Phẫu Thuật Tạo Hình Grabb & Smith’s (Bản Cập Nhật – Kevin C. Chung)

Nerve Conduits
A prodigious amount of research has focused on the development of synthetic nerve guidance conduits
designed to facilitate axonal regeneration across segmental nerve gaps. An ideal nerve conduit needs to
be widely available, have low antigenicity, and be biocompatible. Currently commercially available
conduits are constructed from biocompatible materials such as collagen, polyglycolic acid (PGA), poly-
DL-lactide-co-caprolactone, polyvinyl alcohol, and N-fibroin (silk protein). 35 These materials have
varying degrees of permeability for diffusion of supportive nutrients while providing adequate structural
scaffolding for regenerating axons. The absorbable nature of these conduits limits the associated foreign
body reaction that can result in scar tissue encapsulation and subsequent inhibition of axonal growth. 36
The newest tissue-engineered conduits incorporate structural elements for delivery of molecular- or
cellular-based therapies to optimize regeneration potential. 37 Stem cells and Schwann cells seeded into
nerve conduits have demonstrated significantly better functional outcomes compared with empty
conduits. 38 Controlled release of regenerative neurotrophic factors (e.g., nerve growth factor [NGF],
brain-derived neurotrophic factor [BDNF], neurotrophin-3 [NT3], neurotrophin-4-5 [NT4-5] others) from
conduits has also been shown to be beneficial for axonal growth. 39 There is mounting evidence to support
synthetic nerve conduit reconstruction of short defects in sensory nerves. Specifically, these constructs
have been shown to support successful nerve regeneration across small diameter nerves with gaps up to
3 cm or with large diameter nerves with gaps less than 0.5 cm. In fact, all alternatives to autologous nerve
grafts, including decellularized allografts and tissue-engineered conduits, demonstrate similar efficacy in
reconstruction of sensory nerve defects of less than 3 cm. However, for motor defects or nerve defects that
span more than 3 cm, autologous nerve grafting is still considered the standard of care.
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Nerve Transfers
In proximal nerve defects, functional outcomes following nerve repair or reconstruction at the site of
injury are poor due to the extended length of time and distance until regenerating axons can be expected
to reach their distal targets. The effect of prolonged denervation results in target muscle fibrosis with loss
of motor end plates 40 and senescence of Schwann cells that normally provide trophic support to
regenerating axons. In these cases, nerve transfers can provide regenerating axons from a donor nerve to
the distal aspect of the injured nerve by considerably shorten the time until reinnervation of important
muscles and to preserve function. 41 When done properly, donor site morbidity is minimal and the
procedure can produce predictably good outcomes. 42,43
Nerve transfers are traditionally reserved for restoration of muscle function, but the technique has also
been used in the reconstruction of critical sensory nerves. The most common applications of motor nerve
transfers include the restoration of elbow flexion, shoulder abduction, ulnar-innervated intrinsic hand
function, forearm pronation, and radial nerve function. 44 For example, the thoracodorsal nerve
transferred to the musculocutaneous nerve can restore elbow flexion after brachial plexus injury. This
nerve transfer purposefully sacrifices the motor function to the latissimus dorsi muscle, for which action
can be compensated by other shoulder muscles, to power the more critical contraction of the biceps
brachii, brachialis, and coracobrachialis muscles. The choice of optimal donor nerve for motor transfer is
based on factors such as the quantity of motor axons, proximity to the target muscle, and synergy of
muscle function. 44 Motor fascicles that can be readily separated from a mixed nerve (e.g., the flexor carpi
ulnaris fascicle of the ulnar nerve) can also serve as ideal donor nerves. 44
Sensory nerve transfers are more frequently performed at the level of the distal forearm or palm to restore
critical digit sensation, such as the contact surfaces of the thumb and index finger. For sensory transfers,
suitable donor nerves should innervate noncritical sensory distribution, contain a large number of purely
sensory axons, and be located close in proximity to the target sensory end organs. If possible, the distal
end of a transferred sensory nerve can be coapted end-to-side to an adjacent sensory nerve for some
recovery of sensation in the donor territory. When an end-to-end repair is planned, the donor nerve is
ideally transected as distally as possible and the recipient nerve is transected as proximally as possible to
optimize a tension-free coaptation.
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Recovery
Functional outcomes following nerve repair and reconstruction depend on the degree of nerve injury,
level of injury, and time since injury, as well as number of patient and surgical factors. In 1990,
Sunderland summarized 40 years of clinical experience highlighting the principles of peripheral nerve
repair and expected outcomes 16 : early repairs are better than late; nerve coaptation is better than
interposing nerve grafts; and sharp transection injuries have better outcomes than crush or avulsion
injuries. Younger patients also have better prognosis and distal nerve repairs do better than proximal
repairs. Furthermore, pure sensory or pure motor nerve repairs do better than mixed nerve repairs. 16
After surgical intervention, functional recovery is monitored with serial physical examinations and
electrodiagnostic studies. The most widely used grading system for nerve recovery is the Medical
Research Council Grading System for Nerve Recovery. This system is grades sensory recovery from S0 to
S5 and motor recovery from M0 to M5 based on physical examination findings. 24 The greater the
numerical grade, the greater the functional recovery.
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Neuromas
Any peripheral nerve injury involving transection of axons is at risk for neuroma formation. 45 Neuromas
result from failure of the regenerative growth cone to reach peripheral targets. Sprouting axons that are
unable to reach the distal endoneurial tube will continue to elongate at the site of injury, forming a mass
of disorganized fibroneural tissue containing axons, connective tissue, and scar. 45 Neuromas can form at
the site of axonal disruption along the course of a peripheral nerve (i.e., neuroma-in-continuity) or at the
end of a transected peripheral nerve (i.e., terminal bulb or end neuromas). Neuromas signify the presence
of unsuccessful reinnervation and can often be associated with disabling neuropathic pain.
Efforts to prevent neuroma formation should be considered during management of any nerve injury.
Even small sensory nerves can produce debilitating neuroma pain after transection. Therefore, when
these minor nerves are identified during surgery, formal repair is recommended to prevent aberrant
axonal sprouting and subsequent neuroma formation. When a painful neuroma does develop, a course of
desensitization therapy is warranted as first-line treatment. When the pain is refractory to conservative
measures or if functional recovery is poor, surgical intervention is indicated. Surgery may entail
neurolysis or neuroma resection and interposition nerve graft reconstruction. 46 If the nerve is expendable
(e.g., a noncritical sensory nerve), neurectomy may be considered. Numerous methods have been
explored to prevent neuroma formation, yet there remains no standard for treatment or prevention.
Several surgical approaches utilizing epineurial closure, nerve transposition with muscle implantation,
and neurorrhaphy techniques have all been employed with inconsistent results. 47
Traditional neuroma prevention methods are all aimed at minimizing or masking aberrant nerve
regeneration. However, these methods do not seek to prevent neuroma formation but instead place the
anticipated recurrent neuroma in a less symptomatic location. Newer strategies for neuroma
management provide functional connections for regenerating axons and consequently prevent neuroma
formation. Both targeted muscle reinnervation 48 and regenerative peripheral nerve interface 49 techniques
provide distal physiologic targets (i.e., denervated muscle fibers) for regenerating axons for new
neuromuscular junctions. The number of axons from a regenerating nerve without a functional
connection is greatly reduced, and this results in significantly lower chances of neuroma formation.
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Conclusion
Significant advances in strategies for peripheral nerve repair and reconstruction have improved our
ability to optimize functional outcomes after various types of nerve injury. Accurate diagnosis of the level
and severity of nerve injury is paramount to the selection of the most appropriate treatment. Whenever
possible, direct end-to-end repair of a transected nerve is performed. Nerve autografts remain the
standard option for reconstruction of segmental nerve defects. Continuing research will elucidate the
roles of allografts and nerve conduits in nerve repair, and further development of techniques to diminish
symptomatic neuroma formation will greatly improve functional recovery following peripheral nerve
injury.
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ACKNOWLEDGMENT
This work was supported by the American Association of Plastic Surgeons Academic Scholar Program to
Theodore A. Kung. The content is solely the responsibility of the authors and does not necessarily
represent the official views of the American Association of Plastic Surgeons.
