous joint held in a distracted position
and will have severe pain in the joint with passive range of
motion. Early diagnosis and treatment with antibiotics and
surgical exploration is crucial to prevent permanent joint
destruction. The most common pathogens include Strep­
tococcus species, Staphylococcus species, and Haemophilus
influenzae. In adults, Neisseria gonorrhoeae should also be
considered.
Osteomyelitis is a destructive infection of the bone.
Patients with a history of chronic infections, nonhealing
wounds, or bony nonunions should be evaluated for osteo­
myelitis. Bone biopsy is the definitive diagnostic method to
determine the presence of osteomyelitis. The pathologic ex­
amination of bone biopsy specimen remains the most accu­
rate method of diagnosing osteomyelitis underlying pres­
sure ulcers. Lewis et al34 demonstrated that core needle
bone biopsy is both sensitive and specific for the diagnosis
of osteomyelitis, 73% and 96%, respectively. Bone biopsy has
been shown to be highly sensitive and specific in predicting
which patients undergoing reconstruction with a flap are at
an increased risk for developing postoperative complications
consistent with osteomyelitis. Magnetic resonance imaging
can determine the extent of involvement; the sensitivity and
specificity are 91% and 78%, respectively. Fluorodeoxyglu­
cose positron emission tomography (FDG-PET) imaging can
Fig. 13.4 Osteomyelitis.

SECTION III GENERAL PROBLEMS
104
Coral snakes are responsible for a minority of snake­
bites in the United States.36 The coral snake, Micrurus ful­
vius, found in the southern United States from North Caro­
lina to West Texas, are typically secretive and nonaggressive.
They rarely bite unless provoked, and they envenomate by
chewing their victims rather than injecting. Coral snake bites
are neurotoxic. Often they present as painless, tiny puncture
wounds with negligible surrounding tissue change and are
easy to miss. Systemic symptoms are much more profound
and deadly, with the risk of cranial nerve palsies, respiratory
paralysis, and death. Once systemic symptoms are present,
they are difficult to reverse. Therefore any patient suspected
of being bitten by a coral snake should receive antivenin.
The brown recluse spider (Loxosceles reclusa) is one of
two species of North American spider capable of envenom­
ation. It is generally found throughout the southern United
States. The brown recluse spider bite initially causes local­
ized muscle pain and cramping. Next, blistering, ischemia,
and ulceration may be seen and can ultimately lead to tissue
necrosis. Antibiotic treatment is recommended, and dapsone
100 mg daily for 14 days has been a preferred treatment be­
cause it has both bacteriostatic and bactericidal properties.
However, this must be weighed with the potential side ef­
fects of dapsone in certain patient populations (i.e., hemo­
lysis, methemoglobinemia).
The black widow spider (Latrodectus mactans) is the
other North American spider species capable of envenom­
ation. It is found throughout the United States but is more
commonly found in the south. The black widow spider bite
initially causes sharp pain at the site of two small red spots
(puncture sites) because of a neurotoxic agent. Late findings
include diffuse musculoskeletal pain and cramping, abdomi­
nal pain, vomiting, tremor, and excessive salivation. Treat­
ment is typically aimed at treating symptoms of pain and
muscle cramping with appropriate analgesia and muscle
relaxants. If pain is unbearable or if the patient is immuno­
compromised, black widow spider antivenin (Lyovac) can be
considered, but it is rarely used.
In the southwestern United States, six species of scor­
pions can cause medically significant injuries from a sting.
Affected patients initially have localized severe pain and
hyperesthesia because of the venom’s neurotoxic effects.
Adults can typically be managed symptomatically with cold
compresses over the injured area. However, the neurotoxin
also results in activation of the autonomic nervous system
and depolarization of the neuromuscular junctions. This can
lead to blurry vision, strabismus, dyspnea, wheezing, dys­
phagia, urinary or fecal incontinence, opisthotonos, fever,
and involuntary muscle contractions. These symptoms can
be particularly pronounced in pediatric patients. Admis­
sion is recommended for all pediatric patients with scor­
pion stings for appropriate monitoring given the potential
for airway compromise, sedation, and severe pain. Scorpion
antivenin can be administered if available.
