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

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816
Cerebrovascular anomalies are the most common asso­
ciated finding (72%). Because 8% of these children have a
stroke in infancy, patients should have an MRI to evaluate
the brain and cerebral vasculature. Infants are referred for
ophthalmologic, endocrine, and cardiac evaluation to rule
out these associated anomalies and LUMBAR association
(Lower body infantile hemangioma, Urogenital anomalies,
Myelopathy, Bony deformities, Anorectal malformations,
Renal anomalies).13 The hemangioma is flat, reticular, and
diffusely involves the midline lumbosacral area.
Capillary malformations can be associated with under­
lying anomalies. A lesion involving the parietal or occipital
screening should be considered.11 PHACES association af­
fects 2.3% of patients with infantile hemangioma and con­
sists of a plaquelike lesion in a regional distribution of the
face with at least one of the following anomalies12:
PHACES
Posterior fossa brain malformation
Hemangioma
Arterial cerebrovascular anomalies
Coarctation of the aorta and cardiac defects
Eye/Endocrine abnormalities
Sternal clefting or Supraumbilical raphe
Fig. 45.6 Examples of vascular anomalies that have associated morbidities outside of the area of the lesion. (a) Multiple cutaneous infan­
tile hemangiomas (five or more). (b) Diffuse reticular hemangioma of the lumbosacral area. (c) PHACE association. (d) Heterotopic neural
nodule. (e) Sturge-Weber syndrome. (f) Capillary malformation–arteriovenous malformation. (g) CLOVES syndrome. (h) Klippel-Trénaunay
syndrome.
a
b
c
d
e
f
g
h

817
Chapter 45 Vascular Anomalies
Managing Unfavorable Results
and Complications in Vascular
Anomalies
Resection of vascular anomalies have a higher complica­
tion rate compared to the removal of other benign lesions.
Vascular anomalies cause local ischemia and have increased
blood flow. Consequently, the risk of postoperative infection,
hematoma, and wound dehiscence is elevated (Fig. 45.7).
Surgeons should have a low threshold to use perioperative
antibiotics, drains, and strategies to control blood loss.
After subtotal or complete resection of a vascular anom­
aly, it is generally best to reconstruct the area by advancing
skin flaps or using regional flaps. Skin grafts have a higher
risk of failure if they are placed on a recipient site that con­
tains disease (Fig. 45.8). Grafts placed over an anomaly are
difficult to vascularize because the underlying wound bed
is ischemic.
Less-invasive interventions than resection for vascular
anomalies are also at risk for complications. A common con­
sult from interventional radiology colleagues is to manage
wounds. Sclerotherapy for venous and lymphatic malforma­
tions has a 5% risk of cutaneous ulceration (Fig. 45.9). Embo­
lization of arteriovenous malformation can cause wounds.
Carbon dioxide laser for bleeding lymphatic vesicles has a
high risk for full-thickness skin loss. Wounds are allowed to
heal secondarily; aggressive intervention to close the wound
generally should be avoided. If the scar is unfavorable and
causes a deformity, it can be revised at a later time.
scalp with alopecia and a ring of long hair (“hair collar sign”)
may be a heterotopic neural nodule.5 These lesions have a
50% risk of extending intracranially and contain hetero­
topic leptomeningeal tissue. MRI is obtained to determine
whether a connection to the dura exists and, if present, the
patient is referred to a neurosurgeon. Children with a capil­
lary malformation in the first trigeminal nerve distribution
are at risk for Sturge-Weber syndrome.5 Individuals undergo
MRI to identify leptomeningeal vascular anomalies that can
cause seizures. They are referred for ophthalmology evalu­
ation to rule out ocular abnormalities (glaucoma, choroidal
vascular anomalies). A midline capillary malformation of the
posterior trunk may be associated with an underlying spinal
arteriovenous malformation.14 Patients likely have CLOVES
syndrome (Congenital, Lipomatosis, Overgrowth, Vascular
malformations, Epidermal nevi, and Scoliosis/Skeletal/Spinal
anomalies) or capillary malformation–arteriovenous mal­
formation (CM-AVM).15 Children with CM-AVM also are at
risk for intracranial arteriovenous malformations and may
undergo MRI screening.
Vascular malformation overgrowth conditions should
be recognized, because they may have significant associ­
ated morbidity. Individuals with CLOVES syndrome are at
risk for Wilms tumor and undergo renal ultrasound screen­
ing. Patients with Klippel-Trenaunay syndrome (capillary-
lymphatic-venous malformation of a lower extremity with
overgrowth) may have thrombophlebitis and pulmonary
embolism from a large, embryonic vein.16 Patients undergo
MRI evaluation and removal of this vein.
Fig. 45.7 Wound dehiscence after resection of an infantile hemangioma. This male infant had an ulcerated infantile hemangioma on his
upper extremity. Because of the large wound, pain, and bleeding, the lesion was resected. (a) Preoperative appearance. (b) After removal
of the ulceration. The tumor was too large to resect in one stage and thus serial excision was performed. The skin edges containing residual
hemangioma were approximated. (c) The suture line dehisced, likely because of necrosis of the skin edges (infantile hemangioma causes
ischemia from shunting of arterial blood directly to the venous circulation). (d) The wound margins containing residual hemangioma were
débrided and the area underwent delayed primary closure. The center of the wound was unable to be closed linearly and healed second­
arily. (e) Appearance of the scar.
a
b
c
d
e

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818
Fig. 45.8 Complication after resection of an arteriovenous malformation. After resection, part of the defect was reconstructed with a split-
thickness skin graft that failed. Because the underlying recipient site likely contained an arteriovenous malformation, the area was ischemic
and unable to vascularize the skin graft. (a) Preoperative appearance. (b) After resection. (c) Partial closure and split-thickness skin graft.
(d) Wound after graft failure. (e) External tissue expansion device placed. (f) Postoperative appearance.
a
b
c
d
e
f
Fig. 45.9 Skin necrosis after sclerotherapy. This boy had a diffuse venous malformation of his left face. He underwent sclerotherapy by
an interventional radiologist. Because the venous malformation was superficial and involved the integument, the sclerosant caused full-
thickness skin loss. (a) Magnetic resonance image showing the subcutaneous lesion of the left cheek. (b) Fluoroscopy delineates the venous
malformation during sclerotherapy. (c) Skin necrosis after the procedure. (d) Appearance of the scar after the wound healed secondarily.
a
b
c
d

819
Chapter 45 Vascular Anomalies
and often do not require treatment. Intervention should not
cause a worse deformity than the appearance of the ­lesion.
Patients with complicated vascular anomalies are best
managed in an interdisciplinary center. Physicians treat­
ing these lesions should be aware of associated ­morbidities
outside of the area of the anomaly.
Conclusion
The field of vascular anomalies is difficult, because lesions
look similar and terminology is confusing. Most complica­
tions result from misdiagnosis of the lesion leading to in­
correct treatment. Vascular anomalies are not malignant
References
1. Hassanein AH, Mulliken JB, Fishman SJ, Greene AK. Evalu­
ation of terminology for vascular anomalies in current lit­
erature. Plast Reconstr Surg 2011;127(1):347–351
2. Greene AK, Liu AS, Mulliken JB, Chalache K, Fishman SJ.
Vascular anomalies in 5,621 patients: guidelines for refer­
ral. J Pediatr Surg 2011;46(9):1784–1789
3. Mulliken JB, Glowacki J. Hemangiomas and vascular
malformations in infants and children: a classification
based on endothelial characteristics. Plast Reconstr Surg
1982;69(3):412–422
4. Finn MC, Glowacki J, Mulliken JB. Congenital vascular le­
sions: clinical application of a new classification. J Pediatr
Surg 1983;18(6):894–900
5. Greene AK. Vascular Anomalies: Classification, Diagnosis,
and Management. St. Louis, MO: Quality Medical Publish­
ing; 2013
6. Greene AK. Management of hemangiomas and other vas­
cular tumors. Clin Plast Surg 2011;38(1):45–63
7. Maguiness SM, Liang MG. Management of capillary mal­
formations. Clin Plast Surg 2011;38(1):65–73
8. Greene AK, Perlyn CA, Alomari AI. Management of lym­
phatic malformations. Clin Plast Surg 2011;38(1):75–82
9. Greene AK, Alomari AI. Management of venous malfor­
mations. Clin Plast Surg 2011;38(1):83–93
10. Greene AK, Orbach DB. Management of arteriovenous
malformations. Clin Plast Surg 2011;38(1):95–106
11. Horii KA, Drolet BA, Frieden IJ, et al; Hemangioma Investi­
gator Group. Prospective study of the frequency of hepatic
hemangiomas in infants with multiple cutaneous infan­
tile hemangiomas. Pediatr Dermatol 2011;28(3):245–253
12. Metry DW, Garzon MC, Drolet BA, et al. PHACE syndrome:
current knowledge, future directions. Pediatr Dermatol
2009;26(4):381–398
13. Iacobas I, Burrows PE, Frieden IJ, et al. LUMBAR: associa­
tion between cutaneous infantile hemangiomas of the
lower body and regional congenital anomalies. J Pediatr
2010;157(5):795–801.e1–e7
14. Alomari AI, Chaudry G, Rodesch G, et al. Complex spinal-
paraspinal fast-flow lesions in CLOVES syndrome: analy­
sis of clinical and imaging findings in 6 patients. AJNR Am
J Neuroradiol 2011;32(10):1812–1817
15. Revencu N, Boon LM, Mulliken JB, et al. Parkes Weber
syndrome, vein of Galen aneurysmal malformation, and
other fast-flow vascular anomalies are caused by RASA1
mutations. Hum Mutat 2008;29(7):959–965
16. Kulungowski AM, Fishman SJ. Management of com­
bined
vascular
malformations.
Clin
Plast
Surg
2011;38(1):107–120
Discussion by Juan Carlos Lopez Gutierrez
An international consensus management protocol based
on the vast information recently published and pro­
gressively updated in the field of vascular anomalies is
the key to obtaining a successful outcome in this group
of patients. A physician in a primary care center using
wrong nomenclature and avoiding the help of a multi­
disciplinary team has little chance for an optimal man­
agement of a patient with a complex vascular anomaly.
A revised International Society of Vascular Anoma­
lies (ISSVA) classification of vascular anomalies has been
published.1 Because the updated classification lists a
large number of different diseases, it is presented as a
general table1 (Box 45D.1) containing the main classes
of vascular anomalies and referring to several subtables.
The new ISSVA classification of vascular lesions is
an important contribution to the literature and is meant
to represent the state of the art in vascular anomalies
and should therefore be the only one to be considered
as a useful tool in the communication among vascular
anomalies specialists.
Vascular Tumors
Management of Tufted Angioma,
Kaposiform Hemangioendothelioma,
and Infantile Hemangioma
Tufted angioma (TA) is three times more common than
Kaposiform hemangioendothelioma (KHE) at our insti­
tution. Despite the concurrence of features of both vas­
cular tumors in some patients, they are still considered
as two separate entities.2–7 In fact, we found a lower
tendency of TA to develop Kasabach-Merritt phenom­
enon as well as a nonrandom distribution of TA, with
up to 80% of incidence of this tumor in the mandibular
area (Figs. 45D.1 and 45D.2).

SECTION VI PEDIATRIC AND CRANIOFACIAL SURGERY
820
Box 45D.1
Vascular Tumors
•• Benign vascular tumors
○
○Infantile hemangioma (IH)/hemangioma of
infancy
○
○Congenital hemangioma
–
– Rapidly involuting (RICH)
–
– Noninvoluting (NICH)
–
– Partially involuting (PICH)
○
○Tufted angioma (TA)
○
○Spindle-cell hemangioma
○
○Epithelioid hemangioma
○
○Pyogenic granuloma (also called lobular
capillary hemangioma)
○
○Others
•• Locally aggressive or borderline
○
○Kaposiform hemangioendothelioma (KHE)
○
○Retiform hemangioendothelioma
○
○Papillary intralymphatic angioendothelioma
(PILA), Dabska tumor
○
○Composite hemangioendothelioma
○
○Kaposi’s sarcoma
○
○Others
•• Malignant
○
○Angiosarcoma
○
○Epithelioid hemangioendothelioma
○
○Others
Vascular Malformations
•• Simple
•• Capillary malformations
○
○Lymphatic malformations
•• Venous malformations
○
○Arteriovenous malformations
○
○Arteriovenous fistula
•• Combined
○
○CVM, CLM
○
○LVM, CLVM
○
○CAVM, CLAVM
○
○Others
Benign Vascular Tumors
•• Infantile hemangioma
International Society of Vascular Anomalies Classification
of Vascular Anomalies
Abbreviations: CAVM, capillary-arteriovenous malformation; CLAVM, capillary-lymphatic-arteriovenous malformation; CLM, capillary-
lymphatic malformation; CLVM, capillary-lymphatic-venous malformation; CVM, capillary-venous malformation; LVM, lymphatic-venous
malformation.
In addition, TA is more commonly painful, and hy­
perhidrosis at the site is common. Those findings are not
characteristic of KHE.
If a physician can differentiate between the eight
major lesions he or she will be able to successfully man­
age 95% of patients, but it is also evident that up to 95%
of IH, pyogenic granulomas, congenital hemangiomas,
and KHE will be properly managed by an expert pediat­
ric dermatologist. Probably, the role of the surgeon has
more importance in the management of aggressive or
malignant vascular tumors, potentially fatal entities that
deserve special attention because mistakes in their rec­
ognition can have lethal consequences.8,9 Two patients
with diagnoses of multifocal liver infantile hemangioma
and skin composite hemangioendothelioma died at our
institution from metastatic disease at 1 and 6 years, re­
spectively, after diagnosis despite undergoing radical
resections including orthotopic liver transplantation.
Multifocal liver angiosarcoma and epithelioid heman­
gioendothelioma were finally diagnosed (Figs. 45D.3
and 45D.4).
Different types of sarcomas have a similar prolif­
erative clinical course as IH with significant fast flow
on ultrasound examination. A failure of pharmacologic
Fig. 45D.1 Tufted angioma involving the full left lower limb
without developing Kasabach-Merritt phenomenon.
Fig. 45D.2 Tufted angioma with the typical mandibular area
involvement.

821
Chapter 45 Vascular Anomalies
therapy for what is assumed to be IH is an indication for
immediate biopsy (Fig. 45D.5).
Regarding overtreatment of IH, its management is
currently well protocolized around the world, and oral
propranolol, when administrated in the first month of
life, is successful in IH proliferation arrest in 99% of cases
based on the medical literature and our experience in
more than 300 treated patients.10–14 There is no indica­
tion for intralesional corticosteroids if the IH is treated
with oral propranolol in the first month of life after in­
ternationally recognized guidelines. Only patients with
inappropriate previous management and who are too
late to be treated pharmacologically will be candidates
for surgery. The need of surgical management of IH is
basically the result of a wrongly delayed treatment with
beta-blockers or unresponsiveness to this therapy, cur­
rently estimated at less than 1% of the cases.
The rapid response of IH to propranolol can be help­
ful in the management of radiologically undiagnosed
vascularized tumors located in difficult anatomic areas
where a biopsy can entail significant morbidity. Because
IH is the most common tumor with increased blood sup­
ply in this age group and it responds dramatically to
propranolol, an oral beta-blocker test can be useful to
reduce the need for biopsies when ultrasound and mag­
netic resonance imaging (MRI) cannot ascertain the di­
agnosis of hemangioma or sarcoma among others. Pro­
pranolol is administrated at 3 mg/kg/day for 3 weeks.
The criteria for positive response are reduction of vol­
ume and blood flow, measured by weekly ultrasound
examination. Sarcomas, mesenchymal hamartomas, and
metastatic neuroblastoma do not respond to proprano­
lol and continue to progress, whereas IH always shows
decreased perfusion and size, obviating biopsies in dif­
ficult areas such as the liver, heart, and orbit.
Another pharmacologic agent, rapamycin, is cur­
rently being considered as the first treatment option for
complicated lymphatic, venous, or combined vascular
anomalies. In fact, up to 561 clinical trials are currently
on course related to the use of mammalian target of ra­
pamycin (mTOR) inhibitors in the treatment of vascular
disorders. Sirolimus is a safe and well-tolerated treat­
ment that can reduce symptoms and/or stabilize disease
in patients with severe lymphatic malformation (LM).
In fact, current pharmacological management protocols
for Kasabach-Merritt phenomenon (KMP) are switching
from intravenous (IV) vincristine at 0.05 mg/kg/week to
oral aspirin and ticlopidine at 10 mg/kg/day or to oral
sirolimus at 0.8 mg/m2/dose twice a day with an easier
administration and similar outcome (Fig. 45D.6).
Although the number of patients with KMP treated
with mTOR inhibitors is still limited, response has been
uniformly good in the reported cases as well as in our
six-case experience, with an excellent tolerability and
an easier oral administration.
Fig. 45D.4 Hepatectomy specimen of liver multifocal angio­
sarcoma.
Fig. 45D.5 External ear rhabdomyosarcoma mimicking an in­
fantile hemangioma in a 5-month-old boy.
Fig. 45D.3 Bone metastatic disease 8 years after epithelioid
hemangioendothelioma excision.