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Questions
1. 1. A 23-year-old man is brought to the emergency department 6 hours after sustaining a single
gunshot to the right upper arm. Physical examination shows an open wound and a high radial nerve
palsy. Which of the following is the most appropriate first step in management of potential nerve
injury?
a. Immediate surgical exploration and primary nerve repair if the nerve is lacerated
b. Immediate surgical exploration and repair with a nerve graft if the nerve is lacerated
c. Immediate surgical exploration, resection of devitalized nerve, and suture tagging of the nerve
ends for delayed repair
d. Observation with EMG 6 months after injury followed by exploration and repair if no return
of function
2. A 45-year-old woman is brought to the emergency department after a rollover motor vehicle
accident. Physical examination shows significant soft tissue loss and a median nerve injury at the
wrist. The patient is taken immediately back to the operating room where a 5 cm segmental nerve
gap is observed. Which of the following treatment options is most likely to provide the best long-
term functional outcome for this patient?
a. PGA conduit
b. Acellular allograft reconstruction
c. Collagen conduit reconstruction
d. Peripheral nerve autograft
e. Primary nerve repair
3. A 37-year-old woman presents to clinic with nerve compression of her right ulnar nerve at the
elbow. Both NCS and EMG are planned. Which of the following best indicates loss of motor axons?
a. Decreased distal motor latency
b. Presence of fibrillation potentials
c. Absent PSWs
d. Increased amplitudes
e. Increased conduction velocity
4. A 25-year-old woman presents to clinic 8 months after sustaining a stab wound to her right
forearm with complaints of weakness of grip strength in her right hand. Physical examination
reveals a Tinel sign present over the ulnar aspect of the mid-volar forearm adjacent to a well-healed
laceration. She is taken to the operating room where a neuroma-in-continuity is identified along her
right ulnar nerve. The neuroma is resected, and a 3 cm nerve gap remains. Which of the following is
the most appropriate next step in management?
a. Nerve reconstruction with synthetic nerve conduit
b. Mobilize nerve both proximally and distally and perform primary neurorrhaphy
c. Nerve reconstruction with LABC nerve graft
d. Sural nerve cable grafting
e. Perform tendon transfers to assist with grip
5. A 21-year-old man presents to the emergency department after sustaining a deep laceration to his
left elbow. Physical examination shows decreased function of the ulnar nerve, and the patient is
taken for urgent operative exploration. Following proximal and distal dissection, a 1 cm gap persists
between the proximal and distal nerve ends. Which of the following is the most appropriate next step
in management?
a. Nerve transfer
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b. Primary neurorrhaphy
c. PGA nerve conduit
d. Nerve transposition
e. Sural nerve grafting
6. A 27-year-old man comes to clinic after sustaining a brachial plexus injury in a motorcycle
accident. Nerve transfer to the biceps for restoration of elbow flexion is planned. Which of the
following fascicles or nerves is the most appropriate donor?
a. Distal spinal accessory nerve
b. Medial pectoral nerve
c. Thoracodorsal nerve
d. Palmaris longus fascicle of the median nerve
e. Flexor carpi ulnaris fascicle of the ulnar nerve
7. A 7-year-old girl is brought to the emergency department after sustaining an injury to the left
upper extremity, 3 cm proximal to the antecubital fossa. Which of the following factors is associated
with improved functional outcomes following peripheral nerve repair?
a. Proximal nerve injury
b. Young patient age
c. Increased time between injury and repair
d. Tension at nerve repair
e. Few suture strands used in nerve repair
1. Answer: c. In general, nerve injuries associated with open wounds should be explored and, if
appropriate, repaired early. For example, if the nerve injury resulted from a relatively clean
laceration or wound, it should be explored and repaired immediately. However, in the case of crush
or significant soft tissue injury, like in the case of a gunshot wound, nerve repair should be delayed
until the extent of devitalized tissue can be determined and the soft tissue repair is stable.
2. Answer: d. Peripheral nerve autografts are the most reliable choice for reconstruction of nerve
gaps greater than 3 cm. Autograft use is limited by availability and donor site morbidity from
additional incisions, loss of sensation, and possible neuroma formation. Nerve conduits, such as PGA
conduits, collagen conduits, and acellular allografts are limited in their use in short gaps (<3 cm).
Beyond 3 cm, there is no clinically meaningful regeneration. Lastly, even with extensive mobilization
of the nerve, it is unlikely tensionless primary repair could be performed in a 5 cm nerve gap.
3. Answer: b. There are numerous electrodiagnostic findings suggestive of axonal loss: decreased
CMAP/compound sensory nerve action potential amplitudes, slowed conduction velocity, prolonged
latency, and the presence of fibrillations and PSWs. It should be noted that fibrillations and PSWs do
not become evident for 3 to 6 weeks following an acute nerve injury.
4. Answer: d. Synthetic nerve conduit reconstruction of nerve has not proven effective in gaps longer
than 2 cm and is less effective in motor nerve defects. A tension-free repair is always the goal for
nerve anastomoses but is likely not attainable with a nerve gap of 3 cm. The LABC nerve is the distal
continuation of the musculocutaneous nerve. Given the size of the defect and the need for at least
two cable grafts, this nerve would not be an appropriate donor. The sural nerve is a more
appropriate donor, as it provides sufficient length of graft to enable cable graft reconstruction.
Tendon transfers are a last-resort means of restoring function.
5. Answer: d. Primary neurorrhaphy is performed whenever possible, provided that the repair is free
of any tension at the suture site. Performing primary repair in the setting of a 1 cm segmental nerve
defect would likely result in undue tension at the repair site. Fortunately, the ulnar nerve at the
elbow is unique in that anterior nerve transposition allows significant shortening of the distance
between nerve ends, making tension-less, primary repair possible. Nerve transfers are indicated in
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very proximal nerve injuries where primary repair and grafting are unavailable, or there is concern
that target muscle denervation might occur prior to nerve regeneration. PGA nerve conduits
represent an option for nerve reconstruction without any associated donor site morbidity; however,
recovery outcomes are inferior to that of primary repair and autograft reconstruction. Autologous
nerve
grafts
are
the
gold
standard
for
reconstruction
of
nerve
gaps,
but
nerve
mobilization/transposition and primary repair is preferable if possible.
6. Answer: e. The fascicle of the largest caliber and with the greatest number of motor axons should
be selected as the donor nerve. The other suggested nerve transfers are also possibilities, but the
flexor carpi ulnaris fascicle of the ulnar nerve to biceps (Oberlin procedure) is the most preferable for
this reason.
7. Answer: b. Recovery after peripheral nerve injuries is affected by several patient factors. Younger
patients have better outcomes than older patients. Earlier repairs have also been shown to have
better outcomes than those attempted at later time points. The more distal the injury, the better the
prognosis in terms of functional recovery. Minimal tension and an increasing number of suture
strands crossing the repair site are both associated with improved function.
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References
Lundborg, G, Dahlin, L, Danielsen, N, Zhao, Q. Trophism, tropism, and specificity in nerve regeneration. J Reconstr Microsurg. 1994;10(5):345-
354.
Dellon, AL, Mackinnon, SE. Basic scientific and clinical applications of peripheral nerve regeneration. Surg Annu. 1988;20:59-100.
Lundborg, G. Structure and function of the intraneural microvessels as related to trauma, edema formation, and nerve function. J Bone Joint
Surg Am. 1975;57(7):938-948.Dr. Göran Lundborg describes the extrinsic and intrinsic microvascular anatomy of peripheral nerves and associated
structural changes following peripheral nerve trauma. Any interference with intraneural microcirculation will cause disturbances in nerve function.
The structure and function of the vasa nervorum are of great interest to surgeons who need to know to what extent a peripheral nerve can withstand
various kinds of trauma without loss of blood supply.
Bittner, GD, Schallert, T, Peduzzi, JD. Degeneration, trophic interactions, and repair of severed axons: a reconsideration of some common
assumptions. Neuroscientist. 2016;6(2):88-109.
Lunn, ER, Brown, MC, Perry, VH. The pattern of axonal degeneration in the peripheral nervous system varies with different types of lesion.
Neuroscience. 1990;35(1):157-165.
Bosse, F, Hasenpusch-Theil, K, Küry, P, Müller, HW. Gene expression profiling reveals that peripheral nerve regeneration is a consequence
of both novel injury-dependent and reactivated developmental processes. J Neurochem. 2006;96(5):1441-1457.
Taskinen, HS, Röyttä, M. The dynamics of macrophage recruitment after nerve transection. Acta Neuropathol. 1997;93(3):252-259.
Brück, W. The role of macrophages in wallerian degeneration. Brain Pathol. 1997;7(2):741-752.
Burnett, MG, Zager, EL. Pathophysiology of peripheral nerve injury: a brief review. Neurosurg Focus. 2004;16(5):1-7.
Bhatheja, K, Field, J. Schwann cells: origins and role in axonal maintenance and regeneration. Int J Biochem Cell Biol. 2006;38(12):1995-1999.
Campbell, WW. Evaluation and management of peripheral nerve injury. Clin Neurophysiol. 2008;119(9):1951-1965.
Lundborg, G, Dahlin, LB, Danielsen, N, Nachemson, AK. Tissue specificity in nerve regeneration. Scand J Plast Reconstr Surg. 1986;20(3):279-
283.
Lee, SK, Wolfe, SW. Peripheral nerve injury and repair. J Am Acad Orthop Surg. 2000;8(4):243-252.
Menorca, RMG, Fussell, TS, Elfar, JC. Nerve physiology: mechanisms of injury and recovery. Hand Clin. 2013;29(3):317-330.
Pan, YA, Misgeld, T, Lichtman, JW, Sanes, JR. Effects of neurotoxic and neuroprotective agents on peripheral nerve regeneration assayed by
time-lapse imaging in vivo. J Neurosci. 2003;23(36):11479-11488.
Sunderland, SS. The anatomy and physiology of nerve injury. Muscle Nerve. 1990;13(9):771-784.In this report, Sir Sydney Sunderland summarizes
forty years of clinical experience managing peripheral nerve injuries. Salient peripheral nerve anatomy is reviewed with focus on microstructure,
fascicular distribution and blood supply. The manner in which anatomical features at the suture line influence the outcome of axon regeneration is also
described.
Dedkov, EI, Kostrominova, TY, Borisov, AB, Carlson, BM. Survival of Schwann cells in chronically denervated skeletal muscles. Acta
Neuropathol. 2002;103(6):565-574.
Seddon, HJ. Three types of nerve injury. Brain. 1943;66(4):237-828.This seminal article by Sir Herbert Seddon in 1943 describes three types of
peripheral nerve injuries – neurapraxia, axonotmesis, and neurotmesis – based on the severity of tissue injury, prognosis and time for recovery.