In all bites and stings, antibiotic treatment and tetanus
prophylaxis should also be considered.
of rabies. Should the animal develop signs of rabies, post­
exposure prophylaxis should be initiated. However, if the
animal cannot be located, postexposure prophylaxis should
be considered.
In all patients, tetanus immunization either with booster
or immunoglobulin should be considered depending on the
patient’s immunization history and whether the wound ap­
pears tetanus-prone or not.
Human bites can result from both purposeful and unin­
tentional injury and are more prone to infection than other
animal bites. Clenched fist human bites are the most prone
to infection and typically present with lacerations over the
third, fourth, and fifth metacarpophalangeal joint or proxi­
mal interphalangeal joints of the dominant hand. Patients
who present with this injury pattern have sustained a hu­
man bite unless proven otherwise and must be aggressively
treated. Even if there are no signs of infection, the wound
must be explored to rule out injury to the extensor tendon,
joint capsule, and cartilage. Infecting pathogens of human
bites comprise aerobes including Streptococcus and Staphy­
lococcus species and anaerobes such as Eikenella, Fusobac­
terium, Prevotella, Peptostreptococcus, and Porphyromonas
species.
Snake, Scorpion, and Spider Bites
Venomous snakes are responsible for biting an estimated
seven thousand people in the United States every year. Ap­
proximately 98% of venomous snakebites are caused by
the Crotalidae (pit viper) family of snakes, which includes
rattlesnakes, copperheads, and cottonmouths.36
Not all bites cause envenomation. If fang marks are pres­
ent along with rapid swelling of the extremity, envenom­
ation should be assumed. Immediate first aid should con­
sist of patient reassurance, immobilization of the affected
limb, and placement of the limb on a level plane, but most
important is transportation of the patient to the hospital as
soon as possible.
Snake venoms can be classified as hemotoxic (attack­
ing tissue and blood) or neurotoxic (damaging or destroy­
ing nerve tissue). Pit viper snake venoms are hemotoxic. The
venom causes hemolysis, capillary endothelial cell damage,
third spacing and swelling, and tissue necrosis. Pit viper bites
are classically painful with local swelling and necrosis. Rarely,
patients can develop tense edema of the affected extremity
causing compartment syndrome. If compartment syndrome
develops, fasciotomy is indicated. More commonly, surround­
ing tissue necrosis is present. Immediate débridement of ne­
crotic tissue is not indicated because at times, envenomated
necrotic tissue can recover. Snake venom can greatly worsen
myonecrosis and therefore snake antivenin should be admin­
istered to those patients who do not exhibit allergic sensitiv­
ity. Life-threatening systemic reactions have rarely occurred
but are more common in pediatric patients. This typically
presents as disseminated intravascular coagulation, acute
renal failure, hypovolemic shock, and death.

105
Chapter 13 Surgical Infections
Infections Requiring Plastic
Surgery
The initial management of infected wounds involves ob­
taining quantitative cultures to identify and quantify the
bacteria present. Growth of more than 105 colony-forming
units (CFU) per gram of tissue or per milliliter of wound
fluid is considered as infection. After determination of the
offending organisms by qualitative and quantitative cul­
tures, specific antibiotic therapy can be selected. Topical
antimicrobials can be used to decrease the local bacterial
count in preparation for reconstruction. Débridement of
devitalized tissue may be necessary to control the infec­
tion, improve healing, or prepare for reconstruction (Video
13.1). See Fig. 13.2 for further details on wound manage­
ment.
Soft tissue flaps are believed to possess an antibacterial
property that is independent of vascularity. Applications of
soft tissue flaps include the following:
•• Treatment of open traumatic fractures
•• Osteomyelitis
•• Median sternotomy wounds (Fig. 13.5)
•• Exposed prosthetic joints
•• Vascular prosthesis
•• Abdominal mesh
•• Chronic open wounds
Fig. 13.5 Sternal wound dehiscence.
One such case is illustrated in Fig. 13.6.
Calderon et al37 popularized muscle flaps for use in
the reconstruction of wounds with chronic osteomyelitis.