SECTION VI PEDIATRIC AND CRANIOFACIAL SURGERY
822
a
b
Fig. 45D.6 (a) A lower limb tufted angioma that developed severe Kasabach-Merritt phenomenon. (b) Immediate response to
oral sirolimus administration.
Currently, it is not known whether treatment must
be continued for life or whether resistance to sirolimus
eventually develops. The optimal dose of sirolimus that
should be used and when it is most efficacious to initi­
ate treatment is not known.15–18 The dosage and blood
levels currently used are based on experience with si­
rolimus in the prevention of graft rejection in patients
who have undergone organ transplantation. It is pos­
sible that lower sirolimus levels may be equally effec­
tive, especially in the treatment of lymphatic disease.19,20
Lymphatic Malformations
LMs are the vascular malformations that most com­
monly need treatment at an early age. Only patients
with a minor LM are considered candidates for a “wait
and see” protocol until adulthood. Prenatal treatment
is sometimes indicated, and different fetal procedures
have been reported to prevent airway compromise dur­
ing pregnancy. In fact, the ex utero intrapartum treat­
ment procedure is commonly indicated at delivery to
prevent perinatal hypoxemic episodes. A neonate with
airway involvement in the context of an oral or cervical
LM needs a careful examination by an expert team. Im­
mediate bronchoscopy must be performed to confirm
tracheal infiltration. In this eventuality a tracheostomy
must be considered, because appropriate treatment
will take years. If the upper airway shows signs of com­
pression and not infiltration, total or subtotal surgical
excision remains the best option to achieve a prompt
extubation.
Recently we developed a new strategy in this group
of patients. In case of difficulty for extubation in the
first week of life, we administrate rapamycin at 1 mg/
kg/day for 2 to 3 weeks. Reduction in the volume and
size of the lymphatic mass very often helps in the pro­
cess of extubating the patient, and therefore the sur­
gical or sclerosing procedure can be delayed 6 to 12
months by continuing the patient on sirolimus treat­
ment. Surgical resection of large LM in neonates is a
common cause of neural damage because facial nerve
branches, among others, are difficult to identify, moni­
tor, and preserve.
Given the known significant morbidity and mortal­
ity rates in patients with complicated lymphatic malfor­
mations, future treatment studies need to address these
specific phenotypes.
Similar considerations are currently under study in
the management of potentially fatal vascular anoma­
lies such as blue rubber bleb nevus syndrome, massive
venous or combined lymphatic-venous malformations,
and phosphatase and tensin homolog hamartomas
syndrome.
Conclusion
In summary, the surgeon plays a central role in the
management of vascular anomalies and in the clinical
setting to evaluate the efficacy of systemic antiangio­
genic drugs for the improvement of cosmetic outcomes,
reduction of unfavorable results, and the prevention of
complications.
References
1. Wassef M, Blei f, Adams D, et al; ISSVA Board and
Scientific Committee. Vascular Anomalies Classifi­
cation: Recommendations from the International
­Society for the Study of Vascular Anomalies. Pediat­
rics 2015;136(1):e203–e214
2. Kozakewich HPW, Mulliken JB. Histopathology of
vascular malformations. In: Mulliken JB, Burrows PE,
Fishman SJ, eds. Mulliken & Young’s Vascular Anoma­
lies, Hemangiomas and Malformations. 2nd ed. New
York, NY: Oxford University Press; 2013:480-507

823
Chapter 45 Vascular Anomalies
3. Enjolras O. Classification and management of the
various superficial vascular anomalies: hemangiomas
and vascular malformations. J Dermatol 1997;24(11):
701–710
4. Chu CY, Hsiao CH, Chiu HC. Transformation between
Kaposiform hemangioendothelioma and tufted an­
gioma. Dermatology 2003;206(4):334–337
5. North PE, Waner M, Buckmiller L, James CA, Mihm
MC Jr. Vascular tumors of infancy and childhood: be­
yond capillary hemangioma. Cardiovasc Pathol 2006;
15(6):303–317
6. Osio A, Fraitag S, Hadj-Rabia S, Bodemer C, de Prost
Y, Hamel-Teillac D. Clinical spectrum of tufted angio­
mas in childhood: a report of 13 cases and a review of
the literature. Arch Dermatol 2010;146(7):758–763
7. Le Huu AR, Jokinen CH, Rubin BP, et al. Expression of
prox1, lymphatic endothelial nuclear transcription fac­
tor, in Kaposiform hemangioendothelioma and tufted
angioma. Am J Surg Pathol 2010;34(11):1563–1573
8. Requena L, Sangueza OP. Cutaneous vascular prolifer­
ations. Part III. Malignant neoplasms, other cutaneous
neoplasms with significant vascular component, and
disorders erroneously considered as vascular neo­
plasms. J Am Acad Dermatol 1998;38(2 Pt 1):143–
175, quiz 176–178
9. Wassef M, Hunt SJ, Santa Cruz DJ, Barnhill RL. Vascu­
lar tumors and vascular malformations. In: Barnhill
RL, Crowson AN, Magro CM, Piepkorn MW, eds. Der­
matopathology. 3rd ed. New York, NY: McGraw-Hill;
2010:802-856
10. Léauté-Labrèze C, Hoeger P, Mazereeuw-Hautier J, et
al. A randomized, controlled trial of oral propranolol
in infantile hemangioma. N Engl J Med 2015;372(8):
735–746
11. Liang MG, Frieden IJ. Infantile and congenital heman­
giomas. Semin Pediatr Surg 2014;23(4):162–167
12. Solman L, Murabit A, Gnarra M, Harper JI, Syed SB,
Glover M. Propranolol for infantile haemangiomas:
single centre experience of 250 cases and proposed
therapeutic protocol. Arch Dis Child 2014;99(12):
1132–1136
13. Drolet BA, Frommelt PC, Chamlin SL, et al. Initia­
tion and use of propranolol for infantile hemangi­
oma: report of a consensus conference. Pediatrics
2013;131(1):128–140
14. Marqueling AL, Oza V, Frieden IJ, Puttgen KB. Pro­
pranolol and infantile hemangiomas four years later:
a systematic review. Pediatr Dermatol 2013;30(2):
182–191
15. Lackner H, Karastaneva A, Schwinger W, et al. Sirolim­
us for the treatment of children with various compli­
cated vascular anomalies. Eur J Pediatr 2015;174(12):
1579–1584
16. Nadal M, Giraudeau B, Tavernier E, Jonville-Bera AP,
Lorette G, Maruani A. Efficacy and Safety of Mam­
malian Target of Rapamycin Inhibitors in Vascular
Anomalies: A Systematic Review. Acta Derm Venereol
2016;96(4):448–452
17. Vlahovic AM, Vlahovic NS, Haxhija EQ. Sirolimus for
the treatment of a massive capillary-lymphatico-
venous malformation: a case report. Pediatrics 2015;
136(2):e513–e516
18. Wang Z, Li K, Yao W, Dong K, Xiao X, Zheng S. Success­
ful treatment of kaposiform lymphangiomatosis with
sirolimus. Pediatr Blood Cancer 2015;62(7):1291–
1293
19. Kim D, Benjamin L, Wysong A, Hovsepian D, Teng J.
Treatment of complex periorbital venolymphatic mal­
formation in a neonate with a combination therapy of
sirolimus and prednisolone. Dermatol Ther (Heidelb)
2015;28(4):218–221
20. Hammill AM, Wentzel M, Gupta A, et al. Sirolimus
for the treatment of complicated vascular anomalies
in children. Pediatr Blood Cancer 2011;57(6):1018–
1024

824
CHAPTER
46
Tissue Expansion for Pigmented Lesions
and Other Defects
Bruce S. Bauer and Sara R. Dickie
Large and giant congenital melanocytic nevi present a
unique reconstructive challenge. Nevomelanocytes are
known to penetrate through the full thickness of skin and
into the subcutaneous fat. Often they invade nerve and
blood vessels. On rare occasions they may penetrate fas­
cia, muscle, and internal organs.1,2 Thus excision of the full
thickness of nevus tissue is required to remove most of the
nevus cells and minimize subsequent reappearance of ne­
vus cells with possible long-term sequelae.
The principle of reconstruction is to replace like with
like. Serial excision can often debulk these massive lesions
but rarely removes them completely. Excision and split-
thickness skin graft, if the excision is carried out to the fas­
cial level, can result in both poor aesthetic outcome and
risk of functional disturbance, except for select situations.3
Partial-thickness removal such as dermabrasion, curettage,
chemical peel, and laser treatment all have problems with
recurrence, because these modalities only eliminate the su­
perficial portion of the nevus. Later degeneration of the re­
maining nevus has been reported.4
Avoiding Unfavorable Results
and Complications in Tissue
Expansion
When direct excision and primary closure are not a pos­
sibility, tissue expansion is the workhorse treatment mo­
dality for melanocytic lesions, for large scars, for vascular
lesions, and as an adjunct in reconstruction of some cra­
niofacial deformities. Since 1980, I (B.B.) have dedicated
my practice to refining the techniques used in the treat­
ment of nevi and other skin and soft tissue defects using
tissue expansion.5–7 This vast experience has garnered
a host of successes, as well as some expected and unex­
pected complications, for which effective management
strategies have been developed. This chapter relays this
expertise so the reader can avoid some common mistakes
and successfully manage a variety of complications in­
volving tissue expansion.
Summary Box
Avoiding Unfavorable Results and
Complications
During
Expansion
Complication
Major
Infection
Flap ischemia
Implant exposure or extrusion
Device failure
Minor
Seroma
Wound dehiscence
Pain
Flipped or inaccessible port
Postexpansion
Major
Flap ischemia
Infection
Wound dehiscence
Minor
Delayed wound healing
Scar widening
Flap congestion
Seroma

825
Chapter 46 Tissue Expansion for Pigmented Lesions and Other Defects
specific volumes are not set but are gauged by capillary re­
fill and the feel of the expander. Therefore for nearly all our
patients we plan the removal and reconstruction for 11 to
12 weeks after the expander placement (expansion over 7 to
8 weeks for smaller facial nevi). For smaller expanders or for
smaller defects for which we are using a larger expander but
do not require the full volume of expansion, we shorten the
time as needed. Whether the families decide to come weekly
to the clinic for injections or, more commonly, expand at
home after careful instructions, the parents and doctor must
agree to an open and regular dialog (email, digital images, or
phone communication when needed). In this manner, com­
plications can often be avoided or treated soon enough to
avoid compromising the expander or flap.
Many of our patients perform home expansion. There­
fore they need to be prepared to maintain an open line of
communication with physicians and nurses regarding the
appearance of skin flaps, any fevers, red skin, incision drain­
age, or other issues. We also require photographic documen­
tation to be provided so that an ongoing assessment of the
progress can be made. For patients who elect to undergo
office-based expansion, they need to commit to visit the of­
fice on a weekly basis. Patients who are willing to meet the
aforementioned criteria are considered good candidates for
tissue expansion.
It is vital that patients be made aware of what a fully
inflated expander will look like in a given location. It might
be shocking on first impression, and the management of
these expectations preoperatively is vital. We provide mul­
tiple photographs depicting a variety of cases for patients to
visually gain this understanding. Adult patients who have
employers or professions that would not tolerate the visual
appearance of an expander are encouraged to arrange time
off or reassignment during their expansion. This will ensure
the least disruption to their livelihood, and they can be more
comfortable, improving the chances at a successful outcome.
Some parents prefer to have their children undergo the ex­
pansion process during the summer months to avoid the
social stigma in some scholastic settings. Others choose the
opposite approach so as not to miss any summer activities
such as swimming or camp.
High-risk tissue expansion patients are typically those
who have undergone multiple expansions in the past (Fig.
46.1). Resulting scars and thinner flaps increase the risk
of exposure of the implant. Patients who are prone to in­
fections, such as those with recurrent otitis media, are at
increased risk of expander infection. In these cases we rec­
ommend myringotomy tubes before the start of expansion
to reduce the risk of bacterial seeding via the bloodstream
once the expander has been placed. Other patients may
be prescribed oral antibiotics for the course of expansion
if they have a history of expander infection. Nevus qual­
ity also affects the chances for success. Nevi that have fine
villous hair are found to be at higher risk for infection and
Preoperative Planning and Patient
Selection
Most patients with melanocytic nevi treated with tissue
expansion are children, although we have gained some im­
portant insights from a small group of adult patients. Juve­
nile skin, although elastic, does not have the laxity of adult
skin, and the local flaps used in adults are often difficult in
children. The decision to excise large and giant nevi in chil­
dren is sometimes controversial.8–10 In our practice the ideal
patient is one with a supportive family structure that un­
derstands the involvement required to achieve successful
outcomes using expansion and can take an active role in the
process. Preferably, the patient does not have symptomatic
neurocutaneous melanosis,11 a developmental disability, or
comorbid conditions that may outweigh the benefits of exci­
sion and reconstruction. The patient must also have enough
normal skin with which to expand. This does not require a
certain percentage but needs to be sufficient to undergo se­
rial expansion to reduce the nevus size so that clothing can
cover what remains and provide some social benefit.
There is no ideal age to begin expansion, but in our
practice we have noted that younger patients often toler­
ate expansion very well and have little or no memory of
the process when they are older. Younger patients are often
easier to control and to limit their activities around the time
of surgery to optimize healing. We place expanders in chil­
dren starting at 6 months of age when the anesthetic risk is
low.12,13 Many of our patients approach us via the Internet
or email and the initial consultation is done via pictures or
web-based video conference. For any assessment of a new
patient regarding an expander the surgeon must evaluate
the extent of the defect or lesion to be treated and the avail­
able donor tissue. With experience it becomes easier to es­
timate how much can be accomplished by a single round
of expansion and what defects will require more. Further
assessment of the patient focuses on the donor skin sur­
rounding the lesion. The surgeon must ask: What is the tis­
sue quality? Are there preexisting scars? Are there satellite
lesions? Is there infection or another wound? What struc­
tures will limit the placement or the amount of expansion
that can be achieved? The answers to these questions will
help delineate the number and the size of the expanders to
be used and the ideal placement locations and will identify
potential pitfalls. Cases can be matched against patients with
similar nevus distribution as a guide to the number of ex­
panders and rounds of expansion that might be required to
complete the excision and reconstruction.
Once the size and location of the expanders has been
chosen, the next step is to determine the length of time that
will be required to expand the tissue. We anticipate that
with weekly expander injections, most expanders can be
filled to the desired volume in 10 to 12 weeks. The volumes
vary with the expander size and area to be expanded, and

SECTION VI PEDIATRIC AND CRANIOFACIAL SURGERY
826
Fig. 46.1 A high-risk patient for expanders. (a) He had a large neural nevus of forehead and scalp. (b–d) After multiple rounds of expansion
and initial reconstruction, he presented with residual nevus of the temporal forehead and scar alopecia. (e,f) Two expanders were placed in
the frontal and temporal scalp. The expander on the right temple was exposed through the thin scar and residual nevus. (g–i) Tissue loss
from implant exposure required reconstruction using the expanded frontal scalp, resulting in unfavorable scalp scars and scar alopecia, and
did not achieve sufficient tissue gain to fully excise the residual nevus.
a
b
c
d
e
f
g
h
i
Continued

827
Chapter 46 Tissue Expansion for Pigmented Lesions and Other Defects
sible for the care, making and keeping appointments, and
maintaining an open dialog about early signs of infection or
wound problems. The patient or caregiver possesses equally
half of the responsibility to achieve a good outcome. It is
worth noting that many of the mentioned approaches to in­
cipient infection, or antibiotic regimens in serial expansion
cases, have arisen through careful day-to-day (sometimes
hour-by-hour) observation by the parents.
Tissue expansion can be considered as a continuous pro­
cedure that lasts 3 months rather than simply as a two-stage
reconstructive surgery. Patients or parents who do not grasp
this concept of expansion, fail to appreciate the time com­
mitment, wish to rush the process, or present a controlling
delayed healing at incision sites (even with optimal wound
care the fine hairs seem to incite inflammation and second­
ary infection) (Fig. 46.2). For these lesions and for scar re­
construction, incisions are typically placed outside of the
lesion to prevent these complications. We always stress
trimming or cutting hair that is near incisions to avoid the
buildup of crust, scab, or other irritation that can lead to
local infection.
Finally, the most successful outcomes arise from coop­
erative and collaborative doctor–patient relationships. There
is much that the physician cannot control during the time
the expander is in place. Although it is easy to provide guid­
ance and reassurance, the parent or adult patient is respon­
Fig. 46.1, cont’d (j,k) Repeat expansion with a parietal expander placed in a more posterior position, remote from the scars. (l–n) At 6
months postoperatively, after complete excision of the nevus and revision and reorientation of the scalp scars in a more favorable position.
j
k
l
m
n

SECTION VI PEDIATRIC AND CRANIOFACIAL SURGERY
828
a
b
c
d
e
f
g
Fig. 46.2 A high-risk patient for an expander. (a,b) She had a large hairy nevus of the arm; villous hair texture increases the risk of infec­
tion. An expander was placed through the border of the nevus at the shoulder into the right upper back to expand the parascapular flap.
(c) A red expander developed midway through expansion. (d) An incision drained frank pus. Hair was trimmed from around the incision,
and it was allowed to continue draining. Oral antibiotics were given for the remainder of expansion. (e–g) Expansion was completed and
reconstruction was successful.

