Operative Technique in Plastic Surgery – Kevin C.Chung

(yellow arrow) in situ below the adductor longus. C.
The dissection of the obturator nerve (seen over the
WECK-CEL) extends under the adductor longus to its
branch point. D. The gracilis muscle is split
longitudinally to decrease bulk. E. The length of
gracilis to be used is measured, while the muscle is
still in situ. F. Mattress sutures are placed on the
edges of the gracilis to prevent suture pull-through.
■ Once isolated, a nerve stimulator is used to assess the contractile units of the
muscle. The gracilis can usually be split into medial and lateral components
(TECH FIG 5D).
■ This split occurs along a natural cleavage plane. Spanning vessels between
the muscle segments should be preserved until nerve contraction has been
tested.
■ The nerve is stimulated, and the best contractile segment is prepared for
transfer.
■ In general, no more than one-third to one-half of the muscle is required for
transfer, depending on the size of the child and muscle. Any muscle not
harvested is left in situ.
■ The length of the gracilis needed is then determined using measurements
obtained from the recipient site (described above).
■ A total length measurement (a + b), length proximal to the pedicle (a), and
length distal to the pedicle (b) will be relayed.
■ An additional 1 cm is added to each side to allow for a layer of bolster
sutures to be placed at either end (TECH FIG 5E).
■ A row of mattress sutures of 0-0 Vicryl are placed 1 cm from each end of the
muscle to prevent suture pull-through (TECH FIG 5F).
■ The proximal and distal muscle bellies are severed using bipolar
electrocautery.
■ Once the recipient site is ready, a heparin bolus is given. After 10 minutes,
the vascular pedicle is clipped, and the muscle is transferred to the face.
■ Gracilis Muscle Inset

■ The orientation of the muscle is then determined with consideration of
microvascular anastomosis and the nerve coaptation.
■ The previously placed inset sutures are then placed in the gracilis, just
central on the gracilis to the row of mattress sutures. The muscle is then
parachuted into position at the commissure (TECH FIG 6A).
■ The obturator nerve is then passed through a previously created tunnel to the
upper lip (if using a CFNG) or placed in position to coapt to the nerve to the
masseter.
■ The muscle is then temporarily placed and secured in its final inset position
in preparation for a tension-free anastomosis that will not change after the
final muscle inset.
■ The microvascular anastomosis is then performed, generally vein before
artery.
■ The epineural nerve coaptation is performed. The buccal sulcus incision is
closed at this time.
■ The inset origin of the muscle is secured to the deep tissues and periosteum
of the zygoma using mattress sutures of no. 1 Vicryl again behind the row of
mattress sutures on the gracilis. The muscle should be spread over the inset
origin to prevent excess bulk (TECH FIG 6B).
■ When the muscle is inset, proper tension must be set. If the measurements
have been properly made, the resting position will appear as a slight (20%–
30% of max) smile.
■ A Penrose drain is placed behind the ear by way of a separate stab wound.
■ The cheek flap is closed using 4-0 Vicryl sutures in the dermis and a 5-0
Monocryl plus skin closure (TECH FIG 6C).
TECH FIG 6 • A. The gracilis muscle is parachuted
into position at the commissure. B. The gracilis in the

final position. C. The skin is closed and the area
drained with a Penrose drain.
PEARLS AND PITFALLS
Donor
nerve
evaluation
■ Selection of an appropriate donor nerve for the CFNG is crucial to the
overall success of the operation.
■ The donor nerve should supply the zygomaticus muscles and the
levator anguli oris, with minimal (if any) contributions to the
orbicularis oris.
■ The donor nerve branch taken must have redundancy with other
nearby branches and therefore can (and should) be divided relatively
proximally. This should be determined with a nerve stimulator to avoid
any donor-site weakness.
Muscle
inset
■ An incorrectly inset muscle is nearly impossible to correct.
Unfortunately, this may not be noticed until the muscle starts to
function, months after the initial procedure. Care must be taken to
avoid potential issues by concentrating on the following:
■ Determine the desired vector of pull, and focus on adequate vertical
orientation during inset.
■ Use a row of mattress sutures to prevent pull-through.
■ Avoid excess bulk by splitting the muscle in situ before transfer and by
removing buccal fat.
■ The muscle should be inset with tension to simulate 20%–30% of a
natural smile.
■ Avoid excess bulk by coursing the muscle posterior to the malar
eminence and fanning the muscle out in the temple area.
Inset
insertion
suture
placement
■ Preoperative smile vector analysis is key to creating a pleasing smile
and should be done in the upright position in the holding area.
■ Time and care should be taken to place each suture in the appropriate
position on the upper lip and commissure, avoiding inversion,
eversion, and dimpling.
■ A symmetric nasolabial fold should be created.
Gracilis
harvest
■ Identification of the gracilis is best done by visualizing the obturator
nerve and the medial femoral circumflex vessels traversing underneath
the adductor longus muscle en route to the medial aspect of the

gracilis.
■ The pedicle size can be small but can be followed below the adductor
longus to its origin on the profunda for additional length and diameter.
■ The pedicle is best found by scoring the fascia of the adductor longus
exposing the space below the adductor that contains the medial femoral
vessels and obturator nerve.
■ Donor site seromas are less common in facial reanimation than when
the gracilis is used in breast reconstruction but still warrant placement
of a drain.
■ Lidocaine should not be used as a vasodilator during this portion of the
procedure to avoid any effects on nerve stimulation. Papaverine is
preferred.
POSTOPERATIVE CARE
■ Free muscle transfers are monitored via implantable Doppler probes.
Postoperative flap checks are performed on an hourly basis for 2 days,
followed by every 4 hours for the next 2 days.
■ Our postoperative management follows a gradual increase in activity:
■ Bed rest for 1 day
■ Gradual and slow mobilization thereafter
■ No pressure on the operated side of the face for 6 weeks
■ Perioperative antibiotics are given.
■ Signs of reinnervation are followed in the clinic and can generally be expected
at 2 to 4 months when the nerve to the masseter is used and 6 to 12 months
when a CFNG is used.
■ Once reinnervation is noted on examination, therapy is started. Patients work
with therapists specifically trained in facial reanimation rehabilitation. We
believe this to be critical to success.
■ Exercises done in front of a mirror are useful to provide a feedback
mechanism and improve symmetry. This should be done 2 or 3 times a day for
4 to 5 minutes at a time.
■ Therapy should be continued for a period of 6 months.
OUTCOMES
■ The goal of a functional gracilis transfer is smile recreation using a single
vector pull of the muscle. Thus, limitations exist. A pure symmetric smile is a
lofty goal, but with attention to detail and therapy, dramatic results can be

obtained (FIG 6).
■ Studies have shown improved speech outcomes in patients with Mobius
syndrome after undergoing bilateral gracilis transfers.
COMPLICATIONS
■ Garcia et al. in a pooled data analysis reported a complication rate of 9.6%.7
■ Complications included the following:
■ Postoperative hematoma (3.6%)
■ Infection (3.5%)
■ Vascular compromise (1.4%)
■ Salivary leak (1%)
■ Seroma (0.4%)
■ Long-term failure of the muscle to reinnervate was reported at 1.8%
FIG 6 • Preoperative and 2-year postoperative pictures
of the patient in FIG 4, who underwent a two-stage free
gracilis transfer for a congenital facial nerve palsy.
REFERENCES
1. Garcia RM, Hadlock TA, Klebuc MJ, et al. Contemporary solutions for the
treatment of facial nerve paralysis. Plast Reconstr Surg. 2015;135(6):1025e-
1046e.
2. Westin LM, Zuker R. A new classification system for facial paralysis in the
clinical setting. J Craniofac Surg. 2003;14(5):672-679.
3. Proctor B. The anatomy of the facial nerve. Otolaryngol Clin North Am.
1991;24(3):479-504.
4. Dorafshar AH, Borsuk DE, Bojovic B, et al. Surface anatomy of the middle
division of the facial nerve: Zuker’s point. Plast Reconstr Surg.
2013;131(2):253-257.
5. Fisher MD, Zhang Y, Erdmann D, Marcus J. Dissection of the masseter
branch of the trigeminal nerve for facial reanimation. Plast Reconstr Surg.
2013;131(5):1065-1067.
6. Borschel GH, Kawamura DH, Kasukurthi R, et al. The motor nerve to the
masseter muscle: An anatomic and histomorphometric study to facilitate its use

in facial reanimation. J Plast Reconstr Aesthet Surg. 2012;65(3):363-366.
7. Garcia RM, Gosain AK, Zenn MR, Marcus JR. Early postoperative
complications following gracilis free muscle transfer for facial reanimation: a
systematic review and pooled data analysis. J Reconstr Microsurg.
2015;31(8):558-564.