Muscle flaps were shown to improve blood flow and thus
the delivery of oxygen, immune factors, and systemic anti­
biotics. In an animal model study, Gosain and colleagues38
demonstrated increased oxygen tension in the distal por­
tion of muscle flaps compared with random flaps. Muscle
Fig. 13.6 (a–d) A chronic nonhealing wound 2 years after a lumpectomy. This 53-year-
old woman had a lumpectomy for left-side localized breast cancer and underwent che­
motherapy and radiation therapy postoperatively. She had several risk factors for de­
veloping a surgical-site infection: obesity, insulin resistance, and a history of radiation
exposure. At presentation she had a chronic draining infected seroma cavity. Cultures
were positive for Pseudomonas aeruginosa (more than 105 colony-forming units). She
was treated with antibiotics and Dakin’s solution 0.025% with wet to dry dressings until
repeat quantitative and qualitative cultures were negative.
d
a
c
b

SECTION III GENERAL PROBLEMS
106
Fig. 13.6, cont’d (e–j) Latissimus dorsi flap reconstruction. (e) Preoperatively, the patient was placed in the standing position to delineate
the borders of the latissimus dorsi muscle. (f) The wound was thoroughly débrided and irrigated. (g) Excision of the wound. (h) The remain­
ing soft tissue defect was measured. (i) The skin island was positioned in the center of the muscle, and dissection proceeded just under the
fascia in all directions, keeping the deep layer of fat attached to the muscle. The thoracodorsal neurovascular bundle was identified and the
thoracodorsal nerve was divided. (j) The muscle was flipped into the axilla, avoiding kinking of pedicle, and the flap was prepared for inset­
ting. (k,l) The latissimus dorsi muscle provided well-vascularized tissue to the ischemic chest wall and provided adequate bulk to obliterate
the dead space. The patient had complete resolution of infection on subsequent follow-up.
f
g
e
Iliac crest border
Tip of scapula
h
k
l
j
Cephalad
Subcutaneous fat
Latissimus
dorsi m.
i
Thoracodorsal
neurovascular
bundle
Latissimus
dorsi m.
Serratus
anterior m.

107
Chapter 13 Surgical Infections
equal to or superior to that of muscle in treating infected
wounds or complex defects with bone exposure.
Conclusion
In treating surgical infections, surgeons encounter two types
of problems: infections occurring in wounds from their own
surgeries and infected wounds referred to them. Risk factors
for surgical infection have been identified, and evidence-
based recommendations have been provided to help prevent
infection. Recognition of surgical infection and initiation of
appropriate treatment is essential to limiting patient mor­
bidity and mortality. The field of plastic and reconstructive
surgery continues to develop innovative technology and op­
erative procedures that potentiate the host’s ability to resist
or overcome infection. These therapies have been highly
successful in providing patients who have surgical infections
with innovative and excellent outcomes.
flaps were found to be superior to random flaps in eliminat­
ing bacteria from the wound bed. In a separate study, they
compared bacterial growth within the wound fluid at the
interface of musculocutaneous and fasciocutaneous flaps
and found that despite a higher blood flow and tissue oxy­
gen tension in the fasciocutaneous group, muscle exhibited
a greater ability to reduce the bacterial count. Moreover, his­
tologic examination revealed greater evidence of wound re­
pair, including increased collagen deposition, at the muscle
interface.
Muscle flaps were generally believed to be superior to
fasciocutaneous flaps. Fasciocutaneous flaps, however, of­
fer significant advantages, including simplicity, availability,
and versatility, replacing “like with like” without sacrificing
muscle function. Subsequent studies evaluating fasciocuta­
neous flaps in the treatment of infected wounds have been
promising. Treatment with fasciocutaneous flaps has been
so successful that researchers have suggested that they are
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Accessed on July 3, 2017
Discussion by William Lineaweaver
The chapter identifies three specific interventions that
plastic surgeons can expertly provide to manage surgi­
cal infection: (1) ablation, (2) reconstruction, and (3)
prophylaxis.
Ablation
After a diagnosis of a surgical infection, the treating
surgeon should promptly move toward ablation. Re­
moval of the primary site of infection limits site-spe­
cific damage and aborts the systemic inflammatory
cascades of sepsis.