829
Chapter 46 Tissue Expansion for Pigmented Lesions and Other Defects
Each of these types can safely hold twice the listed vol­
ume, and overexpansion is common. Although custom ex­
panders may be required in the rare expansion of nasal skin,
the concept of shaping an expander to only fit within an area
of normal skin adjacent to the lesion will limit the later size
of the flap. We prefer to use the largest expander that can
safely be placed, because it is better to work with more tis­
sue than less. Although placing a larger expander through
an incision further within the border of a nevus will expand
the nevus as well as normal skin, the result will be to gain
more expansion of the normal skin than can be obtained
with a smaller expander.
The expander preferably has a reinforced backing, which
creates some directional expansion but also allows the initial
excess expander envelope to be folded beneath the backing,
which creates a low profile at the time of placement. The
silicone quality should be soft and pliable to avoid unnec­
essarily sharp folds that can compromise the flap. Saline is
delivered in a controlled fashion via the valve port, which
is placed at some distance from the expander and overlying
firm tissue. Although integrated ports have been used by
some surgeons, we use remote ports in all cases, with none
externalized, despite the fact that the parents typically do
the expander injections. Because the skin overlying the port
can be readily anesthetized with a topical anesthetic, we see
no benefit in externalizing the ports.
Regarding the donor site, the surgeon must match the
color, texture, and contour of the recipient site to maximize
the aesthetic and functional outcome. The donor site tissue
must be free of infection, or have stable scars, to minimize
the risk of expander failure or extrusion. Careful selection
of expander size is imperative in areas with thin donor skin
to avoid expander folds or prominence, which can create
areas of excessive pressure and skin compromise. In most
cases, the expanders are placed through an incision within
the border of the lesion. In cases where expansion has been
used repeatedly and scars are present both at the border of
the remaining nevus and at junctions of prior flaps, the new
attitude toward the surgical plan are often poor candidates.
Patients or parents who appear overly concerned with their
appearance during expansion or refuse to accept scars or any
variation in scarring offer red flags to the surgeon. Even the
most straightforward tissue expander reconstruction can
fail because of a noncompliant or overly controlling patient
personality. By the same token, physicians who do not ap­
preciate the importance of the preoperative plan and cannot
commit the necessary time to the ongoing needs of patients
through the expansion process are bound to fail.
Intraoperative Decision-Making
The ideal goal of tissue expansion is to achieve adequate
tissue coverage with the fewest rounds of expansion. Scars
should be well concealed, avoid contracture or tethering,
and have as little asymmetry as possible. Therefore the
design of an expanded flap is of major importance and is
impacted directly by the orientation of the expander. Al­
though the early dogma of tissue expansion emphasized
designing advancement flaps only, experience over more
than three decades has demonstrated that expanded
transposition and rotation flaps are commonly preferable
because they provide greater versatility in flap design and
range.7,11,14 In addition, the incision for expander place­
ment was originally designed at a right angle to the direc­
tion of expansion, but this approach can greatly limit flap
design in serial expansion cases.
Placement of Expander
Several types of tissue expanders exist based on the shape,
size, and type of filling valve. We most commonly use rect­
angular or loaf-shaped expanders to treat congenital nevi
(as well as virtually all expansion cases). Expander volumes
have a wide range and vary according to the anatomical
site. Standard sizes include 70 mL, 250 mL, 350 mL, 500 mL,
750 mL, 1000 mL, and 1200 mL (Fig. 46.3).
Fig. 46.3 The ideal expanders are smooth rectangular expanders with remote ports. Silicone backing prevents folds and migration of the
expander. Sizes vary depending on the location and tissue requirement.

SECTION VI PEDIATRIC AND CRANIOFACIAL SURGERY
830
low a home expansion protocol, with injections performed
by the parents under the direction of our nursing staff and
surgeons. A broad-spectrum antibiotic is started at the time
of surgery and is continued until the drains are removed. By
maintaining a low threshold for reinstating antibiotic ther­
apy in the presence of suspected infection, most infections
can be controlled before potential loss of the expander.
Expansion
During the expansion process, which lasts 8 to 12 weeks
depending on the size of the expander and amount of ex­
pansion required, close communication with the patient or
family is critical. Although infection of a tissue expander
occurs in 6 to 9% of cases,15–18 it is rarely an indication to
remove a tissue expander. Early identification of symptoms
that indicate a problem often prevents expander loss. Pa­
tients may report fever, pain, drainage, or red skin over the
expander, but equally important is a report of early upper
respiratory infection or temperature elevation in the ab­
sence of any changes in the area of the expander (Fig. 46.4).
In these cases we start antibiotics and observe the patient
closely. If fever or redness persists, we attempt fluid aspira­
tion from the expander pocket. This is done by placing a
needle into the skin above the remote port and pulling back
slightly so the tip of the needle is still under the skin, but
out of the port. Aspiration of as little as 1 mL of fluid will
often allow antibiotic levels to reach affective levels quickly
enough to control the infection and save the expander (Fig.
46.5). This fluid can also be sent for culture to properly ta­
per antibiotic coverage. Finally, in rare instances, persistent
fever or a red expander requires intramuscular or IV anti­
biotics to achieve improvement and salvage the expander.
When patients have an active fever or have any suspected
infection, we hold all expander fills. If and when the pa­
tient improves and fever resolves, we resume expansion 2
to 7 days later. If expander infection persists and is not re­
sponsive to IV antibiotics, the expander is removed. Often,
expanders should be placed through those scars that are
least likely to be stressed by the weight or pull of the new
expander (i.e., away from the most dependent points). In
other cases, like unstable scar, nevus with fine villous hair,
vascular tumor, and craniofacial deformities, the incisions
are planned outside the border of the defect or on occasion
at a distant site.
A pocket is dissected to allow placement of the ex­
pander, with positioning of the port in a separate pocket
over a region with firm skeletal support for ease of outpa­
tient filling. Flap dissection needs to be done with as lit­
tle trauma or stretch to the overlying skin as possible. We
prefer to use Bovie cautery judiciously and rely mainly on
sharp dissection with scissors and blunt finger dissection
of the pocket with precision bipolar cautery. Most flaps are
raised just above the typically avascular fascial plane. The
flap pocket should not be larger than the footprint of the
expander (plus a few centimeters to allow for the previously
mentioned excess width of the unexpanded envelope) to
avoid expander migration. However, it must be large enough
to prevent folds in the expander from pressing into the flap,
which can compromise the blood supply. Once the expander
is placed fully within the pocket, the flap is examined to en­
sure there is no tethering tissue still present. If there is, the
expander is removed and further dissection is performed.
Very limited dissection is done for the placement of
the port so that it does not migrate toward or under the
expander in the postoperative period. The port should be
placed a good distance away from the expander over firm
skeletal tissue. To achieve this we sometimes use a separate
counterincision through which to place the port. This may
be particularly important in later stages of serial expansion
when the site for ideal port placement is shorter than ideal.
Placing the port in a separate pocket and tunneling the tub­
ing through a tunnel no wider than the width of the tubing
can prevent migration of the port. Extension tubing is used
if the distance is greater than the manufactured tube length.
The surgeon should keep in mind that when overexpansion
is expected, the expander may encroach on the injection
port toward the later stage of expansion if the port is placed
too close to the expander initially.
Partial fill of the expander (10–15% of the listed volume)
ensures the expander is properly positioned without sur­
face folds that can cause pressure against the skin flap to be
expanded. It is important to check the patency of the port
before waking the patient. If saline cannot be drawn out or
injected in, the tubing may be kinked or the port flipped
or placed too deeply in the tissue. These problems need to
be addressed before completion of surgery to avoid reop­
eration. Closed suction drains are placed for 3 to 10 days to
control the potential dead space from wide undermining
and to remove serosanguinous fluid. Our preference is to
use 19-gauge butterfly intravenous (IV) lines, reversing the
tubing and cutting holes in the last 4 to 5 cm. The butterfly
needle is inserted in a vacutainer tube for suction.
Serial injections are started 7 to 10 days after insertion
if the skin flaps are in excellent condition and continue on a
weekly basis for 8 to 12 weeks. Most pediatric patients fol­
Fig. 46.4 An infected expander.

831
Chapter 46 Tissue Expansion for Pigmented Lesions and Other Defects
these cases, removal of fluid will improve the skin (Fig.
46.6). When patients or parents are expanding at home, it
is very important to instruct them on proper flap assess­
ment such as skin quality, tension, and capillary refill. At
other times ischemia may be related to the flap design itself
or an overly thin flap. In these cases we place a large, clear,
semiocclusive dressing (such as Tegaderm or Opsite) over
the flap in the area of compromise (see Fig 46.6b) This is
left in place continuously and only replaced if it becomes
dislodged. This extra layer helps to support and protect the
skin. Often after a few days to a week, the vascularity will
improve to the point that expansion can resume. If the skin
some amount of reconstruction can still be performed with
whatever amount of expansion had been gained before the
illness. The surgeon must consider that the flap may be
somewhat compromised by the infectious process, and it
is best to use direct advancement in these cases and not to
attempt transposition of the flap.
Flap ischemia is also rare, but is noted when the flap
has areas of pink or purple discoloration. If this occurs im­
mediately after surgery, expansion is delayed until the flap
recovers. Later in expansion, some color change is normal
as the vascularity of the skin flap is augmented. Late flap
ischemia is typically a result of overzealous expansion. In
a
b
c
Fig. 46.5 (a) This patient developed a red expander with fever partway through expansion. (b) The patient was prescribed oral antibiot­
ics, and fluid was drawn from around the port. The fever abated and expansion continued. (c) The patient is shown at the completion of
expansion before reconstruction.

SECTION VI PEDIATRIC AND CRANIOFACIAL SURGERY
832
a
b
c
d
Fig. 46.6 A young girl with a trunk nevus, after multiple stages of tissue expansion and reconstruction. (a) A nearly fully expanded 500-
mL expander, with the skin flap overlying the abdominal expander appearing stressed. (b) A parent removed 10 mL of saline and applied
a clear semiocclusive dressing. (c) The patient is shown 1 week after the removal of the saline. (d) The flap is shown immediately before
reconstruction without additional fill.

833
Chapter 46 Tissue Expansion for Pigmented Lesions and Other Defects
If the ischemia or incipient flap compromise is related to
a point or a fold in the expander we place one or two layers
of foam tape (such as Microfoam tape, 3M) over the area and
leave it in place. Expansion is continued on a regular sched­
ule. This has the effect of increasing resistance of the skin in
the area of prominence, in effect distributing the pressure
continues to be compromised, to thin, or even to expose the
implant, the dressing can help salvage the remainder of the
flap. If other expanders are in place, the extra support and
protection provided by the dressing allows completion of
expansion by the other expanders, avoiding an additional
trip to the operating room (Fig. 46.7).
a
b
c
d
e
Fig. 46.7 A young patient with a cape nevus. (a–c) Exposure of the expander occurred in two locations. The areas were treated with a clear
semiocclusive dressing to support the remaining flap. Her back expanders continued expansion until complete. (d,e) After reconstruction.

SECTION VI PEDIATRIC AND CRANIOFACIAL SURGERY
834
Expander extrusion is a rare complication and can of­
ten be dealt with in the office. If the expander is exposed
to the point of extrusion, it needs to be removed and the
wound allowed to heal. Repeat expansion can be attempted
over a wider area and lessening the pinpoint stress on the
flap. With the added support of the tape, the fold will even­
tually flatten with ongoing expansion and the skin will often
recover, allowing the foam tape to be removed (Fig. 46.8).
a
b
c
d
e
Fig. 46.8 A young girl with right hemifacial nevus. (a) The neck expander experienced early exposure because of the folds. Support with
a clear semiocclusive dressing failed. (b) Two months after early removal of the expander, the neck was healed. (c) Subsequent expander
placement with prominent folds, treated with foam tape immediately when exposure was recognized. Expansion continued on schedule.
(d) With ongoing expansion, the prominent fold rounded out and the foam tape was discontinued. Expansion continued on schedule.
(e) The patient is shown 1 month after cheek reconstruction with the expanded neck flap.

835
Chapter 46 Tissue Expansion for Pigmented Lesions and Other Defects
used to partially reconstruct the nevus at this time. If the
patient has other expanders in place, the extruded expander
is simply cut from the tubing of the port either in the office
or at home by the parent (Fig. 46.9). The port is left in place
until the remaining expanders are ready to be removed. The
at a later date. If the patient has a single expander, we typi­
cally remove an extruded expander in the operating room
to remove the remote port as well. Nonviable tissue can be
débrided as needed and the flap pocket washed out and
dressed. Any of the expanded flap that is viable can still be
a
b
c
d
e
Fig. 46.9 Expander extrusion. This young male patient had a giant neural nevus of the back. (a) His second round of tissue expansion in­
cluded three expanders, two at the upper back and shoulder, and one on the abdomen. (b) Early in expansion, the right shoulder flap ap­
peared compromised. A clear, semiocclusive dressing was placed. (c) Shortly after treatment began, the skin deteriorated and the expander
extruded. It was cut from the tubing in the office and the port was left in place. (d) The patient is shown 1 week after the extrusion, with
the remaining expanders that were left in place continuing on a routine schedule. (e) The patient is shown 4 weeks after reconstruction
with the remaining flaps and 9 weeks after the extrusion.

SECTION VI PEDIATRIC AND CRANIOFACIAL SURGERY
836
providers. Some older children can also participate in the
expansion process.
Expander Removal and Reconstruction
Once the expander is removed and reconstruction is be­
gun, several key principles help in avoiding complications.
The first is not overextending the flap. Reexpansion is
preferable to overextension of the flap, which may lead to
ischemia, flap loss, and delayed healing. The preferred ap­
proach is to design and transpose the flap before fully ex­
cising the lesion. This prevents the creation of a defect that
may not have enough flap to cover it. We start by making an
incision along the border of the expanded flap and remov­
ing the expander. Flap movement is then determined by its
flexibility and main blood supply. Release of the flap along
its margin, maintaining the capsule in the design, will al­
low rotation advancement or transposition, and the flap
can be inset while the lesion is being sequentially excised.
Although expanded flap movement varies in each body re­
gion, there are typical, reliable designs in each area (head
and neck, trunk, extremity). We have found that it is of the
utmost importance to inset the capsule along with the flap
to improve the venous drainage of the expanded flap. Long
experience has demonstrated how flaps can be extended,
well beyond typical design, as long as the capsule is car­
ried with these extensions (e.g., retrograde extension on an
expanded forehead flap used for coverage of the eyelid and
brow).
Regional Considerations for Flap Design
Scalp
Because the shape and distribution of nevi follow quite
repeatable patterns (and based on decades of long-term
follow-up), the placement of expanders that will result in
the fewest rounds of expansion and optimal hair direction
and coverage have been well established. Follicular density
remaining port is then removed during planned reconstruc­
tion with the other expanded flaps.
Despite a common fear that expanders are fragile or
prone to rupture, this is a very rare complication. Most pa­
tients, once past the immediate perioperative period (3
weeks), can resume normal activities and even play sports.
In the very rare occurrence of device failure, leak, or rup­
ture, depending on the timing, we either proceed to surgical
reconstruction with removal of the failed device or replace
the expander as soon as possible (Fig. 46.10). Both of these
options unfortunately require an unanticipated return to the
operating room, but if identified early and treated, the final
reconstructive goal will be achieved. If the deflation of the
expander is slow, from a pinpoint leak, and the surgery for
expander removal is imminent, then the expander can be
kept near maximal size with daily reinjection.
The remote port can occasionally flip upside down or
otherwise become inaccessible. In these cases, it can often
be turned back to the correct position by digital manipula­
tion. If it has migrated under the expander but is still able
to be located on palpation by retracting the expander, the
port can typically still be accessed as long as the expander
itself can be safely pushed out of the way to avoid inadver­
tent puncture (Video 46.1).
Accessing the port requires passing a needle through
the skin into the port. Topical anesthetic should be used to
anesthetize the skin before each fill. A dollop of lidocaine-
based cream, covered by a clear dressing to prevent inadver­
tent removal of the medication, should be applied 30 min­
utes before the fill. Acetaminophen or ibuprofen can also
be used but are rarely necessary. Some patients who still
feel the needlestick may benefit from cryoanesthesia—us­
ing an ice cube to cool the skin immediately before injection.
Through experience, often the best pain control for children
is distraction. Many families set up elaborate games, bubble
displays, science experiments, and art projects during ex­
pansion; others simply turn on the television. Once children
recognize that expansion is not painful and can actually be
fun, the process is greatly simplified for the parents and care
a
b
Fig. 46.10 Device failure. (a) Early during the expansion, the left back expander decompressed. (b) The expander was replaced, and expan­
sion continued on schedule.