53
CHAPTER
Corneal Neurotization
Joseph Catapano, Ronald Zuker, Asim Ali, and Gregory H.
Borschel
DEFINITION
■ Neurotrophic keratopathy is a degenerative corneal disease caused by
impairment of corneal innervation.1
■ Corneal neurotization involves using functioning sensory nerves from
elsewhere on the face as donor nerves to reinnervate the cornea and restore
corneal sensation and improve ocular surface health.
ANATOMY
■ The cornea is the most densely innervated part of the body.1,2
■ Corneal innervation derives from the ophthalmic branch (V1) of the trigeminal
nerve (CN V).3
■ Lesions may occur anywhere along the course of the corneal innervation
pathway including the pons, the trigeminal (gasserian) ganglion, the
ophthalmic branch, the nasociliary nerves, and the long ciliary nerves.
■ Despite corneal nerve density, the cornea is supplied by relatively few
trigeminal neurons as a single neuron may support hundreds of individual
nerve endings.4–6
■ The corneal innervation is divided into three networks: stromal, sub-basal, and
epithelial.7,8
PATHOGENESIS
■ Corneal sensation is a necessary component of reflexive tearing and blinking,
which prevent corneal injury.
■ Pain ordinarily would prompt patients to seek appropriate treatment after
corneal injuries; however, an insensate cornea leaves patients unaware of their

corneal injury.
■ Repetitive corneal epithelial injury and ulceration cause corneal scarring and
vision loss.9–11
■ Corneal nerves also contain neuromediators that promote corneal epithelial
maintenance and repair.3,11
■ Immediately following corneal denervation, animal models show decreases in
epithelial cell vitality and mitosis, resulting in thinning, breakdown, and
ulceration of the corneal epithelium.12–15
NATURAL HISTORY
■ Neurotrophic keratopathy is one of the most difficult ocular diseases to treat.1
■ Prognosis is dependent on the severity of corneal hypoesthesia and the
presence of other concomitant ocular disorders such as dry eye disease,
exposure keratopathy, and corneal limbal stem cell deficiency.
■ Patients require lifelong treatment and even with optimal management many
develop vision loss and blindness in the affected eye.
■ Inflammation and repeated corneal injury may also result in
neovascularization of the cornea, further impeding vision.
PATIENT HISTORY AND FINDINGS
■ Patients typically present with persistent asymptomatic corneal epithelial
defects.
■ Neurotrophic keratopathy is classified into three stages depending on clinical
findings based on the Mackie classification1:
■ Stage 1: epithelial irregularity with punctate keratopathy and minimal stromal
scarring.
■ Stage 2: epithelial ulceration surrounded by a rim of loose epithelium +/−
stromal swelling.
■ Stage 3: corneal ulceration involving the stroma with risk of corneal
perforation.
IMAGING AND OTHER DIAGNOSTIC STUDIES
■ Diagnosis is based on clinical findings and a patient history of corneal
hypoesthesia or anesthesia with delayed healing and persistence of corneal
epithelial defects.16,17
■ Slit lamp: identifies corneal epithelial abnormalities, including diffuse staining
with fluorescein, epithelial sloughing, and stromal neovascularization.

■ Corneal esthesiometry: measures corneal sensation. This can be performed
with a Cochet-Bonnet aesthesiometer (Luneau, France) by a skilled
ophthalmologist.
■ Schirmer test: used to diagnose concomitant dry eye disease, when needed.
■ In vivo corneal confocal microscopy (IVCCM): documents the absence of
corneal nerve fibers.
DIFFERENTIAL DIAGNOSIS
■ Hallmark for diagnosis is the presence of a corneal ulcer and the absence of
corneal sensation.
■ Possible etiologies of corneal anesthesia and hypoesthesia are as follows:9,16
■ Viral infection (herpes simplex and zoster keratoconjunctivitis)
■ Chemical burns
■ Physical injury to the trigeminal innervation (such as intracranial surgery)
■ Corneal surgery
■ Diabetes
■ Leprosy
■ Topical anesthetic abuse
■ Congenital (such as trigeminal agenesis, cerebellar hypoplasia, brainstem
hypoplasia)
■ Certain disease may also exacerbate neurotrophic keratopathy:
■ Dry eye disease
■ Exposure keratopathy; facial nerve paralysis
■ Corneal limbal stem cell deficiency
NONOPERATIVE MANAGEMENT
■ The goals of treatment are to prevent corneal ulceration and promote epithelial
healing when ulcerations occur.1,16,17
■ Preservative-free topical artificial tears
■ Punctal occlusion
■ Therapeutic contact lenses (eg, the “Boston lens”)
■ Topical antimicrobials
■ Protective tarsorrhaphy
■ If a corneal perforation is suspected, then cyanoacrylate glue or keratoplasty
(cornea transplant) may be indicated.
■ Exacerbating conditions, such as exposure keratopathy and limbal stem cell
deficiency, should be treated.

■ Experimental treatments for persistent ulcerations include topical IGF-1,
substance P, or nerve growth factor (NGF).18–21
SURGICAL MANAGEMENT
■ Surgical management to restore corneal sensation in patients with corneal
anesthesia or hypoesthesia has been described.22–24
■ Samii first decribed a surgical technique to reinnervate the cornea using an
intracranial approach through an osteoplastic frontal craniotomy to guide
regenerating axons directly into the ophthalmic nerve using a long sural nerve
graft and the occipital nerve as donor.
■ Avoiding an intracranial approach, Terzis22 described a technique using the
peripheral nervous system to reinnervate the cornea by directly transferring the
supraorbital and supratrochlear nerves to neurotize the cornea.
■ This technique necessitates a coronal incision and extensive dissection to
access the supratrochlear and supraorbital nerves distally.
■ This technique was then modified by Borschel, Ali, and Zuker,23,24 who were
able to avoid a coronal incision by guiding axons from the proximal
supratrochlear nerve into the anesthetic cornea via a sural nerve graft.
■ This technique uses two small supraorbital incisions.
■ This approach is described in detail in this chapter.
Preoperative Planning
■ Thorough facial sensory nerve examination and mapping must be done in
order to identify potential donor nerves for reconstruction. The authors use an
occupational therapist and Semmes-Weinstein monofilaments to document
facial sensation.
■ All patients should be evaluated by an ophthalmologist to document visual
acuity, overall ocular health, and corneal sensation using Cochet-Bonnet
aesthesiometry.
Positioning
■ The patient is placed in the supine position on the operating table, and the
entire face is prepped and draped (FIG 1).
■ The leg to be used for sural nerve harvest is also prepped and draped.

FIG 1 • We prefer to operate from the head of the bed
with the patient in the supine position. Even with a
thorough sensory examination documenting normal
sensation in the contralateral face, we have found the
donor supratrochlear or supraorbital nerves to be
insufficiently large enough for coaptation on occasion.
For this reason, we prep the patient’s entire face in
case we use the infraorbital nerve as a donor.
T E C H N I Q U E S
■ Sural Nerve Harvest

■ This can be performed using the surgeon’s preference. We prefer using a
nerve stripper device that permits harvesting of the proximal tibial
component of the sural nerve, which usually provides a branch-free graft of
sufficient length.
Identification of the Contralateral Supratrochlear Nerve
■ Any functioning sensory nerve in the face can be used for corneal
neurotization.
■ Many patients have hemifacial sensory deficits associated with neurotrophic
keratopathy. Our preferred technique is to use the contralateral supratrochlear
nerve as a donor. If the ipsilateral supratrochlear or supraorbital nerves are
normal and available, they may be used instead of the contralateral nerves.
■ Two- to three-centimeter supraorbital incisions are made on the medial lower
border of the eyebrows over each eye (TECH FIG 1A).
■ The donor supratrochlear or supraorbital nerve is then identified through this
incision on the donor side (TECH FIG 1B).
■ The supratrochlear nerve is identified deep to the origin of the frontalis
muscle, on the surface of the corrugator supercilii muscle traveling cephalad
from the supratrochlear notch.
■ The supratrochlear notch can often be palpated to guide dissection.
■ Some supratrochlear nerves divide distal to the notch. Both branches can be
incorporated as donors.
Tunneling of the Sural Nerve Graft to the Affected Cornea
■ Once the supratrochlear or supraorbital nerve has been identified, the
contralateral incision over the affected eye is deepened to the level of the
subcutaneous tissue.
■ A fine hemostat is used to bluntly dissect a subcutaneous plane between the
two incisions to provide a passage for the sural nerve graft.
■ With the distal portion of the hemostat through the incision on the affected
eyelid, the distal end of the sural nerve graft is grasped and pulled through
the subcutaneous pocket so that the nerve graft is traversing the incisions,
reversing the direction of the nerve graft for coaptation.
■ A superonasal perilimbal incision is made in the conjunctiva using blunt
scissors, and a small pocket is made in the potential space between the sclera
and Tenon capsule (TECH FIG 2A).