The history of the management of necrotizing fasci­
itis illustrates the primacy of ablation. In 1924 Meleney1
reported a series of patients with necrotizing fasciitis
treated with prompt, thorough incision, drainage, and
débridement. His management was undertaken with­
out benefit of anesthesia, intravenous fluids, or antibi­
otics, but 15 (75%) of his 20 patients survived.1 In 1952
Wilson2 (who appears to have coined the term “necro­
tizing fasciitis” based on the anatomic definition of the
infection) reported 23 patients treated with aggressive
surgical débridement enhanced with anesthesia, intra­
venous fluid replacement, and penicillin. Of his 23 pa­
tients, 21 (91%) survived. Recent reports of treatment
of this disease, complete with all 21st century adjuncts,
still include mortality rates of 9 to 25%.3 Sarani et al4
concluded in a recent review of necrotizing fasciitis that
“mortality is directly proportional to time of [surgical]
intervention.” Surgical excision of infected tissue there­
fore remains as the most important single element in
the treatment of surgical infection. An unfavorable re­
sult at this stage of management is generally related to
incomplete and delayed ablation.
The plastic surgeon brings expanded dimensions
to the strategy of ablation. Wide incision, drainage,
and débridement of necrotizing fasciitis can be daunt­
ing in its magnitude, but the procedure itself is tech­
nically straightforward. Infections in more complicated
circumstances can require sophisticated interventions
based on thorough anatomic knowledge. I once de­
scribed hand infections as “a chess match between the
infecting agents and the surgeon, [with] the patient’s
anatomy being an intricate board.”5 A plastic surgeon
can approach a hand infection with confident strate­
gies of access to tissue planes, bursal spaces, and ten­
don sheaths (Fig. 13D.1).

109
Chapter 13 Surgical Infections
Furlow6 has described plastic surgeons as being “in­
terested in using solutions to problems in one anatomic
area to solve problems in other areas . . . .” This wide
scope of practice certainly applies to a plastic surgeon’s
ability to deal with surgical infections throughout the
body. The plastic surgeon can use a broad set of skills to
explore the anatomies of the face, neck, extremities, and
surgical sites to address the specific locations of surgical
infections.2 Table 13D.1 summarizes the sites of surgical
infections treated in a single series of patients managed
by plastic surgeons.7
Reconstruction
The plastic surgeon’s ability to proceed to reconstruc­
tion even further amplifies the potential for definitive
ablation of surgical infections. The example of tibial os­
teomyelitis serves to make this point.8 Resection of all
involved bone and chronically scarred soft tissue can
be pursued most aggressively with the reconstructive
options of local and microsurgical flaps available to
provide secure coverage and limb salvage9 (Fig. 13D.2).
Beyond defining greater limits of ablation, reconstruc­
tive options can also be integrated into plans to opti­
mize progress toward functional recovery. Table 13D.2
describes the variety of reconstructive procedures
Fig. 13D.1 This patient presented with a neglected pulp ab­
scess of his middle finger. Pus traveled down the flexor sheath
to the midpalmar space, the carpal tunnel, and the deep volar
forearm, all of which required drainage. The radiocarpal joint
was also involved, and dorsal incision with débridement of the
distal pronator muscle and the volar wrist capsule were neces­
sary to drain this space.
Table 13D.1 Sites of surgical
infections
Body region
Cases
Head and neck
14 (9.5%)
Trunk and pelvis
58 (39.5%)
Upper extremity
32 (21.8%)
Lower extremity
43 (29%)
Total
147
Source: Reproduced from Lineaweaver WC, Hui K, Yim K, et al. The
role of the plastic surgeon in the management of surgical infection.
Plast Reconstr Surg 1999;103:1553–1560.
Table 13D.2 Reconstruction
procedures applied to surgical
infection sites after ablation
Primary closure
5
Delayed closure
18
Split-thickness skin graft
15
Full-thickness skin graft
2
Local skin flaps
11
Fasciocutaneous flap
17
Local muscle flaps
26
Microsurgical flaps
28
Flap revisions
4
TOTAL
126
Source: Reproduced from Lineaweaver WC, Hui K, Yim K, et al. The
role of the plastic surgeon in the management of surgical infection.
Plast Reconstr Surg 1999;103:1553–1560.
Fig. 13D.2 This patient initially underwent soft tissue and tibial
resections for long-standing osteomyelitis and chronic scars.