837
Chapter 46 Tissue Expansion for Pigmented Lesions and Other Defects
transposition flaps that are secured at sequential spots to
the periosteum or deeper skeletal structures. For the fore­
head we start by setting the brow position using deep
periosteal anchoring sutures. We then bring the flap to the
landmark and measure the desired height of the hairline at
the temple and midforehead. Excess tissue along the brow
presents as a dog-ear. This is sequentially cut back, but left
attached at the leading edge. The flap is then inset along the
capsule to the periosteum using a permanent suture. This
prevents flap recoil, scar widening, elevation of the brow,
and distortion of the facial features. Brows may have some
asymmetry after scar maturation. This is often corrected
by simple skin excision for symmetry 6 to 12 months later.
For the cheek, we often expand the neck and submental
skin (with the expander positioned medially as close to the
midline as possible). This flap is a transposition flap that
comes up along the nasolabial and nasojugal folds. We tack
the flap using deep periosteal sutures along the margin
at the piriform aperture, the frontal process of the max­
illa, the nasal bones, and the lateral orbital wall. This helps
prevent the flap from migrating away from the eye, nose,
and mouth, which leads to distortion of these important
structures (Fig. 46.11). Although our initial experience fa­
vored expanded rotation flaps based medially, we now use
laterally based transposition and advancement flaps. This
design allows for greater flap movement and significantly
less downward traction on the lower eyelid and nose than
the former design.
Trunk
On the back, scar placement along the midline will help
prevent growth restriction or scoliosis. Large trunk flaps,
on the scalp readily allows expansion to reconstruct more
than half the scalp without the appearance of thinning or
balding. Placement of scars is, however, crucial to the ap­
pearance of normal hairlines. Expansion of the occipital
scalp with a combined transposition and advancement flap
provides the optimal reconstruction of the temporal hair­
line. Ideal scalp scars have adjacent hair falling over them
rather than away. This prevents the appearance of alopecia
once the scar matures. Even a narrow scar on the scalp, if
the hair falls in outlying directions, will appear as a bald
patch. Expanders should be placed below the galea and
above the periosteum. On repeat expansion of the scalp,
the expander is often placed under periosteum because of
scar adhesion of the prior flap. Subsequent expansions may
need to proceed more slowly, because the flaps are gener­
ally less pliable with each round. Hair can become stuck to
the incisions. Mainly this occurs in the first week or two
after expander placement and after the removal. It is vital
that hair be washed and kept trimmed near the incision to
avoid this buildup. Constant scabbing and sticking of hair to
a scalp incision will eventually irritate and erode the inci­
sion and can lead to a dehiscence, infection, and delayed
wound healing (see Fig. 46.1).
Face
It is important to respect the aesthetic units of the face
when planning an expanded flap reconstruction. Ideally
scars should fall along the border regions. It is also impor­
tant to recognize that direct advancement flaps (i.e., cheek)
will often result in distortion of the facial features because
of tethering or pull placed on mobile areas (eyelid, lip)
as the flap heals and gravity takes over. It is best to plan
Fig. 46.11 (a) A young boy with a hemifacial nevus. (b) Two expanders, forehead and neck. The expander port covered with foam tape to
protect the flap during expansion. (c) Two months after reconstruction with a cheek flap and forehead flap. This demonstrates the results
of techniques described in the text to secure the flaps to deeper periosteal structures to prevent flap recoil.
a
b
c

SECTION VI PEDIATRIC AND CRANIOFACIAL SURGERY
838
tion of the location and growth of the breast when she
reaches puberty. For this reason we delay excision and
reconstruction of chest nevi and some upper abdominal
lesions in girls until they reach maturity. For boys, move­
ment of the nipple–areolar complex (NAC) is of less con­
sequence. For males, we typically proceed with trunk re­
construction and, if needed, place expanders in the chest
to reconstruct the neck, upper abdomen, or axillary area.
If the NAC is moved with the expanded flap, we transfer
it to its normal position as a full-thickness graft once re­
construction is complete (Fig. 46.12). The decision to ap­
proach the expansion by allowing initial repositioning of
the NAC is only undertaken when the parents accept the
fact that later repositioning as a free graft will be delayed
until the anterior trunk nevus excision and reconstruc­
tion is nearly complete.
if designed as advancement flaps only, may tent over the
underlying body contour and increase the likelihood of
seroma after expander removal. It is our practice to con­
tinue a compressive elastic fabric wrap for 3 weeks after
reconstruction to help avoid this. Prolonged seroma can
be percutaneously drained if needed. Rarely a scleros­
ing procedure might be considered if seroma is recur­
rent but has only been considered in a single patient over
35 years, and then was not needed. Along the waistline,
scars placed transversely along the lower lumbar area
and lower abdomen are ideal for concealment below the
beltline or a bathing suit. The abdomen is typically ex­
panded and directly advanced as it is in abdominoplasty.
For young girls, attention must be paid to the location of
the breast bud and eventual breast mound. Expansion of
the chest skin in a young girl has the potential for distor­
Fig. 46.12 (a) A male patient with a giant nevus of the abdomen, chest, right arm, and shoulder. (b) After an expanded reconstruction
of the chest and abdomen as well as a free anterolateral thigh flap for the upper arm. At this stage the right nipple–areola complex (NAC)
was located in the midline near the neck. The left NAC was located in the midline below the xiphoid. (c) At age 12 years he underwent free
nipple grafting to the chest.
a
b
c

839
Chapter 46 Tissue Expansion for Pigmented Lesions and Other Defects
to little scarring. Thicker wounds or eschar can then be
treated with wet-to-dry dressings as needed. In the back
specifically, a balance is sought between maximizing ne­
vus excision and how much tension is acceptable on the
distal flap. Small separation at the junction of the T or Y
closures will heal with dressing changes and rarely nega­
tively impact the final outcome. In most cases the resulting
scars will be easily remedied during subsequent rounds
of expansion and nevus excision by a readvancement or
expansion of the flap.
Scar alopecia of the scalp is mainly evident when the
hair direction is unfavorable and the scar is not well con­
cealed. Stable scars can be treated with micro-hair graft­
ing. Alternatively, repeat expansion may be necessary to
reorient the scar location and direction. If another set of
expanders is needed to excise a lesion fully (serial expan­
sion) we usually wait 4 to 6 months between rounds (see
Fig. 46.1).
Managing Unfavorable Results
and Complications in Tissue
Expansion
Putting It All Together
The following case, though not a nevus case, involved mul­
tiple rounds of expansion for scalp and forehead recon­
struction after a dog bite avulsion of at least two thirds
of the scalp and forehead in infancy and treatment with a
split-thickness skin graft to the periosteum. This case is in­
structive in that the choice of expander placement, strategy
of placement, timing of expansion, prevention and treat­
ment of expander exposure, and flap design in both the
forehead and scalp required all the knowledge and experi­
ence discussed in the previous discussion of avoidance and
treatment of complications.
At the time of initial referral the child was 5 years
old; the family provided a history of having had one at­
tempted placement of a tissue expander in the left scalp
with rapid exposure and removal before any expansion
was accomplished. His first of five rounds of expansion
began at age 6 years. The following sections explore the
issues and considerations for each round of expansion and
reconstruction.
First Round
Although he had both left parietal and occipital scalp to
expand, the initial concern was the adherence of the skin
along the border of the normal parietal scalp to the thin
skin graft on the periosteum (Fig. 46.14a–c). The maxi­
mum size expander that could be placed was 350 mL, and
Extremities
We have had success with expander placement in the
extremities,19 but some literature has reported a high
complication rate.17,20 Expanded skin in the arms and legs
will preferentially move circumferentially as opposed to
axially. For this reason, in circumferential or large lesions
we use expanded flaps from the abdomen to reconstruct
the arm and the posterior thigh for the lower leg. In older
children, we approach larger pigmented lesions of the ex­
tremities with free tissue transfer. Once a pedicle or free
flap has been successfully transferred it can be thinned
and rearranged to complete the excision of the lesion if
some remains. Alternatively, an expander can be placed
under the transferred flap to better assist with spreading
and movement of the flap to cover the necessary defect.
Postoperative complications of all expanded flaps, re­
gardless of body region, include delayed healing, flap isch­
emia and loss, flap congestion, wound dehiscence, seroma,
asymmetries, and scar alopecia.17,18 Most small wounds
can be managed with local wound care and dressing
changes. It does bear keeping in mind that expanded flaps
may recoil if not adequately fixed to the deep structures.
If an early dehiscence is noted, especially if it is a result of
a broken suture or trauma and the patient is available for
surgery, débridement and repeat closure may be consid­
ered. Sometimes this can be done in the office using local
anesthesia. For patients who may not be amenable to re­
turning to the operating room, a scar revision or even re­
peat expansion may be required to improve the outcome.
In these cases we wait 6 to 12 months to reexpand a flap
that is near a wide or unstable scar. Flap congestion is
rarely a problem if the capsule has been adequately main­
tained with the flap and its inset prevents it from recoil­
ing. However, there are occasions when congestion can
be seen. In these cases, as with all congested flaps, the
first maneuver is to release any tethering sutures or tis­
sue along the pedicle. Once this is done, if there remains
congestion and the surgeon is confident that the capsule
was well inset, bleeding the flap by needlestick can buy
time until the vascular channels are reestablished. Sub­
cutaneous heparin and/or leeches can also be of benefit,
but we prefer to avoid them on facial flaps and for children.
It is very important to monitor blood loss in children if
blood thinners are used, because they can become anemic
quickly. Before using heparin or leeches, it is advisable to
get a baseline blood count.
Because expanded flaps are delay flaps, both the de­
sign of the flap and the distance the flap will carry dif­
fer significantly from unexpanded flaps. We do occasion­
ally see flap ischemia at the distal edges of the flap (Fig.
46.13). When this occurs the best approach is to keep the
skin very well moisturized with a thick emollient oint­
ment such as Aquaphor. Early epidermolysis will typically
resolve over a number of days with this method and lead

SECTION VI PEDIATRIC AND CRANIOFACIAL SURGERY
840
a
b
c
d
e
f
g
h
i
Fig. 46.13 Ischemia of an expanded flap. (a) Two 750-mL expanders were placed below skin flaps that had been expanded on one prior
occasion. (b,c) After further excision of the trunk nevus and flap advancement, the right flank flap showed signs of ischemia. The flap was
treated with Aquaphor ointment to improve healing in areas of epidermolysis. (d) After 1 week, the distal tip had demarcated and wet-
to-dry dressings were initiated. (e–i) Weekly progress of serial wet-to-dry dressings show complete healing with an acceptable scar. This
patient was subsequently reexpanded and reconstructed with further resection of the nevus and scar.

841
Chapter 46 Tissue Expansion for Pigmented Lesions and Other Defects
Although catching up and completing the expansion
over a 12-week period can be accomplished in most cases,
the small volumes that could be injected, even with an in­
terval of every 4 to 5 days, warranted the extended time.
Once the expander is in place, it is better to take a few weeks
longer to complete expansion to the planned volume than to
move a smaller flap sooner. With the incisions now stable,
the success of further expansion is greater than it may be
by starting again.
At the time of expander removal, the next obstacle was
the difficulty of fixing the flaps to the thin, adherent skin
graft. The posterior flap was advanced and transposed into
the parietal region, while the left flap was primarily an ad­
vancement design (Fig. 14.15d,e). The closure of normal-
thickness scalp to the remnant of normal scalp above the
right ear was uncomplicated, but the thin adherent skin
graft at the medial borders of each flap was difficult to su­
ture securely; however, putting the flaps at excessive ten­
sion by trying to bring the flaps together medially would
put the flaps at risk, especially because there were additional
small scars at the base of each flap. The capsules cannot be
divided at the base of these flaps, nor can the capsule be
scored without significant risk. Healing was uneventful, but
the time between the first and second rounds was increased
to six rather than our typical four rounds.
Second Round
At the second round the expanders were placed in the
occiput where the two prior scalp flaps had joined and
the plan was to overexpand this if possible. The expander
could not be placed through any other incision than at
the border of the defect (Fig. 46.15a), so the incision was
placed where the graft–scalp junction felt thickest and the
incision was kept as short as possible.
Dissection, as always in the scalp, was accomplished
with a malleable retractor slid along the contour of the
head in the subgaleal plane. The tunnel to the ports was
dissected in a similar fashion. Although a smaller expander
could be placed more easily (e.g., 250 mL), the 350 mL ex­
pander provided expansion of the entire area of available
scalp both in the occiput and parietal area. The parietal flap
was large enough to accommodate the expander, but the
skin was relatively inflexible, so little saline could be injected
at the time of placement, and therefore the folded edges of
the expander needed to be carefully positioned to minimize
their prominence.
Dehiscence was a concern, particularly in this first stage,
because the issue of expander prominence was compounded
by the fact that only a single-layer closure was possible along
the anterior border of the parietal flap. To compensate for
the expander prominence and thin layer of coverage, the first
injection of the left scalp flap was delayed for about 3 weeks
(Fig. 14.15b,c). The wound was kept meticulously clean, and
by that time the skin had relaxed enough to accommodate
the fold. The occipital scalp flap was ready for first expansion
at 10 days after placement. However, the expansion for both
flaps was very slow, so the expansion was carried out over an
additional month before they were considered sufficiently ex­
panded to carry out the first scar and graft excision.
Fig. 46.14 (a–c) Three views of the scalp and forehead in a 5-year-old child who suffered scalp, forehead, and facial injuries from a dog
bite at 9 months of age.
a
b
c

SECTION VI PEDIATRIC AND CRANIOFACIAL SURGERY
842
Fig. 46.15 (a) The incisions can be seen for placement of the 350-mL expander beneath the left scalp and occipital scalp. The fullness of
the expander edge can be seen at the anterior border of the parietal scalp adjacent to the scar. (b,c) The expanders are shown at comple­
tion of the 4-month expansion. (d,e) The flaps are in place shortly after the first-stage excision. Maximal advancement and transposition
still required suturing to thin scar and graft.
a
b
c
d
e

843
Chapter 46 Tissue Expansion for Pigmented Lesions and Other Defects
move across the forehead above the normal skin that was
still present for half the vertical height of the right forehead.
The latter skin cannot be expanded and moved upward to­
ward the hairline without distortion of the brow. A 70- to
90-mL expander was placed in the forehead. At this stage,
the movement of all the expanded flaps was still a function
of the multiple scalp scars along the right side of the head,
and at this point the gains were slow (Fig. 46.17c).
Scars continued to stretch at the anterior margin of the
flaps in the right frontal area, and expansion on the left side
was needed primarily to allow continued release of the right
flaps near the midline to allow part of the flap to move in a
forward direction. Although the expansion in the forehead was
uneventful, it was slow and the movement of the expanded
flap was limited by the narrow pedicle at the right temporal
area. Maintaining the capsule on the flap and ensuring that
the capsule was captured in all sutures aided in preserving
this flap. A small distal flap based on the end of the left scalp
flap had been preserved to provide the small additional hair-
bearing tissue to reach forward to the hairline. A distal half
centimeter was lost but healed with basic wound care.
Fourth Round
The fourth round again expanded each hemiscalp flap and
the forehead flap with two 350-mL expanders and one 70- to
through an incision in the postauricular scalp on the right.
This prevented a new incision at the scalp graft junction
and provided two-layer closure. Mistakenly, a 0.5-cm scar
was resected in the area of the latter and closure even with
limited saline in the expander was tight. This maneuver
should be avoided. The flaps now accommodated the 350 mL
expanders easily, and the expansion proceeded more eas­
ily and was completed in a 3-month period (Fig. 46.16a,b).
Placing larger expanders, such as 500 mL, would have risked
the same issue along the attenuated flap margin as was en­
countered in the first stage. Although a specific volume is
not set as a target, the expanders were both expanded to full
capacity. Overexpansion is not uncommon in our cases, but
in this setting, overexpansion was believed to be more likely
to compromise the flap or incision line and thus was not at­
tempted. Although the anterior extension of each flap was
still secured to thin scar and graft, the two expanded flaps
easily reached one another in the midline (Fig. 46.16c–e).
Third Round
The third round of expansion, 6 months after the prior
round, again placed two 350-mL expanders in the scalp and
for the first time placed an expander in the left forehead
(Fig. 46.17a,b). The expansion and movement of the fore­
head skin would be limited by the fact that it would have to
a
b
c
d
e
Fig. 46.16 (a,b) The expansion in round two was considerably easier, and the flaps can be seen at full expansion just before and at surgery.
(c) The result of advancement at completion of the procedure. (d,e) The result 4 months after the second round.

