Atlas Phẫu Thuật Thẩm Mỹ (Tập 2) – Atlas of Cosmetic Surgery

49
Imaging  •  Chapter 5
can be automatic or manual. Auto-white balance (AWB) relies
on the decisions made by the image processor within the cam­
era. Though this is a simple and convenient feature, it is NOT
recommended for medical photography because the results
often vary (Fig. 5-4B). The preferred method is to white bal­
ance the camera as outlined in the camera manual, and save
that white balance setting or profile. Once the white balance
profile is created, it can be used for all photographs taken in
that particular room. Since the necessary steps needed to cre­
ate a custom white balance profile vary greatly among digital
cameras, one should consult the camera owner’s manual.
Megapixels
Digital cameras use light-sensitive electronic image sensors
rather than film to capture a photograph. Megapixels is a term
used to describe how many millions of ‘picture elements’ (pix­
els) are captured by the image sensor. The more megapixels a
camera is capable of recording, the more detail an image will
have. However, purchasing a camera with the most megapixels
available is not necessarily the best option for cosmetic surgery
use. Capturing more megapixels per image increases file size,
image storage times, and image transfer times. Larger files
require additional storage space on both the camera’s memory
card and computer’s hard drive, and can make computers
perform slowly when using image editing software. Although
cameras currently available can take photographs of greater
than 15 megapixels, cameras operating at a mere 1.5–2.5
megapixels often produce images of sufficient resolution for
cosmetic surgery documentation. Slightly higher numbers of
megapixels are recommended for publication or if the image
will be enlarged at a later time for detailed observation.
Submitting images for publication
Modern medical textbooks and journals are now almost all
being produced using digital publishing systems. For this
reason, they can easily accept digital images for submission.
However, most publishers specify parameters for submis­
sion. Authors should refer to the ‘instructions for authors’
section of the publisher’s website or publication and com­
ply with the resolution requirements. Most journals allow
(or require) submission of prints in addition to digitally sub­
mitted images. This step enables accurate color reproduc­
tion. Authors may also be asked to provide signed consent
forms from patients who may be identified from submitted
pictures.
Resolution
In the printing and publication industry, resolution is
generally specified in pixels per inch (ppi). The more ppi
printed on paper, the finer the quality of the reproduction
will appear. For example, a 1×1 inch photograph printed
at 72 ppi will have 72×72 (5184) small dots creating the
image. A 1×1 inch photograph printed at 300 ppi will have
300×300 (90 000) small dots creating the image of the exact
same size. The image printed at 300 ppi will appear more
detailed because it provides more visual information. Dig­
ital images displayed on a computer monitor are generally
at 72 ppi because most computer monitors operate at this
resolution. However, many printers can handle much higher
ppi settings. Digital images that appear large and grainy at
‘100% zoom’ (72 ppi) on a computer monitor can still print
quite nicely, albeit much smaller, at high ppi settings. The
resolution can be changed using a variety of photo-editing
Fig. 5-4  Properly white balanced image
(A) versus auto white balanced image
(B) not correcting for ‘cool’ color ­temperature
of fluorescent lighting in room. (Images
­courtesy of Derm.md [)
A
B

50
Chapter 5
Evaluation of the cosmetic surgery patient
applications. Changing the ppi will not alter the size of the
file because it will still contain the same amount of infor­
mation. For example, a 100 ppi photo that measures 2×2
inches can be converted to a 200 ppi image. The new image
will be 1×1 inch, but the file size will remain unchanged. It
is important to note that different ppis are ideal for different
situations.
For PowerPoint™ presentations, 72 or 150 ppi is a more
than adequate resolution, but for print publication at least
300 ppi is generally necessary to minimize the graininess of
photos. Each publication, whether a journal or textbook, lists
the requirements for submitted images (Table 5-1).
Cataloging digital images
As important as it is to take excellent-quality, consistent
photography, it is equally important to be able to retrieve
those images when they are needed. There are many
­methods which can be used to catalog images. ­Rudimentary
filing systems based upon creating folders on a computer
with patient names or other identifying information have
been used for years. However, this type of filing system
lacks good search capability. There are countless software
solutions available for the cataloging of digital images.
Most cameras come with basic software to do this. There
are several good free or shareware packages available such
as Picasa (Google, Inc., Mountain View, CA) or ACDSee
(ACD Systems International Inc., Miami, FL). These allow
cataloging images by keywords, search features, and image
editing features.
In an office environment, it is helpful to be able to access a
central repository of images from many computers to avoid
duplicating the image database on every computer. For this,
there are a variety of network-ready medical image database
solutions such as Mirror (Canfield Scientific Inc., Fairfield, NJ)
or an application service provider (ASP) model such as
ImageStore for Healthcare (Through The Lens, Inc., Portola
Valley, CA). The difference between network software and
ASP software is that the network software has to be installed
and maintained on computers in the office. When updates
are necessary, they must be installed at the office. On the
other hand, ASP software is not purchased; rather it is paid
for by a monthly subscription. The software and images are
securely accessible via any computer with an Internet con­
nection. Updates to the software are done by the ASP and
are seamless and automatic. Since all of the data is stored
off site, it is protected from unfortunate events at the office.
Many software packages are going to the ASP model includ­
ing electronic health record (HER) software, since it lowers
the physician’s up-front costs and electronic headaches with­
in the office. When choosing an ASP, look for companies with
a growing user base, frequent technology updates, automatic
back-up guarantees, data security insurance, and an option
to have your data sent to you on media such as DVDs for
­additional safekeeping.
Videography
Videography is emerging as an increasingly useful tool in cos­
metic surgery. It can be an invaluable tool to teach residents
and peers the finer technical points of increasingly complex
procedures. It also has the potential for use as an educational
tool for patients to help them better understand the nature of
a procedure. It is important to edit the video used for patient
education into a succinct presentation highlighting the gen­
eral points, while avoiding details that may be found to be
distasteful to a layman. Prior to showing a video to patients,
be sure to ask if they would like to see some footage of the
procedure to better understand what is involved.
• In cosmetic dermatology, monitoring and
documenting both subtle and drastic changes
over time is vital for publishing, research,
­education, and medicolegal reasons. Since
SLR cameras allow for control of many more
settings than compact cameras, they are
the better choice for capturing images with
consistent settings.
• When choosing a macro lens, select one with
a 1:1 or 1:2 subject to film reproduction ratio
and a focal length of 60–100 mm.
• To achieve the most consistent lighting ­during
clinical photography, flash photography is
­recommended. When purchasing an auxiliary
flash unit, select one with a guide number (GN)
of 80 or higher (at ISO 100).
Pearls
• The ‘automatic’ modes in modern SLR and
­compact cameras can produce excellent
results, but inconsistencies in settings made
­automatically by cameras can result in images
that may be difficult to compare. Avoid this by
using manual settings when possible.
• Disable or avoid using the ‘digital zoom’ feature
on one’s camera, since it artificially zooms in by
discarding surrounding image data, resulting in
a lower resolution image. It is best to always use
the optical zoom.
• Avoid the auto white balance feature on the
­camera. It can result in inconsistencies in
the color of the images. Use the manual white
­balance procedure for the camera to set the
white balance for office photography.
• Taking all of office pictures at a very high
­resolution can result in high storage space
needs and long transfer times in moving
images from camera to computer and ­retrieving
the images for viewing. Setting the camera
at 2–2.5 megapixels is adequate for most
­dermatologic office photography.
Pitfalls

51
Imaging  •  Chapter 5
Like photography, videography has made some major
advances in the past decade. Digital format tapes have
become commonplace at the consumer and professional level.
Software for editing digital video is included with practically
all computer operating systems including Mi����������������
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rosoft Windows
and the Mac OS.
While the principles of videography share many similar
aspects with photography, there are some important differ­
ences to note when recording surgical procedures. First, there
must be a clear line of view from the camera to the ­surgical
field at all times during the surgery. This can be accomplished
with several different methods. An assistant dedicated to film­
ing the procedure can move with the camera to vantage points
that allow a clear view of the field. This can be challenging
for the assistant and dangerous in a procedure room since the
likelihood of contamination of the field goes up with the addi­
tional individual in the room trying to get a view of the field.
The preferred method is to use mounting equipment for the
digital video camera such as a jib that suspends the camera
near the field, clamps that mount the camera to the overhead
OR lights (Fig. 5-5), or a high tripod which affords a high view
of the surgical field. All allow a consistent view of the field
with minimal shaking of the camera, allowing for a more
­professional look of the video.
Selecting a video camera depends on the needs of the sur­
geon. Higher-end digital consumer cameras can provide all of
the major features to film basic videos for instructional or edu­
cational use. Look for features such as a firewire and USB-2
connections to easily connect the camera with a computer,
manual white balance, and image stability to minimize image
shake in case the tripod or mount is accidentally bumped dur­
ing taping. A wireless remote is also an essential to pause and
restart the recording or adjust the zoom without inducing cam­
era shake from the pressing of on-camera buttons. A 3 CCD
camera uses three digital sensors instead of one, allowing for
greater color accuracy in video. For even better video resolu­
tion, one can choose a high definition (HD) video camera. This
allows recordings in HD quality. Though rarely necessary for
routine procedures, it may be beneficial for very detailed proce­
dures or to accurately demonstrate microsurgical techniques.
Table 5-1  Reviews guidelines for submitting images to four different dermatology journals as of early 2007
Journal
Photo type
Min. resolution*
Color
mode
Acceptable
formats
Unacceptable
­formats
Archives of
Dermatology
Color
350 ppi at 5” wide
RGB
EPS, JPG (highest
­quality), PSD,
and TIF (without
compression).
BMP, GIF, PCT, and
PNG. No ­images in
Word or ­PowerPoint
files. (May label
images in Power­
Point, but must
submit original photo
too).
Black & White
350 ppi at 5” wide
RGB,
Grayscale
Dermatologic ­Surgery
Color
300 ppi at 5” wide,
1200 ppi with line art
CMYK
Color photos should
be submitted as TIF
or JPG. B&W photos
should be TIF.
Embedded photos
in Word, PowerPoint,
Adobe Illustrator.
(However, line draw­
ings may be made in
these programs).
Black & White
300 ppi at 5” wide,
1200 ppi with line art
Grayscale
Journal of the ­
American Academy
of Dermatology
Color
300 ppi at 5” wide,
1200 ppi with line art
CMYK
EPS, JPEG, PDF,
TIF. Must be created
in graphics software
(e.g. Adobe Photo­
shop, Adobe Illustrator).
Photos and graphics
made in presentation
software (e.g. Power­
Point, ­Microsoft
Word, CorelDraw,
Harvard Graphics).
Black & white
300 ppi, 1200 ppi
with line art
CMYK,
Grayscale
Lasers in Surgery
and Medicine
Color
300 ppi, 600 ppi
with line art
CMYK
Unspecified file
format requirements.
Make sure image
colors mode is
CMYK.
RGB images.
Black & white
300 ppi, 600 ppi
with line art
CMYK,
Grayscale
*Photos that have thin lines/arrows, text, or other ‘drawn’ objects are typically considered to contain ‘line art.’ This may make it necessary to have higher-resolution
images.
This information is subject to change. Review the current ‘instructions for authors’ section for each journal or textbook prior to submitting images.

52
Chapter 5
Evaluation of the cosmetic surgery patient
Lighting
Good lighting is essential during surgical procedures. This can
be provided by the standard surgical lights in the procedure
room. If these are to be used, it is important to perform a
manual white balance using the surgical lighting. Otherwise,
a yellow-orange hue may be present in the recording. Alter­
natively, the surgeon may choose to use less-intense external
lighting. These are standard commercial grade videography
lights which can be mounted on a tripod or with clamps and
project softer light through a diffuser. This is often preferred
when filming minor procedures in examination rooms such as
laser procedures, filler injections, and neurotoxin injections.
These lighting set-ups are relatively inexpensive, light, and
portable.
Audio
There are two options for audio recording that may be used
when filming a procedure. Either the live audio recording can
be played back with the video, or the audio can be narrated
over the original video. Most often, narrations are done at a
future time because the actual video is generally edited down
to remove repetitive and unnecessary scenes. If discussion
during filming is kept to a minimum, the audio track from the
filming can serve as a background for the narration to keep it
sounding natural. This is particularly important for laser pro­
cedures where the sound of the laser firing is important for the
viewer to hear. If live audio is to be used in the final recording,
do not rely on the built-in microphone of most video cameras.
To capture the best audio, the preferred method is to use a
wired or wireless external microphone which can be affixed
to the surgeon’s mask or collar of the gown. This allows for
a clear recording of the voice with minimal ambient sound
from the operating room.
DISCUSSION
Photography tips and techniques
• Obtain a signed informed consent form from the patient
before taking any medical photographs.
• Results are most consistent when there is an ­examination
room dedicated to photography. However, if a ­dedicated
­studio room is not a possibility, good technique can
­compensate for photographs taken in different lighting
­conditions.
Just as patients grant their consent for a procedure, they must
also grant consent to be photographed. Often, the photog­
raphy consent verbiage can be integrated into the procedure
consent form. It should clearly state that the patient allows the
photographs to be used for a variety of purposes ­including
publication and that the patient forfeits any rights to pay­
ments or royalties that may accumulate with use of the image.
Sample photography consent forms, such as those available at
local medical schools and from professional photographers,
can help an office design a photography consent to be inte­
grated into the standard consent forms. Once drafted, it is
advisable to have an attorney review the form. To avoid sepa­
ration of the signed consent from the patient’s pictures, be
sure to ­photograph the consent prior to taking pictures.
Fig. 5-5  A video camera mounting arm fastened with a clamp
to overhead surgical lighting. Care must be taken not to exceed
the weight limits of the surgical lighting arms. Also, clamps must
be ­ ­secured well to avoid having the equipment fall into the surgical
field. (Image courtesy of Derm.md [)
• Edit videos used for patient education to show
only the detail needed to help patients under­
stand the procedure. Too much detail may be
found to be distasteful to sensitive audiences.
• Often, the best way to film a procedure is by
using mounting equipment to allow a favorable
vantage point for the camera. This is usually
from above on a jib or mounted to surgical lights
or mounts.
• When selecting a video camera, look for features
such as a firewire and USB-2 connections to
easily connect the camera with a computer,
manual white balance, and image stability to
minimize image shake in case the tripod or
mount is accidentally bumped during taping.
Pearls
• Dangling cords and caps from cameras can
easily contaminate a surgical field. Be sure to
remove or secure these prior to filming a proce­
dure.
• White balancing prior to turning on the surgical
lights can result in poor color quality. Be sure to
white balance the video camera with the lighting
which will be used during filming.
PITFALLS

53
Imaging  •  Chapter 5
Consistent imaging is important in medical and surgical
photography. Implementing standardized procedures for
photography in a cosmetic surgery office is the best way to
ensure that photographs are consistent. Although it is often
not possible in a very busy practice or in situations where
space is at a premium, creating a secure, private location
in the office that can be used exclusively for photography is
optimal. In designing a studio, emphasis should be placed
on patient comfort, patient privacy, image consistency,
image quality, equipment security, and record-keeping con­
venience. An ideal studio space would meet the following
requirements:

• Spacious. Enough room to fit the entire patient or area of
interest (e.g. face only) into the view of the camera. The
necessary distance between patient and camera will vary
based upon the lens used.

• Lighting. There should be enough light to illuminate the
subject, but not so much that it overwhelms or suppresses
the flash, resulting in comprise of the color balance.

• Window covers. In rooms with windows, opaque
blinds or curtains help ensure patient privacy and keep
ambient light consistent. Otherwise, lighting conditions
can change throughout the day with the sun’s position and
cloud cover.

• Background. Choose a nonreflective solid color such as
black, light blue, gray or green.

• Patient privacy and comfort. Providing patients with
gowns and a private area to change and hang their clothes
reduces anxiety and is appreciated by the patients.

• Equipment security. A locked cabinet or closet that
contains the camera and other accessories ensures that all
items necessary will be at hand. Measuring devices (rulers)
should also be readily available.

• Batteries. Be sure the camera battery charger is near the
storage cabinet for the camera. Ideally, it will be plugged
in and charging a back-up camera battery in case of
failure of the primary battery. Lithium-ion rechargeable
batteries are the best value at this time.

• Writing space. A small desk or table in the photography
area is useful when writing relevant information for the
photographs during the session (e.g. into a log book).
­Clipboards should be available for patients to sign the
consent forms.
The emphasis on consistency of the images used in cos­
metic procedures cannot be overstated. Without consistency,
accurate representations of the results of cosmetic treatments
or procedures cannot be obtained. In addition to the tips men­
tioned previously, a key variable to control between pictures is
the positioning of the patient. Tape or other markings on the
floor can direct the patient and the photographer to stand in
the appropriate locations and standardize distances between
the subject and camera. Log books can document the poses,
camera settings, and exposures made for each patient. Refer­
ring back to the log book can ensure that the same conditions
are used for follow-up pictures. In addition, previous pictures
should be available for comparison when taking follow-up
pictures. The pictures for comparison should be displayed
on a computer screen or printed and placed in the patient’s
chart.
With digital photography, the best way to initially estab­
lish appropriate camera settings is by trial and error. Settings
should be determined for various shooting distances from the
subject. To easily access these standardized settings, they can
be written on a small piece of paper and taped to the back
of the camera or flash. Some high-end digital SLR cameras
allow custom ‘profiles’ of settings to be saved and retrieved
with ease. Once standard settings are established, any staff
member should be able to take consistent photographs.
Instructing the staff on how to eliminate distracters from the
field of view is essential. Using a standard background elimi­
nates most of the distracters behind the patient. Additionally,
clothing, jewelry, and make-up should also be removed when
possible. A black ‘bib’ can be used to cover the clothing and
shoulders of a patient for facial photography. If an irrelevant
object appears in the viewfinder before taking a picture, move
it or take note that it should be cropped out later.
Facial photography of the cosmetic
­patient
Before-and-after photographs provide critical comparison for
the cosmetic practitioner and patient. These photos can help
assess the outcome for the procedure and may help deter­
mine whether or not additional treatments may be beneficial.
When subtle changes are not recognized by the patient, they
can be objectively pointed out by referring to the before-
and-after images. Another situation where before-and-after
photographs are very useful is when a patient complains of
facial asymmetry after a treatment. Often, the asymmetry was
present before the procedure, but is noticed by the patient
only after the treatment. Using the before images, pre-existing
asymmetry can easily be demonstrated to the patient.
To help maintain consistent poses for facial photographs,
a few strategies can be implemented. First, staff should be
instructed on how to position patients for standard photo­
graphic poses. The patient’s body should be turned and aligned
with the direction that they are facing at all times to prevent
distortion of the neck and jaw line. A photographic technique
commonly used by facial surgeons involves five standard views
for each photo session. The five standard views include: right
lateral face, right oblique face, frontal face, left oblique face,
and left lateral face (Fig. 5-6). Since patients differ in height,
it may be necessary to alter the vertical distance between the
camera and the ground. A good rule of thumb is to keep the
lens pointing directly at the mid-face of the patient. However,
the horizontal distance between the patients and the camera
should remain relatively constant for all facial photographs.
This can be achieved by having the photographer and patient
stand at fixed distances from one another by using tape or

54
Chapter 5
Evaluation of the cosmetic surgery patient
other markers on the floor. Taking photos of frontal and
­lateral views of the face is self explanatory. To standardize
oblique views, the most prominent edge of the distal cheek
should be aligned with the distal tip of the nose.
Some cosmetic surgeons prefer to use positioning equip­
ment to consistently position the patient. Chin rests and posi­
tioning aids at fixed distances can be used to help standardize
the pictures. These devices allow exact positioning and subject­-
to-camera distance for every photograph. They usually con­
sist of a chin rest for the patient and occasionally forehead
rests or other positioning implements. Some are designed with
a ­camera mount which rotates around the patient (Fig. 5-7),
while others require that the patient turns to face different
directions while the camera stays in a fixed position.
A
B
Fig. 5-7  The OMNIA positioning system (Canfield Scientific, Inc., Fairfield, NJ). (A) Viewed from the subject’s point of view. (B) Viewed from
the camera’s point of view. Note that the camera and lighting are mounted on a single arm that can rotate around the patient to capture various
poses. (Images courtesy of Derm.md [)
A
B
C
Fig. 5-6  Examples of standard facial views: (A) frontal view, (B) right oblique view, (C) right lateral view. (Images courtesy of Derm.md [www.
derm.md].)

