Các Biến Chứng Trong Phẫu Thuật Tạo Hình Thẩm Mỹ Vùng Mặt

15 Surgical Correction of Congenital Anomalies and Associated Complications 137
managed with tarsorrhaphy. Tarsorrhaphy is also use-
ful intraoperatively to protect the corneas. Papilledema
and disc pallor both signal threatened vision and require
urgent action. In a review of 141 patients with cranio-
synostotic syndromes of Apert, Crouzon, Pfeiff er and Sa-
ethre–Chotzen, Khan et al.30 demonstrated a poor visual
outcome with an acuity of 6/12 Snellen or worse in the
better eye in 39.8% of cases, while 64.6% of cases had
this level of vision or worse in either eye. Tay et al.31 as-
sessed the prevalence and causes of visual impairment
in 71 patients with craniosynostotic syndromes of Ap-
ert, Crouzon, Pfeiff er, Saethre–Chotzen and CFND and
confi rmed Hertle’s fi ndings.28 Causes of visual impair-
ment were amblyopia (16.7%), ametropia (25%), optic
atrophy (16.7%), exposure keratopathy (4.2%), and in-
fantile nystagmus syndrome (4.2%). Overall, 6.3% of the
patients had amblyopia that was attributable to a com-
bination of factors: exotropia (two cases), astigmatism
(two cases), and anisometropic hypermetropia (one
case). 6.3% patients were found to have optic atrophy.
Tay et al. found complete resolution of papilledema in
all six patients with it following decompressive surgery.
Orbital repositioning may result in extraocular mus-
cle dysfunction. In most instances, it resolves sponta-
neously within six months. Persistent problems may
require strabismus surgery for correction. Pulsatile oph-
thalmopathy results from transmitted dural pulsations
after fronto-orbital advancements without orbital roof
reconstruction. In patients older than 9–12 months, the
orbital roofs must have bone grafts. Diamond et al.32 re-
ported the ocular and adnexal complications of unilat-
eral orbital advancement for plagiocephaly. Ptosis was
observed postoperatively in 29% of patients, and stra-
bismus and amblyopia in 18% of the patients. For eye
protection during craniofacial corrective surgery, tar-
sorrhaphy can be performed before surgical draping to
protect the cornea. Otherwise, the eyes must be taped
securely to avoid corneal injury. During surgery, retrac-
tion or pressure on the orbits can cause changes in the
patient’s pulse rate and blood pressure. Accordingly,
during orbital dissection the anesthesiologist should be
alerted to monitor the vital signs with particular care,
so that the surgical team can immediately be informed
of oculocardiac stimulation. Fortunately, the reported
number of complications involving the orbits that result
in loss of vision is less than 1%.

◆Distraction Osteogenesis
Distraction osteogenesis is becoming the treatment of
choice for the surgical correction of many skeletal de-
fi ciencies because of its promise of new bone forma-
tion without donor sites, slow movements allowing for
soft-tissue accommodation, and suitability for growing
patients. Although initially there had been great empha-
sis on a several day postoperative latency period and a
the child is 3 years old before attempting to repair it. By
the time the child is 3, the diploe has formed, and split-
thickness bone grafts can be harvested and used to fi ll in
the defects.26 Defects have also been repaired with dis-
tant bone grafts and a myriad of bone graft substitutes,
such as the previously mentioned CPC (Fig. 15.7A,B).
Visible contour irregularities may require burring to im-
prove appearance.
Postoperative Head Injury or Deformity
The frequency of postoperative head trauma tends to be
age-related, being highest in children who have reached
the crawling and toddler stages. Protective headgear is
recommended at this stage if signifi cant defects persist.
In addition, helmets may be used postoperatively to re-
shape the head further, or they may be used in lieu of
surgery for nonsynostotic plagiocephaly cases. Potential
health risks associated with the use of helmets include
excessive skin breakdown and infection, inappropriate
mechanical restriction leading to altered or impaired
head growth and development, asphyxiation, and head
and neck trauma as well as ocular trauma.27 The parents
should be instructed on how to position their child in
cases of plagiocephaly or advancement repair so that
the child’s sleep position does not add to the forces for
skeletal relapse. Techniques for positioning the child
with rolled towels should be demonstrated. During the
day, parents should be encouraged to keep the child in
a walker-type stroller fi tted with a circumferential rail
that prevents the child from receiving an impact with
hard objects. About 6–12 weeks of healing are required
to achieve good structural support for the repositioned
bone and brain protection. During this critical period,
the child must be watched closely. Daycare may be a
risk in this period. After 3–6 months, the bone is well
fi brosed, and only a hard impact can disrupt the bone
units.
Ocular Complications
The visual system is often signifi cantly involved in cra-
niosynostosis.28 Impaired vision may be an inherent
feature of the pathologic process or occur as a second-
ary complication. In particular, optic disc edema, optic
atrophy, and progressive optic nerve dysfunction may
accompany increased intracranial pressure without evi-
dence of hydrocephalus and with open fontanels. Un-
corrected refractive error (particularly anisometropia),
strabismus, ptosis, and corneal exposure problems are
an invitation to the development of amblyopia.29 If not
reversed, this condition can lead to permanent visual
disability. Proptosis and corneal exposure problems are
a third potentially treatable cause of functional blind-
ness. Prompt involvement of an ophthalmologist in the
care of children with craniosynostosis is essential. Pro-
ptosis resulting in corneal exposure should be urgently

Complications in Facial Plastic Surgery
138
rect way can lead to premature consolidation of the re-
generate formation or lack of regenerate formation after
what appears to be successful distraction. Lack of com-
pliance with activity level restrictions can lead to device
dislodgement. Other causes of failure to form regenerate
are patient factors such as local vascular compromise
and bone metabolism disorders.

◆Cleft Lip and Palate
The location of the cleft lip and palate anomaly leads
to possible impairments of breathing, eating, hearing,
speech, dental relationships, craniofacial growth, and
facial appearance, along with possible psychosocial im-
pairment. There is a lack of data on outcomes to direct
cleft care. Several factors contribute to this problem. The
time lapse between treatment intervention and fi nal
growth result is signifi cant. There are no standardized
national treatment protocols. Most surgeons follow a
protocol that places primary cleft lip repair and tip rhi-
noplasty between three and six months of age. Millard
and Tennison techniques tend to be the ones most com-
monly used. That is followed by palatoplasty at six to
twelve months, usually with some variation of a Langen-
beck, Veaux-Wardill-Kilmer, or Furlow technique. Sec-
ondary speech surgery, if needed, is performed between
the ages of three and seven years. At the age of seven to
eleven years, alveolar bone grafting is frequently neces-
sary. Some patients require orthognathic surgery, and
in selected cases distraction osteogenesis is performed.
Between the ages of 12 and 18 years, secondary rhino-
plasties are indicated in most patients.
Cleft Lip Repair
Initial problems with bleeding, infection, or dehiscence
are rare. Occasionally, signifi cant respiratory distress
may be noted from nasal obstruction, particularly in the
limited distraction rate of 1 mm per day, distraction is
now often started on the fi rst postoperative day after
distracter insertion and at an increased rate of 2 mm
per day without either fi brous union or premature con-
solidation. Mandibular distraction is less invasive than
traditional methods of mandibular reconstruction with
bone grafts and has a signifi cantly reduced morbidity
rate. It may also be done in infancy to avoid or shorten
time with a tracheotomy in cases of micrognathia. An-
terior cranial and maxillary distraction share the above
benefi ts plus the lack of a large anterior cranial fossa
defect with monobloc distraction compared with tra-
ditional advancement. In addition, larger movements
are easier with distraction than with traditional tech-
niques. Pitfalls include improper device and osteotomy
placement, device failure, poor compliance with device
activation, pin track scars, and diffi culties with device
removal after alteration of the anatomy. Complications
can range from infection of the pin track to total failure
of the procedure.
Complications of osseodistraction can be divided into
placement, osteotomy, and removal complications and
distraction process complications. Surgical complica-
tions include those found with traditional osteotomies:
infection, hematoma, brain or ocular injury, facial or
mandibular nerve injury, damage to tooth buds, scars
from visible incisions, and incorrect osteotomy or de-
vice placement (Fig. 15.8). Tooth bud injury can lead to
eruption failure or odontogenic cyst formation.10,33–35
Careful planning and execution are the best ways to
avoid these problems.
Distraction process complications occur during ac-
tivation of the device or in the latency phase. Device
failure includes breakage of the distracter, screw or pin
loosening, and device binding. Condylar displacement
has also been reported.35,36 Distraction can cause pin
migration through the soft tissues and pin tracks in the
skin (Fig. 15.9). Compliance problems with BID or TID
activation with a small tool that must be turned the cor-
Fig. 15.8 Infected extruding fractured distracter.
Fig. 15.9 External distracter pins extruded through the chin.

15 Surgical Correction of Congenital Anomalies and Associated Complications 139
fi ciencies may be addressed with dermal fat grafts or
V–Y mucosal advancement, but mucosa outside of the
wet line can lead to chapping and color mismatch. More
signifi cant defi ciency is due to vertical skin or muscle
defi ciency, and depending on degree, it requires a scar
revision or total lip revision. Severe bilateral cleft lip
vermilion defi ciencies can be corrected with a lower lip
vermilion fl ap.
Cleft-side high peaking of Cupid’s bow or vertical
skin defi ciency without lip notching is commonly seen
early after the Millard rotation advancement repair due
to scar contracture.37 This usually resolves with gentle
massage and scar maturation. If the problem persists
beyond one year postoperatively, then it should be sur-
gically corrected. In cases in which the lip is short by
up to 2 mm, a diamond-shaped excision of the scar and
reclosure can add adequate length. When the whole lip
is short due to scar contracture, total excision of the scar
eliminates contracture and allows for normal alignment.
If additional lengthening is needed, Z-plasties, rotation-
advancement, or triangular fl ap techniques can be used
just in the skin. Greater vertical defi ciency or a shortage
of subcutaneous tissue and muscle necessitates com-
plete revision. If the orbicularis muscle is dehiscent, it
should be released from its abnormal insertions and
approximated. The most severe defects may require an
Abbe fl ap. Less commonly, excess in the vertical dimen-
sion results in a long upper lip. Reduction is achieved
with an excision of the skin and muscle just below the
nasal ala and sill.
Misalignment without signifi cant tissue defi cit can
be corrected by readjustment of available local tissue.
The degree of misalignment again dictates whether
there will be a minor procedure or complete revision.
The most obvious abnormalities include misalignment
of the white roll and the wet line. Popular techniques
include scar excision and reclosure with proper align-
ment, a small asymmetric Z–plasty, V–Y advancement,
and serial excision to move structures with minimal
secondary distortion. Severe misalignment may involve
a complete revision of the lip with mobilization and for-
mal realignment of the muscle and surface structures.
Horizontal abnormalities can result from defi ciency
or excess. A defi ciency in the distance from the low
point of Cupid’s bow to the cleft-side peak is produced
by improper marking in the initial repair. The defi ciency
is very diffi cult to repair and is best avoided. In the bi-
lateral cleft lip, asymmetry can be addressed by mov-
ing the scar on the wider side of the philtrum closer to
the midline. Inadequate undermining and recruitment
of tissue from lateral to medial can lead to excess ten-
sion, hypertrophic scarring, keloids, subcutaneous tis-
sue dehiscence, or a tight lip. Infection or reaction to
suture material can also cause unfavorable scars. This
complication can be improved with a normal straight
scar excision or with the wave line method of Pfeifer.
Dermabrasion may help in mild cases. It is important to
repair of bilateral clefts. The problem responds acutely
to insertion of nasal stents. Twenty-three hour postop-
erative observation is recommended for patients young-
er than four months of age. Avoidance of lip trauma in
the fi rst seven to ten days postoperatively with gentle
feeding techniques and handling helps ensure good
healing with minimal scars.
Cleft lip repair generally involves recruiting tissue
fl anking the cleft to fi ll the cleft-related defects. Com-
plications generally result in the need for a revision. Re-
visions can be divided into small touch-up procedures
for minor defi ciencies and total lip repair revisions for
major problems. Careful analysis of the residual defor-
mity leads to the choice of the appropriate approach.
Residual defi ciencies can be thought of as tissue defi -
ciency problems, tissue distortion problems, or some
combination of both. As is typical, the best management
is proper initial technique to avoid residual problems.
However, even the best hands still have revisions.
Notching of the lip margin (whistle deformity) is a
frequently encountered secondary deformity in cleft
lip patients (Fig. 15.10). It represents some degree of
vertical defi ciency in the lip skin, vermilion, muscle, or
mucosa. Central mucosal defi ciency may be minimized
at the time of the initial unilateral lip repair by back-
cutting the mucosa in the gingivobuccal sulcus along
the medial lip element, where the defi ciency is most
common, and advancing from lateral to medial and infe-
riorly. The resulting mucosal defect in the sulcus quickly
heals secondarily.
There is a natural vermilion defi ciency in clefts
(worse in bilateral clefts) as the wet line fuses with the
white roll at the cleft margin. This is best managed dur-
ing primary repair with vermilion fl aps from the lat-
eral segments being brought into the philtral tubercle.
Vermilion defi ciency can occur under the lip scar(s) or
centrally as a philtral tubercle defi ciency. Minor de-
Fig. 15.10 Whistle deformity.

Complications in Facial Plastic Surgery
140
lip repair. The results support the observation that na-
sal growth on the cleft side of the nose is unaff ected by
early primary nasal surgery and that the vertical length-
ening of the nose by the alar lift technique is preserved
into adult life. Ariyan and Krizek39 recommended suture
fi xation of the cleft-sided lower lateral cartilage to the
non-cleft upper lateral cartilage, while Dingman and
Natvig40 felt suture fi xation to the cleft-sided upper lat-
eral cartilage was superior. Black et al.41 described box
suture fi xation to correct the cleft lateral crus. Many ad-
vocate postoperative nostril stenting to maintain nostril
shape.
Nasal airway obstruction may be caused by irregu-
larity of nasal fl oor on the cleft side, inferior turbinate
hypertrophy into the cleft, a deviated nasal septum
common to nearly all unilateral cleft lip-palates and
many bilateral clefts, and decreased nostril and nasal
cavity size. A 25% diminution of the nasal airway us-
ing pressure fl ow studies was documented by Warren.42
Severe obstruction may necessitate early corrective
nasal surgery (intermediate septorhinoplasty). Caudal
septal defl ection is corrected with minimal dissection
and very conservative septoplasty. The septum is repo-
sitioned to the midline and secured to the nasal spine
with a suture. Most posterior deviation requires limited
septal spur resection. Inferior turbinate reduction and
nasal valve surgery may also be required.
Other secondary cleft nose deformities include a wid-
ened or constricted nostril, hooding in the soft triangle,
inadequate correction of the lower lateral cartilage, and
fl aring of the alar base. A mildly stenotic nostril can be
addressed early through dilation with nasal silicone
stents. Moderate or severe stenosis requires vestibular
surgery, possibly with grafting. The soft-tissue triangle
hooding can be addressed during the primary rhino-
plasty. Later it can be directly excised, resulting in an ex-
ternal scar. Alternatively, once the new high point of the
cleft-side dome has been established during secondary
rhinoplasty, careful closure of the marginal incision un-
der the dome will pull the soft triangle up. Defatting the
cleft-side lateral alar lobule may also help with nostril
narrowing. A wide nostril can be corrected with a sill
excision or V-Y advancement of the alar base. Lower lat-
eral cartilage and tip correction can be performed with
standard open septorhinoplasty techniques. A turned-
out alar base can be improved by a perialar Z-plasty. Tip
asymmetries and dorsal deviations are correctable with
standard open rhinoplasty techniques. Inferior turbinate
reduction and nasal valve surgery may also be required.
Bilateral Cleft Lip Nasal Deformity
The classic bilateral cleft lip nasal deformity is charac-
terized by a poorly projecting bulbous bifi d tip, splayed
alar cartilages, short columella, fl ared alar rims, and a
wide alar base (Fig. 15.12). The nostril rims are oriented
transversely instead of at the usual 45° angle to the fa-
ensure proper alignment of the orbicularis muscle fi bers
and minimal tension. A tight, thin upper lip can often
be corrected by total revision with wide recruitment of
lateral tissue, but an Abbe fl ap or Bruns lip-lengthening
technique may be necessary. An overly wide philtrum
occurs mostly in a bilateral cleft lip and is created when
the philtrum is designed too widely at the initial lip re-
pair (greater than 4–5 mm). Any excess philtrum and
muscle or connective tissue should be excised and the
lip scars medialized.
Unilateral Cleft Lip Nasal Deformity
It is generally the residual associated nasal deformity
that stigmatizes aff ected children rather than the re-
paired cleft lip. The anomalous anatomy of the cleft lip
nose was clearly defi ned in the 1950s by Huff man and
Lierle38 (Fig. 15.11). If the cleft lip is repaired without
correction of the malpositioned alar cartilage, the nos-
tril rim droops on the side of the cleft, the lower border
of the alar cartilage pushes up an oblique ridge within
the vestibule, and the nostril fl ares.
Primary (i.e., synchronous with cleft lip repair) correc-
tion of nasal alar deformity has become commonplace
during the past 25 years and has reduced the severity
of the residual deformity. Primary treatment consists of
correcting the caudal rotation of the alar cartilage at the
time of lip repair. The alar cartilage, with the attached
vestibular lining, is lifted to lengthen the nose on the
side of the cleft. The arch swings forward and establish-
es the vault of the vestibule before closure of the nos-
tril fl oor. McComb and Coghlan37 published an 18-year
follow-up of ten consecutive patients who underwent
primary correction of their cleft lip nasal deformity to
elevate the displaced alar cartilage at the time of cleft
Fig. 15.11 Cleft lip nasal deformity.

15 Surgical Correction of Congenital Anomalies and Associated Complications 141
columella at the expense of creating a scarred, abnormal-
ly wide columella. Inadequate and incomplete correc-
tion, noticeable external scars, an unnatural columellar
appearance, inadequate alar support with resultant ves-
tibular narrowing, external nasal valve collapse, and alar
base asymmetry have all been problems associated with
these techniques. Alar asymmetry and notching, as well
as persistent deformities in the lower lateral cartilages,
may also be seen.53–56 Other procedures involve the use
of external nasal tip and columellar incisions to lengthen
the columella from the tip down rather than from the
lip and sill up. This approach achieves both columel-
lar lengthening and tip narrowing57,58 with the cost of
external incisions and subsequent midline columellar
and tip scars. However, this type of approach is gaining
popularity. Placing an alar base cinch suture improves
the ratio of the nasal length to the alar base width and
creates a more aesthetically pleasing and balanced nasal
contour. Defatting the tip and placing interdomal sutures
improves the bulbous nasal tip and gives it a more nar-
rowed and refi ned shape.
Palatoplasty
The multidimensionality of cleft outcomes includes the
eff ects of the anomaly and its repair on respiration, nu-
trition, speech, hearing, appearance, dental occlusion,
craniofacial growth and psychosocial function. Modifi -
cation of surgical techniques or timing to optimize one
of these variables may induce untoward consequences
in another; for example, it has been shown that delayed
closure of the hard palate, recommended to minimize
maxillary growth disturbances because of palatoplasty,
increases speech impairment.59 The best outcomes are
achieved with an interdisciplinary, coordinated, and
uniform approach to treatment.
Modern palatoplasty techniques have focused on
reducing postoperative velopharyngeal insuffi ciency.
However, negative growth eff ects remain a concern
as well as fi stula rates. Palatal lengthening, improved
muscle function, and reduction of anteroposterior scar
contraction have been goals. The Veau-Wardill-Kilner
pushback operation is aimed at palatal lengthening
by posterior palatal tissue mobilization. In the hope of
improving speech results, the palatal musculature was
reoriented. This operation, popularized by Kriens60 as
intravelar veloplasty, has been adopted by many cleft
surgeons during the past three to four decades. How-
ever, neither anatomical reports nor historical com-
parative data have established the effi cacy of intravelar
veloplasty. The only prospective study in the literature
does not show a statistically signifi cant diff erence that
would warrant its routine application.61
More recently, palatal lengthening and levator retro-
positioning have been combined in the Furlow double-
opposing Z-plasty repair.62 Retrospective studies of the
Furlow palatoplasty by Spauwen et al.,63 Yu et al.,64 and
cial plane. The nose generally forms an obtuse nasola-
bial angle.43 Columellar shortening and poor nasal tip
projection require V-to-Y advancement of tissue from
the upper lip.
Simple techniques include the use of suture fi xation
of the lower lateral cartilage to adjacent nasal structures
after extensive dissection and mobilization. McComb44
described suture fi xation of the lower lateral cartilage to
the nasion and nasal bridge. To maintain the outcome,
others like Cenzi and Guarda45 have advocated nostril
splints to oppose the contractile forces during healing.
Unfortunately, these suturing methods have tended to
result in an inadequate correction of the bilateral cleft lip
nasal deformities, with a high incidence of recurrence.
Structural grafts also help to correct the bilateral cleft
lip nasal deformity. Barsky46 advocated the use of nasal
tip grafts of autologous cartilage to improve tip projec-
tion. Columellar struts are commonly employed. Some
authors47,48 have advocated multiple cartilage and bone
grafts to provide structural support and improve the
projection of the nose.
Columellar lengthening typically requires a combina-
tion of skin lengthening and structural support with car-
tilage grafting and suture techniques. To gain maximum
tip projection, the surgeon must often augment both
the internal structures and the skin envelope. Cartilage
composite grafts support the nasal rim and prevent alar
retraction. Raspall et al.49 used a columellar strut and a
small V-Y advancement from the nasal sill to lengthen
the columella and minimize columellar and philtral inci-
sions. Others have used advanced vestibular fl aps, phil-
tral scars or banked fork fl aps from the prolabium into
the columella, skin or composite grafting, or narrowing
of the nasal tip with central excision of tip skin. Lateral
crural fl aps have similarly been advanced toward the
tip.50–52 The lip, sill, and grafting techniques lengthen the
Fig. 15.12 Bilateral nasal deformity.

Complications in Facial Plastic Surgery
142
drinking and eating, diffi culties with oral hygiene, and
production of socially undesirable sounds. A symptom-
atic fi stula may cause deterioration in speech quality
and intelligibility. Many opinions have been expressed
in the surgical literature concerning which fi stulas are
likely to be symptomatic.68,69 The most common vari-
ables discussed are the size and location of the fi stula.
Larger fi stulas may be associated with more signifi cant
hypernasality and nasal emission, but the size of a fi s-
tula alone does not correlate with the change in speech
symptoms when a fi stula is temporarily obturated or
repaired. This fi nding is supported by data from Hen-
ningsson and Isberg77 that indicated that improvement
in speech is not caused solely by the reduction of air
fl ow through the fi stula. Using videofl uoroscopy, they
demonstrated that the occlusion of a fi stula could cause
concomitant improvement in velopharyngeal valving.
Prior palatal surgery inevitably results in formation
of scarred tissue that often makes successful wound
healing after oronasal fi stula repair problematic. Con-
sequently, the likelihood of recurrent fi stula formation
after an attempted repair is quite high, with reported
rates ranging from 9 to 65%.68,69,78–82 Several options for
fi stula repair have been reported, including paring of
fi stula margins with reclosure, local turnover fl aps,83
tongue fl aps,74,83 buccal fat pad grafting,75,84 pedicled
fl aps from adjacent oral tissue,83 free fl aps,84–91 distrac-
tion osteogenesis,92 tissue expansion,93,94 and free carti-
lage grafts.95–97 The multitude of techniques is testament
to the fact that no particular procedure reliably yields
satisfactory results. Furthermore, these options can re-
quire cumbersome, lengthy procedures and may result
in signifi cant donor-site morbidity, even as they still
carry high rates of recurrence. More recently, Clark et
al.98 and Kirschner et al.99 have successfully used acellu-
lar dermis as an interposition graft in the repair of cleft
palate fi stulae.100
Velopharyngeal Dysfunction
Approximately 20% of children who undergo cleft pal-
ate repair develop speech production disorders, most
commonly velopharyngeal dysfunction, that require
additional intervention.101 This percentage seems in-
dependent of the type of palatoplasty. Velopharyngeal
dysfunction is diagnosed clinically by a constellation of
symptoms that include abnormal nasal resonance (hy-
pernasality), misarticulation, escape of air through the
nose (nasal emissions), and aberrant facial movements
(grimacing). Trost-Cardamone102 has proposed a taxon-
omy for velopharyngeal disorders that is based on caus-
ative factors. Velopharyngeal dysfunction may result
from anatomic, myoneural, and behavioral disorders or
from a combination of these disorders. Although it is
now possible to separate various etiologies of velopha-
ryngeal dysfunction by using instrumental evaluations,
contemporary treatments for velopharyngeal dysfunc-
Sie et al.65 have demonstrated complete resolution or
substantial improvement of velopharyngeal insuffi cien-
cy postoperatively. However, Spauwen et al.63 found no
signifi cant diff erences between the Furlow palatoplasty
and von Langenbeck palatoplasty techniques in respect
to articulatory skills, language comprehension, and lan-
guage production as well as hearing.
Concerning the use of a vomer fl ap, the literature is
contradictory about whether it interferes with maxil-
lary growth. Friede et al.66 presented data that seem to
indicate disturbance of maxillary growth when a vomer
fl ap was used to close the hard palate in infancy. Others
use a vomer fl ap to close the hard palate at the time of
lip repair and have not found signifi cant growth altera-
tion. The Oslo Cleft Palate group believes that the vomer
fl ap allows early closure of the cleft alveolus, thereby de-
creasing the frequency of alveolar nasal fi stulas without
producing signifi cant maxillary growth attenuation.67
Oronasal Fistulas
A palatal fi stula may occur anywhere along the site of
the original cleft as a complication of palatoplasty (Fig.
15.13). The reported incidence of fi stulization varies
widely, ranging from zero to 34% of all patients with re-
paired clefts.68,69 Multiple etiologic factors have been sug-
gested for the formation of oronasal fi stulas, including
wound breakdown secondary to closure site tension,70
infection,71–73 postoperative fl ap trauma,74 hematoma,75
and hypoxemia.76 Care should be taken to avoid pedicle
damage during fl ap elevation. If a fl ap appears ischemic,
it should be explored for tension on the pedicle. Tension
may be reduced by notching the pedicle out of the back
of the hard palate, dissecting a few millimeters of the
pedicle off of the fl ap, circumferential dissection of the
periosteum around the pedicle, and hamulus fracture
or tensor transposition. A palatal fi stula may result in
audible nasal air escape during speech, hypernasality,
increased nasal resonance, nasal regurgitation during
Fig. 15.13 Oronasal fi stula.