SECTION VI PEDIATRIC AND CRANIOFACIAL SURGERY
844
along the leading edge of the right scalp flap was still a risk.
In this round, the incision broke down and the expander
edge was exposed (Fig. 46.18a).
Given the parents’ experience at this time with manag­
ing the expansion and incisions, they managed the enlarg­
ing exposure with Tegaderm and foam tape to minimize the
push of the expander against the opening. Despite a widen­
ing hole, the expander was kept in place for at least a month
while the remaining expansion was completed. With dress­
ing changes and antibiotic coverage, the area never showed
evidence of infection, and the surrounding flaps were
90-mL expander. Although the scalp flaps were now consid­
erably bigger than early on in the process, the multiple small
scars within the larger flaps from the initial injury and in an
area above and behind the right ear put a larger expander at
risk of having folds that would be in regions of scar, or put
expander ports at risk. Ports were, at this stage, often placed
through a small distant incision, with the tubing tunneled
beneath thinner areas of scar but keeping the port promi­
nence in easily palpable positions under healthy skin.
This was the first round of expansion in which the still-
attenuated junction between normal scalp and skin graft
a
b
c
Fig. 46.17 (a) In the third round of expansion, the expanders were placed both in the scalp and for the first time in the forehead. In areas
where it may be difficult to completely smooth the expander beneath the flap it is possible for the edge or a fold of the expander to create
a pressure point that can cause potential flap injury. In these cases, a small piece of foam tape placed over the point will distribute the force
to a wider area. This minimizes the pressure until the expander rounds out with subsequent injections. (b) The expanders at completion
of the 12-week expansion. (c) The manner in which the forehead flap was moved toward the right above the normal segment of forehead
skin above the right brow.
a
b
c
Fig. 46.18 (a) This fourth round of expansion was complicated by breakdown along the anterior scalp border on the right. In an effort to
keep the expander from extruding while completing the expansion on the left scalp and forehead, a clear semiocclusive dressing and foam
tape were used in combination with meticulous cleaning of the scalp and other incisions. (b) The continued advancement of the forehead
flap is seen 1 month postoperatively. (c) The progressive movement of the scalp flaps on the right was complicated by the multiple scars
and efforts to position the flaps to optimize the direction of the hair.

845
Chapter 46 Tissue Expansion for Pigmented Lesions and Other Defects
placed through more normal-thickness skin, and the fore­
head and scalp flap on the left through the incision along
their common scar border. Ports were placed through dis­
tant incisions, and the right expander was placed through
an incision, without any scar excision at the time of place­
ment. Expansion was uneventful, and after 3 months of
expansion, the forehead flap was carried to the border
of the hairline on the left side (Fig. 46.19c–f); the differ­
ence in skin flap thickness required careful inset of the flap
with care to again maintain the capsule in the full border
of the repair. Although there was sufficient scalp to bring
unaffected. At the time of expander removal, the defect on
the right side was closed loosely, and the forehead flap ad­
vanced further across the forehead and above the right fore­
head skin (Fig. 46.18b,c).
Fifth Round
Another break of 8 months was allowed to pass both for
further healing and family schedules. The placement of the
expanders was similar to what had been planned at the
prior surgery (Fig. 46.19a,b). At this point, expanders were
a
b
c
d
e
f
g
Fig. 46.19 (a,b) The appearance at the completion of the fifth round of expansion of the scalp and third round of expansion of the forehead.
(c–f) The scalp and forehead reconstruction at the completion of the procedure. (g) Despite hyperemia, suggestive of potential compromise
of the forehead flap in d, at 1 week postoperatively the flap was healing well and completed the forehead aesthetic subunit.

SECTION VI PEDIATRIC AND CRANIOFACIAL SURGERY
846
levels of expansion experience to work toward successful
treatment of any reconstructive case requiring expansion.
Conclusion
Tissue expansion is a valuable technique and lends itself to
superior reconstruction of various defects and deformities.
Proper planning for the placement of the expander or ex­
panders is one of the most important aspects in avoiding
complications. Although the understanding of flap move­
ment and versatility comes with experience, there are key
principles to success.
the midfrontal hairline an additional centimeter or more,
this would have compromised the distal blood supply to
the forehead flap and can be left to a subsequent day. The
scalp reconstruction was completed, and the expansion of
the larger left flap aided in breaking up the scar line along
the midscalp. The forehead expansion allowed comple­
tion of the aesthetic forehead subunit reconstruction
(Fig. 46.19d,g).
At the completion of this reconstruction, all the princi­
ples of both avoiding complications and dealing with them
had been tested. Each case requires the same thought pro­
cess and same considerations to one degree or another; the
issues reviewed in this chapter will allow surgeons at all
References
1. Arneja JS, Gosain AK. Giant congenital melanocytic nevi.
Plast Reconstr Surg 2007;120(2):26e–40e
2. Rhodes AR, Silverman RA, Harrist TJ, Melski JW. A histo­
logic comparison of congenital and acquired nevomela­
nocytic nevi. Arch Dermatol 1985;121(10):1266–1273
3. Bauer BS, Adler N. Congenital melanocytic nevi. In: Neli­
gan P, ed. Plastic Surgery, Vol 3. 3rd ed. London: Elsevier
Saunders; 2012
4. Zutt M, Kretschmer L, Emmert S, Haenssle H, Neumann C,
Bertsch HP. Multicentric malignant melanoma in a giant
melanocytic congenital nevus 20 years after dermabra­
sion in adulthood. Dermatol Surg 2003;29(1):99–101,
discussion 101
5. Bauer BS, Few JW, Chavez CD, Galiano RD. The role of tis­
sue expansion in the management of large congenital pig­
mented nevi of the forehead in the pediatric patient. Plast
Reconstr Surg 2001;107(3):668–675
6. Bauer BS, Corcoran J. Pediatric tissue expansion. In: Bentz
ML, Bauer BS, Zuker RM, eds. Principles and Practice of
Pediatric Plastic Surgery. St Louis, MO: Quality Medical
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7. Bauer BS, Margulis A. The expanded transposition flap:
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2004;114(1):98–106
8. Arad E, Zuker RM. The shifting paradigm in the man­
agement of giant congenital melanocytic nevi: re­
view and clinical applications. Plast Reconstr Surg
2014;133(2):367–376
9. Bauer BS, Dickie SR, Marghoob AA. The shifting para­
digm in the management of giant congenital melanocytic
nevi: review and clinical applications. Plast Reconstr Surg
2014;134(4):659e–660e
10. Vourc’h-Jourdain M, Martin L, Barbarot S; aRED. Large
congenital melanocytic nevi: therapeutic management
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11. Marghoob AA, Dusza S, Oliveria S, Halpern AC. Number of
satellite nevi as a correlate for neurocutaneous melanocy­
tosis in patients with large congenital melanocytic nevi.
Arch Dermatol 2004;140(2):171–175
12. Tay CL, Tan GM, Ng SB. Critical incidents in paediatric an­
aesthesia: an audit of 10 000 anaesthetics in Singapore.
Paediatr Anaesth 2001;11(6):711–718
13. Murat I, Constant I, Maud’huy H. Perioperative anaes­
thetic morbidity in children: a database of 24,165 an­
aesthetics over a 30-month period. Paediatr Anaesth
2004;14(2):158–166
14. Joss GS, Zoltie N, Chapman P. Tissue expansion tech­
nique and the transposition flap. Br J Plast Surg
1990;43(3): 328–333
15. Adler N, Elia J, Billig A, Margulis A. Complications of
nonbreast tissue expansion: 9 years experience with 44
adult patients and 119 pediatric patients. J Pediatr Surg
2015;50(9):1513–1516
16. Gibstein LA, Abramson DL, Bartlett RA, Orgill DP, Up­
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847
Chapter 46 Tissue Expansion for Pigmented Lesions and Other Defects
Discussion by Ernest K. Manders
Perhaps the first and most important message is that
reconstruction with tissue expansion takes time and
patience. With that understanding, surgeons can ac­
complish great things.
Regarding the age to begin tissue expansion, the
surgeon must be cautious. Expansion certainly begins
earlier than 6 months of age, and cranial sutures do not
need to be closed to start scalp expansion. However,
caution should always dictate when to begin reconstruc­
tion with expansion, because there are no emergency
expansions.
When planning an expansion the surgeon should
look at the available skin and consider where the final
scars should lie. Although advice about the typical du­
ration for an expansion in practice is valuable, in truth
there is no time limit.
The most important guide to length of expansion is
the amount of advancement required and attaining an
expansion large enough to provide that tissue.1–4 The
advancement needed is determined at the first clinical
encounter when tissue expansion is considered. When
families do home expansion it is very helpful to show
them how to measure over the dome of the expansion
mass. By holding flexible tape stretched straight over
the expander, the family member can measure the base
width. By subtracting this second measurement, the
base width, from the arc over the dome, the surgeon
has a ready measure of anticipated advancement of the
expanded flap. Some hemispheric flaps do not properly
advance without release, which is discussed later. Com­
munication by the caregivers by phone or email keeps
the surgeon informed on how much progress is being
made.
Some uses of expansion are inherently more prone
to complications. The character of the nevus is a valid
factor. I would add that expanding near hemangiomas is
fraught with a hazard of infections. If the hemangioma
is weeping and has been inflamed, the wisest approach
may be to excise it, graft the area, and later resurface
with expanded soft tissue.
Cautions regarding selecting patients and families
who are able to cope with the change in appearance
are well founded. Most families can and do very well.
Perhaps even more difficult is gaining an understand­
ing that the expansion cannot proceed with an abso­
lute date on the calendar for tissue advancement. Every­
one must understand that it simply will take the time
it takes. Rushing often leads to complications and less-
than-ideal results.
For placement of expanders, incisions may usually
be made in the lesion to be replaced or at its margin.
The surgeon should be wary, however, of some nevi that
may have an inadequate collagen layer in the dermis.
Such skin does not hold sutures well or heal well. Surgi­
cal wounds in such skin are prone to dehiscence. In my
own experience a linear nevus may often have a defi­
cient dermis.
Crucial to the planning of the expansion is the rec­
ognition of the biomechanics of expansion of the skin.
Because the smallest area containing the largest volume
is a sphere, all expansions approximate a hemisphere.
With a longer base, the mass may resemble a loaf of
bread. It is crucial to planning to understand that al­
though the skin over the expander has increased its di­
mension substantially, the skin at the base perimeter
of the expander has not! Surgeons often advance an
expanded flap over a flat or cylindrical surface only to
find that they cannot use the full extent of the expanded
tissue. The perimeter of the flap is stretched tight, but
there is redundant expanded flap that is not used This
dilemma has led to parallel incisions over the dome of
the expander, making a so-called “caterpillar flap.” This
imposes a lot of unnecessary scarring and should always
be avoided.
The key is to expand halfway around a defect so
that the edge of the expanded flap can advance like the
handle of a bucket over the defect. This also imposes
minimal scar. This concept was the genesis of the crois­
sant design, a crescent-shaped expander whose arms
are meant to enclose the defect.5 There is less expan­
sion at the arms, and usually less tissue is needed there.
The wide middle of the croissant gives the bigger ex­
pansion for advancement across the widest part of the
typical defect. A croissant expander with an adjustable
base was developed and available commercially until
recently when new regulations made it unavailable. The
problem of the tight perimeter of a hemispheric flap is
eliminated when expanding halfway around the defect.
Many surgeons have attempted to half-surround le­
sions using rectangular-base expanders, but this is not
as easy as one might assume. Often a web of tissue be­
tween the two expanders limits expansion and must be
cut away before the full extent of the expansion can be
used.
Another subtlety that can confound surgical plan­
ning is placing expanders in a concavity, such as under
the jawline on the side of the neck. A moment’s reflec­
tion will convince the surgeon that he or she can create a
rather massive expansion below the jawline without ac­
tually having achieved any substantial increase in tissue.
The problem is that the concavity has been converted to
a convexity with no real gain in tissue dimensions. It is
often misleading to look at an expansion below the jaw­
line and think that the flap will advance up the cheek.

SECTION VI PEDIATRIC AND CRANIOFACIAL SURGERY
848
The suggestion in the chapter to use the largest ex­
pander available for the job is spot on. If one does the
math, knowing that the cross section of the expander
will approximate a hemisphere, one can show that the
predicted advancement is about one radius of the ex­
pander, or one half the base width. One can do better
with favorable geometry and lax adjacent tissues, but
this is a good rule for a conservative estimate of the later
advancement possible.
Tissue expanders with stiff bases do simplify place­
ment, and they guide the surgeon in the placement so
that the expander cavity will allow the full expansion of
the device. However, on small children’s limbs, the base
plate may be stiff enough to actually lift off the underly­
ing soft tissue to erode through the overlying skin. It is
better in very small children requiring limb expansion
to use an expander without a stiff base.
Buried remote ports are the safest and most reliable
for children. Remote ports should not be placed over
bony prominences. The mastoid area has been a site for
innumerable port exposures over the years. In adults
integrated injection ports can be of great value. Place­
ment and removal are facilitated. However, these valves
tend to be bigger and harder to insert through small
incisions and under tight tissues such as the scalp and
forehead. When a remote valve is placed through the
same incision as the expander, it must be placed at some
distance from the expander, which will enlarge. An inex­
perienced surgeon will quickly learn to avoid placing a
remote port caudal to a large expander on the trunk or
thigh. Here the expander will reliably slowly move down
over the port, making injection without puncture of the
envelope impossible.
Home-based expansion is an admirable feat. Though
long taught in plastic surgery, few surgeons have
adopted this practice. Of course, this may be applied to
breast reconstruction expansions, too. However, few
surgeons seem willing to institute this thoughtful effi­
ciency. Our experience has taught us that this strategy is
very safe and successful. Anyone treating children with
expansion should consider it, because the process of ex­
pansion in the home is much less intimidating than go­
ing to the doctor’s office for the procedure.
My practice has been to simply have the child rub
an ice cube on the skin over the port. It conditions the
child to be ready for the manipulation of needle inser­
tion and expansion. Cold skin is much less sensitive, and
the experience of needle insertion for injection is gen­
erally very well tolerated. Distraction is the best “local
anesthetic.”
Experience has shown that injecting twice a week
will only get about one third more volume in than inject­
ing once a week. The rate-limiting step is the mammalian
cell, which requires about 22 hours for mitosis. Only a
small fraction are stimulated to begin deoxyribonucleic
acid (DNA) synthesis and mitosis with each expansion,
so patience is required. Parents and patients must un­
derstand that expansion is not just stretching. The sur­
geon must remember that when he or she looks at the ex­
panded skin over the expander, it is under tension. When
creating a breast or in a situation where recoil of skin
when the expander is removed would be distorting, the
surgeon should partially deflate the expander to see what
the resting length of the flap is. Unfortunately plastic sur­
geons have to learn again and again that the dimensions
over a taut expander do not equal the dimensions over a
soft breast implant or a cheek.
Expansion should never cause pain. Children who
can cooperate are instructed to say when it is starting
to feel tight. Years ago my colleagues and I injected with
a transducer and found that by letting the child be our
guide, the pressure may transiently exceed 40 mm Hg,
but it soon fell to 40 mm Hg or below. This is a safe pres­
sure generally, given that capillary pressure is usually
about 32 to 40 mm Hg.
What does one do for an infant who cannot cooper­
ate or in an area that is insensate? There is an easy way
to be safe:
1. Fill through a scalp vein needle.
2. Periodically remove the syringe with the tubing
extended straight up vertically over the needle and
the expander under it.
3. Look at the hub of the needle. When the saline just
makes a drop meniscus at the top of the hub for
syringe connection, the pressure in the expander is
about 20 mm Hg.
I have always used this technique for forehead expan­
sions to avoid injuring the thin and vulnerable frontalis
muscle. If the surgeon is careful in dissection and ex­
pansion, he or she can actually expand a functioning
frontalis that will raise the brow later. This is an im­
portant consideration in removing a nevus from the
forehead.
The suggested use of clear dressings and foam tape
to protect the skin when folds appear in the expansion
are pearls of wisdom, though I have been less successful
in salvaging infected expanders. I agree with using any
advancement possible when removing the expander in
the case of an infection. In my practice aspiration of pu­
rulence from over the injection port has typically been
treated with expander removal, advancement, and a
later reexpansion, if needed. Likewise, I have not left
remote ports in place if removing an infected expander.
The capsule is very important for flap integrity. We
demonstrated using microspheres that an intact cap­
sule doubles the blood flow to an expanded flap.6 The
capsule is the surgeon’s and the patient’s friend and will
make the desired outcome more successful.

