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Lower Extremity Soft Tissue & Cutaneous Plastic Surgery
The flap arrangement shown in Figure 18.12 is infrequently utilized
in comparison to the flap arrangement in Figure 18.13. These rhom­
boid flaps are nearly diametrically opposed to one another. This seems
most well-situated in the majority of circumstances on the lower
extremities.
Triple rhomboid flap
For larger lesions, where closure might be difficult, the triple rhom­
boid flap should be considered (Fig. 18.14). The defect is designed as
a hexagon, or three connected 60° rhombi. The rhomboid flaps can
be planned on the 120° angle, thus six potential flaps are available.
The three flaps are selected for convenience, function and cosmetic
result and all should have their limbs pointing in the same direction
(Fig. 18.15). Large circular defects may be closed with this technique
by simply converting them into hexagons and then, conceptually, the
hexagon can be broken up into three rhomboids.
the rhomboid defect is converted to an M-plasty, which effectively
creates two 30° closures rather than one 60° closure (Fig. 18.11). This
preserves tissue and, because this flap is narrower than the classic
rhomboid flap, tension must be shared by the edges of the defect. The
Webster flap is much more difficult to design and perform and it
appears that there is more tension on the transfer of the flap than with
the Limberg flap.
Double rhomboid flap
The double rhomboid transpositional flap may be used to close a 60°
parallelogram with a 2 : 1 length to width ratio. Closure of defects with
this approach is easy to visualize since the 2 : 1 parallelogram consists
of two 60° rhombi (Fig. 18.12). The double rhomboid principle can
be very useful for closing long defects. It is possible to plan four avail­
able rhomboids on the 120° angles. The rhomboid flaps are then
chosen according to the requirements of the local situation.
Figure 18.8  The rhomboid transposition flap. (A) Flap design around non-infected plantar foot ulceration. (B) Transposition of flap and final closure.
Note that additional revisional surgery has been performed dorsally. (C) Postoperative appearance at 6 weeks.
(Courtesy of Dr Stephen Schroeder.)
A
B
C

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The triple rhomboid flap is even more complicated to plan than
other flaps and it leaves a stellate-shaped scar. This scar is not easy to
merge into natural skin crease lines and is, therefore, conspicuous as
a geometric scar (Fig. 18.16). Employ this technique with prudence
and only in areas where the final scar is inconsequential to the closure
of the defect.
Iida double transposition flap
The flap is described as a bilobed flap but it is designed around a
rhombus of 60° and 120° (Fig. 18.17). This method works well if the
defect can be converted to a rhomboid easily and if the skin of the
defect site is mobile and has allowance. Two triangular flaps are pre­
pared to close the rhombic defect. The first triangular flap has an angle
one-quarter smaller than the rhombic skin defect, and the second one
Figure 18.9  Dufourmentel rhomboid flap. The angle of the flap is
created by a bisecting line between horizontal and diagonal tangents of
the primary defect (dotted lines) and the final side is incised equal in
length and parallel to the long axis of the defect. This decreases the arc
of transposition of the flap.
60°
60°
Figure 18.10  Webster 30° transpositional flap. Similar to Dufourmentel
flap except that the distal angle and flap are both 30°.
60°
30°
30°
Figure 18.11  Webster 30° flap with M-plasty. This design is used to
shorten the length by using an M-plasty at the distal angle.
30°
30°
Figure 18.12  Double rhomboid flap. Two 60° rhomboid designs are
placed together. Four different configurations can be designed depending
upon the flap selection. Uncommon version.
Figure 18.13  Double rhomboid flap. This flap design is more commonly
utilized.
Figure 18.14  Triple rhomboid flap. Six potential flaps are available and
the three that are selected should all rotate in the same direction.
Figure 18.15  Triple rhomboid flap. One of the possible triple rhomboid
flap configurations.

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also has an angle one-quarter smaller than the first one. It is important
to set the rotation of the flap at an appropriate angle. It is also neces­
sary to pay attention to the favorable blood circulation of the flap and
to minimize the dog-ear that occurs after the flap is shifted. Tension
on the flap is almost uniformly diffused by consecutively providing
two triangular limbs for the skin defect site. The rotation angles of the
defect site and the second flap are made <90° to minimize the dog-ear
after the flap is transposed.
This flap method may be used on the foot and leg where skin type,
color and quality compatibility is important. Because the posterior
heel and Achilles tissue is less distensible, skin necrosis is more likely
to occur if excessive tension is applied when a defect in this area is
reconstructed with this flap. As a result, the postoperative scar may be
more prominent or conspicuous. When there is less mobility in the
defect site and thus a risk of causing deviation and deformation of the
adjacent tissues by transposing the flap, it is advisable to draw the first
lobe the same size as the skin defect.
Rhomboid flap with multiple Z-plasty
This flap is designed as a rhomboid, an oblique-angled parallelogram
with unequal adjacent sides of 60° and 120°, with a Z-plasty at oppo­
site ends (Fig. 18.18). This 60–120° rhomboid transpositional flap
has gained wide acceptance and popularity as an excellent-shaped flap
for reconstruction of hypertrophic scar defects and lesions in areas
where the standard rhomboid transposition flap may need a little
assistance with redirecting tension away from the operative wound
to a secondary area of laxity. This technique of repair of excisional
defects is characterized by borrowing the required tissue from two
non-adjacent opposite sides of the defect (Fig. 18.19). Most other
flaps borrow the required tissue from a single adjacent region or all
adjacent directions. The ‘sharing’ of tissue from two opposite regions
A
B
Figure 18.16  Triple rhomboid flap. (A) The lesion is drawn in red. The
hexagon is drawn around the lesion with three rhombi in the interior.
The three flaps are designed from each 120° outer angle with the arms
all going in the same direction. (B) The central hexagon and lesion are
excised. (C) Each flap is incised and mobilized and transferred inward.