TECH FIG 1 • A. We palpate the supratrochlear notch
to mark two incisions over the ipsilateral and
contralateral supratrochlear nerves. As most patients
with corneal anesthesia have hemifacial sensory
abnormalities, we most frequently use the
contralateral supratrochlear nerve as a donor sensory
nerve for corneal neurotization. B. The supratrochlear
nerve is identified below the level of the frontalis
muscle at the location of the supratrochlear notch and
is secured with vessel loop.
TECH FIG 2 • A. Once the sural nerve graft has been
tunneled to the ipsilateral supraorbital incision, an
incision is made into the perilimbal conjunctiva and a
potential space is expanded between the conjunctiva
and sclera. This permits the Wright needle to be
passed from the perilimbal conjunctiva to the

ipsilateral supraorbital skin incision. B. The Wright
needle is passed from the perilimbal conjunctival
incision into the ipsilateral supraorbital skin incision.
The sural nerve graft is then placed within the eye of
the needle, tunneling the sural nerve graft into the
orbit as the needle is withdrawn through the perilimbal
conjunctival incision.
■ A Wright needle (curved ophthalmologic trocar with eyelet) is then used to
pass the sural nerve graft from the supraorbital incision over the affected eye,
below the conjunctiva and Tenon capsule, to be delivered to the perilimbal
incision (TECH FIG 2B).
Dissection of the Sural Nerve Fascicles
■ Under the operating microscope and on the surface of the affected eye, the
sural nerve graft is divided into separate fascicles so that they may be evenly
distributed around the eye to reinnervate the cornea (TECH FIG 3A).
■ We aim to produce three to four fascicles from the sural nerve graft;
however, in many patients, we have used only two fascicles, with good
results.
■ The fascicles are then distributed around the cornea to evenly distribute the
location of regenerating axons into the cornea (TECH FIG 3B).
Tunneling of Fascicles Into the Corneal Stroma
■ Separate perilimbal incisions are then made for each of the fascicles, and
again a small perilimbal pocket is made between the sclera and Tenon
capsule. Each fascicle in then tunneled below the conjuctiva into these
incisions to lie adjacent to the cornea.
■ A corneal scalpel blade is used to make a small scleral tunnel incision 1.0 to
1.5 mm from the limbus and approximately 1.5 mm wide (about twice the
width of the fascicle) into the clear peripheral cornea so that each fascicle can
be tunneled directly into the cornea (TECH FIG 4A).
■ The nerve graft fascicle is then gently placed directly into the stromal pocket
(TECH FIG 4B), and 10-0 absorbable (Vicryl) stitch is placed through the
sclera and the epineurium of the fascicle to keep the fascicle in place.
■ This is then done for each of the fascicles individually.

■ Each of the perilimbal conjunctival incisions are then closed with 10-0
absorbable stitch (TECH FIG 4C) being careful to avoid any exposure of the
fascicles.
TECH FIG 3 • A. Once overlaying the cornea, the
sural nerve graft is dissected into separate fascicles.
B. Once divided into separate fascicles, these are
distributed evenly around the cornea. In our
experience, there are a variable number of fascicles in
the sural nerve. We aim to have at least two fascicles,
with a maximum of four when available. Each fascicle
is then tunneled below the level of the conjunctiva
through perilimbal incisions to surround the eye.

TECH FIG 4 • A. Through each perilimbal incision, an
ophthalmic scalpel is used to make a pocket within the
corneal stroma. B. Once the stromal pocket has been
made, the fascicle is tunneled directly into the corneal
stroma using forceps. In the image, the distal portion
of the sural nerve graft can be seen protruding into the
corneal stroma. Each fascicle is sutured into place
proximal to the stromal pocket using 10-0 absorbable
sutures. C. After the sural nerve fascicle has been
tunneled into the corneal stroma and secured to the
sclera with a 10-0 stitch, the perilimbal conjunctival
incision is sutured closed.
■ A limbal incision and tunneling the nerve fascicles directly into the corneal
stroma may significantly improve nerve regrowth as the limbus may act as a
barrier to corneal nerve ingrowth.
■ The affected eye is then closed with a temporary central tarsorrhaphy suture

to protect the corneal surface after surgery, and this is left in place for 1 to 2
weeks.
■ If a permanent lateral tarsorrhaphy has not been performed previously, it can
be done at this step.
Nerve Coaptation
■ As the final step, the distal portion of the sural nerve graft is coapted to the
supratrochlear nerve in an end-to-end fashion with 10-0 nylon suture or fibrin
glue (TECH FIG 5) or both glue and sutures, depending on surgeon
preference.
■ The supraorbital incisions are closed with a 6-0 subcuticular Monocryl
stitch.
TECH FIG 5 • Once all conjunctival incisions have
been closed, the distal portion of the sural nerve graft
is coapted to the proximal stump of the transected
supratrochlear nerve. We have also done side-to-end
repair; however, we prefer this technique as we have
found the donor site morbidity to be minimal and end-
to-end repair recruits a greater number of donor
sensory axons.

PEARLS AND PITFALLS
Preoperative
considerations
■ A thorough sensory examination is necessary prior to the
operation to identify normal functioning donor nerves.
Acquired vs
congenital
cases
■ Acquired cases usually have straightforward neuroanatomy.
■ Congenital cases often have aberrant anatomy.
■ These cases may have complete absence of any supratrochlear
or supraorbital nerves despite intact glabellar sensation.
■ We have also used the ipsilateral infraorbital nerve to
reconstruct corneal sensation.
Nerve harvest
■ The tibial contribution to sural nerve is usually sufficient length.
This can be harvested through a popliteal incision and a small
counter incision in the midcalf.
Postoperative
considerations
■ Keep postoperative patients out of sports or vigorous activities
for 6 weeks.
■ Patients may experience pain once innervation occurs; this is
actually a positive sign, but they should be warned in advance.
POSTOPERATIVE CARE
■ Patients should be under the care of an ophthalmologist pre-, intra-, and
postoperatively.
■ The intraoperative tarsorrhaphy suture is left in place for 1 week.
■ Patients are provided with postoperative topical medication:
■ Topical tobramycin and dexamethasone ointment until the tarsorrhaphy is
removed
■ Topical moxifloxacin and prednisolone eyedrops
■ Preservative-free lubricating eyedrops
■ Sensory and vision outcomes are monitored regularly by the ophthalmologist.
OUTCOMES
■ To date, there are have been only two series published describing outcomes in
patients with corneal neurotization by Terzis22 and Borschel23,24 and a case
report by Samii.
■ In Terzis’ series, all 6 patients were followed for an average of 16.3 ± 2.42
years and demonstrated significant improvements in corneal sensibility with no
further deterioration of visual acuity or overall corneal health.22

■ In Borschel and Ali’s series, using the described surgical technique for corneal
neurotization, all patients demonstrated significant improvements in corneal
sensation with some patients developing sensation indistinguishable from
normal with Cochet-Bonnet esthesiometry; however, follow-up had not been
carried out far enough to definitively determine vision outcomes.23
COMPLICATIONS
■ Axon regrowth through the nerve graft and into the cornea may take several
months with this sural nerve grafting technique.
■ Using the contralateral supratrochlear nerve results in minimal sensory loss on
the donor side.
■ Inability to regain protective sensation after corneal neurotization may be
caused by unrecognized insufficiency of the donor nerve.
■ Loss of sensation on the lateral ankle and foot after sural nerve harvest is of
minimal functional consequence.
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2. Rozsa AJ, Beuerman RW. Density and organization of free nerve endings in
the corneal epithelium of the rabbit. Pain. 1982;14:105-120.
3. Müller LJ, Marfurt CF, Kruse F, Tervo TMT. Corneal nerves: structure,
contents and function. Exp Eye Res. 2003;76(5):521-542.
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sensitivity to noxious stimuli in trkA knockout mice. Eur J Neurosci.
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immunocytochemical characteristics of trigeminal ganglion neurons projecting
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trigeminal ganglion neurons that innervate the mouse cornea: relevance to
intercellular spread of herpes simplex virus. J Comp Neurol. 1993;327:133-
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7. Al-Aqaba MA, Fares U, Suleman H, et al. Architecture and distribution of
human corneal nerves. Br J Ophthalmol. 2010;94(6):784-789.
8. Marfurt CF, Cox J, Deek S, Dvorscak L. Anatomy of the human corneal
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9. Lambley RG, Pereyra-Muñoz N, Parulekar M, et al. Structural and functional
outcomes of anaesthetic cornea in children. Br J Ophthalmol. 2014:1-7.
10. Ramaesh K, Stokes J, Henry E, et al. Congenital corneal anesthesia. Surv
Ophthalmol. 2007;52(1):50-60.
11. Rosenberg M. Congenital trigeminal anaesthesia. Brain. 1984;107:
1073-1082.
12. Alper M. The anesthetic eye: an investigation of changes in the anterior
ocular segment of the monkey caused by interrupting the trigeminal nerve at
various levels along its course. Trans Am Ophthalmol Soc. 1975;73:313-365.
13. Beuerman R, Schimmelpfennig B. Sensory denervation of the rabbit cornea
affects epithelial properties. Exp Neurol. 1980;69:
196-201.
14. Cavanagh H, Colley A. The molecular basis of neurotrophic keratitis. Acta
Ophthalmol. 1989;192:115-134.
15. Sigelman S, Friedenwald J. Mitotic and wound-healing activities of the
corneal epithelium. Arch Ophthalmol. 1954;52:46-57.
16. Goins KM. New insights into the diagnosis and treatment of neurotrophic
keratopathy. Ocul Surf. 2005;3(2):96-110.
17. Sacchetti M, Lambiase A. Diagnosis and management of neurotrophic
keratitis. Clin Ophthalmol. 2014;8:571-579.
18. Chikama T, Fukuda K, Morishige N, Nishida T. Treatment of neurotrophic
keratopathy with substance-p-derived peptide (FGLM) and insulin-like growth
factor I. Lancet. 1998;351:1783-1788.
19. Brown SM, Lamberts DW, Reid TW, et al. Neurotrophic and anhidrotic
keratopathy treated with substance P and insulinlike growth factor 1. Arch
Ophthalmol. 1997;115:926-927.
20. Bonini S, Lambiase A, Rama P, et al. Tropical treatment with nerve growth
factor for neurotrophic keratitis. Ophthalmology. 2000;107(7):1347-1352.
21. Lambiase A, Rama P, Bonini S, Camprioglio G, Aloe L. Topical treatment
with nerve growth factor for corneal neurotrophic ulcers. N Engl J Med.
1998;338(17):1174-1180.
22. Terzis JK, Dryer MM, Bodner BI. Corneal neurotization: a novel solution to
neurotrophic keratopathy. Plast Reconstr Surg. 2009;123(1):112-120.
23. Elbaz U, Bains R, Zuker RM, et al. Restoration of corneal sensation with
regional nerve transfers and nerve grafts: a new approach to a difficult
problem. JAMA Ophthalmol. 2014;132(11):1289-1295.
24. Bains R, Elbaz U, Zuker R, et al. Corneal neurotization from the