849
Chapter 46 Tissue Expansion for Pigmented Lesions and Other Defects
Consideration of scar placement and the exit angle
of hair in expanded flaps is crucial to getting an opti­
mal result. I would add that the surgeon would always
be well advised to avoid making a T-shaped closure at
a hairline. The intersection of the scar in the scalp with
the scar at the hairline will always widen to make a most
distracting area of alopecia.
Families and patients often need a break from the
process of expansion. This can be appreciated through
both verbal and nonverbal communication. Whenever
possible, however, I encourage following a first expan­
sion with the next stage, having placed expanders at the
time of advancement after the first expansion.7 To be
sure, this is a matter for some judgment. Sometimes nei­
ther the patient nor the tissues are ready for immediate
follow-on expansion.
Over the years I have learned that there are some
areas that do not require expansion:
•• Microtia reconstruction
•• Removal of central facial nevi
•• Forehead reconstruction
Microtia reconstruction does not generally require ex­
pansion. Removal of central facial nevi usually does not
require expansion. A simple reverse facelift-type ad­
vancement will usually suffice, even if more than one
step is required. Likewise, although forehead recon­
struction can be accomplished with expansion, I have
found that taking a split-thickness skin graft from the
parietal scalp and applying this as a sheet graft will usu­
ally give a superb result, almost overnight. Great care
must be exerted to preserve the frontalis muscle. The
donor defect is dressed with irradiated allograft skin,
which separates when reepithelialization is complete.8
Hair growth is evident on shedding of the allograft, and
there is no donor site scar.
Conclusion
Perhaps the greatest and most important lesson of my
experiences is the example of caring, thorough, com­
mitted physicians. Assessing who is a good patient and
appropriate counseling so expectations are realistic
are paramount. Being there for the duration to usher
a patient to a successful result is vitally important. The
results speak for themselves.
Home expansion is easy and reliably successful and
should be encouraged. Careful planning is key for even­
tual success. Planning to surround the defect will allow
easy advancements with a minimum of scar. Preserving
the capsule doubles the blood flow to the flap.
Some patients present special difficulties and even
contraindications to the use of expansion. Certainly this
applies to impatient individuals. Some nevi may not heal
well. Hemangiomas may be colonized, leading to infec­
tions in nearby expander cavities. Microtia reconstruc­
tion generally does not require expansion, although it is
used with great success by some. Central facial lesions
can usually be eliminated with serial advancement of
adjacent normal skin. Forehead reconstruction can be
accomplished with a split-thickness skin graft of scalp
skin with preservation of the frontalis muscle.
References
1. Manders EK, Graham WP III, Schenden MJ, Davis TS.
Skin expansion to eliminate large scalp defects. Ann
Plast Surg 1984;12(4):305–312
2. Manders EK, Schenden MJ, Furrey JA, Hetzler PT, Davis
TS, Graham WP III. Soft-tissue expansion: concepts and
complications. Plast Reconstr Surg 1984;74(4):493–
507
3. Manders EK. Scalp and nasal reconstruction. Adv Plast
Surg 1984;1:113, 117
4. Manders EK, Graham WP III. Alopecia reduction by scalp
expansion. J Dermatol Surg Oncol 1984;10(12):967–969
5. Adjustable Base Tissue Expander. Ernest C. Manders,
Ernest K. Manders, and Thomas Hooker. U.S. Patent No.
5,571,179
6. Manders EK, Mottaleb M, Hetzler PT. Soft tissue expan­
sion. In: Marsh JL, ed. Current Therapy in Plastic and
Reconstructive Surgery. Head and Neck. Philadelphia,
PA: B.C. Decker; 1989:987
7. Manders EK, Da Paula P. Repeated tissue expansions. In:
Grotting JC, ed. Reoperative Aesthetic and Reconstruc­
tive Plastic Surgery. St Louis: Quality Medical Publish­
ing; 1995:137–153
8. GammaGraft. Pittsburgh, PA: Promethean LifeSciences

850
CHAPTER
47

Fractures of the Jaws
Marco Rainer Kesting
The long-term outcome after jaw fractures depends not
only on the type of fracture and the precise restoration of
the broken bone, but also on the integrity of all anatomic
structures neighboring the fracture. Choosing the ap­
propriate surgical approach is an additional key factor for
avoiding complications. This chapter focuses on the man­
agement of upper and lower jaw fractures.
Anatomy of the Jaws and
Types of Fractures
Direct and indirect forces to the lower and upper jaw re­
sult in fractures. Several low-resistant anatomic locations
with thinned bone are prone to fractures. Typical fractures
(Fig. 47.1) of the maxilla include the so-called Le Fort I frac­
ture, in which the maxilla breaks off the midface (A in Fig.
47.1), and sagittal fractures (see B in Fig. 47.1), which in­
volve transverse expansion of the upper jaw. With regard
to the mandibular bone, the parasymphyseal (see C in Fig.
47.1) and the angle (see D in Fig. 47.1) regions are prone
to fractures. The extended root of the lower canine and the
foramen of the mental nerve are responsible for parasym­
physeal fractures, whereas retained wisdom teeth are a de­
terminant in angle fractures. The thin condylar neck (see E
in Fig. 47.1) including the condylar head (see F in Fig. 47.1)
is another fragile region of the mandible. High-velocity
trauma leads to comminuted fractures (see G in Fig. 47.1).
In particular, the uncompleted median symphysis in chil­
dren is highly vulnerable. Pathologic conditions of the bone
such as osteomyelitis or osteonecrosis (see H in Fig. 47.1)
increase the risk of fractures, as does an edentulous, highly
atrophied body of the mandible1,2 (see I in Fig. 47.1).
Aims of Jaw Fracture Reconstruction
The anatomical complex of the upper and lower jaw is
functionally involved in clenching and speaking, but also
plays a significant role for facial aesthetics. Restoration of
painless unlimited mouth opening, laterotrusion, and pro­
trusion is one of the main targets after jaw fracture. Perfect
occlusion should be recovered in dentate patients, and the
harmonic red-white aesthetics of teeth and gingiva should
be reestablished. As a basis for later prosthetic rehabilita­
tion, the accurate positioning of the maxilla and mandible
in the vertical, transversal, and sagittal dimension is always
necessary.3
Unfavorable Results and
Complications in Jaw Fracture
Reconstruction
Undesirable results after treatment of jaw fractures arise,
in most cases, because of deficient clinical and radiologi­
cal diagnostics and insufficient treatment planning.4 To a
lesser extent, poor outcome results from the failure of the
patient to cooperate or from a lack of postoperative care.
Therapeutic Principles
Open reduction and internal fixation (ORIF) is the basic re­
constructive principle in nearly all types of jaw fractures.
Since their development in the 1970s, titanium miniplates
represent the osteosynthesis material of first choice for the
maxilla and for the mandible.5 Fundamental publications

851
Chapter 47 Fractures of the Jaws
the maxilla and the subnasal region. The patient presents
with pseudoprogernia.
Avoidance and Correction
When reducing the fracture, retral positioning of the max­
illa must be avoided, and particular attention should be
paid to the exact positioning of the maxilla. A posteriorly
impacted maxilla must be pulled forward. Significantly de­
layed cases should be reduced with Rowe’s maxillary dis­
impaction forceps. The two-pronged instrument grasps the
maxilla with a palatal blade and a blade positioned in the
nasal cavity. After reduction, meticulous mandibulomaxil­
lary fixation is necessary to secure the occlusal relationship
until osteosynthesis with miniplates is performed.
After ossification of the malpositioned maxilla, a sec­
ondary correction must be carried out. Preoperative plan­
ning is therefore indispensable. First, plaster models from
the maxilla and mandible are made, a checkbite is per­
formed, and the positions of the maxilla with respect to the
temporomandibular joint (TMJ) and the cranial base are de­
termined with a face-bow. To imitate the position of the jaws
and the mandibular movements, upper- and lower-jaw casts
are positioned correctly in an adjustable articulator.
With respect to the posttraumatic and intended fa­
cial profile, occlusion and aesthetics model osteotomy is
have described the buttresses of the facial bones.6 Most
postoperative complications can be avoided when the rules
of miniplating along the natural strains of the bones are
strictly observed. For exceptional cases in which bone has
been sheared off, lag screws might be a therapeutic alterna­
tive. Particular attention must be paid to jaw fractures in
childhood. The jaw bones of children have a high potential
for bone remodeling. Reconstructive principles have to be
modified; closed reduction is a sufficient therapy in many
cases.7 If ORIF is conducted, plate removal must be per­
formed much earlier.
This chapter concentrates on the most challenging types
of jaw fractures, because of their high potential of thera­
peutic failure.
Maxilla Fractures
Le Fort I Fracture
Malposition, Nonocclusion, and Change of
Facial Profile
After the breaking off of the midface, the pterygoid muscles
pull the fractured upper jaw into a dorsal position. Nonoc­
clusion, open bite, and nasal airway restriction result. In the
long term, the facial profile changes by the retral position of
A
A
B
F
E
D
C
H
A
A
B
F
E
D
C
Fig. 47.1 Types of jaw fractures (blue, maxillary fractures; red, mandibular fractures). A,
Le Fort I fracture. B, Sagittal upper jaw fracture. C, Parasymphyseal fracture. D, Angle
fracture. E, Fracture of the condylar process. F, Fracture of the condylar head. G, Com­
minuted fracture. H, Pathologic fracture (osteomyelitis, osteoradionecrosis, medication-
related osteonecrosis). I, Fracture of the atrophic jaw.
I

SECTION VI PEDIATRIC AND CRANIOFACIAL SURGERY
852
Sagittal Fractures of the Maxilla
Sagittal fractures are accompanied by transverse malposi­
tion, resulting in transverse expansion of the maxilla and
nonocclusion. In some cases, sagittal fractures with exten­
sive dislocation cause lacerations of the palatal soft tissues
with oronasal communication.
Avoiding Complications and Surgical
Solutions
The alveolar process is often tilted, which makes it dif­
ficult to achieve a sufficient occlusion solely by maxillo­
mandibular wiring. The fabrication of an individual acrylic
palatal plate might be indicated for better stabilization of
the palatal vault. After this pretreatment, osteosynthesis
performed on the casts. The exact movement of the max­
illa in three dimensions is ascertained and marked on the
model. Occlusal splints, namely a starting splint and a pos­
tosteotomy splint, are made on the basis of the model op­
eration. These splints are fixed between the maxilla and the
mandible during the Le Fort I osteotomy.
Secondary correction of maxilla malpositioning can also
be carried out by virtual planning of a Le Fort I osteotomy.
Once a computed tomography (CT) scan of the middle and
lower face is obtained, the data is prepared with a special
software to gain a virtual three-dimensional model. The re­
quired movement of the maxilla can be simulated, and in­
dividual cutting guides and osteosynthesis material for the
Le Fort I osteotomy can be produced by industrial partners
within a few days.8
Summary Box
Unfavorable Results and Complications Associated with Fractured Jaw Repair
Maxilla Fractures
•• Le Fort I fractures
○
○Malposition and nonocclusion
–
– Open bite
–
– Nasal airway restriction
○
○Facial profile changes
•• Sagittal fractures
○
○Transverse malposition and nonocclusion
○
○Transverse expansion of maxilla
○
○Laceration of palatal soft tissue
○
○Oronasal communication
Mandibular Fractures
•• Plate exposure
•• Injury to mental nerve
•• Injury to root of lower canine
•• Infection
Condylar Process Fractures
•• Malocclusion
•• Condylar absorption
•• Arterial hemorrhage
•• Nonocclusion
•• Reduced mouth opening
•• Limited mandibular movement
•• Osteonecrosis
•• Scarring
•• Facial nerve paralysis
•• Parotid fistulae
•• Infection
•• Scarring stenosis of the auditory canal
•• Dislocation of osteosynthesis material
Comminuted Fractures
•• Discontinuity of the bone
•• Infection (abscesses, cellulitis, osteomyelitis)
•• Nonunion and malocclusion
•• Nerve injury
Pathologic Fractures
•• Class A
○
○Infection
○
○Bone graft loss
○
○Nonunion
•• Class B
○
○Persistent infection
○
○Movable fractured bone segments
○
○Necrosis
○
○Infection of surrounding soft tissue
○
○Soft tissue shortage
○
○Salivary fistula
•• Class C
○
○Infection, pain, and scarring leading to secondary
surgery
Atrophic Jaw Fractures
•• Complication in bone healing
•• Stability loss of mandible
•• Extraoral plate exposure
•• Intraoral plate exposure
•• Fractured osteosynthesis material
Childhood Jaw Fractures
•• Facial asymmetry
•• Malocclusion/open bite
•• Joint ankylosis

853
Chapter 47 Fractures of the Jaws
parasymphyseal fractures. Injuries of these anatomic struc­
tures from incorrect placement of screws and miniplates
can easily be avoided.
Managing Complications
If plate exposure occurs, further infection of the region
must be prevented. Strict oral hygiene must be maintained,
including antiseptic mouthwashes, and the patient must be
seen weekly in the maxillofacial outpatient clinic. Osteo­
synthesis material removal is delayed to at least 2 months
to allow bony consolidation to be completed.
Condylar Process Fractures
The treatment of condylar fractures is a controversial topic.
During the past decade, much effort has been made to im­
prove the outcome of condylar fractures, but after critical
consideration, many of the “new techniques” have been
abandoned as fast as they have emerged. Taking all conflict­
ing points into consideration, the surgeon has the choice
of treating all cases conservatively or performing ORIF on
the other.
Unfavorable Results in Condylar Process
Fracture Treatment
Various complications arise after the fracture and treat­
ment of the condylar neck and head. Functional, aesthetic,
and neurosensory deficits are common.10 Malocclusion, re­
duced mouth opening, and limited mandibular movement
are often associated with the pterygoid lateral muscle pull­
ing at the fractured and nonfractured fragments.1
Malocclusion also results because of the dislocation
of the condylar process and subsequent reduction of ra­
mus height. Osteonecrosis of the condyle might be an un­
favorable result of traumatic or iatrogenic disruption of the
blood supply to the small broken fragment. Surgery-associ­
ated problems include unfavorable scarring and facial nerve
paralysis, mostly of the marginal mandibular branch, after
use of an extraoral approach for ORIF. In addition, parotid
is carried out with miniplates being placed on the frontal
part of the maxilla. Additional problems might arise from
laceration of the palatal gingiva. Primary tension-free clo­
sure is challenging, because mobilization of the palatal
soft tissue is nearly impossible. As an unfavorable result,
a persistent oronasal fistula might occur. Closure of such
fistulas is hampered by scarring. The use of a pedicled
palatine flap and the mobilization of the buccal fat pad
are therapies of the first choice for oronasal fistula closure.
Techniques for the closure of recurrent or extended oro­
nasal fistulas are associated with much more donor site
morbidity and include the tongue flap or a radial forearm
flap (Fig. 47.2).
Mandibular Fractures
Fractures of the Mandibular Body, Angle,
and Symphysis
The treatment of these types of mandibular fractures is
based on the miniplating techniques developed by the group
led by Champy9 in the 1970s. With the exception of the an­
gle region, two monocortical fixed miniplates (four-hole or
six-hole) are placed on the buccal surface of the mandible.
Whereas one plate is fixed below the dental roots, the other
one is fixed at the mandibular base to neutralize moments
of torsion (Fig. 47.3). In the angle region, the muscle sling
of the masseter and medial pterygoid muscles compresses
the strains of the mandibular base. Therefore placement of
a single plate running from the postmolar oblique line to
the buccal molar region is adequate.
Avoiding Complications
If the principles of miniplate osteosynthesis are fulfilled,
complications are rare. Unfavorable results such as plate
exposure can arise when the intraoral incision is placed
directly over the fixed titanium plates. Postoperative smok­
ing and poor oral hygiene are cofactors that increase the
risk of plate exposure. Particular attention must be paid
to the mental nerve and the root of the lower canine in
Fig. 47.2 Persistent oronasal fistula after sagittal fracture of the maxilla. (a) After repeated trials of primary closure. (b) Final closure with
a tongue flap.
b
a

SECTION VI PEDIATRIC AND CRANIOFACIAL SURGERY
854
Exact and reliable control of the post-therapeutic effect
on the posttraumatic state can only be achieved by CT and
CBCT.
Treatment
The condylar fracture classifications of Spiessl et al.12 and
Loukota et al.13 are helpful in determining whether the
fracture should be done operatively and which surgical ap­
proach is the most suitable. The classification by Spiessl et
al.12 (Fig. 47.4) suggests that ORIF is definitely indicated for
healthy adults with type IV and type V fractures (Box 47.1).
Luxation of the condylar head out of the TMJ socket is
associated with a massive loss of vertical height and non­
occlusion and, in bilateral luxations, with the development
of an iatrogenic malpositioning of an adjusting screw and
retral position of the mandible. Therefore the repositioning
of the condylar process and the securing of this position by
osteosynthesis is essential (Fig. 47.5a). The classification by
Spiessl et al.12 does not differentiate between the severity of
dislocation in type II and type III fractures. Dislocated frac­
tures with a deviation of the condylar process of less than
30 degrees can be treated by maxillomandibular fixation
and early functional therapy (Fig. 47.5b). This suggestion
includes, in particular, unilateral cases, cases without loss of
vertical height, and posttraumatic normo-occlusion.
Wired arch bars for maxillomandibular fixation should
be used in all cases with slight dislocation. In type I and
type VI fractures without dislocation, I recommend four
fistulas and sequential infections have been described after a
transcutaneous transparotid approach to the fractured con­
dylar process. Scarring and subsequent stenosis of the audi­
tory canal is also a problem that arises after ORIF of condylar
head fractures through a retroauricular approach.10
The technique of the anatomic repositioning of the con­
dylar head fragments with trapezoid plates and successive
definitive screw fixation to the stable mandible can result in
the dislocation of osteosynthesis material. A via falsa of the
inserted screw with significant harm to surrounding struc­
tures can occur. Although bleeding from the external audi­
tory meatus is common after posterior dislocation of the
condylar head, the penetration of the fractured condyle to
the middle cranial fossa might, in rare cases, result in life-
threatening infections and complications.11
Algorithm for Avoiding Complications
Diagnostics
Modern diagnostics of condylar process fractures should
not rely only on clinical parameters and plain radiographs
such as panoramic and mandible posteroanterior radiogra­
phy. Mandible posteroanterior radiographs might provide
a hint to the grade of dislocation of the fractured segment.
For an exact classification of the segment and determina­
tion of the treatment concept, a further investigation with
a three-dimensional technique (computed tomography
[CT], cone beam computed tomography [CBCT]) is required.
Fig 47.3 Management of mandibular fractures. (a,b) Radiologic diagnostics are performed in two planes with panoramic and mandible
posteroanterior radiographs. (c) Maxillomandibular fixation with screws and wires. (d) Open reduction and internal fixation with miniplates
considering the anatomy.
b
a
d
c

855
Chapter 47 Fractures of the Jaws
I
II
III
VI
V
IV
Fig. 47.4 Fracture types of the mandibular condyle as classified by Spiessl et al, with indications for open reduction and internal fixation
marked in pink.
Box 47.1
Open reduction and internal fixation (ORIF) is rec­
ommended in mandibular condyle fractures with
the following characteristics:
•• Luxated condylar fragment
•• Dislocation of the condyle of more than 30
degrees
•• Massive loss of vertical height
Exceptions to the algorithm can/must be:
•• Posttraumatic normo-occlusion
•• Multimorbid patients with potential life-
threatening risk during narcosis
•• Children younger than 12 years with a high
potential of condylar remodeling
•• ORIF is indicated (even in slight dislocations)
in*:
○
○Patients with alcohol abuse
○
○Patients with epilepsy
Open Reduction and Internal
Fixation Recommendations
*Maxillomandibular fixation could be life-threatening in these patients
because of glossoptosis, vomiting, and aspiration.
a
> 30°
b
Fig. 47.5 Indications for open reduction and internal fixation in frac­
tures of the mandibular condyle. (a) Loss of vertical ramus height.
(b) Dislocation of the condylar fragment of more than 30 degrees.