Final closure provides the unique appearance of this flap. Small dog-ears
are common at each tip but will usually resolve without the need for
additional procedures.
C
Figure 18.17  Iida double transposition flap. Draw an ABCD rhombus
around the lesion at 60° and 120°. Draw bisectors of the prolonged line
CD and the prolonged line BD, and plot point E on the bisector so that
the line DE is equal in length to one side of the rhombus. Plot point F
to make the angle β equal to three-quarters of the angle α (β = 34α).
The DEFG rhombus is drawn as a result. Make point H using the
same procedure, and then make point I to create an angle γ equal to
three-quarters of the angle β (γ = 34β). Using the procedure described
above, two triangular lobes are prepared. Angle β of the first triangle is
one-quarter smaller than angle α, and angle γ of the second triangle is
also one-quarter smaller than angle β. The first lobe is applied to the
target skin defect, and the second lobe is turned sideways to the primary
donor site and reefed to the secondary donor site.
(Redrawn from: Iida, N., Ohsumi, N., Tonegawa, M., et al., 1999. Simple method of
designing a bilobed flap. Plast Reconstr Surg 104, 495–499.)
C
A
E
= 3/4
= 3/4
I
G
F
H
α
α
β
β
β
γ
γ
B
D

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The ‘Reading Man’ transposition flap
This technique basically uses the extra skin relaxation gained with an
unequal Z-plasty maneuver in favor of the defect closure. The proce­
dure is named the ‘Reading Man’ flap because its surgical design
resembles the silhouette of a man who is reading a book held in his
hand (Fig. 18.20). In this technique, two skin flaps are designed in an
unequal Z-plasty manner. To obtain a better resultant scar aligned
with the relaxed skin tension lines, the central arm should be placed
perpendicular to these lines (Fig. 18.20B). The central arm of the
unequal Z-plasty is drawn as an imaginary tangential line passing
through the margin of the circular defect (Fig. 18.20C). The length of
the central arm of the Z-plasty is designed to be 50% longer than the
diameter of the circular defect. From the free end of this line, another
imaginary line is drawn with an angle of 60° (Fig. 18.20D). Then
beginning from the other end of the central arm, a third imaginary
line is drawn with an angle of 45° (Fig. 18.20E). Two skin flaps (f1
and f2) are obtained. The flaps are elevated and flap f1 is transposed
to the defect area and flap f2 is transposed to cover the first flap’s
donor site. The skin flaps are sutured into place resulting in the final
appearance of the incision (Fig. 18.20F).
Figure 18.18  Rhomboid flap with multiple Z-plasty. This flap is designed
as a rhomboid, an oblique-angled parallelogram with unequal adjacent
sides of 60° and 120°, with a Z-plasty at opposite ends.
60°
120°
Figure 18.19  Rhomboid flap with multiple Z-plasty (pig foot). (A) The rhomboid portion is oriented around the lesion to be excised along the axis of
the RSTL. (B) Incisions are made and the rhomboid area is excised. (C) The flaps are mobilized and transposition starts. (D) The final flaps are
transposed and closed.
A
B
C
D
minimizes tension in that direction, while not borrowing from the
remaining regions prevents the distortion of anatomic landmarks
located along that direction. The orientation of the final scar and
direction of tissue tension can be controlled by rotating the rhombic
defect about its central axis.

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Interpolation flaps
An interpolation flap is a two-stage flap in which the base of the flap
does not directly border the recipient site (Fig. 18.23). These flaps are
used when inadequate tissue or skin mobility is present in nearby
tissue to permit coverage of the defect with a primary closure or adja­
cent flap technique. The interpolated flaps are comparable with
The reading man flap is a useful and easy technique for the closure
of circular skin defects located on various lower extremity anatomic
sites. It enables the surgeon to obtain a tension-free skin closure of
large circular defects with minimal healthy skin excision (Fig. 18.21).
COMPARATIVE PROCEDURES
In most cases, when faced with a single lesion that can be excised and
closed with a single flap, the author prefers to use round excision
techniques and rounded flaps as compared with the harsh cornered
rhombus and angled flaps (Fig. 18.22). A comparison of the two
procedures will show the similarities. I will seldom choose the single
or double rhomboid over the single or double-lobed flaps. When the
lobed flaps are performed, I do not have to worry about the corners
and I always prefer the softer final scar appearance. On the other hand,
the potential advantage of the rhomboid flap is that it possesses
straight lines and angles, and it is probably this combination that
prevents scar contracture from having the same effect as in the circular
type of flap. This fact should be taken into consideration in making
the choice between the two methods.
Figure 18.20  The ‘Reading Man’ transpositional flap. (A) Circular defect.
(B) Determining the direction of the central arm of the Z-plasty (dotted
lines). This line should be perpendicular to the relaxed skin tension lines.
(C) The central arm of the Z-plasty is drawn as an imaginary tangential
line passing through the margin of the circular defect. (D,E) Other limbs
of Z-plasty are planned with angles of 45° and 60° according to the
unequal Z-plasty concept. (E) Flap f1 is used to close the defect and
the flap f2 is transposed for closure of the donor site. (F) The final
appearance after incision closure.
(Redrawn from: Mutaf, M., Sunay, M., Bulut, O., 2008. The ‘Reading Man’
procedure. A new technique for the closure of circular skin defects. Reconstr Burns
60 (4), 420–425.)
B
RSTL
d+1/2 %
C
B
D
A
60°
60°
f2
f1
f1
f2
45°
E
F
Figure 18.21  The ‘Reading Man’ transpositional flap. (A) The flap
is drawn out following the guidelines for design. (B) The flaps are
transposed and partially closed to show the approximate final appearance
on a pig foot.
A
B
Figure 18.22  Comparison of rhomboid transposition flap and single-lobe
rotation flap. Note the similarities in appearance at final closure.