supratrochlear nerve with sural nerve grafts: a minimally-invasive approach.
Plast Reconstr Surg. 2015;135(2):397e-400e.

54
CHAPTER
Section XIII: Brachial
Plexus (Obstetrical Injury)
Primary Treatment of
Neonatal Brachial Plexus
Palsy
Bryce R. Bell, Ji-Geng Yan, and Hani Matloub
DEFINITION
■ Injury to the nerves supplying the upper extremity (C5-T1) during the birth
process
■ Epidemiology1
■ Incidence can vary greatly by institution.
■ The most recent nationwide study shows 1.51 per 1000 live births in the
USA.
■ Risk factors1–3
■ Shoulder dystocia
■ Macrosomia (greater than 4–4.5 kg)
■ Instrumented delivery
■ Prior delivery with brachial plexus injury
■ Prolonged labor resulting in hypotonia
■ Tachysystole during labor
■ Use of oxytocin
■ Studies have consistently shown that more than half of patients with neonatal
brachial plexus palsy (NBPP) have no identifiable risk factor.
ANATOMY

■ Normally, the brachial plexus has contributions from C5 to T1.
■ Can have prefixed or postfixed cords with contributions from C4 (22%) and
T2 (1%), respectively
■ Roots combine to form upper (C5/C6), middle (C7), and lower trunks (C8/T1).
■ Near the level of the clavicle, these trunks give off anterior and posterior
divisions to form lateral, medial, and posterior cords, so named for their
relation to the axillary artery. The lateral cord is formed from the confluence of
the anterior divisions of the upper and middle trunks. The posterior cord is
formed from the posterior divisions of all three trunks. Finally, the medial cord
consists of only the anterior division of the lower trunk.
■ Cords then divide into terminal branches (musculocutaneous, axillary, radial,
median, and ulnar).
■ Smaller branches originate from various levels in the brachial plexus and are
important in localizing the level of injury by clinical examination (FIG 1).
■ The sympathetic chain runs along the ventral aspect of the exiting roots and is
often disrupted in root avulsions from the spinal cord. This accounts for the
findings seen in Horner syndrome.
PATHOGENESIS
■ Mechanism of injury
■ Most commonly a downward force on the shoulder causes deviation of the
neck away from the involved extremity. This typically involves at least the
C5-C6 roots but can result in complete plexus injury.
■ More rarely, injury can occur due to extreme cranial traction on the extremity
with neck extension during breech delivery. These injuries often involve the
lower roots.
■ Traditionally, injury was thought to be caused by traction during delivery by
the obstetrician, by either manual or instrumented delivery.
■ However, given that more than half of children with brachial plexus injuries
do not have an identifiable risk factor, some debate exists on the presence of
an intrauterine mechanism of injury that is more difficult to identify. One
study estimated uterine contractions exert up to 9 times greater force on the
shoulder than that applied by the obstetrician.4
■ In addition, Walsh et al. showed no significant decrease in incidence of NBPP
despite structured training on management of shoulder dystocia and a rising
cesarean section rate.5
■ These injuries result in varying degrees of weakness in the ipsilateral

extremity, ranging from subtle weakness to flaccid paralysis.
■ Classifications of Seddon and Sunderland
■ Seddon divided nerve injuries into three categories: neurapraxia,
axonotmesis, and neurotmesis.6
FIG 1 • The most common anatomy of the brachial
plexus. The branching of the brachial plexus can be
highly variable, and a thorough understanding of the
most common variants is crucial prior to proceeding
with brachial plexus exploration.
■ Neurapraxic injuries have a transient loss of conduction, but do not undergo
wallerian degeneration. In axonotmesis, the nerve is still externally in
continuity but undergoes wallerian degeneration due to axonal disruption.
Neurotmesis indicates a complete division of a nerve.
■ Sunderland classified neurapraxia as type I and neurotmesis as type V. The
axonotmesis category is divided into three separate categories, types II to IV,
based on degree of internal injury short of complete division of the nerve.7
MacKinnon and Dellon later added a type VI injury, indicating multiple

degrees of injury in a single cross-sectional area of a nerve.8 This has been
termed a neuroma-in-continuity.
■ Wallerian degeneration occurs in axonotmetic and neurotmetic lesions due to
axonal disruption. While there is some chance of recovery in axonotmetic
lesions depending on the degree of internal injury, neurotmetic lesions will
not recover without surgical repair or grafting.
■ Contractures
■ Denervation leads to a progressive joint contracture due to muscle paralysis.
This joint contracture was generally believed to be caused by muscle
imbalance and fibrosis of denervated muscle groups. However, animal studies
have shown that muscle contracture precedes fibrosis, indicating a separate,
yet to be determined mechanism.9
■ Two types of joint contractures are seen in NBPP patients. The first is due to
overpowering of affected muscles by their antagonists, as is seen with the
internal rotation contracture at the shoulder in Erb palsy. The second is due to
muscle contracture and shortening, as seen in the glenohumeral abduction
contracture caused by the paralyzed deltoid or the elbow flexion contracture
caused by the brachialis in Erb palsy.
■ Global shoulder dysfunction and glenohumeral deformity develop as early as
3 months due to unbalanced forces on the shoulder and may require open or
arthroscopic reduction and tendon transfers for treatment.
■ It has also been shown that each segment of the upper extremity exhibits
decreased length and girth compared to the unaffected extremity.10
NATURAL HISTORY
■ In the past, full recovery had been reported to be as high as 95.7%.11 However,
more recent reports claim less optimistic spontaneous recovery rates in the 60%
to 70% range.12,13
■ Upon closer analysis, it is clear that location and severity of injury, as well as
the degree of spontaneous recovery by 3 to 6 months, can all dramatically
change the prognosis for a given patient. Assessing these factors is essential to
recommending a plan of care to the patient’s parents.
■ In patients with only mild weakness and rapid recovery within weeks,
complete neurologic recovery is highly likely without surgical intervention.
■ However, in patients with a flaccid upper extremity and Horner syndrome
(indicating a complete brachial plexus injury with avulsion), acceptable
recovery is extremely unlikely, and early surgical intervention at about 3