55
Imaging  •  Chapter 5
Photography in the operating suite
Prevention of contamination of the sterile field is necessary
in any operating room setting. Cameras and lenses can act as
fomites, so particular care must be taken to keep them away
from the sterile area. For this reason, the most appropriate
person to act as the photographer in this setting is an assist­
ant who is not scrubbed into the case. Equally important is
that the assistant has an understanding of how to operate the
camera and of what needs to be included in the photos. Fur­
thermore, they should be aware of the location of the camera
strap and other accessory cords connected to the camera at all
times so that these do not dangle and contaminate the field. It
may be necessary to tape these down prior to the initiation of
surgery. A stand or stool for the camera operator may also be
helpful to ensure that proper viewing angles can be achieved
without obstruction by the surgeon or assistant’s hands or
other devices.
The first image of each procedure should contain informa­
tion about the identity of the patient. An identification sticker
or a note card with the patient’s name can be placed in the
camera’s view (but NOT over the sterile field) to essentially
label the series of subsequent images.
A few practice photographs prior to setting up a sterile field
can ensure appropriate exposure and positioning. ­Operating
room lighting is usually different from office lighting, so com­
pensating for this difference early can prevent poor-quality
photographs. To highlight an area of interest in the photo­
graph, such as a small vessel or stitch, it is best to use clean sur­
gical instruments to do so. If gloved hands are a necessary part
of the photograph, be sure to wipe off blood ­before ­allowing
photographs to be shot. Similarly, towels and drapes that are
in the field of view and stained with excess blood should be
­replaced prior to taking photographs. Suction should be main­
tained in deep or rapidly bleeding wounds ­immediately up to
the instant before the picture is taken so as not to obscure
the area of interest. Additionally, areas that have become wet
from irrigation should be patted dry to minimize distracting
reflections.
Finally, when photographing excised or extracted speci­
mens, place them on a clean surgical towel prior to shooting.
Also, photograph the specimen in its correct anatomical ori­
entation with a nonreflective measuring ruler placed next to it.
In case the ruler needs to be cropped out later, be sure not to
place it too close to the specimen.
Conclusion
For medical and cosmetic documentation, the image quality of
photographs taken by digital cameras has reached a level that
is comparable to, if not better than, that of 35 mm cameras.
A good digital SLR camera system that takes photographs at
6–7 megapixels is an investment that will pay for itself in a
relatively short period of time as compared to the cost of film
photography. Mastering the basics of photography to ensure
consistent, high-quality photographs is an invaluable skill for
the cosmetic practitioner. This skill will not only enhance
patient satisfaction, but it will also make the photographs
more valuable as educational tools for patients, staff, students,
and residents.
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emedicine.com/derm/topic561.htm
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surgery sections. Dermatol Surg 2001; 27(4):411–414.
Papier A, Peres MR, Bobrow M, et al. The digital imaging system and
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org/wiki/Ceteris_paribus
• Photograph the signed consent form prior to
­taking pictures of the patient to avoid separation
of the signed consent from the patient’s pictures.
• Tape or other markings on the floor can direct
the patient and the photographer to stand in the
appropriate locations and standardize distances
between the subject and camera.
• Tidy up the surgical field when taking intra­
operative photographs. Gloves and instruments
should be wiped clean with wet sterile gauze.
Any blood on the field can be covered with
a clean drape on top of the current drape.
PEARLS
• Consent form verbiage requirements may
vary from state to state. Have all consent forms
­reviewed by a local attorney.
• Subtle, gradual changes from certain cosmetic
procedures can be difficult for patients to discern.
The use of consistent digital photography makes
it easy to see these changes between before-
and-after photographs.
• Patients often do not notice their pre-existing
facial asymmetry, and may feel that it is a result
of a cosmetic procedure. Use photographs from
before the procedure to help patients appreciate
their natural asymmetry.
PITFALLS

SECTION I
History and Science
Background and history
No one can argue that one of the biggest advances in the last
thousand years of medical history has been the discovery of
local anesthesia. Prior to this, patients had to endure excruciat­
ing pain with procedures that we take for granted today. Even
the toughest of us cannot imagine having a tooth extracted or
an extremity amputated with no anesthesia. Prior to the late
1800s one could get drunk or literally bite the bullet, neither
of which had any effect on pain. I recently read an interesting
article about a .50-caliber bullet found at the site of the Battle
of Ox Hill where the 21st Massachusetts Regiment had fought
at a local cornfield with extreme and horrifying injuries and no
medical care. The bullet has molar tooth cusp imprints, report­
edly from a patient biting during surgery without anesthesia.
Figure 6-1 shows an artist’s rendition of the horror and panic
of such a battlefield amputation complete with a bullet between
the patient’s teeth. Fortunately, we have come a long way in the
last 100 years in terms of pain control. Many doctors still fail to
provide painless procedures for their patients. When we inject
fillers in the lips without anesthesia, we are in effect, asking the
patient to bite the bullet! Those doctors that have mastered
local anesthetic techniques will have happier patients, better
marketing, and less stress. It is very disconcerting to perform
procedures on patients that are white knuckled and shaking.
The surgeon cannot do as good of a job and the experience is
also unpleasant for the patient. Those doctors that provide pain­
less procedures are automatically marketing their practice in a
positive manner, and those doctors that hurt patients are mar­
keting their practice in a negative manner. I recently saw a new
patient for filler injection to the lips. I applied topical anesthesia
and prepared to perform miniblock local anesthetic injections
when the patient asked me what I was doing. I explained that
I don’t perform lip injections without first numbing the lips.
She stated that she had had her lips injected in the past without
local anesthesia. I asked her to humor me and accept the local
anesthesia. The experience was totally painless for her and she
admitted that she had been unnecessarily suffering at the other
doctor’s office. Not only did she return for more treatment, but
she sent me most of her tennis club. Painless doctors get more
patients; remember that!
Cocaine was the first local anesthetic to be widely used in
surgical applications. In the nineteenth century it was report­
ed that the Indians of the Peruvian highlands chewed the
leaves of the coca leaf (Erythroxylon coca) for its stimulating and
exhilatory effects.1–3 It was also observed that these Indians
had numbness in the areas around the lips. In 1859, Albert
Niemann, a German chemist, was given credit for being the
first to extract the isolated cocaine from the coca shrub in a
purified form. When Niemann tasted the substance his tongue
became numb. This property led to one of the most humane
discoveries in all of medicine and surgery. Over two decades
later, Sigmund Freud began treating patients with cocaine
for its physiological and psychological effects. While treating
a colleague for morphine dependence, the patient developed
cocaine dependence.4
Anesthesia
Joseph Niamtu
C h a p t e r
6
p a r t 2
Fig. 6-1  Biting the bullet was apparently utilized as a means of
pain control prior to the advent of anesthesia. With permission from
April Lee,

60
Chapter 6
Cosmetic surgery procedures and techniques
A resident at the University of Vienna Ophthalmologic
Clinic named Koller demonstrated the topical anesthetic
activity of cocaine on the cornea in animal models and on
himself. In an operation for glaucoma Koller used cocaine for
local anesthesia in 1894.
William Halsted was a prominent American surgeon who
investigated the principles of nerve block using cocaine. In
November, 1884, Dr. Halsted performed infraorbital and
­inferior alveolar (mandibular dental block) as well as demon­
strating various other regional anesthetic techniques. ­Halsted’s
self-experimentation with cocaine caused an addiction requir­
ing 2 years to resolve and regain his eminent position in
­surgery and teaching.
Early dentists dissolved cocaine hydrochloride pills in ­water
and drew this mixture up in a syringe to perform nerve infil­
trations and blocks. The extreme vasoconstrictive effects of
cocaine often caused tissue necrosis, but nonetheless provided
profound local anesthesia that revolutionized dentistry and
medicine for ever. Many proprietary preparations of that time
contained cocaine.
By the early 1900s cocaine’s adverse effects became well
recognized. These deleterious effects included profound car­
diac stimulation and vasoconstriction (cocaine blocks the
neuronal reuptake of norepinephrine in the peripheral nerv­
ous system, and myocardial stimulation in combination with
coronary artery vasoconstriction has proven lethal in sensitive
individuals), central nervous system stimulation, and mood-
altering euphoric effect. These effects coupled with the severe
physical and psychological dependence proved to be signifi­
cant drawbacks to cocaine use for local anesthesia.
In 1904, Alfred Einhorn, searching for a safer and less toxic
local anesthetic synthesized procaine (Novocain). Novocain was
the gold standard of topical anesthetics for almost 40 years when
Nils Lofgren synthesized lidocaine (Xylocaine), the first amide
group of local anesthetics. Lidocaine provided advantages over
the ester group (procaine) in terms of greater potency, less aller­
gic potential and a more rapid onset of anesthesia.1,2,5,6
The mechanism of action of local
­anesthetics
Local anesthetics block the sensation of pain by interfering
with the propagation of impulses along peripheral nerve fibers
without significantly altering normal resting membrane poten­
tials.7 Local anesthetics depolarize the nerve ­membranes and
prevent achievement of a threshold potential. A propagated
action potential fails to develop and a conduction blockade
is achieved. The interference of nerve transmission is caused
by blocking the influx of sodium through the excitable nerve
membrane.8
Choice of local anesthetic agents
This chapter relates more to techniques than specific anes­
thetics. Ester-based local anesthetics are known to cause
increased allergic reactions and amide-based local anesthetics
are more commonly used for nerve blocks. Some instances
call for extended local anesthetic duration and agents such
as Bupivicaine or Etidiocaine. Various practitioners favor
­various local anesthetic agents (Table 6-1).
Table 6-1  The qualities and dosage of commonly utilized local anesthetic agents
Agent
Duration of action
Maximum dosage guidelines
Esters
Cocaine
Medium
N/A
Procaine (Novocain)
Short
7 mg/kg
Benzocaine (Cetacaine)
N/A
N/A
Tetracaine
N/A
N/A
Chloroprocaine (Nesacaine)
Short (15–30 min)
800 mg without Epi,
1000 mg with Epi
Amides
Lidocaine (Xylocaine)
Medium (30–60 min)
4.5 mg/kg without Epi,
7 mg/kg with Epi
Mepivacaine (Polocaine/Carbocaine)
Medium (45–90 min)
7 mg/kg to max of 400 mg
Bupivacaine (Marcaine)
Long (120–240 min)
175 mg without Epi,
225 mg with Epi
Etidocaine (Duranest)
Long (120–180 min)
6 mg/kg without Epi,
8 mg/kg with Epi
Prilocaine
Medium (30–90 min)
500 mg without Epi,
600 mg with Epi

61
Anesthesia  •  Chapter 6
Procedures and Techniques
Clinical considerations
Sensory anatomy of the head and neck
The main sensory innervation of the face is derived from
cranial nerve V (trigeminal nerve) and the upper cervical
nerves (Fig. 6-2).
Sensory anatomy of the trigeminal nerve
The trigeminal nerve is the fifth of the twelve cranial nerves.
Its branches originate at the semilunar ganglion (Gasserian
ganglion) located in a cavity (Meckel’s cave) near the apex of
the petrous part of the temporal bone. Three large nerves,
the ophthalmic, maxillary, and mandibular, proceed from the
ganglion to supply sensory innervation to the face (Fig. 6-3).
Often referred to as ‘the great sensory nerve of the head
and neck,’ the trigeminal nerve is named for its three major
sensory branches. The ophthalmic nerve (V1), maxillary nerve
(V2), and mandibular nerve (V3) are literally ‘three twins’
(trigeminal) carrying sensory information of light touch, tem­
perature, pain, and proprioception from the face and scalp
to the brainstem. The commonly used terms ‘V1,’ ‘V2,’ and
‘V3’ are shorthand notation for cranial nerve five, branches
one, two, and three, respectively. In addition to nerves car­
rying incoming sensory information, certain branches of the
trigeminal nerve also contain nerves with motor components
(the ophthalmic and maxillary nerves consist exclusively of
sensory fibers; the mandibular nerve is joined outside the cra­
nium by the motor root.) These outgoing motor components
include branchial motor nerves (nerves innervating muscles
derived embryologically from the branchial arches) as well as
‘hitchhiking’ visceral motor nerves (nerves innervating viscera,
including smooth muscle and glands). The trigeminal nerve
exits the trigeminal ganglion and courses ‘backward’ to enter
the mid-lateral aspect of the pons at the brainstem.9
The ophthalmic nerve (V1) leaves the semilunar ganglion
through the superior orbital fissure. The maxillary nerve (V2)
leaves the semilunar ganglion through the foramen rotundum
at the skull base, and the mandibular nerve (V3) leaves the
semilunar ganglion through the foramen ovale at the skull
base (Fig. 6-3, inset).9 The remainder of this article will only
discuss the sensory components of this nerve system as they
relate to local anesthetic blocking techniques for cosmetic
facial procedures.
Sensory anatomy of the ophthalmic nerve (V1)
The ophthalmic nerve, or first division of the trigeminal, is a
sensory nerve. It supplies branches to the cornea, ciliary body,
and iris; to the lacrimal gland and conjunctiva; to the part of
the mucous membrane of the nasal cavity; and to the skin of
the eyelids, eyebrow, forehead, and upper lateral nose (Fig. 6-3,
V1). It is the smallest of the three divisions of the trigeminal
and divides into three branches, the frontal, nasociliary, and
lacrimal.9 The frontal nerve divides into the supraorbital and
supratrochlear nerves, providing sensation to the forehead
and anterior scalp.
The nasocillary nerve divides into four branches, two
of which supply sensory innervation to the face. These two
branches are the infratrochlear nerve which supplies ­sensation
to the skin of the medial eyelids and side of the nose and the
ethmoidal nerve which gives off a terminal branch called the
external (or dorsal) nasal nerve and innervates the skin of
the nasal dorsum and tip. The lacrimal nerve innervates the
skin of the upper eyelid.
Fig. 6-2  The sensory innervation of the head and neck is derived
from the trigeminal and upper cervical nerves.
Fig. 6-3  The main branches of the trigeminal nerve ­supplying
­sensation to the respective facial areas. The inset shows the
­trigeminal ganglion with the three main nerve branches.

62
Chapter 6
Cosmetic surgery procedures and techniques
Local anesthetic techniques for the scalp
and forehead
The frontal nerve exits through a notch (in some cases a
foramen) on the superior orbital rim approximately 27 mm lat­
eral to the glabellar midline (Fig. 6-4). This supraorbital notch
is readily palpable in most patients. After exiting the notch or
foramen, the nerve traverses the corrugator supercillii muscles
and branches into a medial and lateral portion. The lateral
branches supply the lateral forehead and the medial branches
supply the scalp. The supratrochlear nerve exits a foramen
approximately 17 mm from the glabellar midline (Fig. 6-4) and
supplies sensation to the middle portion of the forehead. The
infratrochlear nerve exits a foramen below the trochlea and
provides sensation to the medial upper eyelid, canthus, medial
nasal skin, conjunctiva, and lacrimal apparatus (Fig. 6-4).10
When injecting this area it is prudent to always use the free
hand to palpate the orbital rim to prevent inadvertent injec­
tion into the globe. To anesthetize this area, the supratroch­
lear nerve is measured 17 mm from the glabellar midline and
1–2 cc of 2% lidocaine 1:100 000 epinephrine are injected
(Fig. 6-5A). The supraorbital nerve is blocked by palpating the
notch (and/or measuring 27 mm from the glabellar midline)
and injecting 2 cc of local anesthetic solution (Fig. 6-5B). The
infratrochlear nerve is blocked by injecting 1–2 cc of local
anesthetic solution at the junction of the orbit and the nasal
bones (Fig. 6-5C). In reality, one can block all three of these
nerves by simple injecting 2–4 cc of local anesthetic solution
from the central brow proceeding to the medial brow. Figure
6-6 shows the regions anesthetized from the above blocks.
Sensory anatomy of the maxillary nerve (V2)
The maxillary nerve, or second division of the trigeminal,
is a sensory nerve that crosses the pterygopalatine fossa then
traverses the orbit in the infraorbital groove and canal in the
floor of the orbit, and appears upon the face at the infraorbital
foramen as the infraorbital nerve.9 At its termination, the nerve
divides into branches which spread out upon the side of the
nose, the lower eyelid, and the upper lip, joining with filaments
of the facial nerve.9 Terminal branches include the following:

• The zygomatic nerve arises in the pterygopalatine fossa,
enters the orbit by the inferior orbital fissure, and divides
at the back of that cavity into two terminal branches, the
zygomaticotemporal and zygomaticofacial nerves.

• The zygomaticotemporal branch runs along the lateral wall
of the orbit in a groove in the zygomatic bone then passes
through a foramen in the zygomatic bone and enters the
temporal fossa. It ascends between the bone and substance
of the temporalis muscle and pierces the temporal fascia
about 2.5 cm above the zygomatic arch where it is distributed
to the skin of the side of the forehead (see Fig. 6-3, V2).

• The zygomaticofacial branch passes along the infero­
lateral angle of the orbit, emerges upon the face through a
foramen in the zygomatic bone, perforates the orbicularis
oculi, and supplies sensation to the skin on the prominence
of the cheek (see Fig. 6-3, V2).
Fig. 6-4  The supraorbital nerve (SO) exits about 27 mm from
the glabellar midline and the supratrochlear nerve (ST) is located
­approximately 17  mm from the glabellar midline. The infratrochlear
nerve (IT) exits below the trochlea.
A
B
C
Fig. 6-5  (A, B, C) The forehead and scalp are blocked by a series of injections form the central to the medial brow.

63
Anesthesia  •  Chapter 6
As the maxillary nerve traverses the orbital floor and exits
the infraorbital foramen, it branches into a plexus of nerves
which has the following terminal branches:

• The inferior palpebral branches ascend behind the orbicu­
laris oculi muscle and supply the skin and conjunctiva of
the lower eyelid (see Fig. 6-3, V2).

• The lateral nasal branches (rami nasales externi) supply
the skin of the side of the nose (see Fig. 6-3, V2).

• The superior labial branches are distributed to the skin of
the upper lip, the mucous membrane of the mouth, and
labial glands (see Fig. 6-3, V2).
Local anesthetic techniques for the
­infraorbital nerve block and branches
of the ­maxillary nerve (V2)
The infaorbital nerve exits the infraorbital foramen 4–7 mm
below the orbital rim in an imaginary line dropped from the
medial limbus of the iris or the pupillary midline. The ante­
rior superior alveolar nerve branches from the infraorbital
nerve before it exits the foramen and thus some patients will
manifest anesthesia of the anterior teeth and gingiva if the
­branching is close to the foramen. Areas anesthetized include
the lateral nose, anterior-medial cheek, lower eyelid and upper
lip on the injected side. This nerve can be blocked by intraoral
or extraoral routes. To perform an infra­orbital nerve block
from an intraoral approach, topical anesthesia is placed on the
oral mucosa at the vestibular sulcus just under the canine fossa
(between the canine and first premolar tooth) and left for several
minutes. The lip is then elevated and a 1 or 1.5 inch, 27–30-
gauge needle is inserted in the sulcus and directed superiorly
toward the infraorbital foramen (Fig. 6-7). The needle does not
need to enter the foramen for a successful block. The anesthetic
solution needs only to contact the vast ­branching around the
foramen to be effective. It is imperative to use the other hand to
palpate the inferior orbital rim to avoid injecting the orbit. Two
to four cubic centiliters of 2% lidocaine with 1:100 000 epine­
phrine are injected in this area for the infraorbital block.
Fig. 6-6  The shaded areas indicate the anesthetized areas from
supraorbital nerve (SO) and supratrochlear nerve (ST) and infra­
trochlear nerve (IT) blocks.
B
Fig. 6-7  (A, B) The intraoral approach for local anesthetic block of
the infraorbital nerve.
A

64
Chapter 6
Cosmetic surgery procedures and techniques
The infraorbital nerve can also be very easily blocked by
a facial approach. This may also be the preferred route in
­dental-phobic patients. A 27–30-gauge, half-inch needle is
used and is placed through the skin and aimed at the foramen
in a perpendicular direction. Two to four cubic centiliters of
local anesthetic solution are injected at or close to the foramen
(Fig. 6-8). Again, the other hand must constantly palpate the
inferior orbital rim to prevent inadvertent injection into the
orbit.
A successful infraorbital nerve block will anesthetize the
infraorbital cheek, the lower palpebral area, the lateral nasal
area, and superior labial regions as shown in Figure 6-9.
The aforementioned techniques may provide anesthesia
to the lateral nasal skin but do not provide anesthesia to the
central portion of the nose. A dorsal (external) nasal nerve
block will supplement nasal anesthesia by providing anesthe­
sia over the area of the cartilaginous nasal dorsum and tip.
This supplementary nasal block is accomplished by palpating
the inferior rim of the nasal bones at the osseous cartilaginous
junction. The dorsal nerve (anterior ethmoid branch of the
nasocillary nerve) emerges 5–10 mm from the nasal midline at
the osseous junction of the inferior portion of the nasal bones
(the distal edge of the nasal bones) (Fig. 6-10). The dotted line
in Figure 6-10 shows the course of this nerve under the nasal
bones before emerging.
Two often overlooked nerves in facial local anesthetic blocks
are the zygomaticotemporal and zygomaticofacial nerves.
These nerves represent terminal branches of the ­zygomatic
Fig. 6-9  Area of anesthesia from unilateral infraorbital nerve block.
B
A
Fig. 6-10  (A, B) The dorsal (external) nasal nerve is blocked
subcutaneously at the osseous-cartilaginous junction of the distal
nasal bones.
B
A
Fig. 6-8  (A, B) The
facial approach for local
anesthetic block of the
infraorbital nerve.