Peripheral nerve surgeons still use this nerve injury classification system today.
Sunderland, S. A classification of peripheral nerve injuries producing loss of function. Brain. 1951;74(4):491-516.In this 1951 classic paper by Sir
Sydney Sunderland, a more complex and specific classification scheme of peripheral nerve injury is introduced. This classification system stratifies
nerve injuries into one of five categories according to severity of injury based on the level of anatomic nerve disruption.
Pfister, BJ, Gordon, T, Loverde, JR, et al. Biomedical engineering strategies for peripheral nerve repair: surgical applications, state of the art,
and future challenges. Crit Rev Biomed Eng. 2011;39(2):81-124.
Dellon, AL, Mackinnon, SE. Nerve repair and nerve grafts. In: Surgery of the Peripheral Nerve. New York, NY: Thieme Medical Publishers; 1988.
Dellon, AL. Management of peripheral nerve problems in the upper and lower extremity using quantitative sensory testing. Hand Clin.
1999;15(4):697-715.
Lipinski, LJ, Spinner, RJ. Neurolysis, neurectomy, and nerve repair/reconstruction for chronic pain. Neurosurg Clin N Am. 2014;25(4):777-787.
Griffin, JW, Hogan, MV, Chhabra, AB, Deal, DN. Peripheral nerve repair and reconstruction. J Bone Joint Surg Am. 2013;95(23):2144-2151.
Robinson, LR. Traumatic injury to peripheral nerves. Muscle Nerve. 2000;23(6):863-873.
Chaudhry, V, Cornblath, DR. Wallerian degeneration in human nerves: serial electrophysiological studies. Muscle Nerve. 1992;15(6):687-693.
He, YS, Zhong, SZ. Acetylcholinesterase: a histochemical identification of motor and sensory fascicles in human peripheral nerve and its use
during operation. Plast Reconstr Surg. 1988;82(1):125-132.
Lundborg, G. A 25-year perspective of peripheral nerve surgery: evolving neuroscientific concepts and clinical significance. J Hand Surg Am.
2000;25(3):391-414.
Tse, R, Ko, JH. Nerve glue for upper extremity reconstruction. Hand Clin. 2012;28(4):529-540.
Cruz, NI, Debs, N, Fiol, RE. Evaluation of fibrin glue in rat sciatic nerve repairs. Plast Reconstr Surg. 1986;78(3):369-373.
Martins, RS, Siqueira, MG, Da Silva, CF, Plese, JPP. Overall assessment of regeneration in peripheral nerve lesion repair using fibrin glue,
suture, or a combination of the 2 techniques in a rat model: which is the ideal choice? Surg Neurol. 2005;64:S10-S16.
Mackinnon, SE, Doolabh, VB, Novak, CB, Trulock, EP. Clinical outcome following nerve allograft transplantation. Plast Reconstr Surg.
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2001;107(6):1419-1429.
Karabekmez, FE, Duymaz, A, Moran, SL. Early clinical outcomes with the use of decellularized nerve allograft for repair of sensory defects
within the hand. Hand. 2009;4(3):245-249.
Moore, AM, Ray, WZ, Chenard, KE, et al. Nerve allotransplantation as it pertains to composite tissue transplantation. Hand. 2009;4(3):239-
244.
Gaudin, R, Knipfer, C, Henningsen, A, et al. Approaches to peripheral nerve repair: generations of biomaterial conduits yielding to replacing
autologous nerve grafts in craniomaxillofacial surgery. Biomed Res Int. 2016;2016(13):1-18.
Lundborg, G, Dahlin, LB, Danielsen, N. Ulnar nerve repair by the silicone chamber technique. Scand J Plast Reconstr Surg Hand Surg.
2009;25(1):79-82.
Kubiak, CA, Kung, TA, Brown, DL, Cederna, PS, Kemp, SWP. State of the art techniques in treating peripheral nerve injury. Plast Reconstr
Surg. 2018;141(3):702-710.
Georgiou, M, Golding, JP, Loughlin, AJ, et al. Engineered neural tissue with aligned, differentiated adipose-derived stem cells promotes
peripheral nerve regeneration across a critical sized defect in rat sciatic nerve. Biomaterials. 2015;37:242-251.
Cui, Q. Actions of neurotrophic factors and their signaling pathways in neuronal survival and axonal regeneration. Mol Neurobiol.
2006;33(2):155-180.
Nath, RK, Mackinnon, SE. Nerve transfers in the upper extremity. Hand Clin. 2000;16(1):131-139.
Lee, SK, Wolfe, SW. Nerve transfers for the upper extremity: new horizons in nerve reconstruction. J Am Acad Orthop Surg. 2012;20(8):506-
517.
Novak, CB, Mackinnon, SE. Distal Anterior interosseous nerve transfer to the deep motor branch of the ulnar nerve for reconstruction of high
ulnar nerve injuries. J Reconstr Microsurg. 2002;18(6):459-464.
Teboul, F, Kakkar, R, Ameur, N, et al. Transfer of fascicles from the ulnar nerve to the nerve to the biceps in the treatment of upper brachial
plexus palsy. J Bone Joint Surg Am. 2004;86A(7):1485-1490.
Dvali, L, Mackinnon, S. Nerve repair, grafting, and nerve transfers. Clin Plast Surg. 2003;30(2):203-221.This article presents a detailed overview of
principles and techniques in peripheral nerve repair and management of segmental nerve gaps. Autogenous nerve grafts, vascularized nerve grafts,
conduits, and allografts are all reviewed. The prinicples and techniques of nerve transfers are also discussed with numerous transfer procedures
described.
Ide, C. Peripheral nerve regeneration. Neurosci Res. 1996;25(2):101-121.
Capek, L, Clarke, HM, Curtis, CG. Neuroma-in-continuity resection: early outcome in obstetrical brachial plexus palsy. Plast Reconstr Surg.
1998;102(5):1555-1562.
Ives, GC, Kung, TA, Nghiem, BT, et al. Current state of the surgical treatment of terminal neuromas. Neurosurgery. 2017;89(3):422.
Souza, JM, Cheesborough, JE, Ko, JH, et al. Targeted muscle reinnervation: a novel approach to postamputation neuroma pain. Clin Orthop
Relat Res. 2014;472(10):2984-2990.
Kubiak, CA, Kemp, SWP, Cederna, PS. Regenerative peripheral nerve interface for management of postamputation neuroma. JAMA Surg.
2018;153(7):681-682.
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C H A P T E R 11
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Principles of Tissue Expansion
Paul F. Hwang and Samuel J. Lin
Key Points
Tissue expansion is a simple technique which has wide-range soft tissue coverage capabilities.
These prosthetics provide broader coverage through changes at the histologic level as well as altering
physiologic properties of the skin.
The epidermal layer thickens in reaction to tissue expansion, whereas the dermal layer becomes
thinner.
Up to 50% of the scalp can be reconstructed utilizing tissue expansion.
Extremities have the highest level of complications when tissue expanders are placed in these
anatomic regions.
Tissue expansion is a simple yet effective tool in one’s armamentarium to reconstruct adjacent cutaneous
and soft tissue defects. This technique takes advantage of the viscoelastic properties of the skin to create
donor material that can truly replace like tissue with like. Its applicability to almost all parts of the body
and even the most complexity of wounds makes this a valuable technique that should be familiar to all
reconstructive surgeons.
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History
The foundation for tissue expansion technique actually has its derivation from distraction osteogenesis.
At the turn of the 20th century, Codvilla applied the principles of external distraction directly to bones
and used this to shortened limbs in stages with traction of medium intensity, thus enabling to overcome
the resistance with a lesser force to distract the bony component. 1 In 1921, Putti continued the work on
refining femur-lengthening technique by pinpointing the need for continuous and elastic forces to
overcome the resistance of the soft tissues. 2 This expansion of soft tissue accommodates newfound limb
lengthening.
One of the earliest descriptions of skin expansion came several years later in 1957 when Neumann
became the pioneering surgeon to first use gradual distention of a rubber balloon through an externally
exposed tube with a stopcock to expand local skin and subcutaneous tissue to reconstruct a partial ear
defect. 3 This technique was revolutionary in that we now have the ability to secure skin that was high in
quality in regard to color and texture with tissue immediately adjacent to the defect, avoiding the need
for harvesting from a remote donor site.
Unfortunately, this case report on tissue expansion did not receive the enthusiastic fervor and legitimacy
as a potential option in reconstructive surgery. More than two decades later, Radovan reinvigorated the
concept of expansion through the use of an internally placed port. 4 Further work by Austad and Rose
elucidated much of the physiology behind tissue expansion through the use of an osmotically driven,
self-inflating expander in a guinea pig model. 5
Since then tissue expansion is now widely accepted and considered a familiar technique for any
reconstructive surgeon. Although a simple technique, understanding of the physiology behind tissue
expansion and special considerations in design make it more intricate in nature. Appreciation of these
concepts is critical to the widespread application of this method to areas all over the body that may not
have been previously possible.
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Biological Effects of Tissue Expansion
At the molecular level, tissue expansion is possible secondary to elaborate intrinsic signaling. The
principle of strain-induced cellular growth involves a network of several integrated cascades that include
growth factors, cytoskeletal structures, and protein kinases. 6 Growth factors such as platelet-derived
growth factor and angiotensin II have been implicated in cell growth. 7,8 Not only are there implications
on cell growth, but also there are other growth factors such as epidermal growth factor (EGF) and
transforming growth factor (TGF) that are involved in cell migration, differentiation, and wound healing.
