Geoffrey 3 C. Gurtner, Peter C. Neligan, Daniel Z. Liu – Plastic Surgery-Craniofacial, Head and Neck Surgery-Pediatric Plastic Surgery. 3-Elsevier (2018)

58
SECTION I
CHAPTER 3 • Facial injuries
may be required, and in many patients turbinate outfracture,
or partial resection of enlarged turbinates, may simultane-
ously be advisable.
Synechiae may form between the septum and the turbinates
in areas where soft tissue lacerations occur and the tissues are
in contact. These may be treated by division and placement
of a Doyle splint between the cut surfaces for a period of 10–14
days.
Obstruction of the nasal vestibule may occur as a result
of malunited fractures of the pyriform margin, especially if
displaced and telescoped medially, or from overlap or lateral
displacement of the nasal septum into the ipsilateral airway.
rhinoplasty is expected for correcting deviation, irregularity,
loss of nasal height, or nasal airway obstruction.
Complications of nasal fractures
Hematomas of the nasal septum, while uncommon, may
result in subperichondrial fibrosis and thickening with partial
nasal airway obstruction. The septum in these cases may be
as thick as 1 cm in areas and may require trimming. In the
case of repeated trauma, the cartilages of the septum may be
largely replaced with calcified or chondrified material. Sub-
mucous resection of thickened portions of the nasal septum
A
B
C
Fig. 3.14  Reduction of a nasal fracture. (A) After
vasoconstriction of the nasal mucous membrane with
pseudoephedrine-soaked pledgets the nasal bones are
“outfractured” with a Boies nasal elevator. (B) The
septum is then straightened with an Asch forceps. Both
the nasal bones and the septum should be able to be
freely dislocated in each direction (C) if the fractures
have been completed. If the incomplete fractures have
been completed properly, the nasal bones may then be
molded back into the midline and remain in reduction
(D). Care must be taken to avoid placing the reduction
instruments into the intracranial space through a
fracture or congenital defect in the cribriform plate.
(E) Steri-Strips and adhesive tape are applied to the
nose, and a splint is applied over the tape. Intranasal
Doyle splints are placed inside the nose to minimize
clot and hematoma in the distal portion of the nose.
D
E

59
Midfacial fractures
presence of closed splinting may not prevent recurrent devia-
tion owing to the release of “interlocked stresses” in carti-
lage.76,77 Any external or internal deformity of significance
may require a corrective rhinoplasty.
Nasoethmoidal orbital fractures
Nasoethmoidal orbital fractures are severe fractures of the
central one-third of the upper midfacial skeleton. They com-
minute the nose, the medial orbital rims, and the pyriform
aperture. Nasoethmoidal fractures are isolated in one-third
and extended in two-thirds of cases to involve either the
frontal bone, zygoma, or maxilla. One-third are unilateral and
two-thirds are bilateral.
The central feature characterizing nasoethmoidal orbital
fractures is the displacement of the lower two-thirds of the
medial orbital rim, which provides the attachment of the
medial canthal ligament. Any fractures that separate this part
of the frontal process of the maxilla with its canthal-bearing
tendon potentially allow canthal displacement.
Surgical pathology
The bones that form the skeletal framework of the nose
are projected backward between the orbits when subjected
to strong traumatic forces. These bones form the junction
between the cranial, orbital, and nasal cavities. A typical cause
of a nasoethmoidal orbital fracture is a blunt impact applied
over the upper portion of the bridge of the nose producing a
crush in the upper central midface. The severity of the impact
or penetrating injuries may burst the soft tissues, producing
an open, compound, comminuted injury. When displacement
of the upper nose and anterior frontal sinus occur, no further
resistance is offered by the delicate “matchbox-like” structures
of the interorbital space; indeed, these structures “collapse
and splinter”.
Interorbital space
The term “interorbital space” designates an area between the
orbits and below the floor of the anterior cranial fossa. The
“interorbital space” contains two ethmoidal labyrinths, one
on each side, and consists of the ethmoidal cells, the superior
and middle turbinates, and a median thick plate of septal
bone and the perpendicular plate of the ethmoid.
Traumatic telecanthus and hypertelorism
Traumatic telecanthus is an increase in the distance between
the medial canthal ligaments. The patient has a characteristic
appearance of telecanthus, where the medial canthal liga-
ments are further apart than normal. The eyes may appear to
be further apart, simulating orbital hypertelorism.78,79 Trau-
matic orbital hypertelorism80 (as opposed to telecanthus) is a
deformity characterized by an increase in the distance between
the orbits and the ocular globe81 and requires bilateral laterally
displaced zygoma fractures in addition to bilateral nasoeth-
moidal orbital fractures.
Clinical examination
The appearance of patients who suffer nasoethmoidal orbital
fractures is typical. A significant frontal impact nasal fracture
is generally present, with the nose flattened and appearing to
Osteotomy of the bone fragments can correct displaced frac-
tures; however, contracture due to shrinkage or loss of soft
tissue lining may require excision of the scar and replacement
with mucosal or composite grafts within the nasal vestibule
or in some cases flap reconstruction.
Residual osteitis or infection of the bone or cartilage is
occasionally seen in compound fractures of the nose. These
conditions are usually treated by repeated conservative
debridements until the infected focus is completely removed.
Secondary soft tissue grafting may restore absent tissue.
Chronic pain is infrequent and usually affects the external
nasal branches of the trigeminal nerve.75
Malunion of nasal fractures is common after closed reduc-
tions, since the exact anatomic position of the bone fragments
is difficult to confirm or achieve by palpation alone, and the
A
Fig. 3.15  (A) Preoperative and (B) postoperative images of a 20-year-old male
who sustained a nasoethmoidal orbital fracture during a wrestling match.
B

60
SECTION I
CHAPTER 3 • Facial injuries
bone reduction. Therefore, canthal ligament reattachment is
required as a separate step, accomplished with its own set of
transnasal wires for each of the bone of the medial orbital rim
and then the canthus. In general, the bony reduction of the
intercanthal distance should be 5–7 mm per side less than the
desired soft tissue distance (Fig. 3.18).
Treatment of nasoethmoidal orbital fractures
Treatment consists of a thorough exposure of the nasal orbital
region by, at most, three incisions: a coronal (or an appropriate
laceration or local upper nasal incision (midline or transverse
radix), a lower eyelid incision, and a gingival buccal sulcus
incision.84 Nasal and forehead lacerations are common but
should not be extended, as the scar deformity from extension
is frequently worse than making a separate incision.
The primary principle underlying open treatment of naso-
ethmoidal orbital fractures involves the preservation of all
fragments of bone and their accurate reassembly. Despite
even anatomic reassembly of the nasal bone fragments,
primary bone grafting is usually necessary to improve the
A
Fig. 3.16  (A,B) Lateral image of 3D craniofacial computer tomography scan of a
type 1 nasoethmoidal orbital fracture injury pattern pre- and post-open reduction
and internal fixation of midface fractures using the inferior alone approach.
B
have been pushed between the eyes. There is a loss of dorsal
nasal prominence, and an obtuse angle is noted between the
lip and columella. Finger pressure on the nose may document
inadequate distal septal or proximal bony support. The medial
canthal areas are swollen and distorted with palpebral and
subconjunctival hematomas. Ecchymosis and subconjunctival
hemorrhage are the usual findings. Crepitus or movement
may be palpated when external pressure is deeply applied
directly over the canthal ligament. A “bimanual examination”
of the medial orbital rim is helpful if the diagnosis is uncertain:
it is performed by placing a palpating finger deeply over one
medial canthal ligament and placing a clamp inside the nose
with its tip directly opposite the pad of the finger. The frontal
process of the maxilla may then, if fractured, be moved
between the index finger and the clamp, indicating instability
and confirming both the diagnosis and the need for an open
reduction. The clamp, if placed under the nasal bones too
anteriorly (and not at the medial orbital rim to medial canthal
ligament attachment), erroneously identifies a nasal fracture
as canthal instability.
Radiographs
CT scans are essential to document the injury. The diagnosis
of a nasoethmoidal orbital fracture on radiographs requires at
a minimum four fractures that isolate the frontal process of
the maxilla from adjacent bones. These include (1) fractures
of the nose, (2) fractures of the junction of the frontal process
of the maxilla with the frontal bone, (3) fractures of the medial
orbit (ethmoidal area), and (4) fractures of the inferior orbital
rim extending to involve the pyriform aperture and orbital
floor. These fracture lines, therefore, define the “central frag-
ment” of bone bearing the medial canthal ligament as “free”
and, depending on periosteal integrity, may displace the
medial orbital rim.
Classification of nasoethmoidal orbital fractures
Nasoethmoidal fractures are classified according to a pattern
established by Markowitz and Manson82 types I–III, according
to the bimanual examination and the CT scan.83
Type I is an incomplete fracture, mostly unilateral but
occasionally bilateral, which is displaced only inferiorly at the
infraorbital rim and piriform margin. Inferior alone approaches
(gingival buccal sulcus +/− inferior orbit) are necessary
(Fig. 3.16).
Type II nasoethmoidal orbital fractures are comminuted
nasoethmoidal fractures with the fractures remaining outside
the area of the canthal ligament insertion. The central frag-
ment may be managed as a sizable bony fragment and
united to the canthal ligament-bearing fragment of the other
side with a transnasal wire reduction. The remainder of the
pieces of the nasoethmoidal orbital skeleton are reduced and
then stabilized by junctional plate and screw fixation to the
frontal bone, the infraorbital rim, and the Le Fort I level of
the maxilla. Type II fractures may be unilateral or bilateral
(Fig. 3.17).
Type III nasoethmoidal orbital fractures either have avul-
sion of the canthal ligament (uncommon) or the fractures
extend underneath the canthal ligament insertion. The frac-
ture fragments are small enough that a reduction would
require that the canthus be detached to accomplish the

61
Midfacial fractures
Fig. 3.17  (A) Frontal 3D craniofacial computer tomography scan of a type II nasoethmoidal orbital fracture injury pattern in a 23-year-old female who sustained craniofacial
injuries following being struck by a motor vehicle as a pedestrian. (B) Pre- and post-open reduction and internal fixation of midface fractures. (C) Postoperative frontal
photograph view of patient approximately 12 months from surgery.
A
B
C
laterally and brought clearly into the surgeon’s view laterally
and next to the nasal bones, where its superficial position
allows turning of the fragment; in this position, drilling and
wire pass through the “central” fragment. Nasal bone frag-
ments can be temporarily dislocated or removed to permit
better exposure of the medial orbital rim segments. Removing
the nasal bones is especially helpful in passing a transnasal
wire from the posterior and superior aspect of one “central”
fragment (medial orbital rim canthal bearing bone fragment)
to the other. The medial orbital rims are then replaced in
anatomic position and then linked with fine wires to adjacent
nasal and frontal bone fragments. Following the placement of
two transnasal wires, one should pass one extra wire per side,
for soft tissue reapproximation to bone. Junctional plate and
screw fixation at the periphery of these reassembled frag-
ments is employed after the initial interfragment wiring is
nasal height and to provide smooth dorsal contour. The bone
onto which the canthal ligament is attached (if comminuted)
may require replacement with a bone graft.
The importance of the “central fragment” in
nasoethmoidal orbital fractures
First, identify and classify what is happening to the bone of
the medial orbital rim which bears the medial canthal liga-
ment as there is a direct relationship between surgical tech-
niques, simplicity of surgery, and outcome of the treatment.
The most essential feature of a nasoethmoidal reduction is
the transnasal reduction of the medial orbital rims by a wire
placed posterior and superior through the bone of the canthal
ligament insertion. The medial orbital rim with its attached
canthal-bearing segment is first dislocated anteriorly and
Fig. 3.18  (A) Frontal 3D craniofacial computer tomography scan of type III nasoethmoidal orbital and a Le Fort II type injury pattern in a 33-year-old who sustained
craniofacial injuries following being thrown off a motorcycle without a helmet. (B) Pre- and post-open reduction and internal fixation of midface and mandibular fractures.
(C) Postoperative frontal photograph view of patient 6 months from surgery.
A
B
C

62
SECTION I
CHAPTER 3 • Facial injuries
zygomatic bone has a quadrilateral shape with several pro-
cesses that extend to reach the frontal bone, the maxilla, the
temporal bone (zygomatic arch), and orbital processes.
Physical diagnosis and surgical pathology of
zygoma fractures
Although the zygoma is a sturdy bone, it is frequently injured
because of its prominent location. Moderately severe blows
are absorbed at the malar eminence and transferred to its
buttresses. Severe blows may cause separation of the zygo-
matic body at its articulating surfaces; these high-energy
injuries dramatically increase the width of the midface. As the
zygoma is disrupted, it is usually displaced in a downward,
medial, and posterior direction, whereas high-energy injuries
displace the zygoma in a posterior and lateral direction
because of disruption of the ligaments in addition to the
fractures. The direction of displacement varies with the direc-
tion of the injuring force and with the pull of the muscles,
such as that of the masseter.
Periorbital and subconjunctival hematomas are the
most accurate physical signs of the orbital fracture always
associated with a complete zygoma fracture. Numbness of
the infraorbital nerve is a common symptom as well. The
infraorbital nerve runs in a groove in the posterior portion
of the orbit and enters a canal in the anterior third of the
orbit, behind the infraorbital rim.90 It may be crushed in a rim
fracture with medial displacement, as the fracture occurs in
the weak area of bone penetrated by the infraorbital foramen.
Direct force to the lateral face may result in isolated frac-
tures of the temporal extension of the zygoma (zygomatic
arch) and the zygomatic process of the temporal bone in the
absence of a fracture of the remainder of the zygoma and its
articulations.
Medial displacement of an isolated arch fracture is usually
observed and may impinge against the temporalis muscle and
coronoid process of the mandible resulting in restricted man-
dibular motion. Fractures in the posterior portion of the
zygomatic arch may enter the glenoid fossa and produce
stiffness or a change in occlusion because of the swelling in
the joint or muscles. In high-energy injuries or gunshots, frag-
ments of bone can be driven through the temporal muscle and
make contact with the coronoid process and precipitate the
formation of a fibrous or bony ankylosis, necessitating exci-
sion of the bone of the coronoid process and scar tissue as a
secondary procedure.
Fracture dislocation of the zygomatic body with sufficient
displacement to impinge on the coronoid process requires
considerable backward dislocation of the malar eminence.
Level discrepancies or step deformities at the infraorbital
margin can usually be palpated in the presence of inferior
orbital rim displacement. The lateral and superior walls of the
maxillary sinuses are involved in fractures of the zygoma, and
torn maxillary sinus lining results in bleeding within the sinus
with unilateral epistaxis. The lateral canthal attachment is
directed towards Whitnall’s tubercle, located approximately
10 mm below the zygomaticofrontal suture, which is a shallow
eminence on the internal aspect of the frontal process of the
zygoma. When the zygoma is displaced inferiorly, the lateral
attachment of the eyelids via the lateral canthal ligament
is also displaced inferiorly giving rise to an antimongoloid
slant of the palpebral fissure. The globe follows the inferior
tightened. It should be emphasized that the transnasal reduc-
tion wires must be passed posterior and superior to the lacri-
mal fossa in order to provide the proper direction of draping
force necessary to create the preinjury bony position and
shape of the canthal ligaments. The transnasal reduction is not
a “transnasal canthopexy”, as it does not involve the canthal
ligament per se. It is a reduction only of the “central bony
fragment” of the nasoethmoidal orbital fracture.
Canthal reattachment
If the canthal ligament requires reattachment (the canthal
tendon is rarely stripped from bone), the canthal tendon85 may
be grasped by one or two passes of 2-0 nonabsorbable suture
adjacent to the medial commissure of the eyelids through a
2–3 mm horizontal incision in the skin directly over the
canthal ligament.86 The 2-0 nonabsorbable suture is then
passed into the internal aspect of the coronal incision, and the
suture is then connected to a separate set of #28 transnasal
wires per side that have been passed transnasally superiorly
and posteriorly to the expected position of the medial canthus.
The transnasal canthal ligament wires are tightened only as
the last step after the bone reduction, and after medial orbital
and nasal bone grafting are completed. Each set of canthal
wires is tightened gently after a manual reduction of the
canthus to the bone with forceps is performed, to reduce stress
on the ligament by the canthal sutures. Each canthal reduction
wire pair is then separately twisted over a screw in the frontal
bone.
Lacrimal system injury
Interruption of the continuity of the lacrimal apparatus
demands specific action. Most lacrimal system obstruction
occurs from bony malposition or damage to the lacrimal
sac or duct.87 The most effective treatment involves initial
satisfactory precise repositioning of fracture segments to
the bony part of the lacrimal system. If transection of the
soft tissue portion of the canalicular lacrimal system has
occurred, it should be repaired over fine silicone tubes with
magnification.88
Complications of nasoethmoidal orbital fractures
The early diagnosis and adequate treatment of nasoethmoidal
orbital fractures achieves optimal aesthetic results with the
lowest number of late complications. Depending on the
quality of initial treatment and the results of healing, further
reconstructive surgery may be required in some cases. Late
complications, such as frontal sinus obstruction, occur in less
than 5% of isolated nasoethmoidal orbital fractures where
damage to the anterior frontal sinus walls has not occurred.
Deformities and nasal functional impairment are late compli-
cations, which can be minimized by early diagnosis and
proper early open reduction. The presence of a nasoethmoidal
orbital fracture may be obscured by the swelling and escape
detection. After several weeks, nasal deformity and enoph-
thalmos are evident.89
Fractures of the zygoma
The zygoma is a major buttress of the midfacial skeleton. It
forms the malar eminence, giving prominence to the cheek,
and forms the lateral and inferior portions of the orbit. The

63
Midfacial fractures
entry of elevators into the orbit as the maxilla and zygoma are
dissected. The infraorbital nerve is protected by the dissection
and is immediately seen after detaching the levator anguli
oris muscle. The zygoma may often be reduced by placing the
tip of an elevator in the lateral aspect of the maxillary sinus
directly behind the malar eminence and levering the body of
the zygoma first outward and then forward. Alternately, a
Carrol–Girard screw (Walter Lorenz Co., Jacksonville, FL) can
be placed in the malar eminence through a percutaneous inci-
sion and manipulated. In gingival buccal sulcus approaches,
after the reduction maneuver has been completed, zygomatic
stability depends upon an incomplete fracture at the zygo-
maticofrontal suture. The floor of the orbit can be inspected
with an endoscope through the maxillary sinus. It is also
possible to tell from a preoperative CT the degree of orbital
floor comminution. Fractures with orbital floor comminution
and significant displacement require an additional inferior
orbital approach.
Fractures with zygomaticofrontal (Z-F) suture diastasis
If the Z-F suture demonstrates diastasis, direct exposure of the
suture permits stabilization through the lateral portion of an
upper blepharoplasty incision (<1 cm) which is made directly
over the Z-F suture 8–10 mm above the lateral canthus. Pal-
pating the frontal process of the zygoma between the thumb
and index finger, the junction of the zygoma with the frontal
bone can be marked precisely in eyelid skin. The incision
should be short and never progress laterally out of the eyelid
skin, as it will scar noticeably. Alternately, the Z-F suture may
be approached through a laceration or by superior dissection
from a subciliary or conjunctival lower lid incision by canthal
detachment. The inferior portion of the orbit may be
approached through a midtarsal, subciliary, or conjunctival
incision. The conjunctival fornix incision produces the least
cutaneous scarring, but the exposure may be restricted by fat
prolapse. The treatment of a zygoma fracture has recently
become quite specific and directed only at areas that require
open reduction for confirmation of alignment or for fixation
(Fig. 3.19).
displacement of the zygoma with a lower (inferior and lateral)
position after fracture dislocation. Double vision is usually
transient in uncomplicated fractures of the zygoma, which
always involve the orbital floor. Diplopia may persist when
the fracture is more extensive, especially if a fracture com-
minutes the inferior orbital floor. Diplopia may result from
muscle contusion, incarceration of perimuscular soft tissue or
actual muscle incarceration (rare in zygoma fractures), or
simply drooping of the muscular sling.
Anterior approaches
The anterior approach may be partial or complete and poten-
tially involves up to three incisions: (1) access to the zygomati-
cofrontal suture; (2) access to the inferior orbital rim; and (3)
access to the zygomaticomaxillary buttress, anterior maxilla,
and malar prominence.
Twenty-five percent of complete fractures of the zygoma
are undisplaced or have such subtle displacement that they
do not benefit from an open reduction. Thirty-five percent of
fracture dislocations of the zygoma result in greensticked
fractures at the zygomaticofrontal suture, and these may be
reduced with a gingivobuccal sulcus incision alone without
exposure of the suture. Forty percent of fracture dislocations
of the zygoma result in complete separation at the zygomati-
cofrontal suture, which may be palpable through the skin over
the upper lateral margin of the orbit. The latter fractures
require exposure through an incision directly over the suture,
i.e., the lateral limb alone of an upper lid blepharoplasty.
Orbital rim and orbital floor exposures may be necessary
based on the fracture patterns visualized on preoperative CT
scans.91
“Minimalist” approaches for fractures without
zygomaticofrontal suture diastasis
In this approach, the gingivobuccal sulcus is opened and the
anterior face of the maxilla and zygoma are degloved. The
infraorbital rim and infraorbital nerve are visualized from an
inferior direction. Palpation with a finger on the rim avoids
Fig. 3.19  (A,B) Frontal 3D craniofacial computer tomography scan of a right zygomaticomaxillary fracture in a 22-year-old male who sustained craniofacial injuries
following a sports-related injury, pre- and post-open reduction and internal fixation of the right zygomaticomaxillary complex and orbital floor fractures. (C) Postoperative
frontal photograph view of patient 3 months following surgery.
A
B
C

64
SECTION I
CHAPTER 3 • Facial injuries
include medial displaced isolated arch fractures and simple
large segment or single piece zygoma fractures in which the
displacement is medial and posterior, without comminution
at the buttresses, and where the fracture at the Z-F suture is
incomplete and nondisplaced. An elevator placed beneath the
malar eminence allows the zygoma to be “popped” back into
position. Palpation is the guide to reduction, such as the
inferior orbital rim. The stability of closed reduction depends
on the integrity of periosteal attachments and principally
“greensticking” at the Z-F suture. The force of contraction
of the masseter muscle may act to create postoperative
displacement.92
Displacement at the Z-F suture93 comminution of the infe-
rior orbital rim or Z-M buttress and lateral displacement of
the zygomatic arch and body are characteristics that were
found to predict a poor result from closed reduction.
Buttress articulations and alignment for complete
open reduction
Six points of alignment with adjacent bone may be confirmed
with complete craniofacial exposures: Z-F suture, infraorbital
rim, zygomaticomaxillary buttress, greater wing of the sphe-
noid, orbital floor, and zygomatic arch. The orbital floor may
require reconstruction with bone or artificial materials such
as Medpor or titanium mesh.
Methods of reduction
The first step that should be considered in complete open
reductions is passing an osteotome through the Z-F suture
after exposing it, mobilizing and thoroughly completing all
fractures. This step is the most neglected step in open reduc-
tion internal fixation (ORIF) of zygomas and routinely simpli-
fies the rest of the reduction.
Reduction through the maxillary sinus
Next, the body of the zygoma is mobilized by displacing it
laterally, completing fractures and achieving free displace-
ment and mobility. A Carroll–Girard screw (Walter Lorenzo,
Jacksonville, FL) may be utilized percutaneously or from an
intraoral approach providing leverage to manipulate the
zygoma. This approach is used by persons who do not com-
plete the fractures.
Temporal approach
A temporal approach for the reduction of zygomatic fractures
was described by Gilles. An elevator is slipped along the
muscle behind the zygomatic arch or under the malar emi-
nence, depending on the areas of reduction required. A small,
2-cm incision placed vertically within the temporal hair heals
with an inconspicuous scar. The elevator must be placed deep
to the deep temporal fascia, visualizing the temporalis muscle.
The bone may be palpated with one hand to document the
accuracy of reduction, while the other hand guides the eleva-
tor into position and corrects the displacement by force
application. Gentle elevation often “clicks” the arch into posi-
tion. Moving the elevator back and forth with repeated eleva-
tion movements may disrupt the periosteum holding arch
fragments together, and an open reduction is then required.
The approach can also be used for reduction of the zygomatic
body.
Coronal incisions (posterior approach)
Fractures with extreme posterior displacement and those with
lateral displacement of the zygomatic arch often benefit from
the addition of a coronal incision. These represent 5% of iso-
lated zygoma fractures. The coronal incision allows exposure
of the entire zygomatic arch, roof of the glenoid fossa, the Z-F
suture, and the lateral orbital wall, which is the area that
confirms proper alignment and medial position of the zygo-
matic arch (Fig. 3.20).
Treatment of fractures of the zygoma
Closed reduction
Remotely, closed reduction techniques were employed for
most zygomatic fractures. In practice, many fractures can be
treated reasonably with closed reduction, and especially
where cost is an issue, this treatment would have to be con-
sidered. Those fractures still amenable to closed reduction
A
Fig. 3.20  (A) Frontal 3D craniofacial computer tomography scan of a high energy
orbito-zygomaticomaxillary complex injury in a 33-year-old who sustained
craniofacial injuries following a high speed motor vehicle collision. (B) Pre- and
post-open reduction and internal fixation of the left orbital and zygomaticomaxillary
complex through anterior and posterior (coronal) approaches.
B