15 Surgical Correction of Congenital Anomalies and Associated Complications 143
operative dehiscence. Certainly there is at least a theo-
retical concern for mediastinal or vertebral spread after
these procedures, but it is rare, even though the posterior
oropharyngeal donor site in pharyngeal fl ap surgery is
typically left open to heal by secondary intention.113
Alveolar Bone Grafting
Patients with clefts through the maxillary alveolus have
osseous discontinuity of the alveolus and maxillary
basal bone. Succedaneous teeth cannot erupt through
the bone defect and may be unstable when fl anking
the bony cleft even if soft-tissue closure of the alveolar
gap has been achieved. Any patient born with a com-
plete cleft should be considered for alveolar grafting.
The benefi ts and goals of this procedure are well recog-
nized and include the stabilization of the maxillary arch,
elimination of oronasal fi stulae, creation of bony sup-
port for subsequent tooth eruption, and reconstruction
of the hypoplastic pyriform aperture and soft-tissue na-
sal base support. Losquadro and Tatum114 more recently
described their results for gingivoperiosteoplasty at the
time of cleft palate repair as a method to reduce or elim-
inate alveolar bone grafting.
Based on its timing, alveolar bone grafting is classifi ed
into primary (before palate repair or in children young-
er than two years of age) and secondary bone grafting
(at any time thereafter). The main concerns with bone
grafting are its eff ect on maxillary growth and the
height and width of the neo-alveolar ridge. Early tech-
niques of primary bone grafting were characterized by
extensive hard palatal dissection around and across the
vomerine-premaxillary suture and led to long-term
midfacial growth disturbance. With more recent modi-
fi cations, there are no diff erences in facial growth be-
tween operated and unoperated patients.115,116
Although the need for secondary augmentation of the
primarily grafted alveolus is reported to be low,117 de-
layed secondary grafting of the cleft alveolus with iliac
cancellous bone has gained widespread acceptance be-
cause of the predictable production of viable bone with
adequate cross-sectional width for tooth eruption, orth-
odontic tooth movement, or endosteal implant place-
ment. This procedure typically provides greater than
80% root coverage of incisors and cuspids adjacent to the
cleft.118 When teeth are present and erupt into the graft-
ed alveolus, often with the aid of surgical exposure and
orthodontic assistance, alveolar bone height is retained.
When teeth are not present to erupt through the graft
within six months, partial resorption of the graft occurs,
even when it is overfi lled intraoperatively.119 However,
total secondary graft failures are uncommon. Poor tissue
quality is the most common reason for compromised
results.119 Other complications include tooth injury or
loss, along with recurrent fi stulization. Complications
at the iliac donor site include bleeding, infection, bowel
or hip joint damage, cutaneous nerve damage, inguinal
tion were developed irrespective of its etiology. The ef-
forts of an international working group to standardize
fl uoroscopic and endoscopic velopharyngeal functional
evaluations103 may permit development of diff erential
treatments based on diff erential diagnosis.
Partial obstruction of the velopharyngeal port is the
unifying feature of most surgical treatments for velo-
pharyngeal dysfunction. Two classes of operations are
currently used to manage velopharyngeal dysfunction:
(1) lengthening and reorienting the muscles of the pal-
ate by retropositioning of the velum (V-Y pushback;
intravelar veloplasty; double-opposing Z-plasty) and
(2) reducing the size of the opening between the nasal
and oral pharynges. Velopharyngeal port reduction can
be accomplished by central obstruction (pharyngeal
fl ap), posterolateral narrowing (sphincter pharyngo-
plasty),104–106 or posterior pharyngeal wall augmenta-
tion.107–109 Although outcome reports for each of these
interventions have been published107–109 that document
variable success rates and associated morbidity, com-
parative data are unavailable. All these procedures are
capable of producing iatrogenic postoperative airway
obstruction. They should be used very cautiously in pa-
tients who are at risk for airway complications because
of cardiopulmonary or neurologic conditions or in pa-
tients who already have airway concerns.
Failure of the pharyngeal fl ap or sphincter pharyn-
goplasty operations results from inadequate obstruc-
tion (persistent hypernasality) or too much obstruction
(mouth breathing, rhinorrhea, increase in ear and sinus
infections, and sleep apnea). Tailoring the intervention to
the patient’s needs based on visualization studies (fl uo-
roscopy and endoscopy) is thought to be one of the best
ways to achieve appropriate obstruction. Attempts have
been made to defi ne the reasons for morbidity and fail-
ure after sphincter pharyngoplasty. Riski et al.110 docu-
mented the necessity for proper anatomic placement of
the myomucosal fl aps that comprised the neosphincter
and the improvement in velopharyngeal function after
attention to anatomic placement during a six-year expe-
rience. Witt et al.107–109 identifi ed the risk of identifi able
syndromes, microretrognathia, or perinatal respiratory
and feeding diffi culties for development of post-sphinc-
ter airway problems and Chegar et al.111 described pha-
ryngeal fl ap modifi cations that resulted in reduced risk of
obstruction from wide pharyngeal fl aps. Persistent air-
way obstruction may necessitate port dilation, revision
surgery, or even removal of the obstructing tissue with
the likely attendant reduction in the speech result. Vari-
ous palatal prosthetic lifts or obturators may be used as
reversible methods of velopharyngeal management. A
comparison of speech outcomes using prosthetic versus
surgical management showed no diff erence for patients
who complied with the prostheses.112 However, because
nearly 30% of patients referred for prostheses did not
comply, surgery was more effi cacious overall. Recognized
infection is uncommon, but it might contribute to post-

Complications in Facial Plastic Surgery
144
tients who underwent microtia repair. He observed chest
deformities in 64% of children under the age of ten years
and 20% in older children. The surgical incision should
be placed in the medial inframammary fold, especially in
female patients. Leaving the deep perichondrium down
during cartilage removal reduces the risk of pneumo-
thorax. The anesthesiologist should perform a Valsalva
maneuver at the time of closing to check for an air leak.
Small pleural tears can be repaired over a suction catheter
that can be removed after airtight wound closure. Tube
thoracostomy is rarely required. Costal cartilage harvest
is associated with signifi cant pain. It is helpful to place a
small-diameter infusion catheter in the wound bed at the
time of graft harvest for instillation of anesthetic solution.
Complications also occur at the ear reconstruction site.
Thinning of the skin fl ap is desirable to enhance visible
cartilage contours. However, too much thinning or pres-
sure dressings may compromise the skin envelope.124,125
Exposure of the carved cartilage framework secondary
to skin fl ap necrosis may necessitate complete removal
of the framework. Small areas of skin loss (less than1
cm) can be treated with topical and systemic antibiotic
therapy as well as limited debridement, but this usually
leads to a contour defect (Fig. 15.14). Infection occurs in
less than 0.5% of cases. Hematoma formation has been
reported in 0.3% of patients.131 The use of stainless steel
wire instead of sutures to coapt the cartilage elements
of the framework has been associated with a higher inci-
dence of construct notching and wire extrusion.132 Long-
term complications include extrusion of suture material
or necrotic cartilage, resorption of cartilage, and poor
anatomic detail (Fig. 15.15). Careful attention to detail
and conservative tissue handling improve results.
ligament separation, scarring, chronic hip pain, gait dis-
turbance and contour defect. Other donor sites have in-
cluded the skull, mandible, ribs, and tibia.

◆Microtia Repair
Malformations of the external ear occur in newborn in-
fants with a frequency of less than 1%. The majority of
those are minor, such as preauricular skin tags. The inci-
dence of isolated microtia is 1:10,000,120 occurring more
often in right ears and in males.121 Whites and blacks
appear to have a lower incidence of microtia than His-
panics and Asians.122 The cause of microtia is thought
to be multifactorial, and most cases are sporadic, with
fewer than 15% having a positive family history. If asso-
ciated with a syndrome (e.g., Treacher-Collins, Golden-
har, etc.) the incidence is higher. Microtia is unilateral in
70% of cases, and the commonest associations are facial
abnormalities and hearing loss. There is no universally
accepted classifi cation system for microtia. One widely
adopted system, originally described by Weerda and
simplifi ed by Aguilar, assigns a grade from I to III based
on the severity of the deformity.121
Auricular Reconstruction with Costal Cartilage
In 1971, Tanzer123 described his four-stage reconstruc-
tion that consisted of (1) lobule transposition, (2) car-
tilage framework carving and placement, (3) elevation
of the ear with postauricular skin grafting, and (4)
tragus construction with conchal excavation. In 1992,
Brent124,125 published his own experience with 600 cases
over 20 years, with a median follow-up of fi ve years. He
describes his four-stage technique that consisted of (1)
framework placement, (2) lobule transposition, (3) tra-
gus construction and conchal excavation, and (4) eleva-
tion of the ear framework. With experience, sequencing
the stages of reconstruction is fl exible depending on the
degree of deformity and the surgeon’s preference. With
regard to timing, there is usually suffi cient rib cartilage
by the age of six years, and the auricle has reached 95%
of its adult size.126 Reconstruction can often begin at an
earlier age if an alloplastic framework is being used, be-
cause there is no need to harvest a large quantity of rib
cartilage.124,125,127,128 An alternative to reconstruction is
the use of a prosthetic ear. Despite the introduction of
osseointegrated prostheses, most patients prefer a rib
graft repair.129 Because the placement of osseointegrat-
ed implants requires the removal of skin and soft tissue
in the area of the repair, future autogenous rib recon-
struction is precluded. However, rib reconstruction does
not prevent later prosthesis placement.
Complications associated with autogenous rib cartilage
graft harvest include a chest scar, a visible anterior chest
wall deformity, pneumothorax, and postoperative pain.
Ohara et al.130 evaluated donor site morbidity in 18 pa-
Fig. 15.14 Neohelix defect from cartilage exposure.

15 Surgical Correction of Congenital Anomalies and Associated Complications 145
Otoplasty
Otoplasty typically refers to surgery to correct an overly
prominent auricle, generally from some combination of
conchal excess and antihelical fold defi ciency. The ap-
proach is usually a postauricular incision or excision,
with cartilage weakening or cutting and suturing. Early
complications after otoplasty include hematoma for-
mation and infection. The incidence of postoperative
hematoma after otoplasty is low. Bleeding results from
local factors, such as an improper dissection plane or in-
adequate hemostasis, and from systemic factors such as
hypertension or undiagnosed coagulopathy. Excessive
pain should prompt exploration of the wound to rule
out a hematoma. If a blood clot is found and removed,
the incision is loosely closed over a passive drain, fol-
lowed by replacement of a conforming dressing or pos-
sibly even sutured dental rolls, along with treatment
by a broad-spectrum antibiotic. If the hematoma is left
untreated, wound infection, perichondritis, chondritis
and postoperative caulifl ower deformity may result.
The risk of infection is reduced by strict observance of
sterile technique, perioperative parenteral and topical
antibiotic administration, and postoperative application
of antibiotic ointment to the suture line.
Patients may be dissatisfi ed with the result of the oto-
plasty; for example, over-correction may put the ear too
fl at against the head, or overly aggressive cartilage weak-
ening techniques may lead to an unnatural operated look
with sharp contours. Over-resection of the central post-
auricular skin can lead to a telephone ear deformity, in
which the ear is close to the head in its middle portion
but projects at the upper and lower poles (Fig. 15.16).
Hypertrophic scarring, hypesthesia, and suture-re-
lated complications such as granuloma formation or
suture exposure are also potential problems. Suture-re-
lated complications such as localized skin infl ammation,
stitch abscess formation, or foreign-body granulomas
are easily dealt with by removal of the off ending su-
ture when the wound has matured. Extrusion of su-
tures is more prevalent with scaphoconchal Mustarde
sutures than with conchomastoid Furnas sutures. If
they are placed too far away from the antihelical fold,
these sutures may then bowstring across the gap, even
becoming exposed and causing both an aesthetic and
functional deformity, particularly for patients who wear
eyeglasses. Over-excision of postauricular skin may re-
sult in tense skin closure and poor suture coverage. Fi-
nally, improper conchomastoid suture placement may
be responsible for anterior displacement of the conchal
cartilage, leading to external auditory canal narrowing.
Relapse or loss of correction is one of the more com-
mon postoperative complications encountered, with
reported rates ranging from 6.5 to 12%.133,134 It is fre-
quently observed with postoperative trauma and car-
tilage-sparing techniques. Improper type, location, or
quantity of sutures may result in excessive tension and
Alloplastic Framework Reconstruction
By using an alloplastic framework, reconstruction may
begin at an earlier age because the size of the child’s rib
cartilage is not an issue. Cronin and Ohmori described
excellent initial aesthetic results from the use of a sili-
cone framework, but long-term follow-up revealed
an unacceptably high failure rate from implant expo-
sure.126 Exposure and subsequent failure may occur
many years after implantation, even with minor trau-
ma. The use of silicone for ear reconstruction has thus
been abandoned. More recently, reconstruction with a
porous polyethylene (MEDPORE, Porex Surgical, Inc.,
Newnan, GA) framework has been advocated with in-
creasing enthusiasm. Porous polyethylene causes min-
imal tissue reaction, and its porosity allows ingrowth
of soft tissue, thereby providing greater stability. The
use of a temporoparietal fascia fl ap that completely
surrounds the porous polyethylene implant has sig-
nifi cantly reduced its initial failure rate,124,125 although
long-term results are lacking127,128 and a lifelong risk of
exposure remains.
Prosthetic Reconstruction
Prosthetic reconstruction usually requires only one op-
erative procedure after removal of the congenitally mal-
formed auricular remnants. Depending on the thickness
of the temporal bone, the implant can be attached to a
bone-anchored abutment or (if there is insuffi cient bone
thickness) to an implant-carrying plate system. Compli-
cations of placement include meningitis, dural penetra-
tion, hemorrhage, and brain injury. Meticulous hygiene
around the transcutaneous abutments is necessary to
avoid infection of the implant site. Implant integration
failure and rejection remain persistent risks. Psycholog-
ical diffi culties might arise from the social impact of the
dislodgement of an auricular prosthesis, in a classroom
setting for instance. Replacement of the prosthetic ear is
required every two to fi ve years.
Fig. 15.15 Poor auricular defi nition and exposed cartilage.

Complications in Facial Plastic Surgery
146

◆Conclusion
Surgery for the correction of congenital anomalies is
both rewarding and challenging. There is a myriad of
presentations, each requiring careful analysis and plan-
ning. Many of the procedures are complex and danger-
ous, requiring specialized training and experience. As
has been stated, prevention is the best way to manage
complications. Attention to detail and early acknowl-
edgment are paramount to complication management.
Thorough preoperative counseling will help to maintain
the patient’s confi dence during the trying times of post-
operative complications.
pull-through of sutures. Other causes of insuffi cient
long-term correction include insuffi cient conchal set-
back or inadequate weakening of particularly infl ex-
ible cartilage. The patient should be made aware of the
consequences of external trauma in the postoperative
healing phase. The untoward eff ect s of external trauma
may be lessened by careful placement of sutures with
attainment of adequate purchase on the anterior peri-
chondrium to avert suture pull-through and by place-
ment of conchotemporal tension-relieving sutures to
help reinforce the correction. Hypertrophic scarring or
keloid formation occurs most commonly in susceptible
individuals of African, Asian, or Scandinavian descent.
Younger patients are also more vulnerable, especially
in the setting of postauricular incisions. Preventive mo-
dalities include avoidance of excessive wound-closing
tension and minimization of tissue trauma or infection.
Management may include steroid injections and scar re-
vision. Persistent paresthesias or sensory defi cits after
otoplasty are rare. Although injury to the greater au-
ricular nerve may give rise to these symptoms initially,
they usually resolve spontaneously over several months.
A more likely symptom relates to cold temperature in-
sensitivity and increased risk of frostbite after otoplasty.
Fig. 15.16 Telephone deformity of the auricle. (Illustration by
Robert Brown.)
PEARLS OF WISDOM
Remain constantly aware of hemostasis and volume replace-
ment throughout infantile craniofacial surgery. Although these
procedures have become routine, they are still very dangerous.
Pay close attention to the security of the endotracheal tube
during craniofacial cases. It is best to avoid reintubation after
the calvarium has been removed.
In distraction osteogenesis, the regenerate is as only as big as
the cross-section of the original osteotomy. Choose a large
area of bone stock to make the osteotomy.
Avoid absorbable skin sutures on primary cleft lip repairs. They
can leave marks on delicate infant skin.
Tension is the enemy of palate repair. Learn multiple maneu-
vers to reduce tension.
Remember that pharyngeal fl aps are intended to partially ob-
struct the nasopharynx. Additional obstruction at the oropha-
ryngeal level can occur if the fl ap is too low or the donor-site
healing narrows the pharynx.
In alveolar bone grafting, it is critical to expose the entire
margins of the bony cleft from the alveolar ridge to the fl oor of
the nose and lateral pyriform crest.
Consider waiting to start microtia correction until the child is
over eight years old. The larger cartilages are easier to work with.
Avoid cartilage cutting techniques until you have become very
comfortable with otoplasty. They are much harder to use to
achieve a natural appearance.
References
1. Shillito J Jr, Matson DD. Craniosynostosis: a review of 519 sur-
gical patients. Pediatrics 1968;41(4):829–853
2. Harrop CW, Avery BS, Marks SM, Putnam GD. Craniosynosto-
sis in babies: complications and management of 40 cases. Br J
Oral Maxillofac Surg 1996;34(2):158–161
3. Kadri H, Mawla AA. Incidences of craniosynostosis in Syria. J
Craniofac Surg 2004;15(4):703–704

15 Surgical Correction of Congenital Anomalies and Associated Complications 147
23. Dujovny M, Aviles A, Anger C. An innovative approach for cra-
nioplasty using hydroxyapatite cement. Surg Neurol 1997;
48(3):294–297
24. Mathur KK, Tatum SA, Kellman RM. Carbonated apatite and
hydroxyapatite in craniofacial reconstruction. Arch Facial
Plast Surg 2003;5(5):379–383
25. Dupoirieux L, Gard C. Hydroxyapatite cement for calvarial
reconstruction. Oral Surg Oral Med Oral Pathol Oral Radiol
Endod 2000;89(2):140–142
26. Psillakis JM, Grotting JC, Casanova R, Cavalcante D, Vasconez
LO. Vascularized outer-table calvarial bone fl aps. Plast Recon-
str Surg 1986;78(3):309–317
27. Littlefi eld TR. Food and Drug Administration regulation of
orthotic cranioplasty. Cleft Palate Craniofac J 2001;38(4):
337–340
28. Hertle RW, Quinn GE, Minguini N, Katowitz JA. Visual loss in
patients with craniofacial synostosis. J Pediatr Ophthalmol
Strabismus 1991;28(6):344–349
29. Gray TL, Casey T, Selva D, Anderson PJ, David DJ. Oph-
thalmic sequelae of Crouzon syndrome. Ophthalmology
2005;112(6):1129–1134
30. Khan SH, Nischal KK, Dean F, Hayward RD, Walker J. Vi-
sual outcomes and amblyogenic risk factors in craniosyn-
ostotic syndromes: a review of 141 cases. Br J Ophthalmol
2003;87(8):999–1003
31. Tay T, Martin F, Rowe N, et al. Prevalence and causes of visual
impairment in craniosynostotic syndromes. Clin Experiment
Ophthalmol 2006;34(5):434–440
32. Diamond GR, Katowitz JA, Whitaker LA, Bersani TA, Bartlett
SP, Welsh MG. Ocular and adnexal complications of unilat-
eral orbital advancement for plagiocephaly. Arch Ophthalmol
1987;105(3):381–385
33. Hurmerinta K, Hukki J. Vector control in lower jaw distrac-
tion osteogenesis using an extra-oral multidirectional device.
J Craniomaxillofac Surg 2001;29(5):263–270
34. Hollier LH, Kim JH, Grayson B, McCarthy JG. Mandibular
growth after distraction in patients under 48 months of age.
Plast Reconstr Surg 1999;103(5):1361–1370
35. Karaharju-Suvanto T, Peltonen J, Laitinen O, Kahri A. The ef-
fect of gradual distraction of the mandible on the sheep tem-
poromandibular joint. Int J Oral Maxillofac Surg 1996;25(2):
152–156
36. Carls FR, Sailer HF. Seven years clinical experience with
mandibular distraction in children. J Craniomaxillofac Surg
1998;26(4):197–208
37. McComb HK, Coghlan BA. Primary repair of the unilateral
cleft lip nose: completion of a longitudinal study. Cleft Palate
Craniofac J 1996;33(1):23–30, discussion 30–31
38. Huff man WC, Lierle DM. Studies on the pathologic anatomy
of the unilateral harelip nose. Plast Reconstr Surg (1946)
1949;4(3):225–234
39. Ariyan S, Krizek TJ. A simplifi ed technique for correction
of the cleft lip nasal deformity. Ann Plast Surg 1978;1(6):
568–574
40. Dingman RO, Natvig P. The infracartilaginous incision for rhi-
noplasty. Plast Reconstr Surg 1982;69(1):134–135
41. Black PW, Hartrampf CR Jr, Beegle P. Cleft lip type nasal
deformity: defi nitive repair. Ann Plast Surg 1984;12(2):
128–138
42. Warren DW. A quantitative technique for assessing nasal air-
way impairment. Am J Orthod 1984;86(4):306–314
4. Nonaka Y, Oi S, Miyawaki T, Shinoda A, Kurihara K. Indication
for and surgical outcomes of the distraction method in various
types of craniosynostosis. Advantages, disadvantages, and cur-
rent concepts for surgical strategy in the treatment of cranio-
synostosis. Childs Nerv Syst 2004;20(10):702–709
5. Kakitsuba N, Sadaoka T, Motoyama S, et al. Sleep apnea and
sleep-related breathing disorders in patients with craniofacial
synostosis. Acta Otolaryngol Suppl 1994;517:6–10
6. Järund M, Lauritzen C. Craniofacial dysostosis: airway ob-
struction and craniofacial surgery. Scand J Plast Reconstr Surg
Hand Surg 1996;30(4):275–279
7. Sculerati N, Gottlieb MD, Zimbler MS, Chibbaro PD, McCarthy
JG. Airway management in children with major craniofacial
anomalies. Laryngoscope 1998;108(12):1806–1812
8. Goodrich JT. Craniofacial surgery: complications and their
prevention. Semin Pediatr Neurol 2004;11(4):288–300
9. Fishman MA, Hogan GR, Dodge PR. The concurrence of hy-
drocephalus and craniosynostosis. J Neurosurg 1971;34(5):
621–629
10. Golabi M, Edwards MS, Ousterhout DK. Craniosynostosis and
hydrocephalus. Neurosurgery 1987;21(1):63–67
11. Renier D, Sainte-Rose C, Marchac D, Hirsch JF. Intracra-
nial pressure in craniostenosis. J Neurosurg 1982;57(3):
370–377
12. Thompson DN, Jones BM, Harkness W, Gonsalez S, Hayward RD.
Consequences of cranial vault expansion surgery for craniosyn-
ostosis. Pediatr Neurosurg 1997;26(6):296–303
13. Fialkov JA, Holy C, Forrest CR, Phillips JH, Antonyshyn OM.
Postoperative infections in craniofacial reconstructive proce-
dures. J Craniofac Surg 2001;12(4):362–368
14. Fearon JA, Yu J, Bartlett SP, Munro IR, Chir B, Whitaker L. In-
fections in craniofacial surgery: a combined report of 567
procedures from two centers. Plast Reconstr Surg 1997;
100(4):862–868
15. Bergsma JE, de Bruijn WC, Rozema FR, Bos RR, Boering G. Late
degradation tissue response to poly(L-lactide) bone plates
and screws. Biomaterials 1995;16(1):25–31
16. Eppley BL, Sadove AM, Havlik RJ. Resorbable plate fi xa-
tion in pediatric craniofacial surgery. Plast Reconstr Surg
1997;100(1):1–7, discussion 8–13
17. Tharanon W, Sinn DP, Hobar PC, Sklar FH, Salomon J. Surgi-
cal outcomes using bioabsorbable plating systems in pediat-
ric craniofacial surgery. J Craniofac Surg 1998;9(5):441–444,
discussion 445–447
18. Imola MJ, Hamlar DD, Shao W, Chowdhury K, Tatum S. Resorb-
able plate fi xation in pediatric craniofacial surgery: long-term
outcome. Arch Facial Plast Surg 2001;3(2):79–90
19. Böstman OM. Osteolytic changes accompanying degradation
of absorbable fracture fi xation implants. J Bone Joint Surg Br
1991;73(4):679–682
20. Eppley BL, Morales L, Wood R, et al. Resorbable PLLA-PGA
plate and screw fi xation in pediatric craniofacial surgery:
clinical experience in 1883 patients. Plast Reconstr Surg
2004;114(4):850–856, discussion 857
21. Mackool R, Yim J, McCarthy JG. Delayed degradation in a re-
sorbable plating system. J Craniofac Surg 2006;17(1):194–
197, discussion 197–198
22. Verret DJ, Ducic Y, Oxford L, Smith J. Hydroxyapatite cement
in craniofacial reconstruction. Otolaryngol Head Neck Surg
2005;133(6):897–899