65
Anesthesia  •  Chapter 6
nerve. The zygomaticotemporal nerve emerges through a
foramen located on the anterior wall of the ­temporal fossa.
This foramen is actually behind the lateral orbital rim ­posterior
to the zygoma at the approximate level of the lateral canthus
(Fig. 6-11).
Injection technique involves sliding a 1.5-inch needle behind
the concave portion of the lateral orbital rim. It is suggested that
one closely examine this area on a model skull prior to attempt­
ing this injection as it will make the technique simpler. To ori­
entate for this injection the doctor needs to palpate the lateral
orbital rim at the level of the frontozygomatic suture (which is
frequently palpable). With the index finger in the ­depression of
the posterior lateral aspect of the lateral orbital rim ­(inferior
and posterior to the frontozygomatic suture) the operator places
the needle just behind the palpating finger (which is about 1 cm
posterior to the frontozygomatic suture (Fig. 6-11). The needle
is then ‘walked’ down the concave posterior wall of the lateral
orbital rim to the approximate level of the lateral canthus. After
aspirating, 1–2 cc of 2% lidocaine 1:100 000 epinephrine are
injected in this area with a slight pumping action to ensure dep­
osition of the local anesthetic solution at or about the foramen.
Again, it is important to hug the back concave wall of the lat­
eral orbital rim with the needle when injecting.
Blocking the zygomaticotemporal nerve causes anesthesia
in the area superior to the nerve including the lateral orbital
rim and the skin of the temple from above the zygomatic arch
to the temporal fusion line (Fig. 6-12).
The zygomaticofacial nerve exits through a foramen (or
foramina in some patients) in the inferior lateral portion of
the orbital rim at the zygoma. If the surgeon palpates the
­junction of the inferior lateral portion of the lateral orbital
rim, the nerve emerges several millimeters lateral to this point.
By palpating this area and injecting just lateral to the finger,
this nerve is successfully blocked with 1–2 cc of local anesthe­
sia (Fig. 6-13). Blocking this nerve will result in anesthesia of a
triangular area from the lateral canthus and the malar region
along the zygomatic arch and some skin inferior to this area
(see Fig. 6-12).10
Total second division nerve block
An efficient and simple technique to obtain hemi-midfacial
local anesthesia is to block the entire second division or maxil­
lary nerve. This will anesthetize the entire hemi-maxilla and
the unilateral maxillary sinus by blocking the pterygopalatine,
infraorbital, and zygomatic nerves and their terminal branches.
This is an easily learned technique involves an intraoral
approach at the posterior lateral palate (Fig. 6-14).
The maxillary nerve block via the greater palatine canal
was first described in 1917 by Mendel.11 The greater ­palatine
foramen is located anterior to the junction of the hard and
soft palate medial to the second molar tooth (Fig. 6-14B).
The foramen is usually found about 7 mm anterior to the
hard and soft palate junction. This junction is seen as a color
change such that the tissue overlying the soft palate is darker
pink than the tissue overlying the hard palate. The key to this
block is to place a 1.5-inch needle through the greater palatine
foramen. It sometimes takes multiple needle sticks to localize
the foramen. Due to the need for multiple sticks the palatal
mucosa in this area is first infiltrated with 0.5 cc of lidocaine
to facilitate painless location of the greater palatine foramen.
A 1.5-inch, 25- or 27-gauge needle is bent to a 45-degree
­angle and will usually easily negotiate the pterygopalatine
canal, thereby placing the local anesthetic solution into the
pterygopalatine fossa. The course of the maxillary division of
the trigeminal nerve (V2) is as follows. The second division
of the trigeminal nerve arises from the Gasserian ganglion in
the ­ medial cranial fossa and exits the skull via the foramen
rotundum (Fig. 6-14C). The nerve then traverses the superior
aspect of the pterygopalatine fossa, where it divides into three
major branches: the pterygopalatine nerve, the infraorbital
nerve, and the zygomatic nerve.12 It is these nerves that are
targeted in this block.
When the foramen is located, the needle should be gently
advanced. If significant resistance is encountered the needle
should be withdrawn and redirected. Approximately 5% of
the population has been shown to have tortuous canals that
B
A
C
Fig. 6-11  (A, B, C) The zygomaticotemporal nerve is blocked by placing the needle on the concave surface of the posterior lateral orbital rim.

66
Chapter 6
Cosmetic surgery procedures and techniques
impede the needle tip and in some patients this technique is
not possible. It is also important to aspirate before injecting
to prevent intravascular injection. When the needle is prop­
erly positioned (usually at a depth of 25–30 mm), the injection
(2–4 mL) should proceed over 30–45 seconds.
Transient diplopia of the ipsilateral eye may occur. This
results from the local anesthetic diffusing superiorly and
­medially to anesthetize the orbital nerves. The patient must
be assured that if this phenomenon occurs, it is transient.
Again, this technique will anesthetize all the terminal
branches of the maxillary nerve with a single injection.
Sensory anatomy of the mandibular nerve (V3)
The mandibular nerve supplies the teeth and gums of the
mandible, the skin of the temporal region, part of the auri­
cle, the lower lip and the lower part of the face (see Fig.
6-3, V3). The mandibular nerve also supplies the muscles of
­mastication and the mucous membrane of the anterior two-
thirds of the tongue. It is the largest of the three divisions of
the fifth cranial nerve and is made up of a motor and sensory
root.9
Sensory branches of the mandibular nerve include:

• The auriculotemporal nerve supplies sensation to
the skin covering the front of the helix and tragus
(see Fig. 6-3).

• The inferior alveolar nerve is the largest branch of the
mandibular nerve. It descends with the inferior alveo­
lar artery and exits the ramus of the mandible to the
­mandibular foramen. It then passes forward in the
mandibular canal, beneath the teeth, as far as the mental
foramen, where it divides into two terminal branches, the
incisive and mental nerves. The mental nerve emerges at
the mental foramen, and divides into three branches; one
descends to the skin of the chin, and two ascend to the
skin and mucous membrane of the lower lip. The buccal
nerve which supplies sensation to the skin over the buc­
cinator muscle.9
Fig. 6-12  The anesthetized areas form zygomaticotemporal (ZT)
and the zygomaticofacial nerve (ZF).
B
A
Fig. 6-13  (A, B) The zygomaticofacial nerve(s) are blocked by injecting the inferior lateral portion of the orbital rim.

67
Anesthesia  •  Chapter 6
Local anesthetic techniques for the mental
nerve block
The mental nerve exits the mental foramen on the hemi-
mandible at the base of the root of the second premolar
(many patients may be missing a premolar due to ortho­dontic
­extractions). The mental foramen is, on average, 11 mm
­inferior to the gum line (Fig. 6-15). There is variability with
this foramen (like all foramina), but by injecting 2–4 cc of local
anesthetic solution about 10 mm inferior to the gum line or
15 mm inferior to the top of the crown of the second ­premolar
tooth the block is usually successful. In a patient without teeth,
the foramen is often located much higher on the jaw and can
sometimes be palpated. This block is performed more supe­
riorly in the denture patient. As stated earlier, the foramen
does not need to be entered as a sufficient volume of local
anesthetic solution in the general area will be effective. By
­placing traction on the lip and pulling it away from the jaw,
the labial branches of the mental nerve can sometimes be
seen ­traversing through the thin mucosa. The mental nerve
gives off labial branches to the lip and chin.
When anesthetized, the distribution of numbness will gener­
ally be the unilateral lip down to the mentolabial fold. ­Depending
on the individual furcating anatomy of that patient’s nerve the
anterior chin and cheek may be involved as well (Fig. 6-16).
A
B
C
Fig. 6-14  The maxillary nerve block is performed by locating the greater palatine foramen (A), inserting a bent needle up the pterygopalatine
canal (B) to inject local anesthetic into the ptergopalatine fossa (C). Notice the needle tip in the pterygopalatine fossa on image (C). As the
second division traverses this area it is blocked at the main trunk.
A
B
Fig. 6-15  The mental foramen is approached intraorally below the root tip of the lower second premolar (A) or from a facial approach (B).

68
Chapter 6
Cosmetic surgery procedures and techniques
The inferior alveolar nerve also supplies sensory innervation
to the chin pad. The mylohyoid nerve may also innervate this
area. To augment or extend the area of local anesthesia on the
chin, an inferior alveolar nerve block (mandibular dental block)
can be performed instead of or with the mental nerve block.
Additionally, local skin infiltration in that area may assist.
Local anesthetic techniques for the inferior
alveolar nerve block (Intraoral)
Almost every person who has ever been to a dentist has had
this block and is aware of its effects, distribution, and dura­
tion. This block is technically more difficult to master, but is
easily learned. The basis of this technique involves the deposi­
tion of local anesthetic solution at or about the mandibular
foramen on the medial mandibular ramus where the inferior
alveolar nerve enters the mandible (Fig. 6-17).
Detailed description of this technique is beyond the scope
of this review article but will be outlined as follows. The ­patient
is seated upright and the surgeon places the index finger on
the posterior ramus and the thumb in the coronoid notch on
the anterior mandibular ramus (Fig. 6-17).
A 1.5-inch, 27-gauge needle is then directed to the medial
mandibular ramus at the level of the cusps of the upper second
molar and the needle is advanced half way between the thumb
and index finger of the other hand, that is grasping the mandi­
ble (Fig. 6-17). Two cubic centiliters of 2% lidocaine, 1:100 000
epinephrine is then injected in a pumping motion to better
the chances of anesthetic solution contacting the nerve and
foramen. The needle can be slightly bent as shown in ­Figure
6-18 to negotiate the sometimes outward curvature of the
Fig. 6-16  The anesthetized areas from a unilateral mental
nerve block. Due to various anatomic factors, the area below the
­mentolabial fold or at the midline may share other innervation.
A
B
Fig. 6-17  (A, B) The target of the needle in the intraoral inferior alveolar nerve block is at the entrance of the nerve in the mandibular foramen
on the medial ramus. The needle can be slightly bent with a medial angle to negotiate the flaring anatomy of the ramus. The mylohyoid nerve
(inferior to needle) may or may not be blocked by this technique, depending upon its level of branching.

69
Anesthesia  •  Chapter 6
mandibular ramus. The surgeon should first aspirate to avoid
intravascular injection. Anesthesia from this block sometimes
takes 5–10 minutes to take effect. Proficiency in this blocking
technique requires practice, but is very useful in cosmetic facial
procedures. In addition, the ispilateral tongue is usually anes­
thetized with this block. The area anesthetized includes the
lower teeth and gums, the chin and skin on the lateral chin.
The inferior alveolar nerve block frequently ­includes the mylo­
hyoid nerve. In some patients the mylohyoid nerve branches
above the area of inferior alveolar injection and in this case
needs a specific mylohyoid nerve block as outlined previously.
Local anesthetic techniques
for the mandibular nerve (V3) block
(Facial Approach)
The mandibular nerve can also be blocked from a deep injec­
tion as the nerve exits the foramen ovale, posterior to the
pterygoid plate (Fig. 6-18, No. 2).13 This technique requires
more experience and has more potential complications than
the intraoral approach.
The technique for performing this block begins with the
patient in supine position with the head and neck turned away
from the side to be blocked. The patient is asked to open and
close the mouth gently so that the operator can identify and
palpate the sigmoid notch. This is the area between the man­
dibular condyle and the coronoid process (Fig. 6-18). This
notch is located about 25 mm anterior to the tragus. If one
places a finger 25 mm anterior to the tragus and opens and
closes the jaw, the mandibular condyle can be palpated with
the jaw open. When the jaw is closed, the finger will be over the
sigmoid notch. A 22-gauge, 8 cm needle is inserted in the mid­
point of the notch and directed slightly cephalic and medial to
angle through the notch until the lateral pterygoid plate is con­
tacted (Fig. 6-18, No. 2). This is usually at a depth of approxi­
mately 4.5–5.0 cm. Spinal needles frequently have measuring
stops that can be adjusted to the position of original contact
of the pterygoid plate. The needle is then withdrawn to a sub­
cutaneous position and carefully ‘walked off ’ the posterior
border of the pterygoid plate (Fig. 6-18, arrows) in a horizon­
tal plane until the needle no longer touches the plate and is
posterior to it. The needle depth should be the same as the
distance on the needle stop marker when the pterygoid plate
was originally contacted. The needle should not be advanced
more than 0.5 cm past the depth of the pterygoid plate
because the superior constrictor muscle of the pharynx can
be pierced easily.13 When the needle is in appropriate position,
5 cc of local anesthetic solution can be administered. The area
anesthetized is shown as ‘V3’ in Figure 6-3. Complications
include hematoma formation and subarachnoid injection.
Again, this block should be learned in a proctored situation
and not be attempted by novice injectors.
Sensory anatomy of the scalp
The anterior scalp is anesthetized by injecting the branches
of V1 (supraorbital and supratrochlear nerves), and V2 (the
zygomaticotemporal nerve). The posterior scalp is ­innervated
by the greater and lesser occipital nerves, and the greater
auricular nerve supplies the lateral scalp (Fig. 6-19).
Fig. 6-18  The mandibular nerve (‘V3’) block places the local anes­
thetic just posterior to the lateral pterygoid plate where the third divi­
sion of the trigeminal nerve exits the foramen ovale. The needle is
walked off the pterygoid plate (1) and the local anesthetic solution is
deposited in the region of the third division of the trigeminal nerve (2).
Fig. 6-19  Innervation of the scalp: 1, supratrochlear nerve;
2, supraorbital nerve(s); 3, zygomaticotemporal nerve; 4, greater
­auricular nerve; 5, lesser occipital nerve; 6, greater occipital nerve.

70
Chapter 6
Cosmetic surgery procedures and techniques
The greater occipital nerve arises from the dorsal rami of
the second cervical nerve and travels deep to the cervical mus­
culature until it becomes subcutaneous slightly inferior to the
superior nuchal line.14 It emerges on this line in association
with the occipital artery, and the artery is the most useful land­
mark for locating the greater occipital nerve (Fig. 6-19).
Local anesthetic techniques to block
the scalp
By performing the ‘brow blocks’ (see Fig. 6-5), the ­ cervical
plexus block (see Fig. 6-21) and the zygomaticotemporal
block (see Fig. 6-11) most of the scalp is anesthetized, with
the exception of the posterior area. This is anesthetized by
blocking the greater occipital nerve. One can also perform a
ring block where wheals of local anesthetic are injected every
several centimeters around the entire scalp at about the level
of the eyebrows. About 30 cc of local is required to perform a
scalp ring block.
Greater occipital nerve block technique
for posterior scalp anesthesia
The most efficient patient position is sitting upright with the
chin flexed to the sternum.15
The nerve is identified at its point of entry to the scalp, along
the superior nuchal line one-third to one-half the distance
between the mastoid process and the occipital protuberance
in the midline (Fig. 6-20).14 Another measurement for locating
the artery is 2.5–3.0 cm lateral to the occipital ­protuberance.16
The patient will report pain upon compression of the nerve:
the point at which maximal tenderness is elicited can be used
as the injection site. A 25-gauge, 5/8-inch needle is used for
the block. The occipital artery is just lateral to the greater
occipital nerve and can be used as a pulsatile landmark. Two
to four cubic centiliters of local anesthetic solution can be
infiltrated on either side of the artery to ensure proximity to
the nerve. Figure 6-22 (below) shows the dermatomes anesthe­
tized by blocking the greater occipital nerve.
Sensory anatomy of the neck
Innervation of the cervical plexus
The cervical plexus is formed from the ventral rami of the
upper four cervical nerves (Fig. 6-21B). Their dorsal and ven­
tral roots combine to form spinal nerves as they exit through the
intervertebral foramen. The anterior rami of C2 through C4
form the cervical plexus. The cervical plexus lies just behind the
posterior border of the sternocleidomastoid ­muscle, giving off
both superficial (superficial cervical plexus) and deep branches
(deep cervical plexus). The branches of the ­superficial cervical
plexus supply the skin and superficial structures of the head
neck, and shoulder. The deep branches of the cervical plexus
innervate the deeper structures of the neck, including the mus­
cles of the anterior neck and the diaphragm (phrenic nerve)
and are not blocked for local anesthetic procedures.
Superficial branches of the cervical plexus
The lesser occipital nerve arises from the second (and some­
times third) cervical nerve and emerges from the deep fascia
on the posterior lateral portion of the head behind the auricle,
supplying the skin and communicating with the greater occip­
ital, the great auricular, and the posterior auricular branch of
the facial nerve.
The greater auricular nerve arises from the second and
third cervical nerves and divides into an anterior and a pos­
terior branch. The anterior branch is distributed to the skin
of the face over the parotid gland, and communicates in the
substance of the gland with the facial nerve.
The posterior branch supplies sensation to the skin over
the mastoid process and on the back of the auricle, except at
its upper part; a filament pierces the auricle to reach its lateral
surface, where it is distributed to the lobule and lower part
of the concha. The posterior branch communicates with the
lesser occipital nerve, the auricular branch of the vagus, and
the posterior auricular branch of the facial nerve.
The cutaneous cervical nerve (cutaneus colli nerve, anterior
­cervical nerve) arises from the second and third cervical nerves
and provides sensation to the anterolateral parts of the neck
(­Fig. 6-21B).
Local anesthetic techniques for the cervical plexus
This technique is used in cosmetic facial surgery to block the
superficial branches of the cervical plexus to anesthetize skin
of the lateral or anterior neck, the posterior lateral scalp and
portions of the periauricular area (see Fig. 6-2).
Fig. 6-20  The greater occipital nerve is in close approximation
to the artery of the same name (1). The nerve can be located by
­palpating the artery and injecting just medial to it (2). Another
­landmark is injecting on the nuchal line, one-third to one-half the
distance between the mastoid prominence and occipital
­protuberance (3 and 5). Number 4 shows the lesser occipital nerve.

71
Anesthesia  •  Chapter 6
C
A
Fig. 6-21  (A) The cervical plexus block is performed by making a line from the mastoid process (1) to the level of the transverse process of C6
(2) then finding the point half way between these two marks (X) just posterior to the sternocleidomastoid (dotted line). (B) Local anesthetic is then
injected perpendicular, superiorly and inferiorly in this region. (C) The greater occipital nerve, which is not part of the cervical plexus.