9,10 Protein kinase C is known to play a crucial role in signal transduction through a cascade of events
through its activation of other proteins by an unknown mechanism. 11
Despite an unknown mechanism, these molecular activities created by mechanical stress translate into the
creep phenomenon. Creep is defined as stretching of a material under a constant load over time. 12 With
regard to tissue expansion, it comes in the form of mechanical and biologic creep. Mechanical creep relies
on the skin’s ability to acutely stretch and increase in surface area during immediate intraoperative tissue
expansion. 13 It is explained by the displacement of fluids out of the collagen network leading to
dehydration of tissues, collagen fiber realignment in a parallel fashion, elastic fibers microfragmentation,
and adjacent tissue migration into the expanded field as a result of the stretching force. 13,14
Biologic creep, on the other hand, derives its significant gain in tissue from increased fibroblast and
collagen synthesis, increased myofilaments, increased mitotic activity, and neovascularization. 13 It is very
much dependent on the chronicity of controlled tissue expansion, as the imposed deformation allows for
stress-relaxation in preventing the tissue from retracting back into its pre-expansive form because of the
formation of new tissue. 15 Essentially, the force required to maintain tissue elongation decreases with
time as the tissue expansion is maintained.
Many of the predictable changes to the layers of the skin and soft tissue are listed in Table 11.1. 11,16,17 Of
special note is the increased vascularity associated with an expanded flap with increased number and
caliber of vessels when compared with a nonexpanded counterpart. 17 This can be attributed to increased
angiogenic factors such as vascular endothelial growth factor (VEGF) expressed in expanded tissues. 18
These factors may also have the same effect seen in delayed flaps. In fact, skin flap viability and capillary
blood flow were similar between expanded flaps and delayed flaps as well as significantly higher than
those of acute random skin flaps raised on the normal skin. 11 In principle, expanded tissues are a form of
a delayed flap.
TABLE 11.1
Changes in Skin and Soft Tissue After Tissue Expansion
Location
Change
Epidermis
Increased mitotic activity
No significant decrease in thickness
Dermis
Dermal thinning
Collagen synthesis markedly increased
Increase fibroblasts and myofibroblasts
Realignment of collagen fibers
Decreased hair follicle density
Muscle
Increased thinning
Function unchanged
Myofibril and myofilament disorganized arrangement
Increased size and number of mitochondria
Fat
Permanent decrease in fat cells and thickness
Fat necrosis and fibrosis may occur with aggressive expansion
Blood vessels
Proliferation of blood vessels with increase venules and arterioles
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Types of Tissue Expansion Devices
Through technological advances, the modern day tissue expander has changed tremendously since the
initial inflatable balloon and external tubing with a stopcock apparatus that was used by Neumann. 3
Currently, there are a multitude of tissue expanders of different types that are available from a variety of
manufacturers (Figure 11.1). The type of expander chosen will depend on the clinical scenario at hand.
FIGURE 11.1 Tissue expanders of various shapes (breast specific, curvilinear, rectangular, oval) and port integration versus
nonintegration.
Each type of tissue expander will have specific characteristics that make them more advantageous to use
in different anatomic sites and situations. The shape of tissue expander will be the first distinction to
make. In general, they can be round, rectangular, or crescent shaped. They can also be further
subcategorized, depending on the manufacturer, into specific types such as angled, ellipsoid, oval, etc. In
addition to shape, the texture of the tissue expander can come into play when deciding which one to
choose. Some studies have shown that capsular formation quality may be better with texture versus
smooth tissue expanders, thus affecting capsular contracture rates when replaced with definitive
implants in breast reconstruction. 19 Finally, the size of the tissue expander will help determine choice
between the different types. Although obvious that a larger expander will accommodate a large eventual
flap, one may be limited in size because of the internal characteristics of the tissues or amount of
cutaneous coverage needed in the end.
Another important feature of the tissue expansion apparatus is the route of expansion needed. Tissue
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expanders are typically accessed through self-sealing, single ports that can serve as a point for injectable
flow in or out, allowing for serial expansions in addition to the fill placed intraoperatively. However, the
port can also be distal to the expander itself or integrated within the apparatus itself. Distal ports have the
advantage of minimizing risk of iatrogenic rupture by accidental puncture. However, they have their
own faults such as manipulation of the port itself (e.g., flipping, migration) if not placed into a proper
pocket as well as obstruction of the tubing in between the port and the expander. Integrated ports have
the obvious advantage of not having the need to make a separate dissection for the port along with any
mechanical issues one would find with the distant ports. However, one has the main issue of iatrogenic
injury to the tissue expander itself with the integrated port. Also, an integrated port is less ideal if there is
lack of coverage secondary to the thinning of overlying soft tissue.
There has been a renewed interest in self-expanding tissue expanders because of logistical considerations.
As tissue expander technology has evolved, so have the logistics for expansion. To decrease clinic time,
costs for travel, and stress on patients, some clinical situations provide for self-expansion at home
through self-injection, 
 and it is proven to be safe and reliable. 20 More recently, the Food and Drug
Administration had cleared for the use of carbon dioxide–filled, remote-controlled tissue expanders for
further convenience of home expansion and obviating the need for percutaneous saline injections in
breast reconstruction. 21 If this technology is applied to tissues expanders of all shape and sizes, this may
eliminate the complications of both distant and integrated ports entirely.
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Surgical Design and Considerations
Tissue expansion not only involves the surgery to place the expander, expansion, and then subsequent
flap placement or permanent implant exchange, but preoperative conditions must be considered. Patient
selection is crucial if a clinician chooses this form of reconstruction. The patient will require a maturity
level and need to demonstrate emotional stability to withstand the pain or discomfort associated with the
expansion as well as temporary additional aesthetic disfigurement. Smoking, radiation, and infections
have a higher risk of wound complications both during the expansion process and afterward. We would
also not consider tissue expansion as a viable option in the need for acute coverage of a defect. If home
self-injectable expansions will be done, adequate education and training must be given to non–health care
attendants.
Even before an incision is made, flap design incorporating placement of incisions in regard to final scars,
direction of flap movement, and proper placement of the prosthesis itself are all critical factors leading to
a successful tissue expander reconstruction. Incisions are typically made at the border of the defect
needing coverage or lesion needing excision. Flaps can be of any type such as advancement, rotation, or
interpositional flaps, but the incision must take into account that the direction of movement will be
perpendicular to the incision placed to maximize flap coverage and minimize tension during expansion.
Proper placement of the expander will be important and what type of port will factor into this. When
placing a distant filling port, one needs to ensure a separate pocket is created that will accommodate the
port, minimize manipulation resulting in migration or flipping, and be placed typically with a posterior
backing with stiff skeletal support if possible to accommodate ease of injection. The injectable port should
be superficial enough to be palpable, not be in an area of pressure or sensitivity, and not be in the line of a
healing incision. Expanders with integrated ports will require a pocket that will account for the port and
its added projection as well as still have durable overlying tissue in anticipation of some of it thinning
during the expansion process. This is important because there are certain integrated tissue expanders
with a significant height/thickness of the expander with the integrated port requiring careful planning for
adequate soft tissue coverage over the expander. During placement, the expander should also be partially
filled to unravel any folds in the device. This allows for a snug fit with the surrounding tissue envelope
and allows for the closure of any dead space. This will help to minimize seroma formation along with
placement of drains. Clinical evaluation of the skin is necessary to ensure that the expander is not
overfilled to compromise the tissues from the start. The incisions made to place the expanders are closed
in layers.
Once the tissue expander has been placed and wounds have healed for 3 weeks, serial expansion can
begin. The expansion schedule will have to be geared toward the individual on a case-by-case basis to
expand with smaller increments on a daily basis. However, realistically, owing to coordination of clinic
schedules and patient transport issues, expansion is typically done on a weekly or biweekly basis until
the goal is met. After each expansion, the skin and subcutaneous tissues should be checked for tightness
and vascularity. The patient should be asked to report pain or discomfort during and after completion of
the serial expansion. If the patient is in any discomfort, the expansion could be stopped and/or fluid can
be taken out until comfortable again. Once the goal is met, it is best to wait 3 to 4 weeks before the
second-staged reconstruction. The second stage may be for permanent implant exchange or flap
placement and to take advantage of the stress-relaxation effect from prolonged positioning after the final
serial expansion.
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Indications by Anatomic Region
Head and Neck
Scalp
Scalp defects can occur secondary to tumor excision, infection, traumatic injury, burns, radiation injury,
or excision of a congenital lesion. Reconstructive goals are to obtain coverage over a reconstructed scalp
(Figure 11.2) as well as realignment of hair-bearing areas if alopecia is involved (Figures 11.3 and 11.4).