65
Midfacial fractures
Plate and screw fixation then unites the segments. In fractures
treated late, the masseter muscle may require division or
mobilization from the inferior surface of the malar eminence
and arch in order to allow the bone to be repositioned supe-
riorly. The masseter muscle contracts in the case of the malre-
duced fracture and may block reduction. Fractures treated
with delay are more safely treated with osteotomy than force-
ful mobilization by blunt forces, which may result in new
undesirable fracture lines radiating into the apex of the orbit,
with cranial nerve injury (blindness).
Complications of zygomatic fractures
Bleeding and maxillary sinusitis
Bleeding into the maxillary sinus is usually of short duration.
It is always prudent to irrigate blood clots from the antrum
and to remove bone fragments, which drop from the orbital
floor and sequester. Rarely, the ostea of the maxillary sinus
will be occluded by the fractures and require endoscopic sinus
surgery. In those patients with pre-existing sinus disease,
acute exacerbation may be a complicating factor.
Late complications
Late complications of zygomatic fractures include nonunion,
malunion, double vision, infraorbital nerve anesthesia or
hypesthesia, and chronic maxillary sinusitis. Scarring may
result from laceration or malpositioned incisions. Generally,
ectropion and scleral show are mild and resolve spontane-
ously. Gross downward dislocation of the zygoma results in
diplopia and orbital dystopia. Usually, more than 5 mm of
inferior globe dystopia is required to produce diplopia. Treat-
ment97 involves zygomatic mobilization by osteotomy with
bone grafting to augment the malar eminence when malar
projection is deficient. The position of the eye must be restored
with intraorbital bone grafts or alloplastic material. Infection
is not common, and usually responds to antibiotics and sinus
or lacrimal drainage.
Impacted fractures of the zygomatic arch which abut the
coronoid process may result in ankylosis. A gunshot wound
is especially prone to this problem. If the zygomatic arch
cannot be repositioned, coronoidectomy through an intraoral
route usually frees the mandible from the ankylosis and
permits normal function. It is important that the patient vigor-
ously exercise to preserve and improve the range of motion
obtained, which may take 6 months.
Orbital complications
Orbital complications consist of diplopia, visual loss, globe
injury, enophthalmos or exophthalmos, and lid position
abnormalities.
Numbness
Persistent anesthesia or hypesthesia in the distribution of the
infraorbital nerve usually lasts only a short time. If total
anesthesia exists for over six months, it is likely that the nerve
is severely damaged or perhaps transected. If the nerve is
impinged by bone fragments, especially in a medially and
posteriorly impacted zygoma fracture, reduction or decom-
pression of the infraorbital canal and neurolysis are sometimes
indicated. Bone spurs or constricting portions of the canal
should be removed so that the nerve has an adequate
Fixation required to achieve stability
Several individuals have examined zygomatic stability fol-
lowing open reduction. Rinehart and Marsh94 studied cadaver
heads and used 1, 2, or 3 miniplates and accessed stability of
non-comminuted zygoma fractures submitted to static and
oscillating loads to simulate the effect of the masticatory
apparatus on postoperative displacement. Neither single
miniplate nor triple wire fixation was enough to stabilize the
zygoma against simulated masseter forces; however, 3 mini-
plates were sufficient, which stabilized the Z-F, Z-M, and
infraorbital rim areas.
Del Santo and Ellis felt that Rinehart and Marsh overesti-
mated the postoperative forces that could be generated by the
masseter muscle and suggested that stability with less than 3
plates would be possible, based upon actual human measure-
ments of bite forces after zygomatic fracture treatment.92
Surgical techniques for fixation following reduction
The authors’ approach varies depending on the complexity of
zygoma fracture pattern and the extent of involvement of the
orbital floor, which can be assessed using preoperative CT
scan.95
If there is minimal involvement of the orbital floor and
no diastasis at the Z- suture, the zygoma is approached
intraorally at the zygomaticomaxillary buttress. It is reduced
using one of the techniques described above, and one plate
fixation technique is sufficient using an L-shaped plate at
the zygomaticomaxillary buttress. If there is diastasis at the
Z-F fracture line, then a short (1 cm) upper blepharoplasty
incision exposes the Z-F fracture line, a portion of the lateral
orbital wall, and the zygomaticosphenoid suture line. Here,
the zygoma has its broadest articulation with the greater wing
of the sphenoid, and therefore direct visualization may be
helpful in confirming anatomical reduction of the zygoma.
Since one can only look through one incision at a time, the
use of temporary interfragment wire positioning at the Z-F
fracture line while holding the zygoma into correct anatomi-
cal reduction at the zygomatic–sphenoid fracture line, inferior
orbital rim, and zygomaticomaxillary buttress allows relative
positioning of the zygoma fracture. The zygomaticomaxillary
buttress followed by the Z-F fracture line may then be plated
sequentially.
In the authors’ experience, the judgment of whether to
open the lower lid rests upon whether (1) there is a large
orbital floor fracture component of the zygoma fracture that
requires replacement, or (2) there remains a significant step-
off at a comminuted inferior orbital rim following fracture
reduction. A lower eyelid transconjunctival incision without
lateral canthoplasty allows reduction and fixation with a low
profile inferior orbital rim plate +/− an orbital floor plate.
Periosteal resuspension of the lower eyelid and cheek is criti-
cally important should eyelid exposure be utilized.96
Delayed treatment of fractures of the zygoma
Repositioning after two weeks frequently requires osteotomy
of the fracture sites to mobilize the zygoma for reduction.
After the bone has been mobilized, an inspection of each
fracture site should be conducted to remove any area of
fibrous ankylosis or any proliferative bone, which was not
present originally, as its presence may prevent proper align-
ment. Rarely, resorption has occurred requiring bone grafting.

66
SECTION I
CHAPTER 3 • Facial injuries
gestive of fractures involving the maxillary bone. The swell-
ing is usually moderate to severe indicating the severity of the
fracture. Malocclusion with an anterior open bite and rotation
of the maxilla suggest a fracture of the maxilla. The maxillary
segment is frequently displaced downward and posteriorly,
resulting in a class III malocclusion and premature occlusion
in the posterior dentition with an anterior open bite. On inter-
nal examination, there may be tearing of the soft tissues in the
labial vestibule of the lip or the palate, findings that indicate
the possibility of an alveolar or palate fracture. Hematomas
may be present in the buccal or palatal mucosa. The face, after
several days, may have an elongated, retruded appearance,
the so-called “donkey-like faces” suggestive of a craniofacial
disjunction. An increase in midfacial length is seen.
Palpation
The bone should be palpated with the tips of the fingers both
externally through the skin and internally intraorally. Bilateral
opportunity for regeneration and relief of pressure. The nerve
must be explored throughout the floor of the orbit so that it
is free from any compression by bone fragments, scar tissue,
or callus. The functional results of this surgery in terms of
pain relief remain unclear.
Anesthesia can be annoying for patients, especially
immediately after the injury. Patients generally partially
accommodate to the neurological deficit. Some spontaneous
reinnervation may occur from adjacent facial regions as well
as regrowth of axons through the infraorbital nerve. Usually
some vague sensation is then present.
Oral–antral fistula
An oral–antral fistula requires debridement of bone or mucosa,
confirmation of maxillary sinus drainage into the nose, and
closure with a transposition mucosal flap for cover. A 2-layer
closure is required. A bone graft may be placed in between
the layers of soft tissue. The buccal fat pad can be mobilized
and sewn into the defect prior to the mucosa being closed over
it. Rarely, a distant flap is required for difficult persistent
fistulae.
Plate complications
Complications include screw loosening or extrusion, plate
exposure requiring removal, and tooth root penetration by
screws. Prominent plates over the zygomatic arch are directly
due to associated soft tissue atrophy (temporalis) and to
malreduction of the zygomatic arch laterally. Probably 10% of
plates placed at the LeFort I level need to be removed for
exposure, non-healing wound, or cold sensitivity. Plate
prominence at the Z-F suture are due to inadequate soft tissue
closure and poor plate selection.98
Midface buttresses
The midface is a system of sinus cavities where certain thicker
areas (or buttresses) provide considerable structural support.
The important midface supporting skeleton consists of hori-
zontal and vertical structural supports connected by thin
plates of bone. In fracture treatment, the thicker pillars are
anatomically reconstructed and repositioned to re-establish
the preinjury facial bone architecture. The vertical supports
consist of the nasal septum in the midline and the nasomaxil-
lary, zygomaticomaxillary, and pterygoid buttresses (Fig.
3.21). The nasomaxillary buttress extends along the pyriform
aperture through the frontal process of the maxilla superiorly
to the internal angular process of the frontal bone. The zygo-
maticomaxillary buttress extends through the bony mass of
the body of the zygoma and through the frontal process of the
zygoma to the external angular process of the frontal bone.
Posteriorly, the pterygoid plates provide posterior stabiliza-
tion of the vertical height of the midface to the skull base.99
The horizontal buttresses of the midface consist of the inferior
orbital rims and the associated orbital floor, the zygomatic
arch and the palate at the level of the maxillary alveolus.100
Clinical examination
Inspection
Epistaxis, bilateral ecchymosis (periorbital, subconjunctival,
scleral), facial edema, and subcutaneous hematoma are sug-
Fig. 3.21  The vertical buttresses of the midfacial skeleton. Anteriorly, the
nasofrontal buttress skirts the piriform aperture inferiorly and composes the bone of
the medial orbital rim superiorly to reach the frontal bone at its internal angular
process. Laterally the zygomaticomaxillary buttress extends from the zygomatic
process of the frontal bone through the lateral aspect of the zygoma to reach the
maxillary alveolus. A component of the zygomaticomaxillary buttress extends
laterally through the zygomatic arch to reach the temporal bone. Posteriorly, the
pterygomaxillary buttress is seen. It extends from the posterior portion of the maxilla
and the pterygoid fossa to reach the cranial base structures. The mandibular
buttress forms a strong structural support for the lower midface in fracture
treatment. This support for maxillary fracture reduction must conceptually be
achieved by placement of both jaws in intermaxillary fixation. The other “transverse”
maxillary buttresses include the palate, the superior orbital rims, and the inferior
orbital rims. The superior orbital rims and the lower sections of the frontal sinus are
also known in the supraorbital regions as the frontal bar and are technically frontal
bone and not part of the maxilla. (From Manson PN, Hoopes JE, Su CT. Structural
pillars of the facial skeleton: an approach to the management of Le Fort fractures.
Plast Reconstr Surg. 1980;66:54.)
Frontal
attachment
Orbital
buttress
Nasoethmoid
region
Nasofrontal
buttress
Zygomatic
buttress
Pterygomaxillary
buttress
Cranial
base
Mandibular
buttress

67
Le Fort classification of facial fractures
these teeth. The position of the teeth may be maintained by
ligating the teeth in the fractured segment to adjacent teeth
with the use of an arch bar and interdental wiring technique.
Fixation of the alveolar segment should be maintained for at
least six to twelve weeks, until clinical immobility has been
achieved.105
Le Fort classification of facial fractures
Le Fort (1901) completed experiments that determined the
areas of structural weakness of the maxilla which he desig-
nated “lines of weakness” where fractures occurred. Between
the lines of weakness were “areas of strength”. This classifica-
tion led to the Le Fort classification of maxillary fractures,
which identifies the patterns of midfacial fractures (Fig.
3.22).106 It should be emphasized that the usual Le Fort fracture
consists of combinations of these patterns in that pure bilateral
Le Fort I, Le Fort II, or Le Fort III fractures are less common
than combination patterns.107 The level of fracture is frequently
higher on one side than the other, and usually the fracture is
more comminuted and extensive on the side of the direct
injury.
Goals of Le Fort fracture treatment
Goals in the treatment of Le Fort fractures include:
1. Restoration of midfacial height and projection.
2. Achieve proper occlusion.
3. Restore the integrity of the nose and orbit.
The structural supports between the areas of the buttresses
and maxillary alveolus are restored to provide proper soft
tissue contour.
Transverse (Guerin) fractures or Le Fort I
level fractures
Fractures which traverse the maxilla horizontally above the
level of the apices of the maxillary teeth section the entire
alveolar process of the maxilla, vault of the palate and the
inferior ends of the pterygoid processes in a single block from
the upper craniofacial skeleton. This type of injury is known
as the transverse, Le Fort I, or Guerin fracture. This horizontal
fracture extends transversely across the base of the maxillary
sinuses and is usually bilateral. The fracture level varies from
just beneath the orbital rim of the zygoma to just above the
floor of the maxillary sinus and the inferior margin of the
pyriform aperture (Fig. 3.23).
Pyramidal fractures or Le Fort II
level fractures
Blows to the central maxilla, especially those involving frontal
impact, frequently result in fractures with a pyramidally
shaped central maxillary segment. This is a Le Fort II “central
maxillary segment”, and the fracture begins above the level
of the apices of the maxillary teeth laterally and posteriorly in
the zygomaticomaxillary buttress and extends through the
pterygoid plates in the same fashion as the Le Fort I fracture.
Fracture lines travel medially and superiorly to pass through
the medial portion of the inferior orbital rim and extend
across the nose to separate a pyramidally shaped central
palpation may reveal step deformities of the zygomaticomax-
illary suture, indicating fractures of the inferior orbital rims.
These findings suggest a pyramidal fracture of the maxilla
and confirm the zygomatic component of a more complicated
injury, such as a Le Fort III fracture. Intraoral palpation may
reveal fractures of the anterior portion of the maxilla or frac-
tured segments of the alveolar bone.
Digital manipulation
Manipulation of the maxilla may confirm movement in the
entire middle third of the face, including the bridge of the
nose. This movement is appreciated by holding the head
securely with one hand and moving the maxilla with the other
hand (see Fig. 3.5). Crepitation may be heard when the maxilla
is manipulated in loose fractures. The manipulation test for
maxillary mobility is not entirely diagnostic because impacted
or greenstick fractures may exhibit no movement but still
possess bone displacement and malocclusion.
Malocclusion of the teeth
If the mandible is intact, malocclusion of the teeth is highly
suggestive of a maxillary fracture. It is possible, however, that
malocclusion relates to a preinjury condition. A thorough
study of the patient’s dentition and dental models and refer-
ence to previous dental records and pictures are helpful.
Cerebral spinal rhinorrhea or otorrhea
Cerebral spinal fluid may leak from the anterior or middle
cranial fossa in high Le Fort fractures and is then apparent in
the nose or ear canal. A fluid leak signifies the presence of a
dural fistula extending from the intracranial subarachnoid
space through the skull and into the nose, pharynx or ear.101
Frequently the drainage is obscured by bloody secretions in
the immediate postinjury period.102,103
Radiological examination
Maxillary fractures are easily demonstrated in craniofacial CT
scans, with the exception that fracture lines in minimally
displaced fractures are more difficult to image. The presence
of bilateral maxillary sinus fluid should always suggest the
possibility of a maxillary fracture.
Treatment of maxillary fractures
Treatment of maxillary fractures is initially oriented toward
the establishment of an airway, control of hemorrhage, closure
of soft tissue lacerations, and placement of the patient in
intermaxillary fixation. The latter manually reduces the frac-
ture, reduces movement and bleeding, and is the single most
important step in the treatment of a maxillary fracture. Post-
operative intermaxillary fixation may not be necessary after
open reduction of large segment maxillary fractures but is
increasingly useful for several weeks after comminuted frac-
ture treatment and in panfacial fractures or palatal fractures,
where rigid stability is difficult to obtain.104
Alveolar fractures
Simple fractures of the portions of the maxilla involving the
alveolar process and the teeth can usually be digitally reposi-
tioned and held in reduction while an arch bar is applied to

68
SECTION I
CHAPTER 3 • Facial injuries
maxillary segment from the superior cranial and midfacial
structures. The fracture line centrally may traverse the nose
high through the upper nasal bones or low through the nasal
cartilages to separate superior cranial from midfacial struc-
tures (Fig. 3.24).
Craniofacial dysjunction or Le Fort
III fractures
Craniofacial dysjunction may occur when the fracture extends
through the zygomaticofrontal suture and the nasal frontal
suture and across the floor of the orbits to effectively separate
all midfacial structures from the cranium. In these fractures,
the maxilla is usually separated from the zygoma, but occa-
sionally (5% of Le Fort III fractures) the entire midface may
be a large single fragment, which is often only minimally
displaced and immobile. These fractures present with “black
A
Fig. 3.23  Frontal 3D craniofacial computer
tomography scan of a Le Fort I type injury
pre- and post-open reduction and internal
fixation.
B
Fig. 3.22  The Le Fort classification of midfacial fractures. (A) The Le Fort I (horizontal or transverse) fracture of
the maxilla, also known as Guerin fracture. (B) The Le Fort II (or pyramidal) fracture of the maxilla. In this
fracture, the central maxilla is separated from the zygomatic areas. The fracture line may cross the nose through
its cartilages or through the middle nasal bone area, or it may separate the nasal bones from the frontal bone
through the junction of the nose and frontal sinus. (C) The Le Fort III fracture (or craniofacial disjunction). In this
fracture, the entire facial bone mass is separated from the frontal bone by fracture lines traversing the zygoma
nasoethmoid, and nasofrontal bone junctions. (From Kazanjian VH, Converse J. Surgical Treatment of Facial
Injuries, 3rd edn. Baltimore MD: Williams & Wilkins; 1974.)
B
A
C
eyes” and with a subtle malocclusion. The Le Fort III segment
may or may not be separated through the nasal structures. In
these fractures the entire midfacial skeleton is incompletely
detached from the base of the skull (a “greensticked” fracture)
(Fig. 3.25).108 Treatment may be successful with arch bars and
elastic traction without open reduction.
Surgical technique
Le Fort I level fractures
In fractures of the Le Fort I type, placing the patient in inter-
maxillary fixation may occasionally be all that is necessary in
the case of a minimally mobile and undisplaced fracture. In
most cases, however, the Le Fort I level should be opened
through a bilateral gingival buccal sulcus incision and the

69
Surgical technique
Fig. 3.24  Frontal 3D craniofacial computer tomography scan of a Le Fort II type
injury pre- and post-open reduction and internal fixation.
cannot be explained by other sources, especially if air-fluid
levels are present. Any foul odor in the nose or on the breath
necessitates inspection, cleaning and return to the operating
room for drainage and irrigation, and a thorough nasal and
oral examination.
Complications of maxillary fractures
Airway
In almost all cases of extensive fractures, the airway is partially
compromised by posterior displacement of the fracture frag-
ments and by edema and swelling of the soft tissues in the
nose, mouth, throat, and floor of the mouth. In some patients,
a nasopharyngeal airway may assist in establishing a route
for ventilation. In other patients, intubation or tracheostomy
may be indicated.
Bleeding
Hemorrhage may be managed by carefully identifying and
ligating vessels in cutaneous lacerations, and by tamponade
A
Fig. 3.25  Frontal 3D craniofacial computer tomography scan of a Le Fort III type
injury pre- and post-open reduction and internal fixation.
B
fractures reduced and stabilized with plate and screw fixation
at the bilateral nasomaxillary and zygomaticomaxillary
buttresses. The primary consideration in Le Fort I fracture
treatment is to re-establish normal dental occlusion. Proper
lower midfacial height and projection are achieved by open
reduction.
Le Fort II level fractures
In the case of a simple Le Fort II level fracture, the patient is
first placed in intermaxillary fixation. The fracture should be
opened at the Le Fort I level through a gingival buccal sulcus
incision and through both lower eyelids to provide reduction
and fixation at the orbit, zygomaticomaxillary and nasomaxil-
lary buttresses, and at the inferior orbital rims. The need for
opening fractures crossing the nose must be assessed by the
CT scan and the displacement at the nasofrontal junction.
Lower nasal fractures often do not need this exposure.
Le Fort III fractures
Open reduction of Le Fort III fractures generally involves
combining procedures at the Le Fort I, Le Fort II, and zygo-
matic levels simultaneously for open reduction and fixation
in a single operation.
Postoperative care of maxillary fractures
The postoperative management of fractures of the maxilla
consists of three times daily dental and oral hygiene, lip
lubrication, mouthwashes, skin care (abrasion and laceration
cleansing), and lubrication with soaps and antibiotic oint-
ments. Provision of adequate nutrition may be accomplished
by a liquid or pureed diet, nasogastric tube, or percutaneous
gastrostomy. The liquid or pureed diet is generally possible
with intermaxillary fixation (IMF) and a soft diet after the IMF
is released.
Cleansing and aspiration of both the nose and mouth is
very important. The presence of a fever in patients with facial
fractures should always prompt a sinus evaluation if the fever

70
SECTION I
CHAPTER 3 • Facial injuries
Malunion
In multiple (complex) panfacial fractures, malunion may
result from inadequate diagnosis, inadequate reduction, or
inadequate fixation. The period of intermaxillary fixation and
observation may need to be longer when the injury is more
comminuted.
Malocclusion
If malocclusion is detected, it may respond to elastic traction.
Once partial healing has occurred, attempts to re-establish
occlusion with elastics may simply extrude or loosen the
teeth. Revision of the reduction after removal of the internal
fixation devices or a new osteotomy may be necessary. When
new (secondary) osteotomies are necessary, generally a Le
Fort I osteotomy for repositioning of the tooth-bearing
segment of the maxilla is preferred as opposed to a higher
level osteotomy. Occasionally, segmental osteotomies of the
maxillary arch may be necessary to achieve optimal dental
relationships.
Nasolacrimal duct injury
The nasolacrimal duct may be transected or obstructed by the
fractures extending across the middle third of the facial skel-
eton between the Le Fort I and Le Fort III levels. Anatomic
repositioning of the fracture fragments of the medial portion
of the maxilla and nasoethmoidal orbital area provides the
best protection against obstruction. Obstruction of the lacrimal
system produces dacryocystitis and may require external
drainage.
Lower facial fractures
Mandible fractures
The prominence, position, and anatomic configuration of the
mandible are such that it is one of the most frequently injured
facial bones. Following automobile accidents, the mandible
is the most commonly encountered fracture seen at many
major trauma centers. The mandible is a movable, predomi-
nantly U-shaped bone, consisting of horizontal and vertical
segments. The horizontal segments consist of the body and
the symphysis centrally. The vertical segments consist of the
angles and rami, which articulate with the skull through
the condyles and temporomandibular joints. The mandible
is attached to other facial bones by muscles and ligaments
and articulates with the maxilla through the occlusion
of teeth.
The mandible is a strong bone but has several weak areas
that are prone to fracture. The body of the mandible is com-
posed principally of dense cortical bone with a small substan-
tia spongiosa through which blood vessels, lymphatics, and
nerves pass. The mandible is thin at the angles where the body
joins with the ramus and can be further weakened by the
presence of an unerupted third molar or a previous dental
extraction.111
The mandible is also weak at the condylar neck, cuspid root
(the longest root), and mental foramen through which the
mental nerve and vessels extend into the soft tissues of the
lower lip. The weak areas for fractures are the subcondylar
area, angle, distal body, and the mental foramen.112–114
in closed midface injuries with anterior–posterior nasopha-
ryngeal packing, manual reduction of the displaced maxilla
and placing the teeth in intermaxillary fixation. Angiographic
embolization and the combination of external carotid and
superficial temporal artery ligation are rarely necessary.
Infection
Maxillary fracture wounds are less complicated by infection
than are mandibular fractures. However, they are contami-
nated at the time of the injury by entry into adjacent sinuses,
fractures of the teeth, and open intraoral wounds. Fractures
passing through the sinuses do not usually result in infection
unless there has been pre-existing nasal or sinus disease, or in
the case of persistent obstruction of the sinus orifice by dis-
placed bone fractures or blood clot. If the maxillary sinuses
are obstructed, a nasal–antral window or endoscopic drainage
of the maxillary sinus by enlarging the orifice may be required.
Cerebrospinal fluid rhinorrhea
High Le Fort (II & III) level fractures may be associated with
fractures of the cranial base or cribriform area, which produce
cerebrospinal fluid (CSF) rhinorrhea and/or pneumocephalus
and may be associated with death.109 Antibiotic therapy may
be utilized in these fractures at the discretion of the attending
surgeon. Although antibiotic prophylaxis in CSF rhinorrhea
has been quite widely employed, it is difficult to prove that
antibiotics have substantially reduced the incidence of men-
ingitis accompanying cerebrospinal fluid rhinorrhea when
administered over a prolonged period. Blowing of the nose
and placement of obstructing nasal packing should be
avoided, and placement of intranasal tubes should avoid the
superior nose.
Blindness
Blindness is a rare complication of any fracture of the orbit
and may complicate fractures of the Le Fort II and III levels.
It is rare for the optic nerve to be severed by bone fragments.
The most common etiology is a traumatic shock to the nerve
or swelling of the nerve within the tight portion of the optic
canal or interference with the capillary blood supply of the
retrobulbar optic nerve by swelling and edema.
Late complications
Specific complications referable to the maxilla include non-
union, malunion, plate exposure, lacrimal system obstruction,
infraorbital and lip hypesthesia or anesthesia, and devitaliza-
tion of teeth. There may be changes in facial appearance due
to differences in midfacial height and projection, or the trans-
verse width of the face, and malocclusion.110
Nonunion and bone grafting
True nonunion of the maxilla is rare and usually follows
failure to provide even the most elementary type of intermax-
illary fixation or open reduction. If nonunion occurs, the
treatment consists of exposure of the fracture site, resection of
the fibrous tissue in the fracture site, reduction of the displaced
segments, removal of any proliferative bone edges, placement
of bone grafts in all the existing bone gaps, and stabilization
by plate and screw fixation.