SECTION VI PEDIATRIC AND CRANIOFACIAL SURGERY
856
Surgical Approach
Loukota et al.13 published a new classification of condylar
fractures in 2005. They defined an anatomic A-line that
crosses the most inferior point of the semilunar incisure of
the mandible. The A-line starts as a perpendicular line to
a tangent touching the most posterior points of the ramus
and the condylar head13 (Fig. 47.6). To define the surgical
approach, The A-line is an extremely helpful tool for deter­
mining the surgical approach (Fig 47.7).
Although numerous approaches to the mandibular con­
dyle have been developed, I rely on three main approaches
depending on the anatomic position of the fracture with
regard to the A-line. Condylar base fractures located infe­
rior to the A-line are reduced via an intraoral approach (Fig.
47.7a), condylar base fractures running through the A-line
are treated by a retromandibular approach (Fig. 47.7b), and
condylar neck fractures superior to the A-line are reduced
via a rhytidectomy-transparotid approach (Fig. 47.7c). The
latter approach can be extended as a preauricular incision
superior to the temporal region if the condylar head region
must be reached (Fig. 47.7d).
bone screws be placed between the roots of the canines and
the first premolar carefully avoiding violation of the teeth
or their roots. During the first postoperative week, maxillo­
mandibular fixation must be ensured by rigid elastics (type
III and IV), after which soft elastics (type VI to VIII) are indi­
cated for another 3 weeks. Soft elastics should allow mouth
opening and alleviate functional therapy. Rigid maxilloman­
dibular fixation should be limited to 2 weeks, especially in
younger patients, to prevent bony ankylosis of the TMJ. Ra­
diographic observations after maxillomandibular fixation
are essential to detect spontaneous dislocation during ma­
nipulation at an early stage. If this occurs, secondary ORIF
is necessary.
Because of the earlier mentioned risks of ORIF in condy­
lar head fractures (condylar head resorption, stenosis of the
auditory canal, facial paralysis, and dislocation of osteosyn­
thesis material), I recommend closed reduction with func­
tional therapy in such cases. If primary therapy results in
nonocclusion, I recommend orthodontic therapy followed by
secondary orthognathic surgery after several months. Loss
of vertical height can be corrected by vertical ramus oste­
otomy.
Fig. 47.7 Recommendation for the surgical approach with respect to the anatomic location of the condylar fracture.
Transoral approach
Retromandibular approach
Rhytidectomy preauricular approach
with temporal extension
Rhytidectomy-transparotid approach
A-line
Fig. 47.6 Anatomic relationship in fractures of the condylar
process. The A-line is a perpendicular line to the mandibular
ramus tangent running through the inferior part of the incisure
of the mandible.
a
b
Rhytidectomy preauricular approach
with temporal extension
Rhytidectomy-transparotid approach

857
Chapter 47 Fractures of the Jaws
bone. Distraction of the anterior mandible is commonly nec­
essary to reduce the dislocated fragments anatomically.
The algorithm recommends a rhytidectomy anteropar­
otid-transparotid approach for condylar neck fractures. To
prevent complications involving the facial nerve, a strictly
subcutaneous preparation is necessary after skin incision.
The capsula of the parotid gland is either saved when car­
rying out an anteroparotid approach or dissected hori­
zontally when a transparotid approach is used. When the
anteroparotid approach is used, dissection is carried out
subcutaneously until the masseter muscle is reached in
front of the gland and until the overlying nerve branches
have become obvious. Attention must be paid to leaving the
excretory duct of the gland intact. The parotid gland is then
retracted backward, and the masseter muscle is cut hori­
zontally between the two nerve branches. The fracture can
be exposed and anatomically reduced. After osteosynthesis,
meticulous control of hemorrhage is essential. Reconnection
of the masseter muscle with 3–0 or 4–0 resorbable suture
is also mandatory to restore its function. A suction drain is
inserted before skin closure to prevent hematoma and he­
matoma-induced facial nerve palsy.
Cutaneous closure is performed with 4–0 or 5–0 non­
resorbable sutures to prevent scarring. The transparotid
approach involves cutting the parotid capsule parallel to
the nerve branches. Nerve branches must be detected by
an electrostimulation device. The incision of the capsule is
marked with sutures to visualize it later. After dissection of
the gland and the masseter muscle, a more direct view of
When approaching a condylar base fracture transorally,
the overview to the backside of the ascending ramus is re­
duced. Nevertheless, correct repositioning of the fragments
is essential, and hooks and retractors are helpful. However,
iatrogenic injuries caused by pulling forces to the retro­
mandibular vein and the accompanying marginal mandib­
ular branch of the facial nerve must be avoided. In the early
2000s, the technique of endoscopic revision of condylar frac­
tures via a transoral approach was commonly cited in the
literature.14,15 However, four main complications are com­
mon with this technique:
1. Arterial hemorrhage
2. Facial nerve injury
3. Nonunion
4. Partial condylar reabsorption
After critical analysis of their results, Arcuri et al.16 believe
that this is not an ideal approach for a subcondylar fracture
but might be an alternative procedure in selected cases.
With the retromandibular approach (Fig. 47.8), the sur­
geon must pay particular attention not to injure the mar­
ginal mandibular branch of the facial nerve. Therefore it is
useful to prepare the retromandibular vein after skin in­
cision (see Fig. 47.8b) and to visualize the nerve (see Fig.
47.8c). The periosteum is cut anterior to the marginal man­
dibular branch, and the fracture is exposed (see Fig. 47.8d).
The vestibular surface and the posterior rim of the ramus
are prepared to obtain a complete overview of the fractured
Fig. 47.8 The retromandibular approach for a condylar base fracture. (a) Preoperative marking of the anatomic landmarks and incision.
(b) Preparation of the retromandibular vein. (c) Exposure of the marginal mandibular branch of the facial nerve anterior to the retroman­
dibular vein. (d) Visualization of the fracture.
b
a
d
c

SECTION VI PEDIATRIC AND CRANIOFACIAL SURGERY
858
been measured by photoelastic analysis, three-dimensional
biomechanical simulation models, and finite element mod­
els.20–22 The results of these investigations stress that two-
plate fixation with 2-mm four-hole miniplates is superior to
all other stabilization techniques.22,23 Meyer and colleagues24
states that “more and more authors advocate the use of two
miniplates. The first is placed in the axis of the condylar
neck as usual, and the second is placed obliquely under the
mandibular notch.”24 In my own experience and in accor­
dance with Meyer,24 two miniplates are needed. After ana­
tomic reduction of the fracture, the first four-hole miniplate
is placed in the axial direction of the condylar neck. With
gracile condylar necks, particular attention should be paid
to ensure that the first plate is placed posteriorly enough for
the second to be positioned anteriorly. Monocortical screws
of 5 mm or 6 mm are used to fix the plate.
After this maneuver, a control of the occlusion is rec­
ommended. If the occlusion is correct, the second plate is
placed (according to the natural strains) 30 degrees in an
anterior direction to the first, and all screws are drilled in
(Fig. 47.10). The gold standard for postoperative control is
three-dimensional radiographic observation by CT or CBCT.
Postoperative radiography is essential, not only for fo­
rensic reasons. Exact and detailed documentation of the pre­
treatment and post-treatment status can be of high value if
complications—such as malocclusion; mastication pain; or
nearthrosis, pseudarthrosis, or ankylosis—arise. Secondary
dislocations of the nonoperated site might occur, especially
in bilateral condylar fractures with unilateral conservative
the fracture becomes visible than via the anteroparotid ap­
proach. However, the masseter muscle must be reattached
and the capsule closed tightly after osteosynthesis. Tight
capsular closure is essential to prevent salivary fistulas that
might occur in about 1% of the cases.17 Treatment of sali­
vary fistulas or sialoceles can be either carried out surgically
by reevaluation of the parotid or conservatively. Acceptable
conservative regimens include, as a first step, compression
bandaging and drainage and, as a second step, the insertion
of a feeding tube for 8 days and additional administration
of antisialogogs.18 A single injection of botulinum toxin type
A to the parotid gland has also been described as a promis­
ing therapy.19
Osteosynthesis
Osteosynthesis is one of the most important, if not the
key procedure in the surgical treatment of condylar frac­
tures. Many osteosynthesis systems are available. Special
osteosynthesis plates and screws have been developed to
fulfill the requirements of the mandibular condyle (e.g., lag
screws, triangular plates, locking plates, resorbable plates).
The system must fit the usually small condylar fragments,
be adaptable via the restricted approach, and withstand
bite forces (Fig. 47.9).
The correct placement of the osteosynthesis mate­
rial into the condyle process and the mandible has been
the matter of myriad investigations. Tensile and compres­
sion forces to the mandible and its condylar process have
Fig. 47.10 Correct angle of 30 degrees between
two 2-mm miniplates in a condylar base fracture.
(a) Intraoperative view after open reduction and inter­
nal fixation. (b) Postoperative control using cone beam
computed tomography.
b
a
Fig. 47.9 Fatigue of osteosynthesis material and consecutive plate
fractures in both condylar regions.

859
Chapter 47 Fractures of the Jaws
fixed with miniplates and screws. Small fragments that are
impractical to fix are removed to prevent dislocation, infec­
tion, and necrosis. Subsequently, a load-bearing reconstruc­
tion plate is placed on the mandibular base to maintain the
mandibular block, particularly when there is a discontinuity
of the bone (Fig. 47.11a–c). If bone segments are missing
and no obvious signs of infection (e.g., contamination with
foreign material) are apparent, I recommend immediate
bone augmentation with autologous transplants from the
iliac crest. Preconditions for immediate bone augmentation
are that the transplants can be fixed effectively and that suf­
ficient soft tissue closure can be achieved. Intravenous an­
tibiotics (amoxicillin and clavulanic acid) are administered
three times daily for 5 days to prevent transplant infection.
If the preconditions for primary augmentation are inap­
propriate, the augmentation is performed in a second op­
eration after wound healing is complete. Massive bone loss
requires bone augmentation and jaw reconstruction with
microvascular transplants. To counteract the effect of the
lack of bone coverage, osteocutaneous grafts are the trans­
plants of choice. Modern three-dimensional planning tools
can anticipate the amount of bone loss via CT and design
custom-made bony transplants virtually. Corresponding cut­
ting guides for bony osteotomy of the recipient and of the
donor site are then manufactured by industrial partners (see
Fig. 47.11b–f).
Infection
As previously mentioned, antibiotic therapy is necessary
for 5 to 7 days for comminuted fractures. Bone necrosis
resulting from small fragments can be avoided if surgical
therapy is carried out as described. Finding and removing
bullets and splinters can be challenging; intraoperative
navigation is a helpful tool for simplifying the retrieval of
foreign materials. Plate exposure and infection typically re­
sult from the lack of soft tissue coverage of the bone and os­
teosynthesis material. Effective cleansing and appropriate
care of the exposed plate might prolong the time until re­
moval is necessary. Early removal of plates is possible from
6 weeks after osteosynthesis, often with no compromise to
the result. If denuded bone cannot be covered adequately,
pedicled soft tissue grafts are harvested to cover the hard
tissue. Curettage and planning of bony edges are essential;
in complex cases, adjacent teeth are extracted to enhance
soft tissue coverage.
Nonunion and Malocclusion
Nonunion typically results from infection or a lack of bony
stabilization. Pseudarthrosis is a possible result. Two strate­
gies are available:
1. If pseudarthrosis is stable and the patient appears satis­
fied with the situation, no further surgery is recom­
mended.
2. If major mobility occurs between the fragments, resta­
bilization with a taller osteosynthesis plate and a bone
graft is indicated.
treatment. Distraction maneuvers during anatomical reduc­
tion can often cause these dislocations. In consequence, sec­
ondary corrections with ORIF have to be performed.
Comminuted Fractures
Avoiding Complications
Comminuted fractures occur after high-velocity trauma
or shotgun injuries. They are characterized by bone that
is crushed into a number of smaller fragments. For this
reason, anatomic repositioning can be extremely difficult.
Osteosynthesis is hampered by the lack of fixation op­
tions for the small bony segments. Because of the trauma
mechanism, comminuted fractures are often associated
with remarkable injuries to the neighboring tissues, with
lacerations of the gingiva and facial skin or even the loss
of soft tissue with subsequent defects. The prevalence of
fractured, loosened, or knocked-out teeth in these types of
injuries is high. Foreign bodies or bullets penetrate soft tis­
sue and bone. In addition to the difficulties of anatomic re­
positioning and stabilization of the bony fragments, several
complications can arise with this type of fracture:
•• Discontinuity of bone
•• Infection, mainly as abscesses, cellulitis, or osteomyelitis
because of the following:
○
○Contaminated foreign bodies such as bullets or
splinters
○
○Inadequate soft tissue closure over denuded bone
○
○Loosened and movable bone fragments
○
○Loosened or dislocated teeth
○
○Absent or insufficient antibiotic therapy
•• Nonunion or malocclusion
•• Nerve injuries
Anatomic Repositioning, Osteosynthesis,
and Discontinuity of Bone
The discontinuity of bone results primarily after traumatic
loss of a bone fragment or secondarily because of infection
and necrosis of a segment. In extended comminuted frac­
tures, a step-by-step approach is recommended to prevent
the previously mentioned complications and unfavorable
outcomes. First, wounds are cleansed with polyhexanide
0.04% or Ringer’s lactate solution via a syringe; then the
surgeon performs a meticulous search for foreign material
and tooth fragments. Foreign material, dental fragments,
and teeth with vertical fractures and pulp exposure are re­
moved.
Teeth in malposition are manually replaced into their
sockets without touching the root region. These teeth are
fixed with interdental titanium-composite splints for sta­
bilization. If occlusion is reproducible, maxillomandibular
fixation is performed, and intraoral soft tissue is closed if
necessary.
Thereafter the mandible is (if possible) stabilized in oc­
clusion, and the fracture is manually reduced via an extra­
oral approach. The separate fragments are first allocated and

SECTION VI PEDIATRIC AND CRANIOFACIAL SURGERY
860
•• Osteomyelitis (OM)
•• Primary jawbone malignancies or bone infiltration of
oral malignancies
•• Jaw metastasis of distant malignancies
•• Extended benign jawbone tumors
•• Extended jaw cysts
•• Postsurgical jaw fracture (e.g., after removal and
osteotomy of an impacted third molar)
Because the reasons for pathologic fracture are diverse, the
treatment of these fractures also differs. Fractures with a
malignant background must be treated differently from
those with a benign background, and fractures caused by
osteonecrosis or infection require specific therapeutic con­
cepts. Obviously, meticulous diagnosis of each fracture is
the key factor in avoiding most of the possible complica­
tions. Clinical examination and panoramic radiography
provide a sufficient diagnostic basis in solely clinical cases
if the surgeon has no doubts of the underlying pathomech­
anism (e.g., in a young patient who has experienced man­
dibular cracking 2 weeks after extended osteotomy of an
In cases with minor malocclusion, orthodontic pretreat­
ment might be successful. Extended malocclusion is treated
after orthodontic and surgical planning by jaw osteotomy,
in both jaws if necessary.
Nerve Injury
Rupture of the mandibular or lingual nerve should immedi­
ately be treated by microsurgical reanastomosis. If tension-
free anastomosis of both nerve endings is not possible, a
sural or greater auricular nerve graft is used.
Pathologic Fractures
Pathologic fractures occur when the jawbone—mainly the
mandible—is weakened because of a pathologic condition.
The most common pathologic conditions that cause frac­
tures include the following:
•• Osteoradionecrosis (ORN)
•• Medication-related osteonecrosis of the jaw (MRONJ)
d
b
c
e
a
f
g
h
i
Fig. 47.11 Primary and secondary treatment of a gunshot injury. (a) Frontal view after primary defect repair with local soft tissue, mid­
face osteosynthesis, and titanium macroplate for mandibular bridging. (b) Three-dimensional frontal view after primary repair. (c) Three-
dimensional basal view after primary repair. (d) Mandibular reconstruction planning with segmentation of a free fibular graft. (e) Virtual
planning of mandibular reconstruction with an osteotomized free fibular flap. (f) The harvested osteocutaneous fibular flap that has been
segmented with respect to virtual planning. (g) The osteosynthesized fibular graft as a neomandible with a stereolithography model as
the reference. (h) Frontal view 6 months after mandibular reconstruction and scar correction. (i) Dental and functional rehabilitation by
implant-supported prosthesis.
d

