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7 Injuries oftheCheek
Fig. 7.1 (a) Left
cheek—parotid gland,
(b) Facial nerve
rotid duct
Sublingual
gland
b
a
Parotid glan
Mandible
Temporal branch
7.2 Parotid Injury
Injuries to the parotid gland and its duct and their
surgical repair have been described in the literature for more than 100 years. The incidence is
low. Lewis and Knottenbelt (1991) found that
only 0.21% of 15,419 patients seen in a trauma
unit had a parotid gland or duct injury. Injuries to
Facial nerve
Marginal
mandibular
branch
the glandular structures are usually associated
with penetrating wounds and often involve concomitant damage to adjacent structures including
the facial nerve, the ear, and the nearby bony
structures (Van Sickels 2009). Common causes
of parotid injuries include penetrating wounds
(sharp instruments—bottle, knife) and perforating wounds (rearms). Adequate diagnosis relies
7.2 Parotid Injury
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on a thorough history, proper physical examination, and imaging studies in order to establish the
exact nature and extent of the damage. It is
important to perform a correct diagnosis and
immediate repair of all injured structures of the
parotid gland in order to avoid the formation of a
cutaneous stula or sialocele (Parekh etal. 1989;
Gahir etal. 2009).
The initial examination aims at recognizing an
injury of the parotid gland or duct, if the injury
crosses the line from the tragus to the upper lip.
The examiner searches for saliva that ows from
the wound. The injection of colored liquid after
cannulation of the intraoral duct conrms the
diagnosis if the colored liquid is seen in the facial
wound. If the test is negative, Lewkowicz etal.
(2002) suggest keeping the catheter in place for
1week. Van Sickels and Alexander (1981) classied the site of ductal injury as follows: injuries
posterior to the masseter muscle, injuries to the
masseter muscle, and injuries anterior to the masseter muscle. This classication is of prognostic
interest because a duct injury has a worse prognosis than a gland injury, with an increased risk
of complications (Parekh etal. 1989). Operative
gland repair must be performed in the acute phase
if an injury of the parotid is suspected. The injury
is treated with direct suturing of the parotid fascia. Postoperatively, some authors recommend
external pressure of the parotid for 48h, placement of an intraoral duct catheter xed to the
buccal mucosa for 2–3weeks, antibiotic prophylaxis, and frequent review to look for complications such as sepsis, sialocele, and stula (Arnaud
et al. 2006). Other authors, however, found no
signicant difference with the use of pressure
dressings (Parekh etal. 1989).
Lewis and Knottenbelt (1991) advised against
acute surgical repair, because of possible risk of
injury to the facial nerve during surgical exploration of the wound. At present, their argument is
less valid because of the progress in microsurgery and suture materials.
Occasionally, parotid injury is missed at the
time of repair of the facial laceration. Furthermore,
there are cases that salivary gland reconstruction
is limited due to considerable loss of glandular
parenchyma and rupture of capsule and duct in
various segments (Junior et al. 2012). In such
cases, a patient may present a parotid effusion
after 24h (Parekh etal. 1989); however, it is not
a well-recognized entity and is often misdiagnosed as a soft-tissue hematoma (Parekh et al.
1989). An inammatory pseudocapsule limits
further extravasation of saliva into the soft tissues, and the patient goes on to develop a sialocele or an external parotid stula. Sialoceles and
stulae are the main sequelae of parotid gland
injuries, as reported by Akinbami (2009) who
conducted a thorough literature review. An external parotid stula usually develops within the
rst week, whereas a sialocele develops
8–14 days post-injury. A careful inquiry may
conrm that both types of injury were preceded
by the development of a parotid effusion that
went unnoticed. Analysis of the uid in uncertain
cases will conrm parotid secretion due to the
very high amylase content (usually exceeding
10,000units/L) (Parekh etal. 1989).
The management of parotid stulae and sialoceles has been controversial (Parekh etal. 1989).
Several authors have used conservative management with uniform success. Landau and Stewart
(1985) reported closure of glandular injury after
5 days of conservative treatment. Parekh et al.