Closure was initially deferred to obtain pathology readings on
the tissue specimens. The medial gastrocnemius muscle was
mobilized for insertion into the bone cavity. Further closure was
achieved by advancing posterior calf tissue as a fasciocutaneous
flap. (Reproduced from Lineaweaver WC, Jacob S, Yan H, et al.
Wound cultures as predictors of complications in reconstructive
flap procedures. Ann Plastic Surg 2011;66:572–574.)

SECTION III GENERAL PROBLEMS
110
Table 13D.3 Effects of wound
bed cultures and antibiotic
prophylaxis on complication
rates of flap procedures
Culture
Uncomplicated
cases
Complicated
cases
−
92%
8%
+
51%
49%
+, effective
antibiotics
91%
9%
+, ineffective
antibiotics
44%
56%
Source: Reproduced from Lineaweaver WC, Jacob S, Yan H, et al.
Wound cultures as predictors of complications in reconstructive
flap procedures. Ann Plastic Surg 2011;66:572–574.
applied to the surgical infection sites listed in Table
13D.1.7 The range of conventional and microsurgical
strategies allows the surgeon to match a procedure to
the details of the wound, deficit, or deformity created
by infections and their treatments.10 An unfavorable
result at this level of treatment can result from faulty
problem analysis, poor procedure selection, or techni­
cal inadequacies.
Prophylaxis
Given the great variety of infections and treatments
available to plastic surgery practice, the plastic sur­
geon should be in a position to productively investi­
gate strategies of prophylaxis when surgical infections
contribute to measurable rates of complications. In a
study of flap procedures performed for acute closure of
excised defects, I found that in my practice, flaps ap­
plied to wound beds with negative bacterial cultures
had a complication rate of 8%, whereas flap procedures
done to wound beds with a positive culture had a 49%
rate of complications. Within the series of flaps done
for defects with positive bacterial cultures, however,
patients who empirically received prophylactic antibi­
otics effective against wound bed bacteria had a signifi­
cantly lower complication rate (9%) than patients who
did not receive antibiotics effective against the bacteria
that eventually grew from the wound bed cultures (57%
complication rate, p < .004 compared with the effec­
tively covered patients).10 These data (summarized in
Table 13D.3) suggest that, in populations of patients
undergoing acute flap reconstruction, positive defect
bed cultures can serve as predictors of complications
Fig. 13D.3 Effective use of prophylactic antibiotics requires defi­
nition of procedures at risk for infection, identification of organ­
isms likely to be involved, and coordinated timing of antibiotic
administration and the surgical procedure.
and that effective antibiotic prophylaxis can substan­
tially decrease complications associated with positive
bacterial cultures taken at the time of flap inset10 (Fig.
13D.3).
A surveillance system established to track organ­
isms cultured from past cases could be used to select
antibiotics likely to be effective in current cases and
establish a data-based system for choosing appropri­
ate prophylactic antibiotics. Based on such large, di­
verse patient populations, plastic surgeons could de­
velop frameworks for specifying prophylactic antibiotic
guidelines that could be applied to surgical sites, indi­
vidual practices, and different surgical strategies. Unfa­
vorable results in the prophylaxis of surgical infection
can result from ineffective antibiotic selection, antibi­
otic complications resulting from unnecessary antibi­
otic administration, and failure to recognize clinical
circumstances in which prophylactic antibiotics could
reasonably be used.
Conclusion
Plastic surgeons have a wide scope of practice and
can therefore effectively treat surgical infections in
almost all anatomic sites. Reconstructive strategies al­
low plastic surgeons to undertake aggressive ablation
and integrate this level of treatment with salvage and
functional rehabilitation. Analysis of plastic surgery
practices can generate large amounts of data that can
be used to identify clinical circumstances with signifi­
cant levels of complications related to surgical infec­
tions and provide empirical foundations for effective
antibiotic prophylaxis in high-risk circumstances.

111
Chapter 13 Surgical Infections
References
1. Meleney F. Hemolytic streptococcus gangrene. Arch
Surg 1924;9:317–364
2. Wilson B. Necrotizing fasciitis. Am Surg 1952;18(4):
416–431
3. Gunter OL, Guillamondegui OD, May AK, Diaz JJ. Out­
come of necrotizing skin and soft tissue infections.