71
Lower facial fractures
the mouth or bring the teeth into proper occlusion (trismus).
The patient may refuse to eat or to brush their teeth, which
then causes discomfort and an abnormal, foul-smelling odor
(fetor oris). Excessive saliva is often produced as a result of
local irritation (drooling). Small gingival or mucosal lacerations
or bleeding between teeth indicate the possibility of a fracture.
These gaps make the fracture compound into the mouth.
Bimanual manipulation of the mandible causes mobility or
distraction at the fracture site, especially when the fracture
occurs in the body or parasymphyseal area. One hand should
stabilize the ramus, while the other manipulates the symphy-
sis or the body area. The fracture will be demonstrated by
abnormal movement, and the condition and the symptom
reinforced by the presence of discomfort. The mandible may
be pulled forward with one hand while the other hand is
placed one finger in the ear canal and one finger over the
condylar process (see Fig. 3.4). Abnormal mobility or crepitus
indicates a fracture in the condylar/subcondylar area or liga-
ment laxity, indicating a temporal mandibular joint injury. The
most reliable finding in the fractures of the mandible, in
dentulous patients, is the presence of a malocclusion. Often, the
most minute malocclusion caused by the fracture is quite
obvious to the patient. The patient may be unable to move the
jaw (dysfunction) and may request liquid foods that require
minimal jaw movement and mastication. Speech is difficult
because of pain on motion of the mandible. Crepitation may
be noticeable by manipulation at the fracture site. Often, the
necessary manipulation produces such discomfort that it is
not wise to demonstrate this physical sign. Swelling is usually
quite obvious and frequently associated with ecchymosis and
a hematoma. Often, an intraoral laceration is present over
fractures in the horizontal portion of the mandible. There is
frequently deviation to one side or the other, a finding that
supports the diagnosis of a fracture. Tenderness over the frac-
ture site is present, especially in the region of the temporo-
mandibular joint. Such localized tenderness is highly
suggestive of a fracture.
Direction and angulation of the fracture line
Kelsey Frye117 described fractures as “favorable” or “unfavor-
able” according to their direction and bevel of displacement
Mandibular movements are determined by the action of
reciprocally placed muscles attached to the bone. When frac-
tures occur, displacement of the segments is influenced by the
pull of the muscles attaching to the segments. The direction
of the fracture line may oppose forces created by these muscles.
Dental wiring and fixation techniques
Arch bars
Prefabricated arch bars are ligated to the external surface of
the dental arch by passing 24- or 26-gauge steel wires around
the arch bar and around the necks of the teeth. The wires are
twisted tightly to individual teeth to hold the arch bars in the
form of the dental arch. If segments of the teeth are missing,
or if anterior support of the arch bar is needed to balance the
forces generated by elastic traction anteriorly, the arch bar
may be stabilized by additional wires passed from the arch
bar to the skeleton (skeletal wires). Suspension wires may be
passed through drill holes at the piriform margin or around
screws. This is particularly applicable in children where the
structure of the teeth tends to render arch bars less stable. The
mandibular arch bar may also be stabilized by wires passed
to a screw at the lower mandibular border or by circum-
mandibular wiring. It cannot be overemphasized that the
stability and alignment of a fracture reduction depends greatly
on the alignment of the teeth achieved by this initial applica-
tion of arch bars.
Newer types of arch bars exist, which utilize fewer points
of contact and fixation, or screws passed into the bone as
anchor for intermaxillary fixation. They are never better than
full arch bars, and commonly achieve less accurate positioning/
control of fracture fragments. Postoperatively, IMF may be
released if the fracture is stable, and the patient is able to
achieve normal occlusion. Our follow-up is at least once a
week until complete healing has occurred (6–8 weeks),
observing occlusion encouraging range of motion and absence
of infection.
IMF screws
This is a rapid method of immobilizing the teeth in occlusion,
given good dentition and uncomplicated fracture types.115 The
number and position of the IMF screws is based on the frac-
ture type, fracture location, and surgeon preference. Screws
must be positioned superior to the maxillary tooth roots and
inferior to the mandibular tooth roots, otherwise transfixation
of teeth may occur.116
Classification
Mandibular fractures are classified according to location (Fig.
3.26), condition of teeth, direction of fracture and favorability
for treatment, presence of compound injury through the skin
or mucosa, and anatomical fracture pattern.
Clinical examination and diagnosis
Pain and tenderness are usually present upon motion over the
fracture and may be noted immediately as a result of injury.
Fractures occurring along the course of the inferior alveolar
nerve may produce numbness in the distribution of the nerve,
which represents numbness of the ipsilateral lower lip (mental
nerve) and ipsilateral teeth. The patient may be unable to open
Fig. 3.26  Classification of mandibular fractures.
Alveolar process
Canine root
Mental foramen
Coronoid
Parasymphysis
Body
Third
molar
Angle
Ramus
Condyle

72
SECTION I
CHAPTER 3 • Facial injuries
displacement and permits light function. ORIF is especially
appealing to patients because the teeth do not need to remain
wired, which permits intake of soft foods, oral hygiene, and
an early return to work. These desirable aspects might not
justify open treatment if external incisions are required which
would produce permanent scars.122
General principles of reduction and fixation
The basic principle underlying all mandibular fracture treat-
ment is superior and inferior border stabilization. The general
method of fracture fixation involves arch bar placement and
the use of a superior border unicortical non-compression mini
plate. The inferior border is aligned and approximated by a
stabilization plate. Comminuted fractures (Fig. 3.28) require
larger fixation plates and include fractures with “bone loss”
and multiple fragments, where the plate itself bears the entire
load of fixation across the fracture or missing bone (load
bearing).
Treatment of class II fractures
In class II fractures, teeth are present on only one side of the
fracture site, and these fractures require open reduction. This
type of fracture may occur in any portion of the horizontal
mandible but frequently is at the angle. The type and strength
of plate needed to control the non-toothbearing fragment and
displacement of the fracture will vary according to the direc-
tion and bevel of the fracture and the position of the teeth,
surrounding muscles, and the absence of comminution.
(Fig. 3.27). The muscular forces on some fracture fragments
are opposed by the direction and bevel of the fracture line.
Thus, in some fractures, the muscular force would pull the
fragments into a position favorable for healing, whereas
in other fractures, the muscular pull is unfavorable and
separation of the fracture fragments occurs by action of
the muscular forces. Mandibular fractures that are directed
downward and forward are classified as horizontally favor-
able (HF) because the posterior group of muscles and the
anterior group of muscles pull in antagonistic directions,
favoring stability at the fracture site. Fractures running from
above, downward, and posteriorly are classified as horizon-
tally unfavorable (HU). The bevel of the fracture may also
influence a displacement medially. If a fracture runs from
posteriorly forward and medially, displacement would take
place in a medial direction because of the medial pull of
the elevator muscles of mastication (vertically unfavorable,
or VU). The fracture that passes posteriorly forward and
laterally is a favorable fracture because the muscle-pull tends
to prevent displacement. It is called a vertically favorable
fracture (VF).
Indications for ORIF of mandibular fractures
1. Favorable or unfavorable class I fractures where stability
is desired.
2. Class II and class III fractures.
3. Comminuted fractures.
4. Displaced fractures and those subject to rotation.
5. Edentulous fractures.
6. The desire to avoid IMF in the postoperative period.
7. Combined fractures of the upper and lower jaws.
8. Uncooperative (head injured) patients.
Treatment of class I fractures
Class I fractures are those in which there are teeth on each
side of the fracture. Although many of these fractures can be
managed by intermaxillary fixation (IMF) alone in “favor-
able” fractures, if function is desired and post-treatment dis-
placement is to be prevented, internal fixation is also preferred.
If IMF alone is to be used, the period of fixation is six
weeks.118,119 Many mandibular fractures, even if favorable, are
best managed by ORIF. Miniplates may be used for non-
comminuted, non-bone gap fractures where impaction of the
bone ends bears a significant portion of the load of fracture
stabilization (load sharing).120,121 This technique prevents
Fig. 3.27  (A,C) The direction and bevel of the fracture line does not resist displacement due to muscle action. The arrows indicate the direction of muscle pull. (B,D) The
bevel and direction of the fracture line resist displacement and oppose muscle action. The direction of the muscle pull in fractures beveled in this direction would tend to
impact the fractured bone ends. (After Fry WK, Shepherd PR, McLeod AC, et al. The Dental Treatment of Maxillofacial Injuries. Oxford: Blackwell Scientific; 1942.)
A
B
C
D
Fig. 3.28  Large reconstruction plate spans fractures of the entire body. (Courtesy
of Synthes Maxillofacial, Paoli, PA.)

73
Lower facial fractures
Extraoral approach to open reduction
The position of an external mandibular incision should always
respect the location of the marginal mandibular branch of the
facial nerve (Fig. 3.29). The subperiosteal dissection technique
also respects neurovascular structures such as the mental
nerve. Careful subperiosteal dissection establishes the extent
and pattern of the fracture, confirming the impression given
from the CT. The fragments at the inferior border of the
fracture are aligned with clamps. The occlusal reduction
should be checked at this point, and loose arch bar wires on
the minor segment are tightened. IMF is then confirmed or
established. Usually, a superior border plate is now utilized
at the upper border of the mandible and fixated with unicorti-
cal screws. The occlusion is again checked, alignment of the
fractures re-confirmed, and a lower border plate and screws
applied. A larger plate may be utilized. Generally, a large plate
is initially “overbent” so that it stands 2–3 mm off the central
fracture site. Screw length may be determined by a depth
gauge, and bicortical placement is preferred. If a larger plate
is used, as the bicortical screws are tightened, the overbent
plate flattens itself against the outer border of the mandible
and reduces the lingual cortex properly. After the fixation is
secure, any initial positioning wires are removed and the
Fractures at the mandibular angle can be treated using a
variety of techniques depending on the complexity of the
fracture pattern.123,124 For simple fractures at the mandibular
angle, the authors’ preferred approach is with a Champy plate
placed monocortically on the oblique ridge or superior border
of the mandible.
Comminuted fractures
Comminution negatively influences stability and generally
increases the degree of fracture displacement. Three to four
screws are utilized for fracture stabilization placed in non-
fractured bone on each side of the entire fracture defect. Upper
and lower border plates are preferred in the horizontal man-
dible and two plates also in the vertical mandible where
possible.
Class III fractures
Class III fractures have no teeth on either side of the fracture.
Non-displaced, immobile fractures conceptually may be
treated by a soft diet with close follow-up. The majority of
class III fractures, however, should be managed with rigid
fixation with superior and inferior border fixation.
Fig. 3.29  (A,B) Intraoperative photograph of comminuted mandibular fracture in a 23-year-old male
following attempted homicidal gunshot wound to the face pre- and post-open reduction and internal fixation
via the extraoral approach using multiple miniplates. (C) Lateral 3D craniofacial computer tomography
postoperative scan following open reduction and internal fixation of comminuted mandibular fractures.
A
B
C

74
SECTION I
CHAPTER 3 • Facial injuries
bone ends. Load-sharing fixation relies on the impaction of
the bone on each side of the fracture to bear the majority of
the functional load with the small plate holding the bone ends
together with force.
Locking plate and screw systems function as “internal
external fixators”, achieving stability by locking the screw to
the plate.128 The potential advantages of these fixation devices
are that precise adaptation of the plate to the underlying bone
is not necessary. As the screws are tightened they “lock” to
the plate, thus stabilizing the segments without the need to
compress the bone to the plate. This makes it impossible for
the screw insertion to alter the reduction. This theoretically
makes it less important to have good plate bending, as non-
locking, large plates must be perfectly adapted to the contour
of the bone. Theoretically this hardware should be less prone
to inflammatory complications from loosening of hardware
since loose hardware propagates an inflammatory response,
permits motion, and promotes infection.
Champy or miniplate system
Mandibular fixation by the use of smaller “mini plates”, as
advocated by Champy, speeded exposure and was more toler-
ant for mandibular shape and occlusion versus more rigid
plate adaption as the screws were tightened.129,130 The mal-
leable plates minimized malreductions from “plate bending
errors” common to stiff larger plates. This technique did not
result in maximum rigidity achieved with the large plates but
was generally sufficient for required immobilization for many
fractures.
Small plates are more “user friendly” than more rigid
systems and rose in popularity to surpass the use of rigid
plate systems. Champy recommended two plates (upper and
lower border) in the anterior (symphysis and parasymphysis)
portion of the mandible and a single plate along the superior
border in the angle and upper border of the distal ramus (Fig.
3.30). The need for additional fixation must be assessed care-
fully, and this technique should be avoided in comminuted
fractures and in the multiply fractured mandible. The tech-
nique can only be used where the bone at the fracture site is
broad enough to be compressed by the plate to bear the
musculature repaired. Care must be taken in suture placement
to avoid the marginal mandibular branch of the facial nerve,
which is located up to 1–2 cm below the inferior edge of the
mandible.125 The platysma muscle and the skin are closed in
layers, and a dependent drain placed. The cutaneous wound
is closed in layers with subcuticular sutures to avoid suture
marks.
Intraoral approach to open reduction
Any fracture in the horizontal or vertical mandible is usually
amenable to an intraoral approach.126
This is the preferred exposure for any symphysis or para-
symphysis fracture and for non-comminuted angle fractures.
The body region is also able to be reduced but may require a
percutaneous trocar approach for drilling and screw place-
ment. In the intraoral approach, the fracture site is exposed
through an appropriately placed mucosal incision. The inci-
sion is generally brought about a centimeter out of the sulcus
on the buccal aspect of the mucosa, and mucosal and muscular
layers separately incised.
Selection of internal fixation devices for mandibular
fractures: how much fixation is enough
Edward Ellis III123,127 clarified the issues regarding selection of
internal fixation devices for mandibular fractures. Normal
bite forces must be initially countered by fixation devices;
however, patients who have sustained mandible fractures do
not generate normal bite forces for months after the injury.
Rigid fixation is defined as internal fixation that is stable
enough to prevent motion of the bony fragments under
normal function. It has been recognized that absolute rigidity
of the bone fragments is not necessary for healing of the
fracture to occur under functional loading. Ellis believes
“functionally stable fixation” is not “rigid” but satisfies the
goals of maintaining fragment alignment and permits healing
during limited active use of the bone. Ellis describes “load-
bearing” fixation as sufficient strength and rigidity that the
device bears the entire loads applied to the mandible seg-
ments during functional activities without impaction of the
Fig. 3.30  (A) Three-quarter view of 3D craniofacial computer tomography preoperative scan on 16-year-old male who sustained a left mandibular angle fracture and right
mandibular parasymphyseal fracture following an altercation. (B) Intraoperative photograph of open reduction and internal fixation of left mandibular angle fracture using the
Champy technique. (C) Three-quarter view of 3D craniofacial computer tomography postoperative scan.
A
B
C

75
Lower facial fractures
between the bone and the direction of the screw should bisect
a 90-degree angle from the bone in a plane parallel to the bone.
Third molars in mandibular angle fractures
Extraction of an impacted third molar must be carefully
considered. In some circumstances, where the third molar is
partially erupted and inflamed, it should be removed at the
time of fracture treatment to avoid potential complications
(Fig. 3.32).111
Otherwise, it makes little sense to remove bone to extract
a fully impacted third molar, as this weakens the bone and
damages mucosa in the area of the fracture. This can expose
the fracture to the intraoral environment, contributing to bone
instability and infection and a less stable fracture by third
molar removal. The fracture site is less vascularized following
third molar removal by virtue of periosteal stripping. Fully
impacted third molars which do not prevent fracture reduc-
tion by minimal displacement of the tooth can be electively
removed when fracture healing is completed.133–135
Antibiotic use
Intravenous administration of antibiotics perioperatively is
recommended especially in patients undergoing delayed
treatment, patients having long operations, patients with
badly contused soft tissue, where the fracture treatment is
delayed and where the tissues are heavily contaminated, and
where multiple intraoral lacerations are present.136,137 It benefits
patients who are medically compromised, have poor nutri-
tional status or systemic illness, or where local conditions of
poor dental hygiene, periodontal, or dental infections increase
the chance of bacterial complications.
Treatment principles of mandibular fractures
1. Establish proper occlusion.
2. Anatomically reduce the fractured bones into their
normal position.
A
Fig. 3.31  (A) Placement of two horizontal lag screws to reduce and stabilize a
parasymphysis fracture using a trocar device. (B) Intraoperative photograph of open
reduction and internal fixation of mandibular symphyseal fracture using lag screws.
(A, Courtesy of Synthes Maxillofacial, Paoli, PA.)
B
Fig. 3.32  Three-quarter view of 3D craniofacial computer tomography
demonstrating malunion and continuity defect of left mandibular angle fracture with
tooth in line of fracture.
majority of the “load” of the fracture. The use of a brief initial
period of rest in IMF (1 week) is used by some practitioners
for soft tissue “rest” and provides an initial period of occlu-
sion where less stress is placed on the fracture and importantly
intraoral wounds and the soft tissue.
Lag screw technique
This technique is indicated in non-comminuted parasymphy-
sis or symphysis fractures,131,132 where a long length of screw
can be tolerated (Fig. 3.31). Generally, these screw lengths
require 35–45 mm anteriorly. A specific technique is utilized
where the first cortex in the bone is over-drilled to the major
diameter (thread width) of the screw. The second segment of
the screw path is drilled to the minor diameter (core width
not including treads) of the screw. Only the screw head will
engage bone in the first section of the path, and therefore, as
the screw is tightened into the second section of the fracture,
the screw head impacts the cortex toward the fracture site.
Generally, two lag screws are recommended for each fracture
to be stable, for if one becomes loose, the fracture would be
unstable by rotation. A sleeve or drill guide is used to protect
soft tissue. Oblique body or angle fractures may be lag screwed
with 2–3 screws for stability. In screw placement, the angle

76
SECTION I
CHAPTER 3 • Facial injuries
exposed must be debrided. Loose or infected teeth should be
removed. Fracture stability must be provided by removal of
current fixation devices and reapplication of longer, stronger
reconstruction plates, whose screw fixation of 3–4 screws in
healthy uninvolved bone outside the fracture area can be
achieved. In the uncommon persistent infection, the surgeon
may wish to convert to external fixation removing all internal
fixation devices, but most cases may be stabilized with the
debridement and application of a long reconstruction plate.
No screws should be placed in an area of questionable bone.
Serial debridement of devitalized bone and soft tissue may
be required to confirm the absence of infection and adequacy
of debridement. Primary or secondary bone grafting is con-
ducted when the soft tissue and local area have been cleared of
infection by debridement, drainage, antibiotics, and mucosal
closure.144
Condylar and subcondylar fractures
One must consider dislocation, angulation between the frac-
tured fragments, fracture override (which translates to ramus
vertical length shortening), fracture angulation, and bone
gaps between the fragments. In children, growth consider-
ations145 create a capacity for both regeneration and remodel-
ing which is not present in later years.146,147 Adults are capable
only of partial restitutional remodeling.
High condylar (intracapsular) fractures (head and upper
neck) are generally treated with closed reduction with a limited
(2 week) period of postoperative IMF, followed by early
“controlled” mobilization utilizing elastics for re-establishing
occlusion in a rest position. Most neck and low subcondylar
fractures with good alignment, reasonable contact of the bone
ends, and preservation of ramus vertical height without condy-
lar head dislocation may be treated by IMF for 4–6 weeks, with
weekly observation of the occlusion for at least 4 additional
weeks after release of fixation in light function or guiding
elastics.148,149 Some shortening of the ramus height is almost
inevitable with a closed approach to condylar/subcondylar
fracture treatment,150–152 which may lead to a premature contact
in the ipsilateral molar occlusion and a subtle open bite in
the contralateral anterior occlusion. Angulation between the
fractured fragments in excess of 30 degrees and fracture gap
between the bone ends exceeding 4–5 mm, lateral override,
and lack of contact of the ends of the fractured fragments
should be a consideration for open reduction in mid or low
subcondylar fractures types (Fig. 3.33).153–157
Edentulous mandible fractures
These fractures represent less than 5% of the mandibular
fractures.158–160 Fractures commonly occur through the most
atrophic portions where the bone is thin and weak. The body
is a common site for fracture, as compared to the angle and
subcondylar region in dentulous patients.161 Many fractures
are bilateral or multiple, and displacement of a bilateral
edentulous body fracture is often severe and a challenging
condition to treat. The fractures in the horizontal mandible
may be closed or open to the oral cavity. Closed fractures
demonstrating no displacement may be treated with a soft
diet and avoidance of dentures; however, in these cases
observation is critical to be sure that healing occurs within
several weeks without further displacement. In practice most
3. Utilize fixation techniques that hold the fractured bone
segments in occlusion and normal position until healing
has occurred. Open reduction internal fixation (ORIF)
can often permit limited function while healing is
occurring.
4. Control infection.
Complications after fracture treatment
Malocclusion
Malocclusion is commonly the result of insufficient or inac-
curate initial alignment. Poorly applied or loose IMF is the
commonest cause, and inadequate reduction, inadequate plate
size, length or strength, contour, or failure (loosening) of fixa-
tion. The most common cause of screw loosening is overheat-
ing of the bone while drilling. Although subtle malocclusions
may sometimes be corrected by elastic traction, grinding the
occlusal facets of the teeth or orthodontics, any significant
malocclusion requires refracture and/or osteotomy.
Hardware infection and screw migration
Loose hardware generally creates soft tissue irritation, pro-
ducing a foreign body response and infection requiring
hardware removal. Many times the fracture has healed and a
repeat osteosynthesis is not necessary. Migration of loose
hardware into soft tissue away from the fracture site occasion-
ally occurs.138
Increased facial width and rotation of the mandible
Broadening of the distance between mandibular angles is
produced by rotation of the lateral mandibular segments
lingually at the occlusal surface of the teeth.139 The distance
between the mandibular angles increases as the mandible
rotates, and the lower face widens. This rotation (aggravated
by tight IMF and the presence of subcondylar fractures) pro-
duces a malocclusion (open bite) of the palatal and lingual
cusps of the molar dentition (which may only be visible from
a lingual location). A characteristic broadening and rounding
of the face occurs, which is aesthetically and functionally
undesirable. It cannot be treated by orthodontics and requires
refracture.140 The use of a long, strong reconstruction (10–12
hole) plate to keep the mandibular angles unrotated and the
width of the mandible at the angles narrow is required.
Non-union
Non-union and pseudoarthrosis are uncommon after plate
and screw fixation.141–143 Their presence may be masked in
presence of rigid fixation. Plate removal may unmask a poor
union, which requires re-fixation of the fracture after thorough
debridement at the site of poor fracture healing and possible
bone grafting of the defect.
Osteomyelitis
Soft tissue infection is common after mandibular fracture
treatment, but true bone infection, osteomyelitis, is not. Local
infection may almost always be managed with drainage
and antibiotics. The fixation must be confirmed as adequate
and intraoral closure inspected, and any instability in the
fracture fixation noted and corrected. Less commonly,
devitalized soft tissue and bone fragments that are dead or

77
Panfacial injuries
Fig. 3.33  (A,B) Lateral view of 3D craniofacial computer tomography on a 20-year-old female involved in a motor vehicle collision who sustained craniofacial injuries,
pre- and post-open reduction and internal fixation of a right mandibular subcondylar fracture via a retromandibular extraoral approach. Note that the patient also had a Le
Fort II type fracture that was treated with closed reduction and interdental fixation. (C) Lateral profile view photograph of patient 1 year postoperatively.
A
B
C
massive edema and soft tissue contamination and rigidity that
follow these injuries. Early treatment is possible when other
systems are not injured or are evaluated to exclude significant
instability. However, no matter how severely the patient is
injured, cutaneous wounds can be cleansed and closed, devi-
talized tissue removed, and the patient placed in intermaxil-
lary fixation. This is the minimum urgent treatment of a
significant maxillary or mandibular injury and may always be
accomplished, despite the condition of the patient.
Presently, a one-stage restoration of the architecture of the
craniofacial skeleton is the preferred method of treatment for
fractures are better treated with a load-bearing plate. The
edentulous mandible is characterized by the loss of the alveo-
lar ridge and the teeth.162 The bone atrophy may be minimal
if there is sufficient height (over 20 mm) of the mandibular
body to ensure good bone healing. In cases with moderate
atrophy, the height of the mandibular body ranges from
10–20 mm, and healing is usually satisfactory but not as
certain as if the height were greater than 20 mm. Small plates
with few screws often fail, as there is insufficient bone to
provide buttressing support for “load-sharing” fracture treat-
ment. The plate must bear the entire load of the fracture, and
a large reconstruction (“locking”) plate with 3–4 screws per
side in healthy bone is recommended (Fig. 3.34). In cases
where the mandibular height is less than 10 mm (severe
atrophy) one can assume that the patient has a disease of
“poor bone healing”. Complications following edentulous
mandible fractures directly parallel the extent of mandibular
atrophy. Obwegeser and Sailer163 in 1973 documented that
20% of the complications in edentulous mandible fractures
were seen in the 10–20 mm mandibular height group, and
80% of the complications (i.e. poor or unsatisfactory bone
union) were experienced in cases demonstrating a mandibular
height less than 10 mm. Virtually no complications were seen
in fractures exceeding 20 mm in height. This experience
caused some authors164,165 to recommend primary bone graft-
ing for the severely atrophic edentulous mandible (less than
10 mm in height).
Panfacial injuries
Conceptually, panfacial fractures involve all three areas of the
face: frontal bone, midface, and mandible. In practice, when
two out of these three areas are involved, the term “panfacial
fracture” has been applied.
Treatment of panfacial fractures
The optimal time and the easiest treatment of these injuries is
within hours of the accident, before the development of
Fig. 3.34  Lateral view of 3D craniofacial computer tomography on a 64-year-old
edentulous female, with a history of osteogenesis imperfecta, who was referred for
treatment of a malunion of a left mandibular fracture. Postoperative open reduction
and internal fixation using a load-bearing mandibular plate and iliac bone grafting
via an extra-oral approach.