(1989) conducted a retrospective study of 51
patients treated for post-traumatic parotid stulae
and sialoceles. During the pilot stage of the study,
the patients were administered nothing orally for
only 5days with Pro-Banthine (anti-sialogogues)
and pressure bandage (Regimen 1). However, due
to the prolonged period required for healing of the
injury with this regimen, the patients were administered nothing orally until complete healing of the
injury (Regimen 2). In terms of the time it took for
healing of the injury, the differences of the two
regimens (24 ± 4days vs. 9.4 ± 0.9days) were
highly signicant (p<0.001). Patients with stulae that persisted beyond 8 days were provided
with parenteral nutrition (2000kcal daily) by the
peripheral route. There were highly signicant differences in the healing period between the different types of injuries. Injuries to the parenchyma or
to minor ducts healed in signicantly less time
(6.3 ± 0.07 days) compared with injuries to a
major intraparotid duct (10.3 ± 1.8days). There
68
7 Injuries oftheCheek
was signicantly greater delay with complete ductal transection (21.5 ±3.7 days) compared with
partial ductal and injury to a major intraparotid
duct (10.2±2.1days). There was no difference in
the mean period for healing between salivary stulae and sialoceles (Parekh etal. 1989).
Suppression of the salivary ow prevents the
autolysis of the soft tissues due to salivary components and avoids infections or delayed healing.
Pharmacologic inhibition of salivary secretion
has been used (Pro-Banthine, atropine) without
success (Parekh et al. 1989). Botulinum toxin
type A was reported to effectively treat Frey’s
syndrome (Bjerkhoel and Trobbe 1997). The
interest in botulinum toxin has been based on its
action in blocking acetylcholine release to reduce
salivary ow. The major secretomotor bers to
the parotid gland are cholinergic parasympathetic. Hence, it can be used as an anticholinergic
agent inlocalized treatment. Vargas etal. (2000)
reported on four patients with persistent postparotidectomy sialoceles who had undergone
various treatment failures. All four patients had
total resolution of sialocele or external salivary
stula within 1 month of treatment. No recurrences were seen after a follow-up of 7 through
13months, and there were no complications, particularly facial nerve weakness. Since then, several authors have reported successful treatment of
post-traumatic sialoceles and stulae with the use
of botulinum toxin type A (von Lindern et al.
2002; Arnaud et al. 2006, 2008; Breuer et al.
2006; Gordin etal. 2010).
Botulinum toxin must be injected into the
supercial part of the parotid gland facing the
mandibular ramus without local anesthesia but
after local asepsis, with a hollow electrode connected to an electromyograph. To avoid injecting
into the masseter, the patient’s mouth should be
closed and the teeth should be clenched (Arnaud
etal. 2006). The electromyographic signal should
be observed and must stay negative. The dose
advocated is 100IU divided among three injection points in the supercial part of the parotid
(Arnaud etal. 2006). Other authors have used a
higher dose (450MU of Dysport, Ipsen Pharma,
Ettlingen, Germany, corresponding with 150IU
of botulinum toxin type A) (von Lindern et al.
2002).
Maintenance injections of 100 IU every
3months were performed by Arnaud etal. (2006)
because of the decrease in efcacy after this
period. The injections may be given at 3-month
intervals minimum to avoid the appearance of
antitoxin antibodies, which can reduce the activity of the toxin (Arnaud etal. 2006). It can take as
long as 9 months for the symptoms to subside
(Arnaud etal. 2008) in cases of extensive gland
and/or duct injury.
Parotid gland and duct injuries which do not
respond to conservative and/or medical treatment
can be treated surgically. Cant and Campbell
(1991) reported resolve of 54% of the sialoceles
and stulae of their patients after conservative
management. The remaining cases were treated
surgically by internal drainage. Other surgical
methods which have been used include duct ligation, section of the auriculotemporal nerve of
Jacobson, and parotidectomy, excision, or cauterization of the stula (Parekh etal. 1989; Arnaud
etal. 2006). Placement of a pigtail catheter and
rapid drainage (Gahir etal. 2011) or placement of
an active vacuum drain, which is left in place for
15 days aiming to form a new salivary duct
(Junior etal. 2012), have been recently reported
in cases of sialoceles, where conservative treatment could not promote clinical resolution.