Complications in Facial Plastic Surgery
148
65. Sie KC, Tampakopoulou DA, Sorom J, Gruss JS, Eblen LE. Results
with Furlow palatoplasty in management of velopharyngeal
insuffi ciency. Plast Reconstr Surg 2001;108(1):17–25, discus-
sion 26–29
66. Friede H, Enocson L, Lilja J. Features of maxillary arch and na-
sal cavity in infancy and their infl uence on deciduous occlu-
sion in unilateral cleft lip and palate. Scand J Plast Reconstr
Surg Hand Surg 1988;22(1):69–75
67. Semb G. A study of facial growth in patients with unilateral
cleft lip and palate treated by the Oslo CLP Team. Cleft Palate
Craniofac J 1991;28(1):1–21, discussion 46–48
68. Cohen SR, Kalinowski J, LaRossa D, Randall P. Cleft palate
fi stulas: a multivariate statistical analysis of prevalence,
etiology, and surgical management. Plast Reconstr Surg
1991;87(6):1041–1047
69. Abyholm FE, Borchgrevink HH, Eskeland G. Palatal fi stulae
following cleft palate surgery. Scand J Plast Reconstr Surg
1979;13(2):295–300
70. Campbell DA. Fistulae in the hard palate following cleft palate
surgery. Br J Plast Surg 1962;15:377–384
71. Jolleys A, Savage JP. Healing defects in cleft palate surgery:The
role of infection. Br J Plast Surg 1962;16:134
72. McClelland RMA, Patterson TJS. The infl uence of penicillin on
the complication rate after repair of clefts of the lip and pal-
ate. Br J Plast Surg 1962;16:144
73. Musgrave RH, Bremner JC. Complications of cleft pal-
ate surgery. Plast Reconstr Surg Transplant Bull 1960;26:
180–189
74. Posnick JC, Getz SB Jr. Surgical closure of end-stage palatal fi s-
tulas using anteriorly-based dorsal tongue fl aps. J Oral Maxil-
lofac Surg 1987;45(11):907–912
75. Honnebier MB, Johnson DS, Parsa AA, Dorian A, Parsa FD.
Closure of palatal fi stula with a local mucoperiosteal fl ap
lined with buccal mucosal graft. Cleft Palate Craniofac J
2000;37(2):127–129
76. Wood FM. Hypoxia: another issue to consider when timing
cleft repair. Ann Plast Surg 1994;32(1):15–18, discussion
19–20
77. Isberg A, Henningsson G. Infl uence of palatal fi stulas on velo-
pharyngeal movements: a cineradiographic study. Plast Re-
constr Surg 1987;79(4):525–530
78. Schultz RC. Management and timing of cleft palate fi stula re-
pair. Plast Reconstr Surg 1986;78(6):739–747
79. Amaratunga NA. Occurrence of oronasal fi stulas in operated
cleft palate patients. J Oral Maxillofac Surg 1988;46(10):
834–838
80. Rintala AE. Surgical closure of palatal fi stulae: follow-up
of 84 personally treated cases. Scand J Plast Reconstr Surg
1980;14(3):235–238
81. Emory RE Jr, Clay RP, Bite U, Jackson IT. Fistula formation and
repair after palatal closure: an institutional perspective. Plast
Reconstr Surg 1997;99(6):1535–1538
82. Muzaff ar AR, Byrd HS, Rohrich RJ, et al. Incidence of cleft pal-
ate fi stula: an institutional experience with two-stage palatal
repair. Plast Reconstr Surg 2001;108(6):1515–1518
83. Bardach J, Salyer K. Surgical Techniques in Cleft Lip and Palate.
Chicago: Year Books; 1987
84. Coghlan K, O’Regan B, Carter J. Tongue fl ap repair of oro-nasal
fi stulae in cleft palate patients. A review of 20 patients. J Cra-
niomaxillofac Surg 1989;17(6):255–259
85. Egyedi P. Utilization of the buccal fat pad for closure of oro-
antral and/or oro-nasal communications. J Maxillofac Surg
1977;5(4):241–244
43. Ozaki W, Chaff oo RA, Vu KC, Markowitz BL. Comprehensive
rhinoplasty technique to correct the bilateral cleft lip nasal
deformity using conchal composite grafts. J Craniomaxillofac
Surg 2006;34(3):150–155
44. McComb H. Primary repair of the bilateral cleft lip nose. Br J
Plast Surg 1975;28(4):262–267
45. Cenzi R, Guarda L. A dynamic nostril splint in the surgery of
the nasal tip: technical innovation. J Craniomaxillofac Surg
1996;24(2):88–91
46. Barsky AJ. Principles and Practice of Plastic Surgery. Balti-
more: Williams and Wilkins; 2007:159–198
47. Ortiz Monasterio F, Ruas EJ. Cleft lip rhinoplasty: the role
of bone and cartilage grafts. Clin Plast Surg 1989;16(1):
177–186
48. Omori M, Takato T, Eguchi T, Mori Y, Tomizuka K. Secondary
correction of the wide nasal root in bilateral nasal deformity
associated with cleft lip in fi ve Oriental patients. Scand J Plast
Reconstr Surg Hand Surg 2003;37(4):216–219
49. Raspall G, González-Lagunas J. Management of the nasal tip
by open rhinoplasty. J Craniomaxillofac Surg 1996;24(3):
145–150
50. Gilles HD, Kilner TP. Hare-lip: operation for correction of sec-
ondary deformities. Lancet 1932;223:1369–1375
51. Gillies HD, Millard DR. The Principles and Art of Plastic Sur-
gery. Boston: Little, Brown & Co; 2007
52. McIndoe A, Rees TD. Synchronous repair of secondary de-
formities in cleft lip and nose. Plast Reconstr Surg 1959;
24:150–161
53. Millard DR Jr. Earlier correction of the unilateral cleft lip nose.
Plast Reconstr Surg 1982;70(1):64–73
54. Rees TD, Guy CL, Converse JM. Repair of the cleft lip-nose:
addendum to the synchronous technique with full-thick-
ness skin grafting of the nasal vestibule. Plast Reconstr Surg
1966;37(1):47–50
55. Vissarionov VA. Correction of the nasal tip deformity follow-
ing repair of unilateral clefts of the upper lip. Plast Reconstr
Surg 1989;83(2):341–347
56. Kirschbaum JD, Kirschbaum CA. The chondromucosal sleeve
for the secondary correction of the unilateral cleft lip nasal
deformity. Ann Plast Surg 1992;29(5):402–407
57. Cho BC, Lee JH, Cohen M, Baik BS. Surgical correction of uni-
lateral cleft lip nasal deformity. J Craniofac Surg 1998;9(1):
20–29
58. Mulliken JB. Repair of bilateral complete cleft lip and nasal
deformity—state of the art. Cleft Palate Craniofac J 2000;
37(4):342–347
59. Bardach J, Morris HL, Olin WH. Late results of primary ve-
loplasty: the Marburg Project. Plast Reconstr Surg 1984;
73(2):207–218
60. Kriens OB. An anatomical approach to veloplasty. Plast Recon-
str Surg 1969;43(1):29–41
61. Marsh JL, Grames LM, Holtman B. Intravelar veloplasty: a pro-
spective study. Cleft Palate J 1989;26(1):46–50
62. Furlow LT Jr. Cleft palate repair by double opposing Z-plasty.
Plast Reconstr Surg 1986;78(6):724–738
63. Spauwen PH, Goorhuis-Brouwer SM, Schutte HK. Cleft pal-
ate repair: Furlow versus von Langenbeck. J Craniomaxillofac
Surg 1992;20(1):18–20
64. Yu CC, Chen PK, Chen YR. Comparison of speech results af-
ter Furlow palatoplasty and von Langenbeck palatoplasty in
incomplete cleft of the secondary palate. Chang Gung Med J
2001;24(10):628–632

15 Surgical Correction of Congenital Anomalies and Associated Complications 149
106. Jackson IT. Sphincter pharyngoplasty. Clin Plast Surg 1985;
12(4):711–717
107. Witt PD, D’Antonio LL, Zimmerman GJ, Marsh JL. Sphincter
pharyngoplasty: a preoperative and postoperative analy-
sis of perceptual speech characteristics and endoscopic
studies of velopharyngeal function. Plast Reconstr Surg
1994;93(6):1154–1168
108. Witt PD, Marsh JL, Muntz HR, Marty-Grames L, Watchmak-
er GP. Acute obstructive sleep apnea as a complication of
sphincter pharyngoplasty. Cleft Palate Craniofac J 1996;33(3):
183–189
109. Witt PD, O’Daniel TG, Marsh JL, Grames LM, Muntz HR, Pil-
gram TK. Surgical management of velopharyngeal dysfunc-
tion: outcome analysis of autogenous posterior pharyngeal
wall augmentation. Plast Reconstr Surg 1997;99(5):1287–
1296, discussion 1297–1300
110. Riski JE, Serafi n D, Riefkohl R, Georgiade GS, Georgiade NG.
A rationale for modifying the site of insertion of the Orti-
cochea pharyngoplasty. Plast Reconstr Surg 1984;73(6):
882–894
111. Chegar BE, Shprintzen RJ, Curtis MS, Tatum SA. Pharyn-
geal fl ap and obstructive apnea: maximizing speech out-
come while limiting complications. Arch Facial Plast Surg
2007;9(4):252–259
112. Marsh JL, Wray RC. Speech prosthesis versus pharyngeal
fl ap: a randomized evaluation of the management of velo-
pharyngeal incompetency. Plast Reconstr Surg 1980;65(5):
592–594
113. Tucker AL, Hubbard JG. Retropharyngeal infection with
disc space involvement and osteomyelitis, following a pha-
ryngeal fl ap operation. Case report. Plast Reconstr Surg
1974;53(4):477–478
114. Losquadro WD, Tatum SA. Direct gingivoperiosteoplasty with
palatoplasty. Facial Plast Surg 2007;23(2):140–145
115. Rosenstein S, Dado DV, Kernahan D, Griffi th BH, Grasseschi
M. The case for early bone grafting in cleft lip and palate: a
second report. Plast Reconstr Surg 1991;87(4):644–654, dis-
cussion 655–656
116. Rosenstein S, Kernahan D, Dado D, Grasseschi M, Griffi th BH.
Orthognathic surgery in cleft patients treated by early bone
grafting. Plast Reconstr Surg 1991;87(5):835–892, discussion
840–842
117. Eppley BL. Alveolar cleft bone grafting (Part I): Primary bone
grafting. J Oral Maxillofac Surg 1996;54(1):74–82
118. Long RE Jr, Paterno M, Vinson B. Eff ect of cuspid position-
ing in the cleft at the time of secondary alveolar bone
grafting on eventual graft success. Cleft Palate Craniofac J
1996;33(3):225–230
119. Cohen M, Polley JW, Figueroa AA. Secondary (intermedi-
ate) alveolar bone grafting. Clin Plast Surg 1993;20(4):
691–705
120. Shaw GM, Carmichael SL, Kaidarova Z, Harris JA. Epide-
miologic characteristics of anotia and microtia in Cali-
fornia, 1989–1997. Birth Defects Res A Clin Mol Teratol
2004;70(7):472–475
121. Aguilar EF III. Auricular reconstruction of congenital micro-
tia (grade III). Laryngoscope 1996; 106(12 Pt 2, Suppl 82):
1–26
122. Forrester MB, Merz RD. Impact of excluding cases with
known chromosomal abnormalities on the prevalence of
structural birth defects, Hawaii, 1986–1999. Am J Med Genet
A 2004;128A(4):383–388
86. Batchelor AG, Palmer JH. A novel method of closing a pala-
tal fi stula: the free fascial fl ap. Br J Plast Surg 1990;43(3):
359–361
87. Chen HC, Ganos DL, Coessens BC, Kyutoku S, Noordhoff MS.
Free forearm fl ap for closure of diffi cult oronasal fi stulas in cleft
palate patients. Plast Reconstr Surg 1992;90(5):757–762
88. Corrêa Chem R, Franciosi LF. Dorsalis pedis free fl ap to close
extensive palate fi stulae. Microsurgery 1983;4(1):35–39
89. Inoue T, Harashina T, Asanami S, Fujino T. Reconstruction of
the hard palate using free iliac bone covered with a jejunal
fl ap. Br J Plast Surg 1988;41(2):143–146
90. MacLeod AM, Morrison WA, McCann JJ, Thistlethwaite S,
Vanderkolk CA, Ryan AD. The free radial forearm fl ap with
and without bone for closure of large palatal fi stulae. Br J
Plast Surg 1987;40(4):391–395
91. Soutar DS, Scheker LR, Tanner NS, McGregor IA. The radial
forearm fl ap: a versatile method for intra-oral reconstruction.
Br J Plast Surg 1983;36(1):1–8
92. Taub PJ, Bradley JP, Kawamoto HK. Closure of an oronasal fi s-
tula in an irradiated palate by tissue and bone distraction os-
teogenesis. J Craniofac Surg 2001;12(5):495–499, discussion
500
93. De Mey A, Malevez C, Lejour M. Treatment of palatal fi stula by
expansion. Br J Plast Surg 1990;43(3):362–364
94. Van Damme PA, Freihofer HP. Palatal mucoperiosteal ex-
pansion as an adjunct to palatal fi stula repair: case re-
port and review of the literature. Cleft Palate Craniofac J
1996;33(3):255–257
95. Matsuo K, Kiyono M, Hirose T. A simple technique for closure
of a palatal fi stula using a conchal cartilage graft. Plast Recon-
str Surg 1991;88(2):334–337
96. Ohsumi N, Onizuka T, Ito Y. Use of a free conchal cartilage
graft for closure of a palatal fi stula: an experimental study
and clinical application. Plast Reconstr Surg 1993;91(3):
433–440
97. Mohanna PN, Kangesu L, Sommerlad BC. The use of conchal-
cartilage grafts in the closure of recurrent palatal fi stulae. Br J
Plast Surg 2001;54(3):274
98. Clark JM, Saff old SH, Israel JM. Decellularized dermal grafting
in cleft palate repair. Arch Facial Plast Surg 2003;5(1):40–44,
discussion 45
99. Kirschner RE, Cabiling DS, Slemp AE, Siddiqi F, LaRossa DD,
Losee JE. Repair of oronasal fi stulae with acellular dermal ma-
trices. Plast Reconstr Surg 2006;118(6):1431–1440
100. Losee JE, Smith DM, Afi fi AM, et al. A successful algorithm for
limiting postoperative fi stulae following palatal procedures
in the patient with orofacial clefting. Plast Reconstr Surg
2008;122(2):544–554
101. Witt PD, D’Antonio LL. Velopharyngeal insuffi ciency and sec-
ondary palatal management. A new look at an old problem.
Clin Plast Surg 1993;20(4):707–721
102. Trost-Cardamone JE. Coming to terms with VPI: a response to
Loney and Bloem. Cleft Palate J 1989;26(1):68–70
103. Golding-Kushner KJ, Argamaso RV, Cotton RT, et al. Stan-
dardization for the reporting of nasopharyngoscopy and
multiview videofl uoroscopy: a report from an International
Working Group. Cleft Palate J 1990;27(4):337–347, discus-
sion 347–348
104. Hynes W. Pharyngoplasty by muscle transplantation. Br J
Plast Surg 1950;3(2):128–135
105. Wilk A, Champy M. [Repair of soft palate defi ciencies in adults
by Orticochea’s method (author’s transl)]. Rev Stomatol Chir
Maxillofac 1981;82(1):22–27

Complications in Facial Plastic Surgery
150
129. Botma M, Aymat A, Gault D, Albert DM. Rib graft reconstruc-
tion versus osseointegrated prosthesis for microtia: a signifi -
cant change in patient preference. Clin Otolaryngol Allied Sci
2001;26(4):274–277
130. Ohara K, Nakamura K, Ohta E. Chest wall deformities and
thoracic scoliosis after costal cartilage graft harvesting. Plast
Reconstr Surg 1997;99(4):1030–1036
131. Walton RL, Beahm EK. Auricular reconstruction for mi-
crotia: Part II. Surgical techniques. Plast Reconstr Surg
2002;110(1):234–249, quiz 250–251, 387
132. Nagata S. Microtia: Auricular Reconstruction. In: Vanderkolk
CA, ed. Plastic Surgery: Indications, Operations, and Out-
comes. St. Louis: Mosby; 2007:1023–1056
133. Adamson PA, McGraw BL, Tropper GJ. Otoplasty: criti-
cal review of clinical results. Laryngoscope 1991;101(8):
883–888
134. Goode RL, Proffi tt SD, Rafaty FM. Complications of otoplasty.
Arch Otolaryngol 1970;91(4):352–355
123. Tanzer RC. Total reconstruction of the auricle. The evolu-
tion of a plan of treatment. Plast Reconstr Surg 1971;47(6):
523–533
124. Brent B. Auricular repair with autogenous rib cartilage grafts:
two decades of experience with 600 cases. Plast Reconstr
Surg 1992;90(3):319–374
125. Brent B. Microtia repair with rib cartilage grafts: a review
of personal experience with 1000 cases. Clin Plast Surg
2002;29(2):257–271, vii
126. Beahm EK, Walton RL. Auricular reconstruction for microtia:
part I. Anatomy, embryology, and clinical evaluation. Plast Re-
constr Surg 2002;109(7):2473–2482, quiz 2482
127. Romo T III, Fozo MS, Sclafani AP. Microtia reconstruction
using a porous polyethylene framework. Facial Plast Surg
2000;16(1):15–22
128. Reinisch J. Microtia reconstruction using a polyethylene im-
plant: An eight-year surgical experience. 2007. Presented at
the 78th Annual Meeting of the American Association of Plas-
tic Surgeons, Colorado Springs, CO.

Orthognathic surgery is widely used to correct con-
genital and acquired dentofacial discrepancies. The
principles of orthognathic surgery were developed for
treatment of facial disharmony and dental malocclusion;
however, the techniques are also useful for consideration
of maxillofacial tumor resection and as therapy for ob-
structive sleep apnea syndrome. Orthognathic surgical
procedures can produce a high degree of satisfaction for
the patient and surgeon, but they remain challenging in
both presurgical planning and surgical execution. The
benefi ts of orthognathic surgery include better masti-
cator function, reduced facial pain, and improved facial
aesthetics. However, numerous complications have been
reported that can be attributed to improper surgical
planning, technical errors, or poor wound healing. These
can be loosely categorized as (1) vascular or nerve inju-
ries, (2) temporomandibular joint dysfunction, (3) bone
or soft-tissue infections, (4) periodontal disease, (5)
change in airway (obstructive sleep apnea) or swallow-
ing function, and (6) psychological problems.
The bulk of this chapter is organized according to the
complications seen in specifi c procedures. By reviewing
the potential pitfalls that may be encountered in each
procedure, this chapter should provide insight to those
who perform orthognathic surgery, including head and
neck surgeons, oral and maxillofacial surgeons, and fa-
cial plastic surgeons.

◆ Common Complications Associated
with Orthognathic Surgery
Complications commonly associated with the spectrum
of orthognathic surgical procedures are listed in Table
16.1. Of these, special attention will be given to infec-
tion and relapse as universal complications associated
with all procedures.
Infection
Infection after orthognathic surgery may be acute or
chronic, local or general. Endogenous bacteria, most
likely a mixture of anaerobic and aerobic bacteria, cause
most postoperative infections. Factors contributing to
this in orthognathic surgery populations may be the us-
age of steroids, the duration of the surgical procedure,
the patient’s age, interference with the blood supply
to the bony segments, dehydration of the wounds, the
presence of foreign bodies or sequestrum, hospitaliza-
tion in large wards, nutrition, hematoma, and smoking.
The surgeon’s experience, a good aseptic technique, and
gentle tissue handling are also relevant factors.1
In the classical wound classifi cation, normal orthogna-
thic surgery wounds fall into the Class II category (clean
contaminated wound). An infection rate of 10% to 15%
can be expected without use of antibiotics, in compari-
son to Class III wounds, with an expected infection rate
of 20% to 30%. In a clean wound (Class I), the probability
of infection is approximately 2%.1 Studies dealing with
infection after mandibular osteotomies report infection
rates ranging from 0% to 18%.2 In maxillary osteotomies,
infection rates lower than 6% are mostly reported,3 but
151
16
Complications in Orthognathic Surgery
Travis T. Tollefson, Shepherd G. Pryor V, and Nicholas W. Rotas
Table 16.1
Orthognathic Surgery Complications
• Infection
• Hardware exposure
• Unanticipated fractures
• Devitalization of teeth
• Malunion and/or nonunion
• Malocclusion
• Injury to teeth
• Gingival recession and/or periodontal complications
• Respiratory decompensation
• Bleeding
• Relapse

Complications in Facial Plastic Surgery
152

◆Complications of Mandibular Surgery
Bilateral Sagittal-Split Osteotomy
The most common procedure to correct mandibular de-
formities is the bilateral sagittal-split osteotomy (BSSO),
which is useful for both mandibular setback or advance-
ment (Fig. 16.1). The most commonly reported compli-
cations for BSSO are listed in Table 16.2.
in the study of Zijderveld et al. (1999),4 a 52.6% infec-
tion rate was found in a placebo medication group with
bimaxillary surgery.
There is some controversy concerning the need for
prophylactic antibiotics,4 and many diff erent practices
exist. The operator must assess dosage, timing, duration
of therapy, and side eff ects when considering the use
of antibiotic prophylaxis. Peterson (1990)5 has outlined
the following principles for the rational use of antibiotic
prophylaxis in orthognathic surgery: (1) The surgical
procedure should involve a signifi cant risk for infection;
increased risk is seen with both bone grafts and wound
class II (10–15%). (2) Proper antibiotics should be select-
ed. (3) Serum concentrations of the antibiotic should be
appropriately high. (4) The chosen antibiotic must be
administered in a correct time sequence. (5) The short-
est eff ective antibiotic exposure should be used.
Relapse
Relapse is an unpredictable risk of orthognathic surgery.
Many studies reporting relapse have limitations of sam-
ple size or the duration of follow-up, involve diff erent
surgical techniques being applied in the same sample,
or suff er from limitations in the application of cephalo-
metric measurements. Relapse may be dental, skeletal,
or both.
In general, mandibular advancement appears to be
stable if rigid internal fi xation is used6–8 and if anterior
facial height is maintained or increased.9 Several factors
may aff ect relapse in mandibular advancements: the
surgeon’s skills; proximal segment control, including
condylar positioning and prevention of proximal seg-
ment rotation; prevention of counterclockwise rotation
of the distal segment in cases with a high mandibular
plane angle; the degree of mandibular advancement;
and the stretching of the perimandibular tissues, includ-
ing skin, connective tissues, muscles and periosteum.10
Mandibular setback is not always stable, and the inclina-
tion of the ramus at surgery appears to have an impor-
tant infl uence on stability.9
The stability of maxillary osteotomies is aff ected by
the magnitude of the anterior movement and the mag-
nitude of the inferior repositioning of the maxilla, the
adequacy of mobilization of the downfractured maxilla
at surgery, the extent of bone contact in the newly es-
tablished position of the maxilla, and the type of fi xa-
tion.11 On the other hand, Louis et al. (1993)12 did not
fi nd any correlation between relapse and the magnitude
of maxillary advancement. The most stable maxillary
procedure is superior repositioning, and forward move-
ment is also reasonably stable. Inferior repositioning is
the least stable, especially if it causes downward rota-
tion of the mandible and stretching of the elevator mus-
cles of the jaw. Proffi t et al. reported that the least stable
orthognathic procedure is transverse expansion of the
maxilla.9
Table 16.2
Bilateral Sagittal-Split Osteotomy (BSSO) Complications
• Unanticipated fracture or unfavorable split
• Nerve injury
• Bleeding (inferior alveolar artery, masseteric artery)
• Proximal segment malpositioning
• Temporomandibular joint dysfunction
• Condylar resorption
• Avascular necrosis
• Interfragmentary incompatibilities
• Distal segment interference with large setbacks.
Fig. 16.1 Illustration of the potential complications that can
occur with the bilateral sagittal-split osteotomy procedure.
(Illustration by Robert Brown.)