Tissue expansion has been widely accepted and used by plastic surgeons in reconstruction of these
medium to large scalp defects. One can use this technique to cover large defects involving up to 50% of
the scalp without significant thinning of the hair-bearing areas. 22 The robust vascular nature of the scalp
along with incorporation of a dominant vessel in the flap design will ensure a durable flap of good hair-
bearing quality. Even though expansion brings upon a decrease in hair density, this is usually
unnoticeable. 23 The expander is typically placed in the subgaleal plane under hair-bearing area. The
expansion process takes weeks to months depending on patient characteristics. Afterward, the expander
is taken out through the initial incision, and the flap is designed in such a way to avoid transection of any
dominant vessels. Capsulectomies are avoided, as they may devascularize the flap. Galeotomies may also
devascularize the flap, but if carefully done, one may preserve the galeal blood supply for easier and
faster expansion of the scalp with fewer expander extrusion complications. 24 There were initial concerns
for cranial skeletal morphology changes; however, studies have shown that temporary cranial molding
occurs with correction in 3 to 4 months. 19 Nonetheless, the rates of extrusion of the tissue expansion of
the scalp in the general adult population is not insignificant, and careful planning must be undertaken at
each step of the way. Tissue expanders that become exposed during the expansion process may be
successfully exchanged with a smaller amount of volume with closure of the wound with subsequent
expansion over time.
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FIGURE 11.2 Tissue expansion after cranial reconstruction. A. Preoperative expansion. B. Expansion phase, front profile. C.
Expansion phase, right lateral profile. D. Postoperative expansion.
FIGURE 11.3 Tissue expansion for hairline restoration. A. Preoperative expansion. B. Postoperative expansion.
(Courtesy of Kerry Latham, M.D.)
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FIGURE 11.4 Tissue expansion for scar alopecia. A. Preoperative expansion, front profile. B. Preoperative expansion, right
lateral profile. C. Intraoperative. D. Postoperative expansion, front profile. E. Postoperative expansion, birds-eye view.
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Forehead
Forehead reconstruction with tissue expanders is a particular challenge as goals are required to
incorporate aesthetic units involving the brow as well as anterior and lateral hairline symmetries.
Resurfacing of the forehead without distortion of these structures will depend upon the size of the defect.
Expansion with direct advancement of tissues can be used to reconstruct 25% to 70% of forehead defects.
25 Anything less may just require serial excisions, and anything more may require going up the
reconstructive ladder to an expanded full-thickness skin graft or even a free flap. Adjacent scalp and
cheek sometimes need to be mobilized to obtain improved symmetry. Brow symmetry and ptosis should
be assessed simultaneously with any flap advancement.
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Face and Neck
The face and neck are obviously highly visible and therefore aesthetically demanding in regard to
reconstructive resurfacing. Tissue expanders can be used and are usually placed in the lateral facial areas
such as in the cheek and neck. Areas such as the neck are ideal donor sites, as they are optimal in quality
similar to the facial skin. 26 Care is taken to maintain intact aesthetic facial subunits and to keep incisions
in aesthetically compliant locations. Typically, an incision is made in a preauricular facelift-type incision
and placement of the expander above the platysma or submuscular aponeurotic system. A distal port is
commonly used and can be placed postauricularly or within the neck. Once the flap is elevated and
rotated into position, careful suture techniques will be needed to maintain the tissue in the area of defect
but also avoid unnecessary tension that would lead to iatrogenic distortion such as lower lid dropping,
oral incompetence, and facial mimetic asymmetry.
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Breast
Postmastectomy Breast Reconstruction
Breast reconstruction using tissue expanders is a common technique that all plastic surgeons are familiar
with. Implant-based reconstruction accounts for almost 65% of all breast reconstructions in the United
States because of its safety, cost-effectiveness, and reliability. 27 In general, after mastectomy, tissue
expanders are placed in a subpectoral or more recently prepectoral position in conjunction with acellular
dermal matrix for supplemental or total coverage. The surgical wounds are allowed to heal, and
expansion is commenced in 2 to 3 weeks on a weekly or biweekly basis until goal breast volume. An
exchange procedure is undertaken to replace the tissue expander with a similar-sized permanent implant.
Although the majority of plastic surgeons in the United States most likely practice placement of tissue
expanders in a subpectoral pocket, prepectoral placement with total acellular dermal matrix coverage has
gained interest, as it foregoes the need to detach the pectoralis muscle. This translates into quicker
postoperative recovery and decreased operative duration for reconstruction. Although long-term studies
are necessary to determine and compare outcomes, some early studies show this technique to be effective
with comparable complication rates to the subpectoral technique. 28 The topic of breast reconstruction
using prosthetic techniques is covered in more detail in Chapter 59.
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Special Considerations: Congenital Anomalies, Gender Identity Disorder (Male to
Female)
Congenital anomalies of the breast consist of Poland syndrome, idiopathic unilateral breast hypoplasia,
or tuberous breast deformity. Although not congenital, breast asymmetry can also be secondary to
trauma or iatrogenic injuries to the breast bud at a young age, leading to an abnormal growth pattern.
Regardless of the etiology, timing of reconstruction and expansion is what that differs between these
cases and in postmastectomy breast reconstruction. One can place the tissue expander once the patient
has stopped growing so there is a goal in mind (i.e., size and shape of the contralateral normal side);
however, this would be a long time for a young adolescent female to live with this unilateral deformity.
Tissue expanders can be used as a temporary but prolonged measure to incrementally expand the size of
the breast as the patient continues to grow. This can continue until the patient reaches the age of maturity
at which time definitive reconstruction with a permanent prosthesis or autologous reconstruction can be
done. Congenital breast anomalies are covered in more detail in Chapter 62.
Male-to-female transgender patients desiring breast augmentation may need tissue expanders to expand
their skin and soft tissues to fit the size of implant they desire. The Endocrine Society recommends
transgender females to delay breast augmentation until at least 2 years of estrogen therapy, as the breasts
continue to grow during that time period. 29 This may not necessarily negate the need for a tissue
expander but would overall allow for the development of a more suitable soft tissue envelope for the final
prosthetic implant.
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Trunk
There is a wide variety of cases for the trunk such as burns, congenital anomalies, traumatic injuries, and
large hernia defects that require reconstruction. Unless it is amenable to excision in three stages or less,
tissue expansion is the reconstructive option of choice when it comes to the back, abdomen, and chest. 30
Expansion of the skin, with or without the underlying fascia, allows for primary closure when necessary.
Subcutaneously placed expanders are used for defects with minimal fascial tension, whereas
intermuscularly placed expanders can close large defects involving the fascia and abdominal
musculature. 31 Although they are uncomfortable and can interfere with daily activities of living, tissue
expansion of the trunk is associated with low rates of morbidity and mortality and high rates of primary
fascial closure and incisions, while hernia recurrences rates appear to be low. 32
Tissue expanders can also be used to expand truncal donor flaps in preparation for use at a different
recipient site. Pre-expanding the flap increases the flap dimension and reduces the flap thickness and
donor site morbidities. Reports of this method of expanding the donor site have been used to create
donor sites that were large enough to fill the defects of various regions such as the lower extremity,
abdominal wall, perineum, and hand. 33-35
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Extremities
Using an extremity as a donor site with tissue expansion is not ideal. They are typically known to have a
disproportionately higher rate of complications when compared with using expanders in other regions of
the body. 36 Most algorithms for tissue expansion to treat upper extremities rely upon the use of tissue
expansion in regional areas such as the back, shoulder, and flank. 37 Lesions of the proximal arm to elbow,
if noncircumferential, do well with expanded transposition flaps from the back or shoulder. If large and
requiring more soft tissue, an expanded free transverse rectus abdominus muscle flap can be an option.
Expanded flaps from the flank and abdomen can serve as good donor sites for lesions of the forearm and
hands, respectively. For the lower extremity, limited mobility of the tissues results in the need for using
more complex reconstructive approaches even for smaller lesions. 38 Expanded transposition flaps, local
flaps, and even free flaps are the mainstream treatments for these difficult cases.
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Complications
Several factors play a role in complications from tissue expansion. These factors depend on patient
characteristics, technique, site of expansion, and the aggressiveness of expansion schedule and volume.
One study showed complications necessitating some form of revision to the original treatment plan in as
high as 39% of cases. 36 However, enough tissue was generated from the expansion itself to complete the
reconstructive plan without affecting final outcomes. Fortunately, most complications from tissue
expansion are minor, consisting of things such as seroma formation, widened scar, discomfort from the
expansion itself, bone resorption, neuropraxia, remnant excessive soft tissue, and other aesthetic
concerns. 11,39,40
Major complications consist of hematoma, infection, implant exposure, implant failure or iatrogenic
injury, and overlying tissue compromise (Table 11.2). Hematomas would require reoperation and
possible explantation, although salvage is an option if found early on. Infections, if minimal, can be
treated with intravenous and oral antibiotic therapy. Persistent and purulent infections may necessitate
explantation. Colonization of the prosthesis can occur with each injection so sterile technique is
mandatory for each expansion. Implant failure can be secondary to the internal failure in the
manufacturing of the device itself or iatrogenic injury. It is important to use a proper-sized needle such as
23 gauge and to access the port at a 90-degree angle to minimize injury to the self-sealing port where
saline can leak from. Finally, it is important to reevaluate the overlying soft tissues every time one
expands the tissue expander. One should check that the skin is not too taut, that capillary refill is present,
and that it is not too uncomfortable for the patient. Rapid expansion is possible but that should not
compromise the vascularity to the flap that can lead to early extrusion.