7.3 Parotid Duct Injury
Treatment of parotid duct injuries varies with the
anatomic location and type of injury involved.
The duct may be injured by sharp or blunt facial
trauma. Moderate-to-severe facial swelling or
clear drainage shortly after injury in the region of
the parotid gland or its duct should alert the clinician to its potential problems.
Lewis and Knottenbelt (1991) investigated the
outcome for nonoperative management of parotid
duct injuries conrmed with methylene blue, in
19 patients. Nine (47%) healed without complications. Short-term salivary stulas complicated
seven wounds (36.8%), and a sialocele occurred
in four (21.1%). All complications resolved
without the need for operative intervention;
therefore, the authors questioned the necessity of
surgical repair of the injured duct (Fig.7.2).
7.4 Facial Nerve Injury
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Most surgeons, however, feel that primary
repair of the injured or completely transected
Stensen’s duct is indicated. The cut ends of the
duct should be identied with the aid of a small
intravenous catheter (Arnaud etal. 2006) or an
epidural catheter (Sujeeth and Dindawar 2011)
introduced into the intraoral salivary orice. The
sutures are placed over the catheter. The material
used is usually 7-0 or 8-0 nylon. Anastomosis is
done microsurgically (Gehrking et al. 1999;
Sujeeth and Dindawar 2011). Direct end-to-end
anastomosis is possible if the defect in the duct is
less than 1cm; otherwise, an interpositional graft
is necessary. Facial vein grafts (Heymans etal.
1999; Jiang et al. 2011), fascia parotidomasse-
teric ap (Jiang etal. 2011), and supercial temporal artery grafts (Chi et al. 2013) have been
used for this purpose. Reconstruction of a traumatically avulsed parotid duct in a 4-year-old
boy with a buccal mucosa pedicle ap has been
recently reported. Short-term result of this
method was encouraging (Raveenthiran 2008).
Jiang etal. (2011) reported the results of primary
repair of the injured parotid duct in 22 patients.
One case was lost to follow-up. Nineteen cases
had a successful reconstruction with good parotid
secretions. Two cases (ca. 9%) had atrophy of the
gland.
If the proximal part of the duct is badly lacerated, radical management by clamping is indicated (Arnaud et al. 2006). The aim of this
method is to induce atrophy of the parotid gland
by the formation of scar tissue, thus preventing
complications of continuous salivary ow such
as sialocele or stula.
If a sialocele or a stula develops, treatment
principles are the same as described in section on
“Parotid Injury”.
7.4 Facial Nerve Injury
The buccal branches of the facial nerve (FN) lie
close to Stensen’s duct. They are frequently
injured in cases of parotid duct injury and should
be repaired if and whenever possible.
Injury to one or more branches of the facial
nerve should be diagnosed by physical examination (Figs.7.3 and 7.4). The latter becomes difcult in unconscious or uncooperative patients. The
location and depth of the injury may help with the
diagnosis in most cases (Vasconez 2001).
Whenever possible, immediate surgical exploration and end-to-end neurorraphy of the tran-
Fig. 7.2 Female patient 3months after injury to the left
cheek. A parotid duct injury was successfully managed
conservatively without surgical repair of the injured duct
Fig. 7.3 Female patient with an injury to the lower cheek
in the direction of the mandibular branch of the facial
nerve. Fortunately, the facial nerve was intact
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7 Injuries oftheCheek
Fig. 7.4 (a) Male
patient with a deepcutting laceration to the
right cheek. (b, c)
Postoperative pictures
1year after repair
showing normal function
of the facial nerve
a
b
c
sected branches of the extra-temporal facial nerve
should be performed. Loupe magnication or
surgical microscope is of great assistance and
should always be used. Identication of the transected nerve stumps traditionally depends mainly
on the surgeon’s experience. Use of a nerve monitoring system (nerve stimulator) facilitates, and
eventually accelerates, detecting of cut ends of
the facial nerve. The time required for detecting
and dissecting each cut end of a facial nerve
branch was reported between 6 and 15 min
(mean, 10 min) after use of such a monitoring
system (Dai etal. 2013).