16 Complications in Orthognathic Surgery 153
with miniplates, making sure the condyle is seated. This
can be challenging even in the hands of an experienced
surgeon. Depending on the stability of the segments,
one may choose to monitor the postoperative occlusion
without intermaxillary fi xation (MMF) or elect to place
the patient in MMF for eight weeks. Counterclockwise
rotation of the proximal segment is the most common
indicator that healing is delayed and that migration of
the fragments has occurred. Periodic radiographs (Pan-
orex) will monitor the condylar and ramal position and
bone healing. A second surgery to create osteotomies
and bone graft may be warranted if nonunion or mal-
union is identifi ed.
Nerve Injury
Nerve injuries in orthognathic surgery can be caused
by indirect trauma (e.g., from compression by surgi-
cal edema), direct trauma with surgical instruments,
or stretching during manipulation of the osteotomized
bone segments.14 The most common sensory nerve in-
jury with BSSO occurs to the inferior alveolar nerve
(IAN) as it courses through the mandibular canal. The
risk of injury to the IAN is a signifi cant disadvantage of
the sagittal-split osteotomy. The incidence of transection
is reportedly 2–3.5%.24 A long-term neurological defi cit
reportedly occurs to some degree in 10–30% of patients,
although not all are symptomatic.25 When a sagittal-split
osteotomy is combined with genioplasty, nearly 70% of
patients have some degree of neurosensory defi cit after
one year.26,27 Patients must accept this tradeoff between
benefi ts and risks before undergoing mandibular surgery.
Several factors have been identifi ed that may predispose
a patient to IAN injury, including age, the magnitude of
mandibular movement, position of the inferior alveolar
nerve, concomitant genioplasty, the surgeon’s skills, and
the degree of manipulation of the IAN.14,28,29 Even with
careful manipulation of the IAN, persistent sensation
disturbances are possible.30–32 The most dependable way
to prevent this complication is a controlled osteotomy
under direct vision. The inferior alveolar nerve is partic-
ularly vulnerable at the anterior aspect of the split, but it
may be damaged anywhere from the pterygomandibular
space to the vertical osteotomy site. Errant and aggres-
sive drilling, sawing, or chiseling can damage the nerve
at any point along its course.
When the IAN has been injured or transected during
a procedure, an immediate attempt should be made to
assess and repair the damage. Options include apposi-
tion of the nerve segments or primary neurorrhaphy,
but proximal and distal nerve segments may need to be
released from the bone as far as the mental foramen to
provide a tension-free closure. There is no reported cor-
relation between operator-observed partial injury and
postoperative neurosensory changes.33 Therefore, ex-
tensive dissection must be weighed carefully, and con-
servative management may be the best choice.
Unanticipated Fracture or Unfavorable Splits
Fractures of the osteotomized segments in BSSO (i.e.,
bad splits) have been reported to occur in 3 to 23% of
cases.13–15 Proper corticotomy technique is the fi rst line
of prevention. Many modifi cations (Hunsuck,16,17 Ep-
ker,18 Wolford19) of the initial procedure by Dal Pont20
have lessened the chance of unfavorable splits. Of great
importance is the position of the burr or saw blade dur-
ing the medial ramus cut that must be angled parallel
to the mandibular occlusal plane. Likewise, adequate
but minimal visualization of the lateral ramus allows
for appropriate positioning of the medial cut and avoids
risking a horizontal ramus fracture. Removal of a small
amount of the internal oblique ridge with a large burr
in the area of the proposed medial ramal cut may en-
hance visualization.21 The vertical lateral corticotomy of
the mandibular body should penetrate only the cortex.
The corticotomy that connects the medial and lateral
corticotomies should be as lateral as possible while still
remaining inside the lateral cortex. The inferior border
osteotomy must be cut through both cortices to enhance
a favorable split. The only time one would not want to
cut through both cortices is when an inferior border saw
is used.22
Some surgeons remove mandibular third molars dur-
ing the BSSO,23,24 but most authors routinely recommend
this at least six months before BSSO surgery. This allows
time for bone healing and helps ensure a favorable split.
Often the third molars are not in the center of the buccal
and lingual plates, thus increasing the chance of an un-
favorable split if they are removed at the time of a BSSO.
Steps to prevent an unfavorable split include careful
use of a bibeveled chisel to complete the split after the
medial and lateral osteotomies. Another technique uses
a Smith spreader to enhance separation of the segments.
While inspecting the bone separation, the surgeon ad-
justs the chisel position to help prevent unfavorable frac-
tures or injury to the inferior alveolar nerve. While the
surgeon separates the bone segments, the nerve is care-
fully released from the proximal segment. A proper split
is ensured when the proximal and distal segments have
independent movement. A fi nger on the medial aspect
can ensure the proximal (condylar) segment is not mov-
ing while minimally moving the distal (tooth-bearing)
segment. This technique prevents transmission of heavy
prying forces to the proximal and distal segments.
If an unfavorable split occurs, it is most important
for the surgeon to decide whether to proceed with the
planned procedure or to return the fragments to their
native location and abort the surgery. If the surgery is
not aborted, the key feature of treatment on an unfa-
vorable fracture is rigid plating. The initial manage-
ment is to ensure that the osteotomy is completed and
that separation of the condylar segment from the distal
(tooth-bearing) segment has occurred. The free frac-
tured pieces are fi xed to the repositioned mandible

Complications in Facial Plastic Surgery
154
erative anesthesia with postoperative hypertension. A
more rapid recovery by the patient has been reported
when major bleeding is avoided.42 Prevention of bleed-
ing begins with the patient history. Reports of prior
bleeding experiences or a family history suggestive of
coagulopathy warrant preoperative coagulation studies.
The most likely sources of bleeding include the inferior
alveolar and the masseteric arteries. The inferior alveo-
lar artery courses with the IAN through the mandibular
canal and is contained within the pterygomandibular
space. Bleeding from this vessel should be treated by
pressure, packing, thrombin spray, and possibly even li-
gation or cautery once the IAN has been identifi ed and
retracted. The masseteric artery is not commonly en-
countered during a controlled dissection.
The facial artery and retromandibular vein are placed
at risk if the lateral mandibular periosteum is violated.
Proper dissection for a BSSO should require very little
lateral mandibular ramal dissection. Transcervical ex-
posure may be necessary to control hemorrhage if pack-
ing, direct control with bipolar cautery, or thrombogenic
agents are unsuccessful. A pressure dressing may be
warranted if immediate postoperative swelling and
hemorrhage are seen. If any signs of airway compromise
or of rapid expansion of the oral cavity or neck occur, an
immediate return to the operating room is warranted
for exploration and evacuation of a hematoma.
Temporomandibular Joint (TMJ) Dysfunction
Temporomandibular joint (TMJ) dysfunction must be
carefully assessed and discussed preoperatively. Al-
though some patients have improvement of symptoms
after orthognathic surgery, others may develop symp-
toms. Fibrous ankylosis or joint hypomobility following
orthognathic surgery has been proposed to be caused
by several factors: immobilization of the TMJ by MMF,43
iatrogenic posterior displacement of the condyle, in-
tra-articular hematoma,44 or excessive stripping of the
periosteum and muscle attachments in the ascending
ramus, which can result in myofi brotic tissue forma-
tion.45 Multiple pharmacologic therapies (e.g., doxycy-
line, vitamin C) have been suggested to help stabilize the
joint and may be helpful.
Condylar Resorption
The importance of the preoperative assessment of TMJ
health with a detailed history, centric-mounted models,
and radiographic exams (lateral cephalogram, baseline
tomographs, and Panorex) must be emphasized (Fig.
16.2). The fi nal outcome of the surgery may be altered if
the condyles are not seated during the modeling. Several
risk factors for condylar resorption after orthognathic
surgery have been proposed. Preoperative morphologi-
cal or functional factors include radiological signs of
osteoarthrosis, TMJ dysfunction, a posteriorly inclined
Some patients may complain of postoperative dysthe-
sia in the distribution of the inferior alveolar nerve. This
is diffi cult to diagnose and manage, and often observa-
tion is employed. If symptoms are relieved by injecting
a nerve block, it may indicate that a nerve decompres-
sion could be helpful. Preoperative discussion with the
patient must emphasize that nerve decompression may
not, however, relieve these symptoms.
Lingual nerve sensory defi cits occur less frequently
than IAN sensory disturbances. The initial postoperative
incidence has been reported between 1% and 19%;34,35
however, lingual nerve sensory defi cits tend to resolve
over time. Tissue retraction along the medial mandible
and bony fi xation methods are the proposed mecha-
nisms of injury.
Facial nerve paralysis is a devastating outcome of
BSSO. De Vriese et al. reported a low incidence (0.26%)
of facial nerve injuries in a series of 1747 BSSO cases.36
Steps to prevent this complication include careful sub-
periosteal elevation and chisel orientation. Facial nerve
injury is more common in mandibular set-back proce-
dures done for prognathism.37 Damage to the marginal
mandibular branch of the facial nerve is a well-known
complication of extraoral approaches to the mandibular
ramus or angle, but these approaches in orthognathic
surgery are rare. The presumed traumatic mechanisms
have included compression caused by retractors placed
behind the posterior ramus, fracture of the styloid pro-
cess, and direct pressure as a result of distal segment
setback. The prognosis is better if there is incomplete
loss of function, and worse if the loss of function is im-
mediate and complete.38
If facial nerve injury is suspected, the surgeon should
provide ample time for the eff ects of local anesthesia to
dissipate. If facial paralysis evolves gradually over a pe-
riod of days, it may be assumed that a complete return
of function will occur over time. If, however, complete
paralysis is encountered early, standard facial nerve
studies are warranted (e.g., nerve excitability testing
or electroneuronography. Evoked electromyography
(EMG) is an additional test that can help predict return
of function.39 Nerve exploration with reanastomosis and
possible sural nerve grafting may be considered. Protec-
tion of the eye with lubrication, moisture chambers, or
eyelid taping should be emphasized to prevent corneal
exposure and keratopathy.
Bleeding
Uncontrolled hemorrhage may result from either a me-
chanical disruption of the blood vessels or a congenital
or acquired coagulopathy.40 The most common cause of
hemorrhage in orthognathic surgery is a lack of surgical
hemostasis.41 Factors contributing to immediate or sec-
ondary hemorrhage may include variations in anatomy
(bone or vascular), aggressive dissection, tearing of the
periosteum during dissection, and hypotensive intraop-

16 Complications in Orthognathic Surgery 155
inferior border wire or a combined superior border wire
and MMF.60
Postoperatively, a physical exam and determination
of the patient’s comfort with occlusion are paramount
to diagnosing malpositioning. Even when there is an
anomaly on a Panorex radiograph, if the patient has no
occlusal complaints, observation may be warranted. A
more serious problem occurs when shifting of the prox-
imal segment becomes evident. There may be shifting of
the mandibular midline or an open bite deformity pres-
ent that indicates malposition of one or both condyles.
This may occur at any time following surgery; however,
if it is noted in the fi rst three weeks, it may be reason-
able to place the patient in MMF again to allow for addi-
tional wound healing and fracture line security. Delayed
malalignment often necessitates surgical intervention
with osteotomies and bone grafting.
Intraoral Vertical Ramus Osteotomy
Intraoral vertical ramus osteotomy (IVRO) may be
used for mandibular setbacks. The operation can be
performed more quickly and with less morbidity than
BSSO, but it off ers less control of the proximal segment
and often results in condylar sag, with resultant open
bite deformity. IVRO is indicated in cases that require
vertical changes between the proximal and distal seg-
ments and involve a mandibular setback on at least one
side. Hemifacial hyperplasia is one example. The most
common complications of IVRO are listed in Table 16.3.
Condylar Sag
Condylar sag is the lack of proper seating of the condylar
head in the glenoid fossa. One method that some sur-
geons use to avoid condylar sag is to overcompensate in
the presurgical workup by providing a posterior open
condyle, a high mandibular plane angle, and a low
posterior-to-anterior facial height ratio.46–51 Contribut-
ing surgical factors include major mandibular advance-
ment, counterclockwise rotation of the mandibular
proximal fragment, rigid internal fi xation with incor-
rect placement of condylar head, or avascular necrosis
of the condyle.46,48,49,51,53–55 Young females (15–30 years)
have a higher risk for condylar resorption than males
and older females.47,48,50,51,56 The incidence of postopera-
tive condylar resorption has been reported to vary from
1% to 31%. This wide range probably refl ects the great
variation in the study populations.46,49,57,59 Rigid fi xation
is the most successful way to avoid osteotomy slippage
and condylar resorption. Postoperative recommenda-
tions are varied and are not standardized. It may be
unwise to reoperate on a patient with condylar resorp-
tion, as further revision osteotomies may compound the
problem. Mandibular splinting may provide relief from
myofascial pain if it is present. If the patients fi t a high-
risk profi le as outlined above, often preoperative splint-
ing by the their orthodontist may help prevent further
condylar resorption.
Proximal Segment Malposition
Prevention of an undesirable proximal mandibular seg-
ment rotation or position begins with careful preopera-
tive planning. Intraoperatively, the inferior border of the
proximal and distal mandibular segments should be
used as a landmark for correct vertical positioning. In-
troduction of a rotational component makes alignment
more diffi cult. The inferior border of the distal or proxi-
mal segment may lie in a diff erent plane if the mandibu-
lar segments are rotated clockwise or counterclockwise.
Rigid fi xation will help to prevent motion and migration
of the planned advancement or setback.59 Fixation of the
proximal segment may also be achieved with either an
Fig. 16.2 (A) Radiograph of the left mandibular condyle depicting severe condylar resorption prior to orthognathic surgery.
(B) Radiograph of same patient showing the resorption of the right condyle.
A
B

Complications in Facial Plastic Surgery
156
Open Bite
Open bite deformity (Fig. 16.3) is relatively common
with IVRO compared with BSSO.66,67 The surgeon has the
least control over the proximal segments with the IVRO
technique. The condyle may be seated properly at sur-
gery but sag inferiorly away from the glenoid fossa dur-
ing healing. This results in a gap above the condyle and
inferior to the glenoid fossa. Once MMF is released, the
masticator muscles reseat the condyle, and an open bite
can occur. Although condylar resorption is a proposed
theory, the circumferential condylar blood supply (in
contrast to the femoral head blood supply) may make
this unlikely.68 Condylar resorption also tends to occur
months or even years postoperatively, making it less
likely that such a mechanism may induce an immediate
open bite deformity.
Body and Symphysis Osteotomy
Osteotomies performed in the body and symphysis usu-
ally pass between teeth and place the inferior alveolar
nerve at risk when posterior to the mental foramen. If
they are anterior to the foramen, then the surgeon needs
to be cognizant of the added rotational forces placed
upon the mandible by the muscles of mastication. Com-
plications for these procedures are listed in Table 16.4.
Malpositioning
Malpositioning is the most common complication as-
sociated with osteotomies of the tooth-bearing section
of the mandible.69 Careful model surgery may enhance
the outcome in the preoperative setting. Intraopera-
tively, rigid fi xation and good splint alignment are rec-
ommended. Most importantly, after fi xation of the
segments, the planned occlusion should be verifi ed as
bite in the planned postoperative occlusion. During
MMF, the posterior space can be built up slightly with
an occlusal wafer. If it is removed before complete heal-
ing, closure of the open bite may rotate the osteotomy
site. On the other hand, if the splint is removed follow-
ing complete healing, the condyles are seated using light
guiding elastics instead of heavy elastics that may place
excessive stress on the condylar head.
Bleeding
The most likely source of excessive bleeding during IVRO
is the masseteric artery as it passes through the sigmoid
notch of the ramus.61 During retraction, it is easy to place
this vessel on stretch, making it diffi cult to identify. Ev-
ery attempt should be made to ligate the vessel directly.
As with BSSO, in IVRO the surgeon must carefully avoid
the facial artery and retromandibular vein.
Nerve Injury
Sensory nerve injury in IVRO is less likely than in BSSO62;
however, careful placement of the vertical osteotomy is
essential to avoid inadvertent injury to the inferior al-
veolar nerve as it enters at the mandibular lingula. The
osteotomy is completed behind the mandibular fora-
men from the sigmoid notch to the posterior border of
the mandible. The IAN may be injured if the proximal
segment slips medial to the distal segment. The vast
majority of postoperative dysthesias will resolve over
12–18 months’ time. Although it has been reported, fa-
cial nerve injury is exceedingly rare in this procedure.63,64
Inappropriate Osteotomy
Subcondylar osteotomy has been reported as a compli-
cation of the IVRO procedure.15,65 A poorly placed pos-
terior osteotomy may cause severe proximal segment
rotation. Proper exposure and direct visualization of
the planned cuts should prevent this complication. One
pearl is to identify the antilingula on the buccal (lateral)
surface of the mandible for orientation of the lingula.
Table 16.3
Intraoral Vertical Ramus Osteotomy (IVRO) Complications
• Condylar sag
• Bleeding
• Nerve Injury
• Inappropriate osteotomy
• Anterior open bite
Fig. 16.3 Photograph of patient’s occlusion with orthodontic
devices in place illustrating an open-bite deformity.

16 Complications in Orthognathic Surgery 157
ed in Table 16.5. Careful dissection of the mental nerve,
reinsertion of the mentalis muscle fi bers (with two-lay-
er closure), stepped soft-tissue incision (soft-tissue inci-
sion at one level and muscle dissection at a lower level
in the chin), and careful subperiosteal dissection plane
will limit these complications.
Nerve Injury
Neuropraxia often occurs after genioplasty. This compli-
cation may be avoided with meticulous technique and
careful surgical planning of the osteotomy sites. Dissec-
outlined on the preoperative workup. If the postopera-
tive occlusion is incorrect, then an early return to the
operating room or consultation with the patient’s or-
thodontist may be helpful.
Periodontal Defects and Devitalized Teeth
Careful surgical technique and planning of soft-tissue
and bony work are essential. The dental papilla should
be well preserved intraoperatively. Avoidance of apical
tooth roots by staying at least 5 mm above or below the
apices of the teeth (depending on the jaw being oper-
ated on) limits pulp injury. Osteotomies between teeth
require at least 3 mm of space, which can be enhanced
with preoperative orthodontic care and planning.70
Endodontic treatment may be necessary. Periodon-
tal and tooth damage may be encountered, especially
in segmental osteotomies. Most problems are caused
by errors in surgical technique, which reinforces the
need for preoperative planning. The design of the soft-
tissue incisions is critical, as vertical incisions in the
area of osteotomy will predictably create periodontal
problems. Trauma to the lingual mucoperiosteum is a
risk. Excessive heat generated by the saw or drill must
be countered by copious irrigation and careful protec-
tion of the soft tissues from injury. Poor oral hygiene
plays some role in periodontal problems. It should be
reemphasized that these problems may be minimized if
an interdental space is created preoperatively by orth-
odontic means.71
Genioplasty
Genioplasty is a challenging and versatile technique that
is useful in isolated cases of horizontal or vertical man-
dibular discrepancies, as well as in combination with
other orthognathic procedures (Fig. 16.4). The compli-
cations most often associated with genioplasty are list-
Table 16.4
Body and Symphysis Osteotomy Complications
• Malpositioning of segments
• Nonunion of segments
• Periodontal defects possibly causing loss of teeth adjacent
to the osteotomy
• Devitalization of teeth, possibly necessitating endodontic
treatment
• Nerve injury
• Loss of entire bony segment due to devitalization and poor
blood supply
Fig. 16.4 Illustration of the potential complications that can
occur with the sliding osseous genioplasty procedure. (Illustra-
tion by Robert Brown.)
Table 16.5
Genioplasty Complications
• Nerve injury (mental nerve)104
• Inferior mandibular border contour irregularity and
unaesthetic contours105
• Chin ptosis and deepening of the labiomental sulcus106
• Gingival recession
• Mandibular sulcus scarring

Complications in Facial Plastic Surgery
158
a critical assessment of the occlusion should then be
made. If the occlusion is not ideal at this stage, adjust-
ments to the osteotomy should be made.
Bleeding
Maxillary osteotomies, especially LeFort I and II osteoto-
mies, have the potential for the most serious bleeding
sequelae in orthognathic surgery. These complications
may present as immediate intraoperative bleeding or
as postoperative swelling or epistaxis. For two-jaw sur-
geries, the authors recommend preoperative type and
screen for at least 2 units of packed red blood cells. Intra-
operative hypotensive anesthesia is also suggested. The
most common sources of hemorrhage are the terminal
branches of the internal maxillary artery, especially the
descending palatine or sphenopalatine artery. Bleeding
from these may be caused by an improper or overly ag-
gressive use of osteotomies, drilling, an oscillating saw,
or downfracture of the maxilla. The downfracture may
even damage the internal carotid artery if a basal skull
fracture ensues that involves areas such as the foramen
lacerum and the carotid canal. Even arteriovenous fi stu-
las are possible.75,76 The anterior and posterior superior
alveolar and nasopalatine arteries are often intention-
tion of the mental nerves will allow for ease of access
and retraction and may help prevent errant injury dur-
ing bony osteotomy. Careful dissection of the mental
nerve, reinsertion of the mentalis muscle fi bers with
a two-layer closure, stepped soft-tissue incision (soft-
tissue incision superiorly and muscle dissection more
inferiorly), and meticulous subperiosteal dissection will
limit these complications.
Chin Ptosis and Aesthetic Concerns
Ptosis of chin soft tissues may be prevented by minimiz-
ing subperiosteal stripping off the mandible and reap-
proximating the mentalis muscles. To prevent descent,
the mentalis may be resuspended to the anterior su-
perior edge of the distal chin, and a pressure dressing
may be applied. Botulinum toxin may be used to treat
temporary asymmetric mentalis deformities and hyper-
activity.72 Long-term dysfunction of the mentalis should
be addressed with resuspension procedures, which have
been reported to include drilling holes in the proximal
mandible for use in securing the mentalis.73
The most common aesthetic concern following genio-
plasty is characterized by indentations on each side of
the genioplasty at the posterior extent of the inferior
border cut (keyhole-shaped mandible). Extending the
inferior osteotomy posteriorly may prevent this compli-
cation; however, this maneuver may place the mental
nerve at greater risk. These irregularities may also be
improved with a secondary contouring procedure.

◆Complications of Maxillary Procedures
LeFort I Osteotomy
The LeFort I osteotomy (Fig. 16.5) has an impressive
list of complications, all of which underscore the tech-
nical challenges encountered with maxillary surgery
(Table 16.6).
Malpositioning
Proper preoperative planning is the only way to ensure
accurate positioning of the maxilla. To achieve an ideal
outcome, the surgeon must obtain mounted models
with accurate centric relation and an accurate midline
assessment. Concomitant mandibular surgery may be
considered. Intraoperative swelling, bleeding, and the
nasotracheal tube location all confuse the picture. The
most common cause of malpositioning after a LeFort I
osteotomy is an inability to seat the mandibular con-
dyles properly. The surgeon must be certain that the
condyles are seated fi rst; then the maxillomandibular
complex may be rotated superiorly into position un-
til the fi rst contact is felt (Dawson’s technique).74 After
fi xation of the maxilla, the jaws should be unwired, and
Fig. 16.5 LeFort 1 osteotomy. (Illustration by Robert Brown.)

16 Complications in Orthognathic Surgery 159
rior nasal packing, then an arteriogram with possible
embolization may be indicated before a return trip to
the operating room. Certainly, removal of MMF and a
tracheostomy may be necessary if bleeding is aff ecting
the patient’s airway.
Vascular Insuffi ciency
Patients with previous palatal surgery (cleft palate) or
previous LeFort I osteotomy and maxillary downfrac-
ture should be evaluated preoperatively for compromise
in their blood supply. Signifi cant palatal scarring is an
indication to preserve one labial artery pedicle. In the
case of a previous LeFort osteotomy, evaluation of the
gingiva may reveal edematous gingiva, which indicates
poor venous return. This knowledge will guide the sur-
geon intraoperatively.
Intraoperative laser Doppler studies can confi rm that
anterior maxillary perfusion decreases gradually dur-
ing downfracture and mobilization. It is recommended
that the surgeon maintain constant vigilance during
the operation to assess anterior perfusion. Intermittent
relaxation will allow the maxilla to reperfuse. Segmen-
tal osteotomies will also compromise blood supply.78 If
severe perfusion defi ciencies are noted during the op-
eration, the surgeon may need to fi x the maxilla rigidly
into its original position and abort the procedure. Se-
vere, prolonged disturbances in blood circulation may
lead to avascular tissue necrosis, which may cause tooth
devitalization, periodontal defects, or even loss of ma-
jor bone segments. Because of the dense network of
anastomoses in the face, this is a rare event, but it may
manifest both in the maxilla and in the mandible, es-
pecially in association with segmental osteotomies. The
anterior part of the maxilla is a zone of special risk.77–80
Preservation of the descending palatine artery was not
found to be critical for maintaining blood fl ow to the
downfractured maxilla in animal studies,80–82 but it has
been recommended that the artery should be preserved
whenever possible and segmentalization of the maxilla
should be minimized. A wide, intact soft-tissue pedicle
is important for the circulation of the downfractured
maxilla. In the mandible, avascular necrosis can usu-
ally be avoided by minimal stripping of the periosteum
and muscle attachments.83 If frank necrosis occurs, then
the wound should be managed conservatively with lo-
cal wound care. Aggressive debridement is not indicated
and may worsen the situation.
Periodontal Defects
Preoperative assessment of planned maxillary move-
ment should alert the surgeon to future forces on the
gingiva. Maintaining a healthy cuff of gingiva attached
to the teeth during the horizontal vestibular incision
will prevent necrosis. Tooth root disruption is avoided
with a carefully planned osteotomy. Following maxil-
ally severed during maxillary surgery. Thrombogenic
substances (e.g., microfi brillar collagen, topical throm-
bin) are often used to assist in hemostasis. Direct liga-
tion of the descending palatine artery is recommended
and is easily accomplished if dissection in a subperios-
teal plane is performed.77
If bleeding occurs posterior to the pterygomaxillary
osteotomy, packing is the best solution. Absorbable
packing may be necessary. Hemorrhage from the inter-
nal maxillary artery may require direct ligation or even
an external approach to the external carotid artery.77
Postoperatively, epistaxis should be treated with nasal
packing, head elevation, and control of hypertension. If
bleeding remains uncontrolled after anterior or poste-
Table 16.6
LeFort I Osteotomy Complications
• Malpositioning107
• Bleeding108
• Infraorbital nerve traction injury
• Vascular compromise109
• Periodontal defects110
• Devitalized teeth110
• Nerve injury78
• Ophthalmic artery injury111
• Nasolacrimal injury112
• Oronasal and oroantral fi stulas89
• Nasal septal deviations
• Maxillary sinusitis
• Poor aesthetic soft-tissue changes
• Injury to the parotid duct
• Unfavorable fractures (pterygoid plate, sphenoid bone,
middle cranial fossa)
• Nonunion
• Eustachian tube dysfunction
• Velopharyngeal incompetence
• Arteriovenous fi stulas (carotid cavernous sinus)
• Dysphagia
• Transverse relapse