months is recommended. Even in the case where there is some degree of
proximal muscle improvement, if the hand is still paralyzed at 3 months, one
should proceed with surgical intervention to reinnervate the hand, as these
patients are unlikely to recover meaningful hand function on their own.
■ The remainder of neonatal brachial plexus patients fall between these two
extremes, and the decision on the appropriate timing for intervention, if any, is
still controversial.
PATIENT HISTORY AND PHYSICAL FINDINGS
■ History should include a detailed maternal gestational history as well as
patient birth history. The physician should seek specific information on the
course of delivery, shoulder dystocia, instrumented delivery, respiratory
distress or signs of hypoxia, and Apgar scores. This information can be helpful
in ruling out other causes of apparent limb weakness or paralysis (ie, cerebral
palsy, infection, fracture of the involved limb).
■ Careful, systematic examination is crucial for making treatment decisions and
comparisons over time. Given the importance of examination over time and the
negative effects of delayed treatment, early referral to a multidisciplinary
brachial plexus clinic is recommended. This will not only facilitate early
surgical intervention when necessary but also ensure that patients receive
prompt physical and occupational therapy to mitigate joint contracture
formation while awaiting recovery.
■ Physical examination should be performed with the child naked from the waist
up to assess the entire upper extremity as well as the neck, chest, back, scapula,
and abdomen. In the infant, physical examination relies heavily on observance
of limb posture, spontaneous motion, neonatal reflexes, and passive motion.
■ Certain postures have traditionally been associated with different levels of
injury. The “waiter’s tip” posture describes a patient with the shoulder
internally rotated, elbow extended, and wrist flexed. This posture would be
suggestive of an upper plexus injury. Inversely, a patient with a lower plexus
injury may have near normal shoulder and elbow function with a flaccid hand.
A totally flaccid extremity indicates a complete brachial plexus injury.
■ Horner syndrome describes a patient with ipsilateral ptosis, meiosis, and
anhidrosis. This is indicative of a preganglionic avulsion from the spinal cord.
■ There are many assessment tools and classification systems that can help
synthesize information from the physical examination and assist in treatment
decision-making. The most commonly used scores include the modified Mallet

scale, the Active Movement Scale, and the Toronto Test Score. All three of
these scores have been assessed for inter- and intrarater reliability.
■ The modified Mallet scale is a widely used measure of global shoulder
function and does not grade specific muscles. It requires that the patient is
mature enough to follow directions.
■ The Active Movement Scale (AMS) is a detailed scoring of 15 different
movements on a scale of 1 to 7. It was developed to quantify motor function in
infants with NBPP and evaluate recovery over time. It can be used as early as 2
to 3 weeks of age by eliciting neonatal reflexes to assess specific joint
movements.15
■ The Toronto Test Score was developed to help predict recovery in children
with NBPP. It can be used in young children who are unable to follow
directions and tests five specific motions: elbow flexion, elbow extension,
wrist extension, thumb extension, and finger extension.14
IMAGING AND OTHER DIAGNOSTIC STUDIES
■ Although the decision to proceed with primary nerve surgery for NBPP is a
clinical one, further diagnostic testing can provide useful information in
development of a surgical plan.
■ Electrodiagnostic testing can be useful in determining preganglionic vs
postganglionic lesions because avulsions will show normal sensory nerve
action potential with no motor nerve conduction at the same level. However,
these studies tend to overestimate the degree of recovery in NBPP and thus are
not routinely used in surgical decision-making.
■ Computed tomography (CT) myelography can also be useful in determining
the presence of root avulsions preoperatively. One study showed 98%
specificity, but only 37% sensitivity for CT myelography in diagnosing root
avulsions if no rootlets are seen traversing the pseudomeningocele.16
■ Another study compared CT myelography to MR myelography and found
similar results for CT myelography to prior studies. However, MR
myelography on a 3T magnet showed equivalent sensitivity and specificity
without the need for lumbar puncture, intrathecal contrast injection, or ionizing
radiation. Therefore, with improvements in technology, many now favor MR
over CT myelography.17
■ Other imaging modalities that some find useful are ultrasound to assess
diaphragmatic motion and chest radiography to look for an elevated
hemidiaphragm. Abnormal findings would indicate phrenic nerve injury. This

is particularly important if one is considering using the phrenic or intercostal
nerves for plexus reconstruction.
DIFFERENTIAL DIAGNOSIS
■ Spinal cord injury
■ Pseudoparalysis
■ Septic joint
■ Upper extremity fracture
■ Cerebral palsy
NONOPERATIVE MANAGEMENT
■ Patients should be referred early to an occupational therapist with experience
in neonatal brachial plexus injuries. Ideally, this therapist will see the patient at
the same time as the surgeon to facilitate communication.
■ Therapy should focus stretching and range of motion of the entire upper
extremity to prevent contractures and maladaptive motions. It is particularly
important to stabilize the scapula during shoulder range of motion and
stretching to make sure motion is truly glenohumeral and not scapulothoracic.
SURGICAL MANAGEMENT
■ The decision to proceed with microsurgical repair or reconstruction of the
brachial plexus is perhaps the most controversial topic in management of
neonatal brachial plexus injuries.
■ As discussed earlier, most surgeons agree that infants with a flaccid extremity,
Horner syndrome, or other signs of a preganglionic avulsion warrant early
exploration and microsurgical intervention.
■ Gilbert and Tassin popularized the absence of biceps function at 3 months as
an indication to proceed with microsurgery.3 However, another study showed
that when biceps function alone was used in decision-making, it would have
incorrectly predicted recovery in 12.8% of cases.14
■ The Hospital for Sick Children reports using AMS for initial evaluation of
infants with NBPP. At 3 months, a conversion is made for scores of elbow
flexion and elbow, wrist, thumb, and finger extension. The converted scores are
then summed. If the score is above 3.5, then observation is continued and the
patient re-evaluated every 3 months for continued improvement. If the patient
fails to improve at each visit or fails the “cookie test” at 9 months, then
microsurgery is scheduled.18

■ After assessing the outcomes of patients managed by observation,
microsurgery, and/or secondary orthopedic procedures (tendon transfer or
external rotation osteotomy), Waters concluded that he would operate on
infants with no return of biceps function by 5 months or a flail arm and Horner
syndrome at 3 months.19
■ We prefer to use the absence of any biceps function at 4 months as a trigger to
proceed with surgery, re-evaluating monthly for continued improvement in
those with some biceps function present at 4 months. Our center has performed
surgery at up to a year for those that present late to our clinic for initial
evaluation without biceps function. In these cases, we are likely to perform a
bypass graft around the neuroma rather than neuroma resection and grafting, to
avoid resecting any regenerated axons.
PREOPERATIVE PLANNING
■ Once the clinical decision is made to proceed with surgery, develop a carefully
considered operative plan that incorporates information from physical
examination, imaging, and electrodiagnostic testing, if obtained.
■ Review the results of the physical examination and imaging to estimate the
number of roots involved and if they are ruptures or avulsions. The former are
often amenable to neuroma resection and grafting, whereas the latter require
neurotization from other levels or extraplexal nerves. If several levels are
involved, prepare for transfer of nerves from outside the plexus to innervate
critical targets for upper extremity function. This may require further workup
with diaphragmatic ultrasound or chest radiographs to determine if the phrenic
nerve or intercostal nerves are a suitable option for extraplexal neurotization.
■ Consider what portion of the plexus is injured in a proximal to distal direction.
Though most injuries are supraclavicular, more distal involvement may require
a clavicular osteotomy and/or extension of the incision to expose the
deltopectoral interval.
■ In the case that the entire plexus is involved, the lower roots are usually
avulsed, and options are limited for reinnervation. Although priority is usually
given to elbow flexion and shoulder stability in adults, in NBPP, some
advocate that priority should be given to grafting nerve roots supplying the
hand because it is a shorter distance to regenerate than in adults, a greater
capacity for healing, and more neural plasticity in the brain. In addition, there
are proven extraplexal nerve transfer options for shoulder and elbow function.
■ Failure to plan for all potential scenarios and their solutions not only prolongs

surgical time but may compromise the ultimate outcome for the patient if
inappropriate decisions are made intraoperatively.
■ The surgeon should request avoidance of muscle paralysis after induction of
anesthesia to allow for assessment of signal transmission across neuromas via
nerve stimulation.
■ In some centers, pathology service is consulted to perform fresh frozen
specimens for evaluation of neuromas to confirm resection to healthy axons
before grafting.
■ Neurology may be consulted for intraoperative evaluation of somatosensory
evoked potentials (SSEPs). This can be extremely helpful when trying to
distinguish between an intact root, an intraforaminal rupture, and an avulsion
from the spinal cord. However, this requires special training on the part of the
interpreting neurologist and is only available in a limited number of centers.
Positioning
■ Some centers begin with the patient positioned in the prone position and
perform bilateral sural nerve harvest prior to exploration. We prefer to begin in
the supine position and perform the brachial plexus exploration prior to
harvest, as this may avoid unnecessary nerve harvest if bilateral sural nerve
grafts are not needed.
■ For plexus exploration and reconstruction, the patient should be positioned
supine with a small, transversely oriented roll placed at the level of the
scapulae to extend the neck and to rotate to the contralateral side of the injury
by improving access to the injured plexus.
■ We also recommend placing the patient’s head at the most proximal extent of
the bed and the ipsilateral shoulder near the edge of the bed to improve
positioning and access for the surgeon and assistants (FIG 2).
■ It is crucial to assure that all bony prominences are well padded, as the
procedure can last up to 12 hours. A Foley catheter with a temperature probe is
also placed for urine output monitoring, fluid management, and avoidance of
hypothermia.
■ The patient should be prepped and draped from the level of the mandible
proximally to just below the nipple on the ipsilateral chest and the ipsilateral
extremity draped free (FIG 3).
■ If considering use of the contralateral C7 nerve root, it will be necessary to
prep and drape the contralateral chest and neck as well. In addition, both legs

should have a tourniquet placed on the thigh and be prepped and draped for a
possible sural nerve harvest.
FIG 2 • The patient is positioned with the head at the
most proximal extent of the bed and the ipsilateral
shoulder near the edge of the bed to improve
positioning and access for the surgeon and assistants.
A transverse roll should be placed posteriorly at the
level of the scapulae to allow neck extension and
rotation away from the injured side.
Approach
■ Although some surgeons use a straight incision paralleling the upper border of
the clavicle for exposure, we prefer the use of an L-shaped incision.
■ The proximal limb follows the posterior border of the sternocleidomastoid
(SCM) muscle, and the transverse limb follows the superior border of the
clavicle.
■ We believe this improves access to the neural foramina to assess for proximal
rupture vs avulsion from the spinal cord during initial exploration or end-to-
side neurotization into the phrenic nerve, if necessary.