When the proximal and distal stumps of the
facial nerve are available, they should be identied and repaired the earliest possible. Seventytwo hours post-injury, the neurotransmitter stores
required for motor end-plate depolarization are
irreversibly depleted and the target muscles no
longer respond to stimulation of the distal nerve
stump (Rovak etal. 2004). Limited mobilization
of the stumps is occasionally necessary, so that a
tension-free end-to-end neurorraphy can be
achieved, which is the “gold standard” technique.
The effect of surgical timing on functional outcomes of traumatic facial nerve paralysis was
investigated by Kim etal. (2010). The nal functional gains in early-operated patients were
3.7±0.59 on the House-Brackmann (HB) scale
and 75.6±10.88 on the Sunnybrook scale. The
outcome of late-operated patients was 2.17±0.52
on the HB scale and 34.7 ± 16.95 on the
Sunnybrook scale, and that of non-operated
patients was 2.0 ± 0.63 on the HB scale and
26.8±6.27 on the Sunnybrook scale. The author’s
results demonstrated that patients operated on
7.4 Facial Nerve Injury
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71
early regained considerable facial function,
whereas late exploration did not result in positive
outcomes and no difference was observed compared with conservative treatment.
Direct end-to-end coaptation of the facial
nerve and its branches should be attempted for
gaps up to 1cm. Piza-Katzer etal. (2004) raised
this limit to 1.5cm, having successfully repaired
three patients with a transected trunk and branches
of the facial nerve by removal of the supercial
part of the parotid gland. When the proximal and
distal cut stumps are clearly identiable but the
intervening gap is too wide to effect a tension-free
repair, a nerve graft is indicated. Once the stumps
have been dissected and trimmed to the level of
healthy fascicles, the nerve defect may be repaired
in an end-to-end fashion with an interpositional
free nerve graft. The greater auricular nerve, the
medial antebrachial cutaneous (Rovak etal. 2004)
or lateral antebrachial cutaneous nerve, and the
sural nerve are all acceptable donors.
Consideration should be given to nerve diameter
matchup in optimal nerve reconstruction
(McElwee etal. 2021). Grafting as early as possible obtains the best results (Barrs 1991). Possible
reasons are the ease of handling with less scarring
and nerve stump resection and a trend of axon
counts towards a lower regeneration rate in more
delayed grafts, as was shown in an experimental
study in micro-pigs (Barrs 1991).
Xg et al. (2011) reviewed a series of 104
patients who underwent surgical repair of transected peripheral facial nerve injuries. Seventytwo patients underwent primary neurorraphy, and
32 underwent facial nerve grafting. In the facial
nerve neurorraphy group, House-Brackmann
(HB) I, HB II, HB III, and HB IV function were
achieved in 56.9%, 16.9%, 23.1%, and 3.1% of
patients, respectively. The regional grades
showed that the recovery rates of HB I and II
were 27.3% in the forehead, 97.6% in the eye
region, 97.9% in the midface, and 78.6% in the
mouth region. In the facial nerve grafting group,
HB grades I, II, III, and IV were achieved in
16.7%, 20.8%, 29.2%, and 33.3% of patients,
respectively. By regional HB grades, HB I and II
rates were 37.5% in the forehead, 73.7% in the
eye region, 72.7% in the midface, and 44.4% in
the mouth region. The facial nerve anastomosis
group had a higher HB I and II recovery than
facial nerve grafting group (p=0.002). Factors
that inuenced clinical outcomes were the site
and range of facial nerve injury, the time postonset until repair, and the age of the patients (Xg
etal. 2011).
Long-term outcome after primary repair of
traumatic facial nerve injuries was investigated
by Frijters etal. (2008). Sixteen out of 27 patients
operated on for traumatic facial nerve lesions
responded to an invitation for standardized questionnaires (Facial Disability Index, Short FormHealth Survey), physical examination
(Sunnybrook Facial Grading System), and clinical photographs. The mean follow-up was
9.2years. Mean Facial Disability Index Physical
and Social scores were 86 and 81, respectively,
indicating good subjective facial functioning.