Complications in Facial Plastic Surgery
160
spontaneously. Persistent epiphora seems to be more
common with high LeFort osteotomies.87 Disruption of
the nasolacrimal duct88 and nasal septal deviations78 are
the primary causes. Treatment of these complications is
cause-specifi c.
Oronasal and Oroantral Fistulas
Large (greater than 8 mm) maxillary advancements in-
crease the risk of relapse and soft-tissue breakdown. Oro-
nasal fi stulas are slightly more common than oroantral.
Perhaps the cause of this is the greater tension placed on
the palatal mucosa as the maxilla is widened.89 The key
to prevention of these fi stulas is protection of the nasal
mucosa. Excessive tension at closure or mucosal tears in-
crease the risk of fi stula. Postoperatively, patients should
be careful to avoid nose blowing to prevent subcutane-
ous emphysema. Proper oral hygiene and use of a loose
obturator are often recommended as initial treatment of
a fi stula. Decongestants, nasal sprays, and antibiotics may
all assist with patient comfort and maxillary sinus health.
Fistulas that persist after six months may be treated with
surgical procedures, including a buccal fat pad, a tongue
fl ap, or a facial artery musculomucosal fl ap.90
Nasal Septal Deviation
Preoperative evaluation of the symmetry, function, and
appearance of the nose will help guide the postopera-
tive management of it. Deviation of the nasal septum
secondary to maxillary osteotomy has been associ-
ated with increased airway resistance and aesthetic
complaints.89 The anterior edge of the nasal spine rises
superiorly as it progresses toward the nasopalatine fo-
ramen. It then arcs and falls posteriorly. If the maxilla
is repositioned anteriorly, this arc will create buckling
in the caudal nasal septum that may be addressed with
a slight trim of the septum inferiorly. During advance-
ment, both the inferior surface caudal septum and the
superior surface of the ANS should be contoured to pre-
vent deviation.91 A 2–0 permanent suture may be used
to reaffi x the caudal septum in the midline by drilling
a small hole in the nasal spine or appropriate midline.
Postoperative deviation may need to be corrected dur-
ing a separate operation. If deviation is noted in the
immediate postoperative period, gentle manipulation
or nasal packing may guide healing, but this is noto-
riously unreliable compared with good intraoperative
technique.
Unacceptable Soft-Tissue Changes
A preoperative discussion of the changes of the nasal ap-
pearance with maxillary advancement is imperative to
prepare the patient for possible secondary procedures. At
least three to six months of healing following orthogna-
thic surgery are advocated before septorhinoplasty with
lary advancement, grafting with bone or an alloplast is
often helpful. Postoperative periodontal disease may be
prevented with standard hygiene and good nutrition;
however referral to a periodontist is an option.
Nerve Injury
Nerve injuries in maxillary downfracture can be di-
vided into sensory, motor, secretory motor, and special
sensory (optic nerve) injuries. Mastery of local anato-
my is essential. During the procedure, sensory changes
that are secondary to retraction injury are expected.
The infraorbital, anterior, middle, and posterior su-
perior alveolar, nasopalatine, and descending pala-
tine nerves are all at risk. Despite a direct cut to the
nerve, neurosensory innervation returns to the palate,
gingiva, and teeth in nearly all cases. Approximately
25% of cases will have persistent hypesthesia.84 Care-
ful monitoring of fracture planes will typically prevent
motor nerve injury. However, the optic nerve, nasocili-
ary nerve, and cranial nerves III and VI may be at risk
due to postoperative hematoma or seroma collection.
Injury to these nerves is rarely recognized at the time
of surgery.
Postoperatively, reassurance is recommended if neu-
rosensory defi cits present themselves. Cases of abducens
nerve (VI) palsy have been reported, and all spontane-
ously resolved.85 Oculomotor nerve (CN III) injury has
also occurred and resolved in the postoperative period.86
Blindness has also been reported.78 In one case, multiple
sphenoid and middle cranial fossa fractures were seen
on postoperative CT scans. Retrobulbar hematoma was
blamed for the other two cases.78 Blindness persisted in
one patient with a hematoma and in the patient with
multiple sphenoid fractures. Finally, xerophthalmia has
been seen secondary to injury of the secretory fi bers
of the abducens nerve.78 Supportive therapy is recom-
mended in this situation.
Ophthalmic and Nasolacrimal Injuries
Ophthalmic complications are rare sequelae of maxil-
lary osteotomies. They include decreased visual acuity,
extraocular muscle dysfunction, neuroparalytic kerati-
tis, and nasolacrimal problems.78 These injuries appear
to be caused by indirect trauma to the neurovascular
structures during the pterygomaxillary fractures that
extend to the base of the skull. Use of topical sympatho-
mimetics and injectible vasoconstrictive agents can re-
sult in pupil dilation and confuse the postoperative eye
examination. Visual acuity testing should be performed,
and ophthalmologic consultation to assess globe pres-
sures must be obtained without hesitation. In the ex-
treme case of frank proptosis, lateral canthotomy and
high-dose steroids must be instituted.
Most patients undergoing maxillary downfracture
experience some measure of epiphora that resolves

16 Complications in Orthognathic Surgery 161
(including cavernous sinus fi stulas),101 dysphagia,102 and
condylar resorption.103 These complications may be re-
lated to surgical technique or to other unknown factors.
Anterior Maxillary Segmental Osteotomy
Complications of anterior maxillary segmental osteot-
omy include vascular complications and hemorrhage in
the maxilla.
Bleeding
Severe hemorrhage has been previously documented
with both maxillary and mandibular surgery. Massive
hemorrhage is rare, but it is possible during the oste-
otomy of the posterior maxilla or if the cut is incomplete
and one attempts to force the maxilla to downfracture
and produces a fracture at the base of the skull. Bleeding
may also occur from careless use of chisels or saws in
the posterior maxilla. This can result in direct or indirect
vascular injury to the major vessels in the neck or skull
base, including the internal carotid artery and internal
jugular vein. Eff orts should be made to direct osteoto-
mies properly in the pterygoid plates and to downfrac-
ture the maxilla without excessive force. This principle
becomes paramount in revision procedures involving a
maxillary osteotomy, as previous procedures could have
easily created unusual fusion lines. Other vessels at risk
include the internal maxillary artery, the posterior su-
perior alveolar artery, and the greater palatine artery.
Stretch injury of the internal carotid artery is also pos-
sible secondary to positioning. During neck extension,
the carotid is compressed upon the vertebral column.
Adding a rotational component to the neck for exposure
places the vessel at risk for postoperative thrombosis.
Mortality associated with thrombosis of the internal
carotid has been estimated at 40%, with an additional
52% of the patients being left with a serious neurologi-
cal defi cit.
Following a LeFort I osteotomy, delayed bleeding may
occur immediately after surgery or as late as nine days
postoperatively. The vessels most frequently involved
are the greater palatine artery, the internal maxillary,
and the pterygoid plexus of veins.

◆Conclusion
Orthognathic surgery requires astute preoperative as-
sessment, careful preoperative planning and surgical
modeling, and accurate surgical management to pre-
vent common complications. When choosing the proce-
dures with the patient, the orthognathic surgeon must
weigh the risks with the ultimate goals by considering
the patient’s global health, tobacco use, and previous
surgical procedures. Intraoperative vigilance is impera-
tive to prevent alar necrosis from nasotracheal or na-
alar base reductions. Excessive maxillary movements
will aff ect lip position, amount of incisor tooth showing
at rest, fullness of the upper lip, and alar base support.
Unfavorable Fractures
Unusual fractures have been noted, including complete
vomer avulsion,92 pterygoid plate fracture,93 sphenoid
bone fracture,94 and middle cranial fossa fracture.95
Good surgical exposure and completion of all planned
osteotomy cuts are paramount to prevent non-ideal
fracture planes.
Nonunion (Delayed Union)
Nonunion and delayed union were far more common
before rigid fi xation.96 Mobility or poor bony contact can
incite a fi brous union or delayed union. Likewise, if max-
illary mobility persists, vertical bone resorption may oc-
cur, causing foreshortening of the maxillary height with
unplanned and untoward aesthetic results.
Transverse Relapse
Transverse relapse is a phenomenon associated with
multiple-piece maxillary osteotomy.97 When transverse
relapse occurs, we get a constriction of segments toward
the midline with occlusal prematurities that result in an
open bite clinically. If a multiple-piece LeFort osteotomy
is done, the segments need to be adequately mobilized
or grafted to keep them apart. Surgically assisted rapid
palatal expansion has been shown to be eff ective as a
separate procedure before a LeFort I osteotomy.98
Associated Functional Complications
Eustachian tube dysfunction is possible after any pala-
tal procedure, because the levator veli palatini and the
tensor veli palatini have been repositioned. Therefore,
many patients complain of fullness in the ears, de-
creased hearing, and pain. Postoperative decongestants,
nasal sprays, and reassurance are essential. Routine mi-
croscopic evaluation is mandatory to rule out serous
otitis media and the need for tympanostomy tube man-
agement of the middle ear space.
Velopharyngeal dysfunction has been shown to oc-
cur to a minor degree after every maxillary osteotomy.99
However, it is much more common following advance-
ment in patients with a cleft palate.100 Preoperative eval-
uation by a speech pathologist is essential to document
the degree of insuffi ciency, and the surgeon must have
a thorough discussion with the patient and the family
about its possible worsening following advancement.
Also, further consultation is required to discuss adjunc-
tive procedures that can be performed postoperatively
to correct the issue. Other complications present in the
literature are rare instances of arteriovenous fi stulas

Complications in Facial Plastic Surgery
162
9. Lee DY, Bailey LJ, Proffi t WR. Soft tissue changes after supe-
rior repositioning of the maxilla with Le Fort I osteotomy:
5-year follow-up. Int J Adult Orthodon Orthognath Surg
1996;11(4):301–311
10. Smith GC, Moloney FB, West RA. Mandibular advancement
surgery. A study of the lower border wiring technique for
osteosynthesis. Oral Surg Oral Med Oral Pathol 1985;60(5):
467–475
11. Baker DL, Stoelinga PJ, Blijdorp PA, Brouns JJ. Long-term sta-
bility after inferior maxillary repositioning by miniplate fi xa-
tion. Int J Oral Maxillofac Surg 1992;21(6):320–326
12. Louis PJ, Waite PD, Austin RB. Long-term skeletal stability af-
ter rigid fi xation of Le Fort I osteotomies with advancements.
Int J Oral Maxillofac Surg 1993;22(2):82–86
13. van Merkesteyn JP, Groot RH, van Leeuwaarden R, Kroon FH.
Intra-operative complications in sagittal and vertical ramus os-
teotomies. Int J Oral Maxillofac Surg 1987;16(6):665–670
14. Ylikontiola L, Moberg K, Huumonen S, Soikkonen K, Oikar-
inen K. Comparison of three radiographic methods used to
locate the mandibular canal in the buccolingual direction be-
fore bilateral sagittal split osteotomy. Oral Surg Oral Med Oral
Pathol Oral Radiol Endod 2002;93(6):736–742
15. O’Ryan F. Complications of orthognathic surgery. Oral Maxil-
lofac Surg Clin North Am 1990;2:593
16. Hunsuck EE. A modifi ed intraoral sagittal splitting tech-
nic for correction of mandibular prognathism. J Oral Surg
1968;26(4):250–253
17. Hunsuck EE. A method of intraoral open reduction of frac-
tured mandibles. J Oral Surg 1967;25(6):533–541
18. Epker BN. Modifi cations in the sagittal osteotomy of the man-
dible. J Oral Surg 1977;35(2):157–159
19. Wolford LM, Bennett MA, Raff erty CG. Modifi cation of the
mandibular ramus sagittal split osteotomy. Oral Surg Oral
Med Oral Pathol 1987;64(2):146–155
20. Dal Pont G. Retromolar osteotomy for the correction of progna-
thism. J Oral Surg Anesth Hosp Dent Serv 1961;19:42–47
21. Bays RA. Arthrotomy and Orthognathic Surgery for TMD. In:
Kraus SL, ed. Temporomandibular Disorders, 2 ed. New York:
Churchhill Livingstone; 1994:237
22. Wolford LM, Davis WM Jr. The mandibular inferior border
split: a modifi cation in the sagittal split osteotomy. J Oral
Maxillofac Surg 1990;48(1):92–94
23. Epker BN, Wolford LM. Modifi ed Sagittal Ramus Osteotomy.
In: Epker BN, Wolford LM, eds. Dentofacial Deformities: Sur-
gical Orthodontic Correction. St. Louis: CV Mosby; 1980:66
24. Turvey TA. Intraoperative complications of sagittal osteotomy
of the mandibular ramus: incidence and management. J Oral
Maxillofac Surg 1985;43(7):504–509
25. Panula K, Finne K, Oikarinen K. Incidence of complications
and problems related to orthognathic surgery: a review of
655 patients. J Oral Maxillofac Surg 2001;59(10):1128–1136,
discussion 1137
26. Lindquist CC, Obeid G. Complications of genioplasty done
alone or in combination with sagittal split-ramus osteotomy.
Oral Surg Oral Med Oral Pathol 1988;66(1):13–16
27. Walter JM Jr, Gregg JM. Analysis of postsurgical neurologic
alteration in the trigeminal nerve. J Oral Surg 1979;37(6):
410–414
28. Westermark A, Bystedt H, von Konow L. Inferior alveolar
nerve function after sagittal split osteotomy of the mandible:
correlation with degree of intraoperative nerve encounter
sogastric tubes, external scars, cautery burns, nerve or
vascular injury, or excessive vascular compromise of the
bony segments. When complications arise, the surgeon
must address the concerns of the patient as well as act
promptly to prevent negative long-term sequelae.
PEARLS OF WISDOM
Meticulous preoperative planning and model surgery will help
to limit bony segment malposition.
Prevention of an unfavorable split depends on proper cortical
bone cuts that extend through the inferior mandibular border.
The most common sensory nerve injury in the bilateral
sagittal-split osteotomy is to the inferior alveolar nerve.
In the vertical ramus osteotomy, an improperly seated condyle
in the glenoid fossa (condylar sag) can result in a postoperative
open bite deformity.
A common cause of poor maxillary positioning in LeFort I
osteotomy is inadequate seating of the condyles.
Severe proximal segment rotation in the vertical ramus oste-
otomy can be prevented by direct visualization of the planned
cuts and by identifi cation of the antilingula on the buccal
(lateral) surface of the mandible for orientation of the lingula.
References
1. Spaey YJ, Bettens RM, Mommaerts MY, et al. A prospective
study on infectious complications in orthognathic surgery. J
Craniomaxillofac Surg 2005;33(1):24–29
2. Martis C, Karabouta I. Infection after orthognathic surgery,
with and without preventive antibiotics. Int J Oral Surg
1984;13(6):490–494
3. Perko M. Maxillary sinus and surgical movement of maxilla.
Int J Oral Surg 1972;1(4):177–184
4. Zijderveld SA, Smeele LE, Kostense PJ, Tuinzing DB. Preopera-
tive antibiotic prophylaxis in orthognathic surgery: a ran-
domized, double-blind, and placebo-controlled clinical study.
J Oral Maxillofac Surg 1999;57(12):1403–1406, discussion
1406–1407
5. Peterson LJ. Antibiotic prophylaxis against wound infec-
tions in oral and maxillofacial surgery. J Oral Maxillofac Surg
1990;48(6):617–620
6. Van Sickels JE, Richardson DA. Stability of orthognathic sur-
gery: a review of rigid fi xation. Br J Oral Maxillofac Surg
1996;34(4):279–285
7. Dolce C, Hatch JP, Van Sickels JE, Rugh JD. Rigid versus wire
fi xation for mandibular advancement: skeletal and den-
tal changes after 5 years. Am J Orthod Dentofacial Orthop
2002;121(6):610–619
8. Keeling SD, Dolce C, Van Sickels JE, Bays RA, Clark GM, Rugh
JD. A comparative study of skeletal and dental stability be-
tween rigid and wire fi xation for mandibular advancement.
Am J Orthod Dentofacial Orthop 2000;117(6):638–649

16 Complications in Orthognathic Surgery 163
comitantly with superior repositioning of the maxilla. J Oral
Maxillofac Surg 1984;42(4):238–242
46. Kerstens HC, Tuinzing DB, Golding RP, van der Kwast WA. Con-
dylar atrophy and osteoarthrosis after bimaxillary surgery.
Oral Surg Oral Med Oral Pathol 1990;69(3):274–280
47. Moore KE, Gooris PJ, Stoelinga PJ. The contributing role of
condylar resorption to skeletal relapse following mandibular
advancement surgery: report of fi ve cases. J Oral Maxillofac
Surg 1991;49(5):448–460
48. Merkx MA, Van Damme PA. Condylar resorption after orthog-
nathic surgery. Evaluation of treatment in 8 patients. J Cranio-
maxillofac Surg 1994;22(1):53–58
49. Bouwman JP, Kerstens HC, Tuinzing DB. Condylar resorption
in orthognathic surgery. The role of intermaxillary fi xation.
Oral Surg Oral Med Oral Pathol 1994;78(2):138–141
50. Arnett GW, Milam SB, Gottesman L. Progressive mandibular
retrusion—idiopathic condylar resorption. Part I. Am J Orthod
Dentofacial Orthop 1996;110(1):8–15 Review
51. Hoppenreijs TJ, Freihofer HP, Stoelinga PJ, Tuinzing DB, van’t
Hof MA. Condylar remodelling and resorption after Le Fort I
and bimaxillary osteotomies in patients with anterior open
bite. A clinical and radiological study. Int J Oral Maxillofac
Surg 1998;27(2):81–91
52. Hwang SJ, Haers PE, Zimmermann A, Oechslin C, Seifert B,
Sailer HF. Surgical risk factors for condylar resorption after
orthognathic surgery. Oral Surg Oral Med Oral Pathol Oral Ra-
diol Endod 2000;89(5):542–552
53. Schellhas KP, Wilkes CH, Fritts HM, Omlie MR, Lagrotteria LB.
MR of osteochondritis dissecans and avascular necrosis of
the mandibular condyle. AJR Am J Roentgenol 1989;152(3):
551–560
54. Moore KE, Gooris PJ, Stoelinga PJ. The contributing role of
condylar resorption to skeletal relapse following mandibular
advancement surgery: report of fi ve cases. J Oral Maxillofac
Surg 1991;49(5):448–460
55. Cutbirth M, Van Sickels JE, Thrash WJ. Condylar resorption af-
ter bicortical screw fi xation of mandibular advancement. J Oral
Maxillofac Surg 1998;56(2):178–182, discussion 183
56. Kerstens HC, Tuinzing DB, Golding RP, van der Kwast WA. Con-
dylar atrophy and osteoarthrosis after bimaxillary surgery.
Oral Surg Oral Med Oral Pathol 1990;69(3):274–280
57. Moore KE, Gooris PJ, Stoelinga PJ. The contributing role of
condylar resorption to skeletal relapse following mandibular
advancement surgery: report of fi ve cases. J Oral Maxillofac
Surg 1991;49(5):448–460
58. De Clercq CA, Neyt LF, Mommaerts MY, Abeloos JV, De Mot
BM. Condylar resorption in orthognathic surgery: a ret-
rospective study. Int J Adult Orthodon Orthognath Surg
1994;9(3):233–240
59. Bays RA, Fisher KL. Evaluation of condylar position and rigid
fi xation of sagittal split osteotomies. American Association of
Oral and Maxillofacial Surgeons, Anaheim, CA 1987. Abstract.
60. Singer RS, Bays RA. A comparison between superior and in-
ferior border wiring techniques in sagittal split ramus oste-
otomy. J Oral Maxillofac Surg 1985;43(6):444–449
61. Tuinzing DB, Greebe RB. Complications related to the intra-
oral vertical ramus osteotomy. Int J Oral Surg 1985;14(4):
319–324
62. Zaytoun HS Jr, Phillips C, Terry BC. Long-term neurosensory
defi cits following transoral vertical ramus and sagittal split
osteotomies for mandibular prognathism. J Oral Maxillofac
Surg 1986;44(3):193–196
and other variables in 496 operations. Br J Oral Maxillofac
Surg 1998;36(6):429–433
29. Van Sickels JE, Hatch JP, Dolce C, Bays RA, Rugh JD. Eff ects of
age, amount of advancement, and genioplasty on neurosen-
sory disturbance after a bilateral sagittal split osteotomy. J
Oral Maxillofac Surg 2002;60(9):1012–1017
30. Jones DL, Wolford LM, Hartog JM. Comparison of methods to as-
sess neurosensory alterations following orthognathic surgery.
Int J Adult Orthodon Orthognath Surg 1990;5(1):35–42
31. Jääskeläinen SK, Peltola JK, Forssell K, Vähätalo K. Evaluating
function of the inferior alveolar nerve with repeated nerve
conduction tests during mandibular sagittal split osteotomy.
J Oral Maxillofac Surg 1995;53(3):269–279
32. Westermark A, Englesson L, Bongenhielm U. Neurosensory
function after sagittal split osteotomy of the mandible: a
comparison between subjective evaluation and objective
assessment. Int J Adult Orthodon Orthognath Surg 1999;
14(4):268–275
33. Cunningham LL, Tiner BD, Clark GM, Bays RA, Keeling SD,
Rugh JD. Surgeon’s assessment of nerve damage vs. patients’
report of neurosensory defi cit. J Dent Res 1995;74(Special
Issue):156
34. Schendel SA, Epker BN. Results after mandibular advance-
ment surgery: an analysis of 87 cases. J Oral Surg 1980;38(4):
265–282
35. Jacks SC, Zuniga JR, Turvey TA, Schalit C. A retrospective
analysis of lingual nerve sensory changes after mandibular
bilateral sagittal split osteotomy. J Oral Maxillofac Surg 1998;
56(6):700–704, discussion 705
36. de Vries K, Devriese PP, Hovinga J, van den Akker HP. Facial
palsy after sagittal split osteotomies. A survey of 1747 sag-
ittal split osteotomies. J Craniomaxillofac Surg 1993;21(2):
50–53
37. Van Sickels JE, Tucker MR. Prevention and Management of
Complications in Orthognathic Surgery. In: Peterson LJ, ed.
Principles of Oral and Maxillofacial Surgery. Philadelphia: JB
Lippincott; 1992:1465
38. Jones JK, Van Sickels JE. Facial nerve injuries associated with
orthognathic surgery: a review of incidence and management.
J Oral Maxillofac Surg 1991;49(7):740–744 Review
39. Blumenthal F, May M. Electrodiagnosis. In: May M, ed. The
Facial Nerve. New York: Thieme; 1986:1
40. Christiansen RL, Soudah HP. Disseminated intravascular coag-
ulation following orthognathic surgery. Int J Adult Orthodon
Orthognath Surg 1993;8(3):217–224
41. Lanigan DT, Hey JH, West RA. Major vascular complications of
orthognathic surgery: hemorrhage associated with Le Fort I os-
teotomies. J Oral Maxillofac Surg 1990;48(6):561–573
42. Neuwirth BR, White RP Jr, Collins ML, Phillips C. Recovery
following orthognathic surgery and autologous blood trans-
fusion. Int J Adult Orthodon Orthognath Surg 1992;7(4):
221–228
43. Ellis E III, Hinton RJ. Histologic examination of the temporo-
mandibular joint after mandibular advancement with and
without rigid fi xation: an experimental investigation in
adult Macaca mulatta. J Oral Maxillofac Surg 1991;49(12):
1316–1327
44. Nitzan DW, Dolwick MF. Temporomandibular joint fi brous an-
kylosis following orthognathic surgery: report of eight cases.
Int J Adult Orthodon Orthognath Surg 1989;4(1):7–11
45. Gallagher DM, Bell WH, Storum KA. Soft tissue changes as-
sociated with advancement genioplasty performed con-

Complications in Facial Plastic Surgery
164
83. Bell WH, Schendel SA. Biologic basis for modifi cation of
the sagittal ramus split operation. J Oral Surg 1977;35(5):
362–369
84. de Jongh M, Barnard D, Birnie D. Sensory nerve morbidity
following Le Fort I osteotomy. J Maxillofac Surg 1986;14(1):
10–13
85. Watts PG. Unilateral abducent nerve palsy: a rare complica-
tion following a Le Fort I maxillary osteotomy. Br J Oral Maxil-
lofac Surg 1984;22(3):212–215
86. Carr RJ, Gilbert P. Isolated partial third nerve palsy following
Le Fort I maxillary osteotomy in a patient with cleft lip and
palate. Br J Oral Maxillofac Surg 1986;24(3):206–211
87. Keller EE, Sather AH. Quadrangular Le Fort I osteotomy: surgi-
cal technique and review of 54 patients. J Oral Maxillofac Surg
1990;48(1):2–11, discussion 12–13
88. Tomasetti BJ, Broutsas M, Gormley M, Jarrett W. Lack of
tearing after Le Fort I osteotomy. J Oral Surg 1976;34(12):
1095–1097
89. Sher MR. Treatment of oro-antral-nasal fi stula after anterior
maxillary osteotomy. J Oral Surg 1980;38(3):212–214
90. Pribaz J, Stephens W, Crespo L, Giff ord G. A new intraoral fl ap:
facial artery musculomucosal (FAMM) fl ap. Plast Reconstr
Surg 1992;90(3):421–429
91. Bays RA, Timmis DP. Techniques for Maxillary Orthognathic
Surgery. In: Peterson L, ed. Principles of Oral and Maxillofa-
cial Surgery. Philadelphia: JB Lippincott; 1991:1349
92. Smith KS, Heggie AA. Vomero-sphenoidal disarticulation
during the Le Fort I maxillary osteotomy: report of case. J Oral
Maxillofac Surg 1995;53(4):465–467
93. Robinson PP, Hendy CW. Pterygoid plate fractures caused by
the Le Fort I osteotomy. Br J Oral Maxillofac Surg 1986;24(3):
198–202
94. Lanigan DT, Romanchuk K, Olson CK. Ophthalmic complica-
tions associated with orthognathic surgery. J Oral Maxillofac
Surg 1993;51(5):480–494 Review
95. Precious DS, Goodday RH, Bourget L, Skulsky FG. Pterygoid
plate fracture in Le Fort I osteotomy with and without ptery-
goid chisel: a computed tomography scan evaluation of 58
patients. J Oral Maxillofac Surg 1993;51(2):151–153
96. Schendel SA, Eisenfeld JH, Bell WH, Epker BN. Superior repo-
sitioning of the maxilla: stability and soft tissue osseous rela-
tions. Am J Orthod 1976;70(6):663–674
97. Bell WH, Jacobs JD, Quejada JG. Simultaneous repositioning
of the maxilla, mandible, and chin. Treatment planning and
analysis of soft tissues. Am J Orthod 1986;89(1):28–50
98. Kuo PC, Will LA. Surgical-orthodontic treatment of maxil-
lary constriction. Oral Maxillofac Surg Clin North Am 1990;
2:751–759
99. Kummer AW, Strife JL, Grau WH, Creaghead NA, Lee L. The
eff ects of Le Fort I osteotomy with maxillary movement on
articulation, resonance, and velopharyngeal function. Cleft
Palate J 1989;26(3):193–199, discussion 199–200
100. Schwarz C, Gruner E. Logopaedic fi ndings following advance-
ment of the maxilla. J Maxillofac Surg 1976;4(1):40–55
101. Habal MB. A carotid cavernous sinus fi stula after maxillary
osteotomy. Plast Reconstr Surg 1986;77(6):981–987
102. Gaukroger MC. Dysphagia following bimaxillary osteotomy.
Br J Oral Maxillofac Surg 1993;31(3):189–190
103. de Mol van Otterloo JJ, Dorenbos J, Tuinzing DB, van der Kwast
WA. TMJ performance and behaviour in patients more than
6 years after Le Fort I osteotomy. Br J Oral Maxillofac Surg
1993;31(2):83–86
63. Egyedi P, Houwing M, Juten E. The oblique subcondy-
lar osteotomy: report of results of 100 cases. J Oral Surg
1981;39(11):871–873
64. Guralnick W, Kelly JP. Palsy of the facial nerve after in-
traoral oblique osteotomies of the mandible. J Oral Surg
1979;37(10):743
65. Van Sickels JE, Tucker MR. Prevention and Management of
Complications in Orthognathic Surgery. In: Peterson LJ, ed.
Principles of Oral and Maxillofacial Surgery. Philadelphia: JB
Lippincott; 1992:1465
66. Eckerdal O, Sund G, Astrand P. Skeletal remodeling in the TMJ
after oblique sliding osteotomy of the mandibular rami. Int J
Oral Maxillofac Surg 1986;15:233-239
67. Hall HD, Chase DC, Payor LG. Evaluation and refi nement of
the intraoral vertical subcondylar osteotomy. J Oral Surg
1975;33(5):333–341
68. Boyer CC, Williams TW, Stevens FH. Blood supply of the tem-
poromandibular joint. J Dent Res 1964;43:224–228
69. Hale RG, Timmis DP, Bays RA. A new mandibulotomy tech-
nique for the dentate patient. Plast Reconstr Surg 1991;87(2):
362–364
70. Dorfman HS, Turvey TA. Alterations in osseous crestal height
following interdental osteotomies. Oral Surg Oral Med Oral
Pathol 1979;48(2):120–125
71. Karras SC, Wolford LM. Augmentation genioplasty with
hard tissue replacement implants. J Oral Maxillofac Surg
1998;56(5):549–552
72. Papel ID, Capone RB. Botulinum toxin A for mentalis muscle
dysfunction. Arch Facial Plast Surg 2001;3(4):268–269
73. Zide BM, McCarthy J. The mentalis muscle: an essential com-
ponent of chin and lower lip position. Plast Reconstr Surg
1989;83(3):413–420
74. Dawson PE. Centric relation. Its eff ect on occluso-muscle har-
mony. Dent Clin North Am 1979;23(2):169–180
75. Lanigan DT, Hey JH, West RA. Major vascular complications of
orthognathic surgery: hemorrhage associated with Le Fort I os-
teotomies. J Oral Maxillofac Surg 1990;48(6):561–573
76. Mehra P, Cottrell DA, Caiazzo A, Lincoln R. Life-threatening,
delayed epistaxis after surgically assisted rapid palatal ex-
pansion: a case report. J Oral Maxillofac Surg 1999;57(2):
201–204
77. Lanigan DT, West RA. Management of postoperative hemor-
rhage following the Le Fort I maxillary osteotomy. J Oral Max-
illofac Surg 1984;42(6):367–375
78. Lanigan D, Hey J, West RA. Aseptic necrosis of the maxilla: re-
port of 36 cases. J Oral Maxillofac Surg 1990;48(2):142–156
Review
79. Epker BN. Vascular considerations in orthognathic surgery.
I. Mandibular osteotomies. Oral Surg Oral Med Oral Pathol
1984;57(5):467–472
80. Lanigan DT, Loewy J. Postoperative computed tomography
scan study of the pterygomaxillary separation during the Le
Fort I osteotomy using a micro-oscillating saw. J Oral Maxil-
lofac Surg 1995;53(10):1161–1166
81. Bell WH, Fonseca RJ, Kenneky JW, Levy BM. Bone healing and
revascularization after total maxillary osteotomy. J Oral Surg
1975;33(4):253–260
82. Bell WH, You ZH, Finn RA, Fields RT. Wound healing after
multisegmental Le Fort I osteotomy and transection of the
descending palatine vessels. J Oral Maxillofac Surg 1995;
53(12):1425–1433, discussion 1433–1434