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CONCLUSION
All lower-extremity cutaneous defects should be viewed critically and
the options of second-intention healing, skin grafts, rotation flaps,
advancement flaps, transposition flaps and interpolation flaps consid­
ered carefully. When primary closure cannot be performed, flaps give
the surgeon the opportunity to close defects with adjacent tissue that
offers good color and texture match. These flaps may yield functional
and cosmetic results that are superior to those provided by secondary-
intention healing and skin grafts.
Smoking, aspirin, excessive alcohol intake and anticoagulant use
are relative contraindications to the use of transposition flaps as they
interfere with the healing of the flaps and, therefore, increase the
incidence of flap complications. Herbal supplements containing such
substances as gingko biloba or salicylates also have some anticoagu­
lant activity that may delay healing. The use of these substances
should be dealt with prior to surgery so that they may be discontinued
several weeks prior to the procedure.
transposition flaps in that the flap is pivoted and lifted over an area
of normal skin to reach the defect. The base of the transposition flap
is adjacent to the defect, while the base of the interpolated flap is
located at a distance from the defect. This arrangement results in a
bridge of tissue, or pedicle, between the flap base and the defect that
must be removed in a second stage after vascularity is established
between the wound and the overlying flap. The pedicle is usually
separated from the flap tip between 2 and 3 weeks, depending upon
the flap location. At that time, the donor site is revised and the inset
flap is closed. Additionally, the previous sutures in the initial donor
site and flap tip are removed. The patient is then rescheduled for final
suture removal in another 2 weeks.
Interpolation flaps are uncommon on the lower extremity, but may
be useful around prominent bony areas such as the malleoli, first and
fifth metatarsophalangeal area and posterior heel (Fig. 18.24). The
malleoli flaps use tissue from the ankle area to repair the bony promi­
nences. The metatarsophalangeal flaps use tissue from the dorsal foot
region to cover the joints, and the posterior heel flaps use skin from
the medial or lateral heel region to repair defects in the back of the
heel. A major consideration for interpolated flaps is the need for
multiple-staged surgical intervention and special consideration must
be taken regarding patient compliance of the pedicle care during the
interval between the two surgeries.
Figure 18.23  Interpolation flap. (A) The flap is outlined and elevated.
(B) The flap tip is inset into the defect and the primary donor site is
closed. (C) Once the flap has revascularized, it is divided at the pedicle.
(D) The donor site is revised and inset flap is closed.
A
B
C
D
Figure 18.24  Interpolation flap. Illustrated option at medial malleolus
area; first stage of the procedure.
FURTHER READING
Aasi, S.Z., Leffell, D.J., 2005. Bilobed
transposition flap. Dermatol Clin 23 (1),
55–64.
Akyurek, M., Safak, T., 2002. Direct closure of
radial forearm free-flap donor sites by
double-opposing rhomboid transposition
flaps. J Reconstr Microsurg 18, 33–36.
Bauer, B.S., Margulis, A., 2004. The expanded
transposition flap: shifting paradigms based
on experience gained from two decades of
pediatric tissue expansion. Plast Reconstr
Surg 114 (1), 98–106.
Bechara, F.G., Al-Muhammadi, R., Sand, M.,
et al., 2007. A modified corner stitch for
fixation of flap tips. Dermatol Surg 33 (10),
1277–1279.
Borges, A.F., 1981. The rhombic flap. Plast
Reconstr Surg 67, 458–466.
Bray, D.A., 1983. Clinical applications of the
rhomboid flap. Arch Otolaryngol 109,
37–42.

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Chatrath, V., Rohrer, T., 2002. Transposition
flaps. eMedicine 2, 1–33.
Choi, K.H., Kim, S.Y., Kim, G.M., 2010.
Rhombic transposition flap: its
modification and application in skin tumor
surgery. Korean J Dermatol 48 (1), 8–16.
Christensen, J.C., Dockery, G.L., 1986. Flap
classification and survival factors: current
concepts. Clin Podiatr Med Surg 3,
579–588.
Clark, J.M., Wang, T.D., 2001. Skin flaps,
design. eMedicine 10, 1–21.
Congdon, G.C., Altman, M.I., Aldridge, J.,
1988. A comparison of transpositional
neurovascular skin flaps for reconstruction
of diabetic heel ulcerations. J Foot Surg 27,
127–129.
Cook, J.L., 2005. Reconstructive utility of the
bilobed flap: lessons from flap successes
and failures. Dermatol Surg 31 (8 pt 2),
1024–1033.
Cuono, C.B., 1984. Double Z-rhombic repair
of both large and small defects of the upper
extremity. J Hand Surg 9, 197–201.
Dockery, G.L., 1992. Principles of forefoot
plastic surgery. In: Butterworth, R., Dockery,
G.L. (Eds), A color atlas and text of forefoot
surgery. Mosby, Chicago, pp. 1–34.
Dockery, G.L., Christensen, J.C., 1986.
Principles and descriptions of design of
skin flaps for use on the lower extremity.
Clin Pod Med Surg 3, 563–577.
Downs, B.W., Clark, J.M., Wang, T.D., 2008.
Skin flaps, design. eMedicine Online.
Available at:
com/article/875968-overview
Dufourmentel, C., 1962. Le fermture des
pertes de substance limitees le lambeau
de rotation en losange. Ann Chir Plast 7,
61–66.
Feng, Y., Hu, M., Yan, H., et al., 2011. Repair
of dorsal defects over the middle phalanx
and proximal interphalangeal joint with a
transposition flap from the dorsum of the
proximal phalanx. J Hand Surg Am 36 (5),
864–869.
Hoy, E.A., Schwartz, R.A., Granick, M.S., et al.,
2003. Closure of complicated wounds.
eMedicine 12, 1–13.
Iida, N., Kotake, A., 2011. A new surgical
procedure for little toe polysyndactyly
without skin graft. Ann Plast Surg 67 (2),
167–169.
Iida, N., Ohsumi, N., Sakai, M., 1997. A
trilobed flap for reconstruction of nasal
skin defects. Plast Reconstr Surg 100,
991–995.