72
Chapter 6
Cosmetic surgery procedures and techniques
The technique involves laying the patient back with the
sternocleidomastoid flexed. “The mastoid process and the
transverse process of C6 (Chassaignac’s tubercle (approximate
level of the cricoid cartilage) (Fig. 6-21A) are marked and a
line is drawn connecting the two points.” Local anesthetic is
injected half way between these two marks, just behind the
sternocleidomastoid muscle. The local anesthetic is injected
at this midpoint superiorly and inferiorly. This line is divided
in half at the posterior border of the sternocleidomastoid to
determine the injection point. Another technique is to simply
bisect the distance from the origin and insertion of the ster­
nocleidomastoid without osseous landmarks. The success of
this block involves a larger volume of local anesthesia diffus­
ing and spreading out over a larger area rather than absolute
accuracy of the nerve position. Three to five cubic centiliters
of local anesthetic solution is injected subcutaneously with the
needle perpendicular to the skin. The needle is then redirected
superiorly and another 3–5 cc are injected. ­Finally, the nee­
dle is then directed inferiorly and another 3–5 cc are injected.
Figure 6-21B shows the areas anesthetized by a ­cervical plexus
block.
Phrenic nerve involvement is rare with superficial cervi­
cal plexus block (more common with deep cervical blocks)
but technically possible as C3, C4, and C5 innervate the
diaphragm. Healthy patients can tolerate a hemiparaly­
sis of the diaphragm but caution must be used in patients
with cardio­pulmonary problems as assisted ventilation may
be required. It must be kept in mind that a bilateral block
could potentially deinnervate the entire diaphragm. To
prevent unwanted spread of local anesthetic solution, this
injection is just ­subcutaneous in placement and never done
­bilaterally.
Selected area blocks
Anesthesia for the ear
Four nerve branches supply sensory innervation to the ear.
The anterior half of the ear is supplied by the auriculotem­
poral nerve, which is a branch of the mandibular portion of
the trigeminal nerve. The posterior half of the ear is inner­
vated by two nerve branches derived from the cervical plexus:
the great auricular nerve and the lesser occipital nerve (Fig.
6-22). The auditory branch of the vagus nerve innervates the
concha and external auditory canal.
Although these nerves can be individually targeted with
blocks, a circumferential infiltration (ring block) will ­anesthetize
the entire ear, except the concha and the external auditory
canal which are innervated by the vagus nerve. The needle
is inserted into the skin at the junction where the earlobe
attaches to the head. The anesthetic should be infiltrated while
the needle is advanced to the subcutaneous plane. Infiltration
is made in a hexagonal pattern around the entire periphery of
the ear (Fig. 6-22). The conchal bowl and external auditory
canal will need separate infiltration. One should aspirate (as
with all injections) prior to injection to prevent intravascular
injection.
Anesthesia for the nose
The nose receives innervation from multiple nerves. The root,
bridge, and the upper portion of the side of the nose are inner­
vated by the supratrochlear and infratrochlear nerve and the
infraorbital nerve supplies the skin on the side of almost half
of the lower nose. The external nasal branch of the anterior
ethmoidal nerve (dorsal nasal nerve) exits between the nasal
bone and the lateral nasal cartilage to supply the skin over the
dorsum of this part of the nose to the tip.
Anesthetic techniques for blocking the nose vary with the
type of procedure being performed. To block the external
nasal structures (the bridge and tip) bilateral blocks of the
following nerves are performed: infraorbital, supratrochlear,
infratrochlear, and the dorsal nasal nerves.
For internal nasal surgery such as rhinoplasty or nasal
trauma the aforementioned blocks are performed in conjunc­
tion with the following. The second division maxillary block is
valuable in providing supplemental anesthesia. This is shown
in Figure 6-14. For septal anesthesia local anesthetic solution
Fig. 6-22  Blocking the entire ear (with the exception of the area
supplied by the vagus nerve) can be performed by inserting the
­needle at the black dots and infiltrating along the dotted lines. This
will anesthetize the terminal branches of the auriculotemporal nerve,
the lesser occipital nerve, and the anterior and posterior branches
of the greater auricular nerve. The main trunks of these nerves could
be blocked as detailed in the text but this terminal infiltration
technique may be more convenient.

73
Anesthesia  •  Chapter 6
is deposited 1 cm in front of the sphenoid rostrum to block
the posterior and superior branches of the sphenopalatine
nerve (Fig. 6-23). Bending a 1.5-inch needle will improve
­visualization while injecting. The infiltrations are performed
from posterior to anterior to prevent needle puncture bleeding
from obscuring the field. Infiltration can also be made into the
inferior turbinates.
Blocking the lips
Minimally invasive cosmetic surgery techniques such as filler
injections may require local anesthesia of the lips. Although
the doctor could perform bilateral infraorbital and mental
nerve blocks, they present disadvantages. Many practitioners
are uncomfortable with these blocks and they can be unpleas­
ant for the patient. In addition, this combination of blocks will
render a large area of the face insensate for several hours which
is disconcerting to patients. A simple technique for obtaining
anesthesia of the upper and lower lips is to inject 0.5 cc incre­
ments of 2% lidocaine with 1:100 000 epinephrine across the
vestibule of the anterior maxilla and mandible (­Fig. 6-24). This
simple technique is performed as follows. First, topical anesthe­
sia is applied to the anterior and mandibular sulcus for several
minutes. Next, a ½-inch, 30-gauge needle is used to deposit
0.5 cc increments of anesthesia in 4–5 areas between the canine
teeth. This technique will provide profound anesthesia in the
perioral area which is usually sufficient for filler injection.
Figure 6-25 shows the area anesthetized by using the infil­
tration technique in both lips. Although profound anesthesia
may extend from the nasal tip to the chin, some patients can
still feel pain at the lateral portions of the lips, but usually
tolerate injection.
Tumescent anesthesia
Dermatologist Jeffery Klein developed the concept of tumescent
local anesthesia and thereby revolutionized outpatient liposuc­
tion as well as enhanced other cosmetic procedures. The word
‘tumescent’ means swollen and firm. By injecting a large vol­
ume of very dilute lidocaine (local anesthetic) and epinephrine
(capillary constrictor) into subcutaneous fat, the targeted tissue
becomes swollen and firm, or tumescent. The tumescent tech­
nique is a method that provides local anesthesia to large vol­
umes of subcutaneous fat and thus permits liposuction totally
by local anesthesia. The tumescent technique eliminates both
the need for general anesthesia and the need for i.v. narcotics
and sedatives. The tumescent technique for liposuction (1) pro­
vides local anesthesia, (2) constricts capillaries and prevents sur­
gical blood loss, (3) ­provides fluid to the body by subcutaneous
injection so that no i.v. fluids are needed.18 Depending upon
the clinical requirements, a tumescent anesthetic solution may
contain a 5- to 40-fold dilution of lidocaine found in commer­
cially available formulations of local anesthesia. Commercial
solutions of lidocaine used by dentists and anesthesiologists
Fig. 6-23  Septal anesthesia is performed to block branches of the
sphenopalatine nerve and constrict the vascular supply.
A
B
Fig. 6-24  A simple vestibular infiltration technique to the upper (A) and lower (B) lips can assist cosmetic techniques such as the injection of
fillers.

74
Chapter 6
Cosmetic surgery procedures and techniques
typically contain 1 gram of lidocaine and 1 milligram of
epinephrine per 50 milliliters of saline. In contrast, tumescent
solutions of local anesthesia contain approximately 1 gram of
lidocaine and 1 milligram of epinephrine in 1000 milliliters
of saline. This is a 20-fold dilution of the commercial version
of lidocaine and epinephrine.18 Tumescent liposuction totally
by local anesthesia has proven to be extremely safe despite the
use of unprecedented large doses of lidocaine and epinephrine.
The explanation for this remarkable safety is the extreme dilu­
tion of the tumescent local anesthetic solution. Large volumes
of dilute epinephrine produce intense constriction of capillar­
ies in the targeted fat, which in turn greatly delays the rate of
absorption of lidocaine and epinephrine. Undiluted lidocaine
and epinephrine is absorbed into the bloodstream in less than
an hour. Tumescent dilution causes widespread capillary con­
striction which causes the absorption process to be spread over
24 to 36 hours. This reduces peak concentration of lidocaine
in the blood, which in turn reduces the potential toxicity of
a given dose of lidocaine. Dentists typically use ­concentrated
­epinephrine which may cause a rapid heart rate if the epine­
phrine is rapidly absorbed. When very dilute tumescent epine­
phrine is used, the widespread vasoconstriction slows the rate
of epinephrine absorption, which in turn prevents an increase
in heart rate.18 Profound vasoconstriction (shrinkage of cap­
illary blood vessels) results from the ­tumescent infiltration of
a large volume of dilute epinephrine into subcutaneous fat.
Tumescent vasoconstriction is so complete that liposuction
can be done with virtually no blood loss. In contrast, the older
forms of liposuction used before the invention of the tumes­
cent technique were associated with so much surgical blood
loss that autologous blood transfusions were often routine.
Because the vasoconstriction delays lidocaine absorption, the
local anesthetic remains in place in the fat for many hours. This
prolonged anesthesia permits surgery for up to 10 hours after
infiltration, and provides 24–36 hours of significant postop­
erative analgesia. Maximum recommended lidocaine dosage
is 40–55 mg/kg for tumescent liposuction when lidocaine is
greatly diluted. This is a relatively large dosage compared to the
7 mg/kg which is widely accepted as the ‘safe maximum dose
for lidocaine with epinephrine’ that anesthesiologists use for
nondiluted lidocaine for nerve blocks such as epidural blocks.18
Because tumescent local anesthesia lasts so long, tumescent
liposuction is less painful and more pleasant than liposuction
under general anesthesia or i.v. sedation. With tumescent local
anesthesia, patients are able to avoid the postoperative nausea
and vomiting associated with general anesthesia. Tumescent
anesthesia is so efficient at providing fluid to the body that it
is unnecessary to use i.v. fluids. There is a risk of dangerous
fluid overload if excessive i.v. fluids are given to a tumescent
liposuction patient.18 Figure 6-26 shows tumescent anesthesia
Fig. 6-25  This shows the approximate area anesthetized with the
vestibular anesthesia technique.
Fig. 6-26  These images show tumescent anesthesia solution being injected in the submental (A) and preauricular (B) areas.

75
Anesthesia  •  Chapter 6
used in a facelift procedure. Figure 6-27 shows the patient after
the tumescent injection and Figure 6-28 shows the bloodless
facelift flap elevated after tumescent anesthesia infiltration.
Blocking the entire face
Although many cosmetic facial procedures are performed
with i.v. sedation or general anesthesia, many can be per­
formed with only local anesthetic techniques if one masters
the blocks described in this chapter. Although this author
usually uses i.v. sedation for facelift, chemical peel, and laser
resurfacing, he has performed these procedures with only local
anesthesia. Even when using i.v. sedation or general anesthe­
sia a prudent surgeon will utilize local anesthetic techniques.
This allows the anesthetist to maintain the patient with less
medication or gas and provides postoperative pain control.
Figure 6-29 shows the various dermatomes providing sensa­
tion to the head and neck. By realizing the nerves that supply
these areas a customized ‘anesthetic map’ may be made by the
surgeon applicable to the operated areas.
Using the picture in Figure 6-29 the surgeon can create a
formula for which blocks are required for what procedure. An
example would be to select a procedure, let’s say ­endoscopic
brow and forehead lift. Look at Figure 6-29 and see what
blocks correspond with which dermatomes. For the ­endoscopic
brow one would need to block bilaterally ST, SO, GO, LO, AT
and ZT. Remember, due to anatomic variables, crossover may
be needed with adjacent dermatomes, but Figure 6-29 should
be a good map and starting point.
Summary
A firm knowledge of the sensory neuroanatomy of the head
and neck can benefit the practice of cosmetic facial surgery for
both the surgeon and the patient. Although the pathways of
sensation for the head and neck are complex, they can be easily
and safely blocked by reviewing the basic innervation patterns.
Fig. 6-27  The face has been injected with tumescent anesthetic
solution prior to facelift surgery.
Fig. 6-28  A lipocutaneous facelift flap has been elevated after
­tumescent anesthetic solution. Note the bloodless field achieved
with the tumescent technique.
Fig. 6-29  The major sensory dermatomes of the head and neck.
AC, anterior cervical cutaneous colli; AT, auriculotemporal; B,
­buccal; EN, external (dorsal) nasal; G, greater auricular; GO, greater
occipital; IO, infraorbital; IT, infratrochlear; LO, lesser occipital;
M, mental; SO, supraorbital; ST, supratrochlear; ZF,
­zygomaticofacial; ZT, zygomaticotemporal (Diagram adapted from
Larrabee and Msakielski17).

76
Chapter 6
Cosmetic surgery procedures and techniques
The entire sensory apparatus of the face is supplied by
the trigeminal nerve and several cervical branches. There
exist many patterns of nerve distribution anomaly, cross-
­innervation, and individual patient variation; however, by
following the basic techniques outlined in this chapter the
­cosmetic surgeon should be able to achieve pain control of
the major dermatomes of the head and neck.19–22
REFERENCES
  1. Hersh EV, Condouis GA. Local anesthetics: a review of their
pharmacology and clinical use. Compend Contin Educ Dent 1987;
8:374–382.
  2. Jastak JT, Yagiela JA, Donaldson D. Local anesthesia of the oral cavity.
Philadelphia: WB Saunders; 1995.
  3. Covino BG, Vassalo HG. Chemical aspects of local anesthetic agents.
In: Kitz RJ, Laver MB, eds. Local anesthetics: mechanism of action and
clinical use. New York: Grune & Stratton; 1976:1–11.
  4. Hersh EV. Local anesthetics. In: Fonseca RJ, ed. Oral and maxillofacial
surgery. Philadelphia: WB Saunders; 2000:58–78.
  5. Yagiela JA. Local anesthetics. In: Dionne RA, Phero JC, eds.
Management of pain and anxiety in dental practice. New York:
Elservier; 1991:109–134.
  6. Malamed SF. Handbook of local anesthesia, 4th edn. St. Louis: Mosby;
1997.
  7. Aceves J, Machne X. The action of calcium and of local anesthetics
on nerve cells and their interaction during excitation. J Pharmacol Exp
Ther 1963; 140:138–148.
  8. Stricharatz D. Molecular mechanisms of nerve block by local
anesthetics. Anesthesiology 1976; 45:421–441.
  9. Gray H. Anatomy of the human body, 13th edn. Philadelphia: Lea &
Febiger; 1918:1158–1169.
10. Zide BM, Swift R. How to block and tackle the face. Plast Reconst Surg
1998; 101:840–851.
11. Mendel N, Puterbaugh PG. Conduction, infiltration and general
anesthesia in dentistry, 4th edn. 140 New York: Dental Items of Interest
Publishing Co; 1938:140.
12. Mercuri LG. Intraoral second division nerve block. Oral Surg 1979;
47:9–13.
13. Brown DL. Atlas of regional anesthesia. Philadelphia;
WB Saunders; 1999:170.
14. Bonica TT, Buckley FO. Regional anesthesia with local anesthetics. In:
The management of pain. Philadelphia: Lea Febiger; 1990:1883–1966.
15. Wheeler AH. Theraputic injections for pain management. 2001.

16. Gmyrek R. Local anesthesia and regional nerve block anesthesia. 2002.

17. Larrabee W, Msakielski KH. Surgical anatomy of the face. New York;
Raven Press; 1993:83.
18. http// (accessed 2-8-05).
19. Niamtu J. Local anesthetic blocks of the head and neck for cosmetic
facial surgery, part I. A review of basic sensory neuroanatomy. Cosmet
Dermatol 2004; 17(8):515–522.
20. Niamtu J. Local anesthetic blocks of the head and neck for cosmetic
facial surgery, part II. Techniques for the upper and midface. Cosmet
Dermatol 2004; 17(9):583–587.
21. Niamtu J. Local anesthetic blocks of the head and neck for cosmetic
facial surgery, part III. Techniques for the maxillary nerve. Cosmet
Dermatol 2004; 17(10):645–647.
22. Niamtu J. Local anesthetic blocks of the head and neck for cosmetic
facial surgery, part IV. Techniques for the lower face. Cosmet Dermatol
2004; 17(11):714–720.

Office-based Sedation
and Monitoring
Rodney L. Trytko
C h a p t e r
7
Key Points
n Sedation continuum
n Common sedation techniques
n Sedation and anesthesia risks
n Perioperative clinical consideration
n Pain management
n Nausea and vomiting management
n Recovery care
p a r t 2
HISTORY AND SCIENCE
Background and history
Nearly 85% of all surgical procedures are performed outside
of the hospital and that number is growing.1 Anesthesiologists
have responded to this new office-based setting by applying
expertise gained in other ambulatory settings. New anesthetic
medications are extremely short acting and have minimal side
effects. Smaller and more portable monitoring and resusci­
tation equipment is now available. Fast emergence and early
discharge have become the norm.
Despite all the advances and enthusiasm, serious concerns
regarding safety have been raised. Moderate sedation is no
longer considered completely safe.2 Office-based procedures
associated with general anesthesia may have a significantly
higher mortality rate than expected.3,4 For these reasons, a
number of entities have developed guidelines for sedation and
surgery in the office-based setting. The American Society of
Anesthesiologists (ASA) has published guidelines for ‘Sedation
and Analgesia for Non-anesthesiologists’ and ‘Office-Based
Anesthesia’ (Appendixes A and B).5,6 The American Medi­
cal Association and the American College of Surgeons have
published guidelines for office-based surgery.7,8 In addition;
many state medical boards have actively promulgated rules
and statutory changes to regulate office-based surgery.1
Basic science
A continuum exists for sedation that ranges from anxiolysis
to general anesthesia (Fig. 7-1). No discrete interval exists
­between the various levels of sedation. Too much medication
can rapidly convert moderate sedation into general anesthesia
and expose the patient to the risks associated with an ­unsecured
airway and a lack of protective reflexes (Table 7-1).
Anxiolysis describes a state of drug-induced depres­
sion of consciousness in which patients respond normally to
teaching points
n If you do not feel comfortable sedating a patient,
strongly consider performing the procedure in
a hospital.
n Patients are very creative about what they consider
to be ‘clear liquids.’
n The most important monitor is a trained
individual solely watching the patient and doing
nothing else.
n Always check airway equipment to ensure that it
is functioning and of proper size.
n The first response to apnea is always physical
– open the airway.
n The end of the procedure is a particularly danger­
ous time for a sedated patient

78
Chapter 7
Cosmetic surgery procedures and techniques
verbal commands, either alone or accompanied by light
­tactile stimulation. Protective airway reflexes, patent airway,
spontaneous ventilation, and cardiovascular function are
maintained. No additional care is currently recommended
for anxiolysis.
Moderate sedation describes a state of drug-induced de­
pression of consciousness in which patients respond purposefully
to verbal commands, either alone or accompanied by light
tactile stimulation. Protective airway reflexes, patent airway,
spontaneous ventilation, and cardiovascular function are
­usually maintained. Conscious sedation, monitored anesthe­
sia care (MAC), and ‘sedation and analgesia’ are all equivalent
terms.
Moderate sedation allows patients to tolerate and ­sometimes
forget unpleasant procedures. It also facilitates procedures in
uncooperative patients who are not particularly ­uncomfortable
but are required to not move. It is not, however, a substitute
for adequate local or regional anesthesia.
Deep sedation describes a state of drug-induced depression
of consciousness in which patients respond purposefully to
verbal commands in response to repeated or painful stimulation.
Protective airway reflexes, patent airway, and spontaneous
ventilation may not be maintained. Deep sedation is rarely a
desirable state in an office-based setting.
General anesthesia is a medically controlled state of uncon­
sciousness and amnesia. If the only response to stimulation is
withdrawal, a condition of general anesthesia exists. It is asso­
ciated with a loss of protective airway reflexes, the inability to
maintain a patent airway independently, and cardiovascular
instability. The patient under general anesthesia is completely
dependent upon the anesthesiologist for resuscitation during
and after the surgical procedure.
Providing general anesthesia in an office-based setting
can be time consuming, risky, and expensive. Many offices
lack noninvasive monitoring and emergency resuscitation
equipment, recovery facilities, or appropriate perioperative
nursing personnel. Many offices also lack adequate suction
for anesthetic trace gas scavenging; therefore, the utilization
of an anesthesia machine may be problematic. Given the
appropriate equipment and personnel, general anesthesia can
be administered in an office-based setting as in any ambula­
tory surgery center or hospital.
The practice of pediatric sedation in an office-based setting
is controversial and probably should be avoided.
Clinical studies
Moderate sedation
Moderate sedation techniques for office-based procedures
­typically combine a short-acting sedative-hypnotic (mida­
zolam or propofol) and a short-acting narcotic (fentanyl). The
goal is to provide a comfortable situation for the patient and
the ­operating practitioner while minimizing recovery times.
Patient apprehension, recall, and the pain associated with
the procedure should be reduced or eliminated. In order to
achieve these goals, a combination of medications is usually
necessary.
The simplest technique involves incremental doses of
midazolam and fentanyl.9,10 An alternative technique is to
carefully titrate the level of sedation with a propofol infu­
sion. Propofol infusions require heightened surveillance be­
cause of propofol’s propensity to rapidly produce anesthesia
and apnea. Propofol’s package insert (Diprivan®, Astra­
Zeneca 4-01) states that it ‘should be administered only by
persons trained in the administration of general anesthesia
and not involved in the conduct of the surgical/diagnostic
procedure.’ The ASA has developed guidelines for the safe
use of propofol.11
Anxiolysis
Moderate
sedation
Deep
sedation
General
anesthesia
Fig. 7-1  Sedation continuum.
Table 7-1  Sedation definitions
Minimal sedation
(Anxiolysis)
Moderate sedation
(Conscious sedation)
Deep sedation
General anesthesia
Responsiveness
Normal response
to verbal stimulation
Purposeful response
to verbal or tactile
stimulation
Purposeful response
following repeated or
painful stimulation
Unarousable, even with
painful stimulus
Airway
Unaffected
No intervention required
Intervention may be
required
Intervention often
required
Spontaneous ventilation
Unaffected
Adequate
May be inadequate
Frequently inadequate
Cardiovascular function
Unaffected
Usually maintained
Usually maintained
May be impaired