16 Complications in Orthognathic Surgery 165
109. Parnes EI, Becker ML. Necrosis of the anterior maxilla fol-
lowing osteotomy. Oral Surg Oral Med Oral Pathol 1972;
33(3):326–330
110. Vedtofte P, Nattestad A. Pulp sensibility and pulp necrosis af-
ter Le Fort I osteotomy. J Craniomaxillofac Surg 1989;17(4):
167–171
111. Reiner S, Willoughby JH. Transient abducens nerve palsy fol-
lowing a Le Fort I maxillary osteotomy: report of a case. J Oral
Maxillofac Surg 1988;46(8):699–701
112. Shoshani Y, Samet N, Ardekian L, Taicher S. Nasolacrimal
duct injury after LeFort I osteotomy. J Oral Maxillofac Surg
1994;52(4):406–407
104. Lindquist CC, Obeid G. Complications of genioplasty done
alone or in combination with sagittal split-ramus osteotomy.
Oral Surg Oral Med Oral Pathol 1988;66(1):13–16
105. O’Ryan F. Complications of orthognathic surgery. Oral Maxil-
lofac Surg Clin North Am 1990;2:593
106. Park HS, Ellis E III, Fonseca RJ, Reynolds ST, Mayo KH. A ret-
rospective study of advancement genioplasty. Oral Surg Oral
Med Oral Pathol 1989;67(5):481–489
107. Frost DE, Koutnik AW. Alternative stabilization of the maxilla
during simultaneous jaw-mobilization procedures. Oral Surg
Oral Med Oral Pathol 1983;56(2):125–127
108. Lanigan DT, Hey JH, West RA. Major vascular complications of
orthognathic surgery: hemorrhage associated with Le Fort I os-
teotomies. J Oral Maxillofac Surg 1990;48(6):561–573

166
Even though the scalp possesses less anatomic and
physiologic complexity than other areas of the head
and neck, microscopic hair transplantation is a highly
technical procedure, with results that are highly visible.
As such, there is always the potential for troublesome
events. Any adverse outcome in a modern hair restora-
tion practice may create temporal and economic bur-
dens for surgeons, but unfulfi lled expectations may be
psychologically devastating for patients.
Hair restoration techniques have evolved, and the
types of complications and the manner in which they
occur have changed accordingly. Before 1990, scalp re-
ductions, fl aps, and plug grafting were the procedures
of choice. Common problems included fl ap death, wide
scalp scars, misdirected hair, and conspicuous unsightly
pluggy hair grafts. Today, most hair restoration compli-
cations occur with microfollicular grafting and the at-
tendant challenge of producing thick, natural looking
hairlines without accompanying donor site morbidity.
The incidence of hair transplant complications has
declined as knowledge, training, and practitioner skills
have increased, and the majority of cases proceed with-
out adversity.1 However, because many transplants are
performed in procedure rooms rather than accredited
operating rooms, complications undoubtedly are un-
derreported. In addition, the presence of sensational
marketing campaigns may lead prospective patients to
arrive with fantastic and often unrealistic expectations.
Because these hopes cannot be always met with current
methods, failure to meet patient expectations will be
considered.
This chapter is divided into three sections covering
preventative strategies, intraoperative complications,
and postoperative complications. Complications involv-
ing donor and recipient areas will be discussed sepa-
rately, and because we still rely upon scalp reductions
for targeted cases, the challenges associated with fl aps
and reductions and ways to conquer them will also be
discussed.2,3

◆Prevention Strategies
Patient Expectations and Transplant Design
It cannot be overstated that the transplant surgeon
should personally and diligently inform each candidate
of the realistic expectations for the procedure as well
as any potential adverse outcomes. Patients must be
informed that maximum hair density may be achieved
only by undergoing more than a single procedure.
Many other intangibles contribute to the complexity of
results, and hair color, curl, scalp complexion and fu-
ture hair loss are all important factors infl uencing the
outcome. Therefore, even with lengthy preoperative
discussions and comprehensive consent forms, it is still
idealistic to believe that each patient will develop a true
appreciation of the anticipated results. Any patient who
cannot clearly comprehend the limitations of micro-
scopic hair transplantation should not be considered an
appropriate candidate. Because hair loss is usually pro-
gressive with age, many advanced transplant surgeons
are apprehensive about transplanting patients under
the age of 25 years. In some instances, hair loss preven-
tion is a far more important strategy than hair restora-
tion. Convincing an emotionally distraught 20-year-old
of this approach can be very diffi cult. It is perfectly ap-
propriate to insist a relative or close friend be present
during the initial consultation (or series of consulta-
tions). Although a hair restoration complication may
not manifest until balding has progressed, it is the
responsibility of the initial surgeon to use the utmost
discretion. With regard to hairline design, it is impera-
tive to stress the importance of the temporal recession
instead of a straight line. In addition, transplanting ag-
gressively low in the forehead will ultimately result in
extremely unfavorable results.
An additional challenge occurs with women, for they
commonly suff er from postoperative anagen and telogen
effl uvium (shock loss). Regrowth may not occur for over
17
Overcoming Adversities in
Hair Restoration
John E. Frank

17 Overcoming Adversities in Hair Restoration 167
Despite the high dosages of lidocaine administered in
hair transplantation, toxicity is surprisingly rare. How-
ever, the surgeon must be aware of the standard dos-
ages (lidocaine without epinephrine is 5 mg/kg, or up
to 7 mg/kg if given with epinephrine) and the signs and
symptoms of toxicity—the progression of tongue par-
esthesia, light-headedness, and changes in vision lead-
ing to unconsciousness and possible seizure. Should
this occur, the patient should be immediately moved to
an acute care center where serum lidocaine levels can
be drawn (toxicities may be observed at 6 mcg/ml but
more commonly occur once levels exceed 10 mcg/ml)7
and where the patient’s cardiopulmonary status can be
secured.
Preoperatively, patients should be also screened for
prior episodes of fainting. Vasovagal syncope may oc-
cur, most commonly during the application of local an-
esthesia. The high frequency of this event during hair
transplantation may be related to the fact that middle-
aged males constitute the largest demographic for pa-
tients undergoing this procedure. Systemic, nonspecifi c
β-blockers can potentiate the injected epinephrine and
cause toxic hypertension. Although this complication is
unusual, no surgeon should ever hesitate to postpone
a procedure until the patient is converted to a cardiac-
specifi c β-blocker.8

◆ Identifi cation and Management
of Intraoperative Complications
Anesthesia
One of the earliest problems encountered in hair trans-
plantation is an anxious patient intolerant of the admin-
istration of local anesthesia. Depending upon the facility
and the resources available, sedation may be useful. A
small preoperative dose of a benzodiazepine is optimal.
Other options include lorazepam or diazepam, both
which have an onset of less than 30 minutes and a dura-
tion of several hours. Proven techniques for decreasing
the pain of the administration of local anesthetic include
buff ering with sodium bicarbonate, warming, and hyp-
nosis.9,10 A one part in ten bicarbonate dilution and tem-
peratures may be titrated to fi nd the most gentle and
least irritating solution possible. What may appear as a
trivial matter for the highly skilled surgeon is actually
an invaluable opportunity to set the tone for the entire
procedure and further the relationship with the patient.
Diff erent techniques and devices are available for deliv-
ering local anesthesia. Nothing, however, can substitute
for the slow, gentle, and relaxed delivery by the surgeon
or his delegate.
The epinephrine component of the local anesthetic
frequently precipitates episodes of anxiety and tachy-
one year’s time, leading to a very uncomfortable waiting
period for both the patient and the surgeon. Hair and
scalp surgery may exacerbate any telogen effl uvium oc-
curring preoperatively. Shock loss may be limited by use
of some preventative strategies, such as administering
preoperative minoxidil, limiting the amount of intra-
operative epinephrine, and gentle tissue handling with
minimization of damage to surrounding follicles.4 Un-
fortunately, there is no proven preventative remedy, and
this fact must be communicated to all patients at risk.
Assessment of the prevailing hair cell cycles via preop-
erative hair pull tests and microscopic hair pluck root
exams helps to diff erentiate between the typical min-
iaturization associated with male- and female-pattern
hair loss and effl uvium, as well as to determine other
dermatologic conditions of the hair and scalp5. This
knowledge is important and may identify some patients
as poor hair transplant candidates. A sound understand-
ing of these tests and dermatologic conditions is incum-
bent upon any hair transplant surgeon.
Another concern should be individuals requesting ver-
tex or crown transplants. Although many advances have
been made with regard to the design of the crown, such
as the whorl pattern, it is still very diffi cult to achieve
thick, natural coverage in this area.6 Patients must be
clearly informed of this challenge and the necessity of
multiple procedures. The potential for progressive hair
loss is also very high in this area, so surgeons are fore-
warned to proceed carefully. It is possible that the entire
donor supply may be usurped after several transplant
sessions, leaving no reserves for the anterior scalp. The
vertex is also more diffi cult to cover because of the illu-
sion of less hair when the crown is observed from above.
A basic tenet of microscopic hair transplant is that valu-
able donor hair should be allocated in a front-to-back
pattern. In contrast, frontal hair tends to cover balder
areas posteriorly, especially when viewed anteriorly. In
all cases, it is recommended to reiterate the patient’s re-
quests preoperatively, and it may also be helpful to de-
pict the plan with a simple line drawing.
Anesthesia
A major advantage of microfollicular hair transplanta-
tion is that the entire procedure may be completed us-
ing local anesthesia only. However, substantial risk is
present when large dosages of anesthetics are applied.
As with any cosmetic procedure, the surgeon’s tolerance
for withholding an operation on a medically fragile pa-
tient should be low. For individuals who may have low
amounts of coagulants, whether from aspirin, ibupro-
fen, coumadin, clopidogrel (Plavix), other NSAIDS, vita-
mins, or natural supplements, a test procedure using a
small number of grafts may furnish clues as to what to
expect from the defi nitive larger procedure.

Complications in Facial Plastic Surgery
168
to harvest extra tissue, then it becomes prudent to avoid
the postauricular area entirely. Also, prior to re-incising,
it may be helpful to leave the closure sutures intact as
they will act as tissue retractors.
Hair Graft Handling
Surgical assistants have a very important role in hair
transplantation. Following removal of the donor strip
by the surgeon, assistants must use special care while
transferring, dissecting, storing, and placing the grafts.
Once removed from the body, hair follicles are extreme-
ly sensitive to insults from crushing and desiccation.15,16
A small amount of subdermal fatty tissue should be re-
tained around each follicular unit, as this will serve to
protect the fragile follicle; binocular microscopy will aid
in this process.17 Each graft must be sized appropriately
to fi t snugly into the recipient openings. Grafts that are
too large will be traumatized during placement, and
grafts that are too small will not adequately fi ll the re-
cipient site. Optimally, the graft cutting stations should
physically reside in the procedure room so patient-to-
patient crossover is avoided.
Recipient Sites
The surgeon may encounter technical complications
while creating recipient incisions or while placing the
grafts. One of the fi rst challenges is initiating and sus-
taining profound anesthesia. Patients who experience
pain throughout the procedure are likely be hyperten-
sive, with subsequent oozing and graft popping. This
will ultimately aff ect the fi nal outcome. Oral, intramus-
cular, and intravenous analgesics may mitigate these
cardia. Premixed and commercially available packaged
local anesthetics with epinephrine are rarely problem-
atic; however, surgeons may encounter side eff ects
when mixing greater than 1 mg of epinephrine in 30
cc of saline. In addition, paradoxical rebound vasodila-
tion may also occur, causing graft popping and oozing so
that many surgeons commonly avoid these “super juice”
solutions.
Antihypertensive medications should be available, but
they are rarely required. Sedatives may be more useful
in calming a patient and subsequently decreasing blood
pressure and heart rate. Local maneuvers such as Val-
salva and deep breathing are helpful. In the absence of a
bruit or history of cardiovascular disease, a carotid mas-
sage may also be used. Patients with a history of anxiety
or diffi culty with local anesthesia may benefi t from a
benzodiazepine or even a 0.1 mg oral dose of clonidine
if they are tachycardic or hypertensive.
Donor Morbidity
Bleeding or other intraoperative complications of the
donor area are rare. Many surgeons limit the amount of
cautery to prevent damage to the surrounding hair fol-
licles. Intraoperative hematomas are unusual, but if they
are suspected, they should be explored and any bleed-
ing vessel ligated.
Wound closure and edge approximation may be prob-
lematic if the width of the harvest is excessive, since
the scalp is relatively inelastic. This is especially true
in repeat procedures. Typically, elliptical incisions will
close when the width of excision remains less than 1.2
cm. It may also be helpful to measure the elasticity of
the donor area before excision.11–13 In the event of dif-
fi cult wound approximation, wide undermining should
mobilize the edges suffi ciently to allow closure. Pulling
the edges together with a penetrating towel clamp may
also be helpful. Interestingly, it has been postulated that
the scar resulting from an unclosed wound that heals
by secondary intention will ultimately be no wider than
the scar of a wound closed with excessive tension. The
postauricular area is typically the most diffi cult area
to close and usually heals with the most scarring (Fig.
17.1). Narrowly tapering the elliptical incision toward
the mastoid may be helpful. Paradoxically, scalps that
have the greatest elasticity and are easiest to close may
ultimately lead to the widest scarring. This may be a
manifestation of the Ehlers-Danlos syndrome.14
Finally, despite careful calculation and measurement
of the donor strip, it is common for the calculated num-
ber of harvested micro grafts not to match exactly the
anticipated number of promised recipient sites. This
may require opening the already-sutured donor site and
harvesting additional tissue. The surgeon should care-
fully consider the extra trauma that additional tissue
harvesting creates, as this will invariably increase the
tension across the wound. Should the surgeon choose
Fig. 17.1 The retroauricular area is most prone to develop
wide donor scarring, especially after multiple procedures.

17 Overcoming Adversities in Hair Restoration 169
of this complication preoperatively, the sight of postop-
erative facial edema may be unsettling to patients. Be-
sides the use of corticosteroids, it is helpful to reassure
the patient calmly that this is common and that it will
simply resolve with time. After several days, very few
patients experience any pain in the recipient area.
Donor Site
Donor site complications may arise in the immedi-
ate postoperative period, over several weeks, or over
months as the wound remodels. During the fi rst two
weeks, it is not uncommon for patients to complain
about donor site discomfort. This usually resolves with
suture removal. Although staples are easier to place,
they are more uncomfortable than traditional sutures.21
During the weeks to months following suture removal,
localized areas of thickening may arise. These are typi-
cally caused by retained suture remnants or dermal
elements. It may be diffi cult to distinguish suture mate-
rial from hair keratin fi bers. Localized wound irritations
may be treated with widely available commercial 1–2%
topical triamcinolone cream.
Total wound dehiscence may also occur. This is more
likely to occur in patients undergoing repeat procedures
where scar tissue is present and the tension across the
wound is high. If this occurs, local wound hygiene is
important while the wound granulates and heals by
secondary intention. Once the wound has completely
epithelialized, a sizable scar will be evident, because
most of the follicles will have been destroyed. This can
truly be a problematic issue for patients and hair res-
toration surgeons. Unfortunately, most scar revision
techniques fail, ultimately resulting in a persistent, life-
long occipital scar that can, practically speaking, only be
camofl auged by hair styling techniques in the back of
the scalp. Because local fl aps in this area have not prov-
en successful in eliminating donor scars, surgeons have
been left with few options, such as actually transplant-
ing hair from the temporal area into the occipital scar or
tattooing the scarred dermis with permanent ink as a
way to conceal the bare scar.
Other localized wound complications confound-
ing hair surgeons are hypertrophic scarring, pyogenic
granuloma, and arteriovenous fi stula formation. Hy-
pertrophic scarring may be treated with serial Kenalog
(Bristol-Myers Squibb, Princeton, NJ) injections; how-
ever, overuse of concentrated Kenalog injections may
cause skin depressions secondary to atrophy of the
subdermal fat. Pyogenic granulomas should be treated
with local wound care and silver nitrate cauterization
(Fig. 17.2). An arteriovenous (AV) fi stula may present
anywhere from several days to several weeks postop-
eratively. This will typically be perceived as a slightly
painful swelling in the area of the donor excision. On
examination, a pulsating mass confi rms the diagnosis.
Some operators choose to allow this to resolve sponta-
circumstances. The eff ects of lidocaine will diminish
with time, and frequent reapplication or stacking of in-
jections will prevent the lidocaine from wearing off and
disrupting the placement process. As the sensory nerves
run most superfi cially in the dermis, deeper infi ltration
of anesthesia will miss the intended nerves and will also
dissipate more easily through the deeper dermis and
subcutaneous fat. Therefore, the thin subcutaneous ad-
ministration of local anesthesia is mandatory.
Matching the size and the depth of the recipient in-
cisions will minimize problems with graft placement.
The grafts must fi t easily yet snugly into each opening.
Excessively skinny grafts will yield poorer survival.18 At
some point, however, every surgeon will be faced with
grafts that tend to pop during the placement period. The
cause of this problem may be hypertension or vascular
oozing. Additionally, graft popping occurs secondary to
inherent skin properties. Increasing the concentration of
the “super juice” (dilute epinephrine in normal saline)
may ameliorate this condition. However a balance must
be struck; excessive volumes and concentrations of epi-
nephrine may cause transient tachycardia or potentially
diminish blood fl ow and hamper healing. In addition,
rebound hyperemia should be expected following liber-
al use of concentrated epinephrine solutions. Excessive
graft popping may be also technique- and operator-de-
pendent. Surgeons should familiarize themselves with
the various techniques for graft placement.19
Intraoperative headache may be treated with analge-
sics; however, the pain may also be alleviated by simply
removing the circumferential dressing. Ketorolac 15 to
30 mg IM or IV may be helpful. Regardless of the pa-
tient’s blood pressure or coagulation status, the trans-
planted grafts may continue to elevate or pop. This is
probably more related to dermal elasticity, and a gentle
pressure dressing may be applied. Alternatively, a salon
hair dryer set to low heat should serve to limit popping
until the openings coagulate and dry. At home, patients
should be instructed to use direct pressure if oozing oc-
curs. Optimally, patients should keep the grafted area as
moist as possible by using a misting spray bottle. This
will prevent excessive crusting during the postoperative
phase.

◆ Diagnosis and Management of
Postoperative Complications
General
During postoperative days 2–6, edema migrates from
the top of the scalp to the forehead and throughout the
soft tissues of the face. This commonly results in peri-
orbital ecchymosis and facial edema. The edema may
be limited by mixing triamcinolone 40 mg with the lo-
cal anesthesia of the recipient area.20 Nonetheless, even
when the surgeon is diligent about notifying the patient

Complications in Facial Plastic Surgery
170
Following any donor wound complications, a wider
scar may form. In fact, even in uncomplicated surgeries
patients will have a range in the size of the donor scar. A
larger scar is often seen after repeat procedures; there-
fore, some surgeons will choose to harvest in a com-
pletely separate area, either above or below the original
scar. It may be easier to camoufl age several fi ne lines
as opposed to a single wide scar (Fig. 17.5). Although
several scar-reduction techniques are available, con-
verting a widened scar to an invisible line is extremely
diffi cult, as previously mentioned. Simple scar excision
neously; however, the most eff ective treatment for an
uncomfortable AV fi stula is a local excision and ligation
of the feeding vessel.22
Patients may inquire about the potential for keloid
formation (Fig. 17.3). Fortunately, the occurrence of ke-
loids is extremely rare. More commonly, a donor area
may undergo signifi cant telogen effl uvium or shock loss.
Although the donor area is less noticeable, any amount
of shock loss can be extremely unnerving (Fig. 17.4).
The surgeon at this point is obligated to off er gentle re-
assurance that the hair will in fact grow back.
Fig. 17.2 A pyogenic granuloma is noted in the left side of a
patient’s donor area. This was treated with serial silver nitrate
cauterization.
Fig. 17.3 Keloid formation is rare, and this formation devel-
oped after an attempted scar revision.
Fig. 17.4 Telogen and anagen effl uvium developed in the
donor area. It is more diffi cult to conceal in this patient with
short hair.
Fig. 17.5 Stacked donor scars may be more cosmetically ap-
pealing than one large scar.

17 Overcoming Adversities in Hair Restoration 171
The eschar may be left intact as a biologic dressing un-
til granulation tissue forms. If the wound is small, the
edges may contract to cover the area completely; other-
wise, the wound will heal by secondary intention. Tis-
sue expansion may be used to create enough tissue for
primary closure. Several weeks should elapse before a
conservative attempt to add additional grafts.
During the months following the procedure, epider-
mal inclusion cysts occur in at least 10% of all follicu-
lar unit transplant cases.33 Ironically, the occurrence of
cysts may herald the growth of the new grafts. Patients
should be instructed on procedures for home hygiene
using topical rubbing alcohol and warm compresses.34
Most cysts will be self-limiting; however, larger cysts
may require incision and drainage. Persistent cysts oc-
casionally progress to scalp infections requiring oral an-
tibiotics. Rarely will this lead to loss of grafts.
Unfortunately, there is not yet a proven way to predict
the occurrence of anagen and telogen effl uvium (shock
loss) nor a way to limit its severity. Parsely recommends
minimizing the packing in already dense areas, and Kas-
simir has tried using minoxidil.4,30 Because of the unpre-
dictability of this possible temporary outcome and its
potential for emotional distress, all patients should be
carefully counseled regarding it.
Patients should expect new hair growth between the
second and fi fth month; however, individual deviations
may occur (Table 17.1). Growth may be delayed be-
yond six months. Simple reassurance is helpful during
follow-up exams, and demonstration of early growth
with a microscopic device may be helpful. If the ulti-
mate growth is less than expected, then several causes
should be investigated. Poor handling may have created
crush injury or desiccation. The quality of the donor hair
may also have been poor. The surrounding hair may be
may be tempting; however, donor scar revisions have
a low aesthetic yield. Despite the will of a surgeon de-
termined to do big cases, conservative donor excision
minimizes donor scarring by limiting the tension across
the wound. Once again, the retroauricular area tends
to have the widest scarring, and careful preoperative
planning will minimize this problem. Prepare for a wid-
ened scar when harvesting below the external occipital
protuberance, as tension from the extensor muscles of
the neck may contribute to widening. Deep fi xation su-
tures may serve to decrease tension across the wound
and theoretically prevent the scar from widening.23,24 A
small series of running 30°, 45°, or 60° Z-plasties or M-
plasties may serve to break the line as well as to convert
the angle of the tension across the wound from horizon-
tal to vertical. In patients with ample donor supply, hair
may be transplanted into the scar to help camoufl age
the donor scar.3 Other methods of repair, such as using
tissue expansion or trichophytic excisions, have been
infrequently described.25–27
Recipient
Complications in the recipient area are rare in the fi rst
two postoperative days. Some patients may report
bleeding from some of the incision sites. They should be
instructed to apply gentle pressure. Oozing beyond 48
hours is unusual and should raise concern for a bleeding
abnormality. Scabbing is to be expected. However, if the
grafted areas are kept moist with either a saline-based
spray or an ointment, then the crusts and scabs resolve
by day 7. Crusts and scabs may be gently removed, but
prolonged crusting should not be confused with the
development of seborrheic plaques. In this event, treat-
ment is targeted at the proliferating Malassezia yeast
(formerly Pityrospirum ovale) and may include an anti-
fungal shampoo, pyrithione zinc, topical corticosteroid,
or 20% salicylic acid.28,29
Crusting may also conceal recipient wound healing
abnormalities. One such problem is frontal central ne-
crosis (Fig. 17.6). Although it is considered a rare com-
plication, its true incidence is unknown, for many cases
may go unreported.30 The exact cause is also unclear.
Rousso postulates that prolonged numbness may lead to
itching and self-excoriation, while Seager feels that ne-
crosis is the result of a compromised blood supply from
exceedingly dense packing.31,32 A necrotic area should be
treated with local wound care and antibiotics, culturing
any evidence of purulence. The objective of the oral an-
tiobiotic is to minimize the bacterial load of normal skin
fl ora in the infected area while granulation tissue forms.
However, one is advised to inspect the wound routinely
for evidence of advancing cellulitis, particularly in any
patient with compromised blood fl ow, such as a patient
with type 1 diabetes. Should cellulitis occur, the antibi-
otics should be carefully adjusted based upon cultures
and sensitivities, with IV antibiotics used if necessary.
Fig. 17.6 Frontal central necrosis.