Iida, N., Ohsumi, N., Tonegawa, M., et al.,
1999. Simple method of designing a
bilobed flap. Plast Reconstr Surg 104:
495–499.
Iida, N., Watanabe, A., 2011. Rhomboid flap
with multiple Z-plasty for treatment of
hypertrophic scar on the pubic area. J Plast
Reconstr Aesthet Surg 64:818–821. Available
at:
20951106
Jackson, I.T., 1976. Flaps design and
management. In: Calnan, J. (Ed.), Recent
advances in plastic surgery. Churchill
Livingstone, New York, pp. 153–172.
Kandel, E.F., Bennett, R.G., 2001. The effect of
stitch type on flap tip blood flow. J Am
Acad Dermatol 44 (2), 265–272.
Kimyai-Asadi, A., Goldberg, L.H., 2005. Island
pedicle flap. Dermatol Clin 23 (1),
113–127.
Larrabee, W.F., 1990. Design of local skin flaps.
Otolaryngol Clin North Am 23, 899–923.
Larrabee, W.F., Holloway, G.A., Sutton, D.,
1984. Wound tension and blood flow in
skin flaps. Ann Otol Rhinol Laryngol 93,
112–115.
Larrabee, W.F., Trachy, R., Sutton, D., et al.,
1981. Rhomboid flap dynamics. Arch
Otolaryngol 107, 755–757.
Limberg, A.A., 1966. Design of local flaps. In:
Gibson, T. (Ed.), Modern trends in plastic
surgery. Butterworths, London, pp. 38–61.
Lister, G.C., Gibson, T., 1972. Closure of
rhomboid skin defects: the flaps of Limberg
and Dufourmentel. Br J Plast Surg 25,
300–312.
Mashhadi, S.A., Loh, C.Y., 2011. A reliable
method of applying a circumferential
dressing. Int Wound J 8 (3), 320–321.
Mathes, S.J., Hansen, S.L., 2005. Flap
Classification and Applications. In: Mathes,
S.J., Plastic surgery, Vol. I: General
principles, 2nd edn. Saunders, Philadelphia,
pp. 365–482.
Mellette, J.R., Ho, D.Q., 2005. Interpolation
flaps. Dermatol Clin 23 (1), 87–112.
Monheit, G.D., 1980. The rhomboid
transposition flap re-evaluated. J Dermatol
Surg Oncol 6, 464–470.
Mutaf, M., Sunay, M., Bulut, O., 2008. The
‘Reading Man’ procedure. A new technique
for the closure of circular skin defects.
Reconstr Burns 60 (4), 420–425.
Paragas, L.K., Attinger, C., Blume, P.A., 2000.
Local flaps. Clin Pod Med Surg 17,
267–318.
Ramsey, M.L., 2002. Pedicle/interpolation
flaps. eMedicine 6, 1–22.
Ramsey, M.L., Kozic, H., 2009. Pedicle/
interpolation flaps. eMedicine 10, 1–10.
Rohrer, T.E., Bhatia, A., 2005. Transposition
flaps in cutaneous surgery. Dermatol Surg
31 (8 Pt 2), 1014–1023.
Rossi, A., Jeffs, J.V., 1980. The rhomboid flap
of Limberg – a simple aid to planning. Ann
Plast Surg 5, 494–496.
Seyhan, T., Caglar, B., 2008. ‘Reading man flap’
design for reconstruction of circular
infraorbital and malar skin defects.
Dermatol Surg 34 (11), 1536–1543.
Storm, T.R., Lee, M.S., 2001. Plastic and
reconstructive surgery. In: Banks, A.S.,
Downey, M.S., Martin, D.E., et al. (Eds),
McGlamry’s comprehensive textbook of
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Williams & Wilkins, Philadelphia,
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Stough, D.B., Stough, D.B., 1990. Triple
rhomboid flap for crown alopecia
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543–548.
Tschoi, M., Hoy, E.A., Granick, M.S., 2005.
Skin flaps. Clin Plast Surg 32 (2),
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Tschoi, M., Hoy, E.A., Granick, M.S., 2009.
Skin flaps. Surg Clin N Am 89 (3),
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Ulkur, E., Acikel, C., Evinc, R., et al., 2006. Use
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Von Heimburg, D., Hendricks, H.P., Pallua, N.,
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Warren, S.E., Snell, G.F., 1986. Complex
wound closure, excisional biopsy, and
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Webster, R.C., Davidson, T.M., Smith, R.C.,
1978. The thirty degree transposition flap.
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Wilhelmi, B.J., Blackwell, S.J., Mancoll, J.S.,
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CHAPTER CONTENTS
Introduction
207
Historical background
207
Skin anatomy
208
Skin graft physiology
209
Skin contraction in skin grafts
210
Indications for skin grafting
211
Decision ladder for wound closure
211
Split-thickness skin grafts vs full-thickness
skin grafts
211
Donor site locations
211
Instrumentations for split-thickness skin graft
harvesting
212
Preoperative preparation of the recipient bed
212
Intraoperative preparation of the recipient bed
213
Technique of split-thickness skin graft donor site
harvesting with power instrumentation
213
Meshing and pie-crusting
215
Application of the split-thickness skin graft
216
Dressing the skin graft
216
Postoperative care
217
Full-thickness skin grafts
217
Donor site locations: full-thickness skin grafts
218
Full-thickness skin graft harvesting
218
Full-thickness skin graft dressing
218
Postoperative care
218
Donor site healing
218
Graft storage
220
Skin graft complications
220
Summary
220
INTRODUCTION
Skin grafting is a fairly modern adjunct to surgical therapy and has a
distinct role in reconstructive surgery of the foot and ankle. A graft is
defined as any free tissue that is transplanted.1 A skin graft is the sepa­
ration of all or a portion of the skin from its donor site and local
blood supply, followed by transplantation to a recipient site.2 The
transplanted skin subsequently relies entirely on the recipient site’s
blood supply for survival.