TABLE 11.2
Complications From Tissue Expansion
Major
Infection
Implant exposure
Implant failure
Soft tissue compromise
Hematoma formation
Minor
Seroma formation
Widened scar
Patient discomfort/pain
Excess soft tissue
Aesthetic concerns
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Questions
1. A 13-year-old girl comes to the office 16 months after a scalding hot oil–burn injury to the scalp. At
the time of injury, the patient was treated with debridement and skin grafting. On examination, the
patient had an area of well-healed skin graft encompassing approximately 45% of the scalp total
surface area. Which of the following is the best approach to reconstruction the scalp to effectively
address the area of alopecia?
a. Free tissue transfer with latissimus muscle flap
b. Serial excision and closure
c. Tissue expansion
d. Rotational flap
e. Hair transplantation
2. Which layer of the soft tissue thickens during tissue expansion?
a. Muscle
b. Epidermis
c. Dermis
d. Subcutaneous fat
3. What factor is responsible for the increased vascularity and angiogenesis found in animal studies
following tissue expansion?
a. VEGF
b. EGF
c. TGF
d. Angiotensin II
4. What is true of prepectoral breast reconstruction with tissue expanders/implants when compared
with submuscular placement?
a. Prepectoral tissue expansion results in less acute and chronic pain
b. It leads to lower aesthetic outcomes and patient satisfaction
c. Overall complications are higher in prepectoral breast reconstruction.
d. Animation deformity is a common complaint after this technique.
5. Flaps developed from expanded skin
a. Have thickening of the dermis
b. Have thinning of the epidermis
c. Decrease in collagen density
d. Decrease angiogenesis
e. Act as flaps that underwent a delay phenomenon
1. Answer: c. Replacing like with like, in this case scalp tissue with scalp tissue, would be most ideal
because of the hair-bearing qualities of scalp tissue. Tissue expansion can effectively reconstruct up
to 50% of scalp tissue loss. Free tissue transfer with a latissimus muscle flap would give a more
durable coverage; however, the lack of hair would resemble the previous alopecia defect. If this were
a smaller wound, serial excision and closure may have been an option. A rotational flap with the
remaining scalp will not be able to fully cover the entire defect in regard to anatomic landmarks,
borders, and zones of normal hair-bearing 
 scalp. Hair transplantation works in pathology such as
male pattern baldness as the recipient site is ready to receive follicular units in a fresh bed of tissue
for growth. In this patient, the skin graft site is a terrible recipient bed to accept follicular units.
2. Answer: b. Out of all the soft tissue layers, only the epidermal layer has been found to reliably
increase in thickness. Examination at the microscopic level showed this to be primarily due to the
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hyperkeratosis that was present within this layer. Studies have also shown there to be increased
mitotic activity within the epidermis. This was not seen in the dermis along with thinning of this
layer as well. Fatty tissue and muscle decrease in thickness considerably with some permanence.
3. Answer: a. Temporary hypoxia caused by the pressure of the expander leads to an increase in
vascularity and angiogenesis. This was associated with an increased expression of VEGF. EGF has
been shown to lead to actin depolymerization and the formation of membrane ruffles to eventually
induce cell proliferation through the microfilament system. TGF has been reported to eventually
manipulate morphology, migration, and wound healing by enhancing fibroblast growth and
stimulation of extracellular matrix production. Angiotensin II has been reported to play a role in
strain-induced cell growth.
4. Answer: a. Prepectoral tissue expander placement leads to 
 decreased acute pain, as it negates the
need for a submuscular dissection of the pectoralis muscle. Subsequently, pain is also decreased as
the tissue expansion occurs above the muscle. Aesthetic outcomes and patient satisfaction have been
relatively the same despite prepectoral or submuscular breast reconstruction. Overall complications
including flap necrosis, implant exposure, implant infection and total explantation rates have been
shown to be similar as well. Animation deformity is actually less in this patient population.
5. Answer: e. Random flaps developed on tissues that were expanded undergo a delay phenomenon.
These flaps have an increased likelihood of survival because of this. The dermis actually thins
because of tissue expansion and conversely the epidermis thickens. Collage density remains the same
and increased angiogenesis occurs.
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References
Codvilla, A. On the means of lengthening, in the lower limbs, the muscles and tissues which are shortened through deformity. Am J Orthop
Surg. 1905;2:353-357.
Putti, V. The operative lengthening of the femur. JAMA. 1921;77:934-935.
Neumann, CG. The expansion of an area of skin by progressive distention of a subcutaneous balloon. Plast Reconstr Surg. 1957;19:124-130.This
article describes the use of a buried inflatable rubber balloon that was gradually distended to supply soft tissue coverage of a subtotally avulsed ear. At
2 months, this allowed for a 50% increase from its original surface area. Although just a case report, this article laid the foundation for future
acceptance of tissue expansion as a legitimate form of reconstruction.
Radovan, C. Breast reconstruction after mastectomy using the temporary expander. Plast Reconstr Surg. 1982;69:195-208.The author describes
his operative technique which laid the foundation for current day two stage immediate breast reconstruction. In this article, he reviews his experience in
reconstructing 68 patients.
Austad, ED, Rose, GL. A self-inflating tissue expander. Plast Reconstr Surg. 1982;70:588.The authors developed a silicone expandable implant that
used differential osmotic gradients to drive self-inflation of the expander. This work was essential to fully understanding the physiological properties
behind tissue expansion.
De Filippo, RE, Atala, A. Stretch and growth: the molecular and physiologic influences of tissue expansion. Plast Reconstr Surg. 2002;109:2450-
2562.
Wilson, E, Mai, Q, Sudhir, K, et al. Mechanical strain induces growth of vascular smooth muscle cells via autocrine action of PDGF. J Cell Biol.
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Sudhir, K, Wilson, E, Chatterjee, K, et al. Mechanical strain and collagen potentiate mitogenic activity of angiotensin II in rat vascular smooth
muscle cells. J Clin Invest. 1993;92:3003.
Sporn, M, Roberts, A. Transforming growth factor-B: recent progress and new challenges. J Cell Biol. 1992;119:1017.
Mustoe, TA, Pierce, GF, Thomason, A, et al. Accelerated healing of incisional wounds in rats induced by transforming growth factor-B.
Science. 1987;237:1333.
Takei, T, Mills, I, Azai, K, et al. Molecular basis for tissue expansion: clinical implications for the surgeon. Plast Reconstr Surg. 1998;102:247-
258.
Gibson, T. Physical properties of skin. In: McCarthy, J , ed. Plastic Surgery. Philadelphia, PA: WB Saunders; 1990:209-211.
Johnson, TM, Lowe, L, Brown, MD, et al. Histology and physiology of tissue expansion. J Dermatol Surg Oncol. 1993;19:1074-1078.This is a
review of the histological and physiological changes that occur during tissue expansion. Expansion is shown to result in epidermal hypertrophy,
decrease in dermis, muscle and adipose thickness, and bone resorption. This article attempts to define tissue expansion at the microscopic level in order
to better understand the properties behind tissue expansion and its subsequent effect grossly.
Wilhelmi, BJ, Blackwell, SJ, Mancoll, JS, et al. Creep vs. stretch: a review of the viscoelastic properties of skin. Ann Plast Surg. 1998;41:215-219.
Wee, SS, Logan, SE, Mustoe, TA. Continuous versus intraoperative expansion in the pig model. Plast Reconstr Surg. 1992;90:808-814.
Sasaki, GH, Pang, CY. Pathophysiology of skin flaps raised on expanded pig skin. Plast Reconstr Surg. 1984;74:59-67.
Cherry, GW, Austad, E, Pasyk, K, et al. Increased survival and vascularity of random pattern skin flaps elevated in controlled, expanded
skin. Plast Reconstr Surg. 1983;72:680.
Lantieri, LA, Martin-Garcia, N, Wechsler, J, et al. Vascular endothelial growth factor expression in expanded tissue: a possible mechanism of
angiogenesis in tissue expansion. Plast Reconstr Surg. 1998;101:392-397.
Kuriyama, E, Ochiai, H, Inoue, Y, et al. Characterization of the capsule surrounding smooth and textured tissue expanders and correlation
with contracture. Plast Reconstr Surg Glob Open. 2017;5:e1403.
Mohmand, MH, Sterne, GD, Gowar, JP. Home inflation of tissue expanders: a safe and reliable alternative. Br J Plast Surg. 2001;54:610-614.
Morrison, KA, Asherman, BM, Asherman, JA. Evolving approaches to tissue expander design and application. Plast Reconstr Surg.
2017;140:23S-29S.
MacLennan, SE, Corcoran, JF, Neale, HW. Tissue expansion in head and neck burn reconstruction. Clin Plast Surg. 2000; 27:121-132.
Kabaker, SS, Kridel, RW, Krugman, ME, et al. Tissue expansion in the treatment of alopecia. Arch Otolaryngol Head Neck Surg. 1986;112:720-
725.
El Sakka, DM. Tissue expanders in post-burn alopecia: with or without galeotomies? Ann Burns Fire Disasters. 2015;28:210-214.
Gosain, AK, Zochowski, CG, Cortes, W. Refinements of tissue expansion for pediatric forehead reconstruction: a 13-year experience. Plast
Reconstr Surg. 2009;124:1559-1570.
Hu, X, Zeng, G, Zhou, Y, Sun, C. Reconstruction of skin defects on the mid and lower face using expanded flap in the neck. J Craniofac Surg.
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Bertozzi, N, Pesce, M, Santi, P, et al. Tissue expansion for breast reconstruction: methods and techniques. Ann Med Surg (Lond). 2017;21:34-44.
Jafferbhoy, S, Chandarana, M, Houlihan, M, et al. Early multicenter experience of pre-pectoral implant based immediate breast
reconstruction using Braxon® . Gland Surg. 2017;6:682-688.Pre-pectoral placement of tissue expanders in breast reconstruction is a relatively new
technique. This article is a prospective study of 78 immediate breast reconstructions showing this to be an effective technique with complication rates
comparable to subpectoral placement. Further long-term studies will be necessary to validate these results.