78
SECTION I
CHAPTER 3 • Facial injuries
Order of the procedure
Various sequences have been suggested such as “top to
bottom”, “bottom to top”, “outside to inside”, or “inside to
outside”. In reality, it does not make any difference what the
order is as long as the order and sequence make logical sense
and lead to a reproducible, anatomically accurate bone recon-
struction. In our experience, it is more predictable to stabilize
the occlusion in comminuted fractures by relating the ana-
tomically aligned maxilla to the mandible than by relating the
inferior maxilla to the superior maxilla. The frontal bone is
managed first with any brain injury, then the upper midface
beginning with the central nasoethmoid area and progressing
to the zygoma, emphasizing control of facial width. The
mandible is managed next, linking all segments through
required exposures with wires temporarily, then achieving
mandibular width by relating it to an anatomically reduced
and stabilized maxillary dental arch.
Complications of panfacial fractures
Complications of panfacial fractures include complications
referable to the bone and the soft tissue. The most common
bony facial deformities following midface fracture treatment
relate to lack of projection, enophthalmos, malocclusion, and
increased facial width (Fig. 3.35).
The most common soft tissue deformities are descent,
diastasis, fat atrophy, ectropion, thickening, and rigidity. Lack
of periosteal closure over the zygomaticofrontal suture pro-
duces the appearance of temporal wasting because of the gap
in the temporal aponeurosis with skeletalization of the frontal
process of the zygoma (Fig. 3.36). High incisions for arch
exposure made higher in the deep temporal fascia require
dissection through fat to reach the zygomatic arch and cause
fat atrophy by direct fat damage (interference with the middle
temporal blood supply).
Fig. 3.35  Lack of restoration of the preinjury appearance, even if the underlying
bone is finally replaced into its proper anatomic position, is the result of scarring
within soft tissue. Examples of soft tissue rigidity accompanying malreduced
fractures include the conditions of enophthalmos, medial canthal ligament
malposition, short palpebral fissure, rounded canthus, and inferiorly displaced
malar soft tissue pad. The lower lip has a disrupted mentalis attachment. Secondary
management of any of these conditions is more challenging and less effective than
primary reconstruction. A unique opportunity thus exists in immediate fracture
management to maintain expansion shape and position of the soft tissue envelope
and to determine the geometry of soft tissue fibrosis by providing an anatomically
aligned facial skeleton as support. Excellent restoration of appearance results from
primary soft tissue positioning.
Fig. 3.36  “Skeletonization” of the frontal process of the zygoma from failure to
close the temporal fascia to the orbital periosteum over the frontal process.
panfacial injuries, where severe comminution and multiply
fractured facial bones characterize the injury.
Open reduction of all fracture sites is performed with plate
and screw fixation, adding bone grafts to bone defects.
Although local incisions may be useful in selected cases,
regional incisions such as the coronal, transconjunctival, and
upper and lower gingival buccal sulcus provide complete
exposure. An exposure may be avoided when a suitable lac-
eration already exists.
In each subunit of the face, the important dimension to be
considered first is facial width. In less severe fractures, correc-
tion of facial width is not challenging and an “anterior”
approach is sufficient. Control of facial width in more severe
injuries requires more complete dissection and alignment of
each fracture component utilizing all the peripheral and
cranial base landmarks. Reconstructions which emphasize
control of facial width are in fact the principle which recipro-
cally restores facial projection.
The timing and technique of soft tissue reduction are criti-
cal. Repositioning of the bone and replacement of the soft
tissue onto the bone at its correct anatomical location must be
accomplished before the soft tissue has developed significant
memory (internal scarring) in the pattern of the unreduced
bone configuration. Soft tissue replacement requires (1)
layered closure of the soft tissues and (2) reattachment of the
closed soft tissue to the facial skeleton precisely at several
points on the anatomically assembled craniofacial skeleton.

79
Gunshot wounds of the face
Intermediate and high velocity ballistic
injuries to the face
Shotgun pellets have a large mass and are considered inter-
mediate energy deposit projectiles. They travel at speeds of
approximately 1200 feet per second and when grouped in a
close distribution, at close range, are capable of causing
massive injury. In civilian practice, many of these injuries
represent shotgun wounds or high-energy rifle injuries, and
they often result from suicide attempts and assaults. Close
range shotgun wounds are characterized by extensive soft
tissue and bone destruction.
Intermediate and high velocity ballistic injuries to the face
must be managed with a specific treatment plan that involves
stabilization of existing bone and soft tissue in anatomic posi-
tion, and maintenance of this bone and soft tissue stabilization
throughout the period of soft tissue contracture and bone and
soft tissue reconstruction. Wounds from intermediate and
high-energy missiles usually demonstrate areas of both soft
tissue and bone loss, as well as areas of soft tissue and bone
injury. It is important to reassemble the existing bone and soft
tissue as completely as possible, and then serial surgical
debridement ”second-look” procedures, re-open the soft
tissue to define additional areas of soft tissue necrosis, drain
hematoma and/or developing fluid collections or infection,
and assure bone integrity. These “second-look” procedures
are imperative if primary reconstruction is attempted. Thus,
the emphasis is on primary soft tissue, “skin to skin” or “skin
to mucosa” closures, with stabilization of existing bone frag-
ments in anatomical position. Re-exploration for additional
debridements occur at 48-hour intervals, or at an interval
determined until soft tissue loss ceases and wound hematoma
and fluid collections are controlled. Then, reconstruction
proceeds immediately.
In cases where composite tissue loss of bone and soft tissue
occur, techniques utilizing free tissue transfer of bone and
soft tissue are preferred (Fig. 3.37A–F).170,171 The use of local
tissue advanced over the mismatched cutaneous segment of
the free flap ultimately provides the best cutaneous aesthetic
result.172
Postoperative care
Patients with large segment fractures may be adequately
stabilized by plate and screw fixation and permit early release
of intermaxillary fixation. Patients with comminuted midface
or panfacial fractures are best served by varying periods of
postoperative intermaxillary fixation of three to four weeks in
addition to plate and screw fixation.
Gunshot wounds of the face
While some authors advocate delayed reconstruction of
gunshot and shotgun wounds of the face, immediate recon-
struction166,167 and immediate soft tissue closure with serial
“second-look” procedures is the current standard of care.168
Recent experience documents the safety and efficacy of imme-
diate soft tissue closure and bone reconstruction in an ana-
tomically correct position. These two principles prevent soft
tissue shrinkage and loss of soft tissue position and provide
improved functional and aesthetic results with shorter periods
of disability and an improved potential for rehabilitation both
functionally and aesthetically. The philosophy of delayed
closure of these difficult wounds is no longer appropriate,
creates additional soft tissue deformity, and delays effective
rehabilitation of the affected individuals, some of whom
represent suicide attempts.
Ballistic injuries are classified into low, medium, and high-
energy injuries.169 In formulating a treatment plan for ballistic
injuries, it is helpful to identify the entrance and exit wounds
and the presumed path of the bullet and to appreciate the
mass and velocity of the projectile so that the extent of internal
areas of tissue injury can be predicted. Conceptually, the areas
of soft tissue and bone injury and areas of soft tissue loss and
bone loss must be individually assessed and noted (four sepa-
rate components) for each injury. The areas of injury and the
areas of loss are each precisely outlined, which allows a treat-
ment plan to be developed for early and intermediate treat-
ment for the lower, middle, and upper face.
Low velocity gunshot wounds
Low energy deposit ballistic weapons usually involve projec-
tiles that have a limited mass and travel at speeds of less than
1000 feet per second. In general, low velocity gunshot wounds
involve little soft tissue and bone loss and have limited associ-
ated soft tissue injury outside the exact path of the bullet. It
is thus appropriate that they be treated with immediate defini-
tive stabilization of bone and primary soft tissue closure.
Limited debridement of bone and soft tissue are necessary.
Small amounts of bone may need to be debrided and replaced
with a primary bone graft, which can be performed primarily
in the upper face. Because of the lack of significant associated
soft tissue injury, little potential for progressive death or
progressive necrosis of soft tissue exists, and these injuries
may be treated as “facial fractures with overlying lacerations”
both conceptually and practically.
Bonus images for this chapter can be found online at

Fig. 3.1 Cutaneous incisions (solid line) available for open reduction and
internal fixation of facial fractures. The conjunctival approach (dotted line) also
gives access to the orbital floor and anterior aspect of the maxilla, and exposure
may be extended by a lateral canthotomy. Intraoral incisions (dotted line) are
also indicated for the Le Fort I level of the maxilla and the anterior mandible.
The lateral limb of an upper blepharoplasty incision is preferred for isolated
zygomaticofrontal suture exposure if a coronal incision is not used. A horizontal
incision directly across the nasal radix or vertical incision along the glabellar
fold is the one case in which a local incision can be tolerated over the nose. In
many instances, a coronal incision is preferable unless the hair is short or the
patient is balding.

80
SECTION I
CHAPTER 3 • Facial injuries
33. Rodriguez ED, Stanwix MG, Nam AJ, et al. Twenty-six-year
experience treating frontal sinus fractures: a novel algorithm
based on anatomical fracture pattern and failure of
conventional techniques. Plast Reconstr Surg. 2008;122:
1850–1866. Landmark article describing the longest experience
with treating frontal sinus fractures provides an algorithm
for its treatment based on their outcomes, to minimize long-term
complications.
59. Iliff N, Manson P, Katz J, et al. Mechanisms of extraocular muscle
injury in orbital fractures. Plast Reconstr Surg. 1999;103:787–799. A
comprehensive human, cadaveric, and animal study into the effects of
orbital fractures on extraocular muscles and their intramuscular
vasculature to help understand mechanisms of diplopia and muscle
injury.
64. Girotto J, Gamble B, Robertson B, et al. Blindness following
reduction of facial fractures. Plast Reconstr Surg. 1998;102:
1821–1834. Landmark article to define the incidence of blindness
following facial fracture repair.
79. Tessier P, Guiot G, Rougerie J, et al. [Cranio-naso-orbito-facial
osteotomies. Hypertelorism]. Ann Chir Plast. 1967;12:103–118. An
article by the father of craniofacial surgery describing the possibilities of
an intracranial approach for orbital reconstructive surgery.
82. Markowitz B, Manson P, Sargent L, et al. Management of the
medial canthal tendon in nasoethmoid orbital fractures: the
importance of the central fragment in treatment and classification.
Plast Reconstr Surg. 1991;87:843–853. Landmark article on the
classification types of nasoethmoid-orbital region. Knowledge of this
fracture pattern classification assists with the treatment of this complex
surgical condition.
100. Manson P, Clark N, Robertson B, et al. Subunit principles in
midface fractures: the importance of sagittal buttresses, soft tissue
reductions and sequencing treatment of segmental fractures. Plast
Reconstr Surg. 1999;103:1287–1306. Landmark article describing the
authors’ extensive experience in the treatment of midfacial injuries and
the importance of correct realignment of bone and soft tissues to improve
facial fracture treatment.
Access the complete reference list online at

Fig. 3.37  (A,B) Frontal photographs of a 34-year-old male following a self-inflicted gunshot wound injury to the face demonstrating severe midfacial and mandibular
fractures. (C) Intraoperative photographs following open reduction and internal fixation of mandibular fractures using a load-bearing mandibular plate and a monocortical
miniplate fixation via an extraoral approach. (D,E) Frontal 3D craniofacial computer tomography scan of the patient pre- and post-open reduction and internal fixation of
midfacial and mandibular fractures. (F) Postoperative photograph 1 year following surgery.
A
B
C
D
E
F

81
Gunshot wounds of the face
106. LeFort R. Etude experimentale sur les fractures de la machoire
superieur. Rev Chir Paris. 1901;23:208, 360, 479. Original article
describing the various fracture patterns associated with traumatic
craniofacial injury. We associate the author’s name to the different types
of fracture patterns recognized.
129. Champy M, Lodde JP, Schmidt R, et al. Mandibular osteosynthesis
by miniature screwed plates via a buccal approach. J Maxillofac
Surg. 1978;6:14–21. Original article describing the use of monocortical
plates for the treatment of mandibular fractures; lines of osteosynthesis
are defined.

81.e1
References
References
1. <
tables/12s1103.pdf>.
2. Zelken JA, Khalifian S, Mundinger GS, et al. Defining predictable
patterns of craniomaxillofacial injury in the elderly: analysis of
1,047 patients. J Oral Maxillofac Surg. 2014;72:352–361.
3. Mithani SK, St-Hilaire H, Brooke BS, et al. Predictable patterns of
intracranial and cervical spine injury in craniomaxillofacial
trauma: analysis of 4786 patients. Plast Reconstr Surg.
2009;123:1293–1301.
4. Elahi MM, Brar MS, Ahmed N, et al. Cervical spine injury in
association with craniomaxillofacial fractures. Plast Reconstr Surg.
2008;121:201–208.
5. Stacey DH, Doyle JF, Gutowski KA. Safety device use affects the
incidence patterns of facial trauma in motor vehicle collisions: an
analysis of the National Trauma Database from 2000 to 2004. Plast
Reconstr Surg. 2008;121:2057–2064.
6. Davis JW, Bennick L, Kaups K, Parks SN. Motor vehicle restraints:
primary versus secondary enforcement and ethnicity. J Trauma.
2002;53:225–228.
7. Murphy RX Jr, Birmingham KL, Okunski WJ, Wasser T. The
influence of airbag and restraining devices on the patterns of facial
trauma in motor vehicle collisions. Plast Reconstr Surg.
2000;105:516–520.
8. Lee R, Robertson B, Manson P. Current epidemiology of facial
injuries. Semin Plast Surg. 2003;16:283.
9. Dediol E. The role of three-dimensional computed tomography in
evaluating facial trauma. Plast Reconstr Surg. 2012;129:354e–355e.
10. Rowe LD, Brandt-Zawadzki M. Spatial analysis of midfacial
fractures with multidirectional and computed tomography:
clinicopathologic correlates in 44 cases. Otolaryngol Head Neck Surg.
1982;90:651.
11. Gentry LR, Manor WF, Turski PA, Strother CM. High-resolution
CT analysis of facial struts in trauma: (1) normal anatomy (2)
osseous and soft tissue complications. AJR AM J ROENTGENOL.
1983;140:523, 542.
12. Luka B, Brechtelsbauer D, Gellrich N, Konig M. 2-D and 3-D
reconstruction of the facial skeleton: an unnecessary option or a
diagnostic pearl? Int J Oral Maxillofac Surg. 1995;21:99–103.
13. Manson PN, Crawley WA, Yaremchuk MJ, et al. Midface fractures:
advantages of immediate extended open reduction and bone
grafting. Plast Reconstr Surg. 1985;76:1.
14. Manson P, Iliff N. Management of blowout fractures of the orbital
floor: early repair of selected injuries. Surv Ophthalmol.
1991;35:280–291.
15. Bellamy JL, Mundinger GS, Flores JM, et al. Facial fractures of the
upper craniofacial skeleton predict mortality and occult
intracranial injury after blunt trauma: an analysis. J Craniofac Surg.
2013;24:1922–1926.
16. Derdyn C, Persing JA, Broaddus WC, et al. Craniofacial trauma:
an assessment of risk related to timing of surgery. Plast Reconstr
Surg. 1990;86:238–245, discussion 246–247.
17. Schenck NL. Frontal sinus disease. III Experimental and clinical
factors in failure of the frontal osteoplastic operation. Laryngoscope.
1975;85:76.
18. Hybels RL, Newman MH. Posterior table fractures of the frontal
sinus: I. An experimental study. Laryngoscope. 1977;87:171.
19. Gerbino G, Roccia F, Benech A, Caldarelli C. Analysis of 158
frontal sinus fractures: current surgical management and
complications. J Craniomaxillofac Surg. 2000;28:133–139.
20. Jacobs JB. 100 years of frontal sinus surgery. Laryngoscope.
1997;107:1–36.
21. Rohrich R, Hollier L. Management of frontal sinus fractures:
changing concepts. Clin Plast Surg. 1992;19:219–232.
22. Bellamy JL, Molendijk J, Reddy SK, et al. Severe infectious
complications following frontal sinus fracture: the impact of
operative delay and perioperative antibiotic use. Plast Reconstr
Surg. 2013;132:154–162.
23. Bordley JE, Bosley WR. Mucocoeles of the frontal sinus: causes
and treatment. Ann Otol Rhinol Laryngol. 1973;82:696.
24. Donald PJ. The tenacity of frontal sinus mucosa. Otolaryngol Head
Neck Surg. 1979;87:557–566.
25. Stanwix MG, Nam AJ, Manson PN, et al. Critical computed
tomographic diagnostic criteria for frontal sinus fractures. J Oral
Maxillofac Surg. 2010;68:2714–2722.
26. Burstein F, Cohen S, Hudgins R, Boydston W. Frontal basilar
trauma: classification and treatment. Plast Reconstr Surg.
1997;99:1314.
27. Chen KT, Chen CT, Mardini S, et al. Frontal sinus fractures: a
treatment algorithm and assessment of outcomes based on 78
clinical cases. Plast Reconstr Surg. 2006;118:457–468.
28. Choi M, Li Y, Shapiro SA, et al. A 10-year review of frontal sinus
fractures: clinical outcomes of conservative management of
posterior table fractures. Plast Reconstr Surg. 2012;130:
399–406.
29. Bell RB, Dierks E, Brar P, et al. Protocol for the management of
frontal sinus fractures with emphasis on preservation. J Oral
Maxillofac Surg. 2007;65:825–839.
30. Heller EM, Jacobs JB, Holliday RA. Evaluation of the nasofrontal
duct in frontal sinus fractures. Head Neck. 1989;11:46.
31. Stanley RB, Becker TS. Injuries of the nasofrontal orifices in frontal
sinus fractures. Laryngoscope. 1987;97:728–731.
32. Kakibucci M, Fukada K, Yamada N. A simple method of
harvesting. A thin iliac bone graft for reconstruction of the orbital
wall. Plast Reconstr Surg. 2003;111:961.
33. Rodriguez ED, Stanwix MG, Nam AJ, et al. Twenty-six-year
experience treating frontal sinus fractures: a novel algorithm based
on anatomical fracture pattern and failure of conventional
techniques. Plast Reconstr Surg. 2008;122:1850–1866. Landmark
article describing the longest experience with treating frontal sinus
fractures provides an algorithm for its treatment based on their outcomes,
to minimize long-term complications.
34. Barkowski SB, Krzystkowa KM. Blowout fracture of the orbit.
Diagnostic and therapeutic considerations, and results in 90
patients treated. J Maxillofac Surg. 1982;10:155–164.
35. Collins A, McKellar G, Momnsour F. Orbital injuries: a historical
overview. Oral Maxillofac Surg Clin North Am. 1993;5:409–418.
36. Sosin M, De La Cruz C, Mundinger GS, et al. Treatment outcomes
following traumatic optic neuropathy. Plast Reconstr Surg.
2016;137:231–238.
37. Erling B, Iliff N, Robertson B, Manson P. Footprints of the globe: a
practical look at the mechanism of orbital blowout fractures, with
a revisit to the work of Raymond Pfeifer. Plast Reconstr Surg.
1999;103:1313–1316.
38. Burm JS, Chung CH, Oh SJ. Pure orbital blowout fracture: new
concepts and importance of medial orbital blowout fracture. Plast
Reconstr Surg. 1999;103:1839–1849.
39. Woo KS, Cho PD, Lee SH. Reconstruction of severe medial orbital
wall fractures using titanium mesh plates by the pericaruncular
approach. J Plast Surg Hand Surg. 2014;48:248–253.
40. Manson P, Iliff N, Robertson B. The hope offered by early surgical
treatment to those patients whose blowout fractures demonstrate
tight muscle restriction or true muscle incarceration. Plast Reconstr
Surg. 2002;109:490–495.
41. Wachler BSB, Hold JB. The missing muscle syndrome in blowout
fractures: an indication for surgery. Ophthal Plast Reconstr Surg.
1998;14:17–19.
42. Jordan DR, Allen LH, White J, et al. Intervention within days for
some orbital floor fractures: the white-eyed blow-out fracture.
Ophthal Plast Reconstr Surg. 1998;14:379–390.
43. Yang JW, Woo JE, An JH. Surgical outcomes of orbital trapdoor
fracture in children and adolescents. J Craniomaxillofac Surg.
2015;43:444–447.
44. Chen CT, Chen YR. Application of the endoscope in orbital
fractures. Semin Plast Surg. 2002;16:241–251.
45. Sandler N, Carran R, Ochs M, Beatty R. The use of maxillary sinus
endoscopy in the diagnosis of orbital floor fractures. J Oral
Maxillofac Surg. 1999;57:399–403.