The skin is the largest organ of the body consisting of epidermis
and dermis. Skin grafts incorporate all of the epidermis and varying
depths of the dermis. A full-thickness skin graft consists of the epidermis
and the entire dermis, while a split-thickness skin graft consists of the
epidermis and a variable portion of the dermis. According to the thick­
ness of the dermis, split-thickness skin grafts are described as thin,
intermediate or thick. A thin split-thickness skin graft consists of the epi­
dermis and approximately 0.008–0.012 inches of dermis. An interme­
diate split-thickness skin graft consists of epidermis and approximately
0.012–0.016 inches of dermis, whereas a thick split-thickness skin graft
consists of epidermis and 0.016–0.020 inches of dermis.2,3
An autograft (autogenous graft) is transferred from donor to recipi­
ent site in the same individual. An allograft (homograft) is transferred
from one person to another within the same species. A xenograft (het­
erograft) is from a different species (e.g. porcine), while an isograft is
from one genetically identical person to another (e.g. identical twins)
(see Ch. 20).
HISTORICAL BACKGROUND
Although the first accounts of skin grafts are prior to 2500 BC, Reverdin,
in 1869, was the first to report his success with thin skin grafts fol­
lowed by allografts in 1872.4,5 Others followed with reports of their
techniques: Ollier’s thin split-thickness skin grafts (1872), Wolfe’s
©2012 Elsevier Ltd.
Skin grafts
Peter A. Blume
Chapter
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epithelium arranged in distinct layers called strata. The strata from
deep to superficial are the stratum germinativum (basal layer); the
stratum spinosum (prickle cell layer); the stratum granulosum; the
stratum lucidum (only present on palms and soles) and the stratum
corneum.8 These strata represent different stages in the life cycle of the
keratinocytes produced in the stratum basale. The keratinocytes
migrate superficially to the stratum corneum and eventually slough
off in approximately 19 days. The epidermis is avascular mostly con­
sisting of keratinocytes. Scattered in the deeper layers of the epidermis
are melanocytes, Merkel cells and Langerhans cells (Fig. 19.1) (see Chs
2 and 3).9–12
The dermis is divided into two distinct layers: the superficial or
papillary layer and the deep or reticular layer.9,10,12–14 The papillary
layer contains widely separated, delicate, collagenous elastic and
full-thickness skin grafts (1875), Thiersch’s thin split-thickness skin
grafts (1886) and Krause’s full-thickness skin grafts (1893). Not until
the twentieth century did the current concepts, developments and
refinements of skin grafting come to exist due to many investigators
making contributions in understanding graft physiology, as well as
advancements in hardware and instrumentation.6,7
SKIN ANATOMY
The skin envelops the entire surface of the body and consists of two
layers: the outermost thinner layer is the epidermis and the innermost
thicker layer is the dermis. The epidermis is stratified squamous
Figure 19.1  Skin anatomy. Cross-section of skin anatomy representing the levels of thin (0.008–0.012 inches); medium (0.012–0.016 inches) and thick
(0.016–0.020 inches) split-thickness skin grafts and full-thickness skin grafts.
Epidermis
Dermis
Subcutaneous fat
Artery
Nerve
Vein
Full thickness
skin grafts
Split thickness
skin grafts
Thick
Medium
Thin
Free nerve endings
Hair follicle
Hair shaft
Sebaceous gland
Eccrine sweat gland

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SKIN GRAFT PHYSIOLOGY
The process of take of a skin graft is the revascularization and reattach­
ment of the skin graft to the recipient site.2 Skin grafts are a form of
tissue transplantation requiring adherence and the formation of a new
blood supply from the recipient bed. The three phases to skin graft
healing are: (1) the phase of serum imbibition (plasmatic circulation);
(2) the phase of revascularization, a combination of neovascularization
and inosculation and (3) the phase of organization.2,20,21
The phase of serum imbibition is also known as plasmatic circulation
because no true circulation exists between the graft and the recipient
bed. Fibrinogen-free serum, not plasma, passively enters the graft and
therefore, the phase is best termed serum imbibition.2,20,22–27 Initially,
the graft is avascular and dependent upon the fluid from the recipient
bed for nutrition. After placement of the graft, an effusion of clear
fluid from the host bed deposits a light fibrin clot tenuously adhering
the graft to the host bed.2,12,22,23,28,29 A fibrinogen-free suspension of
erythrocytes enters the capillaries of the overlying skin at approxi­
mately 24 h as the graft capillaries dilate. This influx of fluid into the
graft results in edema over the first several days until venous and
lymphatic circulation develop at about day 9 after graft applica­
tion.2,22,23,29 This early phase of wound healing is not nutritional,
rather it functions to keep the graft humid and the graft vessels open
for more efficient revascularization. During this initial phase, it is
critical to keep the graft recipient bed interface as close as possible
in order to optimize the movement of fluid from the host bed to
the graft.
The concept of prewounding the recipient bed refers to the stimula­
tion of serum and blood vessels in the recipient bed prior to the
permanent placement of the skin graft on the bed.30 Prewounding may
be accomplished by applying a porcine graft or another biologic dress­
ing temporarily to the recipient site prior to application of the perma­
nent graft.18,31 Loading the skin graft with nutrient fluid before its
application onto the graft bed allows the nutrient fluid to be taken up
by the graft before application onto the recipient bed.27 Loading is
accomplished by harvesting the skin graft and immediately replacing
the graft to the donor site for 24 h increasing the graft’s ability to
withstand the ischemic period. The importance of these techniques
relates to the patient with vascular insufficiency at the recipient bed.