FIG 3 • The patient is prepped and draped from the
level of the mandible proximally to just below the nipple
on the ipsilateral chest, with the ipsilateral arm draped
free. The incision is marked along the posterior border
of the sternocleidomastoid (SCM) with the transverse
limb following the superior border of the clavicle.
T E C H N I Q U E S
■ Exposure
■ The expected incision should be marked out clearly and hashed for correct
closure at the conclusion of the case (see FIG 3). Formerly, our center
injected the line of the incision with epinephrine diluted 1 to 400 000 to
minimize blood loss during initial dissection. However, we have found that
with careful dissection using electrocautery, epinephrine infusion is not
necessary and eliminates a potential source of error in appropriate dilution.
■ Dissection is taken down through the platysma with meticulous care to
coagulate superficial vessels, attempting to minimize blood loss during the
case. The flap is raised in the plane just below the platysma and reflected
superolaterally to expose the posterior triangle. This is tied back with suture
for retraction throughout the case.

■ At this point, it may be necessary to reflect the clavicular head of the SCM
and ligate the nearby external jugular vein to improve exposure of the
anterior and middle scalene muscles and the more proximal nerve roots. The
clavicular head of the SCM should be tagged and repaired at the conclusion
of the case.
■ Moving laterally, the omohyoid is either divided at its tendinous portion or
tagged and retracted. The omohyoid is a consistent marker for the level of the
suprascapular notch.
■ During this exposure, the branches of the cervical plexus extending across
the clavicle to the upper chest will be encountered and divided. With careful
dissection, these can be traced proximally to identify the C4 root and then
excised and used as additional nerve graft.
■ There will be a fat pad at the level deep to the omohyoid that should be
released from the clavicle, tagged, and reflected superolaterally. This should
be repaired back to the clavicle during closure.
■ Additionally, the transverse cervical vessels will cross the surgical field and
may need to be ligated and cut to facilitate access to the supraclavicular
brachial plexus.
■ After this, the upper and middle trunks are often visible exiting between the
anterior and middle scalene muscles. The junction of the C5 and C6 roots is
the most common site for neuroma formation and is often visible now
(TECH FIG 1A).
■ Identify the phrenic nerve running in a cranial-to-caudal direction along the
lateral border of the anterior scalene, and trace this proximally to its
contribution from the C4 nerve root. Frequently the phrenic nerve gives off a
contribution to the C5 nerve root. The identity of the phrenic nerve can be
confirmed using a nerve stimulator and watching for contraction of the
diaphragm. One should notify the anesthesia team to hold respiration during
phrenic nerve stimulation to avoid confusion.
■ This should give two markers confirming the levels of the brachial plexus. In
many cases, the phrenic nerve is entrapped in scar tissue as it passes over the
involved plexus, and care should be taken not to injure or excise it during
dissection or neuroma resection.
■ Often the anterior and middle scalene muscles are also included in the scar
around the brachial plexus, and careful dissection is required to separate them
and adequately expose the roots and the neural foramina (TECH FIG 1B).

■ Once the levels have been appropriately identified, begin dissecting the C5
nerve root proximally to determine continuity all the way to the spinal cord.
The branch to the long thoracic nerve should be identified during dissection
of C5-C7 and protected initially. However, some or all of these branches may
need to be sacrificed later during neuroma resection and grafting in the case
of very proximal injuries.
■ Carry out the same dissection proximally for C6-T1, inspecting closely for
intraforaminal rupture or avulsion from the spinal cord. Again, the scalene
muscles must be dissected free from the neuroma to allow enough retraction
to inspect the more caudal C8 and T1 roots. In addition, caudal to C7, the
subclavian vein and clavicle will need to be retracted to improve exposure.
Take care to avoid violating the pleura just distal to T1.
■ If there is uncertainty regarding whether or not a preganglionic avulsion
exists, either a specimen can be sent for pathologic assessment to evaluate for
involvement of the dorsal root ganglion or SSEPs can be evaluated if
neurology service is available.
TECH FIG 1 • A. With the superficial dissection
complete, the upper and middle trunks are often
visible exiting between the anterior and middle
scalene muscles. The junction of the C5 and C6 roots
is the most common site for neuroma formation, and
the neuroma is often visible now. B. In more severely
scarred cases, accurate identification of individual
roots and determining which levels are intact,

ruptured, or avulsed is often difficult. A nerve
stimulator and intraoperative electrodiagnostic testing
can be helpful.
■ Next, dissect from proximal to distal along the cranial border of the C5 root
and upper trunk to locate the suprascapular nerve exiting posteriorly toward
the suprascapular notch. It is classically described as branching from the
upper trunk. However, recent cadaver studies have shown that it often
branches at or after the split of the anterior and posterior divisions of the
upper trunk (most often from the posterior division) and can even have
contributions from both the anterior and posterior divisions of the upper
trunk.20
■ Continue laterally to identify the anterior division of the upper trunk and
potentially the lateral pectoral nerve depending on its level of branching. This
is traditionally described as branching from the lateral cord. However, it most
often originates from the anterior division of the upper trunk rather than the
lateral cord proper.20
■ Next dissect from the C7 root distally to identify the middle trunk with its
anterior and posterior divisions. Continue this dissection distally until nerves
are free of neuroma.
■ Carry out the same dissection of the lower trunk distally to its anterior and
posterior divisions and, if necessary, to the medial cord. Identify its branches
as you dissect distally. It will be necessary to carefully dissect and retract the
clavicle and subclavian vein during this portion of the dissection.
■ Once all components of the plexus are identified, a nerve stimulator should
be used to determine which portions of the brachial plexus are transmitting
sufficient signals distally. Catalogue this information clearly and carefully to
avoid neglecting essential functions during reconstruction.
■ If infraclavicular access is also needed, this incision can be joined laterally
with a standard deltopectoral incision near the coracoid process.
■ Once the conjoined tendon is identified, the tendon can be tagged, cut, and
reflected to expose the lateral, posterior, and medial cords as well as their
terminal branches. This will be repaired at the conclusion of the case.
■ Neuroma Resection With Nerve Grafting

■ Although neurolysis alone of a neuroma-in-continuity was performed in the
past, it is no longer recommended due to inferior outcomes when compared
to neuroma resection and grafting.21 Therefore, if it is determined that there
is insufficient signal transmission across a neuroma, then resection and
grafting should be performed.
■ As mentioned in the prior section, careful dissection should be performed
proximal and distal to the site of injury to ensure that there is a complete
understanding of the injured structures. Do not presume a normal appearing
nerve root proximal to a neuroma is not avulsed based solely on visual
appearance. It is possible to have a two-level injury with avulsion from the
spinal cord and a neuroma distally.
■ Begin by sectioning the midportion of the neuroma and then at what appears
to be normal nerve proximally and distally. Many centers will tag these
specimens for orientation and send them for frozen section by the pathology
department to determine whether the proximal and distal extent of the
resection is free of fibrosis. Alternatively, perform an initial resection under
loupe magnification, and then under the operating microscope, inspect the
fascicular pattern to assess the adequacy of resection. Regardless, grafting to
healthy stumps proximally and distally is important to assure fibrosis does
not impair axon regeneration.
■ Next, assess the length of nerve graft necessary to bridge each defect. This
number will need to be multiplied by the number of cables necessary to
match the size of the nerves being grafted. After a determination of the total
length of graft needed, sural nerve harvest can be performed on one or both
legs. This can be done open or endoscopically depending on surgeon
preference and training. These techniques are described elsewhere in this
text.
■ If avulsions make grafting impossible at some levels, existing roots should
be preferentially grafted to the medial and then posterior cords to restore
hand function. Extraplexal nerve transfers can be used to reliably restore
shoulder and elbow function in these cases, as will be described below.
■ Coaptation of the nerves can be carried out using 9-0 or 10-0 nylon suture or
fibrin glue depending on surgeon preference (TECH FIG 2).