Surg Infect (Larchmt) 2008;9(4):443–450
4. Sarani B, Strong M, Pascual J, Schwab CW. Necrotizing
fasciitis: current concepts and review of the litera­
ture. J Am Coll Surg 2009;208(2):279–288
5. Lineaweaver W. Hand infections. In: Cohen M, ed.
Mastery of Plastic and Reconstructive Surgery. Bos­
ton: Little Brown; 1994:1467–1479
6. Furlow LT Jr. Plastic surgery: generic or proprietary?
Plast Reconstr Surg 1992;90(6):1059–1060
7. Lineaweaver WC, Hui K, Yim K, et al. The role of the
plastic surgeon in the management of surgical infec­
tion. Plast Reconstr Surg 1999;103(6):1553–1560
8. Anthony JP, Mathes SJ, Alpert BS. The muscle flap in
the treatment of chronic lower extremity osteomyeli­
tis: results in patients over 5 years after treatment.
Plast Reconstr Surg 1991;88(2):311–318
9. Lineaweaver WC. Problem analysis in reconstructive
surgery. In: Wei FC, Mardini S, eds. Flaps and Recon­
structive Surgery. Philadelphia: Saunders-Elsevier;
2009:4–7
10. Lineaweaver WC, Jacob S, Yan H, Zhang F. Wound cul­
tures as predictors of complications in reconstruc­
tive flap procedures. Ann Plast Surg 2011;66(5):572–
574

CHAPTER
26
112
The skin is the largest organ of the human body and through
its numerous complex functions provides a protective bar­
rier against the environment. It can protect against harmful
chemicals, pathogenic organisms, and ultraviolet radiation
while at the same time regulating temperature, maintain­
ing water balance, and producing Vitamin D. A disrupted
skin barrier provides a unique challenge to the clinician,
because wound healing is a complex and intricate process.
Management of wounds places a tremendous burden
on patients’ quality of life while also contributing signifi­
cantly to health care costs. An estimated 6.5 million people
in the United States suffer from chronic wounds each year,
amounting to an estimated 6 to 15 billion dollars in annual
U.S. health care costs.1 With an aging population present­
ing with various comorbidities (i.e., diabetes mellitus), there
has been a striking increase in the number of patients seek­
ing treatment for wound-related problems. Because of these
various factors, cutaneous wound healing has become an
important topic of ongoing research and debate on an inter­
national level. There is tremendous pressure on the medi­
cal system to provide and develop cost-effective therapies.
Wound healing involves many complicated and delicate
interactions to successfully transition from an acute phase
to the subsequent proliferation and remodeling phases.
When ideal local and systemic conditions are not met, acute
wounds have the potential to move from the acute to chronic
wounds, requiring the clinician to have a thorough under­
standing of outside interventions to bring these wounds
back into the healing cascade.
Avoiding Unfavorable Results
and Complications in Wound
Management
Understanding the Wound-Healing
Cascade
Optimal management of wounds requires a complete un­
derstanding of the wound-healing cascade. Humans, like
other mammals, are evolutionarily optimized for expedient
healing in suboptimal, dirty conditions. Consequently, the
end result of wound healing is scar formation with contrac­
tion and replacement of a defect with a collagen-rich ma­
trix, as opposed to regeneration of damaged or lost tissue.2
The process of wound healing has been divided into
three phases that may occur in sequence or simultaneously:
1. Inflammation
2. Proliferation
3. Maturation
Hemostasis, which has been described as its own phase
or as a component of inflammation, occurs initially with
local vasoconstriction, activation of the extrinsic coagula­
tion pathway, and formation of a fibrin plug that forms a
scaffold for platelet aggregation. Platelets contribute to the
subsequent inflammatory phase by producing cytokines
(i.e., tumor growth factor-β [TGF-β] and platelet-derived
Wound Management
Aditya Sood, Vasanth S. Kotamarti, and Mark S. Granick
CHAPTER
14

113
Chapter 14 Wound Management
Patient-Specific Considerations
Understanding the pathophysiology contributing to a
specific wound includes the contributing patient factors.
Diabetes is one of the most common etiologies of chronic
wounds. Long-term hyperglycemia leads to the develop­
ment of neuropathy, microvascular and macrovascular
disease, and capillary and arteriole basement membrane
thickening. Patients often repeatedly traumatize insensate
areas, and vascular disease contributes to local ischemia.