Theoretically, prewounding and loading increase the chance of success­
ful skin graft take but are rarely performed.27,30,32 Of these two tech­
niques, however, prewounding the site is the more beneficial. If a
porcine graft or biologic dressing fails to produce the desired stimula­
tory effect on a wound, then at least the patient is spared a donor site
wound.30
The phase of serum imbibition lasts approximately 48 h if the graft
covers a fresh wound, but may be extended if placed over a poorly
vascularized wound or shortened if the recipient site has already
reached the proliferative phase. Split-thickness skin grafts may take
well even after four days of ischemia, whereas full-thickness skin grafts
can survive up to approximately five days of ischemia.12,29,33 The most
common complication leading to graft failure is hematoma or seroma
formation within this period. A 19-gauge needle may be used to aspi­
rate the hematoma and reestablish graft-host apposition. The viability
of the graft is dependent upon the succinct attention to hematoma
and seroma formation.
The second phase of skin graft healing is the phase of revascularization
divided into neovascularization and inosculation.2 Controversy exists
as to which one dominates. Neovascularization is the outgrowth of
blood vessels from the recipient bed into the graft dermis at a rate of
2 mm/day. The new vessels grow into the graft from the host bed with
simultaneous degeneration of the old vessels in the graft.2,22,23,28,29 New
vessel growth can occur as primary neovascularization or secondary
reticular fibers enmeshed with capillaries. The papillary layer exhibits
dermal papillae protruding into the epidermis. These papillae are
reflected in the epidermis as epidermal ridges producing fingerprints.
The reticular layer consists of connective tissue fibers more densely
interwoven and coarser than in the papillary layer. Less dense regions
produce skin tension lines. Elastin is distributed throughout the
dermis. The elastin is more closely interlaced in the reticular
layer.9,10,12,14 Connective tissue cells including fibroblasts are often
associated with mast cells and pigment-bearing melanophages and are
distributed throughout the dermis in normal skin.
Two types of glands are present in the dermis: sweat (sudoriferous)
glands and sebaceous glands. Sweat glands are subdivided into eccrine
and apocrine. Eccrine glands are tubular glands coiled at the base of
the dermis and primarily secrete an odorless hypotonic solution.
These glands are located mainly in the plantar and palmar skin
and are controlled by the sympathetic nervous system.14 Apocrine
sweat glands are located in the axillary and anogenital areas. The
ducts of these glands terminate in hair follicles and secrete substances
with fatty and proteinaceous components. Apocrine sweat gland
secretions are odorless. Bacteria enzymatically breakdown apocrine
sweat gland secretions resulting in a musky odor. Full-thickness skin
grafts regain the use of most sweat glands, while full-thickness flaps
regain all of their original sweat glands. During the period when sweat
glands are separated from their innervation after grafting, approxi­
mately 10 months, the graft lacks lubrication, therefore the use of an
emollient is crucial.15,16 Split-thickness skin grafts generally lack sweat
glands, thus, long-term lubrication with emollients is necessary for
graft survival and the prevention of breakdown. Attention must be
directed towards long-term hydration and stress protection in order
to prevent the formation of junctional scar tissue and skin graft
breakdown.
Sebaceous glands fill with fat granules and eventually disintegrate
secreting sebum, which in turn lubricates the hair, maintains supple
skin and protects the skin from friction injury. Sebum also provides a
barrier to moisture loss. Sebaceous glands are not found in the palmar
or plantar skin.12,14 Sebaceous glands may be present in full-thickness
skin grafts but are often absent from split-thickness skin grafts because
they are located deeper in the dermis. Sebaceous glands are not
dependent upon autonomic innervation and if present in the graft,
their function returns within several weeks.16
The vascular anatomy of the skin is entirely in the dermis and con­
sists of a superficial (papillary) plexus and a deep (reticular) plexus.
The epidermis is entirely dependent upon the dermis for its blood
supply. The superficial plexus arborizes as it reaches the dermal papil­
lae.17 It is believed split-thickness skin grafts can re-establish circula­
tion faster and more efficiently than full-thickness skin grafts because
the harvest is more superficial in the dermis.17,18 In split-thickness skin
grafts, the number of transected vessels is increased, and the number
of portals available for recipient bed penetration is increased, thus
revascularization of the skin graft occurs sooner.
Cutaneous sensation consists of Meissner’s corpuscles, Pacinian cor­
puscle receptors, root hair plexuses and free nerve endings.16,19 Meiss­
ner’s corpuscles are located in the dermal papillae and relay afferent
light touch information.19 Their location implies that they may be
spared in both full-thickness skin grafts and all split-thickness skin
grafts. Pacinian receptors are located in the deeper dermis or hypoder­
mis and relay deep pressure information. Pacinian receptors are
spared in full-thickness skin grafts and possibly in thick split-thickness
skin grafts. Root hair plexuses relay hair motion. The hair root is in
the deeper dermis and spared in full-thickness skin grafts but severed
in split-thickness skin grafts. Free nerve endings are present through­
out the dermis and sense painful stimuli. The free nerve endings are
typically spared resulting in pain sometimes being heightened after
grafting.16

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Lower Extremity Soft Tissue & Cutaneous Plastic Surgery
to affect the speed or quality of reinnervation.16 Many factors impede
axon ingrowth and the development of functional innervation includ­
ing proximal nerve injury to a recipient site, scar tissue, infection, deep
penetrating wounds, and hematoma formation. The application of
several small grafts versus one large graft can adversely affect the rein­
nervation process.16,37 The return of pain sensation may be atypical in
pattern with the presentation of hyper- or hypoesthesia.
Split-thickness skin grafts rarely contain functioning sweat (eccrine)
glands, whereas full-thickness skin grafts contain some functioning
sweat glands.12,14,16,28 Transferred sweat glands assume the behavior of
the recipient bed sweat glands. Grafts that lack sensation are often
devoid of functioning sweat glands. Sebaceous gland function is not
dependent upon innervation.28 Split-thickness skin grafts often lack
sweat glands and have a higher propensity towards dyshydrosis, there­
fore, topical rehydration is necessary. Sebum begins to appear at 3–4
weeks and supplementation with topical emollients may be decreased.