81.e2
SECTION I
CHAPTER 3 • Facial injuries
46. Saunders CJ, Whetzel TP, Stokes RB, et al. Transantral endoscopic
orbital floor exploration: a cadaver and clinical study. Plast
Reconstr Surg. 1999;900:575–581.
47. Bales N, Baganlisa F, Schlegel G. A comparison of transcutaneous
incisions used for exposure of the orbital rim and orbital floor: a
retrospective study. Plast Reconstr Surg. 1992;90:85.
48. Converse JM. Discussion: a randomized comparison of 4 incisions
for orbital fracture treatment. Plast Reconstr Surg. 1981;67:736, 737.
49. Holtman B, Wray RC, Little AG. A randomized comparison of 4
incisions for orbital fractures. Plast Reconstr Surg. 1981;67:731–735.
50. Heckler FR. Subciliary incision and skin muscle flap for orbital
fractures. Ann Plast Surg. 1983;10:309–313.
51. Manson P, Ruas E, Iliff N, Yaremchuk M. Single eyelid incision for
exposure of the zygomatic bone and orbital reconstruction. Plast
Reconstr Surg. 1987;79:120.
52. Ball JB Jr. Direct oblique sagittal CT of orbital wall fractures. AJR
Am J Roentgenol. 1987;148:601–608.
53. Manson P, Iliff N, Vander Kolk C, et al. Rigid fixation of orbital
fractures. Plast Reconstr Surg. 1990;86:1103–1109.
54. Jackson IT, Pellett C, Smith JM. The skull as a bone graft donor
site. Ann Plast Surg. 1983;11:527.
55. Rubin MM. Trochlear nerve palsy simulating an orbital blowout
fracture. J Oral Maxillofac Surg. 1992;50:1238–1239.
56. Rutman MS, Harris GJ. Orbital blowout fracture with ipsilateral
fourth nerve palsy. Am J Ophthalmol. 1985;100:343–344.
57. Wojno TH. The incidence of extraocular muscle and cranial nerve
palsy in orbital floor blowout fractures. Ophthalmology.
1987;94:682–687.
58. Biesman BS, Hornblass A, Lisman R, Kazlas M. Diplopia after
surgical repair of orbital floor fractures. Ophthal Plast Reconstr
Surg. 1996;12:9–16, discussion 17.
59. Iliff N, Manson P, Katz J, et al. Mechanisms of extraocular muscle
injury in orbital fractures. Plast Reconstr Surg. 1999;103:787–799. A
comprehensive human, cadaveric, and animal study into the effects of
orbital fractures on extraocular muscles and their intramuscular
vasculature to help understand mechanisms of diplopia and muscle
injury.
60. Kawamoto HK Jr. Late posttraumatic enophthalmos: a correctable
deformity? Plast Reconstr Surg. 1982;69:423.
61. Mathog R, Hlustrom R, Nesi F. Surgical correction of
enophthalmos and diplopia: a report of 38 cases. Arch Otolaryngol
Head Neck Surg. 1989;115:169.
62. Vaca EE, Mundinger GS, Kelamis JA, et al. Facial fractures with
concomitant open globe injury: mechanisms and fracture patterns
associated with blindness. Plast Reconstr Surg. 2013;131:
1317–1328.
63. Magarakis M, Mundinger GS, Kelamis JA, et al. Ocular injury,
visual impairment, and blindness associated with facial fractures:
a systematic literature review. Plast Reconstr Surg.
2012;129:227–233.
64. Girotto J, Gamble B, Robertson B, et al. Blindness following
reduction of facial fractures. Plast Reconstr Surg. 1998;102:1821–
1834. Landmark article to define the incidence of blindness following
facial fracture repair.
65. Kohn R. Lacrimal obstruction after migration of an orbital floor
implant. Am J Ophthalmol. 1976;82:934.
66. Raschke GF, Rieger UM, Bader RD, et al. Standardized
anthropometric evaluation of ectropion repair results. J Craniofac
Surg. 2012;23:1032–1037.
67. Chen CT, Wang TY, Tsay PK, et al. Traumatic superior orbital
fissure syndrome: assessment of cranial nerve recovery in 33 cases.
Plast Reconstr Surg. 2010;126:205–212.
68. Stranc MF, Robertson LA. Classification of injuries to the nasal
skeleton. Ann Plast Surg. 1979;2:468.
69. Motomura H, Muraoka M, Tetsuji Y, et al. Changes in fresh nasal
bone fractures with time on computed tomographic images. Ann
Plast Surg. 2001;47:620–624.
70. Pollack RA. Nasal trauma. Clin Plast Surg. 1992;19:
133–147.
71. Burm JS, Oh SK. Indirect open reduction through cartilaginous
incisions and intranasal Kirschner wire splinting in comminuted
nasal fractures. Plast Reconstr Surg. 1998;102:342–349.
72. Won Kim S, Pio Hong J, Kee Min W. Accurate firm stabilization
using external pins: a proposal for closed reduction of unfavorable
nasal bone fractures and their simple classification. Plast Reconstr
Surg. 2002;110:1240–1246.
73. Yabe T, Muroka M. Treatment of saddle type nasal fracture injury
Kirshner wire fixation of the nasal septum. Ann Plast Surg.
2004;53:89–92.
74. Rohrich RJ, Adams WP Jr. Nasal fracture management: minimizing
secondary nasal deformities. Plast Reconstr Surg. 2000;106:
266–273.
75. McNeil RA. Traumatic nasal neuralgia and its treatment. Br Med J.
1963;2:536–537.
76. Fry HJH. Interlocked stresses in human nasal septal cartilage. Br J
Plast Surg. 1966;19:276–278.
77. Fry HJH. The importance of the septal cartilage trauma. Br J Plast
Surg. 1967;20:392–402.
78. Mulliken JB, Kaban LB, Ezvans CA, et al. Facial skeletal changes
following hypertelorbitism correction. Plast Reconstr Surg.
1983;62:116.
79. Tessier P, Guiot G, Rougerie J, et al. [Cranio-naso-orbito-facial
osteotomies. Hypertelorism]. Ann Chir Plast. 1967;12:103–118.
An article by the father of craniofacial surgery describing the possibilities
of an intracranial approach for orbital reconstructive surgery.
80. Markowitz B, Manson P, Yaremchuk M, et al. High-energy orbital
dislocations: the possibility of traumatic hypertelorism. Plast
Reconstr Surg. 1991;88:20–29.
81. Converse JM, Smith B, Wood-Smith D. Orbital and naso-orbital
fractures. In: Converse JM, ed. Reconstructive Plastic Surgery. Vol. 2.
2nd ed. Philadelphia: W.B. Saunders; 1977:748–793.
82. Markowitz B, Manson P, Sargent L, et al. Management of the
medial canthal tendon in nasoethmoid orbital fractures: the
importance of the central fragment in treatment and classification.
Plast Reconstr Surg. 1991;87:843–853. Landmark article on the
classification types of nasoethmoid-orbital region. Knowledge of this
fracture pattern classification assists with the treatment of this complex
surgical condition.
83. Robinson TJ, Stranc MF. The anatomy of the medial canthal
ligament. Br J Plast Surg. 1970;23:1–7.
84. Sargent LA. Nasoethmoid orbital fractures: diagnosis and
treatment. Plast Reconstr Surg. 2007;120:16S–31S.
85. Anderson RL. The medial canthal tendon branches out. Arch
Ophthalmol. 1977;95:2051–2052.
86. Rodriguez RI, Zide BM. Reconstruction of the medial canthus. Clin
Plast Surg. 1988;15:255–262.
87. Gruss JS, Hurwitz JJ, Ink NA, Kasei E. The pattern and incidence
of nasolacrimal injury in naso-ethmoidal orbital fractures: the role
of delayed assessment and dacryocystorhinostomy. Br J Plast Surg.
1985;38:116–121.
88. Anderson RL, Edwards JJ. Indications, complications and results
with silicone stents. Ophthalmology. 1979;86:1474–1487.
89. Manson P, Iliff N. Posttraumatic orbital repositioning. p. 108–201,
Keating-Stewart, WB, Martin-Dunitz, London, 1999.
90. Hwang K, Suh MS, Chung IH. Cutaneous distribution of the
infraorbital nerve. J Craniofac Surg. 2004;15:3–5.
91. Kelley P, Hopper R, Gruss J. Evaluation and treatment
of zygomatic fractures. Plast Reconstr Surg. 2007;120:
5S–15S.
92. Del Santo F, Ellis E, Throckmorton GS. The effects of zygomatic
complex fracture on masseteric muscle force. J Oral Maxillofac Surg.
1992;50:791–799.
93. Larson OD, Thompson M. Zygomatic fracture: a simplified
classification for practical use. Scand J Plast Reconstr Surg.
1978;12:55–58.
94. Rinehart G, Marsh J, Hemmer K. Internal fixation of malar
fractures: an experimental biophysical study. Plast Reconstr Surg.
1989;84:21–25.

81.e3
References
95. Ellis E 3rd, Perez D. An algorithm for the treatment of isolated
zygomatico-orbital fractures. J Oral Maxillofac Surg.
2014;72:1975–1983.
96. Phillips JH, Gruss JS, Wells MD, Chollet A. Periosteal suspension
of the lower eyelid and cheek following subciliary exposure of
facial fractures. Plast Reconstr Surg. 1991;88:145–148.
97. Longakre M, Kawamoto H. Evolving thoughts on correcting
posttraumatic enophthalmos. Plast Reconstr Surg. 1998;101:889–906.
98. Francel TJ, Birely BC, Ringelman PR, Manson PN. The fate of
plates and screws after facial fracture reconstruction. Plast Reconstr
Surg. 1992;90:568–573.
99. Manson PN, Su CT, Hoopes JE. Structural pillars of the facial
skeleton. Plast Reconstr Surg. 1980;66:54–62.
100. Manson P, Clark N, Robertson B, et al. Subunit principles in
midface fractures: the importance of sagittal buttresses, soft tissue
reductions and sequencing treatment of segmental fractures. Plast
Reconstr Surg. 1999;103:1287–1306. Landmark article describing the
authors’ extensive experience in the treatment of midfacial injuries and
the importance of correct realignment of bone and soft tissues to improve
facial fracture treatment.
101. Raaf J. Post-traumatic cerebrospinal fluid leaks. Arch Surg.
1967;95:648–651.
102. Lewin W. Cerebrospinal fluid rhinorrhea in closed head injuries.
Br J Surg. 1954;42:1–18.
103. Morley TP, Hetherington RF. Traumatic cerebrospinal fluid
rhinorrhea and otorrhea, pneumocephalus and meningitis. Surg
Gynecol Obstet. 1957;104:88–98.
104. Chen CH, Wang TY, Tsay PK, et al. A 162-case review of palatal
fracture: management strategy from a 10-year experience. Plast
Reconstr Surg. 2008;121:2065–2073.
105. Manson PN, Shack RB, Leonard LF, et al. Sagittal fractures of the
maxilla and palate. Plast Reconstr Surg. 1983;72:484–489.
106. LeFort R. Etude experimentale sur les fractures de la machoire
superieur. Rev Chir Paris. 1901;23:208, 360, 479. Original article
describing the various fracture patterns associated with traumatic
craniofacial injury. We associate the author’s name to the different types
of fracture patterns recognized.
107. Manson PN. Some thoughts on the classification and treatment of
Le Fort fractures. Ann Plast Surg. 1986;17:356–363.
108. Romano JJ, Manson PN, Mirvis WE, et al. LeFort fractures without
mobility. Plast Reconstr Surg. 1990;85:355–362.
109. Bellamy JL, Mundinger GS, Reddy SK, et al. Le Fort II fractures
are associated with death: a comparison of simple and complex
midface fractures. J Oral Maxillofac Surg. 2013;71:1556–1562.
110. Girotto J, Makenzie E, Fowler C, et al. Long term physical
impairment and functional outcomes following complex facial
fractures. Plast Reconstr Surg. 2001;108:312–328.
111. Lee J, Dodson T. The effect of mandibular third molar risk and
position on the risk of an angle fracture. J Oral Maxillofac Surg.
2000;58:394–398.
112. Hagan EH, Huelke DF. An analysis of 319 case reports of
mandibular fractures. J Oral Surg. 1961;19:93–104.
113. Huelke DF, Burdi AR. Location of mandibular fractures related to
teeth and edentulous regions. J Oral Surg. 1964;22:396–405.
114. Huelke DF, Burdis AR, Eugene CE. Association between
mandibular fractures and site of trauma, dentition and age. J Oral
Surg. 1962;20:478–481.
115. Cornelius CP, Ehrenfeld M. The use of MMF screws: surgical
technique, indications, contraindications, and common problems
in review of the literature. Craniomaxillofac Trauma Reconstr.
2010;3:55–80.
116. Borah GL, Ashmead D. The fate of teeth transfixed by
osteosynthesis screws. Plast Reconstr Surg. 1996;97:726–729.
117. Frye WK, Sheppard PR, McLeod AC, Parfitt GJ. The Dental
Treatment of Maxillofacial Injuries. Oxford: Blackwell Scientific
Publications; 1942.
118. Amaratunga NA. Mouth opening after release of
maxillomandibular fixation in fracture patients. J Oral Maxillofac
Surg. 1987;45:383.
119. Amaratunga NA. The relation of age to the immobilization period
required for healing of mandibular fractures. J Oral Maxillofac Surg.
1987;45:111–113.
120. Edwards TJC, David DJ, Simpson DA, Abbott AH. The
relationship between fracture severity and complication rate in
miniplate osteosynthesis of mandibular fractures. Br J Plast Surg.
1994;47:210–211.
121. Tuovinen V, Norholt SE, Pedersen SS, Jensen J. A retrospective
analysis of 279 patients with isolated mandible fractures treated
with titanium miniplates. J Oral Maxillofac Surg. 1994;52:931–935.
122. Finn RA. Treatment of comminuted mandibular fractures by
closed reduction. J Oral Maxillofac Surg. 1996;54:320–327.
123. Ellis E 3rd. Treatment methods for fractures of the mandibular
angle. Int J Oral Maxillofac Surg. 1999;28:243–252.
124. Haug RH, Serafin BL. Mandibular angle fractures: a clinical and
biomechanical comparison-the works of Ellis and Haug.
Craniomaxillofac Trauma Reconstr. 2008;1:31–38.
125. Dingman RO, Grabb WC. Surgical anatomy of the mandibular
ramus of the facial nerve based on the dissection of 100 facial
halves. Plast Reconstr Surg. 1962;29:266–272.
126. Chuong R, Donoff RB, Guralnick WC. A retrospective analysis of
327 mandibular fractures. J Oral Maxillofac Surg. 1983;41:305–309.
127. Ellis E. Selection of internal fixation devices in mandibular
fractures: How much fixation is enough? Semin Plast Surg.
2002;16:229–241.
128. Herford AS, Ellis ES. Use of locking reconstruction bone plate for
mandibular surgery. J Oral Maxillofac Surg. 1998;56:1261–1265.
129. Champy M, Lodde JP, Schmidt R, et al. Mandibular osteosynthesis
by miniature screwed plates via a buccal approach. J Maxillofac
Surg. 1978;6:14–21. Original article describing the use of monocortical
plates for the treatment of mandibular fractures; lines of osteosynthesis
are defined.
130. Champy M, Kahn JL. Fracture line stability as a function of the
internal fixation system (Discussion). J Oral Maxillofac Surg.
1995;53:801.
131. Forrest C. Application of minimal access techniques in lag screw
fixation of fractures of the anterior mandible. Plast Reconstr Surg.
1994;104:2127–2134.
132. Niederdellmann H, Schili W, Duker J, Akuamoa-Boateng E.
Osteosynthesis of mandibular fractures using lag screws. Int J Oral
Surg. 1976;5:117–121.
133. Amaratunga NA. The effect of teeth in the line of mandibular
fractures on healing. J Oral Maxillofac Surg. 1987;45:312, 314.
134. Neal DC, Wagner WF, Alpert B. Morbidity associated with teeth in
the line of mandibular fractures. J Oral Surg. 1978;36:859–862.
135. Shetty V, Freymuller R. Teeth in the fracture line. J Oral Maxillofac
Surg. 1989;47:1303–1306.
136. Mundinger GS, Borsuk DE, Okhah Z, et al. Antibiotics and facial
fractures: evidence-based recommendations compared with
experience-based practice. Craniomaxillofac Trauma Reconstr.
2015;8:64–78.
137. Zallen RD, Curry JT. A study of antibiotic usage in compound
fractures. J Oral Surg. 1975;33:431–434.
138. Francel T, Birely B, Ringleman P, Manson PN. The fate of plates
and screws after facial fracture reconstruction. Plast Reconstr Surg.
1992;90:505–573.
139. Ellis E III, Tharanon W. Facial width problems associated with
rigid fixation of mandibular fractures. J Oral Maxillofac Surg.
1992;50:87–94.
140. Manson PN. Facial fractures. In: Perspectives in Plastic Surgery. St
Louis: Quality Medical Publishing; 1988:1–36.
141. Haug R, Schwimmer A. Fibrous union of the mandible: a review
of 27 patients. J Oral Maxillofac Surg. 1994;52:832–839.
142. Bochlogryos PN. A retrospective study of 1,521 mandibular
fractures. J Oral Maxillofac Surg. 1985;43:597–599.
143. Bochlogryos PN. Non-union of fractures of the mandible. J
Maxillofac Surg. 1985;13:189.
144. Benson PD, Marshall MK, Engelstad ME, et al. The use of
immediate bone grafting in reconstruction of clinically infected

81.e4
SECTION I
CHAPTER 3 • Facial injuries
mandibular fractures: bone grafts in the presence of pus. J Oral
Maxillofac Surg. 2006;64:122–126.
145. Cascone P, Sassano P, Spalcaccia F. Condylar fractures during
growth: a followup of 16 patients. J Craniofac Surg. 1999;10:87–92.
146. Hoving J, Boering G, Stegenga B. Long-term results of nonsurgical
management of condylar fractures in children. J Oral Maxillofac
Surg. 1999;28:429–440.
147. Norholt SE, Krishnan V, Sindet-Pederson S, Jensen I. Pediatric
condylar fractures. A long term follow up of 55 patients. J Oral
Maxillofac Surg. 1993;51:1302–1310.
148. Baker AW, McMahon J, Moos KF. Current consensus on the
management of fractures of the mandibular condyle. Int J Oral
Maxillofac Surg. 1998;27:258–266.
149. Zide MF, Kent JN. Indications for open reduction of mandibular
condyle fractures. J Oral Maxillofac Surg. 1983;41:89–98.
150. Assael L. Open versus closed reduction of adult mandibular
condyle fractures: an alternative interpretation of the evidence. J
Oral Maxillofac Surg. 2003;61:1333–1339.
151. Ellis E. Complications of mandibular condylar fractures. Int J Oral
Maxillofac Surg. 1998;27:255–257.
152. Haug RH, Assael L. Outcomes of closed versus open treatment of
mandibular condylar process fractures. J Oral Maxillofac Surg.
2001;59:370–375.
153. Ellis E III, Throckmorton GS. Treatment of mandibular condylar
process fractures: biological considerations. J Oral Maxillofac Surg.
2005;63:115–134.
154. Al-Moraissi EA, Ellis E 3rd. Surgical treatment of adult
mandibular condylar fractures provides better outcomes than
closed treatment: a systematic review and meta-analysis. J Oral
Maxillofac Surg. 2015;73:482–493.
155. Zachariades N, Mezitis M, Mourouzis C, et al. Fractures of the
mandibular condyle: a review of 466 cases. Literature review,
reflections on treatment and proposals. J Craniomaxillofac Surg.
2006;34:421–432.
156. Haug RH, Brandt MT. Closed reduction, open reduction and
endoscopic assistance: current thoughts on the management of
mandibular condyle fractures. Plast Reconstr Surg.
2007;120:90S–102S.
157. Chen CT, Lai JP, Tung TC, Chen YR. Endoscopically assisted
mandibular subcondylar fracture repair. Plast Reconstr Surg.
1999;103:60–65.
158. Barber HD. Conservative management of the fractures atrophic
edentulous mandible. J Oral Maxillofac Surg. 2001;59:789–791.
159. Buchbinder D. Treatment of fractures of the edentulous mandible,
1943 to 1993: a review of the literature. J Oral Maxillofac Surg.
1993;51:1174–1180.
160. Marciani RD. Invasive management of the fractured atrophic
mandible. J Oral Maxillofac Surg. 2001;59:392–395.
161. Amaratunga NA. A comparative study of the clinical aspects of
edentulous and dentulous fractures. J Oral Maxillofac Surg.
1988;46:3–5.
162. Halazonetis JA. The “weak” regions of the mandible. Br J Oral
Surg. 1968;6:37.
163. Obwegeser HL, Sailer HF. Another way of treating fractures of the
atrophic edentulous mandible. J Oral Maxillofac Surg. 1982;40:23.
164. Eyrich GKH, Gratz KW, Sailer HF. Surgical treatment of fractures
of the edentulous mandible. J Oral Maxillofac Surg.
1997;55:1081–1087.
165. Faeone PA, Haedicke GJ, Brooks G. Maxillofacial fractures in the
elderly: a comparative study. Plast Reconstr Surg. 1990;83:443–448.
166. Gruss JS, Phillips JH. A early definitive bone and soft tissue
reconstruction of major gunshot wounds of the face. Plast Reconstr
Surg. 1991;87:436–450.
167. Clark N, Birely B, Manson PN, et al. High-energy ballistic and
avulsive facial injuries: classification, patterns, and an algorithm
for primary reconstruction. Plast Reconstr Surg. 1996;98:583–601.
168. Robertson B, Manson P. The importance of serial debridement and
second look procedures in high-energy ballistic and avulsive facial
injuries. Oper Tech Plast Reconstr Surg. 1998;5:236–246.
169. Goodman JM, Kalsbeck J. Outcome of self-inflicted gunshot
wounds of the head. J Trauma. 1965;5:636–642.
170. Rodriguez E, Martin M, Bluebond-Langner R, et al. Microsurgical
reconstruction of post-traumatic high-energy maxillary defects:
establishing the effectiveness of early reconstruction. Plast Reconstr
Surg. 2007;120:103S–117S.
171. Rodriguez E, Bluebond-Langner R, Park J, Manson P. Preservation
of contour in periorbital & midfacial craniofacial microsurgery:
reconstruction of the soft tissue elements and skeletal buttresses.
Plast Reconstr Surg. 2008;121:1738–1747.
172. Fisher M, Dorafshar A, Bojovic B, et al. The evolution of critical
concepts in aesthetic craniofacial microsurgical reconstruction.
Plast Reconstr Surg. 2012;130:389–398.

SECTION II • Head and Neck Reconstruction
4 
Surgical treatment of migraine headaches
Ali Totonchi and Bahman Guyuron
SYNOPSIS
■ Approximately 30 million Americans suffer from migraine headaches
(MH), and lifetime prevalence is estimated to be 11–32%, including
18% of women and 6% of men.
■ Medical management is the first line of treatment, but poorly controlled
or uncontrolled MH can be treated surgically, specifically since severe
migraine could be disabling.
■ Before considering a patient for surgical management, they should be
evaluated by a neurologist/headache specialist for diagnosis and
medical management.
■ In the surgical evaluation of patients with MH, the trigger site can be
confirmed by botulinum toxin A (BTX-A) injection or nerve block. If the
history or computed tomography (CT) scan findings are strongly
indicative of a specific trigger site, this step can be bypassed.
■ The four major trigger sites are frontal, temporal, occipital,
and nasal.
■ In the frontal trigger site, the supraorbital and supratrochlear nerves
can be irritated by adjacent structures like frowning muscles, vessels,
bands over the supra-orbital notch, or bony tunnel, and this area is
treated by freeing the nerve from all possible irritating structures and
placement of fat graft.
■ The temporal trigger site is treated by avulsion/decompression of the
zygomaticotemporal branch of trigeminal nerve (ZTBTN) as it emerges
from deep temporal fascia.
■ The occipital trigger site is located in the posterior part of the neck
where the greater occipital nerve is passing through the semispinalis
capitis muscle and trapezius fascia and crosses over the occipital
artery; treatment includes partial resection of the muscle/fascia,
padding the nerve with a subcutaneous fat flap, and resection of the
artery adjacent to the nerve.
■ Theory behind the rhinogenic trigger point is that nasal mucosa
containing a rich nervous supply can be irritated due to contact point
or pressure from an entrapped air pocket. Rhinogenic trigger site is
treated with septoplasty, elimination of contact points between the
turbinate and the septum or nasal side wall, reduction of enlarged
turbinates, and removal of concha bullosa.
■ Less common trigger sites like the auriculotemporal nerve, lesser
occipital nerve, third occipital nerve, or any distal branches of all of
the above mentioned nerves could act as a trigger site often due to
irritation by a blood vessel or fascial band.
Access the Historical Perspective section online at

Introduction
Headaches are the seventh leading presenting complaint in
ambulatory medical care in the US.1 In most neurology clinics,
headache, the majority of which is migraine, is the most
common chief complaint. Nearly 30 million Americans suffer
from MH, and lifetime prevalence is estimated to be 11–32%
across several countries. Eighteen percent of women and 6%
of men are involved, and two-thirds of these patients do not
benefit from over-the-counter medications. In women, MHs
are more common than asthma (5%) and diabetes (6%) com-
bined. Many of the available prophylactic medications harbor
side effects such as sedation, paresthesia, weight gain, cogni-
tive impairment, and sexual dysfunction. The cost of migraine
treatment and loss of time from work associated with MH
impose a major economic burden on the patient and society,
collectively exceeding $13 billion.1–11
Basic science/disease process
The diagnostic criteria of MH are shown in Table 4.1. There
are two subtypes of migraine: migraine with aura and
migraine without aura. Auras develop over 5–20 min but last
for less than 60 min and are followed by a migraine headache.
One out of three patients with MH experiences aura. MHs are
usually frontotemporal, typically unilateral, and are charac-
terized by recurrent attacks of pulsating, intense pain associ-
ated with nausea and photophobia. Traditional, non-surgical
treatment of MH can be non-pharmacologic or pharmacologic.
Non-pharmacologic treatment of MH consists of avoidance

83
Basic science/disease process
norepinephrine reuptake inhibitors), and antiepileptics
(e.g., Topiramate, valproic acid).12,13
Opioid-containing analgesics are not recommended in
the treatment of migraine. Barbiturate-containing analgesics
should be avoided in migraine patients as well. Both of these
classes of medications have a very strong potential for causing
“medication overuse headache”.
Medication overuse headache, which is also sometimes
called “rebound” headache, based on the International Head-
ache Society definition, is a headache that occurs more than
15 days per month, developing as consequence of regular
use of abortive headache medication. All of the abortive
medications, including simple analgesics and migraine-
specific medication (Triptan and Ergots), can cause medication
overuse headaches if used frequently and generally beyond
3 months.
of triggers, which commonly include artificial sweeteners,
monosodium glutamate, and nitrate containing foods or
alcohol. Sometimes application of pressure, cold, or heat can
mitigate or abort the migraine headaches.
Pharmacologic treatment can be further subdivided into
acute abortive and prophylactic treatment:
■ Acute abortive treatment consists of simple analgesics
like acetaminophen, nonsteroidal anti-inflammatory, or
migraine specific abortive medications, which includes
Triptan or Ergots. The first-line acute abortive treatment
is the use of Triptans or NSAIDs, sometimes together,
although intravenous antiemetics and ergotamine can be
used as well.
■ Preventive treatment consists of antihypertension
medications (beta-blockers, Ca++ blockers),
antidepressants (tricyclic antidepressants or serotonin-
Table 4.1  The constellation of symptoms that aid in the diagnosis of migraine headache trigger sites
Frontal
Temporal
Rhinogenic
Occipital
Starting location
of pain
Frontal area
Temple area
Behind the eye
At the point of exit of the
greater occipital nerve
from the semispinalis
capitis muscle (3.5 cm
caudal to the occipital
tuberosity and 1.5 cm
off the midline)
Time
Usually in the afternoon
Patient usually wakes up in
the morning with pain
Patient commonly wakes
up with pain in the
morning or at night
Not specific
Exam,
observation
Strong corrugator muscle
activity causing deep frown
lines on animation
The points of emergence of the
supraorbital and
supratrochlear nerves from
corrugator muscle or the
foramen are tender to the
touch
Patients usually have eyelid
ptosis on the affected side at
the time of active pain
Pressure on these sites may
abort the headache during the
initial stages
Application of cold or warm
compresses on these sites
often reduces or stops the
pain
The pain is usually imploding in
nature
Stress-related
Sometimes associated with
tenderness of the
temporalis or masseteric
muscle
Clenching/grinding
Rubbing or pressing the
exit point of the
zygomaticotemporal
branch of the trigeminal
nerve from the deep
temporal fascia can stop
the pain in the beginning
Application of cold or
warm compresses to
this point may reduce or
stop the pain
The pain is characterized
as imploding
Stress-related
Commonly triggered by
weather changes
Rhinorrhea on the
affected side
Allergy-related
Hormone-related,
menstrual cycle-related
The pain is usually
described as
exploding
Muscle tightness
Heavy exercise-related
Compression of this site
can stop the pain in
the early stage; at the
later stage, this point is
tender
Application of cold or
heat at this site may
result in some
improvement in the
pain
Stress-related
CT scan
Concha bullosa, septal
deviation with contact
between the turbinates
and the septum, and
septa bullosa
CT, computed tomography.