Hyperglycemia further affects the physiology of the wound
environment through the formation of advanced glyca­
tion end-products (AGEs), changes in cell morphology and
function, and alteration of immune function and cytokine
expression in the wound environment. Management of hy­
perglycemia in diabetic patients has been shown to have a
significant impact on healing times of leg and foot ulcers.4
Chronic venous insufficiency (CVI) is another common
cause of chronic wounds and is therefore important to rec­
ognize for its unique implications in wound treatment. CVI
may originate from venous reflux or obstruction. Although
reflux is the more prevalent cause in CVI-related ulceration,
obstruction carries a higher risk of ulcer development and a
more rapid disease course. Both mechanisms establish dis­
ease by elevating hydrostatic pressure in the venous system,
which leads to inflammation and a subsequent increase in
ambulatory venous pressure. Altered shear stress and me­
chanical forces placed on both the microscopic and mac­
roscopic venous systems in CVI induce proinflammatory
responses from the endothelium that directly contribute
to ulcer development. Inflammation, with the subsequent
expression of matrix metalloproteinases (MMPs) and cy­
tokines, damages not only venous structures including the
glycocalyx, endothelium, vein wall, and vein valve, but also
surrounding tissues like the dermis. Destruction of the der­
mis eventually leads to skin changes and ulcer formation.
growth factor [PDGF]).3 Infiltration of leukocytes follows,
with neutrophils arriving within a few hours and serving
both an antimicrobial function as well as a proteolytic func­
tion. Within two days, macrophages (attracted by platelets
in the fibrin clot), keratinocytes at the wound edge, fibro­
blasts, and other monocytes arrive and perform most of the
débridement of nonviable tissue necessary for the advance­
ment of the healing process. In addition to their phagocytic
role, macrophages are essential as antigen-presenting cells
and possibly as sources for numerous potent growth fac­
tors. Ironically, studies have suggested that neutrophils
may not be necessary for proper wound healing, but the
absence of macrophages results in significant healing dis­
ruption.2
The proliferative phase begins with the arrival of fibro­
blasts 48 to 76 hours after injury. Within the first week, fi­
broblasts begin to produce extracellular matrix for granu­
lation tissue formation by depositing type III collagen, and
the collagen content of the wound increases until around 6
weeks. During this time, keratinocytes and endothelial cells
proliferate, creating granulation tissue and epithelialization
on the surface. Fibroblasts migrate along new vessels cen­
trally into the wound, facilitating the complete coverage of
the wound bed with granulation tissue.
Remodeling and maturation is characterized by reorga­
nization and replacement of the randomly oriented type III
collagen typical of granulation tissue with linearly oriented
type I collagen associated with scar tissue. This process con­
tinues until the ratio of type III to type I collagen is 4:1, equal
to that of normal skin. Fibroblasts in the wound differentiate
into myofibroblasts, theorized to cause wound contraction,
which serves to reduce the size of the defect or wound. Dur­
ing this time, T cells play an important role in overcoming
local infections. By 2 years, the process of wound maturation
is complete, and the tensile strength of the new scar tissue
is around 80% of the preinjury state.3
Summary Box
Factors Impeding Wound Healing
Endogenous
•• Local tissue hypoxia
○
○Chronic venous insufficiency (CVI)
○
○Peripheral arterial occlusive diseases (PAOD)
○
○Microangiopathy
○
○Disturbed lymphatic drainage
•• Chronic metabolic disorder
○
○Metabolic disorder
○
○Malnutrition
•• Immune system dysfunction
•• Neoplasm
○
○Primary tumors
○
○Metastases
Exogenous
•• Colonization with microbes
•• Persistent necrosis
•• Trauma
•• Chemical/physical agents
○
○Chemical agents
○
○Drugs
○
○Ionizing radiation
○
○Chronic mechanical forces
○
○Thermal

SECTION III GENERAL PROBLEMS
114
by leukocytes (especially neutrophils), endothelial cells, and
fibroblasts. Although normally functioning to target and de­
stroy pathogens, ROS unchecked in chronic wounds directly
damage cell membranes and structural proteins, promoting
the expression of proinflammatory cytokines, chemokines,
and proteolytic enzymes.2
Both local and systemic factors may contribute to
chronic wound development. Infection is the most com­
monly implicated factor.9 Other local factors include tissue
hypoxia and edema, repeated trauma, history of irradiation,
and presence of necrotic tissue. Systemic factors include dia­
betes mellitus, malnutrition, immunodeficiency, and cer­
tain medications.9 Local tissue hypoxia is caused by impaired
perfusion and edema, which may result from chronic ve­
nous insufficiency (CVI), peripheral arterial occlusive dis­
eases (PAOD), microangiopathies, and disturbed lymphatic
drainage. The three most common causes of chronic wounds
are CVI, diabetes mellitus, and pressure necrosis.2
Chronic wounds increase the risk for neoplastic transfor­
mation of local tissues through an unclear mechanism.2 The
most common neoplasm presenting in chronic wounds is
squamous cell carcinoma, suggesting that keratinocytes are
especially vulnerable to malignant transformation.2 These
lesions most often present as an enlarging ulceration in a
preexisting chronic wound or scar (i.e., Marjolin’s ulcer). A
primary tumor, especially in sun-exposed areas, or meta­
static tumor can also present as a nonhealing wound. Biop­
sies of suspicious wounds are warranted.