Full-thickness skin grafts remain smooth and pliable throughout the
entire period.
SKIN CONTRACTION IN SKIN GRAFTS
Two types of skin contraction occur with skin grafting. Primary con­
traction occurs when the graft is removed from the donor site. It is
more pronounced in full-thickness skin grafts than in split-thickness
skin grafts owing to the elastin fibers present in the dermis.18,34,39–41
The more dermis present in the graft, the more passive recoil of the
elastin fiber occurs. Full-thickness skin grafts retract approximately
44%, intermediate split-thickness skin grafts retract approximately
22% and thin split-thickness skin grafts retract approximately 9%.8,28,42
Tension applied to the graft when applied to the recipient bed rees­
tablishes graft length and width.
Secondary contraction takes place after the graft is placed on the
recipient bed.41 Secondary contraction results from the host bed
myofibroblasts within the wound pulling the skin graft. Full-thickness
skin grafts are more resistant to secondary contraction than split-
thickness skin grafts. The greater the percentage of dermis in the
graft, the less the skin graft contracts secondarily. Histologic evalua­
tion of secondary contraction reveals that it is a function of the
life cycle length of myofibroblasts present in the wound. Initial
invasion of myofibroblasts is equal in full-thickness skin grafts,
split-thickness skin grafts, and in granulating wounds. It has been
observed that the myofibroblast life cycle is much shorter in full-
thickness skin grafts as compared with split-thickness skin grafts,
therefore, the greater the relative thickness of graft dermis, the
speedier the myofibroblast life cycle.41 Relative thickness refers to the
percentage of dermis in the graft. In addition to the shorter myofi­
broblast life cycle, the enzyme prolylhydroxylase necessary for colla­
gen synthesis is inhibited to a greater degree in full-thickness skin
grafts compared to split-thickness grafts, thus, full-thickness skin grafts
resist secondary contraction better than thin split-thickness skin
grafts.12,18,28,29,34,43
Secondary contraction at joint levels and weight-bearing surfaces
have clinical pitfalls associated with them, including decreased range
of motion and pigmentation changes. It may be necessary to appro­
priately splint an area and institute early physical therapy to maintain
function where contracture could lead to decreased range of motion.
In general, full-thickness skin grafts have better pigmentation matches
than do split-thickness skin grafts. The thinner the graft, the greater
the chance of pigmentation changes. Split-thickness skin grafts may
result in hyperpigmentation due to an altered ratio of pigment pro­
ducing to non-pigment producing cells affecting darker skinned indi­
viduals more.12,16,18,28,34 Although pigmentation is a concern with facial
neovascularization. Primary neovascularization occurs with close
contact between the recipient bed and graft. New vessels reach out
from the recipient bed, penetrate the holes left by the graft vessels and
proliferate into this framework revascularizing the graft. By 24 h, new
vessels invade approximately one-sixth of the thickness of the graft
dermis and by 48 h, reach the dermal-epidermal junction.2,28,29 Blood
enters the graft during this phase and the graft turns a pinkish hue
caused by fine extravasations on the undersurface of the graft signify­
ing anastomoses are being formed. The development of vascular anas­
tomoses with the flow of blood into the graft inhibits vascular
proliferation in the recipient bed, a negative feedback mechanism.28,29
The graft margins are usually devoid of anastomoses caused by a lack
of graft-host apposition. When vascular proliferation remains unin­
hibited, secondary revascularization occurs.28,29 The ischemic period
is extended during secondary revascularization and many irreversible
degenerative processes occur within the graft. When inhibition of
vascular growth is absent, the capillary buds grow into the graft in a
fashion that differs from that of normal skin, such that the graft heals
with a smooth, fibrotic, tight, silvery sheen on its surface. In larger
grafts, it is common for both types of revascularization to exist. Ino­
sculation occurs where circulation is restored in the original graft
vessels through anastomoses with the recipient bed vessels.2,12,28,29
A predominance of new capillary channels within the graft dermis
suggests an active neovascularization process.2,12,28,29
The phase of organization begins when the graft has fully adhered to
the recipient bed.2 The graft now functions in a similar manner to
native peripheral skin. The graft match and durability is a function of
the percentage of dermis transplanted. This phase begins with adher­
ence of the graft to the host, while the recipient bed produces exudate
containing plasma, erythrocytes and leukocytes.12,28,29 The fibrinogen
in this exudate precipitates into fibrin, allowing for adherence of the
graft to the host bed. The subsequent fibrinogen-free serum penetrates
the fibrin layer and enters the graft dermis providing nourishment and
perhaps creating a moist environment for the graft to survive in until
a blood supply can be established.27 Leukocytes enter the dermis and
eventually focus on degenerating appendages and epidermis.12,27–29
Leukocytes remain until there is a reestablishment of circulation.
Fibroblasts infiltrate the layer of fibrin and leukocytes from
day 4 through day 8, as the fibrin clot is resorbed and reorganized. By
day 9, the fibroblasts, along with the new vasculature, have anchored
the deep layers of the dermis to the recipient bed.
Veins begin filling at approximately day 6, with venous outflow
noted by day 9.28,29 Lymphatic vessels fill between days 4 and 7, and
show definitive evidence of the existence of lymphatic flow on the
9th postoperative day.12,28,29 This delicate process of revascularization
can be affected by shearing forces or hematoma formation at
the graft site. The revascularization process can be positively affected
with a strict perioperative regimen. This should include elevation of
the extremity in order to decrease edema, strict bed rest and close
adherence to intraoperative hemostasis by way of ligation and
cauterization.18,34
During the first 25–30 days after graft application, the graft nerves
degenerate.16,35,36 At approximately 2 months, reinnervation begins
with pain sensation returning first, followed by touch, hot and cold
distinction and finally, the ability to perspire.16,37,38 Completion of this
process may take as long as 1.5–2 years. Graft reinnervation is most
complete in full-thickness skin grafts and least complete in thin split-
thickness skin grafts, yet the rate of sensation return is most rapid in
thin split-thickness skin grafts and slowest in full-thickness skin grafts.