84
SECTION II
CHAPTER 4 • Surgical treatment of migraine headaches
Patient selection
Trigger sites
Currently, we have identified four common trigger sites: (1)
frontal triggers, where glabellar muscles, vessels, and possible
fascial band or bony tunnel in the supraorbital rim compress
or irritate the supratrochlear and supraorbital nerves and
causes frontal headaches; (2) temporal triggers, where com-
pression of ZTBTN by contraction of the temporalis muscle,
fascia, or the artery causes inflammation of the nerve and
leads to temporal headaches; (3) occipital triggers, where the
semispinalis capitis muscle, trapezius fascia, and occipital
artery can irritate the occipital nerve and cause occipital head-
aches; and (4) septonasal triggers, where intranasal structures
compress the trigeminal end branches and cause paranasal
and retrobulbar headaches.
There are several less common trigger sites, many of which
are at the intersections of nerves and arteries, such as the
superficial temporal artery and the auriculotemporal nerve.
The lesser occipital nerve and the third occipital nerve can
also act as trigger sites.26,27 In addition to the above-mentioned
trigger points, the end branches of the nerve discussed previ-
ously could be irritated by a blood vessel, or less commonly
by a fascial band, and act as a trigger point.
The role of botulinum toxin injection
BTX-A (Botox, Allergan, Irvine, CA) or abobotulinumtoxin A
(Dysport, Medicis Aesthetics, Scottsdale, AZ) blocks the
release of acetylcholine at the neuromuscular junction. A
deadly neurotoxin produced by Clostridium botulinum, its
In practice, opioids and barbiturate-containing analgesics
by far are the most common reason for medication overuse
headache. The prevalence of medication overuse is reported
between 50 and 70% in different tertiary headache clinics.
In general, these groups of patients are not ideal candidates
for surgical treatment of migraine headache, until they
have been off these medications and cleared for surgery by
the neurologists or there are clear plans for detoxification
after surgery.
Diagnosis and patient presentation
Preoperative history and examination
Surgical treatment of MH should only be considered after the
diagnosis of MH is confirmed by a neurologist and more
serious causes of headaches have been excluded. The proper
surgical candidate is someone whose headaches are not
controlled with traditional medical treatment and who has
an acceptable surgical risk. Pregnant and nursing women
are also typically excluded from surgical consideration. The
constellation of symptoms leads the examiner to suspect the
potential trigger site (Table 4.1), which is further validated by
physical examination.28,31 The salient piece of information that
helps to identify the trigger site is the site from which the pain
starts. The patient is asked to complete a migraine form asking
a number of critical questions. Keeping a monthly diary of
MH prior to the surgery will provide more reliable informa-
tion than patient recall.
Hypertrophy of the corrugator supercilii muscle with verti-
cal frown lines is a common finding and might be obvious in
patients with a frontal trigger site (Fig. 4.1). The nasal exam
includes a physical exam with or without endoscopic exami-
nation, which must be performed to detect septal deviation
and turbinate hypertrophy with contact points between the
septum and turbinates, concha bullosa, and septa bullosa, and
the findings are confirmed using a CT scan of the septum and
sinuses (Fig. 4.2).
Fig. 4.1  Example of corrugator supercilii muscle hypertrophy.
A
Fig. 4.2  (A) Combination of a large spur protruding into the left inferior turbinate,
right middle turbinate concha bullosa, and extensive sinus disease. (B) Significant
enough deviation of the septum to the left to touch the lateral wall of the nose and
the left middle turbinate along with mild maxillary sinus disease. Bilateral concha
bullosa of the middle turbinates and Haller’s cell.
B

84.e1
Historical perspective
Historical perspective
Surgical attempts to treat MH date back to 1931. Walter Dandy
removed the inferior cervical and first thoracic sympathetic
ganglions in two patients.14 Interestingly, he was able to
eliminate MH in both of these patients. However, this pioneer
work lacked scientific significance due to a small patient
sample size, absence of a control group, and an extremely
short follow-up period.
Resection of the greater superficial petrosal nerve in the
treatment of various types of unilateral headaches was sug-
gested by Gardner et al. in 1946.15 Twenty-six patients under-
went surgery, nine of whom were felt to have unilateral MH,
including seven women and two men. All patients with MH
observed either complete elimination or significant improve-
ment. Two patients had initial improvement, but the MH
recurred after 7–8 months. The patients, however, reported a
reduction in tear production and dryness of the nose. Some
patients developed corneal ulcerations.
Total resection of the trigeminal nerve within the cranial
base (trigeminal neurectomy) has also been advocated. Anes-
thesia of the ipsilateral hemiface, dryness of the cornea,
corneal ulceration, and loss of vision may ensue after such a
complex procedure.
Murillo, in 1969, introduced resection of the temporal
neurovascular bundle for control of MH.16 This surgery
included removal of the superficial temporal artery and
auriculotemporal nerve. The procedure was effective in elimi-
nation of MHs in 30 of 34 patients. This report, however, did
not include the length of follow-up, nor was there a control
group for this clinical trial.
An occipital neurectomy was suggested for patients with
occipital MH and neuritis by Murphy in 1969.17 This operation
was performed on 30 patients. Eighteen patients had excellent
results, seven had good results, three had fair, and two patients
had poor results. Many of these patients, however, had less
than 1 year of follow-up. Murphy’s report did not indicate the
incidence of anesthesia or paresthesia in the occipital region,
nor did it outline any other adverse effects resulting from the
surgery.
The elimination of MH in two patients who underwent
endoscopic forehead rejuvenation with resection of the cor-
rugator supercilii muscle prompted our team to conduct a
retrospective study on patients who had undergone endo-
scopic forehead lift.18 Thirty-nine out of 249 patients fulfilled
the International Headache Society criteria for MH (Box 4.1).
Twenty-nine patients (74.4%; all women) experienced
migraine without aura, whereas 10 patients (25.6%; one man
and nine women) had migraine with aura. Thirty-one of 39
patients (79.5%) experienced either complete elimination or
improvement of the MHs immediately after surgery. The
follow-up period averaged 47 months (5–122 months).
The results of the few published studies on the effects of
BTX-A (Botox, Allergan, Irvine, CA) on MH19–22 and the above-
mentioned study led us to the conclusion that the corrugator
supercilii muscle must have a major role in the elimination/
reduction of MH, since deactivation of this muscle was the
only common denominator of these observations. As a result,
a prospective pilot study was designed.23 Twenty-nine patients
who were confirmed to have MH (2–12 MHs per month)
underwent injection of 25 U Botox into each corrugator
supercilii muscle: 16 observed complete elimination of MHs,
eight noted significant improvement, and five had minimal to
no response. Twenty-two of 24 patients responded favorably
to the injection of Botox; surgical decompression of the supra-
orbital and supratrochlear nerves was done by removal of the
corrugator supercilii and depressor supercilii muscles. This
group included 18 women and four men ranging in age from
24 to 58 years old. The ZTBTN was also detached. Of the 22
patients who underwent surgery, 21 (95.5%, P < 0.001)
observed an improvement in MH. Ten patients (45.5%, p <
0.01) noted elimination of MHs, and 11 (50.0%, P < 0.004)
noted a significant improvement. The average intensity of
MH for the entire surgical group was reduced from 8.9 to 4.1
(P < 0.04) on an analogue scale of 1–10, and the frequency
changed from 5.2 to an average of 0.8 (P < 0.001) per month.
When the group with improvement only was analyzed, the
intensity fell from 9.0 to 7.5 and the frequency changed from
5.6 to 1.0 MHs per month. Only one patient failed to notice
BOX 4.1  Migraine headache diagnostic criteria
Migraine without aura
A. At least five attacks fulfilling criteria B–D
B. Headache attacks lasting 4–72 h (untreated or unsuccessfully
treated)
C. Headache has at least two of the following characteristics:
a. Unilateral location
b. Pulsating quality
c. Moderate or severe pain intensity
d. Aggravation by or causing avoidance of routine physical
activity (e.g., walking or climbing stairs)
D. During headache at least one of the following:
a. Nausea and/or vomiting
b. Photophobia and phonophobia
E. Not better accounted for by another ICHD-3 diagnosis
Migraine with aura
A. At least two attacks fulfilling criteria B and C
B. One or more of the following fully reversible aura symptoms:
1. Visual
2. Sensory
3. Speech and/or language
4. Motor
5. Brainstem
6. Retinal
C. At least two of the following four characteristics:
1. At least one aura symptom spreads gradually over 5 min,
and/or two or more symptoms occur in succession
2. Each individual aura symptom lasts 5–60 min
3. At least one aura symptom is unilateral
4. The aura is accompanied, or followed within 60 min, by
headache
D. Not better accounted for by another ICHD-3 diagnosis, and
transient ischemic attack has been excluded
(Adapted from International Headache Society website: http://

Classification-III-ICHD-III-2013-Beta.pdf)

84.e2
SECTION II
CHAPTER 4 • Surgical treatment of migraine headaches
an improvement. Shortly after, the rhinogenic and the greater
occipital trigger sites were discovered as major trigger sites
on those who did not have complete elimination of MHs after
injection of BTX-A, bringing the number of major trigger sites
to four. Anatomical studies were performed,24,25 and minor
trigger sites were also identified.26
A prospective randomized study was conducted27 on 125
patients diagnosed with MHs: 100 were randomly assigned
to the treatment group, and 25 served as controls. Patients in
the treatment group were injected with BTX-A for identifica-
tion of trigger sites. Eighty-two of the 89 patients (92%) in the
treatment group who completed the study demonstrated at
least 50% reduction in MH frequency, duration, or intensity
compared with the baseline data; 31 (35%) reported elimina-
tion and 51 (57%) experienced improvement over a mean
follow-up period of 396 days. In comparison, three of 19
control patients (15.8%) recorded a reduction in MH during
the 1-year follow-up (P < 0.001), and no patients observed
elimination.
In 2009, a placebo-controlled study with sham surgery was
completed by our team.28 Seventy-five patients with moder-
ate to severe MH were randomly assigned to receive either
actual or sham surgery in their predominant single trigger
site. Fifteen of 26 in the sham surgery group (57.7%) and 41
of 49 in the actual surgery group (83.7%) experienced at least
50% reduction in MH. Furthermore, 28 of 49 patients in the
actual surgery group (57.1%) reported complete elimination
of MH, compared with only one of 26 patients in the sham
surgery group (3%) (P < 0.001). Compared with the control
group, the actual surgery group demonstrated statistically sig-
nificant improvements in all validated MH measurements at
1 year.
In another study from Vienna, Austria,29 the authors fol-
lowed our initial report24 and removed the corrugator super-
cilii muscle through a transpalpebral incision. The lead author
of this report, a plastic surgeon who suffered from MHs,
persuaded another colleague to operate on him following the
initial methods developed by our group. Having enjoyed a
successful outcome, he commenced the study summarized
here. From the entire group of 60 patients, 17 (28.3%) reported
total relief from migraine, 24 (40%) significant improvement,
and 19 (31.6%) minimal or no change in their MHs after a
minimum follow-up period of 6 months. This study included
only a single-site surgery before the other trigger sites were
discovered. These reports were later confirmed by Poggi
et al.30 In 2011, a 5-year follow up was published by Guyuron
et al. which showed that 88% of the patients had experienced
a positive response to the surgery after 5 years. Twenty-nine
percent reported complete elimination of migraine headache,
59% noticed a significant decrease, and 8% experienced no
significant change.49 From the above-mentioned studies, it is
evident that whenever the peripheral-to-central trigeminal
pathway is interrupted, relief of migraine pain can be expected
in most patients.

85
Patient selection
severe trigger site based on the patient’s reported symptoms
and physical examination. This is most often the corrugator
supercilii muscle. First, 12.5 U BTX-A is injected with a long
30-gauge, 1-inch needle into the glabellar muscle sites through
a single deep subcutaneous horizontal injection. Patients then
keep a headache diary and refrain from taking prophylactic
migraine medication unless contraindicated. Response to the
injection over the subsequent 4 weeks will direct the next step.
If the headache disappears completely, it means the injected
site is likely to be the sole trigger site. If the headaches are
improved but not eliminated, it means that the patient has
additional trigger sites. If the patient does not respond to the
injection, it means that the headaches are not likely to be
triggered from the initial injection site (Fig. 4.3). Often the
patients will report elimination of the headaches from that
trigger site but continuation of headaches in the temporal,
retrobulbar, or occipital headaches. The other common trigger
sites are injected 1 month apart, up to a maximum of three
injections. Those patients with trigger sites that observe at
least 50% reduction in intensity or frequency of the headache
from baseline are considered for surgical intervention.28 Nerve
clinical utility in MH has been gaining popularity over the last
two decades.22,23
BTX-A was first introduced over three decades ago as a
treatment for strabismus32–35 and since has been used in many
neuromuscular conditions, including oromandibular dysto-
nia, laryngeal dystonia, cervical dystonia, writer’s cramp,
hemifacial spasm, and for aesthetic reasons.36,37
Since the original reports regarding the use of BTX-A for
treatment of headache19–21 and subsequent reports for its use
in the determination of trigger sites,23 the review of the neurol-
ogy literature is contradictory in terms of success rate, possibly
because these studies were not specific about the location of
the injection.38–41 Recent practice for prophylactic migraine
headache treatment using BTX-A is based on PREEMPT I and
PREEMPT II double blind, placebo-controlled randomized
trials is profoundly flawed because of lack of focus on the
anatomy of the nerve and muscle and using 12 inch length
needle for the injection that fails to reach the intended ana-
tomical deep structures.50,51
When BTX-A is used to identify trigger sites, the sites are
injected systematically, starting with the most common and
Fig. 4.3  Algorithm for diagnosis of migraine headache (MH) using botulinum toxin. Trigger sites are injected with 12.5 U botulinum toxin A with a 1-inch (2.5-cm)
30-gauge needle. Improvement is operationally defined as a 50% reduction in headache intensity or frequency from the baseline for 4 weeks. (Redrawn from Guyuron B,
Kriegler JS, Davis J, et al. Comprehensive surgical treatment of migraine headaches. Plast Reconstr Surg 2005;115:1–9.)
B
Improvement
A & C
Improvement
C
Improvement
B & C & ST
B & C
Improvement
A & B & C
Improvement
A & B
Improvement
No change
A
Elimination
Elimination
Elimination
No change
A = Most common trigger site
B = Next most common trigger site
C = 3rd most common trigger site
SD = Septal deviation
ET = Enlarged turbinates
S&T = Septum & Turbinates
= Identified trigger site(s)
Improvement
Inject site A
Inject site B
Inject site B
No change
No change
Inject site C
Inject site C
Elimination
Inject site C
Inject site C
SD & ET
SD & ET
A & B & ST
Elimination
No change
SD & ET
SD & ET
A & ST
Elimination
No change
No change
SD & ET
SD & ET
SD & ET
SD & ET
B & ST
ST
C & ST
A & C & ST
A & B & C & ST
Elimination

86
SECTION II
CHAPTER 4 • Surgical treatment of migraine headaches
supercilii muscle comes into view first. This muscle is lighter
in color than the corrugator supercilii and it is also less friable.
The muscle is then removed as thoroughly as possible. The
corrugator supercilii muscle is identified next by its position
over the supraorbital rim, as well as its darker color compared
with the orbicularis oculi and depressor supercilii muscles. A
small communicating vein is often seen between the supraor-
bital and supratrochlear vessels, deep to the muscle. Almost
consistently, a nerve branch can be identified which pierces
the muscle. This nerve is followed to its origin in the supra-
orbital region while the muscle is lifted. The corrugator
supercilii muscle is removed in a medial to lateral fashion as
thoroughly as possible using electrocautery. Sometimes multi-
tooth forceps serve effectively to avulse the muscle completely
around the nerve, while the supraorbital and supratrochlear
nerves are preserved. Through this approach, supraorbital
and supratrochlear vessels are dissected off the nerves, cauter-
ized using a bipolar cautery, and removed. The supraorbital
notch also is evaluated for possible compression points by a
fascial band or possible presence of bony tunnel. A preopera-
tive peri-nasal CT scan can help with identification and loca-
tion of the main and the accessory bony tunnel. If present,
these are unroofed. If the accessary foramen is very deep, the
related branch is removed. Fat is harvested from the medial
compartment of the upper eyelid and grafted to the site of the
resected muscle. The fat graft serves three purposes: (1) it
minimizes contour irregularity resulting from a thorough
muscle resection; (2) it protects the exposed nerve branches;
and (3) it minimizes the recurrent muscle function. The graft
is sutured to the periosteum with 6-0 Monocryl suture, and
the skin incision is sutured with 6-0 plain catgut.44,45
Postoperatively, the patient is allowed to resume light
activities on day 1, regular activities on day 7, and heavy
exercise after 3 weeks. Patients observe a reasonable amount
of edema and ecchymosis, which usually subside in 10–14
days.
Complications
The most common complication with this approach includes
itching of the forehead and frontoparietal scalp, which usually
lasts several weeks to several months. Rarely, this may persist
for a year or two. Every patient experiences some anesthesia
or paresthesia immediately after surgery. This includes the
entire forehead and anterior scalp. This paresthesia nearly
always resolves if the nerves have been preserved. There is a
risk of asymmetry and dynamic imperfections if the muscle
is not removed thoroughly and evenly.
Endoscopic approach
For the patients who have optimal or short forehead length
and experience migraine headaches in the forehead and
temple, an endoscopic approach is preferred. After proper
preparation of the face under sedation, the incision sites are
marked. There are a total of five or six incisions, each one
measuring 1–1.5 cm in length depending on the thickness of
the scalp – one or two frontal incisions and two on either
temple located 7 and 10 cm from the midline, all placed within
the hair-bearing skin. For patients with a normal or short
forehead, one midline incision is used. In patients with a
borderline long forehead or excessively curved contour, two
blocks could be used similarly, but the timing of the injections
is difficult since it has to be done while the patient has migraine
headaches to be meaningful. Lack of positive response to the
nerve block or BTX-A does not mean that the patient is not a
good candidate for surgery. When the patient has allodynia
or the patient has established (centralized) migraine attack the
response to the nerve block could be negative.
The primary side effect of BTX-A injected into the temporal
area is atrophy of the temporal muscles and related hollowing
of the temples and the reported hourglass deformity.42 This
disuse atrophy is temporary, and patients should be counseled
appropriately. Eyelid ptosis is the second most common
complication. Theoretically, strabismus might happen because
of the high dose and deep injection in the temple or brow
areas. Some patients have developed antibodies to BTX-A,
rendering it relatively ineffective. This has been estimated to
occur in 7% of treated patients.35,43 The use of non-A botulinum
toxins for patients resistant to type A is currently being
investigated.35
While BTX-A had a major role in the detection of the trigger
sites and as the prognosticator during the initial phases of the
development of this procedure, we currently do not use it
routinely due to the cumbersome course of injections
which becomes impractical while caring for out-of-the-region
patients, increasing cost and delaying potential elimination in
patients who otherwise would benefit from the surgery. A
nerve block will serve a similar role if it is injected while the
patient is in the early stages of the migraine cascade. The
constellation of symptoms can serve as reliably as BTX-A in
the detection of the trigger sites.52
Surgical technique
Deactivation of frontal trigger site
In the frontal trigger site, the supraorbital and supratrochlear
nerves are passing through the glabellar muscles, including
the corrugator supercilii, depressor supercilii, and procerus.
The nerves could be irritated by this group of muscles, vessels
traveling with the nerves through bony supraorbital foramen
or under the fascial band beneath the supraorbital notch. The
goal of surgery is to prevent irritation of the nerves by all of
these structures, complete and thorough resection of the
muscle is suggested for a favorable outcome.19 The approach
can be either transpalpebral44,45 or endoscopic. The endoscopic
approach is a better choice for those who suffer from MH
triggered from both temporal and frontal sites.
Transpalpebral approach
Under intravenous sedation or general anesthesia, the face is
prepped and draped. The upper tarsal crease is marked on
each eyelid, with an incision length of approximately 1 inch
(2.5 cm), unless a concomitant blepharoplasty is planned. For
the latter indication, a conventional blepharoplasty incision is
utilized. Local anesthesia (0.5% lidocaine with 1 : 100 000 epi-
nephrine) is infiltrated into the eyelid. A skin incision is made
with a 10 blade and is extended through the orbicularis
muscle. The plane between the orbicularis muscle and the
septum is identified, and dissection is continued cephalically
with a pair of baby Metzenbaum scissors. The depressor