The mean Sunnybrook Facial Grading System
score was 74 indicating adequate facial functioning. Mean physical and mental health scores
(Short Form–36 Health Survey) were comparable with normative data. The results of this study
demonstrated that long-term outcome of primary
end-to-end repair of traumatic facial nerve injuries is functionally and emotionally good.
Initial facial movements after facial nerve
anastomosis or grafting were visible after
5.41± 1.80 months, whereas voluntary electromyographic activity occurred on average
4.52±1.31months after the operation (GuntinasLichius etal. 2006).
After nerve injury, an exaggerated neuroinammatory process may hinder neuron regeneration and recovery. Immunomodulation using
corticosteroids has been shown in animal studies
to improve facial nerve injury outcomes
(Lieberman etal. 2011; Seth etal. 2012). Toros
et al. (2013) used a combination of hyperbaric
oxygen (HBo) and methylprednisolone (MP) to
treat facial nerve injury in rats. Lower axonal
degeneration, lower vascular congestion, and a
larger diameter of axons were observed in the
animal group treated with combined HBO+MP
compared to animals treated with one agent only.
Another pharmacological agent having been
shown to have a benecial effect on recovery of
72
7 Injuries oftheCheek
facial nerve function is nimodipine, a calcium
channel blocker. Angelov etal. (1996) and later
Lindsay etal. (2010) demonstrated that the number of sprouted motoneurons in nimodipinetreated rats after facial nerve anastomosis was
twice as high as in the control group. Nimodipine
improved recovery of whisking after facial nerve
crush (Lindsay et al. 2010). Recently, Scheller
and Scheller (2012) reported an improved function of the facial nerve in 13 patients treated with
orally administered nimodipine. Facial nerve
function up to House-Brackmann grades I–II was
observed in all patients within a period of
2 months after the beginning of treatment
(p=0.00027).
Natural biological conduits containing seed
cells have been widely used as an alternative to
nerve grafts for nerve gap reconstruction. Recent
experimental work has shown benecial effects
on nerve regeneration and functional restoration,
and thus conduits could represent an alternative
approach for the reconstruction of facial nerve
defects. Sun etal. (2011) used artery and Wang
etal. (2011) used vein grafts and transdifferentiated mesenchymal stem cells to repair facial
nerve gaps in rats and rabbits, respectively. In
both studies, transected axon regeneration was
accelerated and remyelination was better compared to the control groups. Semere etal. (2014)
successfully used a collagen absorbable biological conduit to bridge a 1cm traumatic gap of the
buccal branch of the facial nerve. The limited
data of allografts in FN repair reveals suboptimal
outcomes compared with direct neurorraphy, but
allografts are still a feasible option when an autograft is not an option (McElwee etal. 2021).
Occasionally, facial function tends to recover
spontaneously in injuries lying medial to a line
drawn from the lateral canthus of the eye to the
lateral corner of the mouth. This could be attributed to the variable spatial arrangement of the
facial nerve, whereby individual facial muscle
bers can possess multiple motor end plates that
arise from different branches of the nerve (Rovak
et al. 2004). This duplicity in innervation and
more consistent facial nerve topography may
lead to a greater degree of recovery with more
medial, or peripheral, injuries and also contribute
to greater success with nerve repair (Rovak etal.
2004). In some cases, trigeminal neo-
neurotization may be the cause for spontaneous
return of facial function (Cheney etal. 1997).
Facial nerve repair is frequently complicated
by synkinesis (the abnormal, simultaneous contraction of a group of muscles with voluntary or
involuntary facial expression occurring when
regenerating axons innervate unintended targets)
or dyskinesis (the unintended facial muscle contractions occurring when axons inappropriately
innervate the intended target). Synkinesis can
affect eating, drinking, and speaking and can be
socially distressing because of facial asymmetry
and disruption of intended emotional expressions
(Beurskens et al. 2010). This phenomenon, however, is more likely to occur with more proximal
(intratemporal) injuries, due to a lack of funicular
structure within the intratemporal facial nerve
(Yamada etal. 2010).