Meyer, WJ, Webb, A, Stuart, CA, et al. Physical and hormonal evaluation of transsexual patients: a longitudinal study. Arch Sex Behav.
1986;15:121-138.
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Arnja, JS. Gosain, AK. Giant congenital melanocytic nevi of the trunk and an algorithm for treatment. J Craniofac Surg. 2005;16:886-893.
Wooten, KE, Ozturk, CN, Ozturk, C, et al. Role of tissue expansion in abdominal wall reconstruction: a systematic evidence-based review. J
Plast Reconstr Aesthet Surg. 2017;70:741-751.
Alam, NN, Narang, SK, Pathak, S, et al. Methods of abdominal wall expansion for repair of incisional herniae: a systematic review. Hernia.
2016;20:191-199.
Monsivais, SE, Webster, ND, Wong, S, et al. Pre-expanded deep inferior epigastric perforator flap. Clin Plast Surg. 2017;44:109-115.
Wang, C, Zhang, J, Yang, S, et al. Pre-expanded and prefabricated abdominal superthin skin perforator flap for total hand resurfacing. Clin
Plast Surg. 2017;44:171-177.
Liu, Y, Zang, M, Zhu, S, et al. Pre-expanded paraumbilical perforator flap. Clin Plast Surg. 2017;44:99-108.
Antonyshyn, O, Gruss, JS, Mackinnon, SE, et al. Complications of soft tissue expansion. Br J Plast Surg. 1988;41:239-250.
Margulis, A, Bauer, BS, Fine, NA. Large and giant congenital pigmented nevi of the upper extremity: an algorithm to surgical management.
Ann Plast Surg. 2004;52:158-167.
Kryger, ZB, Bauer, BS. Surgical management of large and giant congenital pigmented nevi of the lower extremity. Plast Reconstr Surg.
2008;121:1674-1684.
Bennett, RH, Hirt, M. A history of tissue expansion: concepts, controversies and complications. J Dermatol Surg Oncol. 1993;19:1066-1073.
Casanova, D, Bali, D, Bardot, J, Legre, R, Magalon, G. Tissue expansion of the lower limb: complications in a cohort of 103 cases. Br J Plast
Surg. 2001;54:310-316.
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C H A P T E R 1 2
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Principles of Procedural Sedation and Local and
Regional Anesthesia
Neal Moores and Jayant P. Agarwal
Key Points
Local anesthetics differ widely in potency, toxicity, and duration of action.
Epinephrine can be used in digits and end organs, if used safely.
Local anesthetic dosing differs significantly when used in tumescent solution, relative to standard
use as a soft tissue infiltrate.
Regional blockade techniques facilitate conduct of complex procedures without the need for general
anesthesia.
Sedation is an important tool for the plastic surgeon.
Local anesthetics may be applied topically, injected subcutaneously, or injected in the area of major
peripheral nerves. There are a variety of local anesthetics available, which differ in onset, duration,
allergenicity, and toxicity. For office-based procedures, peripheral nerve blocks and sedation that may be
administered without the need of endotracheal intubation are increasingly relevant in contemporary
plastic surgery practice.
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Pharmacokinetics
Mechanism of Action
Local anesthetic drugs enter the neuronal cell by passive diffusion in the nonionic state. Once inside the
cell, they inhibit sodium channel function and thereby prohibit the cell from achieving threshold potential
and thus preventing signal transduction. It is important to note that the aforementioned reliance on
passive diffusion has significant ramifications in clinical practice. The highly acidic (and charged) nature
of inflamed wounds severely inhibits the diffusion of local anesthetics into nerve cells. For this reason,
infiltrative anesthesia may be much less effective in inflamed tissue, and alternate methods may be
required. 1–3
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Pharmacology
Local anesthetics are classified as either amides or esters. The different chemical behavior (metabolism,
allergenicity) of the drugs depends on the presence of this amide or ester linkage. Esters include procaine
(novocaine), chloroprocaine, tetracaine, and cocaine. Amides include lidocaine, mepivacaine, prilocaine,
bupivacaine (Marcaine), and etidocaine. 2,3
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Metabolism
Esters are metabolized by hydrolysis in the plasma by pseudocholinesterase. Amide anesthetics are
metabolized in the liver. 3
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Allergenicity
A true allergic reaction to local anesthetic is extremely rare. In a Danish case series, over 5 years, no
patients referred for allergy testing relating to local anesthetics tested positive for a true allergy. 4 Patients
with allergic reactions to local anesthetics are more likely reacting to preservatives in the preparations
such as para-aminobenzoic acid. 3 In patients who do demonstrate allergy to local anesthetics, allergy to
esters are far more common than to amides.
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Potency
Local anesthetic potency is determined primarily by the degree of lipid solubility of the drug. This is
because the local anesthetic molecule must enter and traverse the neuronal cell membrane to take effect.
In clinical settings, however, other factors such as vasodilatory activity, addition of epinephrine, and the
tissue redistribution properties of the different local anesthetics also have some effect on potency. 3
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Duration of Action
Duration of action is largely determined by the rate at which the infiltrated local anesthetic is cleared to
the intravascular space away from the desired target tissue. This is determined by the vasodilatory
activities of the various drugs. The more vasodilation the drug causes, the faster the drug is cleared from
the interstitial space and the shorter the duration of action.
The addition of vasoconstrictors (epinephrine) helps to significantly prolong the duration of action of
local anesthetics. Epinephrine causes vasoconstriction and thus delays the clearance of the local anesthetic
from the interstitium. Epinephrine is most commonly added to local anesthetics in concentrations of
1:100,000 to 1:200,000. The addition of epinephrine to a plain lidocaine solution will augment the duration
of action from 30 to 60 minutes to 1.5 to 6 hours. See Table 12.1 for the effect of additional epinephrine on
various local anesthetics. 3
TABLE 12.1
Dosage and Duration Characteristics of the Local Anesthetics When Used for Infiltration Anesthesia (e.g., Infiltration Around the
Periphery of a Skin Lesion Before Excision)
Drug
Plain Solution
Epinephrine-Containing Solution
Concentration (%)
Maximal Dose (mg)
Duration (min)
Maximal Dose (mg)
Duration (min)
Duration
Procaine
Chloroprocaine
1.0–2.0
800
15–30
1,000
30–90
Moderate Duration
Lidocaine
0.5–1.0
300
30–60
500
120–360
Mepivacaine
0.5–1.0
300
45–90
500
120–360
Prilocaine
0.5–1.0
500
30–90
600
120–360
Long Duration
Bupivacaine
0.25–0.5
175
120–240
225
180–420
Etidocaine
0.5–1.0
300
120–180
400
180–420
Reprinted with permission from Strichartz, GR, Covino, BG. Local anesthetics. In: Miller, RD, ed. Anesthesia. 4th ed. New York, NY: Churchill
Livingstone; 1994.
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Clinical Application
Peripheral Nerve Blocks
Blockade of a single targeted nerve is generally referred to as a minor nerve block, whereas blockade of
two or more nerves or a nerve plexus is referred to as a regional block.
Examples of common minor nerve blocks include infraorbital, mental, median, and ulnar nerve blocks.
These are commonly utilized in plastic surgery for minor office procedures and for laceration repair in
the emergency department. Examples of regional nerve blocks include brachial plexus block, femoral
nerve block, and transversus abdominis plane block (TAP block). These may be utilized to anesthetize
entire limbs or body regions with a single cutaneous puncture. Regional nerve blocks are most commonly
performed by anesthesia providers under ultrasound guidance. Tables 12.2 and 12.3 show the maximal
dose, onset, and duration of action of the commonly used local anesthetics for minor and major nerve
blocks.
TABLE 12.2
Dosage and Duration Characteristics of the Local Anesthetics When Used for Minor Nerve Blocks (e.g., Median Nerve Block at the
Wrist)
Drug
Plain Solutions
Epinephrine-Containing
Solutions
Usual Concentration
(%)
Usual Volume
(mL)
Dosage
(mg)
Average Duration
(min)
Average Duration (min)
Procaine
2
5–20
100–400
15–30
30–60
Chloroprocaine
Lidocaine
Mepivacaine
1
5–20
50–200
60–120
120–180
Prilocaine
Bupivacaine
0.25
5–20
12.5–50
180–360
240–480
Etidocaine
0.5
5–20
25–100
120–240
180–420
Reprinted with permission from Strichartz, GR, Covino, BG. Local anesthetics. In: Miller, RD , ed. Anesthesia. 4th ed. New York, NY:
Churchill Livingstone; 1994.
TABLE 12.3
Dosage and Duration Characteristics of the Local Anesthetics When Used for Major Nerve Blocks (e.g., Axillary Block of the
Brachial Plexus)
Drug With Epinephrine
1:200,000
Usual Concentration
(%)
Usual Volume
(mL)
Maximal Dose
(mg)
Usual Onset
(min)
Usual Duration
(min)
Lidocaine
1–1.5
30–50
500
10–20
120–240
Mepivacaine
1–1.5
30–50
500
10–20
180–300
Prilocaine
1–2
30–50
600
10–20
180–300
Bupivacaine
0.25–0.5
30–50
225
15–30
360–720
Etidocaine
0.5–1.0
30–50
400
10–20
360–720
Tetracaine
0.25–0.5
30–50
200
20–30
300–600
Reprinted with permission from Strichartz, GR, Covino, BG. Local anesthetics. In: Miller, RD , ed. Anesthesia. 4th ed. New York, NY:
Churchill Livingstone; 1994.