87
Surgical technique
After the incisions are made with a number 15 scalpel, they
are deepened to the deep temporal fascia using the spread-
ing effects of the baby Metzenbaum scissors. The dissection
continues using an Obwegeser periosteal elevator, and the
EAD is inserted to allow the endoscope to be introduced.
The periosteum is raised posteriorly and cephalically. Once
dissection is completed on the right side, it is repeated on the
left side.
A subperiosteal dissection is then carried out to the supra-
orbital rim, lateral orbital rim, and zygomatic and malar
arches under endoscopic visualization. The dissection is
continued immediately superficial to the deep temporal fascia
until the Zygomaticotemporal branch is exposed (Fig. 4.4). It
is absolutely crucial to the safety and success of this operation
to avoid dissection too superficial to the deep temporal fascia.
This means that no fat should be left attached to the deep
temporal fascia. Grasping forceps or a long hemostat is used
to dissect and avulse the nerve. It is important to avulse as
much length of the nerve as possible to prevent re-coaptation.
Often a segment of the nerve measuring around 2 cm is
removed. Any bleeding vessels are coagulated, and the proxi-
mal nerve end is allowed to retract into the temporalis muscle
to reduce the risk of neuroma formation. In our recent study,
the results of nerve decompression have been shown to be the
same as nerve avulsion.53 The decompression will include
removing the vessels accompanying the nerve and temporalis
fasciotomy around the nerve.
The periosteum and arcus marginalis are released in the
lateral orbital and supraorbital regions on patients older than
midline incisions are utilized. Xylocaine containing 1 : 100 000
epinephrine is injected in the non-hair-bearing skin and
Xylocaine containing 1 : 200 000 epinephrine is injected in
the hair-bearing skin. The Endoscopic Access Device (EAD;
Applied Medical Technology, Cleveland, OH) is used for hair
control and to facilitate insertion of the endoscopic equipment
by keeping the wound margin apart. The dissection is per-
formed in the subperiosteal plane down to the supraorbital
and lateral orbital rims, and the zygomatic arch. The proce-
dure for ZTBTN resection is described below and requires
exposure of the zygomatic arch. For corrugator resection,
attention is concentrated in the glabellar area. Once the supra-
orbital and the supratrochlear nerves and corrugator muscle
groups are exposed, the periosteum is then released laterally,
leaving the central portion intact over the mid-glabellar area
to prevent too much elevation of the medial eyebrows. The
corrugator and depressor muscles, along with vessels, are
removed as thoroughly as possible while the operating sur-
geon’s non-dominant index finger is compressing the soft
tissues against the grasper from the outside. Through this
approach, the supraorbital rim is evaluated for any possible
compression point and presence of fascial band or bony
tunnels which are released using a 2 mm percutaneous osteo-
tome, if present. Fat harvested from the temporal region is
delivered to the corrugator site using the technique described
by our group.45,46 To harvest the fat, the junction of the zygo-
matic arch with the malar body is identified, a small rent in
the deep temporal fascia is created cephalad to the arch, and
the fat is harvested while the assistant is compressing on the
buccal area.
Fascial sutures of 3-0 polydioxanone are placed for suspen-
sion of the temple area further laterally and cephalically to
achieve some eyebrow lift, if needed. The suture suspends the
superficial temporal fascia from the deep temporal fascia.
Incisions are repaired with 5-0 polyglactin (Vicryl) and 5-0
plain catgut.24
Complications
Alopecia can rarely occur at the port sites. Every patient
experiences complete anesthesia immediately after surgery;
however, permanent paresthesia or anesthesia is unlikely.
Transient itching might happen after surgery. Inadequate
resection of muscle may result in recurrence of the symptoms,
and dynamic irregularity or dimpling can occur on anima-
tion.47 The temporal branch of the facial nerve can rarely be
injured during the dissection. This is exceedingly rare and
would result in only a temporary paralysis.
Deactivation of temporal triggers
Temporal headaches are triggered primarily by irritation of
the zygomaticotemporal branch of the trigeminal nerve by the
muscle, fascia, or the vessels.
After appropriate preparation of the head and face, four
1–1.5-cm incisions are marked – two on each temple, usually
7 and 10 cm from the midline and one in the midline, only
if the glabellar trigger site deactivation is also intended.
Otherwise, the two most lateral incisions are used. The fore-
head, temple, and malar regions are then injected with 1%
lidocaine with 1 : 100 000 epinephrine. The hair-bearing scalp
is injected with 0.5% lidocaine with 1 : 200 000 epinephrine.
A
Fig. 4.4  Endoscopic view of the zygomaticotemporal branch of the trigeminal
nerve. (A) The dissection is performed using a periosteal elevator. (B) The nerve
can be seen superficial to the deep temporal fascia just under the grasping forceps.
B

88
SECTION II
CHAPTER 4 • Surgical treatment of migraine headaches
in contact with the nerve are cauterized using bipolar cautery
and removed. A 2 × 2-cm subcutaneous flap, based caudally,
is elevated and passed under the nerve to isolate the nerve
from muscle (Figs. 4.5J & 4.5K). Usually after incision of the
skin and on the way of dissection to the semispinalis muscle,
the third occipital nerve is encountered; in this case, the nerve
is avulsed on each side and allowed to retract into the muscle.
After completion of the procedure on the opposite side, the
two subcutaneous flaps are sutured to the deepest portion of
the midline raphe (Figs. 4.5L & 4.5M) using a 5-0 Monocryl
suture. A single TLS drain is placed on the left side using a
trocar and passed to the right side under the midline raphe
(Fig. 4.5N). A total 0.5 mL of a Kenalog 40-mg solution is
injected in the perineurium and along the course of the nerves.
The wound is irrigated and repaired with 5-0 Monocryl to
reattach the subcutaneous tissue to the midline raphe and
eliminate the dead space. (Fig. 4.5O). The skin is repaired
using 5-0 plain catgut running locked sutures.
Complications
Infection or bleeding is rare after this procedure. Reattaching
the skin to the midline raphe reduces the chance of seroma
formation. Temporary anesthesia and paresthesia are expected.
Permanent anesthesia and paresthesia are unlikely. Every
patient experiences a slight depression in the removed muscle
site. However, since this is covered with hair, patients are not
concerned about this.
Septonasal triggers
Septonasal triggers must be considered when the pain mostly
starts from behind the eyes, commonly triggered by weather
or hormonal changes, especially when the pain is daily, is
worse in the morning, or injection of BTX-A in other trigger
sites results in no change or results in improvement without
resolution. The main pathologic actors are (1) deviated septum
with a spur which is in contact with a turbinate; (2) presence
of concha bullosa; and (3) Haller’s cell. The main goal of
surgery is to eliminate the contact point or decompress the
concha bullosa.
The face is prepped and draped after the induction of
general anesthesia. The nose is packed with cocaine-soaked
gauze and is infiltrated with 0.5% lidocaine with 1 : 200 000
epinephrine initially and 0.5% lidocaine containing 1 : 100 000
epinephrine after a few minutes. An L-shaped incision is
made on the left side of the septum, and the mucoperiosteum
is elevated. After extending the L shape incision through the
quadrangle cartilage, the opposite mucoperiosteum is ele-
vated. The deviated portion of the cartilaginous septum and
perpendicular plate of the ethmoid and vomer bone are
removed, and the straight portion of the cartilage is placed
back in the site. It is crucial to remove any existing spurs and
eliminate any contact points between the turbinates and the
septum. The mucoperiosteal flap is sutured back into place
with 5-0 chromic running sutures. Doyle stents are placed in
each side and fixated to the membranous septum with 4-0
Prolene sutures.
The Doyle stents are removed in 3–8 days. The patient
may resume light activities on postoperative day 1, heavy
activities on postoperative day 7, and strenuous activities in
3 weeks.
35 to facilitate some rejuvenation.23 The endoscopic devices
are removed, and a single hook is placed on either side of the
caudal portion of the incision. A 3-0 PDS suture is used to fix
the superficial and intermediate temporal fascia to the deep
temporal fascia laterally. Skin incisions are repaired with 5-0
poliglecaprone (Monocryl) and 5-0 plain catgut interrupted
stitches.
Patients are allowed to return to light activities the next
day, to regular activities within 7 days, and to strenuous
exercise within 3 weeks.
Complications
Every patient experiences transient anesthesia and paresthesia
in the temple area postoperatively. Permanent anesthesia and
paresthesia are rare. Alopecia around the incisions can occur,
and often is temporary. Injury to the temporal branch of the
facial nerve may rarely cause paralysis of the frontalis muscle.
This complication is usually short-lasting as well. A neuroma,
although a possibility after the avulsion of the nerve, has not
been observed after this surgery.
Deactivation of occipital triggers
A 4-cm midline incision is designed in the hair-bearing caudal
occipital region while the patient is seated. After induction
of anesthesia, the patient is placed in a prone position with
the shoulders raised by a gel roll and the neck stabilized.
The area around the incision is shaved to a total width of
approximately 3 cm. The incision site is then infiltrated with
1% lidocaine with 1 : 100 000 epinephrine (Fig. 4.5A). The skin
incision is made with a number 10 scalpel, and hemostasis is
achieved with coagulation cautery. The incision is taken to the
midline raphe (Fig. 4.5B), and the trapezius fascia is incised
about 0.5 cm lateral to midline (Fig. 4.5C), leaving the midline
raphe intact. The trapezius muscle, which rarely reaches the
midline, has obliquely oriented fibers and, if encountered,
it is divided and retracted laterally; the semispinalis capitus
muscle fibers are identified by their vertical orientation and
their location directly underneath the fascia. The semispinalis
muscle is then further exposed following retraction of the
trapezius fascia, and dissection is continued under the fascia
with a pair of Metzenbaum scissors. The trunk of the greater
occipital nerve is easily located approximately 1.5 cm from
the midline and 3 cm caudal to the occipital protuberance
(Fig. 4.5D). Munion clamps are used to isolate the nerve. A
vessel loop is placed around the nerve for retraction (Fig.
4.5E). A full-thickness, 2.5-cm long piece of the muscle is dis-
sected medial to the nerve and is transected cephalically and
caudally using cautery in the coagulation mode. The muscle
resection is considered complete when no muscle fibers
remain medial to the nerve (Figs. 4.5F & 4.5G). A small portion
of the trapezius fascia and muscle immediately overlying the
nerve is then removed (Figs. 4. 5H & 4.5I). The nerve is traced
laterally ensuring that no fascial bands, which may cause
compression, remain superficial to the nerve, similar to carpal
tunnel release. Occasionally, the nerve bifurcates within the
muscle. In this case, it is necessary to remove muscle fibers
between the two branches.
Dissection is continued laterally and superiorly along the
direction of the nerve until the nerve reaches the subcutane-
ous adipose tissue. The occipital artery or its branches that are

89
Surgical technique
A
B
C
D
E
F
G
H
I
J
K
L
Fig. 4.5  Surgical technique for release of the occipital nerve for occipital migraines. (A) The 1.6-inch (4-cm) incision is designed in the caudal occipital region. (B) The
incision is taken to the midline raphe, and (C) the trapezius fascia is incised slightly away from the midline; the semispinalis muscle fibers can be identified by their vertical
orientation. (D) Dissection continues subfascially and superficial to the muscle, and the trunk of the occipital nerve will be seen approximately 0.6 inch (1.5 cm) lateral to
the midline and 1.2 inch (3 cm) caudal to the occipital protuberance. (E–G) A 1-inch (2.5-cm) length of muscle is dissected medial to the nerve and transected. (H–L) A
flap is designed to be placed under the nerve to protect it. (M) The flap is sutured to the midline raphe, and (N) a drain is placed. (O) The incision is closed in layers while
attaching the subcutaneous flap to the midline raphe.
M
N
O

90
SECTION II
CHAPTER 4 • Surgical treatment of migraine headaches
relationship between the peripheral nerve branches with the
blood vessels.
These peripheral trigger points could be addressed under
local anesthesia. After preparation and draping the area, a
small incision is made over the tender point which corre-
sponds to the Doppler signal, dissection is carried down, and
usually some type of nerve–vessel crossover could be found
in the area. Blood vessels are dissected off the nerve and
excised after cauterization. Occasionally, a fascial band is also
identified in the area, which could be released. (Fig. 4.6). The
small nerve branch is removed to augment the chance of
elimination.
Complications
Bleeding and infection are very rare. Temporary anesthesia in
the area could happen. Neuroma is very unlikely and, if it
occurs, it is excised and the nerve is buried in the muscle.
Conclusion
A patient who presents for surgical treatment for migraine
headaches should have a thorough headache evaluation.
Trigger sites are then identified by the constellation of the
presenting symptoms, CT of the peripheral sinuses, and
finding the Doppler signal. For frontal trigger sites, corrugator
muscle group resection is performed. For temporal trigger
sites, the ZTBTN is avulsed. For occipital trigger sites, the
semispinalis capitis muscle medial to the greater occipital
nerve is resected. Septoplasty and turbinectomy is performed
in patients who have evidence of septal deviation and enlarged
turbinates with contact points, and whose clinical profile sug-
gests septal and turbinate related migraine triggers.
In some cases, the inferior turbinates are enlarged or have
a contact point with the septum and require reduction. The
inferior turbinate is infiltrated with 0.5% lidocaine containing
1 : 200 000 epinephrine, and 0.5% lidocaine containing 1 : 100 000
epinephrine after a few minutes. Turbinate scissors are used
to resect the inferior turbinates conservatively, leaving normal
turbinate size behind. A partial in-fracture is performed and
the area is cauterized. A patient who has concha bullosa or
significant enlargement of the middle turbinates will require
partial or complete resection of the middle turbinates. Using
the sharp end of the septal elevator, the mucosa overlying the
turbinate is incised and peeled off over the medial half of the
turbinate. The medial wall of the concha bullosa is resected,
raw margins are cauterized, and Doyle stents are inserted.
Turbinate reduction could also be performed using a zero
degree scope and 4.3 mm microshaver KPS.
Complications
Temporary dryness of the nose occurs in 12% of our patients.
At this time, we have not observed permanent dryness. Syn-
echiae and sinus infection are rare. A small percentage of
patients experience postoperative epistaxis, which, if signifi-
cant enough, is treated with desmopressin (DDAVP) 0.3
microgram/kg of body weight dissolved in 50 cc saline and
infused over 45 min without having to pack the nose.48
Less common trigger points
The auriculotemporal nerve, lesser occipital nerve, third
occipital nerve, and end branches of the other main nerves in
the scalp or temporal area could act as trigger sites. Blood
vessels are the most common reason for nerve irritation,
although fascial bands also can act as trigger sites.
Trigger points in the scalp or lateral temporal area are
evaluated by asking the patients to put their fingertip over the
pain starting point or maximum tender point. This area is
marked, and using a handheld Doppler machine, a vascular
signal is almost invariably identified. Having a blood vessel
signal over the tender points is suggestive of a close
A
B
Fig. 4.6  Exploration of peripheral trigger points: (A) use of handheld Doppler in tender point, (B) artery and nerve relationship,
Box 4.1 Migraine headache diagnostic criteria
Bonus content for this chapter can be found online at

91
Conclusion
C
D
(C) dissection process, (D) nerve after excision of artery.
Fig. 4.6, cont’d
18. Guyuron B, Varghai A, Michelow BJ, et al. Corrugator supercilii
muscle resection and migraine headaches. Plast Reconstr Surg.
2000;106:429–434, discussion 435–437. In this retrospective review,
migraine headache status was assessed in patients undergoing forehead
rejuvenation procedures involving resection of the corrugator supercilii. A
strong correlation between corrugator removal and relief of migraine
headaches was demonstrated.
23. Guyuron B, Tucker T, Davis J. Surgical treatment of migraine
headaches. Plast Reconstr Surg. 2002;109:2183–2189. This is a
prospective trial evaluating a surgical approach (corrugator resection,
transection of the zygomaticotemporal branch of the trigeminal nerve, and
temple soft-tissue repositioning) to managing migraine headaches. A
significant improvement in symptomatology was demonstrated with
surgery, and preoperative Botox injection was demonstrated to be useful in
predicting this response.
24. Totonchi A, Pashmini N, Guyuron B. The zygomaticotemporal
branch of the trigeminal nerve: an anatomical study. Plast Reconstr
Surg. 2005;115:273–277.
25. Mosser SW, Guyuron B, Janis JE, et al. The anatomy of the greater
occipital nerve: implications for the etiology of migraine headaches.
Plast Reconstr Surg. 2004;113:693–697, discussion 698–700. It is
theorized that trigger points along the greater occipital nerve may
contribute to migraine headache symptomatology. This anatomic study
assesses the course of the greater occipital nerve to enhance the efficacy of
chemodenervation procedures.
26. Dash KS, Janis JE, Guyuron B. The lesser and third occipital nerves
and migraine headaches. Plast Reconstr Surg. 2005;115:1752–1758,
discussion 1759–1760.
27. Guyuron B, Kriegler JS, Davis J, et al. Comprehensive surgical
treatment of migraine headaches. Plast Reconstr Surg. 2005;115:1–9.
In this randomized prospective clinical trial, Botox injections were used to
identify migraine headache trigger sites in diagnosed migraine sufferers.
Site-specific surgical releases were shown to reduce migraine symptoms
significantly compared to controls.
28. Guyuron B, Reed D, Kriegler JS, et al. A placebo-controlled surgical
trial of the treatment of migraine headaches. Plast Reconstr Surg.
2009;124:461–468. This is a double-blind, sham surgery-controlled clinical
trial that demonstrates the efficacy of trigger-point-specific surgical
management of migraine headaches.
31. Guyuron B, Tucker T, Kriegler JS. Botulinum toxin A and migraine
surgery. J Plast Reconstr Surg. 2003;112(suppl):171S–173S, discussion
174S-176S.
Access the complete reference list online at

91.e1
References
References
1. Lipton RB, Stewart WF, Diamond S, et al. Prevalence and burden of
migraine in the United States: Data from the American Migraine
Study II. Headache. 2001;41:646–657.
2. Lipton RB, Bigal ME, Diamond M, et al. Migraine prevalence,
disease burden, and the need for preventive therapy. Neurology.
2007;68:343–349.
3. Lipton RB, Steward WF, Diamond S, et al. Prevalence and burden
of migraine in the United States: Data from the American Migraine
Study II. Headache. 2001;41:646–657.
4. Stewart WF, Shechter A, Rasmussen BK. Migraine prevalence: A
review of population-based studies. Neurology. 1994;44(suppl
4):S17–S23.
5. Henry P, Auray JP, Gaudin AF, et al. Prevalence and clinical
characteristics of migraine in France. Neurology. 2002;59:232–237.
6. Patel NV, Bigal ME, Kolodner KB, et al. Prevalence and impact of
migraine and probable migraine in a health plan. Neurology.
2004;63:1432–1438.
7. Adeney KL, Flores JL, Perez JC, et al. Prevalence and correlates of
migraine among women attending a prenatal care clinic in Lima,
Peru. Cephalalgia. 2006;26:1089–1096.
8. Mattsson P, Svardsudd K, Lundberg PO, et al. The prevalence of
migraine in women aged 40–74 years: a population-based study.
Cephalalgia. 2000;20:893–899.
9. Rozen TD. Migraine prevention: What patients want from
medication and their physicians (a headache specialty clinic
perspective). Headache. 2006;46:750–753.
10. Young WB, Hopkins MM, Shechter AL, et al. Topiramate: A case
series study in migraine prophylaxis. Cephalalgia. 2002;22:659–
663.
11. Hu XH, Markson LE, Lipton RB, et al. Burden of migraine in the
United States: Disability and economic costs. Arch Intern Med.
1999;159:813–818.
12. Peres MFP, Silberstein S, Moreira F, et al. Patients’ preference for
migraine preventive therapy. Headache. 2007;47:540–545.
13. Lim C. Headache, migraine. In: Ferri F, ed. Ferri’s Clinical Advisor
2007: Instant Diagnosis and Treatment. 9th ed. Philadelphia: Mosby
Elsevier; 2007.
14. Dandy WE. Treatment of hemicrania (migraine) by removal of the
inferior cervical and first thoracic sympathetic ganglion. Johns
Hopkins University Bull. 1931;48:357–361.
15. Gardner WJ, Stowell A, Dutlinger R. Resection of the greater
superficial petrosal nerve in the treatment of unilateral headache. J
Neurol. 1947;4:105–114.
16. Murillo CA. Resection of the temporal neurovascular bundle for
control of migraine headache. Headache. 1968;8:112–117.
17. Murphy JP. Occipital neurectomy in the treatment of headache. Md
State Med J. 1969;18:62–66.
18. Guyuron B, Varghai A, Michelow BJ, et al. Corrugator supercilii
muscle resection and migraine headaches. Plast Reconstr Surg.
2000;106:429–434, discussion 435–437. In this retrospective review,
migraine headache status was assessed in patients undergoing forehead
rejuvenation procedures involving resection of the corrugator supercilii. A
strong correlation between corrugator removal and relief of migraine
headaches was demonstrated.
19. Binder W, Brin MF, Blitzer A, et al. Botulinum toxin type A (BTX-A)
for migraine: An open label assessment. Mov Disord. 1998;13(suppl
2):241.
20. Wheeler AH. Botulinum toxin A: Adjunctive therapy for refractory
headaches associated with pericranial muscle tension. Headache.
1998;38:468.
21. Jankovic J, Brin MF. Botulinum toxin: Historical perspective and
potential new indications. Muscle Nerve Suppl. 1997;6:S129.
22. Behmand R, Tucker T, Guyuron B. Single site botulinum toxin
injection for elimination of migraine trigger points. Headache.
2003;43:1085–1089.
23. Guyuron B, Tucker T, Davis J. Surgical treatment of migraine
headaches. Plast Reconstr Surg. 2002;109:2183–2189. This is a
prospective trial evaluating a surgical approach (corrugator resection,
transection of the zygomaticotemporal branch of the trigeminal nerve, and
temple soft-tissue repositioning) to managing migraine headaches. A
significant improvement in symptomatology was demonstrated with
surgery, and preoperative Botox injection was demonstrated to be useful in
predicting this response.
24. Totonchi A, Pashmini N, Guyuron B. The zygomaticotemporal
branch of the trigeminal nerve: an anatomical study. Plast Reconstr
Surg. 2005;115:273–277.
25. Mosser SW, Guyuron B, Janis JE, et al. The anatomy of the greater
occipital nerve: implications for the etiology of migraine headaches.
Plast Reconstr Surg. 2004;113:693–697, discussion 698–700. It is
theorized that trigger points along the greater occipital nerve may
contribute to migraine headache symptomatology. This anatomic study
assesses the course of the greater occipital nerve to enhance the efficacy of
chemodenervation procedures.
26. Dash KS, Janis JE, Guyuron B. The lesser and third occipital nerves
and migraine headaches. Plast Reconstr Surg. 2005;115:1752–1758,
discussion 1759–1760.
27. Guyuron B, Kriegler JS, Davis J, et al. Comprehensive surgical
treatment of migraine headaches. Plast Reconstr Surg. 2005;115:1–9.
In this randomized prospective clinical trial, Botox injections were used to
identify migraine headache trigger sites in diagnosed migraine sufferers.
Site-specific surgical releases were shown to reduce migraine symptoms
significantly compared to controls.
28. Guyuron B, Reed D, Kriegler JS, et al. A placebo-controlled surgical
trial of the treatment of migraine headaches. Plast Reconstr Surg.
2009;124:461–468. This is a double-blind, sham surgery-controlled clinical
trial that demonstrates the efficacy of trigger-point-specific surgical
management of migraine headaches.
29. Dirnberger F, Becker K. Surgical treatment of migraine headaches
by corrugator muscle resection. Plast Reconstr Surg.
2004;114:652–657.
30. Poggi JT, Grizzell BE, Helmer SD. Confirmation of surgical
decompression to relieve migraine headaches. Plast Reconstr Surg.
2008;122:115–122.
31. Guyuron B, Tucker T, Kriegler JS. Botulinum toxin A and migraine
surgery. J Plast Reconstr Surg. 2003;112(suppl):171S–173S, discussion
174S-176S.
32. Scott AB, Rosenbaum A, Collins CC. Pharmacologic weakening of
extraocular muscles. Invest Ophthalmol. 1973;12:924–927.
33. Scott AB. Botulinum toxin injection into extraocular muscles as an
alternative to strabismus surgery. J Pediatr Ophthalmol Strabismus.
1980;17:21–25.
34. Scott AB. Botulinum toxin injection of eye muscles to correct
strabismus. Trans Am Ophthalmol Soc. 1981;79:734–770.
35. Brin MF. Botulinum toxin: chemistry, pharmacology, toxicity, and
immunology. Muscle Nerve Suppl. 1997;6:S146–S168.
36. Carruthers A, Carruthers J. Cosmetic uses of botulinum A exotoxin.
Adv Dermatol. 1997;12:325–347.
37. Guyuron B, Huddleston SW. Aesthetic indications for botulinum
toxin injection. Plast Reconstr Surg. 1994;5:913–918.
38. Mathew NT, Jaffri SF. A double-blind comparison of
onabotulinumtoxina (Botox) and topiramate (Topamax) for the
prophylactic treatment of chronic migraine: a pilot study. Headache.
2009;49:1466–1478.
39. Silberstein SD. Preventive migraine treatment. Neurol Clin.
2009;27:429–443.
40. Cady RK. OnabotulinumtoxinA (botulinum toxin type-A) in the
prevention of migraine. Expert Opin Biol Ther. 2010;10:289–298.
41. Shuhendler AJ, Lee S, Siu M, et al. Efficacy of botulinum toxin type
A for the prophylaxis of episodic migraine headaches: a meta-
analysis of randomized, double-blind, placebo-controlled trials.
Pharmacotherapy. 2009;29:784–791.
42. Guyuron B, Rose K, Kriegler JS, et al. Hourglass deformity after
botulinum toxin type A injection. Headache. 2004;44:262–264.
43. Greene P, Fahn S, Diamond B. Development of resistance to
botulinum toxin type A in patients with torticollis. Mov Disord.
1994;9:213–217.
44. Guyuron B, Michelow BJ, Thomas T. Corrugator supercilii muscle
resection through blepharoplasty incision. Plast Reconstr Surg.
1995;95:691–696.