When the proximal facial nerve stump is not
available for primary repair, a cross-facial nerve
graft may be employed (Scaramella 1996).
Branches of the contralateral facial nerve, usually
the one causing elevation of the upper lip, are
exposed, severed, and coapted in an end-to-end
fashion with a sural autograft 20–22 cm long.
The latter is passed through a subcutaneous tunnel in the upper lip, delivered to the contralateral
side and coapted to the contralateral nerve
branches, if the procedure can be done shortly
after the initial injury. Otherwise, it is banked in
the preauricular region in preparation for a free
muscle transfer.
Facial nerve defects that are not amenable to
repair using the ipsilateral or contralateral facial
nerve must rely on innervation from an alternative source. The hypoglossal, trigeminal, and
spinal accessory nerves have all been used; however, donor-site morbidity is high and includes
swallowing and speech problems and tongue
hemiatrophy. A pure end-to-side anastomosis
(without section of the hypoglossal nerve)
between the hypoglossal nerve and facial nerves,
using sural interpositional grafts or mobilizing
the intratemporal facial nerve to the neck, in
patients with facial palsy restored facial symmetry and tone at rest and achieved facial reanima-
7.5 Cheek Defects
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73
tion after 8 months in two patients (Koh et al.
2002). Partial tongue atrophy and tongue hemi-
paresis are still observed after end-to-side hypoglossal-facial nerve anastomosis (Venail et al.
2009).
When facial musculature has seen denervated
for more than a year, motor end plates are usually
irreversibly lost, and surgical attempts at reinnervation are usually futile. Regional muscle transfer, free muscle transfer, or simply static
procedures may be used to achieve facial symmetry, prevent drooling, and restore the patient’s
ability to express emotion with the facial musculature. New techniques including bioengineered
nerve grafts, and further research on the characteristics of the facial musculature, will contribute
to the future surgical management of facial nerve
injuries.
7.5 Cheek Defects
Traumatic cheek defects which cannot be primarily closed require tissue for closure. Patient,
defect, and potential donor site factors must be
carefully considered in the restoration of cheek
form and function. A number of techniques are
available to choose, depending also on the personal preference and experience of the reconstructive surgeon.
Small-to-moderate defects can be recon-
structed with traditional locoregional aps (e.g.,
cervicofacial ap) or newer aps and techniques
(modication of the Mustardé ap, a technique of
supercial muscular aponeurotic system plication to achieve primary closure of larger defects),
which have recently been reviewed (Jowett and
Mlynarek 2010).
Large defects usually result from gunshot
injuries. According to a classication proposed
by Clark etal. (1986), cheek defects present in
lower midface and mandible patterns of
involvement.
Gunshot injuries cause signicant soft-tissue
and bone defects. The extent of soft-tissue damage, immediately after injury, is typically not
wholly apparent (Kaufman et al. 2009). High
rates of signicant tissue necrosis, ischemia, and
infection may complicate reconstructive efforts.
An appropriate reconstructive approach involves
three stages: initial stabilization (of fractured
bones which are usually present), denitive softtissue reconstruction, and potentially secondary
renement. In the past, surgeons opted for
delayed reconstruction, whereas contemporary
efforts frequently use immediate, denitive
reconstruction (Gruss et al. 1991; Clark et al.
1986; Kaufman etal. 2009).
Initial management follows the algorithmic
advanced trauma life support (ATLS) protocol.
Maintenance of a patent airway is the primary
concern. Accurate and directed control of bleeding vessels avoids clamping critical structures.
When this is not possible, angiographic embolization by an interventional radiologist should be
carried out to denitively control the bleeding.
Neurological evaluation is a critical part of the
initial management. Cervical spine stabilization,
done at the beginning, is kept until cleared both
clinically and radiographically. A careful assessment of soft-tissue status, sensory disturbances,
and any facial nerve decits as well as a complete
ophthalmological evaluation (visual acuity, light
and red perception, ocular motility, pupillary
reactivity, examination of the conjunctiva and
eyelids) are crucial steps of the initial management. Computed tomography (CT) is the gold
standard for determining the extent of bony
injury.