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Topical Anesthesia
Topical anesthesia is used by many surgeons to lessen the discomfort of injectables such as hyaluronic
acid filler or Botox. These topical agents will provide dermal anesthesia if applied far enough in advance
and in sufficient aliquots, although clinical experience with these drugs may at times be disappointing.
Topical anesthesia is commonly utilized in the pediatric population to lessen the pain associated with
cutaneous puncture associated with intravenous (IV) placement or local anesthetic administration.
Eutectic mixture of local anesthetics is a combination of 25 mg lidocaine and 50 mg prilocaine per gram.
The drug is best applied 30 to 60 minutes prior to the procedure and may be serially reapplied to keep the
skin saturated, or it is often applied and then covered with an occlusive dressing to assist in absorption. 5
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Infiltration of Local Anesthetics
Most often, local anesthesia is achieved by simple subcutaneous infiltration of local anesthetic. Here, local
anesthetic is infiltrated into the tissues immediately adjacent to the wound or planned incision. Specific
nerves are not targeted, only those sensory nerve endings immediately surrounding the surgical field.
The addition of epinephrine in this setting is invaluable for hemostasis in vascular tissue beds and for
prolonging the effect of the drug by preventing clearance to the intravascular space.
Because of the drug’s acidity, infiltration of local anesthetic can itself be a painful experience. Anesthetics
are prepared in a range of pH from 3.5 to 7.0, which serves to lengthen the drug’s shelf life. It is known
that hydrogen ions stimulate peripheral nociceptors, and thus the infiltrated acid causes pain. 6 It is
hypothesized that the time required for the body to alkalinize the solution to a physiologic pH that will
facilitate diffusion into the neuron prolongs the duration to efficacious anesthesia. 6 Furthermore,
alkalinization may serve to augment the amount of nonionized drug available for neuronal cell uptake. 7
Buffered lidocaine solutions have been demonstrated to improve patient comfort and satisfaction in
double-blind randomized controlled trials. 8 Table 12.1 shows the maximal dose and duration of local
anesthetics when used for infiltrative anesthesia.
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Toxicity of Local Anesthetics
Toxicity of local anesthetic is related to the specific anesthetic being utilized, as well as the tissue it is
utilized in. Tissues that are more vascular may carry higher risk of intravascular injection, or the local
anesthetic may be more efficiently cleared to the intravascular space thereby inducing systemic toxicity.
Clinically, when toxic reactions occur, it is often the result of inadvertent intravascular injection or
administration of too large a dose. Furthermore, intravascular injection of epinephrine may cause its own
complications or confuse the presentation of local anesthetic toxicity. It is essential that the syringe be
aspirated prior to injection to confirm that the needle tip is not intravascular. Repeat aspirations should
be performed serially during infiltration to further avoid this complication.
Local anesthetics induce both central nervous system (CNS) and cardiovascular system (CVS) toxicities.
CNS toxicity occurs at a lower dose range than CVS toxicity. Although CNS toxicity is more common,
CVS toxicity is more dangerous and more challenging to treat.
CNS toxicity includes light-headedness, tinnitus, tremors, numbness of the lips or tongue, restlessness
and CNS depression, seizures, apnea, and loss of consciousness at high doses. Benzodiazepines, which
alter the seizure threshold for lidocaine, may be used either as treatment for these symptoms or as
pretreatment when large doses are anticipated. 9
Although rarely observed in the clinical setting, CVS toxicity of local anesthetics can be life-threatening
and difficult to treat. Local anesthetics depress myocardial activity by acting directly on the myocardium
as well as the conduction system of the heart. Local anesthetic also acts on vascular smooth muscle to
induce vasodilation. Hypotension, tachycardia, bradycardia, arrhythmias, or cardiac arrest may be
observed as a result. The longer acting local anesthetics such as bupivacaine (Marcaine) may induce very
difficult-to-treat cardiac complications owing to the drugs’ special affinity for myocardial tissue and long
half-life. Protracted periods of resuscitation have been observed resulting from bupivacaine cardiac
toxicity. 10
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Epinephrine Infiltration and End Organ Perfusion
It was previously believed that epinephrine should be omitted from anesthetic solutions injected in
proximity to end arteries (e.g., fingers, toes, and penis) because of the danger of ischemic necrosis. Recent
experience and research contradicts this notion. It is now accepted that epinephrine is safe for infiltration
in proximity to end arteries such as in the digits and in fact may improve visualization in the surgical
field and reduce painful tourniquet use. Infiltrated epinephrine in end organ anesthesia is now
considered safe, and a number of studies to date have demonstrated the safety and efficacy of this
intervention in digital anesthesia. 11,12 In cases where epinephrine has been infused in the digit and
concern persists, the epinephrine effect may be reversed with phentolamine, but most often this is
unnecessary because simple observation will suffice and perfusion will gradually return as the
epinephrine wears off.
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Tumescent Technique for Liposuction
Clinical experience with tumescent technique for local anesthetic infiltration has cast new light on toxicity
associated with local anesthetic infiltration. The tumescent technique uses highly dilute concentrations of
local anesthetic with epinephrine (1:500,000–1:100,000) in normal saline or lactated Ringer solution.
Contrary to long-accepted maximum safe doses of 7 mg/kg lidocaine, in the tumescent technique, doses
of up to 35 mg/kg lidocaine are routinely safely administered. 13 However, these dose parameters are
dependent on the tissues subjected to the infiltration. For example, in the face, which is considerably
more vascular than the abdomen, clearance of tumescent doses of lidocaine to the intravascular space
occurs much more quickly and toxicity may be faster. Peak serum lidocaine levels may occur as late as 10
to 14 hours after initial injection, as it has been demonstrated that only approximately 20% of infiltrated
local anesthetic is removed along with the lipoaspirate. 14,15 Although large local anesthetic doses are
routinely utilized in practice with the tumescent technique in the trunk and extremities, until a safe
maximum dose is more completely defined, the recommended dose by the manufacturer is no more than
7 mg/kg.
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Treatment of Local Anesthetic Toxicity
The initial treatment of a patient suffering local anesthetic toxicity is supportive. This includes airway
control and oxygenation with 100% FiO2. Hypercarbia can worsen CNS toxicity, and in the convulsing
patient, hyperventilation with 100% oxygen may alter the seizure threshold and terminate the seizure. If
needed, the patient may also be intubated. If seizure activity persists, diazepam (0.1 mg/kg) or thiopental
(2 mg/kg) have also proven effective. 9,16
In the case of hypotension resulting from local anesthetic toxicity, interventions are again initially
supportive. IV fluids should be started and, if needed, vasopressors (phenylephrine) or inotropes to
maintain the blood pressure. In the case of cardiac collapse, in addition to supportive measures, a lipid
rescue protocol should be initiated, as resuscitative measures may be prolonged owing to the long half-
life of the local anesthetic drugs. 16
Intralipid, an infusible 20% lipid emulsion developed for IV nutrition (total parenteral nutrition), is now a
studied and efficacious intervention in local anesthetic overdose. It has been incorporated since 2008 into
safety protocol guidelines in the United States for the management of local anesthetic–induced
cardiotoxicity. During the resuscitative effort, a 20% lipid emulsion infusion can initially be bolused
(1.5 mL/kg) and subsequently infused. The mechanism is not well understood, but it is hypothesized that
augmenting the intravascular lipid concentration creates a lipid sink and acts to draw the lipid-avid local
anesthetic out of the myocardial tissue to the intravascular space, where it may be metabolized by the
liver or circulating plasma esterases. 17
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Cocaine
Cocaine is the only local anesthetic that induces a vasoconstrictive, rather than vasodilatory response. It is
uncommonly used in clinical practice today owing to its CNS stimulant effects including euphoria,
behavioral stimulation, and arousal. The drug is readily absorbed through the mucous membranes.
Numerous deleterious side effects are associated with the drug including tachycardia, hypertension,
mydriasis, tremors, and perspiration. Cocaine is known to simultaneously augment cardiac output while
also inducing coronary vasoconstriction, which may increase the risk of myocardial infarction. 18 Cocaine
has in the past been utilized in nasal surgery for its vasoconstrictive properties. The safe maximum dose
for nasally administered cocaine solution is 1.5 mg/kg. 18,19
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Liposomal Bupivacaine
A liposomal bupivacaine formulation is now Food and Drug Administration (FDA) approved for use in
postsurgical analgesia. Marketed under the name Exparel by Pacira Pharmaceuticals, it uses DepoFoam
technology to encapsulate bupivacaine in multivesicular liposomal particles. These liposomes are slowly
degraded, gradually releasing local anesthetic for up to 72 hours after injection. FDA approval of the drug
was based on several early placebo-controlled trials in bunionectomy and hemorrhoidectomy for which
improved pain control was demonstrated in hours 0 to 24 after injection. However, no significant benefit
was observed in either trial in the hours 24 to 72. 20,21
Applications of liposomal bupivacaine are now broad. Exparel is commonly used for postoperative
analgesia in abdominoplasty, peripheral nerve blockade, pharyngoplasty, and any application where
extended analgesia is desired following surgical intervention. The drug is FDA approved for local
infiltration to improve postoperative pain control and for interscalene brachial plexus blockade following
shoulder surgery. 22
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