TECH FIG 2 • After confirming intact roots and
adequate neuroma resection, use the available graft
material to reinnervate as many priority targets as
possible.
■ Accessory (CN XI) to Suprascapular Nerve
Transfer
■ If you cannot graft directly to the suprascapular nerve from the upper trunk
or the C5/C6 root, either because of avulsion of the upper roots or the need to
divert those roots to other targets, external rotation of the shoulder can be
restored through transfer of CN XI.
■ Trace the transverse cervical artery posteriorly to where it enters the
trapezius muscle. Localize the accessory nerve using a nerve stimulator.
■ Next, trace the accessory nerve distally, past its innervation of the upper and
middle portions of the trapezius. Mobilize and then cut the nerve, making
sure there is sufficient length to reach the stump of the suprascapular nerve.
The stump of the suprascapular nerve should be prepared such that it is as
close as possible to its origin while still resecting to healthy axons.
■ Transpose the accessory nerve over to the suprascapular nerve stump, and
coapt the two using either nylon suture or fibrin glue, depending on surgeon
preference (TECH FIG 3).

TECH FIG 3 • The spinal accessory nerve is followed
caudally to the branch to lower trapezius, where it is
transected and rotated laterally to innervate the
suprascapular nerve.
■ Ulnar to Musculocutaneous Nerve Transfer
■ If the lower trunk and medial cord are intact and the patient has
demonstrated full ulnar nerve function preoperatively, a portion of the ulnar
nerve can be used to reanimate the biceps muscle.
■ Beginning at the inferior border of the pectoralis major tendon, make a
longitudinal incision on the medial arm about 8 cm long. Dissect down to the
biceps fascia, and separate it from coracobrachialis (TECH FIG 4A).
■ Identify the motor branch to the biceps, which is about 13 cm distal to the
acromion.22 Dissect this as far proximally into the musculocutaneous nerve
as possible, and then transect it for transfer to the ulnar nerve.

TECH FIG 4 • A. The incision is marked beginning at
the inferior border of the pectoralis major tendon and
extended distally along the medial border of the
biceps tendon. B. After isolating the fascicles of the
ulnar nerve to FCU as distally as possible, transect
the motor branch to biceps as proximally as possible
to assure there is no tension on the repair.
■ Dissect posteriorly to locate the median and then ulnar nerves. If there is any
confusion, a nerve stimulator can be used to differentiate the two.
■ Using the microscope, make an epineurotomy in the ulnar nerve, and harvest
two fascicles from the ulnar nerve. Use the nerve stimulator to confirm that
they contain motor fibers, and section them distally enough that they can be
transposed anteriorly to meet the biceps motor branch without tension.
■ Coapt the ulnar nerve fascicles to the biceps motor branch under the
microscope using either nylon suture or fibrin glue (TECH FIG 4B). Some
surgeons will perform a similar transfer of median fascicles to the FCR flexor
carpi radialis (FCR) to the motor branch to the brachialis in conjunction with
this procedure for added elbow flexion strength.
■ Intercostal to Musculocutaneous Nerve Transfer
■ If the ulnar nerve is not an option for restoration of elbow flexion, two to
three intercostal nerves can be transferred in a similar manner.
■ If you have already made the incision in the deltopectoral groove to expose
the infraclavicular plexus, then you can extend this inferomedially across the
chest. If not, then make an anterior axillary incision and extend your incision

inferomedially, perpendicular to the ribs down to the level just inferior to the
nipple. Retract the pectoralis major tendon superiorly to expose the
musculocutaneous nerve at its take off from the lateral cord. It should be
sectioned here and mobilized for later coaptation with the cables from the
intercostal nerves (TECH FIG 5A).
■ Limit resection of the fat and the associated lymph nodes in the axillary
fossa. However, dissect sufficiently to expose the involved structures and a
more direct line for coaptation of the intercostal and musculocutaneous
nerves.
■ Dissect down to the ribs. It may be necessary to release portions of the origin
of the pectoralis major and serratus anterior muscles. These should be tagged
for repair at the conclusion of the case.
■ Expose the second, third, and fourth ribs subperiosteally. The intercostal
nerves from roots T2 to T4 are inferior to their respective ribs after dissecting
through the external and internal intercostal muscles.
■ Carefully dissect the intercostal nerves anteriorly to the mammary line and
posteriorly to the point where they will be transposed toward the
musculocutaneous nerve.
■ Cut the intercostal nerves about 1 cm medial to the mammary line, and
carefully mobilize each nerve posteriorly such that there is sufficient length
to reach the musculocutaneous nerve in the axilla.
■ Coapt the intercostal nerves as a cable graft to the musculocutaneous nerve
as far distal as possible without tension or kinking, to minimize the distance
for regeneration. Coaptation can be performed with nylon suture or fibrin
glue, per surgeon preference (TECH FIG 5B).
■ Make sure that you there is no tension on the nerve coaptation site with the
arm in 90 degrees of abduction and 90 degrees of external rotation.

TECH FIG 5 • A. Mark out an anterior axillary incision,
and extend your incision inferomedially, perpendicular
to the ribs down to the level just inferior to the nipple.
B. Cut the intercostal nerves about 1 cm medial to the
mammary line, and carefully mobilize each nerve
posteriorly such that there is sufficient length to reach
the musculocutaneous nerve in the axilla. These will
be transferred to the musculocutaneous nerve as a
cable.
■ Radial to Axillary Nerve Transfer
■ For this procedure, we prefer the patient to be flipped prone with the
involved extremity prepped into the field and forearm either at the side or
resting on the lower back. As mentioned before, paralysis should be avoided
after induction of anesthesia to allow for use of the nerve stimulator.
■ Make a J-shaped incision from the lateral border of the scapula, following
the posterior border of the deltoid and extending down the posterior aspect of
the upper arm (TECH FIG 6A).
■ Dissect down to the fascia overlying the triceps and deltoid, watching for the
lateral cutaneous branch of the axillary nerve. This can be used to trace
proximally to the axillary nerve as it passes through the quadrangular space.

■ Transect the axillary nerve just proximal to the teres minor motor branch,
and transpose the nerve distally.
■ Find the radial nerve as it passes through the triangular space, and trace it as
distally to locate the motor branch the medial head of the triceps muscle.
Transect the nerve as distally as possible such that there is sufficient length
for tension-free repair.
■ Transpose the triceps nerve branch proximally. Remove the lateral cutaneous
nerve from the axillary nerve.
■ Under the microscope, coapt the triceps motor branch to the axillary stump
using nylon suture or fibrin glue. 8-0 or 9-0 suture is appropriate. Intercalary
grafts are usually not needed (TECH FIG 6B).
■ Abduct and rotate the arm to make sure that there is no tension on the repair
with shoulder motion.
TECH FIG 6 • A. A J-shaped incision is marked from
the lateral border of the scapula, following the
posterior border of the deltoid and extending down the
posterior aspect of the upper arm allowing exposure of
the axillary nerve in the quadrangular space and the
radial branch to the medial head of the triceps distally.
B,C. The branch to the medial head of the triceps is
transected as distally as possible and transposed
proximally to meet the motor branch of the deltoid. A
branch to the lateral or long head of the triceps could
also be used if better for coaptation. No branch has
been shown to be functionally superior to the others.

PEARLS AND PITFALLS
Preoperative
planning
■ Develop a complete understanding of the injury prior to surgery,
as well as a plan with multiple alternatives. This facilitates
efficiency during a long procedure and minimizes the chance of
overlooking important targets for reinnervation.
Exploration
■ It is crucial to fully explore each involved nerve root to its
insertion in the spinal cord, even if it is involved in neuroma
distally. Grafting from an avulsed nerve root assures complete
failure of the surgery at that level.
Neuroma
resection
■ Use available resources to confirm adequate neuroma resection
as grafting to a fibrotic nerve ending will limit or completely
block nerve regeneration.
Reconstruction
■ When there are limited intact nerve roots for grafting,
preferentially graft to the lower trunk and medial cord as there
are no proven extraplexal transfers for animating the hand but
multiple options for extraplexal transfers for the shoulder and
elbow.
Therapy
■ Appropriate therapy before and after surgery is at least as
important as a technically excellent repair or reconstruction.
Maintaining full passive motion of all involved joints gives the
recovering neuromuscular units the best chance to succeed. A
strong relationship with a trusted occupational therapist,
experienced in brachial plexus injury, is crucial for success.
POSTOPERATIVE CARE
■ Acute phase (0–4 weeks)
■ Place the patient in cervical collar and shoulder immobilization dressing for 3
weeks in order to protect repairs. We perform weekly dressing changes in our
therapy clinic to monitor the incisions as well as for skin breakdown in the
axilla and between the forearm and abdomen.
■ After 3 weeks of immobilization, begin gentle active and passive range-of-
motion exercises for the neck, scapula, shoulder, elbow, and hand. We
recommend two formal therapy visits per week initially.
■ Subacute phase (4 weeks to 2 years)