91.e2
SECTION II
CHAPTER 4 • Surgical treatment of migraine headaches
45. Guyuron B, Knize DM. Corrugator supercilii resection through
blepharoplasty incision. Plast Reconstr Surg. 2001;107:604–607.
46. Guyuron B, Rose K. Harvesting far from infratemporal fossa. Plast
Reconstr Surg. 2004;114:245–249.
47. Guyuron B. Endoscopic forehead rejuvenation: limitations, flaws,
and rewards (reply). Plast Reconstr Surg. 2007;119:1116–1119.
48. Totonchi A, Eshraghi Y, Beck D, et al. Von Willebrand Disease:
Screening, Diagnosis, and Management. Aesthet Surg J.
2008;28:189–194.
49. Guyuron B, Kriegler JS, Davis J, Amini SB. Five-year outcome of
surgical treatment of migraine headaches. Plast Reconstr Surg.
2011;127(2):603–608.
50. Diener HC, Dodick DW, Aurora SK, et al.; PREEMPT 2 Chronic
Migraine Study Group. OnabotulinumtoxinA for treatment of
chronic migraine: results from the double-blind, randomized,
placebo-controlled phase of the PREEMPT 2 trial. Cephalalgia.
2010;30(7):804–814.
51. Aurora SK, Dodick DW, Turkel CC, et al.; PREEMPT 1 Chronic
Migraine Study Group. OnabotulinumtoxinA for treatment of
chronic migraine: results from the double-blind, randomized,
placebo-controlled phase of the PREEMPT 1 trial. Cephalalgia.
2010;30(7):793–803.
52. Liu MT, Armijo BS, Guyuron B. A comparison of outcome of
surgical treatment of migraine headaches using a constellation of
symptoms versus botulinum toxin type A to identify the trigger
sites. Plast Reconstr Surg. 2012;129(2):413–419.
53. Guyuron B, Harvey D, Reed D. A Prospective Randomized
Outcomes Comparison of Two Temple Migraine Trigger Site
Deactivation Techniques. Plast Reconstr Surg. 2015;136(1):
159–165.

SECTION II • Head and Neck Reconstruction
5 
Scalp and forehead reconstruction
Julian J. Pribaz and Edward J. Caterson
SYNOPSIS
■ The scalp and forehead are specialized components of the uppermost
part of the head. Although at first glance they appear to be quite
different, with the scalp being static hair-bearing tissue and the
forehead being hairless with significant mimetic function, they both
share a similar layered anatomy remembered by the mnemonic,
“SCALP”.
■ The convexity of the skull results in increased tautness of the overlying
soft tissues, which causes increased tension in repairs after injury,
and making flap repair more complex.
■ There is a rich blood supply from branches of both the external and
internal carotid systems, which allows closure of wounds with
moderate tension and the safe transfer of flaps as long as the
vascularity is respected.
■ There are some unique and specific pathological processes as well as
other general conditions, both benign and malignant, affecting the
scalp and forehead.
■ The goal of all reconstruction is to obtain the best possible outcome,
which is ideally achieved by using “like” tissue, which is in limited
supply. This is feasible for smaller lesions, which can be reconstructed
with local tissue transfers. Larger wounds will leave secondary donor
defects requiring skin grafting. There are few regional flap options. For
very large or complex defects, free tissue transfers are the best
solution.
■ The subunit principle should be used to design the ideal method of
reconstruction to maximize the outcome. The scalp with its hair-
bearing feature can be considered as its own extensive subunit, while
the forehead is best considered as several different subunits,
depending on the location and mobility of the soft tissues.
■ In forehead reconstruction, care should be taken to avoid any
displacement of the surrounding mimetic or mobile anatomical features,
especially the eyebrow, upper eyelid, and glabella at its inferior border.
■ Secondary procedures are indicated to maximize the aesthetic
outcome for both scalp and forehead reconstruction. For the scalp,
this mainly involves restoration of hair-bearing tissue, often performed
with the use of serial tissue expansion; for the forehead, this involves
restoring any displaced surrounding landmarks, and obtaining a
smooth homogeneous surface.
Introduction
The scalp and forehead are a very specialized and unique
component of the upper most part of the head and neck. It is
dome-shaped and covers the cranium and the underlying
brain. Although at first glance, the forehead and scalp looked
quite different, mainly due to the hair-bearing character of the
scalp, the underlying structures are remarkably similar with
some regional difference that impact the approach to recon-
struction. Its exposed nature makes it especially vulnerable to
all forms of trauma, direct sun exposure with its long-term
sequelae, as well as some unique disorders that give rise to
pathological conditions that can result in challenging defects
that can be difficult to repair. This is due in part to the tautness
of tissue compounded by the convexity of the scalp and
forehead.
Fortunately, there is a very rich blood supply which
permits elevation of hardy flaps that can withstand moderate
tension which is typically encountered when covering convex
surfaces. Nonetheless, careful analysis of each defect, a sound
knowledge of the anatomy, especially the blood supply, and
the use of templates and patterns are invaluable in design-
ing appropriate flaps which can result in a satisfactory
outcome.
In this chapter we will review the relevant anatomy, disease
processes, patient selection, and options for reconstruction
with the goal of developing some algorithms to assist in this
process. We will consider the overlapping similarities of the
scalp and forehead, but then consider the reconstructive
options separately.
Basic science/disease process
Anatomy
The scalp and forehead constitute a significant area of the
head and neck which is proportionally greater in children

93
Basic science/disease process
The galea aponeurotica is a fibrous aponeurosis that extends
and connects the occipitalis muscles posteriorly and the
frontalis muscles anteriorly. Laterally, the temporoparietal
fascia is an extension of the galea and, anterolaterally, the
galea is confluent with the superficial muscular aponeurotic
system (SMAS) of the face.4 The muscles within this layer
consist of the paired frontalis muscles anteriorly and occipi-
talis muscles posteriorly and the auricularis muscles laterally.
The frontalis muscles originate from the galea and insert into
the dermis of the brow. Contraction of the frontalis causes
elevation of the eyebrows producing horizontal wrinkle lines
in the forehead. Anteriorly, the frontalis muscles blend with
the procerus and corrugator supercilii muscles as well as the
upper aspects of the orbicularis oculi muscles. The paired
corrugator supercilii muscles arise from the frontal bone near
the superomedial orbital rim and then pass superolaterally
through the fibers of the orbicularis oculi and the frontalis
muscles before inserting into the medial eyebrow skin. The
corrugator muscle is the brow depressor pulling the brow
medially and inferiorly producing vertical glabella wrinkles.
The procerus muscle is a thin muscle that inserts into the
glabella and lower mid forehead. It is a brow depressor
forming horizontal nasal root creases.
In the posterior scalp, the paired occipitalis muscles take
origin from the superior nuchal line and mastoid and insert
into the galea. There are also three auricular muscles on each
side of the scalp – the anterior, superior, and posterior auricu-
lar muscles. They take their origin from the temporalis fascia
than in adults. A thorough understanding of the surgical
anatomy of the scalp and forehead is vital to the reconstruc-
tive surgeon. This compound unit extends from the superior
orbital rims anteriorly to the nuchal line posteriorly. Laterally,
it extends from each frontal process of the zygoma and zygo-
matic arch anteriorly, the ear centrally and mastoid process
posteriorly. The most obvious attribute of the scalp is that it
is hair-bearing. The forehead is typically the area devoid of
hair and is best considered as a separate unit, extending
between the side-burns laterally and the supraorbital ridges
and glabella inferiorly. Superiorly, the boundary between the
forehead and scalp depends on the hairline which is variable
with age and gender.
Scalp
The scalp and forehead are often considered as a single unit
due to its similar composition of tissue layers, which can be
remembered by the mnemonic “SCALP”, where S is the skin,
C is the subcutaneous tissue, A is the aponeurotic layer, L is
the loose areolar tissue, and P is the pericranium. However,
there are regional differences in relative tissue composition
that impact reconstruction (Fig. 5.1).1–3
The outermost layer of the scalp is the skin, containing hair
follicles; sebaceous and sweat glands that extend into the
dermis and laterally, in the temporal region, are located just
superficial to the temporoparietal fascia. There are septa con-
necting the dermis and deep aponeurotic layer.
Fig. 5.1  Layers of the scalp: S, skin; C, subcutaneous tissue; A, aponeurotic layer; L, loose areolar tissue; and P, pericranium. (Reproduced from TerKonda RP, Sykes JM.
Concepts of scalp and forehead reconstruction. Otolaryngol Clin North Am. 1997;30:519–539.)
Skin
Subcutaneous
fat
Galea
Loose areolar
tissue
Pericranium
Frontalis muscle
Superior
temporal line
Superficial temporal fascia
(temporoparietal fascia)
Temporalis muscle
Superficial
temporal fat pad
Deep temporal
fascia (temporalis
muscle fascia)

94
SECTION II
CHAPTER 5 • Scalp and forehead reconstruction
muscle. Its main part overlies the temporalis muscle, and
inferiorly it splits into superficial and deep layers. The super-
ficial layer attaches to the anterior aspect of the zygomatic
arch, and the deeper layer fuses with medial aspect of the
zygomatic arch. This is the plane of dissection for access to
the zygomatic arch in cases of zygomatic fractures (Gillies
approach) and for raising bicoronal flaps to expose the cranio-
facial skeleton. Dissection deep to this layer avoids injury to
the frontal branch of the facial nerve as it passes over the
zygomatic arch within the fascia (Fig. 5.4).
The temporalis muscle is a large strong fan shaped muscle
of mastication, which originates from the temporal fascia and
skull and inserts into the coronoid process of the mandible. It
receives its blood supply from the deep temporal branches of
the internal maxillary artery. It is commonly used to provide
a moderate sized muscle flap that may be used for orbital,
palate, and cheek reconstruction, as well as a functional flap
for facial reanimation (which is described in other chapters of
this volume).
Forehead
The forehead extends from the superior orbital ridge and
glabella inferiorly and is bounded by the hairline laterally and
superiorly. The exact height of the forehead depends on the
anterior hairline and varies with age and gender. It has a
similar SCALP layered composition to the scalp, with some
variation in different regions.
and mastoid bone and insert into of the perichondrium of the
external ear (Fig. 5.2).
Beneath the galea is a loose areolar layer that is very thin
over the vertex that becomes thicker laterally where it joints
the temporoparietal fascia. It is at this level of loose areolar
tissue that scalping injuries occur. Historically, scalps were
taken as trophies of war, but in modern times similar scalping
injuries are produced when hair gets entangled in industrial
machinery. The deepest layer of the scalp is the pericranium
or periosteum of the cranium. This is a well vascularized layer
firmly adherent to the skull in the region of the cranial sutures.
The temporal region of the scalp has additional specialized
layers and attributes (Fig. 5.3). The hair-bearing skin typically
is the last to lose its hair in cases of male pattern baldness. The
temporoparietal fascia (TPF) is an extension of the galea and
is closely applied to the skin and the hair follicles and has a
rich blood supply which passes on its deep surface. Anteriorly,
the frontal branch of the facial nerve passes in this layer. There
is a deeper, thin subgaleal fascial layer which can be delami-
nated from the TPF, which can be useful to expand the width
of vascularized fascial coverage as may be required in total
ear cartilaginous construct coverage.
Deep to this is the deep temporal fascia which is thick and
fuses with the periosteum superiorly above the temporalis
Fig. 5.2  Extrinsic muscles of the ear – anterior auricular, superior auricular, and
posterior auricular muscles. (Reproduced from Agarwal CA, Mendenhall SD,
Foreman KB, et al. The course of the frontal branch of the facial nerve in relation to
fascial planes: an anatomic study. Plast Reconstr Surg. 2012;125:532–537.)
Auricularis
anterior
Tragicus
Antitragicus
Concha
Helicis minor
Helicis major
Auricularis superior
Auricularis posterior
Antihelix
Fig. 5.3  Anatomy of the temporal region.
Bone
Pericranium
Deep temporal artery
Temporalis muscle
Temporalis muscle fascia
Loose areolar tissue
Superficial temporal artery
and vein
Tempoparietal fascia
Subcutaneous tissue
Skin
Middle temporal artery

95
Basic science/disease process
carotid artery, and they enter the forehead at the supraorbital
rim and pass through the frontalis muscle at the brow and run
in the subcutaneous plane. They anastomose laterally with the
anterior branch of the superficial temporal artery.
The superficial temporal artery is the largest of the scalp
vessels and is a terminal branch of the external carotid artery.
It passes through the superficial lobe of the parotid in front of
the ear running with the auriculotemporal nerve. The vessels
run within the superficial temporal fascia and divide into
anterior and posterior branches. It supplies blood on the
temporal and central scalp, anastomosing anteriorly with
the supraorbital and supratrochlear and posteriorly with the
posterior auricular and occipital vessels.
The occipital artery provides blood supply to the posterior
scalp above the nuchal line. It is a branch of the external
carotid passing through the vertebral muscles and between
trapezius and sternomastoid into the occipitalis muscle and
divides into medial and lateral branches. The mastoid and
post-auricular region is supplied by the posterior auricular
artery, the smallest of the main vessels of the scalp (Fig. 5.6).
The venous drainage of the scalp is by veins that parallel
and accompany the main arteries. Venous blood also flows
through diploë of the cranium to the dural sinuses by emis-
sary veins. The supratrochlear and supraorbital veins drain
into the ophthalmic vein. Laterally, the venous drainage
passes through the parotid gland and joins the maxillary vein
to form the retromandibular vein. The post-auricular veins
join the posterior division of the retromandibular vein to form
the external jugular vein. The occipital veins drain into the
deep cervical vertebral venous plexus.
Scalp lymphatics are located in the subdermal and subcu-
taneous layers. There are no lymph nodes in the scalp region.
The lymphatic drainage is towards the parotid gland and into
the pre- and post-auricular lymph nodes, as well as into the
upper cervical and occipital nodes.9
Fig. 5.4  Course of the frontal branch of the facial nerve. Cross section at the level
of the zygomatic arch. (Reproduced from Agawal CA, Mendenhall SD, Foreman KB,
et al. The course of the frontal branch of the facial nerve in relation to fascial planes:
an anatomic study. Plast Reconstr Surg. 2012;125:532–537.)
Temporalis muscle
Periosteum
Masseter muscle
Superficial layer
of deep temporal
fascia
Superficial temporal
fascia
Innominate
fascia
SMAS
Parotid-
masseteric
fascia
Frontal branch
facial nerve
Fig. 5.5  Aesthetic subunits of the forehead region. L=lateral, C=central,
SB=suprabrow, G=glabella, T=temporal. (Redrawn from Jackson IT. In: Local Flaps
in Head and Neck Reconstruction, 2nd edn. St. Louis: Quality Medical Publishing;
2007.)
L
SB
SB
L
C
G
T
In 1957, Gonzalez-Ulloa proposed the concept of the aes-
thetic units of the face and in his view, the whole forehead
was considered to be a single subunit.5 Subsequent authors
have further modified and refined this concept subdividing
the forehead into additional subunits. We believe that the
description by Ian Jackson is the best to date.6 This divides the
forehead into a central subunit (which can be further divided
into paramedian and lateral components), the supraorbital
and glabella subunit, and the temporal subunits (Fig. 5.5).
Although the basic anatomy is similar in these different sub-
units, there are local differences in the thickness and mobility
of the tissue layers that allow different reconstructive strate-
gies and flap options in the different subunits, that can
enhance the outcomes in forehead reconstruction. The goal of
reconstruction is to avoid distortion to the anatomical land-
marks and boundaries of the forehead, especially the eyebrow
inferiorly and the hairline superiorly and laterally.7,8
Blood supply
The blood supply of the scalp and forehead is rich, coming
from five paired arteries that form a rich network within the
subcutaneous plane. Contributions come from both the inter-
nal and external carotid system. Anteriorly, the paired supra-
orbital and supratrochlear vessels arise from the internal
carotid system. Laterally, the superficial temporal and, poste-
riorly, the posterior auricular and occipital vessels are branches
of the external carotid system.
The supraorbital and supratrochlear vessels arise from the
ophthalmic artery, which is the first branch of the internal

96
SECTION II
CHAPTER 5 • Scalp and forehead reconstruction
Innervation
The motor innervation to the muscles of the forehead comes
from the frontal (also called temporal) branch(es) of the facial
nerve (VII cranial nerve). There are often several branches,
and these emerge from the parotid 2.5 cm anterior to the
tragus and pass in the loose areolar plane just deep to the
SMAS layer crossing the midportion of the zygomatic arch
and then 1.5 cm lateral to the orbital rim to reach the under-
side of the frontalis muscle.10 The corrugator muscles are also
innervated by the temporal branch of the facial nerve, whereas
the procerus muscle is innervated by the deep buccal branch
of the facial nerve. The occipitalis muscle is innervated by the
posterior auricular branch of the facial nerve. This originates
from the facial nerve as it exits the stylomastoid foramen. The
temporalis muscle is innervated by two branches from the
third or mandibular division of the trigeminal nerve.
The sensory nerve supply to the anterior scalp and forehead
comes by the supratrochlear and supraorbital nerves which
originate from the ophthalmic or first division of the trigemi-
nal nerve. The supratrochlear nerve exits the orbit between
the pulley of the superior oblique and the supraorbital
foramen. It passes beneath the corrugator muscles and sup-
plies the medial forehead, the upper eyelid, and conjunctiva.
The supraorbital nerve exits the frontal bone through the
supraorbital foramen and then divides into a superficial and
deep branch. The superficial branch penetrates the frontalis
muscle and courses superiorly in the subcutaneous plane to
the vertex of the scalp. The deep branch passes laterally
between the periosteum and deep aspect of the frontalis
muscle to supply the temporoparietal scalp (Fig. 5.7).11
The lateral orbit, temple, and scalp are supplied by the
zygomaticofacial and zygomaticotemporal nerves which are
branches of the maxillary or second division of the trigeminal
nerve. The pre-auricular scalp is supplied by the auriculotem-
poral nerve which is a branch of the mandibular or third
division of the trigeminal nerve.
Fig. 5.6  Arterial and nerve supply of the scalp.
Supratrochlear nerve
Lesser occipital
nerve
Occipital artery
Posterior auricular
artery
Superficial temporal
artery
Supraorbital artery
Supratrochlear artery
Auriculotemporal
nerve
Supraorbital nerve
Greater occipital nerve
Third occipital nerve
Fig. 5.7  The course of the deep branch of deep (SON-D) and superficial (SON-S)
division of the supraorbital nerve. The deep branch superiorly or obliquely across
the forehead between the galeal aponeurotica and the periosteum and by the
mid-forehead level found between 0.5 and 1 cm medial to the superior temporal
crest. It pierces the galea just before the coronal suture (CS). The superficial branch
passes through the lower frontalis muscle to run over the surface of the muscle.
TBr, terminal branch; STL, superior temporal line of the skull. (Reproduced from
Knize DM. A study of the supraorbital nerve. Plast Reconstr Surg.
1995;96:564–569.)
SON-S
SON-D
STL
CS
TBr
The posterior scalp is supplied by the greater occipital and
the third occipital nerve which are branches of the dorsal rami
of the cervical spinal nerves. These emerge from the suboc-
cipital triangle, 3 cm below the occipital protuberance and
1.5 cm lateral to the midline and supplies the posterior scalp
to the vertex.
Disorders of the scalp and forehead
Scalp and forehead defects may result from a variety of con-
genital and acquired etiologies. The problems may be acute
(lacerations, burns, avulsions, etc.) requiring immediate atten-
tion, or more elective, requiring work up and careful planning.
The scalp is very vascular and bleeding can be excessive,
requiring expeditious wound closure, which is usually the
best way to obtain hemostasis.
The defects may be small or extensive, partial or full-
thickness loss with possible loss of the underlying bone as
well (Box 5.1).
Congenital and neonatal indications
These include aplasia cutis congenita, hemangiomas and
vascular malformations, extravasation injuries and other rare
conditions.

97
Disorders of the scalp and forehead
BOX 5.1  Disorders of the scalp and forehead
Congenital
A. Aplasia cutis congenita
B. Nevus sebaceous of Jadassohn
C. Nevoid basal cell nevus syndrome
D. Congenital melanoma
E. Dysplastic nevus syndrome
F. Giant hairy nevus
G. Xeroderma pigmentosa
H. En coup de sabre
I. Vascular malformations
J. Autoimmune
K. Scleroderma
Neoplastic
A. Malignant
1. Basal cell carcinoma
2. Squamous cell
3. Malignant melanoma
4. Sarcoma
B. Benign
1. Lipoma
2. Dermatofibroma
3. Keratoacanthoma
4. Neurofibroma
5. Epidermal inclusion cyst
6. Trichoepithelioma
7. Hemangioma
8. Syringoma
Infectious
A. Localized
1. Bacterial
a. Folliculitis decalvans
b. Leprosy
2. Viral
3. Fungal
a. Kerion
b. Tinea capitis
B. Systemic
Acquired
A. Traumatic
1. Physical
2. Burns
a. Thermal
b. Chemical
c. Electrical
d. Radiation
Aplasia cutis congenita is a rare sporadic congenital defor-
mity of unknown etiology, but it is thought to be a malforma-
tion of the neural tube leading to failure of differentiation of
the skin in early embryonic life and can present with a range
of subtotal to total absence of the skin, underlying fat, skull,
dura, and occasionally underlying brain. In most cases it
involves the vertex and the ulcers may be single or multiple.
At birth, these defects are usually covered with a thin fragile
membrane and are generally treated conservatively with
dressing changes and allowed to heal by secondary intention,
if small. Larger defects with absence of deeper structures are
susceptible to infection, meningitis, sagittal sinus thrombosis,
and hemorrhage, and may be life threatening and need to be
formally closed with a flap. If allowed to heal by secondary
intention, an atrophic hairless scar will result, which can be
excised when the child is older. These children need to be
carefully followed, especially if there is delayed healing with
repeated breakdown, as the chronic wound may undergo
malignant degeneration many years later, requiring aggres-
sive resection, and complex reconstruction (Fig. 5.8).12,13,14
Hemangiomas and vascular malformations may also
occur on the scalp and can present very challenging recon-
structive problems.15 The clinical findings and management
are described in other chapters.
Intravenous fluid extravasation, especially in a neonate, is
also fairly common due to use of scalp veins for fluid admin-
istration in the neonate. Generally, these small wounds are
treated conservatively.
Traumatic defects
These range from simple lacerations to scalp avulsions and
include thermal, electrical, and radiation burn injuries. With
lacerations, basic principles of management are followed,
obtaining a careful history and physical examination to iden-
tify possible associated injuries such as underlying skull
fractures. The wound itself is managed by irrigation, debride-
ment, and hemostasis. After debridement, closure may be
difficult and it may be necessary to utilize some galeal scoring
to achieve primary repair. Smaller defects may be managed
conservatively with dressing changes and allowed to heal by
secondary intention. However, the best way of achieving
hemostasis is with wound closure. Larger defects may require
skin grafting or local or distant flaps. Complex local flap
reconstruction is best not performed at an acute stage but
secondarily.
Partial and total scalp avulsion can be very challenging, but
since the advent of microsurgery, the best option is to replant
the scalp if at all possible. The level of avulsion is usually in
the plane between the galea and the periosteum and may
include parts of the forehead, eyebrows, upper lids, and also
ears.16 In 1976, Miller et al. reported the first successful total
scalp replantation by microvascular anastomosis.17 Microsur-
gical replantation should be attempted as this is the only way
of restoring “normal”; there is no other way of adequately
replacing the very specialized hair-bearing tissue.
Replantation can be very tedious and demanding, and
there can be considerable blood loss, especially once the flap
is initially revascularized. Blood should be available, and to
expedite matters, a two-team approach is used, with one team
dissecting the amputated part to identify the arteries (one
superficial temporal artery can perfuse the entire scalp), and
a second team to prepare the recipient site and vein grafts
which are often needed. It can be difficult to identify the
collapsed veins in the amputated part, but once the scalp is
revascularized, the veins become very apparent with quite
profuse bleeding. At least one artery and two veins should be

98
SECTION II
CHAPTER 5 • Scalp and forehead reconstruction
Fig. 5.8  Aplasia cutis congenita: the appearance in the neonatal period (A) and 30 years later (B), when a
squamous cell cancer developed in the unstable skin. A CT scan shows a lack of scalp and cranium (C). The SCC
and unstable skin was excised by neurosurgery (D) – it involved the dura and was close to the sagittal sinus. A
dural patch was used to repair the dura (E) and a free TRAM flap is designed to repair this extensive defect (F).
The Free TRAM is well healed and two tissue expanders are in place beneath adjacent normal hair-bearing scalp
(G). After expansion, the TRAM flap is de-epithelialized (H) and the expanded flaps advanced to cover the central
alopecia. The intraoperative (I) and later appearance (J) with full hair coverage is shown.
A
B
C
D
E
F
G
H
I
J