79
Office-based sedation and monitoring  •  Chapter 7
The typical total dosages of medication vary considerably
among patients but do correlate with the procedure duration.
Recovery is typically rapid (10 min) with a minimum amount
of delirium and confusion. The most common ­complications
are nausea and vomiting, which fortunately occurs in a
­minority of patients. Discharge times are longer for patients
who developed nausea and vomiting, younger patients, and
patients receiving preoperative oral sedation.
General anesthesia
General anesthesia can be administered with potent
­inhalational anesthetic gases (e.g. desflurane, isoflurane, and
sevoflurane), total intravenous anesthesia (TIVA), or a com­
bination of both. With general anesthesia, the patients are
asleep, the surgical field is steady, and the time requirements
for the operating practitioner are substantially reduced.
Administering potent inhalational anesthetics requires an
aesthesia machine and suction capabilities to scavenge trace
anesthetic gases.
TIVA techniques do not require an anesthesia machine,
and are associated with minimal complications and extremely
rapid recoveries.12–18 TIVA also offers advantages over inha­
lational anesthesia in terms of patient satisfaction, lower costs,
and improved recovery profile. Most TIVA techniques utilize
a propofol infusion that is supplemented with fentanyl or
­another short-acting narcotic.
Postoperative care
Surgery represents a form of premeditated injury that is always
associated with pain and frequently associated with nausea.
Pain is an unpleasant sensory and emotional experience asso­
ciated with actual or potential tissue damage. Nausea is an
­unpleasant sensation associated with the awareness of the urge
to vomit. These symptoms are frequently feared by patients,
can delay discharge, and are a leading cause of ­unanticipated
hospital admission.19
Recovery is a continual process. Patients cannot be consid­
ered fully recovered until they have returned to their preoper­
ative physical and mental status. Respiratory depression in the
early postoperative period is a significant risk to all patients
after sedation.20 Postoperative monitoring must continue
­until the patient meets accepted discharge criteria.21,22 The
requirement for oral intake and voiding before discharge has
been questioned, and this issue remains controversial. Quality
postoperative nursing care is the single most important factor
to ensure rapid discharge.23
Sedation and anesthesia risk
The overall risk of general anesthesia has dramatically de­
clined because of the advances in anesthesia techniques.
Currently, the risk of death from general anesthesia is less
than 1 in 185 000.24
Contrarily, the risk associated with moderate ­ sedation
appears to be increasing. The ASA Closed Claims study has
demonstrated an increasing number of annual ­malpractice
litigation actions involving serious injuries associated
with monitored anesthesia care (almost always moderate
­sedation, Fig. 7-2).2 In this study, the severity of injury for
such claims was comparable to general anesthesia, with
41% of the claims being for death or permanent brain
damage. The most common cause of injury was respira­
tory ­depression as a result of oversedation. Most injuries
­occurred in sicker elderly patients who received a combi­
nation of two or more drugs. Nearly half of the injuries
were judged to be preventable with the use of additional or
better ­monitoring.
Studies of office-based surgery also demonstrate significant
safety concerns. In a large survey of plastic surgeons, 95 lipo­
suction-related fatalities in nearly half a million procedures
yielded a normalized fatality rate of 19.1 per 100 000.25 In
another study, surgical procedures performed in offices and
ambulatory surgery centers were associated with a tenfold
­increased risk of adverse incidents and death.3 Other authors
have questioned the latter study.4
Discussion
Sedation can generally be safely administered to healthy adults
in an office-based setting. For moderate sedation, the ASA’s
Sedation and Analgesia guidelines should be meticulously fol­
lowed in order to ensure patient safety. General anesthesia can
be administered to healthy adult patients in an office-based
setting with a rapid discharge to home.
Private physician offices have been relatively slow to adopt
safety improvements that have swept the rest of the country.
The public will likely become more educated on the prob­
lems associated with office-based procedures. Regulators will
­demand that safety is proven to be equivalent to the hospital
setting. The future will demonstrate that many procedures
now performed in an ambulatory surgery center or a hospital
can be safely performed in the office-based setting.
MAC
General
Regional
60%
50%
40%
30%
20%
10%
0%
Death or
permanent brain
damage
Permanent
disabling
Temporary non-
disabling
Fig. 7-2  Severity of injury in monitored anesthesia care (MAC),
general, and regional anesthesia claims.

80
Chapter 7
Cosmetic surgery procedures and techniques
PROCEDURES AND TECHNIQUES
Preoperative clinical considerations
Patient selection
The ASA classifies patients according to preoperative physi­
cal status with classes I to V (Table 7-2). The ASA Closed
Claims study has demonstrated that for moderate sedation,
age greater than 70 years, and ASA physical status III to
V result in a higher risk of litigation.2 Physical status has
also been demonstrated to correlate inversely with general
anesthesia outcomes; therefore, general anesthesia should
be limited to lower-risk patients (ASA I and II) in an office-
based setting.26
Preprocedure preparation
Patients should be informed of the associated risks and
agree to the administration of sedation before the proce­
dure begins. All reasonably possible complications should be
discussed.
A preoperative history should include the following:

1. Abnormalities of the major organ systems

2. Previous adverse experience with moderate sedation,
and regional and general anesthesia

3. Current medications and drug allergies

4. Time and nature of last oral intake

5. History of tobacco, alcohol, or substance use or abuse
Patients should undergo a focused physical examination
including auscultation of the heart and lungs, and an evalua­
tion of the airway. Airway evaluation is performed in order to
identify patients who are likely to be difficult to intubate.
Airway evaluation includes the following three criteria:

1. Relative tongue size. Mallampati utilized three classifications
for describing the relative size of the tongue (Fig. 7-3).27
The Mallampati classification is best obtained with the
patient in the sitting position with the head in full extension,
tongue out, and with phonation.28

2. Mandibular space size. This is the space that is anterior to
the larynx where the tongue must be displaced in order to
intubate the patient under direct vision.

3. Atlanto-occipital joint extension. Such extension aligns the
laryngeal and oral axes.
Only patients who are Mallampati class I or II who possess
a mandibular space (tip of larynx to tip of mandible) greater
than 6  cm and demonstrate an atlanto-occipital extension
greater than 35% should be considered candidates for office-
based procedures.29
Preprocedure testing should be guided by the patient’s un­
derlying medical condition and the likelihood that the results
will affect the management of sedation. Patients scheduled for
surgeries do not need routine laboratory tests.30 Other test­
ing (including laboratory, ECG, and chest X-rays) should be
considered only for specific indications.
Procedural techniques
Procedure guidelines and standards
The ASA has developed guidelines for preoperative fasting
and the use of pharmacologic agents to reduce the risk of
pulmonary aspiration.31 Preoperative fast should be at least
2 hours for clear liquids, and 6 hours for all other liquids
and solid foods. Medications may be given at their usual
times with a sip of water. The routine use of medications
Table 7-2  ASA physical status classification
Category
Description
I
Healthy patient
II
Mild systemic disease; no functional limitation
III
Severe systemic disease; definite functional
limitation
IV
Severe systemic disease that is a constant
threat to life
V
Moribund patient unlikely to survive 24 hours
with or without operation
Class I
Class II
Class III
Class IV
Fig. 7-3  Mallampati classification.27

81
Office-based sedation and monitoring  •  Chapter 7
to reduce the risk of pulmonary aspiration is not recom­
mended.
The ASA has also published a number of guidelines and
standards pertinent to office-based sedation and ­ surgery
­(Appendixes A, B, and C).5,6,32 The guidelines include
­recommendations for basic monitoring equipment, appropri­
ate personnel, and emergency medications and equipment.
These guidelines are widely accepted and should be meticu­
lously followed.
Moderate sedation
Most moderate sedation techniques involve the following
steps:

1. Establish an intravenous line.

2. Administer fentanyl 0.05–1 μg/kg i.v. p.r.n. and

3. Administer midazolam 0.5–1 mg i.v. p.r.n. and/or

4. Administer continuous propofol infusion (25–50 μg/kg/min),
increasing at increments of 5 μm/kg/min p.r.n. Rarely more
than 150 μg/kg/min is needed.
All medications (Appendix D) should be carefully titrated
to achieve the desired level of sedation. The typical total
dosages of medication correlate significantly with procedure
duration as well as patient age, sex, and weight.
A designated individual should be present to monitor the
patient throughout the procedure. This individual should
be able to recognize all complications associated with seda­
tion, understand the pharmacology of the agents that are
­administered, and understand the role of pharmacologic
­antagonists for opioids and benzodiazepines. In addition, at
least one individual with advanced life-support skills should
be immediately available.
General anesthesia
Because of the risks and multiple system instabilities associ­
ated with general anesthesia, an anesthesiologist should be
present at all times. Techniques utilize a potent inhalational
anesthetic gas, TIVA, or some combination of both. TIVA
does not require an anesthesia machine or the need for trace
anesthetic gas scavenging equipment, both advantages for the
office-based setting (Fig. 7-4). A guideline for TIVA is listed in
Appendix E.
Perioperative risk management
The primary complication associated with sedation is airway
mismanagement. A particularly dangerous combination of
apnea and unresponsiveness occurs when sedative-hypnotics
and narcotics are utilized simultaneously. In addition, air­
way obstruction at the level of the oral pharynx is frequently
caused by the relaxation of the normal tone of the genio­
glossus muscle.
Upon recognizing hypoventilation or apnea, the open air­
way algorithm should be followed until the patient returns to
a stable state of unassisted respiration and adequate oxygen
saturation (Fig. 7-5).
Fig. 7-4  W. Phillip Werschler, MD, is
­performing laser facial resurfacing under
total intravenous anesthesia (TIVA) at the
Spokane Dermatology Clinic, Spokane,
Washington.

82
Chapter 7
Cosmetic surgery procedures and techniques
The first response to a suspected hypoventilation or apnea
should be an immediate attempt to open the airway. Most
of the time, a simple chin lift will relieve the obstruction
and stimulate the patient to begin breathing. If the problem
­persists, the next steps include pharmacologic reversal agents
and positive-pressure ventilation.
As previously stated, combinations of sedatives and narcot­
ics are much more likely to cause hypoventilation or apnea.
While pharmacologic reversal agents are available for narcot­
ics and benzodiazepines, usually only reversing the narcotic
is necessary to restore adequate ventilation. Small doses of
naloxone are usually effective.
If positive-pressure mask ventilation is indicated, one per­
son should hold the face while maintaining a mask seal and a
chin lift/jaw thrust, while the other person squeezes the bag.
If ventilation is not adequate, various pharyngeal airways
(oral and nasal) may relieve the obstruction. A variety of ob­
turator airways (Laryngeal Mask Airway or Combitube) can
also be immediately inserted. Laryngeal mask airways (LMAs)
are placed blindly and obturate the airway at the level of the
larynx (Fig. 7-6). Adult LMAs typically are sizes 3 to 5.
Many of these situations are true emergencies. Airway man­
agement experts should be immediately summoned anytime air­
way obstruction is not immediately and completely reversed.
Postoperative clinical considerations
Pain management
The single most reliable indicator of the existence and inten­
sity of acute pain is the patient’s self-report. Once postopera­
tive pain has occurred, pain assessment should be frequent
and simple. Surgical causes of unexplained pain should be
considered and excluded. Treatment should then be initiated
utilizing the pharmacological analgesic therapies. Patients
Chin lift/jaw thrust
No respirations present
Spontaneous respiration
present
Ventilate with supplemental
oxygen
Insert pharyngeal
airway
Ventilate
Endotracheal
intubation
Keep airway open.
Place in the recovery
position and monitor
vital signs
Fig. 7-5  Open airway algorithm.
A
B
Fig. 7-6  Laryngeal mask airway (LMA). (A) An LMA. (B) Diagram
of an LMA in proper position to obturate the airway at the level of the
larynx.

83
Office-based sedation and monitoring  •  Chapter 7
with severe pain that cannot be easily or adequately control­
led may need to be admitted to an acute care facility.
The Agency for Healthcare Policy and Research (AHCPR)
has developed guidelines for acute postoperative pain manage­
ment (Fig. 7-7).33 These guidelines recommend the following:

1. A collaborative, interdisciplinary approach to pain control

2. An individualized, proactive pain control plan developed
preoperatively by patients and practitioners

3. Assessment and frequent reassessment of the patient’s
pain

4. Use of both drug and non-drug therapies to control
and prevent pain

5. A formal, institutional approach to management of
acute pain with clear lines of responsibility
A large prospective study examined the patterns of pain in
over 10 000 ambulatory surgery patients.34 Severe pain was
Assess resources for pain
management
Preoperative patient
assessment
Develop collaborative
plan
Patient (and family)
preparation and preoperative
intervention
Preoperative pain
Analgesia
No preoperative pain
Intraoperative anesthesia and
analgesia
Initiate preemptive measures
for postoperative pain control
Postoperative management
Termination of operative
anesthesia/analgesia
Significant pain consistent with
surgical trauma
No pain or
pain not requiring
intervention
No pain or
pain requiring
intervention
Initiate postoperative analgesia
or adjust dose/interval of
preoperative analgesic
Reassess
Surgical
evaluation
Unacceptable
side effects or
inadequate
analgesia
No
Assess: Did intervention
produce satisfactory
pain relief
Treat
Yes
Optimize dose
interval
Satisfactory response
Discharge planning
Change drug,
Interval, dose,
route, modality; add
adjuvant; or
treat side effects
A
B
Fig. 7-7  AHCPR pain treatment flowcharts.33

84
Chapter 7
Cosmetic surgery procedures and techniques
more prevalent in younger healthy male patients, and the
type and length of the surgery were significant factors. Not
­surprisingly, procedures performed under local anesthesia had
a negligible amount of postoperative pain, far less than if the
procedures had been performed under general anesthesia.
Administering adequate local anesthesia at an operative site
minimizes postoperative pain by blocking local pain fibers and
nociceptors, and by providing preemptive analgesia.
Opioids are, more than other medications, almost ideal
analgesics (Table 7-3). In a study of painful ambulatory
­surgeries, equipotent doses of fentanyl were compared with
morphine in the treatment of postoperative pain.35 Morphine
produced the best quality of analgesia but was associated with
an increased incidence of postoperative nausea and vomit­
ing (PONV), the short duration of fentanyl was not associ­
ated with faster discharge times, and most patients receiving
­fentanyl required additional oral analgesic medications.
Since opioids have many undesirable side effects that offset
their benefits, multimodal methods to manage postoperative
pain have become very popular. Multimodal methods com­
bine opioids with local anesthesia and nonopioid analgesics
(Table 7-4).37
Operative pain is multifactorial. Pain management inter­
ventions at different levels in the peripheral and central nerv­
ous systems will facilitate a synergism between different
classes of drugs. This synergism permits the use of lower
effective doses of each drug and thereby reduces the asso­
ciated side effects. Multimodal pain management can lead
to significantly shorter discharge times, lower incidence of
PONV, and nearly complete postoperative pain relief.
Aspirin and acetaminophen are two popular nonopioid an­
algesics with a vast history of efficacy. Unlike aspirin, acetami­
nophen does not damage the gastric mucosa or inhibit platelet
aggregation; however, acute and chronic overdoses can cause
hepatic necrosis.38
Nonsteroidal antiinflammatory drugs (NSAIDs) should
always be considered when treating acute pain, especially
when inflammation is involved. They work by inhibiting the
enzyme cyclooxygenase (COX). Two isoforms of COX have
been identified. COX-1 isoenzyme is normally found in blood
vessels, the stomach, and kidneys. COX-2 is induced in
­peripheral tissues by inflammation.
Patients may vary in their relative response to various
NSAIDs; therefore, if a patient does not experience an ade­
quate response to one agent, another may be considered. The
most common side effects related to NSAIDs are hematological
­effects (inhibition of platelet aggregation), gastrointestinal ef­
fects (dyspepsia, ulcerations, bleeding, or perforation), and renal
insufficiency. All NSAIDs should be used cautiously in patients
with congestive heart failure, chronic renal insufficiency, cirrho­
sis with ascites, volume depletion, and multiple myeloma.
NSAIDs celecoxib (Celebrex), parecoxib (Dynastat), ro­
fecoxib (Vioxx), and valdecoxib (Bextra) selectively inhibit the
COX-2 enzyme. Given the current controversies over the car­
diovascular risks associated with these medications, caution is
indicated until further studies are performed.39 While there is
no evidence that the use of these medications for acute pain
is associated with additional risks, there is also little evidence
that they offer any significant benefit compared to other
­nonopioid analgesics.40
Table 7-3  Selected opioid analgesics36*
Medication
Oral dose
(mg)
Parental dose**
(mg)
Comment
Precaution and
contraindications
Fentanyl
None
0.1
Duragesic patch 25 μg/h roughly
equivalent to sustained-release
morphine 45 mg/d
12-hour delay in
onset and offset of
transdermal patch;
use short-acting agent
when initiating patch
Hydromorphone
7.5
1.5
Slightly shorter duration
than morphine
Meperidine
300
75
Slightly shorter duration
than morphine
Normeperidine (metabolite)
accu­mulates; do not use in
children or patient receiving
monoamine oxidase
inhibitors
Morphine
30
10
Long-acting preparation available
Oxycodone
20
None
*For all opioids: use caution in patients with asthma, hepatic failure, impaired ventilation.
**Intramuscular doses for acute pain in adults. For single intravenous boluses, use half the intramuscular dose.

85
Office-based sedation and monitoring  •  Chapter 7
Other classes of medications may enhance the effects of
opioids. Benzodiazepines are effective in patients whose pain
is compounded by excessive anxiety. Clonidine may reduce
postoperative opioid requirements.41 Some antihistamines,
such as hydroxyzine, are effective adjuncts to opioids. Fi­
nally, glucocorticoids are potent antiinflammatory agents that
­significantly reduce postoperative pain as well as nausea and
vomiting.42
Postoperative nausea and vomiting
management
Postoperative nausea and vomiting (PONV) remains a com­
plication of ambulatory surgery that is not only distressing
to the patients but may delay or prevent discharge. Patients
with a history of motion sickness or PONV are particularly
distressed with the thought of experiencing PONV after an
operative procedure. Despite recent advances in antiemetic
therapies, nearly a third of patients have PONV during the
first 24 hours after surgery.43
The goals of PONV management are to accurately predict
which patients are at high risk to develop PONV in order to
initiate prophylactic treatment, reduce baseline risk factors,
and treat PONV symptomatically when it occurs (Fig. 7-8).44
Patient characteristics associated with a higher incidence of
PONV are female gender, history of PONV, nonsmoking,
and use of postoperative opioids.45 The incidence of PONV
with the presence of none, one, two, three, or all four of these
risk factors is approximately 10%, 20%, 40%, 60%, and 80%,
respectively. The method of anesthesia and the length of sur­
gery have a significant effect on PONV, and these factors seem
to be far more significant than the type of surgery.
A reduction in baseline risk factors is the most effective
strategy for reducing PONV.46 A list of these strategies is
­included in Table 7-5.
Antiemetic agents are also effective in decreasing the
incidence of PONV when administered prophylactically.
Prophylaxis is only recommended for patients at moderate
to high risk for PONV. Patients at low risk for PONV are
usually not given PONV prophylaxis unless they are at risk
for medical sequelae from vomiting (i.e. patients with wired
jaws or increased intracranial pressure or who are having
fundoplication surgery).
In general, combination therapy is superior to monotherapy
for PONV prophylaxis and is indicated in high-risk pa­
tients.47,48 Drugs with different mechanisms of action should
Table 7-4  Selected nonopioid analgesics36
Medication
Average oral
analgesic dose (mg)
Maximum daily
dose (mg)
Plasma
half-life (h)
Comments
Acetaminophen
500–1000
4000
2–3
Hepatotoxicity in large
doses
Aspirin
500–1000
4000
0–25
Do not use in children
with viral illness
Ibuprofen
200–400
2400
2–2∙5
Indomethacin
25
100
2
High incidence of side
effects
Ketorolac (Toradol)
30–60 mg i.m. or 30 mg
i.v. initial; 15 or 30 mg i.v.
or i.m. subsequent
150 first day; 120
thereafter
6
Limit treatment to
5 days; compares to
6–12 mg of morphine
Naproxen (Naproxen)
250–500
1250
12–15
Evaluate risk of
PONV in
surgical patient
Low
Moderate
High
No prophylaxis is a
medical
sequelae from
vomiting
Consider regional
anesthesia
otherwise, reduce
baseline risk factors
Patients at
moderate risk
Patients at
high risk
Consider antiemetic
prophylaxis with
monotherapy (adults)
or combination therapy
(children and adult)
Initiate combination
therapy with 2 or 3
prophylactic agents
from different classes
Fig. 7-8  Algorithm for the management of PONV.

