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techniques that do not address potential axonal regrowth. While
allograft reconstruction can help prevent subsequent neuromas
during primary nerve reconstruction at the time of trauma, in this
case a symptomatic neuroma had already formed and was
being treated secondarily.
2. Answer: b. Symptomatic neuromas are a common cause of
pain after nerve injury. After initial injury, the distal nerve end
undergoes Wallerian degeneration and the proximal end
attempts to regenerate toward the distal nerve target.
Unsuccessful, disorganized regeneration of the proximal nerve
end results in neuroma formation. Pain centralization is when
peripheral nerve derangements propagate into heightened
sensitivity and abnormal central processing of peripheral nerve
pain. Reinnervation of denervated muscle describes the process
behind targeted muscle reinnervation (TMR) and regenerative
peripheral nerve interfaces (RPNIs).
3. Answer: a. Targeted muscle reinnervation (TMR) has been
shown in both prospective and prospective, randomized trials to
reduce residual limb pain and phantom limb pain, as well as
improve functional and patient-reported outcome scores when
compared with conventional neuroma excision and muscle
burying. Regenerative peripheral muscle interfaces (RPNIs),
Agonist-antagonist myoneural interface (AMI), and reset
neurectomy have been shown in retrospective studies to
decrease residual and phantom limb pain but have never been
studied in a randomized, prospective fashion.
VIDEO LEGENDS
Video 9.1. TMR of ulnar digital nerve to dorsal interosseous motor
branch. Stimulation of ulnar digital nerve after coaptation resulting in
contraction of dorsal interosseous muscle.
REFERENCES
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neuroma following initial amputation for traumatic digital
amputation. J Hand Surg Am. 2018;43(1):86.e1-86.e8.
2. Fried K, Govrin-Lippmann R, Rosenthal F, Ellisman MH, Devor
M. Ultrastructure of afferent axon endings in a neuroma. J
Neurocytol. 1991;20(8):682-701.
3. Karsy M, Watkins R, Jensen MR, Guan J, Brock AA, Mahan MA.
Trends and cost analysis of upper extremity nerve injury using the
national (Nationwide) inpatient sample. World Neurosurg.
2019;123:e488-e500.
4. Arnold DMJ, Wilkens SC, Coert JH, Chen NC, Ducic I, Eberlin KR.
Diagnostic criteria for symptomatic neuroma. Ann Plast Surg.
2019;82(4):420-427.
5. Benne MI, Simpson KH. Gabapentin in the treatment of
neuropathic pain. Palliat Med. 2004;18(1):5-11.
6. Restrepo-Garces CE, Marinov A, McHardy P, Faclier G, Avila A.
Pulsed radiofrequency under ultrasound guidance for persistent
stump-neuroma pain. Pain Pract. 2011;11(1):98-102.
7. Wu J, Chiu DT. Painful neuromas: a review of treatment
modalities. Ann Plast Surg. 1999;43(6):661-667.
8. Eberlin KR, Ducic I. Surgical algorithm for neuroma management:
a changing treatment paradigm. Plast Reconstr Surg Glob Open.
2018;6(10):e1952.
9. Ducic I, Mesbahi AN, Ainger CE, Graw K. The role of peripheral
nerve surgery in the treatment of chronic pain associated with
amputation stumps. Plast Reconstr Surg. 2008;121(3):908-914.
discussion 915-907.
nerve allografts. Hand Clin. 2016;32(2):127-140.
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the body with processed nerve allografts: results from a large
multicenter study. Microsurgery. 2020;40(5):527-537.
analysis of nerve gap repair: comparative effectiveness of
allografts, autografts, and conduits. Plast Reconstr Surg. Publish
ahead of print 2022.
Mackinnon SE. Limitations of conduits in peripheral nerve repairs.
Hand (N Y). 2009;4(2):180-186.
versus microsurgical neurorrhaphy: 2-year follow-up of a
prospective, blinded clinical and electrophysiological multicenter
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Neuroma-in-continuity: a review of pathophysiology and
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neuroma resection and muscle implantation. Plast Reconstr Surg.
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Treatment of painful hand neuromas by their transfer into bone.
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treatment of neuromas improves patient-reported pain,
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depression, and quality of life. Plast Reconstr Surg. 2017;139(2):407-
418.
treatment of painful residual limb neuroma in lower extremity
amputees. J Orthop Trauma. 2015;29(9):e321-e325.
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neuroma formation after finger amputation. J Hand Surg Br.
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M. Neuroma prevention by end-to-side neurorraphy: an
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Application of a porcine small intestine submucosa nerve cap for
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CHAPTER 10 Principles of Tissue
Expansion
Anureet K. Bajaj and Nicole Z. Sommer
KEY POINTS
Tissue expanders are used for the coverage of defects in
the treatment of congenital anomalies, burn
reconstruction, breast reconstruction, abdominal wall
reconstruction, and following traumatic injuries.