Denitive reconstruction is undertaken when
the patient has stabilized (usually within 24–48h
post-injury). Gruss etal. (1991) and Clark etal.
(1986) reported favorable results after early
denitive reconstruction of extensive gunshot
wounds. These authors argued that immediate
reduction of dead space through early soft-tissue
reconstruction enhances delivery of essential
nutrients and promotes wound healing, provides
more robust biologic coverage, and improves
immunoreactivity. Furthermore, the indications
and necessity for secondary corrections are
reduced. An increased incidence of wound contracture was observed when delayed reconstruction was performed, which resulted in
signicantly more structural and functional
deformity (Vasconez etal. 1996).
74
7 Injuries oftheCheek
Initial surgical management of gunshot injuries involves decontamination and debridement
of clearly necrotic tissue. When tissue viability is
questionable, it should be allowed to heal naturally with ensuing necrotic areas debrided, if necessary, every 48h. Irrigation, eventually with a
pulsed lavage system, is recommended for more
extensive wounds or those with a great deal of
contamination (Fig.7.5).
Correction and stabilization of underlying
skeletal fractures are the next step to be undertaken. It is helpful to place the zygomatic arch
early in the procedure in order to restore the
width of the face (Gruss et al. 1991; Kaufman
etal. 2009). If a mandibular fracture is present,
reestablishing mandibular continuity and occlusion rst is advisable (Kaufman et al. 2009).
Defects larger than 5mm should be bone grafted.
Depending on the nature of the defect, iliac crest,
cranium, and rib are all reasonable options. The
use of free bula aps has been reported recently
(Pereira etal. 2012). Vascularized bone is usually
not critical for reconstruction, as long as healthy
vascularized soft tissue is used to repair the defect
(Gruss et al. 1991). Soft-tissue closure often
requires free tissue transfer. Advances in microvascular technique have established free ap
transfer as the gold standard in the reconstruction
of severe facial trauma (Gruss etal. 1991; Clark
etal. 1986; Kaufman etal. 2009). In other large
series of severe facial trauma patients, however,
only a few patients (14.2%) underwent free tissue
transfer (Pereira etal. 2012).
Traditionally, free rectus abdominis muscle
and musculocutaneous ap and omentum aps
were used for reconstruction of large cheek
defects (Gruss et al. 1991). The radial forearm
fasciocutaneous and the latissimus dorsi musculocutaneous ap have also gained popularity
(Danino etal. 2009; Sun etal. 2012). The anterolateral thigh ap is the most commonly applied
free ap in some practices (Kaufman etal. 2009).
Inherently thin, fasciocutaneous aps are highly
pliable and must accurately re-create cheek contour. The radial forearm ap has the disadvantage
of leaving an unsightly donor scar when used for
resurfacing of a large cheek area. Soft tissue-only
reconstructions tend to droop according to some
a
b
c
Fig. 7.5 (a) Female patient with heavily contaminated wound to the left cheek. A Penrose drain for irrigation was
placed during initial repair at a district hospital. (b, c) The same patient 9 and 12months postoperatively
References
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75
authors’ experience (Kaufman etal. 2009). They
postulate that it is preferable to incorporate bone
and soft tissue in composite defect reconstruction
using osteocutaneous aps, if that is possible
(Kaufman et al. 2009). Although recent reports
link denitive free ap reconstruction with a
decreased need for revisional surgery, the majority of patients still request some form of secondary corrective procedure. Besides the common
problems, like poor cosmesis from undesirable
scarring patterns, unique to this group of patients
is “skeletonization” of the reconstruction and
soft-tissue atrophy (Kaufman et al. 2009). The
temporalis muscle ap turned down has proven
to be a successful solution of adding bulk to the
cheek.
Local tissue advancement has been historically preferred; however, recent advances in
microsurgical technique have permitted distant
free ap transfers, which improve cosmesis and
function. This has resulted in a reduced number
of surgical procedures in order to achieve an
acceptable postoperative result. However, longterm functional and cosmetic complications may
still occur. A systematic algorithm is essential to
help manage these complex and diverse cheek
injuries.
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