■ Monitor active and passive range of motion and return of muscle function.
■ Review and adjust home therapy program to emphasize the importance of
consistency in performing exercises at home and to address any developing
contractures early.
OUTCOMES
■ Outcomes in brachial plexus surgery can be highly variable depending on the
number of levels involved, the number of avulsion injuries, and the willingness
or ability of the patient’s family to participate in therapy.
■ In patients undergoing nerve transfer or grafting, it may take 6 to 9 months to
see any function in the involved muscle groups. Continued improvement can
be seen for 2 to 4 years as patients continue to make gains in strength and
coordination.
■ It should be emphasized repeatedly to parents that therapy must continue at
home until the child reaches skeletal maturity. Excellent early outcomes can be
lost if therapy is neglected for any period of time, especially during a growth
spurt.
COMPLICATIONS
■ Injury to major vessels of the neck and upper extremity
■ Failure to recover function after plexus reconstruction
■ Pneumothorax
■ Seroma formation
■ After axillary dissection during nerve transfers
■ With thoracic duct injury when exploring the left brachial plexus
REFERENCES
1. Foad SL, Mehlman CT, Ying J. The epidemiology of neonatal brachial plexus
palsy in the United States. J Bone Joint Surg Am. 2008; 90(6):1258-1264.
2. Abzug JM, Kozin SH. Evaluation and management of brachial plexus birth
palsy. Orthop Clin North Am. 2014;45(2):225-232.
3. Gilbert A, Brockman R, Carlioz H. Surgical treatment of brachial plexus birth
palsy. Clin Orthop Relat Res. 1991;(264):39-47.
4. Gonik B, Walker A, Grimm M. Mathematic modeling of forces associated
with shoulder dystocia: a comparison of endogenous and exogenous sources.
Am J Obstet Gynecol. 2000;182(3):689-691.
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injury: comparison of incidence and antecedents between 2 decades. Am J
Obstet Gynecol. 2011;204(4):324.e1-324.e6.
6. Seddon HJ. A classification of nerve injuries. Br Med J. 1942;2(4260):
237-239.
7. Sunderland S. A classification of peripheral nerve injuries producing loss of
function. Brain. 1951;74(4):491-516.
8. Mackinnon SE. New directions in peripheral nerve surgery. Ann Plast Surg.
1989;22(3):257-273.
9. Nikolaou S, Liangjun H, Tuttle LJ, et al. Contribution of denervated muscle to
contractures after neonatal brachial plexus injury: not just muscle fibrosis.
Muscle Nerve. 2014;49(3):398-404.
10. Bae DS, Ferretti M, Waters PM. Upper extremity size differences in brachial
plexus birth palsy. Hand (N Y). 2008;3(4):297-303.
11. Greenwald AG, Schute PC, Shiveley JL. Brachial plexus birth palsy: a 10-
year report on the incidence and prognosis. J Pediatr Orthop. 1984;4(6):689-
692.
12. Hoeksma AF, ter Steeg AM, Nelissen RGHH, et al. Neurological recovery in
obstetric brachial plexus injuries: an historical cohort study. Dev Med Child
Neurol. 2004;46(2):76-83.
13. Pondaag W, Malessy MJA, van Dijk JG, Thomeer RTWM. Natural history of
obstetric brachial plexus palsy: a systematic review. Dev Med Child Neurol.
2004;46(2):138-144.
14. Michelow BJ, Clarke HM, Curtis CG, et al. The natural history of obstetrical
brachial plexus palsy. Plast Reconstr Surg. 1994;93(4):675-680.
15. Curtis C, Stephens D, Clarke HM, Andrews D. The active movement scale:
an evaluative tool for infants with obstetrical brachial plexus palsy. J Hand
Surg [Am]. 2002;27(3):470-478.
16. Chow BC, Blaser S, Clarke HM. Predictive value of computed tomographic
myelography in obstetrical brachial plexus palsy. Plast Reconstr Surg.
2000;106(5):971-977.
17. Tse R, Nixon JN, Iyer RS, et al. The diagnostic value of CT myelography,
MR myelography, and both in neonatal brachial plexus palsy. AJNR Am J
Neuroradiol. 2014;35(7):1425-1432.
18. Clarke HM, Curtis CG. An approach to obstetrical brachial plexus injuries.
Hand Clin. 1995;11(4):563-580.
19. Waters PM. Comparison of the natural history, the outcome of microsurgical
repair, and the outcome of operative reconstruction in brachial plexus birth

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649-659.
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and lateral pectoral nerves within the brachial plexus. Plast Reconstr Surg.
2014;133(1):20e-27e.
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using a part of ulnar nerve for C5-C6 avulsion of the brachial plexus:
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237.

55
CHAPTER
Secondary Neonatal
Brachial Plexus Palsy
Reconstruction
Joshua M. Adkinson
DEFINITION
■ Neonatal brachial plexus palsy (NBPP) results from injury to any brachial
plexus nerve root (C5-T1) during a difficult delivery.1,2
■ Persistent paralysis and progressive spasticity, contractures, joint instability,
and bony deformities of the upper extremity may occur in children with
incomplete recovery of nerve function.
■ The type, severity, and manifestations of NBPP vary greatly between patients
and surgical options for treatment must be individualized.
ANATOMY
■ Most commonly, the C5C6 roots are involved (Erb palsy), leading to deficits of
shoulder abduction and external rotation (supraspinatus, infraspinatus, and
deltoid), elbow flexion (biceps brachii, brachialis), and forearm supination
(supinator).
■ C7 involvement causes paralysis of the subscapularis, teres major (TM),
clavicular head of the pectoralis major (PM), brachioradialis (BR), extensor
carpi radialis longus (ECRL) and brevis (ECRB), and possibly extensor carpi
ulnaris and extensor digitorum communis (EDC). This leads to the classic
“waiter tip” posture,3 with deficits of wrist and finger extension.
■ Rarely, the C8T1 roots alone are affected (Klumpke palsy), leading to
weakness/paralysis in the wrist/finger flexors and hand intrinsic muscles.
■ Complete plexus involvement (C5-T1) leads to a flail extremity.
PATHOGENESIS

■ Between 50% and 92% of patients with NBPP experience complete recovery
of function without primary nerve reconstruction.1,4–8 In those with persistent
deficits, the clinical findings will vary over time.
■ Secondary deformities are impacted by the severity of the initial nerve injury,
extent of muscle recovery, patient age at presentation, and previous treatments.
■ In addition to paresis/paralysis of affected muscles, co-contracture of
antagonistic muscles can occur in patients with partial recovery.9 This may lead
to contracture and/or joint deformity.
■ The most common posture in children with NBPP is internal rotation of the
shoulder, flexion of the elbow, supination of the forearm, and ulnar deviation of
the wrist, with variable involvement of the fingers.10 Many children also
develop a limb-length discrepancy.
PATIENT HISTORY AND PHYSICAL FINDINGS
■ The preoperative evaluation of children with secondary NBPP deformities
includes a detailed history, an assessment of functional limitations, and
measurements of active and passive range of motion.
■ Grading function
■ No grading systems are universally recommended for assessment of elbow,
forearm, wrist, and hand function in patients with NBPP.
■ Physical Examination
■ Function is observed, active and passive ranges of motion are documented,
and muscle strength is assessed with and without gravity.
■ Elbow
■ Co-contracture of the elbow flexors and extensors are assessed. Dislocation
of the radial head and proximal ulna are noted.
■ Forearm
■ Long-standing supination or pronation deformities may lead to fixed
contracture of the interosseous membrane (IOM). Continued growth can then
lead to bowing of the radius and ulna, dorsal dislocation of the distal ulna,
and/or posterior dislocation of the radial head.
■ Wrist
■ Ulnar deviation is common because of paralysis of the ECRL and ECRB.
■ Hand
■ Limited metacarpophalangeal (MCP) joint extension is common, as is thumb
instability.11

IMAGING
■ Anteroposterior and lateral radiographs of the elbow or wrist may be obtained
to evaluate for joint subluxation/dislocation or articular deformities (FIG 1).
NONOPERATIVE MANAGEMENT
■ All patients should undergo physical therapy, with the goal of muscle
strengthening and full passive range of motion of the elbow, forearm, wrist, and
fingers.
■ Orthoses are used to maintain anatomic joint alignment and to prevent
contracture.
■ Botox injection into spastic musculature is effective for temporary (3–6
months) muscle weakening.
SURGICAL MANAGEMENT
■ Surgical options include tendon transfers, arthrodeses, osteotomies,
muscle/tendon releases, and functioning muscle transfers.
■ Secondary reconstruction of the elbow, forearm, wrist, and hand is considered
in children older than 4 years with incomplete recovery of upper extremity
function after primary reconstruction or in those who present after the optimal
window for nerve reconstruction.10,12–15
FIG 1 • Right radial head dislocation (arrow) in long-