Complications in Facial Plastic Surgery
172
known problems include pitting, ridging, cobbleston-
ing, improper hair/scalp angling, and excessively curly
or kinky hair growth. Hair styling may camoufl age some
problems, but ultimately the surgeon always has the op-
tion to excise unwanted hair or to add additional grafts
to create blending. The same concepts are true for re-
pairing older techniques, such as the hairline with un-
sightly multifollicular plugs. Experienced transplant
surgeons have developed several elegant techniques for
repairing undesirable results from prior procedures by
either completely or partially excising standard grafts
(hair plugs) and transplanting smaller, microscopic
grafts in the immediate area.14,35–37 The basic idea is to
break up all or parts of the older hair plug (standard
graft) using a small dermatologic circular biopsy punch,
reprocess the grafts, and reinsert smaller, follicular unit
grafts and thereby create a new, blended hairline.

◆Flaps and Scalp Reduction
Fairly recent surveys conducted by the International So-
ciety of Hair Restoration Surgery revealed that only 1.2%
of all surgical hair restoration procedures involve alo-
pecia reductions or fl aps.38 Many current hair surgeons
may not even be familiar with the techniques. By way
of review, the classic temporoparietal fl ap (Juri fl ap or
Fleming-Mayer fl ap) is a pedicled fl ap using a terminal
branch of the superfi cial temporal artery. Hair-bearing
scalp is transferred to the frontal hairline, and several
separate fl aps may allow the transfer of large amounts of
thick hair. Although the transferred hair yields complete
density, the fl ap delivers far from satisfactory aesthetic
results by today’s standards. Complications associated
with the Juri fl ap, such as necrosis, asymmetry, and
faulty hair direction, spawned techniques designed to
correct them.39 Because of their marginal aesthetics and
elevated risk of complications, as well as the advance-
ment of micrografting, Juri fl aps have become relatively
obsolete except in rare instances associated with trauma
or burn scars.
On the other hand, alopecia reductions may still be
useful in selected cases of alopecia. Diff erent designs ex-
cise unwanted bald scalp while advancing hair-bearing
tissue. Serial excisions as well as tissue expansion will
maximize the size of the reduction. The techniques are
useful for revising scars and reconstructing scalp de-
fects.40,41 Infection, hematoma, and implant exposure
are all possible complications when tissue expanders
are used. In addition, the complications of any scalp
reduction procedure include diminished density of the
surrounding hair and a visible scar. Perhaps the most
troubling cosmetic deformity is the development of a
“slot defect,” with hair falling unnaturally away from the
scar (Fig. 17.7). Frechet describes using a triple transpo-
sition fl aps to deal with the slot formation (Fig. 17.8).2
experiencing continued hair loss, making it very diffi -
cult to determine the fi nal results. On occasion, despite
meticulous technique, the graft counts may have been
tallied incorrectly. In any event, it may be very diffi cult
to quantify the fi nal outcome. Practically speaking, this
fi nal step of graft placement requires the highest level
of skill and technical acumen. To enable the greatest
graft survival, the surgeon must ensure patient comfort
and safety as well as facilitating a perfect environment
for the technicians, including brilliant lighting, magni-
fi cation, precision instruments, and logistics. Hairpiece
wearers have notoriously poor or delayed growth. Sev-
eral reasons have been postulated; however, current
dogma is to limit the amount of time the patient wears
the hairpiece postoperatively, and the hair should be
fi xed to the scalp only with clips—hair adhesives should
be avoided. Anecdotal evidence supports the notion that
artifi cial hair should not be worn in the immediate post-
operative period (during the fi rst 3–5 days); however,
this often presents social limits for patients, and they
have been known to place hairpieces directly on the
healing grafts. The same is true preoperatively, when
patients are encouraged to maximize the health and
natural state of the scalp follicle environment by limit-
ing the time they wear their hairpiece. More scientifi c
work needs to be completed that studies the eff ect of
scalp hygiene on hair growth. As the tools for measuring
postoperative results for hair transplant and other aes-
thetic surgeries evolve, patients should be encouraged
to maintain meticulous scalp hygiene and to avoid any
unnecessary traction on the grafts.
Even with robust growth, surgical errors may still oc-
cur in the planning and design. Poor outcomes include
asymmetry or perhaps the placement of grafts in areas
that were not acceptable to the patient. Patients also
have been known to change their minds. It may be help-
ful to ask patients to sign a copy of the preoperative
design, either on a drawing or a marked photograph.
Obviously, this should be done before any sedation is
administered. Finally, despite excellent growth and ex-
ecution of a well-designed transplant, each individual
graft may still appear cosmetically unsatisfactory. Some
Table 17.1
Growth Problems
Poor growth
Handling errors, weak donor,
continued hair loss, count er-
ror, ergonomics, hairpiece
Poor planning
Asymmetry, too low, too
straight, wrong area
Individual graft problem
Pitting, cobblestoning, wrong
angles, kinky

17 Overcoming Adversities in Hair Restoration 173
References
1. Adler SC, Rousso D. Evaluation of past and present hair re-
placement techniques. Aesthetic improvement, eff ectiveness,
postoperative pain, and complications. Arch Facial Plast Surg
1999;1(4):266–271
2. Frechet P. A new method for correction of the vertical scar ob-
served following scalp reduction for extensive alopecia. J Der-
matol Surg Oncol 1990;16(7):640–644
3. Epstein JS. Hair transplantation in women: treating female
pattern baldness and repairing distortion and scarring from
prior cosmetic surgery. Arch Facial Plast Surg 2003;5(1):
121–126
4. Kassimir JJ. Use of topical minoxidil as a possible adjunct to
hair transplant surgery. A pilot study. J Am Acad Dermatol
1987;16(3 Pt 2):685–687
5. Olsen E. In: Disorders of Hair Growth: Diagnosis and Treat-
ment. New York: McGraw-Hill; 2004:77–81
6. Ziering C, Krenitsky G. The Ziering whorl classifi cation of scalp
hair. Dermatol Surg 2003;29(8):817–821, discussion 821
7. Klein J. Cytochrome P450 3A4 and Lidocaine Metabolism. In:
Klein JP, ed. Tumescent Techniques. St. Louis: Mosby; 2000:
131–140
8. Zhang CBD, Banting DW, Gelb AW, Hamilton JT. Eff ect of
beta-adrenoreceptor blockade with nadolol on the dura-
tion of local anesthesia. J Am Dent Assoc 1999;130(12):
1773–1780
9. Nusbaum BP. Techniques to reduce pain associated with hair
transplantation: optimizing anesthesia and analgesia. Am J
Clin Dermatol 2004;5(1):9–15
10. Hammond D. Hypnotic Inductions. In: Hammond DC, ed.
Hypnotic Induction and Suggestion. Chicago: American Soci-
ety of Hypnosis; 1998:20–44
11. Feldman C. Tissue laxity based on donor tissue ballooning.
Hair Trans Forum Intl 2001;11(4):119

◆Conclusion
This chapter has described the complications of hair
restoration and techniques for their prevention and mit-
igation. Despite proper planning and execution, experi-
enced transplant surgeons will still encounter patients
whose expectations have not been met. Maintaining
close follow-up and good communications should limit
the problems when unexpected results or complica-
tions occur. As always, avoidance of complications is the
best practice.
Fig. 17.7 This photograph shows the slot defect that may oc-
cur after a reduction performed to alleviate vertex alopecia.
Fig. 17.8 The slot defect may be repaired with the transposi-
tion of three hair-bearing fl aps, allowing both coverage of the
slot as well as a natural direction of the hair falling inferiorly.
PEARLS OF WISDOM
Preparing hair restoration patients to have realistic expectations
will help tremendously with patient satisfaction.
Patients must understand that hair loss is progressive and
that most hair restoration patients will require more than one
procedure.
It is always easier to add additional hair than to attempt cor-
recting poorly placed grafts.
The best hair results occur when patients are relaxed and at
ease.
When there is doubt, a preliminary test procedure using ap-
proximately 100 grafts may allay the fears of both the surgeon
and patient.
Promising new techniques using Follicular Unit Extraction
(FUE) and automation devices will undoubtedly be associated
with newer, but hopefully less serious, complications.

Complications in Facial Plastic Surgery
174
hair-bearing skin. Plast Reconstr Surg 2000 Apr;105(5):1866-
1870, discussion 1871
28. Cotterill P. Seborrheic dermatitis. Hair Trans Forum Intl
1997;7(6):13
29. DeAngelis YMG, Gemmer CM, Kaczvinsky JR, Kenneally DC,
Schwartz JR, Dawson TL Jr. Three etiologic facets of dan-
druff and seborrheic dermatitis: fungi, sebaceous lipids,
and individual sensitivity. J Investig Dermatol Symp Proc
2005;10(3):295–297
30. Parsley W. Management of the Postoperative Period. In: Un-
ger WP, ed. Hair Transplantation. New York: Marcel Dekker;
2004:562
31. Rousso DE. Repostoperative frontal central necrosis. Hair Trans
Forum Intl. 1999;9(5):158
32. Seager DJ. Pitfalls of Follicular Un it Hair Transplantation and
How to Avoid Them In: Unger WP, ed. Hair Transplantation.
New York: Marcel Dekker; 2004:409–410
33. Whiting DA, Stough DB. Posttransplant epidermoid cysts
secondary to small graft hair transplantation. Dermatol Surg
1995;21(10):863–866
34. Barrera A. Micrograft and minigraft megasession hair trans-
plantation results after a single session. Plast Reconstr Surg
1997;100(6):1524–1530
35. Epstein JS. Revision surgical hair restoration: repair of unde-
sirable results. Plast Reconstr Surg 1999;104(1):222–232, dis-
cussion 233–236
36. Vogel JE. Correcting problems in hair restoration surgery:
an update. Facial Plast Surg Clin North Am 2004;12(2):
263–278
37. Swinehart JM. Hair repair surgery. Corrective measures for
improvement of older large-graft procedures and scalp scars.
Dermatol Surg 1999;25(7):523–528, discussion 529
38. International Society of Hair Restoration Surgery. Hair Resto-
ration Surgical Procedures by Type of Procedure. Practice Cen-
sus Statistics, 2005:18
39. Brandy DA. Corrective hair restoration techniques for the
aesthetic problems of temperoparietal fl aps. Dermatol Surg
2003;29(3):230–234, discussion 234
40. Epstein JS. The role of tissue expansion in hair transplant sur-
gery: presentation of two unique cases. Hair Trans Forum Intl
2002;12(3):108–109
41. Ramirez A, Kabaker SS. Reducing the female forehead without
hair transplantation. Hair Trans Forum Intl 2004;14(2):93–94
12. Mayer ML. P.T., Scalp Elasticity Scale. Hair Trans Forum Intl
2005;15(4):122–123
13. Bosley LL, Hope CR, Montroy RE, Straub PM. Reduction of male
pattern baldness in multiple stages: a retrospective study. J
Dermatol Surg Oncol 1980;6(6):498–503
14. Bernstein RM, Rassman WR, Rashid N, Shiell RC. The art of re-
pair in surgical hair restoration part I: basic repair strategies.
Dermatol Surg 2002;28(9):783–794
15. Kim J, Hwang S. The Eff ects of Dehydration, Preservation Tem-
perature and Time, and Hydrogen Peroxide on Hair Grafts. In:
Unger WP, ed. Hair Transplantation. New York: Marcel Dekker;
1995:285–286
16. Greco JF, Kramer RD, Reynolds GD. A “crush study” review of mi-
crograft survival. Dermatol Surg 1997;23(9):752–755
17. Cooley JE, Vogel JE. Follicle trauma and the role of the dissect-
ing microscope in hair transplantation: A multicenter study.
Dermatol Clin 1999;17(2):307-312, viii; discussion 312-313
18. Seager DJ. Micrograft size and subsequent survival. Dermatol
Surg 1997;23(9):757–761, discussion 762
19. Whitworth JM, Stough DB, Limmer B, et al. A comparison of
graft implantation techniques for hair transplantation. Semin
Cutan Med Surg 1999;18(2):177–183
20. Gholamali A, Sepideh P, Susan E. Hair transplantation without
post-operative edema. Hair Trans Forum Int 2005;15(5):149,
158
21. Bernstein RM, Rassman WR, Rashid N. A new suture for hair
transplantation: poliglecaprone 25. Dermatol Surg 2001;
27(1):5–11
22. Davis AJ, Nelson PK. Arteriovenous fi stula of the scalp second-
ary to punch autograft hair transplantation: angioarchitec-
ture, histopathology, and endovascular and surgical therapy.
Plast Reconstr Surg 1997;100(1):242–249
23. Seery GE. Hair transplantation: management of donor area.
Dermatol Surg 2002;28(2):136–142
24. Bernstein RM, Rassman WR, Rashid N, Shiell RC. The art of re-
pair in surgical hair restoration—part II: the tactics of repair.
Dermatol Surg 2002;28(10):873–893
25. Brandy DA. Intricacies of the single-scar technique for donor
harvesting in hair transplantation surgery. Dermatol Surg
2004;30(6):837–844, discussion 844–845
26. Seery GE. Improved scalp surgery results by controlling ten-
sion vector forces in the tissues by galea to pericranium fi xa-
tion sutures. Dermatol Surg 2001;27(6):569–574
27. Seyhan A, Yoleri L, Barutçu A. Immediate hair transplantation
into a newly closed wound to conceal the fi nal scar on the

A
Abducens nerve palsy, LeFort I osteotomy and, 160
Abscess
with hypersensitivity to bovine collagen, 14
management of, 34
orbital, after upper eyelid blepharoplasty, 54
Accreditation Association for Ambulatory Health Care
(AAAHC), 26
Advanta, 100
Air embolism, in surgical treatment of craniosynostosis,
133
Airway(s). See also Nasal airway obstruction
management of, 23, 25
problems, with craniofacial dysostoses, 132
Alar distortion(s), after skin resurfacing, 43
Alar retraction, 30f, 31, 36
correction of, 84–86, 84f–85f
Alopecia
after browlift, 73–74
after facelift, 94
with facial reanimation, 128
reduction, 172, 173f
Alveolar bone grafting
in cleft repair, 143–144
primary, 143
secondary, 143
Amblyopia, in child with craniofacial dysostoses, 137
Ambulatory surgery, accreditation for, 26
American Association for Accreditation of Ambulatory
Surgical Facilities (AAAASF), 26
American College of Surgeons, guidelines for offi ce-
based surgery, 24, 26
American Society of Anesthesiologists
guidelines for offi ce-based surgery, 24, 26
Physical Status classifi cation, 22, 22t, 23t
Ametropia, in child with craniofacial dysostoses, 137
Amoxicillin, indications for, 33
Analgesics, 20
for hair transplantation, 167, 168–169
Anaphylactic shock, with hypersensitivity to bovine
collagen, 14
Anesthesia
adverse outcomes of, 18t
causes of, 17–18
data on, 17
complications of, 17–28
patient factors and, 22–23
duration of surgery and, 24–25
for hair transplantation, 167–168
medications for, complications of, 18–22
outcomes of, 17–18
pearls, 26
personnel for, 17
safety of, 17, 26
Anisocoria, 114
Antibiotic(s)
with orthognathic surgery, 151–152
perioperative
in facelift, 95
for facial implant-related infection, 99
in rhinoplasty, 87–88
for postoperative infection, 34
prophylactic, 33–34
Anticoagulants, perioperative management of, 91, 91t, 99
Antiemetics, indications for, 18
Anxiety, in hair transplantation, 167–168
Anxiolytics, 20
as premedication, 18–19
Apraclonidine eyedrops
adverse eff ects and side eff ects of, 12
indications for, 12, 16
ArteFill, 13
Arteriovenous fi stula, in hair transplant donor site,
169–170
175
Index
Note: Page numbers followed by f and t indicate fi gures and tables, respectively.

Index
176
after facial reanimation, 129
Blood loss, in surgical treatment of craniosynostosis,
133
Body dysmorphic disorder, 6–7, 6t, 49
Botox. See Botulinum toxin
Botulinum toxin
and brow ptosis, 11–12, 11f
bruising with, 10
complications of
management of, 10–12
prevention of, 10
systemic, 12
edema caused by, 10
immunogenicity of, 10–11
injection, pearls, 16
intraparotid injections, after parotid duct injury, 120
pain caused by, 10
serotype A, 10–12
serotype B, 11
serotypes of, 10
for wound immobilization during healing, 31
Botulism, 12
Brain
anatomy of, 133, 133f
contusion, in surgical treatment of craniosynostosis,
133
growth of, craniosynostosis and, 133
hemorrhage, in surgical treatment of
craniosynostosis, 133
Brain injury
in browlift, 76, 76f
traumatic, 118
Bronchoconstriction, anesthesia-related, 21
Bronchodilation, anesthesia-related, 21
Browlift. See also Brow rejuvenation
alopecia after, 73–74
brain injury in, 76, 76f
endoscopic, 68, 69f
adverse outcomes with, 71, 71t
hairline-lowering, sensory nerve dysfunction
after, 73
hairline-preserving, sensory nerve dysfunction
after, 73
pearls, 77
facial nerve injury in, 71–72, 72f
in facial reanimation, 127–128, 128–129
fi xation devices
and granuloma formation, 75, 76f
infl ammatory nodules caused by, 75, 75f
fi xation failure, 75
and hairline, 70
hairline distortion after, 73–74
hardware failure after, 75–76, 76f
hematoma after, 73
in facial reanimation, 128
historical perspective on, 68
inadequate brow correction after, 74–75
Artery(ies)
direct cutaneous, 30
musculocutaneous, 30
ASA. See American Society of Anesthesiologists
Aspiration pneumonitis, prevention of, 18
Aspirin, perioperative management of, 34–35, 79, 91,
91t, 99
Astigmatism
eyelid hemangioma and, 54
after upper eyelid blepharoplasty, 54–55
B
BDD. See Body dysmorphic disorder
Benzodiazepines, 20
in hair transplantation, 167–168
Bicitra. See Sodium citrate
Bilateral sagittal-split osteotomy. See Mandibular
osteotomy(ies), bilateral sagittal-split
Bite abnormalities. See also Malocclusion; Open bite
deformity
with mandibular condylar fractures, 108–109
Bleeding. See also Hemorrhage
abnormalities, preoperative evaluation for, 79
with anterior maxillary segmental osteotomy, 161
in bilateral sagittal-split mandibular osteotomy, 154
and blepharoplasty, 49, 53–54, 58–59
drug-related, 34–35, 91, 91t
with facial implant, prevention of, 99
in intraoral vertical ramus mandibular osteotomy, 156
with LeFort I osteotomy, 158–159, 161
of locoregional facial fl ap, 34–35
after lower eyelid blepharoplasty, 58
deep orbital, 58–59
superfi cial, 58
postoperative
with rhinoplasty, 88
after upper eyelid blepharoplasty, 53–54
retrobulbar
with facial reanimation, 129
after upper eyelid blepharoplasty, 53–54
in rhinoplasty, 79
Blepharoplasty
lower eyelid. See Lower eyelid blepharoplasty
upper eyelid. See Upper eyelid blepharoplasty
Blepharoptosis, 51–52
acquired, 51–52
botulinum toxin and, 11–12
pearls, 16
classifi cation of, 51
mild, 51
moderate, 51
severe, 51
after upper eyelid blepharoplasty, 54
Blindness
after blepharoplasty, 53, 59
in child with craniofacial dysostoses, 137
after facial fractures, 113

Index 177
light, 40
for postinfl ammatory hyperpigmentation, 42, 42t
medium, 40, 41
Chemoexfoliation, 40
Chemosis, after blepharoplasty, 54, 59–60, 59f
Chiari malformation, 132
Chin
implants for, 100–102
bone erosion with, 101, 101f
complication rates, 101t
infection of, 102
removal of, 101–102, 102f
ptosis, after genioplasty, 158
Chlorhexidine, and cornea, 52
Chloroprocaine, pharmacology of, 20t
Ciprofl oxacin, indications for, 34
Clavulanate, indications for, 33
Cleft lip, repair
complications of, 138–144
horizontal abnormalities after, 139–140
misalignment after, 139
overly wide philtrum after, 140
pearls, 146
postoperative care for, 138–139
revisions, 139
and scarring, 139–140
techniques for, 138
timing of, 138
and vermilion defi ciency, 139
vertical defi ciency after, 139
whistle deformity after, 139, 139f
Cleft lip nasal deformity
bilateral, 140–141, 141f
unilateral, 140, 140f
Cleft palate, repair. See also Palatoplasty
and alveolar bone grafting, 143–144
complications of, 138–144
oronasal fi stulas after, 142, 142f
pearls, 146
techniques for, 138
timing of, 138
velopharyngeal dysfunction after, 142–143
Clindamycin, indications for, 33–34
Clonidine, in hair transplantation, 168
Closure
primary, 29
by secondary intention, 29, 32
indications for, 35
Cocaine
duration of action of, 19t
maximum dose of, 19t
Collagen
bovine, 12
hypersensitivity to, 14, 98
as dermal fi ller, 12
human, 12
porcine, 12
inappropriate brow correction after, 74–75
infection after, 73
pitfalls of, 71
scars after, 74
sensory nerve injury in, 72–73
trichophytic incisions in, 74, 74f
venous congestion after, 73
Brow ptosis, 70
botulinum toxin and, 11–12, 11f
pearls, 16
Brow rejuvenation, 68, 69f. See also Browlift
endoscopic, 68
and open trichophytic, combined, 68
pearls, 77
historical perspective on, 68
patient selection for, 68–70
preoperative evaluation for, 68–70
preoperative photographs, 71
BSSO. See Mandibular osteotomy(ies), bilateral sagittal-
split
BT-A. See Botulinum toxin
BTX. See Botulinum toxin
Bupivacaine
cardiotoxicity of, 19
duration of action of, 19t
with epinephrine
duration of action of, 19t
maximum dose of, 19t
maximum dose of, 19t
pharmacology of, 20t
C
Calcium hydroxylapatite, 13
Calcium phosphate cement, in cranioplasty, 136, 136f
Calvarium
defects, related to elevated intracranial pressure with
craniosynostosis, 134, 134f, 135f
persistent defects, after craniofacial reconstruction,
136–137
Candida infection, after skin resurfacing, 45
Canthal dystopia, 62, 64f
Canthoplasty, complications of, 62, 64f
Capnographic monitoring, intraoperative, 25
Cardiac complications, correlates of, 22–23, 23t
Cardiac Risk index, Revised, 22–23, 23t
Cephalosporin(s), indications for, 33
Ceramics, for facial implant, 97
Cerebrospinal fl uid, leak
with frontal sinus fracture, 118
with surgical treatment of craniosynostosis, 135
Cheek
lacerations, 119–120, 119f
soft-tissue of, trauma to, repair of, 116
Chemical peel(s)
complications of, 39–40, 41f
deep, 40, 41
erythema after, 47