86
Chapter 7
Cosmetic surgery procedures and techniques
be used in order to optimize efficacy. Current antiemetic
medications, doses, and timing for administration are listed
in Table 7-6.44
Patients who are given prophylactic antiemetic therapy for
PONV and subsequently develop PONV should be treated
with an agent from a different pharmacological class than
the medication used for prophylaxis. When PONV occurs
more than 6  h after surgery, repeat dosing of 5-HT3 antago­
nists (dolasetron, granisetron, and ondansetron) should be
considered.
Nonpharmacologic
therapies
acupuncture
(electro-
­acupuncture, transcutaneous electrical nerve stimulation,
acupoint stimulation, and acupressure) may be considered in
adults.49
Recovery care and discharge
The end of the procedure is a particularly dangerous time for
a sedated patient. Noxious stimulation is a natural antagonist
to respiratory depression by opioids and other sedative agents.
Respiratory depression may become evident after the noxious
stimulation associated with a procedure ceases or decreases in
intensity.
Postoperative care of the patient encompasses three phases
of recovery care: early recovery as the patient emerges from
sedation, intermediate recovery where the patient achieves cri­
teria for discharge home, and late recovery or post-discharge
recovery when the patient achieves full recovery from both
surgery and sedation. Intraoperative monitoring should be
continued into the recovery period at regular intervals during
the first two of these phases until the patient is discharged.
Extremely rapid recovery from sedation can be expected.
Patients should be assessed immediately upon emergence
to determine which phase of recovery should be initiated.
Objective discharge criteria should be documented before
appropriate monitoring is terminated and the patient is
discharged.21 While it is the physician’s responsibility to
­ensure that all patients satisfy discharge criteria, the ­nursing
staff may discharge patients according to formal discharge
criteria (Appendix F).
Those rare patients who do not meet the discharge cri­
teria in a reasonable amount of time should be transferred
to a hospital under continuous monitoring. Fortunately,
­hospital admissions after ambulatory surgery are extremely
­uncommon.50
REFERENCES
  1. Non-Hospital Surgical Setting Advisory Work Group Report
(Washington State Department of Health). 2005.
  2. Bhananker S, Posner K, et al. Injury and liability associated with
monitored anesthesia care: a closed claims analysis. Anesthesiology
2006; 104(2):228–234.
  3. Vila H, Soto R, et al. Comparative outcomes analysis of procedures
performed in physician offices and ambulatory surgery centers. Arch
Surg 2003; 138:991–995.
  4. Venkat AP, Coldiron B, et al. Lower adverse event and mortality rates in
physician offices compared with ambulatory surgery centers: a reappraisal
of Florida adverse event data. Dermatol Surg 2004; 30(12 Pt 1):
1451–1453.
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a report by the American Society of Anesthesiologists task force on
sedation and analgesia by non-anesthesiologists. Anesthesiology 1996;
84:459–471.
  6. Guidelines for Office-based Anesthesia. Approved by the American
Society of Anesthesiologists’ House of Delegates on October 13, 1999.
  7. Guidelines for Optimal Office-based Surgery, 2nd edn. Chicago:
American College of Surgeons; 1996.
  8. Office-Based Surgery Regulation. Approved by the American Medical
Society’s House of Delegates in June 2003.
  9. Marcus JR, Tyrone JW, et al. Optimization of conscious sedation in
plastic surgery. Plast Reconstr Surg 1999; 104:1338–1345.
10. Abeles G, Warmuth IP, et al. The use of conscious sedation for
outpatient dermatologic surgical procedures. Dermatol Surg 2000;
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11. Statement on the Safe Use of Propofol. Approved by ASA House of
Delegates on October 27, 2004.
12. Trytko RT, Werschler WP. Total intravenous anesthesia for office-based
laser facial resurfacing. Lasers Surg Med 1999; 25:126–130.
13. Friedberg BL. Propofol-ketamine technique: dissociative anesthesia for
office surgery. Anesth Plast Surg 1999; 23:70–75.
14. Rudner R, Jalowiecki P, et al. Conscious analgesia/sedation with
remifentanil and propofol versus total intravenous anesthesia with
fentanyl, midazolam, and propofol for outpatient colonoscopy.
Gastrointest Endosc 2003; 57(6):657–663.
Table 7-6  Antiemetic doses and timing for administration in adults
Drug
Dose
Timing
Granisetron
0.35–1 mg i.v.
At end of surgery
Dolasetron
12.5 mg i.v.
At end of surgery
Ondansetron
4–8 mg i.v.
At end or surgery
Dexamethasone
5–10 mg i.v.
Before induction
Dimenhydrinate
1–2 mg/kg i.v.
Prochlorperazine
5–10 mg i.v.
At end of surgery
Promethazine
12.5–25 mg i.v.
At end of surgery
Scopolamine
Transdermal
patch
Applied prior
evening or 4 h
before end of
surgery
*When a dose range is presented, the smallest dose is recommended.
Table 7-5  Strategies to reduce baseline risk
Use of regional anesthesia
Use of propofol for induction and maintenance of anesthesia
Use of intraoperative supplemental oxygen
Use of hydration
Avoidance of nitrous oxide
Avoidance of volatile anesthetics
Minimization of intraoperative and postoperative opioids
Minimization of neostigmine

87
Office-based sedation and monitoring  •  Chapter 7
15. Montes FR, Trillos JE, et al. Comparison of total intravenous anesthesia
and sevoflurane-fentanyl anesthesia for outpatient otorhinolaryngeal
surgery. J Clin Anesth 2002; 14(5):324–328.
16. Dershwitz M, Michalowski P, et al. Postoperative nausea and vomiting
after total intravenous anesthesia with propofol and remifentanil or
alfentanil: how important is the opioid? J Clin Anesth 2002; 14(4):
275–278.
17. Ozkose Z, Yalcin Cok O, et al. Comparison of hemodynamics, recovery
profile, and early postoperative pain control and costs of remifentanil
versus alfentanil-based total intravenous anesthesia (TIVA). J Clin
Anesth 2002; 14(3):161–168.
18. Visser K, Hassink EA, et al. Randomized controlled trial of total
intravenous anesthesia with propofol versus inhalation anesthesia
with isoflurane-nitrous oxide: postoperative nausea with vomiting and
economic analysis. Anesthesiology 2001; 95(3):616–626.
19. Chung F, Mezei G. Factors contributing to a prolonged stay after
ambulatory surgery. Anesth Analg 1999; 89:1352–1359.
20. Tiret L, Hatton F, Desmonts JM, et al. The implications of a national
study of risk of anesthesia. Health Policy 1988; 9:331–336.
21. Marshall SI, Chung F. Discharge criteria and complications after
ambulatory surgery. Anesth Analg 1999; 88:508–517.
22. Chung F. Recovery pattern and home-readiness after ambulatory
surgery. Anesth Analg 1995; 80:896–902.
23. Pavlin DJ, Rapp SE, Polissar NL, et al. Factors affecting discharge time
in adult outpatients. Anesth Analg 1999; 89:75.
24. Bodenheimer T. The American health care system – the movement for
improved quality in health care. N Engl J Med 1999; 340:488–492.
25. Grazer FM, de Jong RH. Fatal outcomes from liposuction: census survey
of cosmetic surgeons. Plast Reconstr Surg 1999; 105:436–446.
26. Schneider AJL. Assessment of risk factors and surgical outcomes. Surg
Clin North Am 1983; 63:1113.
27. Mallampati SR, Gatt SP, et al. A clinical sign to predict difficult
intubation: a prospective study. Can J Anaesth 1985; 32:429–434.
28. Lewis M. What is the best way to determine oropharyngeal classification
and mandibular space length to predict difficult intubation?
Anesthesiology 1994; 81:69–75.
29. Tse JC. Predicting difficult endotracheal intubation in surgical patients
scheduled for general anesthesia: a prospective blind study. Anesth Analg
1995; 81:254–258.
30. Narr BJ, Warner ME, et al. Outcomes of patients with no laboratory
assessment before anesthesia and a surgical procedure. Mayo Clin Proc
1997; 72:505.
31. Practice guidelines for preoperative fasting and the use of
pharmacologic agents to reduce the risk of pulmonary aspiration:
application to health patients undergoing elective procedures. American
Society of Anesthesiologists’ report on November 26, 2002.
32. Basic Monitoring Standards. Approved by the American Society of
Anesthesiologists’ House of Delegates on October 21, 1986 and last
amended on October 23, 1996.
33. Acute pain management guidelines panel. Acute pain management:
operative or medical procedures and trauma. Clinical practice guideline.
AHCPR Pub. No. 92-0032. Rockville, Md: Agency for Healthcare
Policy and Research. Public Health Service, US Dept. of Health and
Human Services, Feb. 1992.
34. Chung F, Ritchie E, Su J. Postoperative pain in ambulatory surgery.
Anesth Analg 1997; 85:808–816.
35. Claxton AR, McGuire G, et al. Evaluation of morphine versus fentanyl
for postoperative analgesia after ambulatory surgical procedures. Anesth
Analg 1997; 84:509–514.
36. Omoigui S. The anesthesia drugs handbook, United States. St Louis:,
Mosby-Year Book; 1995.
37. Elia N, Lysakowski C, et al. Does multimodal analgesia with
acetaminophen, nonsteroidal antiinflammatory drugs, or selective
cyclooxygenase-2 inhibitors and patient-controlled analgesia morphine
offer advantages over morphine alone?: meta-analyses of randomized
trials. Anesthesiology 2005; 103(6):1296–1304.
38. Whitcomb DC, Block GD. Association of acetaminophen
hepatotoxicity with fasting and ethanol use. JAMA 1994; 272:1845–
1850.
39. Schror K, Mehta P, Mehta JL. Cardiovascular risk of selective
cyclooxygenase-2 inhibitors. J Cardiovasc Pharmacol Ther 2005;
10(2):95–101.
40. White P. Changing role of COX-2 inhibitors in the perioperative
period: is parecoxib really the answer? Anesth Analg 2005; 100:1306–
1308.
41. Park J, Forrest J, Kolesar R, et al. Oral clonidine reduces postoperative
PCA morphine requirements. Can J Anaesth 1996; 43:900–906.
42. Romundstad L, Breivik H, et al. Methylprednisolone reduces pain,
emesis, and fatigue after breast augmentation surgery: a single-dose,
randomized, parallel-group study with methylprednisolone 125 mg,
parecoxib 40 mg, and placebo. Anesth Analg 2006; 102(2):418–425.
43. Carroll NV, Miederhoff P, Cox FM, et al. Postoperative nausea and
vomiting after discharge from outpatient surgery centers. Anesth Analg
1995; 80:903–909.
44. Gan T, Meyer T, et al. Consensus guidelines for managing postoperative
nausea and vomiting. Anesth Analg 2003; 97:62–71.
45. Apfel CC, Laara E, Koivuranta M, et al. A simplified risk score for
predicting postoperative nausea and vomiting. Anesthesiology 1999;
91:693–700.
46. Habib A, White W, et al. A randomized comparison of a multimodal
management strategy versus combination antiemetics for the prevention
of postoperative nausea and vomiting. Anesth Analg 2004; 99:77–81.
47. Habib A, Gan T. Combination therapy for postoperative nausea and
vomiting: a more effective prophylaxis? Ambulatory Surg 2001; 9:
59–71.
48. Eberhart LH, Morin A, et al. Droperidol and 5-HT3-receptor
antagonists, alone or in combination, for prophylaxis of postoperative
nausea and vomiting: a meta-analysis of randomized controlled trials.
Acta Anaesthesiol Scand 2000; 44:1252–1257.
49. Lee A, Done ML. The use of nonpharmacologic techniques to prevent
postoperative nausea and vomiting: a meta-analysis. Anesth Analg 1999;
88:1362–1369.
50. Twersky RS. Admissions following ambulatory surgery: outcome in
seven urban hospitals. Ambulatory Surg 1995; 3:141–146.

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Cosmetic surgery procedures and techniques
Appendix A
PRACTICE GUIDELINES FOR SEDATION AND ANALGESIA
BY NON-­ANESTHESIOLOGISTS
I.  Patient evaluation
Clinicians administering sedation and analgesia should be familiar with relevant aspects of the patient’s medical history includ­
ing: (1) abnormalities of the major organ systems, (2) previous adverse experience with sedation/analgesia, as well as regional
and general anesthesia, (3) current medications and drug allergies, (4) time and nature of last oral intake, and (5) history of
tobacco, alcohol, or substance use or abuse. Patients presenting for sedation and analgesia should undergo a focused physical
examination including auscultation of the heart and lungs and evaluation of the airway. Pre-procedure laboratory testing should
be guided by the patient’s underlying medical condition and the likelihood that the results will affect the management of seda­
tion and analgesia.
II.  Preprocedure preparation
Patients should be informed of and agree to the administration of sedation and analgesia before the procedure begins. Patients
undergoing sedation and analgesia for elective procedures should not drink fluids or eat solid foods for a sufficient period of time
to allow for gastric emptying before their procedure.
III.  Monitoring
Level of Consciousness: The response of patients to commands during procedures performed with sedation and analgesia serves as a
guide to their level of consciousness. Spoken responses also provide an indication that the patients are breathing. Patients whose
only response is reflex withdrawal from painful stimuli are likely to be deeply sedated, approaching a state of general anesthesia,
and should be treated accordingly.
Pulmonary Ventilation: Ventilatory function usually can be effectively monitored by observation of spontaneous respiratory
activity or auscultation of breath sounds. Impedance plethysmography may fail to detect airway obstruction.
Oxygenation: Hypoxemia during sedation and analgesia is more likely to be detected by oximetry than by clinical assessment alone.
Hemodynamics: Early detection of changes in patients’ heart rate and blood pressure may enable practitioners to detect problems
and intervene in a timely fashion, reducing the risk of cardiovascular collapse.
IV.  Recording of monitored parameters
Patients’ ventilatory and oxygenation status and hemodynamic variables should be recorded at a frequency to be determined
by the type and amount of medication administered as well as the length of the procedure and the ­general condition of the
­patient. At a minimum, this should be: (1) before the beginning of the procedure, (2) after administration of sedative and
­analgesic agents, (3) on completion of the procedure, (4) during initial recovery, and (5) at the time of discharge. If recording is
performed automatically, device alarms should be set to alert the care team to critical changes in patient status.
V.  Availability of a staff person dedicated solely to patient monitoring and safety
A designated individual, other than the practitioner performing the procedure, should be present to monitor the patient through­
out procedures performed with sedation and analgesia. This individual may assist with minor, interruptible tasks.
VI.  Training of personnel
Individuals responsible for patients receiving sedation and analgesia should understand the pharmacology of the agents that are
administered, as well as the role of pharmacologic antagonists for opioids and benzodiazepines. Individuals monitoring patients
receiving sedation and analgesia should be able to recognize the associated complications. At least one individual capable of
establishing a patent airway and positive-pressure ventilation, as well as a means for summoning additional assistance, should be
present whenever sedation and analgesia is administered. It is recommended that an individual with advanced life-support skills be
immediately available.
VII.  Availability of emergency equipment
Pharmacologic antagonists as well as appropriately sized equipment for establishing a patent airway and providing positive-
­pressure ventilation with supplemental oxygen should be present whenever sedation and analgesia is administered. Advanced
airway equipment and resuscitation medications should be immediately available. A defibrillator should be immediately available
when sedation and analgesia is administered to patients with significant cardiovascular disease.

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Office-based sedation and monitoring  •  Chapter 7
VIII.  Use of supplemental oxygen
Equipment to administer supplemental oxygen should be present when sedation and analgesia is administered. If hypoxemia is
anticipated or develops during sedation and analgesia, supplemental oxygen should be administered.
IX.  Use of multiple sedative and analgesic agents
Combinations of sedative and analgesic agents should be administered as appropriate for the procedure being performed and the
condition of the patient. Ideally, each component should be administered individually to achieve the desired effect (e.g. additional
analgesic medication to relieve pain, additional sedative medication to decrease awareness or anxiety). The propensity for combina­
tions of sedative and analgesic agents to potentiate respiratory depression emphasizes the need to appropriately reduce the dose of
each component as well as the need to continually monitor respiratory function.
X.  Titration of sedative and analgesic medications to achieve the desired effect
Intravenous sedative and analgesic drugs should be given in small, incremental doses that are titrated to the desired end points of
analgesia and sedation. Sufficient time must elapse between doses to allow the effect of each dose to be assessed before subsequent
drug administration. When drugs are administered by non-intravenous routes (e.g. oral, rectal, and intramuscular), allowance
should be made for the time required for drug absorption before supplementation is considered.
XI.  Intravenous access
In patients receiving intravenous medications for sedation and analgesia, vascular access should be maintained throughout the
procedure and until the patient is no longer at risk for cardiorespiratory depression.
XII.  Reversal agents
Specific antagonists should be available whenever opioid analgesics or benzodiazepines are administered for sedation and analge­
sia. Before or concomitantly with pharmacologic reversal, patients who become hypoxemic or apneic during sedation and anal­
gesia should: (1) be encouraged or stimulated to breathe deeply, (2) receive positive-pressure ventilation if spontaneous ventilation
is inadequate, and (3) receive supplemental oxygen. After pharmacologic reversal, patients should be observed long enough to
ensure that cardiorespiratory depression does not recur.
XIII.  Recovery care
After sedation and analgesia, patients should be observed until they are no longer at increased risk for cardiorespiratory depression.
Vital signs and respiratory function should be monitored at regular intervals until patients are suitable for discharge. Discharge
criteria should be designed to minimize the risk of central nervous system or cardiorespiratory depression after discharge from
observation by trained personnel.
Appendix B
GUIDELINES FOR OFFICE-BASED ANESTHESIA
Quality of care
• The facility should have a medical director or governing body that establishes policy and is responsible for the activities of the
facility and its staff. The medical director or governing body is responsible for ensuring that facilities and personnel are adequate
and appropriate for the type of procedures performed.
• Policies and procedures should be written for the orderly conduct of the facility and reviewed on an annual basis.
• The medical director or governing body should ensure that all applicable local, state, and federal regulations are observed.
• All healthcare practitioners and nurses should hold a valid license or certificate to perform their assigned duties.
• All operating room personnel who provide clinical care in the office should be qualified to perform services commensurate with
appropriate levels of education, training, and experience.
• The anesthesiologist should participate in ongoing continuous quality improvement and risk management activities.
• The medical director or governing body should recognize the basic human rights of its patients, and a written document that
describes this policy should be available for patients to review.

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Chapter 7
Cosmetic surgery procedures and techniques
Facility and safety
• Facilities should comply with all applicable federal, state and local laws, codes and regulations pertaining to fire prevention, building
construction and occupancy, accommodations for the disabled, occupational safety and health, and disposal of medical waste and
hazardous waste.
• Policies and procedures should comply with laws and regulations pertaining to controlled drug supply, storage, and administration.
Patient and procedure selection
• The anesthesiologist should be satisfied that the procedure to be undertaken is within the scope of practice of the healthcare practi­
tioners and the capabilities of the facility.
• The procedure should be of a duration and degree of complexity that will permit the patient to recover and be discharged from the facility.
• Patients who by reason of pre-existing medical or other conditions may be at undue risk for complications should be referred to an
appropriate facility for performance of the procedure and the administration of anesthesia.
Perioperative care
• The anesthesiologist should adhere to the ‘Basic Standards for Preanesthesia Care,’ ‘Standards for Basic Anesthetic Monitoring,’
‘Standards for Postanesthesia Care’ and ‘Guidelines for Ambulatory Anesthesia and Surgery’ as currently promulgated by the
American Society of Anesthesiologists.
• The anesthesiologist should be physically present during the intraoperative period and immediately available until the patient has
been discharged from anesthesia care.
• Discharge of the patient is a physician responsibility. This decision should be documented in the medical record.
• Personnel with training in advanced resuscitative techniques (e.g. ACLS, PALS) should be immediately available until all patients
are discharged.
Monitoring and equipment
• At a minimum, all facilities should have a reliable source of oxygen, suction, resuscitation equipment, and emergency drugs.
Specific reference is made to the ASA ‘Guidelines for Nonoperating Room Anesthetizing Locations.’
• There should be sufficient space to accommodate all necessary equipment and personnel and to allow for expeditious access to the
patient, anesthesia machine (when present), and all monitoring equipment.
• All equipment should be maintained, tested, and inspected according to the manufacturer’s specifications. Back-up power sufficient
to ensure patient protection in the event of an emergency should be available.
• In any location in which anesthesia is administered, there should be appropriate anesthesia apparatus and equipment which allow
monitoring consistent with ASA ‘Standards for Basic Anesthetic Monitoring’ and documentation of regular preventive maintenance
as recommended by the manufacturer.
• In an office where anesthesia services are to be provided to infants and children, the required equipment, medication, and resuscita­
tive capabilities should be appropriately sized for a pediatric population.
Emergencies and transfers
• All facility personnel should be appropriately trained in and regularly review the facility’s written emergency protocols.
• There should be written protocols for cardiopulmonary emergencies and other internal and external disasters such as fire.
• The facility should have medications, equipment, and written protocols available to treat malignant hyperthermia when triggering
agents are used.
• The facility should have a written protocol in place for the safe and timely transfer of patients to a pre-specified alternate care
­facility when extended or emergency services are needed to protect the health or well-being of the patient.
Appendix C
BASIC MONITORING STANDARDS
Standard I
Qualified anesthesia personnel shall be present in the room throughout the conduct of all general anesthetics, regional anesthetics,
and monitored anesthesia care.