Expanders have multiple advantages including the ability
to replace like tissue with like, and no requirement for
advanced technology such as microscopes or
microsurgical instrumentation.
Tissue expanders alter the physiology of the expanded
tissue on the cellular level.
Tissue expansion procedures by necessity require two
operations—one to place the expander and a second to
remove the expander and perform the definitive
reconstruction.
Tissue expanders can be used in all areas of the body;
however, those placed in the extremities and those used
for genital reconstruction have higher complication rates.
To overcome some of the disadvantages of tissue
expansion, further advancements will continue with
regard to the development of external expanders, selffilling expanders, and patient-controlled expansion.
INTRODUCTION
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Tissue expansion is an important step on the reconstructive ladder. It
is a mechanical process that uses the viscoelastic properties of the
skin to increase the surface area of local or regional tissue. In this
manner, tissue that is similar, if not exactly like the tissue needing
replacement, can be used to reconstruct the defect. Replacing like
tissue with like can facilitate a superior result in match of color and
texture without the need for free tissue transfer. By necessity, tissue
expanders imply a two-stage procedure at a minimum—one to place
the expander and a second to remove the expander and perform the
definitive reconstruction.
HISTORY
Tissue expansion has its origins in distraction osteogenesis in the
early 1900s. Codvilla applied this concept to external distraction of
bones. Putti further refined this concept by understanding that a
constant load also was necessary to overcome the resistance of the
soft tissues.
1,2
The first clinical use of expansion in the soft tissues was described
by Neumann in 1957 when he used a rubber balloon under the skin
with an external stopcock to expand local tissue for reconstruction of
a traumatic ear defect.3 This original work on tissue expansion
occurred with little notice until Radovan and Austad independently
developed tissue expanders in 1975. Radovan described a
subcutaneous expander with an internal port for breast
reconstruction. Austad developed a self-inflating tissue expander
using osmotic gradients.4-7 Further investigation led to a better
understanding of the physiological process behind tissue expansion.
PHYSIOLOGY
Multiple changes occur to the overlying tissues during the expansion
process. Mechanical stress causes creep, which is defined as
stretching of a material under constant load over time.
Tissue expansion involves biologic and mechanical creep. Biologic
creep develops with a constant expansion. It creates tissue gain
from increased fibroblast and collagen synthesis, increased
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myofilaments, increased mitotic activity, and neovascularization.
8
The extended deformation of tissue allows for stress relaxation and
formation of new tissue. Stress relaxation is the concept that the
force required to maintain the skin at stretch to a fixed length
decreases over time.
Mechanical creep is the constant load that is applied to the skin,
allowing its extension over time. The stress force of expansion leads
to a parallel realignment of collagen fibers, microfragmentation of
elastic fibers, and adjacent tissue migration.
Expanded tissues also experience increased vascularity with
increased expression of angiogenic factors including vascular
endothelial growth factor (VEGF). Expanded flaps have similar
viability and capillary blood flow as delayed flaps—essentially, an
expanded flap is a form of a delayed flap.
9,10
All of these changes to the tissues that occur with a tissue
expansion return to the normal state during the 4 to 6 weeks
following removal of the expander. See Table 10.1 for changes in
tissues.
TABLE 10.1. CHANGES IN SKIN AND SOFT TISSUE AFTER
TISSUE EXPANSION
Location Change
Epidermis Mitotic activity in epidermis—increase
Epidermis thickens initially and then returns to
normal
Hair follicles may be compressed but are not
damaged
Melanocyte activity may initially increase
Dermis Dermal thickness decreases
A capsule forms around the implant
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Increase in collagen content
Subcutaneous
tissue
Decreased adiposity in the subcutaneous
tissue
Muscle
atrophy
Muscle atrophy occurs regardless if expander
placed above or below the muscle; the
skeletal muscle returns to normal after
removal
Vascularity Increased vascularity, by increase in the
number and caliber of vessels; this is believed
to occur because of temporary hypoxia and
mechanical stress
Effects to
bone
Bony deformation occurs but resolves with
removal of the expander
TYPES OF TISSUE EXPANDERS
Integrated Versus Remote Port
Most expanders have a self-sealing port which is the point of flow
into or out of the expander to allow for serial expansion. The fill port
can be either integrated into the expander itself, which is seen
commonly in expansion for breast reconstruction, or distal to the
expander connected by tubing. The integrated ports have the
advantage of not requiring extra dissection for the port placement but
do have risk of iatrogenic damage to the expander itself. Distal ports
that sit at a distance from the expander decrease this risk of
iatrogenic rupture but can also have issues including difficulty filling
the port because of flipping of the port or kinking of the tubing. Distal
port expanders tend to be safer in areas of thin overlying tissue and
also allow for external placement of the port. In breast
reconstruction, some expanders can become the definitive implant
when the port is removed at a separate procedure after expansion is
complete.
11
Expander Fill
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