Index
178
head deformity after, 137
head protection after, 137
historical perspective on, 132
and infection, 135
morbidity and mortality rates with, 132
ocular complications of, 137
pearls, 146
persistent skull irregularities and defects after,
136–137
and pneumocephalus, 133
and postoperative head injury, 137
preoperative imaging for, 134–135
resynostosis after, 132
risks of, 132
timing of, 132–133
Croton oil, and Epstein-Barr virus keratitis, 46
CT. See Computed tomography
D
Dacron, characteristics of, 97, 98t
Dacryocystitis, 117
Dacryocystography, 117
Dacryocystorhinostomy, 117
Dantrolene, for malignant hyperthermia, 22
Dehiscence
of hair transplant donor site, 169
of levator aponeurosis, 52
of locoregional facial fl ap, 35
prevention of, 35
risk factors for, 35
Dermabrasion, complications of, intraoperative, 39
Dermal fi ller(s). See also Calcium hydroxylapatite;
Collagen; Hyaluronic acid; Poly-L-lactic acid
bruising caused by, 14
clinical applications of, 12
complications of, 12, 13–15
edema caused by, 14
erythema caused by, 14
hypersensitivity to, 14
injection, pearls, 16
necrosis due to, 14
treatment protocol for, 14, 14t
pain caused by, 14
vascular occlusion caused by, 14
Desfl urane, 21
Diabetes mellitus, and facelift, 91
Diazepam, preoperative, in hair transplantation, 167
Diplopia
chronic, 115
after lower eyelid blepharoplasty, 58
mechanical causes of, 112
neurogenic causes of, 112
after orbitozygomatic trauma, 112–113
Distraction osteogenesis
complications of, 137–138, 138f
pearls, 146
Drain(s), for locoregional facial fl ap, 34
Commissuroplasty, in facial reanimation, 130–131, 130f
Communication
in avoidance of complications, 2–3, 3t
with dissatisfi ed patient, 8–9
eff ective, four Es of, 8
and informed consent, 90
and patient dissatisfaction, 90
postoperative, 7–8
in preoperative consultation, 5, 7
Complications, surgical
avoidance of, 2–3, 3t
causes of, 2
defi nition of, 2
in facial plastic surgery
defi nition of, 2
unique signifi cance of, 1–2
factors aff ecting, 1
pearls, 4
surgeon’s response to, 3–4
Computed tomography
craniofacial, for surgical planning, 114
preoperative, for surgical treatment of
craniosynostosis, 134–135
Computer imaging, preoperative
for facial implants, 98
for rhinoplasty, 78
Congenital craniofacial surgery
complications of, 132–137
defi nition of, 132
Conscious sedation, 21
Consultation, preoperative, 5
Cornea
abrasion of, 52
intraoperative protection of. See also Corneal
shield(s)
in child with craniofacial dysostoses, 137
thermal injury to, 52–53
Corneal refl ex, absence of, and facial paralysis, 126
Corneal shield(s), 52, 60
Corticosteroids, indications for, after skin resurfacing,
43–44
Cosmoderm, 12
Cosmoplast, 12
Cranioplast, characteristics of, 97, 98t
Craniosynostosis
anatomic alterations due to, complications caused by,
134–135
and hydrocephalus, 134
and intracranial pressure, 134
surgical treatment of
and air embolism, 133
anatomical considerations in, 134–135
blood loss in, 133
complications of, 132–137
and CSF leak, 135
foreign materials used in, complications due to,
135–136, 136f

Index 179
Epicanthal fold(s)
with naso-orbital-ethmoid fractures, 116–117
after upper eyelid blepharoplasty, 55
Epidermal inclusion cyst(s), in hair transplant recipient
site, 171
Epidermolysis, 32, 33f
Epinephrine
in hair restoration, 167–168
in local anesthetics, 20
in rhinoplasty, 79
Epiphora
LeFort I osteotomy and, 160
with naso-orbital-ethmoid fractures, 117
Epistaxis, postoperative, with rhinoplasty, 88
Epstein-Barr virus, keratitis, 46
Erythema
in normal wound healing, 43, 47
persistent, after skin resurfacing, 47
in scar formation, 43, 47
treatment of, 47
Etidocaine, pharmacology of, 20t
Exophthalmometer
Hertel, 113
Naugle, 113
External ear, malformations of, epidemiology of, 144
Extraocular muscle(s), dysfunction, LeFort I osteotomy
and, 160
Eye(s)
examination of, in blepharoplasty patient, 52
globe axis, 111, 111f
globe malpositions, 110
globe projection, measurement of, 113
irrigation of, during blepharoplasty, 52
management of, in facial paralysis, 126–127
Eyebrow(s). See also Brow rejuvenation
asymmetries of, 70, 70f
descent of, 50
examination of, before brow rejuvenation, 70–71
ptosis. See Brow ptosis
and upper eyelid skin redundancy, 50
youthful position of, 50
Eyelid(s)
edema, unilateral, 52
fl ap reconstruction, preoperative planning for, 31
hypesthesia, after blepharoplasty, 55
injuries to, with naso-orbital-ethmoid fractures, 117
lower. See also Lower eyelid blepharoplasty
anterior lamella
forced upward traction test, 62–64
shortening of, 62–64, 65f
vertical inadequacy, 62–64, 65f
elevation of, in facial paralysis, 127, 128
horizontal laxity, 62, 63f, 64f
management of, in facial paralysis, 126–127, 127f
middle lamella
shortening, 64–65
vertical inadequacy, 64–65
Dressing(s)
biologic, 43
with facial implant, 99
for locoregional facial fl ap, 34
and prevention of dehiscence, 35
for skin breakdown after resurfacing, 43
Drug(s). See also Medications
photosensitizing, 41–42, 41t
Dry eye syndrome
after blepharoplasty, 50, 50f, 59–60
and facial paralysis, 126
prevention of, 60
risk factors for, 59
treatment of, 60
Dura
anatomy of, 133, 133f
tears, and CSF leak, with surgical treatment of
craniosynostosis, 135
Dural sinus(es), anatomy of, 133, 133f
Dyspigmentation, after skin resurfacing, 40–42
Dysport. See Botulinum toxin
E
Ear(s). See also Microtia
postoperative complications of, 36
telephone deformity, 145, 146f
EBV. See Epstein-Barr virus
Ecchymosis, periorbital
after hair transplantation, 169
after upper eyelid blepharoplasty, 53, 53f
Eclabium, 36
Ectropion, 36
facial reanimation and, 128, 129
after skin resurfacing, 43, 44, 44f
Edema, 21
eyelid, unilateral, 52
facial, after hair transplantation, 169
nasal, after rhinoplasty, 82
prolonged, after facial implantation, 99
in skin fl ap, reduction of, 32
Education of patient(s), and eff ective communication,
8
Electrocautery
bipolar, 31, 34
in rhinoplasty, 79
corneal injury due to, in blepharoplasty, 52–53
monopolar, and fi re risk, 25
Empathy, and eff ective communication, 8
Endotine, 129
Engagement, and eff ective communication, 8
Enlistment, and eff ective communication, 8
Enophthalmos
defi nition of, 110
and diplopia, 112–113
posttraumatic, 110–111
correction of, 115
Entropion, facial reanimation and, 129

Index
180
for chin, 100–102
complications of
implant-related, 100
by material, 100, 101t
patient-related, 97–98
prevention of, 97–98
rates, 100, 101t
related to surgical technique, 98–100
by site, 100, 101t
edema with, 99
hematoma with, 98
hypersensitivity reaction to, 98
ideal, characteristics of, 97, 98t
infection with, 99–100
mandibular, 100–102
migration/extrusion, 99, 99f
nerve injury with, 99
for orbitozygomatic trauma, complications of, 114,
115f
pearls, 105
postoperative care with, 99–100
preoperative evaluation for, 97–98
preoperative photographs, 97–98
seroma with, 99
Facial nerve
buccal branch, injury to, 31
in facelift, 93
diagnostic testing, before facial reanimation, 126
frontotemporal branch, injury to, in facial
implantation, 99
injury to, 31
in bilateral sagittal-split mandibular osteotomy,
154
in endoscopic browlift, 71–72, 72f
in facelift, 93
in intraoral vertical ramus mandibular osteotomy,
156
recovery from, 93
traumatic, 119–120, 119f
management of, in surgical treatment of
craniosynostosis, 134
marginal mandibular branch, injury to
in facelift, 93, 93f
in facial implantation, 99
surgical anatomy of, in endoscopic browlift, 71–72,
72f
temporal branch, injury to, 31
in facelift, 93
zygomatic branch, injury to, 31
in facelift, 93
Facial paralysis
after bilateral sagittal-split mandibular osteotomy,
154
causes of, 125
and eyes, 126–127, 127f
and implant extrusion, 127, 127f
and lower face, 127, 128, 130–131
Eyelid(s)
lower (continued)
retraction
after blepharoplasty, 60–66
facial reanimation and, 129
volume collapse, 61–62, 62f, 63f
management of, in facial paralysis, 126–127, 127f,
128, 129
ptosis, 70, 71f
with compensatory brow elevation, 70, 70f
skin abnormalities, after upper eyelid blepharoplasty,
55
upper. See also Upper eyelid blepharoplasty
asymmetries of, 52
assessment of, 51
lagophthalmos, after blepharoplasty, 55
loading (weighting), in facial reanimation, 128, 129
management of, in facial paralysis, 126
procedures for, in facial reanimation, 128, 129
ptosis, 51–52
after facial reanimation, 128, 129
after upper eyelid blepharoplasty, 54
skin redundancy, assessment of, 50
Eye shield(s), 39, 52, 60
F
Face. See also Midface
lower
management of, in facial paralysis, 127, 128,
130–131
nerve grafts in, in facial paralysis, 127, 128, 130
sling or muscle transfer for, in facial paralysis, 127,
128, 130
soft-tissue trauma, 119–120, 119f
complications of, 119
unique signifi cance of, 1–2
Facelift
alopecia after, 94
hairline distortion after, 93–94, 94f
hematoma after, 91–92, 92f, 93f
hypesthesia after, 94
infection after, 94–95
informed consent for, 90
motor nerve injuries in, 93, 93f
parotid fi stula after, 94
pearls, 96
preoperative considerations in, 90–91
principles of, 90
sensory nerve injury in, 94
skin fl ap necrosis after, 91–92, 92f, 95
Facial implant(s)
allograft, 97
alloplastic, characteristics of, 97, 98t
autologous, 97
autologous lipotransfer for, 104–105, 104f
biocompatibility of, 97
characteristics of, 97, 98t

Index 181
planning for, 30–31
vascularity, factors aff ecting, 91
historical perspective on, 30
locoregional
advantages and disadvantages of, 29
bleeding from, 34–35
blood supply to, 32
complications of
prevention of, 29
risk factors for, 29
site-specifi c, 36
dehiscence of, 35
ischemia, 31–33, 33f
pearls, 37
preoperative planning for, 30–31
survival, improving, 32
random, 30, 32
vascular anatomy of, 30
Fleming-Mayer fl ap, for hair restoration, 172
Fluid replacement, 21
Forehead
deformity, posttraumatic, 118
length changes, after browlift, 74, 74f
Fracture(s). See also specifi c fracture
delayed union of, 107–108
healing, 106, 107–108
fi brous ingrowth in, 107–108
osteogenesis in, 107–108
Frontal bone, osteomyelitis, 118
Frontal sinus
cranialization, 118
complications of, 118
endoscopic surgery in, 118–119
fractures of, 117–119
anterior table, with or without displacement/
comminution, 118
bitabular, with signifi cant disruption of posterior
table, 118
classifi cation of, 118
complications of, 118
late presentation of, 118–119
endoscopic management of, 118–119
follow-up, 118–119
outfl ow tract involvement, with intact posterior
table, 118
treatment of, 117–119
Frontal sinusitis, 118
G
Garlic, and bleeding risk, 49
General anesthesia, 21, 23–24
Genioplasty
aesthetic concerns after, 158
chin ptosis after, 158
complications of, 157–158, 157f, 157t
Gingko, and bleeding risk, 49
Ginseng, and bleeding risk, 49
and midface, 127, 130–131
nonsurgical management of, 126
and previous radiation therapy, special
considerations for, 127
reinnervation
spontaneous, 127
techniques for, 127, 130
special considerations in, 127, 127f
Facial reanimation
browlifting in, 127–128, 128–129
complications of, 125
intraoperative, 127–128
perioperative, 128–131
postoperative, 128–131
prevention of, 125–127
lower face in, 127, 128, 130–131
lower lid elevation in, 127, 128
lower lid procedures in, 127–129
nerve repair in, 127, 128, 130
pearls, 131
planning for, 125–127, 126t
preoperative evaluation for, 125–127, 126t
principles of, 125
procedures for, 125, 125f
recurrent asymmetry after, 130
upper lid loading in, 128, 129
upper lid procedures in, 128, 129
Facial trauma
pearls, 120
in pediatric patient, pearls, 120
repair
complications of, 106–120
pearls, 120
Facial width
fi xation of mandibular fractures and, 108
increased, with orbitozygomatic fractures, 111
Fainting, in hair restoration, 167
Fat, autologous, for facial implant, 104–105, 104f
Fat embolism, 104
Fee(s), refund of, 9
Fentanyl, 20–21
Fibrin glue, indications for, 34
Fire
laser-induced, 39
surgical
prevention of, 25
risk of, 25
Flap(s)
axial, 30, 32
defi nition of, 30
facial
complications of, 30, 30f
design of, 30–31
immobilization during healing, 31
medical conditions aff ecting, 91
necrosis, 91–92, 92f, 95
pearls, 37

Index
182
pearls, 173
postprocedure care for, 169, 171
preoperative evaluation for, 166–167
recipient site
complications, 168–169
postoperative, 171–172
frontal central necrosis, 171, 171f
management of, 168–169
postoperative bleeding, 171
scabbing, 171
seborrheic plaques, 171
wound healing abnormalities, 171, 171f
results
factors aff ecting, 166
repair/revision of, 172
“super juice” and, 168, 169
techniques for, 166
transplant design for, 166–167, 172
vasovagal syncope and, 167
vertex/crown, challenges of, 167
for women, 166–167
Hashimoto’s thyroiditis, 51
Headache, intraoperative, in hair transplantation, 169
Headgear, after surgical treatment of craniosynostosis,
137
Helmet(s), after surgical treatment of craniosynostosis,
137
Hematoma
with browlift, 73
in facial reanimation, 128
epidural, in surgical treatment of craniosynostosis,
133
with facelift, 91–92, 92f, 93f, 95
with facial implant, 98
with locoregional facial fl ap, 34
lower eyelid, with facial reanimation, 129
with lower eyelid blepharoplasty, 58
superfi cial, 58, 59f
mid and lower face, with facial reanimation, 130
subdural, in surgical treatment of craniosynostosis,
133
in surgical treatment of craniosynostosis, 133
Hemorrhage. See also Bleeding
from dural sinus injury, 133
after lower eyelid blepharoplasty, 58
deep orbital, 58–59
orbital
signs and symptoms, 59
treatment of, 59
postoperative, with rhinoplasty, 88
retrobulbar
with facial fractures, 113–114
management of, 113–114, 114t
physical fi ndings with, 113
after upper eyelid blepharoplasty, 53–54
and vision loss, 113
Hemostasis, with locoregional facial fl ap, 34
Glaucoma, acute angle closure, 53
Glycolic acid peel, 40
Goal(s), of facial plastic surgery
patient’s, 5
surgeon’s, 5
Gold, for facial implant, 97
Gore-Tex
characteristics of, 97, 98t
facial implant, 100
complications of, 100, 100f
for mentoplasty, 100–102
malar implant, 102–103
nasal implant, 103, 103f
Granulomata. See also Pyogenic granuloma
with autologous lipotransfer, 104–105, 104f
browlift fi xation device and, 75, 76f
with dermal fi llers, 13, 13f, 15
eyelid, after blepharoplasty, 60, 60f
mycobacterial, 60, 60f
Great auricular nerve
injury to, 31
in facelift, 94
surgical anatomy of, 31
H
HA. See Hyaluronic acid
Hair
shock loss, after hair transplantation, 166–167, 170,
170f, 171
telogen effl uvium, after hair transplantation, 166–167,
170, 170f, 171
Hairline
browlift and, 70
design, in hair restoration, 166
distortion of
after browlift, 73–74
in facelift, 93–94, 94f
Hair restoration
alopecia reduction or fl aps in, 172, 173f
anesthesia for, 167–169
candidates for, 166
complications of, 166
intraoperative, 167–169
postoperative, 169–172
prevention of, 166–167
donor morbidity in, 168, 168f
donor site
discomfort in, 169
postoperative complications, 169–171, 170f
scarring, 168, 168f, 169, 170–171, 170f
wound dehiscence, 169
fainting in, 167
graft popping in, 168–169
hair graft handling in, 168
hair growth after, 171–172, 172t
intraoperative headache in, 169
patient expectations for, 166–167

Index 183
after facelift, 94–95
with facial implant, 99–100
intracranial, with frontal sinus fracture, 118
of malar implant, 102–103, 103f
with mandibular fracture, 106–107
of nasal implant, 103, 103f
after orthognathic surgery, 151–152
postoperative, 34f
risk factors for, 33–34
prevention of, 33–34
after rhinoplasty, 87–88
after skin resurfacing, 44–46, 44t, 45f, 46f
microbiology of, 44, 44t
risk factors for, 44
with surgical treatment of craniosynostosis, 135
after upper eyelid blepharoplasty, 54
Inferior alveolar nerve, injury to
in bilateral sagittal-split mandibular osteotomy,
153–154
in intraoral vertical ramus mandibular osteotomy, 156
Informed consent, for facelift, 90
Infraorbital nerve, injury to, 31
Intracranial pressure
elevated, and erosion of skull bones, 134, 134f, 135f
in surgical treatment of craniosynostosis, 134
Intraoral vertical ramus osteotomy. See Mandibular
osteotomy(ies), intraoral vertical ramus
Ischemia
defi nition of, 32
postoperative, of locoregional facial fl ap, 32–33, 33f, 34
Isofl urane, 21
IVRO. See Mandibular osteotomy(ies), intraoral vertical
ramus
J
Joint Commission on Accreditation of Healthcare
Organizations (JCAHO), 26
Juri fl ap, for hair restoration, 172
Juvederm Ultra, 13
Juvederm Ultra Plus, 13
K
Keloids, 35
after facelift, 95
in hair transplant donor site, 170, 170f
Kenalog, for granulomata, 15
Keratitis
corneal exposure, with facial paralysis, 126, 129
neuroparalytic, LeFort I osteotomy and, 160
risk factors for, in facial paralysis, 126
Keratoconjunctivitis sicca, 50
Keratopathy, exposure-related, in child with
craniofacial dysostoses, 137
L
Lacrimal gland
anatomy of, 51
Herbal therapy
and bleeding risk, 49
perioperative management of, 34–35, 49, 79, 91, 91t
Herpes simplex virus, infection, after skin resurfacing,
45–46, 46f
Herring’s phenomenon, 52
Hertel exophthalmometer, 113
Histamine (H2) antagonists, preoperative indications
for, 18
HSV. See Herpes simplex virus
HTS (hypertrophic scars). See Scar(s)
Hyaluronic acid
as dermal fi ller, 12–13
formulations of, 12–13
hypersensitivity to, 14
injection technique for, 15
nonanimal stabilized, 13
Tyndall eff ect with, 15
Hyaluronidase, 15
Hydrocephalus, in surgical treatment of
craniosynostosis, 134
Hydroxyapatite, for facial implant, 97, 98t
Hylaform, 13
Hylaform Plus, 13
Hyperpigmentation. See also Postinfl ammatory
hyperpigmentation
with autologous lipotransfer, 104–105, 104f
after skin resurfacing, 40
Hypersensitivity reaction, to bovine collagen, 14, 98
Hypertension
and facelift complications, 91–92
and hair transplantation, 168–169
Hypertrophic scars. See Scar(s)
Hypoglobus, 113, 113f
defi nition of, 110
posttraumatic, 111
Hypoglossal-facial nerve graft, in facial reanimation,
130
Hypophthalmos, 110, 113, 113f
Hypopigmentation, after skin resurfacing, 42
Hypotension, anesthesia-related, 21
Hypothyroidism
causes of, 51
orbital changes in, 51
Hypoventilation
intraoperative, 25
monitoring for, 18, 25
I
IAN. See Inferior alveolar nerve
Ibuprofen, perioperative management of, 79
Infantile nystagmus syndrome, in child with
craniofacial dysostoses, 137
Infection(s)
with autologous lipotransfer, 104
after browlift, 73
of chin implants, 102

Index
184
amide, 19–20, 20t
cardiovascular toxicity, 19
central nervous system toxicity, 19
duration of action of, 19, 19t
ester, 19–20, 20t
for hair transplantation, 167–168, 168–169
maximum dose of, 19, 19t
pearls, 26
pharmacology of, 20t
in rhinoplasty, 79
toxicity, 19
Lorazepam, preoperative, in hair transplantation, 167
Lower eyelid blepharoplasty
complications of, 58–66
lower eyelid retraction after, 60–66
anterior lamellar shortening and, 62–64, 65f
etiology of, 60
horizontal laxity and, 62, 63f, 64f
middle lamellar shortening and, 64–65
orbicularis paralysis and, 60–61, 61f
prominent globe and, 65–66, 66f
psychological factors and, 66
relationship of globe to its bony support and,
65–66, 66f
volume collapse and, 61–62, 62f, 63f
pearls, 67
preoperative evaluation for, 58
psychological factors and, 66
M
MAC. See Monitored anesthesia care
Macropore, in craniofacial surgery, problems related to,
136
Magnetic resonance imaging, preoperative, for surgical
treatment of craniosynostosis, 134–135
Malar fl attening, with orbitozygomatic fractures, 111
Malar implants
complication rates, 101t
complications of, 102–103, 103f
infection of, 102–103, 103f
Malassezia, in hair transplant recipient site, 171
Malignant hyperthermia, 21–22
Malignant Hyperthermia Association, 22
Malignant Hyperthermia Hotline, 22
Malocclusion
with mandibular fractures, 108–109
with maxillary fractures, 117
treatment of, 109
Mandibular fracture(s)
condylar, 108–110
bilateral, 108
in pediatric patient, 110
treatment of, 109
unilateral, 108
fi xation of, and facial width, 108
hypesthesia after, 108
and infection, 106–107
Lacrimal gland (continued)
lobes, 51
prolapse of, 51
Lacrimal system, injury to, with naso-orbital-ethmoid
fractures, 117
Lagophthalmos, after upper eyelid blepharoplasty, 55
Laryngotracheal anomalies, with craniofacial
dysostoses, 132
Laser
complications of, intraoperative, 39
fi re caused by, 39
safety precautions with, 39
skin resurfacing, complications of, 41, 42, 42f
Leech therapy, 32
LeFort I osteotomy
associated functional complications, 161
bleeding with, 158–159, 161
complications of, 158–161, 158f, 159t
maxillary malpositioning after, 158
and nasal septal deviation, 160
nasolacrimal injury with, 160
nonunion (delayed union) with, 161
ophthalmic complications of, 160
and oronasal fi stulas, 160
pearls, 162
and periodontal defects, 159–160
soft-tissue changes after, 160–161
transverse relapse after, 161
unfavorable fractures with, 161
and vascular insuffi ciency, 159
Levator aponeurosis
dehiscence of, 52
factors aff ecting, 51
function, assessment of, 51–52
intraoperative injury, in upper eyelid blepharoplasty,
54
Lidocaine
duration of action of, 19t
with epinephrine
duration of action of, 19t
maximum dose of, 19t
for hair transplantation, 167, 168–169
maximum dose of, 19t
pharmacology of, 20t
toxicity, signs and symptoms of, 167
in tumescent liposuction, 24
Lines of maximal extensibility, 30–31
Lingual nerve, injury to, in bilateral sagittal-split
mandibular osteotomy, 154
Lip deformity(ies), after skin resurfacing, 43
Liposuction, tumescent, 24
Lipotransfer, autologous, for facial augmentation,
104–105, 104f
Listening, refl ective, 7–8
LME. See Lines of maximal extensibility
Local anesthetic(s)
allergy to, 19–20

Index 185
photosensitizing, 41–42, 41t
MEDPOR, characteristics of, 97, 98t
Meningitis, with frontal sinus fracture, 118
Mental nerve, management of, in genioplasty, 157–158
Mentoplasty
implants for, 100–102
submental approach, 101
transoral approach, 101
Meperidine, 20
Mepivacaine
duration of action of, 19t
maximum dose of, 19t
pharmacology of, 20t
Mersilene
for augmentation mentoplasty, 102
characteristics of, 97, 98t
Methylparaben, 20
Metoclopramide, 18
MH. See Malignant hyperthermia
Microtia
associated abnormalities, 144
epidemiology of, 144
grading of, 144
repair
by alloplastic framework reconstruction, 145
by auricular reconstruction with costal cartilage,
144, 144f, 145f
complications of, 144–146
otoplasty for, 145–146
pearls, 146
by prosthetic reconstruction, 145
syndromic, 144
unilateral, incidence of, 144
Midazolam, 20–21
Midface, management of, in facial paralysis, 127,
130–131
Midfacial fractures, 117
Milia, 36
formation of, 55
management of, 55
natural history of, 55
after upper eyelid blepharoplasty, 55, 55f
Minimally invasive techniques. See also Botulinum
toxin; Collagen; Dermal fi ller(s); Hyaluronic
acid
complications of, 10
popularity of, 10
Miniplates, resorbable, for cranial fi xation, 135–136
MIO. See Maximal interincisal opening
MMF. See Maxillary-mandibular fi xation
Monitored anesthesia care, 23–24
pitfalls of, 25
Morbidity and mortality (M&M) conference, 3–4
MRI. See Magnetic resonance imaging
Mucocele, with frontal sinus fracture, 118
Mucopyocele, with frontal sinus fracture, 118
Muscle relaxants, 21
malunion of, 108
and nerve injury, 108
nonunion of, 108
subcondylar, 108–110
treatment of, 106
biomechanical considerations in, 106–107
Mandibular implants, 100–102
bone erosion with, 101f, 102
complications of, 102
Mandibular osteosynthesis line, 106, 107f
Mandibular osteotomy(ies)
bilateral sagittal-split
bleeding with, 154
complications of, 152–155, 152f, 152t
condylar resorption after, 154–155, 155f
nerve injury in, 153–154
and proximal segment malposition, 155
temporomandibular joint dysfunction after, 154
unanticipated fracture with, 153
unfavorable splits in, 153
body and symphysis
complications of, 156–157, 157t
and devitalization of teeth, 157
malpositioning of segments in, 156–157
periodontal defects after, 157
intraoral vertical ramus
bleeding with, 156
complications of, 155–156, 156t
condylar sag after, 155–156
inappropriate osteotomy in, 156
nerve injury in, 156
open bite deformity after, 156, 156f
pearls, 162
Mandibular surgery. See also Genioplasty; Mandibular
osteotomy(ies)
complications of, 152–158
infection after, 151
relapse after, 152
Marcaine. See Bupivacaine
Marlex mesh, characteristics of, 97, 98t
Maxillary fractures, 117
delayed union, 117
malunion, 117
nonunion, 117
Maxillary hypoplasia, and negative vector, 127, 127f
Maxillary-mandibular fi xation, 107–108, 109–110, 117
Maxillary osteotomy(ies). See also LeFort I osteotomy
anterior segmental, complications of, 161
pearls, 162
Maxillary surgery. See also LeFort I osteotomy
complications of, 158–161
infection after, 151–152
relapse after, 152
Maximal interincisal opening, 110
Medications
perioperative management of, 34–35, 79
for facelift, 91, 91t