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Office-based sedation and monitoring  •  Chapter 7
Appendix D
COMMONLY UTILIZED MEDICATIONS FOR CONSCIOUS SEDATION
Fentanyl
• Narcotic
• IV onset 1 to 2 min, peak 5 to 15 min, and duration 30 to 60 min
• Advantages: great analgesic, rapid onset, and used in morphine-allergic patients
• Disadvantages: chest wall rigidity, and opioid adverse effects
• IV dose for adults: 0.5 to 1 μg/kg. Repeat doses: half of initial dose
Flumazenil (Romazicon)
• Competitive inhibitor of benzodiazepines at the GABA receptor
• IV onset <1 min, peak 2 to 10 min, and duration 45 to 90 min
• Cautions: sudden and complete reversal could cause anxiety, tremors, and seizures
• IV dose: 0.2 mg, wait 30 sec; then 0.3 mg, wait 30 sec; then 0.5 mg, wait 60 sec. May continue to give 0.5 mg to total of 3 mg
Midazolam (Versed)
• Benzodiazepine
• IV onset 1 to 2 min, peak 3 to 5 min, and duration 20 to 60 min
• Advantages: excellent amnestic, rapid onset, short duration, and many routes
• Disadvantages: expense and respiratory depression.
• IV dose for adults: 0.5 to 1 mg. Repeat doses: half initial dose
Naloxone (Narcan)
• Competitive inhibitor of opioids at their receptors
• IV onset 1 to 2 min, peak 5 to 15 min, and duration 30 to 90 min
• Cautions: sudden complete reversal of opioids could cause severe hypertension, ventricular dysrhythmias, and pulmonary edema
• IV dose: 0.05 to 0.1 mg every 2 to 3 min
Propofol
• Sedative-hypnotic agent
• IV onset of 40 sec, peak 1 min, and duration 5 to 10 min
• Boluses rapidly produce anesthesia due to lipophilicity
• Potential for adverse effects of profound hypotension and cardiorespiratory depression
• IV dose: 25 to 150 μg/kg/min
Standard II
During all anesthetics, the patient’s oxygenation, ventilation, circulation, and temperature shall be continually evaluated.

1. Oxygenation:

• An oxygen analyzer shall measure the concentration of oxygen in the patient’s breathing system with a low oxygen concentra­
tion limit alarm in use.

• A quantitative method of assessing oxygenation, such as pulse oximetry, shall be employed.

2. Ventilation: Adequacy of ventilation shall be continuously monitored. If an endotracheal tube is placed, its correct positioning
must be verified by clinical assessment and by identification of carbon dioxide in the expired gases.

3. Circulation:

• Electrocardiogram shall be continuously displayed.

• Arterial blood pressure and heart rate shall be determined and evaluated at least every five minutes.
In addition to the above, circulatory function shall be continually evaluated by at least one of the following: palpation of a pulse,
auscultation of heart sounds, monitoring of a tracing of intra-arterial pressure, ultrasound peripheral pulse monitoring, or pulse
plethysmography or oximetry.

4. Body temperature: There shall be a readily available means to continually measure the patient’s temperature.

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Chapter 7
Cosmetic surgery procedures and techniques
Appendix E
TOTAL INTRAVENOUS ANESTHESIA
• 1. ASA class I–II adults without gastroesophageal reflux symptoms. ASA Basic Monitoring Standards followed.
• 2. Equipment available


a.  Oxygen source


b.  Laryngoscope, endotracheal tube, LMA, and face mask


c.  Positive-pressure breathing device immediately available


d.  Defibrillator


e.  Suction immediately available
• 3. Premedication


a.  Glycopyrrolate 0.2 mg IV


b.  Ondansetron 4 mg IV prn
• 4. Induction


a.  Preoxygenation


b.  Midazolam 2.5 to 5 mg IV prn


c.  Fentanyl 1 to 2 μg/kg, remifentanil 0.5 to 1 μg/kg., or alfentanyl 10 to 20 μg/kg IV.


d.  Propofol 2 to 2.5 mg/kg IV
• 5. Laryngeal mask airway (LMA) insertion
• 6. Maintenance


a.  Propofol 50 to 250 μg/kg/min IV


b.  Fentanyl 25 μg IV prn, remifentanil 0.05 to 0.25 μg/kg/min, or alfentanyl 0.25 to 0.50 μg/kg/min
• 7. Remove LMA when awake
Appendix F
MODIFIED POSTANESTHESIA DISCHARGE SCORING SYSTEM

1.  Vital signs

2  Within 20% of preoperative levels

1  20% to 40% of preoperative value

0  40% of preoperative level

2.  Activity, mental status

2  Oriented and steady gait

1  Oriented or steady gait

0  Neither

3.  Pain, nausea, vomiting

2  Minimal

1  Moderate

0  Severe

4.  Surgical bleeding

2  Minimal

1  Moderate

0  Severe

5.  Intake and output

2  PO fluids and voided

1  PO fluids or voided

0  Neither
The total score is 10. Patients scoring ≥9 considered fit for discharge to home.

UNDERSTANDING SKIN-TYPE
CATEGORIES
The practice of treating the skin, particularly facial skin, with
cosmetic products to alter its function or appearance dates
back thousands of years to the ancient civilizations in Egypt,
Greece, and Rome and has survived through various tradi­
tional means to the present day. Currently, in fact, such prac­
tices are big business. The modern skin care product market
has its more direct roots planted firmly in the early twentieth
century as represented by the fierce competition between cos­
metics entrepreneurs Elizabeth Arden and Helena Rubinstein
and, later, Estée Lauder. During the early 1900s, Helena
Rubinstein identified four basic skin types, characterizing the
skin as dry, oily, combination, or sensitive. These designations
remained virtually unchallenged through the remainder of
the century and into the current one. During the same period,
the industry has evolved rapidly, with the emergence of ‘cos­
meceuticals’ – which refers to cosmetic products that may
confer some biological function in the skin – and has been
accompanied by exorbitant sales figures. The most recent
data show that sales of skin care cosmeceuticals in the US
were projected to gross $6.4 billion in 2004, representing an
increase of 7.3% from the previous year.1 A diverse array of
skin care products available on the market account for this
tremendous sales figure.
A deeper, more nuanced understanding of skin types
would aid patients/consumers in identifying the products best
suited for their particular skin type. In fact, some products are
now categorized based on the skin types for which they are
designed. Two of the skin types noted by Rubinstein comprise
merely one dichotomous parameter of an innovative method
of classifying skin type. Indeed, there are four parameters by
which to characterize facial skin types: dry or oily; sensitive
or resistant; pigmented or nonpigmented; and wrinkled or
unwrinkled (tight). For practitioners to make appropriate skin
care recommendations, or for patients to accurately self-assess
their skin type, all four parameters must be considered. That is,
assessing skin based on all four parameters yields 16 poten­
tial skin-type permutations. For example, a person with dry,
sensitive, pigmented, wrinkled skin would have substantially
different skin care needs than an individual with oily, resistant,
nonpigmented, unwrinkled skin.
This chapter will characterize the four parameters, focusing
on basic science and defining traits, thereby offering a summary
of the 16 skin-type variations. Variability is an important con­
cept here. Skin types are not necessarily static. A move to a
different climate, stress fluctuations, pregnancy, menopause,
and other significant exogenous and endogenous events can
trigger changes in skin type. The Baumann Skin Typing Sys­
tem (BSTS) is based on a questionnaire designed to ascertain
skin type taken for baseline identification and again after
­significant life changes. The questionnaire is a novel method
to accurately identify a person’s Baumann Skin Type (BST).2
SKIN HYDRATION
Oily (O) versus Dry (D)
The etiology of xerosis, or ‘dry skin,’ is complex and multi­
factorial, but the phenomenon is usually described as skin
characterized by dull color (typically gray-white), rough tex­
ture, and an increased amount of ridges.3 The factors thought
to be most influential in contributing to dry skin are stra­
tum corneum lipids, sebum, natural moisturizing factor, and
aquaporin. The role of the stratum corneum (SC), particularly its
capacity to maintain skin hydration, is the most significant fac­
tor to consider in the mechanism of dry skin development.
Topical Skin Care
Leslie Baumann
C h a p t e r
8
P a r t 2

94
Chapter 8    Cosmetic surgery procedures and techniques
To understand the etiology of dry skin, one should picture
the stratum corneum as a ‘bricks and mortar’ structure; the
‘bricks’ represent the keratinocytes and the ‘mortar’ repre­
sent stacks of protective lipid bilayers surrounding the
­keratinocytes. The three main groups of compounds that com­
prise the ‘mortar’ are ceramides, fatty acids, and cholesterol.
These three primary constituent groups, when present in the
proper quantity and balance, form a three-dimensional array
that surrounds the individual keratinocytes and protects them.
In addition, the lipid bilayer prevents transepidermal water
loss (TEWL) from the SC and keeps it watertight (Fig. 8-1).
Patients with dry skin have been demonstrated to exhibit a
perturbation in this lipid bilayer of the SC, which is linked
to elevated fatty acid levels and reduced ceramide levels.4 It
is likely that cytokines play a role in this protective process as
well, helping to maintain SC homeostasis.5
However, when the SC is impaired, the result is xerosis,
because of the incapacity to maintain water, and sensitivity
because of increased susceptibility to influence by external
factors. Specifically, flaws or insufficiencies in the skin barrier
cause increases in TEWL. Abnormal desquamation of cor­
neocytes results,6 i.e. skin scaling, as the outer layers of the
SC have intact desmosomes because the enzymes required for
desmosome metabolism are inhibited by inadequate hydra­
tion. At the same time, the superficial SC desmoglein I levels
remain high. The resultant abnormal desquamation mani­
fests in visible aggregations of keratinocytes rendering the
skin rough and dry in appearance.7 Various extrinsic factors,
including ultraviolet radiation, detergents, acetone, chlorine,
and protracted water exposure or immersion, can disrupt the
lipid bilayer. Local changes in pH have also been suggested in
recent studies to account for the initial cohesion and ultimate
desquamation of corneocytes from the SC surface. These
changes are thought to selectively activate various extracel­
lular proteases in a pH-dependent manner.8
The maintenance of water within skin cells is ­dependent
on natural moisturizing factor (NMF). NMF is an intracellular, hy­
groscopic compound released by lamellar bodies in the ­upper
levels of the SC. It is derived from the breakdown of the pro­
tein filaggrin, which confers structural support and strength to
the lower SC layers. In outer layers of the SC, specifically in
the stratum compactum, filaggrin is broken down by a poorly
understood cytosolic protease into free amino acids, particu­
larly arginine, glutamine (glutamic acid), and histidine.9 These
water-soluble compounds remain inside the keratinocytes and
potently bind to water molecules. In addition to these amino
acids and their derivatives, filaggrin consists of lactic acid,
urea, citrate, and sugars. Aspartate protease (cathepsin) is
­believed to be responsible for the pace of filaggrin breakdown
and the amount of extant NMF.10 Cathepsin, it is worth not­
ing, can be affected by changes in external humidity. The re­
sult is fluctuations in NMF production depending on climate.
Over the course of several days, usually, once an individual
enters a low-humidity environment, NMF production acceler­
ates.11 In addition, NMF formation is inhibited by ultraviolet
radiation. Surfactants can also denude the skin of NMF. In
addition to xerosis, NMF deficiency is associated with ichthyo­
sis vulgaris. There are no products or procedures available yet
that can be used to artificially regulate NMF production.
Aquaporin-3 (AQP3) allows water transfer between the
­keratinocytes. AQP3 belongs to the family of homologous
integral membrane proteins that selectively facilitate water
transport, as well as small neutral solutes such as glycerol
and urea, across biological membranes.12 Other aquaporins
are well known to play a water transport mediation role in
kidney and lung epithelia and 10 types of aquaporins have
been cloned in mammals. The existence of a pore in the
center of each aquaporin molecule has been demonstrated
through structural analyses. AQP3, which is present in the
kidney collecting ducts and epidermis, as well as the urinary,
NMF
Cholesterol, ceramides and fatty acids
Aquaporin 3
Keratinocytes
Fig. 8-1  Skin hydration is influenced by the presence of intracellular lipids, aquaporin-3 and natural moisturizing factor.

95
Topical skin care  •  Chapter 8
respiratory, and digestive tracts, is a member of a subclass of
­aquaporins, known as aquaglyceroporins, which, in addition
to water, transport glycerol, urea, and other small solutes. In
2002, AQP3 was shown to be expressed copiously in the plas­
ma membrane of human epidermal keratinocytes.13 In the
skin, it is thought that the water conduction function occurs
along an osmotic gradient below the SC, where high AQP3-
mediated water permeability is exhibited. Specifically, AQP3
water clamps viable epidermal layers to enhance the hydra­
tion of those layers beneath the SC.
In terms of AQP3 activity, evidence suggests a high concen­
tration of solutes (Na+, K+, and Cl�−) and a low concentration
of water (13–35%)14 in the superficial SC, generating in the
steady-state gradients of solutes and water from the skin sur­
face to the viable epidermal keratinocytes.15–17 The molecular
mechanisms of fluid transport across epidermal keratinocyte
layers remains poorly understood along with the relationship
between keratinocyte fluid transport and SC hydration, de­
spite the extensive study of transepithelial fluid transport in
kidneys and lungs. AQP3 is thought to enhance transepider­
mal water permeability to guard the SC against the effects of
evaporative water loss from the skin surface and/or to dissem­
inate water gradients throughout the epidermal keratinocyte
layer.13 Researchers investigating the functional expression
of AQP3 in human skin demonstrated that, consistent with
AQP3 involvement, mercurials and low pH inhibited the
water permeability of human epidermal keratinocytes.13
In a study considering skin phenotype in transgenic mice lack­
ing AQP3,18 AQP3-null mice exhibited significantly reduced
water and glycerol permeability, establishing that AQP3 func­
tions as a plasma membrane water/glycerol transporter in the
epidermis. In most skin areas of the null mice, ­conductance
measurements revealed substantially lower SC water ­content.
Because water transport across AQP3 is slower in skin com­
pared to other tissues, though, epidermal cell water perme­
ability should not be considered an important determinant
of SC hydration.19 As yet, Ajuga turkestanica extract is the only
compound that has been shown to enhance the activity of
AQP3.20 The herb Ajuga turkestanica is also included as an
ingredient in a high-end line of skin care products. ­Eventually,
AQP3 might be pharmacologically manipulated to treat skin
conditions resulting from excess or diminished hydration.
Sebum, the oily secretion of the sebaceous glands that con­
tains wax esters, sterol esters, cholesterol, di- and triglycerides,
and squalene,21 is known to impart an ‘oily’ aspect to the skin
and play a significant role in acne development. An important
source of vitamin E, sebum is believed to protect the skin from
environmental factors and contribute to dry skin when in de­
creased supply.22 Interestingly, however, low sebaceous gland
activity has not been shown to correlate with xerosis develop­
ment. Indeed, sebum production plays a more complicated
role in the etiology of this condition. It has been previously
assumed that sebum does not affect epidermal permeability
barrier function primarily because skin with a small number
of sebaceous glands, e.g. as in prepubertal children, exhibits
normal basal barrier function.23 In fact, prepubertal children
(between 2 and 9 years old) often present with eczematous
patches (pityriasis alba) on the face and trunk that, coinci
dentally, do not appear with the onset of sebaceous gland activity.
In addition, barrier function and SC lamellar membranes are
not influenced24 by sebaceous glands involuted pharmacologi­
cally with supraphysiologic doses of isotretinoin.25,26 Likewise,
SC function is not disturbed by denuding the skin of sebum
using ether.
Even though sebum levels do not alter barrier function,
sebum may still play a pathophysiologic role in xerosis in
individuals that experience dry skin not accompanied by in­
creased sensitivity (dry, resistant [DR] types according to the
BSTS). It is known that lipids from meibomian glands, which
are modified sebaceous glands found in the eyes, help pre­
vent dryness by preventing tear evaporation.27,28 It is not
unreasonable to speculate, then, that sebum-derived fats
create a lipid film over the skin surface, thereby preventing
TEWL. This theory is buttressed by a study assessing per­
meability barrier homeostasis and SC hydration in asebia
J1 mice that exhibit sebaceous gland hypoplasia.29 The nor­
mal barrier function observed in these sebum-deficient mice
is due to the consistent levels of ceramides, free sterols, and
free fatty acids – the three most important barrier lipids –
as well as the persistence of normal SC extracellular mem­
branes. The asebia J1 mice were found to have reduced SC
hydration, however. Significantly, these findings suggest that
an intact intercellular membrane bilayer system is sufficient
for permeability barrier homeostasis, but does not necessarily
provide for normal SC hydration. Interestingly, the investiga­
tors discovered that the topical application of glycerol restored
normal SC hydration. Sebaceous gland-derived triglycerides
(TGs) are hydrolyzed to glycerol before transport to the skin
surface in normal skin. In sebum-deficient individuals, replac­
ing this glycerol may be a suitable approach to alleviating skin
dryness. Glycerol has also been demonstrated as effective in
accelerating SC recovery.30
Patients rarely complain about decreased sebum produc­
tion, but increased sebum production, which results in oily
skin that can lead to acne, is a common complaint. Sebum
production levels are influenced by several factors. The age-
related component is well known, with levels usually low dur­
ing childhood, rising in the mid to late teens, and generally
remaining stable for decades until declining in the seventh and
eighth decades as endogenous androgen production falls.31
Diet, stress, hormone production, and genetics also influence
sebum production. In a study of 20 pairs each of identical
and non-identical like-sex twins, roughly equivalent sebum
excretion rates with significantly divergent acne severity was
observed in the identical twins, whereas both parameters dif­
fered significantly among the non-identical twins, suggesting
that genetic factors as well as exogenous factors influenced
lesion development.32 While oral retinoids are known to have
the capacity to shrink sebaceous glands, topical retinoids have
not yet been demonstrated to exhibit this activity.