861
Chapter 47 Fractures of the Jaws
marginal mandibular branch of the facial nerve. If the bony
contact between the fractured parts is limited, a cancel­
lous bone graft must be inserted into the fracture region
to stimulate osteogenesis. If an extended cyst or an ex­
tended osteotomy defect has caused the fracture and no
signs of infection are apparent, an autologous cortical bone
graft from the iliac crest can stabilize the region. The cor­
tical bone graft has limited osteoinductive and osteogenic
potential compared with a cancellous bone graft, but in
addition to its stabilizing effect, it might provide enough
vertical bone height for subsequent dental implantation.
This autologous bone graft is fixed to the bone fragments
by screws or miniplates. Administration of antibiotics and
meticulous suturing, particularly when using an intraoral
approach, is necessary to prevent infection, bone graft loss,
and nonunion. The insertion of a nasogastric tube for the
first 8 days can be discussed with the patient.
Class B
In contrast to class A fractures, those caused by ORN,
MRONJ, and OM are associated with infected bone. How­
ever, the infected bone is not the only issue. Persistent bone
infection, movable fractured bone segments, and con­
secutive necrosis potentially lead to infection of the sur­
rounding soft tissue. The soft tissue becomes macerated,
and intraoral and extraoral dehiscence with exposed bone
occurs. Long-term infections cause penetrating intraoral
or extraoral leakages with a salivary fistula, which itself
maintains infection. In the case of ORN, the radiation dam­
age to the tissue and its concomitant poor perfusion and
scarring display an additional restriction to reconstructive
surgery. These pose significant reconstructive challenges.
To prevent breakdown of the reconstructive procedure, the
surgeon must integrate a multitude of factors into the sur­
gical plan.
Bony Resection
Necrotic bone requires radical resection to prevent later
reinfection at the resection margins. The assessment of ne­
crotic and healthy bone by clinical judgement is not simple
in any patient. Novel techniques such as intraoperative
fluorescence-guided bone resection, CT imaging, or mag­
netic resonance imaging (MRI) have been demonstrated to
be helpful tools.25,26 With the use of CT, virtual resection of
the affected bone and virtual reconstruction planning are
now possible.27
Bony Reconstruction
Autologous bone must be transplanted to regain bone con­
tinuity after segmental jaw resection. As previously men­
tioned, the wound bed in OM cases, but particularly with
MRONJ and ORN, is perfused insufficiently, and thus the
healing process of the transplant is impaired. When using
impacted lower wisdom tooth). In all other cases, CT is
mandatory and prevents surprises for the surgeon. If the
patient has a history of malignancy or a known metastasiz­
ing neoplasia, positron emission tomography (PET) might
influence the therapeutic concept. Finally, a biopsy of the
fractured region is performed to determine metastasis and
the type of neoplasia or benign tumor, cyst, osteonecrosis,
or osteomyelitis.
The patient’s general condition is discussed with the
general practitioner, the anesthetist, the patient himself,
and sometimes the attending oncologist. Based on these
evaluations, the pathologic fracture can be treated as a pal­
liative case with the main focus of attention on pain reduc­
tion and prevention of emerging infections, or, as in the case
of a healthy adolescent suffering from a pathologic fracture
attributable to a jaw cyst or after wisdom tooth removal,
full jaw reconstruction and prosthetic rehabilitation. Pa­
tients with pathologic fractures can be subdivided into three
classes according to the origin of the fracture (Box 47.2).
I have developed a therapeutic algorithm for each class
that minimizes the risk of failure.
Class A
The ideal treatment for healthy individuals includes ad­
justment of the occlusion via maxillomandibular fixation,
anatomic reduction of the fracture, and osteosynthesis
(typically with a load-bearing 2.3-mm or 2.5-mm recon­
struction plate rather than miniplates). If possible, the plate
should be placed at the mandibular base via an intraoral
approach. Transbuccal fixation or fixation with a 90-degree
angled screwdriver may ease insertion. Postmolar fractures
should be treated by an extraoral approach with special at­
tention paid to minimizing scarring and avoid violating the
Box 47.2
Class A: Benign cysts, benign tumors, and postsur­
gical fractures
•• Limited form
•• Extended form
Class B: Osteomyelitis, osteoradionecrosis, and
medication-related osteonecrosis of the jaw be­
cause of osteoporosis
Class C: Primary malignancy or metastasis from
distant neoplasia or medication-related osteone­
crosis of the jaw because of metastasizing malig­
nancy (stable disease)
•• Palliative
•• Nonpalliative cases
Classes of Pathologic Fracture

SECTION VI PEDIATRIC AND CRANIOFACIAL SURGERY
862
These patients commonly have peripheral vascular disease
that could exclude the harvest of a FFF. To prevent compli­
cations, the pedal pulse must be palpated and CT angiogra­
phy of the lower limb performed. Patients with obliterated
lower leg vessels must be excluded from the FFF procedure
but might be suitable for flaps harvested from the scapular
region.
Soft Tissue Shortage, Salivary Fistula
Sufficient soft tissue coverage is critical in bony recon­
struction of ORN or MRONJ. Contact of the bone trans­
plant with the oral environment will lead to infection and
consecutive transplant loss. Therefore the management
of patients with preexisting intraoral or extraoral leak­
ages and salivary fistulas is extremely delicate. The sur­
geon should favor osteocutaneous flaps over osseous flaps
in reconstruction planning. If soft tissue is lacking after
bone insertion, I apply the sandwich technique.28 The bone
transplant is “wrapped” and covered with two skin flaps:
one intraorally and the other extraorally. The skin flaps can
originate from an osteocutaneous flap (FFF) for intraoral
coverage and a second microvascular pedicled soft tissue
flap (radial forearm or anterolateral thigh flap) for extra­
oral coverage. If not enough recipient vessels are present
for two microvascular flaps (as is often the case in preoper­
ated and irradiated necks with ORN), pectoralis major flaps
or deltopectoral flaps are excellent alternative procedures
for extraoral closure.
unvascularized bone grafts or bone substitutes, the surgeon
therefore must anticipate a high rate of transplant infection
and subsequent transplant loss. Microvascular bone trans­
plantation is the preferred method. Iliac crest transplants
pedicled on the deep circumflex iliac artery (DCIA) provide
enough bone height for mandibular body reconstruction
(Fig. 47.12). The DCIA transplant is an ideal transplant for
patients with OM with minor soft tissue problems. The
iliacus/internal oblique muscle cuff protecting the DCIA is
suitable for the coverage of small intraoral soft tissue de­
fects. The short vascular pedicle can be anastomosed to
the branches of the internal jugular vein and the external
carotid artery.
Alternative microvascular bone grafts embrace flaps
from the scapular region pedicled either on the circumflex
scapular artery or on a branch of the thoracodorsal artery.
These flaps only provide a small amount of thin bone but
allow the additional harvest of a soft tissue island. In con­
trast to the osteocutaneous free fibular flap (FFF) used for
osteocutaneous jaw reconstruction, flaps from the scapular/
parascapular/scapular tip region are an option. Several oste­
otomies can be performed with the FFF, which makes exten­
sive-length bone reconstruction (e.g., from the ipsilateral to
the contralateral mandibular angle) possible.
Particularly in patients with ORN or MRONJ who have
a shortage of soft tissue, one or two skin pedicles can be in­
tegrated into the flap, which will be perfused by skin perfo­
rators of the fibular artery. ORN often originates from head
and neck cancer, which is mainly caused by heavy smoking.
Fig. 47.12 Mandibular fracture caused by osteomyelitis and mandibular rehabilitation by a microvascular iliac bone graft. (a) Panoramic
radiograph revealing chronic osteomyelitis and a pathologic fracture in the left mandibular body after wisdom tooth removal in a 48-year-
old male patient. (b) Harvest of an iliac bone graft pedicled on the deep circumflex iliac vessels. (c) Mandibular reconstruction by micro­
vascular reanastomosed iliac bone graft.
c
b
a

863
Chapter 47 Fractures of the Jaws
Class C
Pathologic fractures originating from oral neoplasm or
metastasis are, in most cases, a sign of advanced tumor
growth. In suspected cases of advanced oral cancer, CT im­
aging (head and neck, thorax, and abdomen) and biopsy
are necessary, and the case should be discussed with an
interdisciplinary oncology board. Even if tumor growth
suggests primary radiotherapy therapeutic strategies, the
surgeon may prefer a “surgery-first” concept. The unfavor­
able results of performing radiotherapy on a fractured jaw,
such as infection, pain, and scarring, will require secondary
surgery, which is then much more difficult and a offers a
questionable outcome.
If the patient has a medical history of a distant malig­
nancy or if a jaw biopsy identifies metastasis of a distant
tumor, additional PET, PET with CT, or PET with magnetic
resonance tomography is necessary. These techniques help
to differentiate between a single metastasis and many. The
goal of therapy in the latter case could be altered from recon­
struction to pain reduction. A similar approach might be rea­
sonable in patients with MRONJ with bone metastases who
have undergone antiresorptive therapy with bisphosphonates
or receptor activator of nuclear factor kappa-B ligand (RANKL)
inhibitors. However, many such patients with disease are sta­
ble for years and present in good health. After critical dis­
cussions with the involved oncologist and the patient, recon­
structive concepts such as FFF grafts might also be suitable. Of
course, preoperative diagnosis has to exclude bone metastasis
into the bone transplant. In contrast, palliative patients in a
reduced health condition should only be treated when they
experience intense pain because of the mobile bone. The cut­
ting of the bony stumps and the removal of necrotic tissue in
an operation of short duration helps to reduce pain symptoms
and improves the quality of life significantly.
Conclusion
From my point of view, three therapeutic strategies are
available for group C patients, and the final strategy chosen
should be substantially influenced by the general health
and oncological status of the patient. The recommenda­
tions for each group are summarized in Table 47.1.
Atrophic Jaw Fractures
Loss of teeth and subsequent edentulism is accompanied
by the resorption of the alveolar ridge. Cawood and How­
ell30 have characterized the changes in shape of the alveolar
process of 300 edentulous jaws. A reduction not only of the
vertical bone height but also of the horizontal axis is de­
scribed in their classification. With the loss of bone, the sta­
bility of the bone decreases, and the weakened mandible is
particularly prone to fracture. Luhr et al31 have categorized
atrophied mandibles by their vertical height in panoramic
radiographs because complications in bone healing are di­
rectly correlated with loss of mandibular height. Class I is
graded between 16 and 20 mm, class II between 11 and
Microvascular Procedures
As mentioned previously, sufficient recipient vessels are
the key factor for microvascular reconstruction. Patients
with a history of multiple neck surgeries, patients being
heavily irradiated in the head and neck region, and patients
with external carotid artery stenosis or occlusion pose a
major problem for reconstruction of a pathologic fracture.
Pathologic fractures in such patients urgently require pre­
operative CT angiography to determine the status of the
neck vessels.29 This diagnostic tool provides a strong base
for any decisions that I make with regard to reconstruc­
tive strategy. The surgeon can determine preoperatively
whether to anastomose two microvascular flaps or to har­
vest a deltopectoral flap, which side of the neck can be used
for anastomosis, and which side of a fibula should be used
to place a skin island intraorally or extraorally. Occasion­
ally, clinical examination and CT angiography reveal that
there are no reliable recipient arteries on either side of the
external carotid system.
In addition, venous anastomosis to the internal or ex­
ternal jugular vein might not seem possible because of ex­
treme scarring. In my experience, preoperative ultrasound
can help locate a sufficient superficial or deep branch of the
transverse cervical artery. To overcome problems with insuf­
ficient venous recipient vessels, anastomosis to the cephalic
vein is a possible alternative. The cephalic vein is prepared
by starting from the deltopectoral groove in a distal direc­
tion to the elbow, where it can be ligated and switched in a
proximal direction to the neck region. If the flap pedicle is
too short to reach the recipient veins or arteries, a saphe­
nous interposition vein must be grafted.
Alternative Strategy to Bony Reconstruction
Some patients are unwilling to have an autologous micro­
vascular bony harvest for personal or occupational reasons.
Others patients have long bony defects but have severe pe­
ripheral vascular disease, gait disturbances, or other factors
that hamper bony microvascular reconstruction. For this
group, an alternative to bony, especially FFF, reconstruc­
tion must be offered. I recommend the use of a 2.5-mm re­
construction plate for bridging the bony gap, although this
technique can be associated with long-term complications.
The most common problem is that, particularly in the chin
region of ORN cases, the thinned soft tissue harmed by
scarring, radiation, and infection is prone to plate exposure.
To prevent this drawback, the plate must be bent exactly.
This can be achieved by preoperatively bending the plate on
a patient-specific three-dimensional model of the mandi­
ble created based on the CT. Bending the plate in slight ret­
roposition is helpful. Intraoral plate exposure is a common
complication, because the thin irradiated mucosa does not
provide enough bulk to cover the plate. Therefore the plate
can be protected within the oral cavity with a bulky soft
tissue flap. I recommend an anterolateral thigh flap rather
than a pectoralis major flap. A radial forearm flap is typi­
cally too thin to prevent long-term exposure.

SECTION VI PEDIATRIC AND CRANIOFACIAL SURGERY
864
thesis material will be covered by a large amount of soft tis­
sue and is therefore not prone to plate exposure. During the
preparation and exposure of the fracture, the surgeon must
be careful to not denude the bone and to keep the perios­
teum attached to the bone. Thus perfusion to the mandible
can be kept intact.
Open Reduction and Internal Fixation
with Macroplate Osteosynthesis
The basic principle for ORIF in atrophied mandibles is that
the thinner the bone, the thicker the osteosynthesis plate.
Therefore miniplate osteosynthesis should be avoided.33,34
An atrophic mandible is not able to bear a load itself. Rigid
internal fixation and the use of a load-bearing plate is the
best way to treat fractures of the atrophic mandible success­
fully.32 Once the fracture ends are exposed, I fix the fracture
with a miniplate to establish bony continuity in a precise
manner. In contrast to “normal” mandibular fractures, ex­
tensive removal of the periosteum should be avoided to
ensure perfusion of the bone. Subsequently, a 2.3-mm or
2.5-mm rigid macroplate can be used for osteosynthesis
(Fig. 47.13). Prebending the plate based on a three-dimen­
sional model of the patient’s mandible is preferred over the
use of angular stable plates with locking screws if the bend
15 mm, and class III less than 10 mm.31 Depending on the
loss of vertical and horizontal dimensions, the contact
area between the fractured bone endings is dramatically
reduced in atrophied jaws. Additional drawbacks for the
healing of atrophied fractured mandibles relate to the re­
maining cortical bone, which is dense, sclerotic, and poorly
perfused.32 For this reason, therapeutic strategies must dif­
fer completely from those of normal mandibular fractures.
Two fundamental aspects should be considered to prevent
unfavorable results:
1. Extraoral approach
2. ORIF with macroplate osteosynthesis
Extraoral Approach
Fractures of an atrophied mandible should be treated
through an extraoral approach if the gingiva is intact. Os­
teosynthesis material should not be placed under the gin­
giva because mechanical irritation may occur from food
intake or a rocking dental prosthesis. Even if patients are
instructed to eat a soft diet or not to use their dental pros­
thesis, compliance might be insufficient. Most patients
with jaw atrophy are of advanced age, are multimorbid, or
have dementia. With an extraoral approach the osteosyn­
Table 47.1 Therapeutic algorithm for patients with pathologic fractures
caused by oral cancer or by medication-related osteonecrosis of the jaw after
bone metastasis
General condition/oncologic status
Recommended surgery
Oral malignancy
Stable distant cancer with bone metastasis
ASA status I or II
No gait disturbance
Resection of infected or necrotic bone plus reconstruction with
microvascular bone graft (and an additional vascularized soft tissue
flap as necessary)
Chronic metastatic cancer
ASA status I, II, III
Gait disturbance
Resection of infected or necrotic bone with a reconstruction plate for
bridging the bony gap (and an additional vascularized soft tissue flap as
necessary)
Oncologically palliative situation
ASA status III and IV
Resection of infected or necrotic bone, removal and planing of bony
edges, and no osteosynthesis
Abbreviation: ASA, American Society of Anesthesiologists.
Fig. 47.13 Macroplate osteosynthesis in an atrophic mandibular
fracture with an extraoral approach.