Managing Unfavorable Results
and Complications in Wound
Management
Evaluation of Wound Care Needs
Any patient with a chronic wound requires a thorough his­
tory and examination before embarking on a course for
therapy. Preexisting concurrent illnesses, such as diabe­
tes, malnutrition, renal failure, and immunosuppression,
need to be optimized. In 2004 a framework for creating an
optimal wound bed was developed using the current un­
derstanding of wound physiology, and the principles were
organized into the acronym “TIME.”10,11 (Box 14.1). These
guidelines help to direct the removal of exogenous barriers
A mainstay of CVI-related ulcer treatment is compression
therapy. Patients may also benefit from endovascular and
surgical management which target both ulcer healing and
prevention of ulcer recurrence.5
Another important consideration is patients’ nutritional
status. Malnourished patients cannot meet the high met­
abolic demands required for wound healing and have im­
paired immune function.6
Patient age is another important factor to consider in
wound healing; an impaired stress response has been noted
with increasing age. Cells in the local wound environment
experience a significant stress from inflammation, reac­
tive oxygen species, proteolytic environments secondary
to bacteria, ischemia, and ischemia-reperfusion cycles. An
adequate stress response is therefore necessary for the cells
in the wound environment to respond appropriately. How­
ever, elderly patients are known to respond poorly to severe
stresses like major burns, and aged cells have been noted to
experience broadly altered gene expression that results in
impaired response to stresses. Aged cells may more rapidly
enter a state of replicative senescence in response to expo­
sure to stress and cytokines. A potential way to address this
issue is aggressive débridement, which removes cells in the
wound margins that may have lost replicative potential and
converts a chronic wound into an acute wound.7
Acute Wound Versus Chronic Wound
Acute Wound
An acute wound is one in which the normal healing pro­
cess as described previously progresses normally without
disruption. These wounds can be from penetrating or blunt
trauma, chemical exposure, temperature exposure, en­
venomation, surgical or iatrogenic causes, and others. The
mechanism of injury determines the nature of the damage
and thus may affect the necessary interventions. Common
to all types of wounds, management involves preparation
of the wound for optimal healing and prevention of chronic
wound development.8
Chronic Wound
Chronic wound development is the most prevalent wound-
healing problem in humans. Failure to progress through
the normal phases of wound healing result in persistent
disruption of the skin barrier. These wounds remain in a
chronic inflammatory state instead of forming and remod­
eling new tissue. This deregulated inflammation is pro­
moted by unbalanced proteolytic activity and a highly pro-
oxidant environment.
Matrix metalloproteinase (MMP) expression from ac­
tivated keratinocytes at the wound edge, fibroblasts, endo­
thelial cells, and macrophages is induced by proinflamma­
tory cytokines. Not only does excess MMP activity impair
the production of new matrix, but it also targets and inacti­
vates growth factors. The highly pro-oxidant environment
is a consequence of reactive oxygen species (ROS) formation
Box 14.1
T = Tissue management
I = Infection/inflammation control
M = Moisture balance
E = Edge of wound
Framework for Creating
the Optimal Wound Bed