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Chapter 8    Cosmetic surgery procedures and techniques
Skin care for the O–D parameter
Ideal skin in terms of the oily versus dry continuum can be
best characterized as exhibiting an intact SC with an intact
barrier, sufficient NMF levels, normal expression of AQP3,
and balanced sebum secretion. Elevated sebum secretion is
typically responsible for causing skin to fall on the oily side of
the spectrum, whether or not acne develops. If acne is present,
the BST profile for such an individual would emerge as OS
(oily, sensitive) because acne-infiltrated skin is characterized
by heightened sensitivity (see next section). For the OS type,
skin care would be geared toward decreasing sebum levels
with retinoids, reducing skin bacteria with antibiotics, benzoyl
peroxide or other antimicrobials, and using antiinflamma­
tory ingredients. Oily skin not accompanied by acne, an oily,
resistant (OR) type, would be treated with the intention of
decreasing sebum production, unless other parameters such
as dyspigmentation and wrinkling were factors (see following
sections). Oral ketoconazole33 and oral retinoids34 have effec­
tively reduced sebum secretion, but such results have not been
demonstrated yet with topical products. Sebum-absorbing
polymers and talcs are also helpful in camouflaging sebum in
OR skin.
Skin that is dry and exposed excessively to the sun is likely
characterized by an impaired skin barrier and diminished
NMF. For such skin, treatment should concentrate on skin
barrier repair and changes in sun exposure, such as avoidance
or at least providing adequate sun protection.
Regardless of the particular circumstances pertaining to an
individual’s dry skin etiology, all patients with dry skin should
abstain from using harsh foaming detergents, found in laundry
and dish cleansers as well as body and facial cleansers, which
remove hydrating lipids and NMF from the skin. All dry skin
patients should also avoid prolonged baths, especially in hot
or chlorinated water. In addition, those with very dry skin are
urged to use humidifiers in low-humidity environments and
apply moisturizers 2–3 times daily and after bathing.
In addition to the pharmacologic and practical steps out­
lined above that target some of the specific causes of dry skin,
there are numerous over-the-counter (OTC) moisturizers (e.g.
occlusives, humectants, and emollients) available that help
hydrate the skin. In fact, this class of agents, according to a
recent US survey, is the third most frequently recommended
type of OTC topical skin care product.35 Further, just as the
BSTS can assist in the proper identification of the most suit­
able products for individual patients, knowledge of the differ­
ences among moisturizer types is integral to proper product
selection. Moisturizers are typically packaged as oil-in-water
emulsions, such as creams and lotions, and water-in-oil emul­
sions such as hand creams.
Occlusives
Typically oily compounds that can dissolve fats, occlusives coat
the SC to impede TEWL. Many occlusive ingredients also
impart an emollient effect; therefore, these compounds are
particularly suited for treating dry skin. Petrolatum and min­
eral oil are common ingredients that have been frowned upon
unjustly by the emerging organic movement. Used as a skin
care product since 1872, petrolatum is considered one of the
best moisturizers and is often used as a gold standard by which
other occlusive ingredients are compared.36 A water vapor loss
resistance 170 times that of olive oil is associated with petro­
latum,37 however, its greasy texture can render some products
that contain it cosmetically unacceptable to some consumers.
Paraffin, squalene, silicone derivatives (dimethicone, cyclome­
thicone), soybean oil, grapeseed oil, propylene glycol, lanolin,
lecithin, stearyl stearate, and beeswax are among the other
frequently used occlusive ingredients.38,39 Lanolin, derived
from the sebaceous secretions of sheep, contains cholesterol (a
key SC lipid), and can coexist with SC lipids as solids and liq­
uids at physiologic temperatures. However, lanolin has devel­
oped a reputation as a sensitizer, considered undeserved by
some as it has been shown to be a weak allergen,40 and may
be disliked by others for containing animal products. Several
moisturizers are now labeled ‘lanolin-free,’ but the ingredient
remains widely used. Propylene glycol (PG), an odorless liq­
uid with antimicrobial and keratolytic properties, functions as
both an occlusive and a humectant. It has been demonstrated
to improve the cellular penetration of some drugs, includ­
ing steroids and minoxidil. Although PG itself is considered
a weak sensitizer, it may contribute to contact dermatitis by
facilitating the penetration of other allergens.41
Significantly, none of these agents confer lasting or linger­
ing effects. Once removed from the skin, TEWL returns to the
previous level. Occlusives are usually combined with humect­
ant ingredients because reducing TEWL by more than 40%
poses a risk of maceration with increased levels of bacteria.42
Humectants
Humectants are water-soluble and hygroscopic compounds.
That is, these ingredients can attract water from the external
environment, in conditions with at least 80% humidity, as well
as from the underlying skin layers. In low-humidity conditions,
however, humectants may take water from the deeper epider­
mis and dermis, thereby increasing TEWL and exacerbating
skin dryness.43 For this reason, humectants are more effective
in combination with occlusives. Emollient properties have also
been associated with several humectants.44 Because they pre­
vent product evaporation and thickening, thus enhancing the
shelf-life of the products in which they are contained, humect­
ants are often included as ingredients in cosmetic moisturizers.
By drawing water into the skin, humectants engender a minor
swelling of the SC, yielding a perception of smoother skin
with fewer wrinkles. Appearances can be deceiving, though,
as these products do not confer long-term anti-wrinkling
effects. But some humectants provide other benefits; some
exhibit bacteriostatic activity.45 Glycerin and glycerol are the
most effective humectant ingredients. Other commonly used
humectants include sorbitol, sodium hyaluronate, sodium and
ammonium lactate, sodium pyrrolidine carboxylic acid, urea,

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Topical skin care  •  Chapter 8
propylene glycol, alpha hydroxy acids, panthenol, gelatin,
honey, and other sugars.39
Glycerin
A potent humectant, glycerin has a hygroscopic capacity
similar to that of NMF.3 In a 5-year study comparing two
high-glycerin moisturizers to 16 other popular moisturiz­
ers applied to 394 patients with severe xerosis, investigators
found that the high-glycerin products were the most effective
because they rapidly restored dry skin to normal hydration
and their effects lasted longer than all the other moisturiz­
ers, which included formulations containing petrolatum.46 As
revealed by ultrastructural analyses of skin treated with high-
­glycerin preparations, glycerin expands the SC by augmenting
­corneocyte thickness and creating greater distance between
corneocyte layers.47 Glycerin also stabilizes and hydrates
cell membranes and the enzymes needed for desmosome
degradation.46
Urea
An end product of protein metabolism in mammals, the main
nitrogen-containing constituent of urine, and a component of
NMF, urea exhibits humectant and mild antipruritic effects.48
Urea has been incorporated as an ingredient in hand creams
since the 1940s.49 Several studies have demonstrated that
combining urea with hydrocortisone,50 retinoic acid,51 and
other agents facilitates penetration by these agents. Although
some disagreement has been expressed regarding this capac­
ity of urea, the Cosmetic Ingredient Review Expert Panel
recently noted that urea does exhibit the ability to increase
the percutaneous absorption of other chemicals, and also
labeled urea as safe for use in cosmetic products.52 In terms
of efficacy, a double-blind clinical study comparing 3% and
10% urea cream revealed the study formulations to be more
effective in dry skin than the vehicle control. Although the
creams were reported to be equally effective, the 10% cream
reduced TEWL but the 3% cream had no impact on TEWL,
which was unchanged.53
Hydroxy acids
Alpha hydroxy acids (AHAs) are naturally occurring organic
acids that function as humectants and exfoliants. The most
commonly used AHAs in moisturizing formulations are gly­
colic acid, derived from sugar cane, and lactic acid, derived
from sour milk. They were also the first to become commer­
cially available. For the last three decades, topical preparations
containing AHAs have been known to impart a significant
influence on epidermal keratinization.54 In one study, gly­
colic acid was shown to exert a photoprotective effect.55 The
FDA considers products that penetrate the dermis and initi­
ate biologic action there to be drugs rather than cosmetics;
there is evidence that AHAs, found in numerous cosmetics, do
actually penetrate to the dermis. Derived from willow bark,
wintergreen leaves and sweet birch, salicylic acid, the lone
beta hydroxy acid (BHA), is a chemical exfoliant ­available in
­synthetic form in several topical products.56 BHA does not
have any humectant properties. Its role in the treatment of dry
skin is to aid the desquamation process by affecting corneocyte
cohesiveness at the lowest levels of the SC. AHAs and BHA
are both able to do this by affecting pH, and act by degrading
desmosomes, thereby promoting desquamation.57,58
Lactic acid
This AHA is unusual insofar as it is a constituent of NMF.
Lactic acid was first used as dermatologic therapy in 1943
to treat ichthyosis,59 and has been found in vitro and in vivo
to augment ceramide production by keratinocytes.60,61 In a
double-blind, vehicle-controlled study using an 8% L-lactic
acid formula, the AHA surpassed the vehicle as a treatment
for photoaged skin, with statistically significant improvements
in skin roughness, mottled hyperpigmentation, and sallow­
ness.62 Lactic acid is often combined with urea, which helps
increase the penetration of lactic acid.
Emollients
Primarily composed of lipids and oils, emollients are sub­
stances added to cosmetics to hydrate, soften, and smooth the
skin. These compounds function by filling in the gaps between
desquamating corneocytes to render a smooth surface.63
Emollient products improve cohesion, facilitating a flattening
of the curled edges of individual corneocytes.3 This, in turn,
yields a smoother surface, reducing friction while enhancing
light refraction. Notably, there are various classes of emol­
lients, including astringent, dry, fatting, and protective, as well
as protein rejuvenators.39 Many emollients function as both
humectants and occlusive moisturizers. Occlusive ingredients
that also impart an emollient effect include lanolin, mineral
oil, and petrolatum.
To summarize: Occlusives coat the SC and reduce TEWL;
humectants attract water from the outer atmosphere, hydrat­
ing the skin; and emollients soften and smooth the skin. Mois­
turizers are considered very safe, generally, and are associated
with few reports of side effects. Allergic contact dermatitis has
been reported from the use of products containing preserva­
tives, perfumes, solubilizers, sunscreens, and some other classes
of compounds. Some specific ingredients linked to contact
dermatitis include lanolin, propylene glycol,64 vitamin E,65
and Kathon CG.
Collagen and polypeptide ingredients
While several expensive moisturizers contain collagen that
manufacturers contend can replace the collagen lost due to
aging, most of the collagen ‘extracts’ have a molecular weight
of 15 000 to 50 000 daltons even though only substances
with a molecular weight of 5000 daltons or less can actually
penetrate the SC.42 The collagen and other hydrolyzed pro­
teins and polypeptides do create a film on the skin that fills
in surface irregularities once the product dries. The tempo­
rary film confers a subtle stretching out of fine skin wrinkles.
Adding humectants can further enhance the slightly plumper

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Chapter 8    Cosmetic surgery procedures and techniques
appearance. These products have little or no effect on TEWL,
but are typically labeled as moisturizers as well as firming
creams.
SKIN SENSITIVITY
Sensitive (S) versus Resistant (R)
Individuals with resistant skin rarely experience erythema
(unless overexposed to the sun) or acne (unless stress or hor­
monal fluctuations intervene). Most skin care products can be
used by people with resistant skin without cause for concern
regarding adverse reactions (e.g. acne, rashes, or a stinging
response). Likewise, however, many products are ineffective
on individuals with resistant skin, who are thought to have an
exceedingly high threshold for penetration. As a result, such
individuals may not be able to detect differences among cos­
metic skin care formulations as most products are too weak to
cross the potent SC to confer salutary effects.
Sensitive skin is a much more complex entity. In recent
years, it has been reported that more than 40% of people pre­
senting to a dermatologist complain of having sensitive skin.66
Most such patients are healthy women of child-bearing age.
The incidence of sensitive skin appears to decline with age.
Although there are numerous cosmetic products available on
the market that are intended and touted for sensitive skin,
there are variations in the sensitive skin presentation. Spe­
cifically, there are four discrete types of sensitive skin: acne
type (manifesting in a tendency to develop acne, black heads,
or white heads); rosacea type (characterized by a proclivity
toward recurrent flushing, facial redness, and experiencing
hot sensations); stinging type (predilection to feeling sting­
ing or burning sensations); and allergic type (prone to exhibit
­erythema, pruritus, and skin flaking).
Each of these subtypes presents a unique set of treatment
challenges to the practitioner as products intended for sensitive
skin are not necessarily suited for all sensitive skin subtypes.
Nevertheless, these four subtypes share one common element:
inflammation. Consequently, reducing and eliminating inflam­
mation is at least part of the focus in any sensitive skin treat­
ment regimen. Treatment is more complicated for patients
that present with more than one subtype of sensitive skin.
Acne type
In the US, between 40 and 50 million people suffer from acne
(Figs 8-2, 8-3) on an annual basis.67 Most of these individu­
als, approximately 70–80%, are adolescents and young adults
between the ages of 11 and 25 years.68 The majority of the
remainder of patients suffering from acne is ­represented by
adult women, who exhibit a hormonal component to their
acne. The pathogenesis of this prevalent and quite vis­
ible, therefore, stressful condition unfolds from the dynamic
­interplay of four primary factors: elevated sebum produc­
tion; clogged pores, resulting from dead keratinocytes inside
the hair follicles clinging together more than in those with­
out acne (increased sebum production may also contribute to
the adhering of these skin cells); the presence of the bacteria
Propionibacterium acnes; and inflammation. Although acne can
develop in a wide array of idiopathic presentations or result
from various contributing factors, the sine qua non feature is
the adherence of dead keratinocytes in the hair follicles due
to elevated sebum production, resulting in the clogging of
the follicle and the emergence of a papule or pustule. The
cascade proceeds with P. acnes migrating into the hair follicle,
assailing the amassed sebum and dead keratinocytes. In turn,
this provokes the release of cytokines and other inflammatory
factors that evokes the inflammatory response resulting in the
characteristic redness and pus development. Indeed, high lev­
els of primary cytokines, chemokines, and other inflammatory
markers are typically associated with chronic inflammatory
skin conditions such as acne.5
Fig. 8-2  Comedones as seen in the acne subtype.
Fig. 8-3  Papules and pustules as seen in the acne subtype.

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Topical skin care  •  Chapter 8
Generally, treatment focuses on the four primary etio­
logic factors, specifically decreasing sebum production (with
retinoids, oral contraceptives, or stress reduction), unclogging
pores (with retinoids, AHAs, or BHA), eliminating bacteria
(with benzoyl peroxide, sulfur, antibiotics, or azelaic acid), and
reducing inflammation.
Rosacea type
Tens of millions of people, usually adults between 25 and
60 years of age, are affected by rosacea (Fig. 8-4) in the US on
an annual basis. This acneiform condition shares some symp­
toms with the common scourge of adolescence, specifically
facial redness, flushing, and papules, but is distinguished by the
development of prominent telangiectases. Topical treatment
of rosacea is primarily focused on not triggering or aggravat­
ing the condition, and using antiinflammatory ingredients to
decrease the dilation of the blood vessels, which is the primary
manifestation. The aim is to influence a dynamic etiologic
pathway by, specifically, decreasing vascular reactivity, reducing
free radicals, suppressing immune function, and inhibiting eosi­
nophilic activity, degranulation of mast cells, and the arachi­
donic acid pathway. Eosinophils are pleiotropic multifunctional
leukocytes that contribute to initiating and promoting various
inflammatory responses.69 Mast cells often colocalize to areas of
eosinophil-mediated disease.70 Feverfew, sulfur, zinc, sulfaceta­
mide, quadrinone, niacinamide, salicylic acid, arnica, licorice
extract, licochalcone, cucumber extract, aloe vera, colloidal
oatmeal, chamomile, and witch hazel are among the most effec­
tive antiinflammatory ingredients in the numerous available
formulations.71 Antibiotics, immune modulators, and steroids
are also used by prescription for antiinflammatory treatment.
Stinging type
Several tests are available to identify ‘stingers’ or the sting­
ing propensity, which is a nonallergic neural sensitivity phe­
nomenon that some people experience in reaction to ­various
­triggers (Fig. 8-5). The lactic acid stinging test is a widely
accepted approach for assessing individuals who report invis­
ible and subjective cutaneous irritation, which is not neces­
sarily associated with erythema as many patients feel stinging
without experiencing redness.72 Rosacea patients manifest­
ing facial flushing, however, are more susceptible to stinging
from lactic acid exposure.73 Patients with the stinging sub­
type of sensitive skin should avoid topical products contain­
ing alpha hydroxy acids (particularly glycolic acid), benzoic
acid, bronopol, cinnamic acid compounds, Dowicel 200, for­
maldehyde, lactic acid, propylene glycol, quaternary ammo­
nium compounds, sodium lauryl sulfate, sorbic acid, urea, or
vitamin C.
Allergic type
A recent epidemiologic survey in the UK found that, over
the course of 1 year, 23% of women and 13.8% of men
experienced an adverse reaction to a personal care product
(e.g. deodorants and perfumes, skin care products, hair care
products, and nail cosmetics).74 Various studies show that
approximately 10% of dermatologic patients who are patch
tested (typically for anywhere from 20 to 100 ingredients) are
revealed to be allergic to at least one ingredient common in
cosmetic products.74 Fragrances and preservatives are the
most common allergens and the 20–60 age group, mostly
women, comprise the majority experiencing such reactions.75
Fig. 8-4  Facial flushing and telangiectases characteristic of the
rosacea subtype.
Fig. 8-5  Stinging may or may not be accompanied by facial
redness.

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Chapter 8    Cosmetic surgery procedures and techniques
Overexposure to skin care products renders individuals more
prone to allergic reactions. In addition, patients with an
impaired SC, as manifested by xerosis, are more susceptible
to topical allergens.76
While discussing the specific needs of the eight sensitive
skin-type permutations is somewhat beyond the scope of this
chapter, it is worth summarily noting some of the fundamen­
tal needs of four of the more common sensitive skin types.
Oil control is essential for people with oily, sensitive skin.
An acne or rosacea treatment regimen is also likely necessary.
Those with dry, sensitive skin require therapy to repair the
skin ­barrier. Wrinkle treatment or prevention is ideal for peo­
ple with aged or wrinkled, sensitive skin. Finally, pigmented,
sensitive skin requires removal of the pigment and prevention
of additional pigmentation.
SKIN PIGMENTATION
Pigmented (P) versus Nonpigmented (N)
This skin parameter refers not to race, but, rather, the ten­
dency to develop unwanted hyperpigmentations or dyschro­
mias on the face or chest (Fig. 8-6). According to the BSTS,
an individual with such a propensity would be considered to
have ‘P’-type skin. In a discussion of topical skin care, pig­
mentary changes that can be improved with skin care prod­
ucts as opposed to lesions that require excision or treatment
beyond skin care (e.g. congenital nevi, seborrheic keratoses)
should be the focus. For example, melasma, solar lentigos,
ephelides, and postinflammatory hyperpigmentation can
be treated with skin care products and procedures. In fact,
these are significant problems on which patients spend a
good deal of money. In order to consider the topical prod­
ucts best suited to the treatment of unwanted pigmentation,
it is incumbent upon practitioners to understand the origin of
pigmentation.
Melanocytes produce melanin (skin pigment) and then
transfer the pigment via melanosomes to keratinocytes.
Melanogenesis is induced by UV radiation exposure and
represents the skin’s defense to additional UV-caused dam­
age. Melanocytes react to UV radiation by increasing the
production of melanin and its transfer via melanosomes to
keratinocytes,77 which ultimately manifests in skin darken­
ing. Melanin itself is derived from the enzymatic breakdown
of tyrosine by tyrosinase into DOPA and then dopaqui­
none, ultimately yielding two melanin types (eumelanin
and pheomelanin).78 Eumelanin, which is more abundant,
consistently correlates with the visual phenotype.79 Melano­
cytes produce more melanin in darker-skinned people; the
melanosomes are larger to accommodate more melanin
and, thus, are broken down at a slower rate than in lighter-
skinned people.80 Typically, approximately 30 ­keratinocytes
are attached to one melanocyte. Melanosome-containing
melanocytes interdigitate with keratinocytes. If the ­protease-
activated receptor (PAR)-2 is activated, the keratinoc­ytes
engulf the melanosome and the melanin is absorbed in
the keratinocytes.81 PAR-2, which is expressed in ke­ratino­
cytes but not melanocytes, is a seven transmembrane
G-protein coupled receptor activated by a serine protease
cleavage.
There are two primary pathways toward impeding the
formation of skin pigmentation: inhibiting tyrosinase, which
prevents the formation of melanin, and blocking the trans­
fer of melanin into keratinocytes. Soybean trypsin inhibitor
(STI) and Bowman-Birk inhibitor (BBI), which are proteins
found in soy, have been identified as agents that can inhibit
skin pigmentation. In addition to having demonstrated de­
pigmenting activity, these soy proteins have also been shown
to prevent UV-induced pigmentation both in vitro and in
vivo.82 According to Paine et al., STI and BBI exert these
effects by inhibiting the cleavage of PAR-2. By hindering this
cleavage, STI and BBI are thought to influence melanosome
transfer into keratinocytes, thereby affecting pigmentation. It
is the PAR-2 that is thought to regulate pigmentation through
interactions between keratinocytes and melanocytes.83
­Niacinamide, a derivative of vitamin B3, has also been
­demonstrated to block melanosome transfer from melano­
cytes to keratinocytes.84
Indeed, soy and niacinamide are considered the most effec­
tive PAR-2 blockers, thus useful in inhibiting melanin transfer
to keratinocytes. Vitamin C, hydroquinone, kojic acid, arbu­
tin, mulberry extract, and licorice extract are effective tyrosi­
nase inhibitors. While there are two approaches to preventing
melanin formation, there are three types of topical products.
In addition to the tyrosinase inhibitors and PAR-2 block­
ers, exfoliating agents (e.g. AHAs, BHA, and retinoids) and
Fig. 8-6  Solar lentigos on the face of a pigmented skin type. Note
the ‘pigmented’ designation refers to the presence of unwanted
pigmented lesions and not to ethnicity.