It is generally believed that reinnervation begins at the margins and
then centralizes.16 In all types of sensation, the graft tends to assume
the sensory pattern of the recipient bed.16,37 Grafts placed over perios­
teum or muscle develop poor sensation.16 Placement of the graft nerve
fibers parallel to the direction of the ingrowing nerves does not appear

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potential inability of the graft to withstand these forces may result in
tissue breakdown or painful junctional scars. Bony deformities and
biomechanical abnormalities often create increased shear in areas
which are normally non-weight-bearing with minimal peak pressures.
Examples include the Charcot foot and intrinsic minus disease of the
diabetic foot. Care must be taken to avoid skin grafting in these
regions which would normally not pose a problem.
DECISION LADDER FOR WOUND CLOSURE
The goal of wound healing is gaining the best possible closure through
the least morbid means. The decision for wound closure depends
upon the location of the wound and host factors (i.e. tissue extensibil­
ity and the individual’s healing potential). From the least complex to
the most complex, the clinician should consider the following: (1)
allowing the wound to close by secondary intention; (2) application
of various wound care products like alginates, hydrocolloids, hydro­
gels or platelet-derived growth factors, as an adjunct to secondary
intention; (3) primary closure of the wound; (4) local random flaps;
(5) skin grafting; (6) local fasciocutaneous or myofasciocutaneous
flaps; (7) island flaps or (8) free tissue transfers.17,18,34,53,63–70 Wound
evaluation coupled with the knowledge of various closure techniques
and their indications will provide the surgeon with the tools to achieve
a successful closure.
SPLIT-THICKNESS SKIN GRAFTS VS
FULL-THICKNESS SKIN GRAFTS
Split-thickness skin grafts have some advantages and disadvantages
when compared to full-thickness skin grafts. First, the thinner the skin
graft is, the greater the chance of graft take since there are a greater
number of transected vessels through which revascularization occurs.
Split-thickness skin grafts take easier and faster than full-thickness
skin grafts. Second, there is less primary contraction with thinner
grafts, since there are fewer elastin fibers in thinner skin grafts resulting
in less primary recoil.12,28,29 Full-thickness skin grafts and, to a lesser
degree, thick split-thickness skin grafts have more primary contraction.
Third, there is greater secondary contraction in thinner grafts, caused
by an increased myofibroblast life cycle and increased prolylhydroxy­
lase activity. Full-thickness skin grafts and, to a lesser degree, thick
split-thickness skin grafts undergo less secondary contraction. Fourth,
there are fewer functioning sweat glands in split-thickness skin grafts
because sweat glands are in the deep dermis and transected split-
thickness skin grafts bring only a portion of the duct and none of the
gland. Full-thickness skin grafts and, to a lesser degree, thick split-
thickness skin grafts have more functioning sweat glands. Since
split-thickness skin grafts vary in thickness, their healing qualities
fall somewhere between those of a full-thickness skin graft and a thin
split-thickness skin graft. The characteristics of each graft must be kept
in mind when deciding which type and thickness of skin graft is
optimal for a particular reconstruction.
Donor site locations
Split-thickness skin grafts can be harvested from a variety of areas of
the body. Ideally, the harvest site should be an area of the body that
is hidden from view in warm weather recreational clothing due to
donor site scarring.12,34 Common harvest sites include the buttocks,
thighs, abdomen, calf, and medial arch of the foot (Fig. 19.2).2,71,72
reconstruction, it is not a major issue in the lower extremity. Function
is the most important parameter for pedal reconstruction.
INDICATIONS FOR SKIN GRAFTING
A vast array of indications exists for skin grafting in foot and
ankle reconstructive surgery. Sterile ulcerations, burns, traumatic
soft tissue loss, defects from flap donor sites, tumor resections,
soft tissue defects from incisional drainage and desyndactylization
are some of the common indications for skin grafts in the lower
extremity.44–51
The decision tree for wound closure should always include skin
grafting as one of its options. Primary closure of a wound should only
be attempted if appropriate, while other wounds require flap closure
and skin grafting. Consideration of the anatomic location and multi­
ple comorbidities need to be evaluated prior to skin grafting. Wound
closure should be individualized for the wound or defect taking all
factors into account.18,52–54
Skin grafts can be applied to dermis, fascia, periosteum, perichon­
drium, peritenon or paratenon but not to cortical bone without peri­
osteum or tendon without tendon sheath. An exception to this rule
exists if the width of the exposed tendon or bone is <5 mm.18,34 In
this instance, the graft receives enough nourishment from the sur­
rounding tissue allowing it to survive. The application of a skin graft
to an acute wound with exposed fat may desiccate and fail, therefore,
it is best to delay placement of the graft until abundant granulation
tissue covers the wound.
The wound bed must be sufficiently perfused in order for the graft
to adhere and contract. A thorough non-invasive vascular work-up
including an ankle-brachial index may be required before surgery. If
a patient is diagnosed with moderate to severe vascular disease, a
lower extremity bypass may be necessary.55–58
The ankle-brachial systolic pressure index is the ratio of ankle systo­
lic blood pressure divided by the brachial systolic blood pressure. It
is measured at rest and then after standardized treadmill exercise,
which consists of walking for 5 min at 2 miles/h on a 12% incline. A
normal ankle-brachial index is slightly >1.0. After exercise it should
not drop >20% of the resting index and should return to that baseline
within 3 min of completing the exercise test. An ankle-brachial index,
>1.3 signifies medial vessel calcification common in the diabetic pop­
ulation. An ankle-brachial index <0.92 signifies arterial obstruction.
Moderate to severe claudication occurs with an index between 0.4 and
0.8. Ischemic rest pain occurs when the index is <0.4 and an ankle-
brachial index <0.15 signifies a threatened limb. A resting ankle-
brachial index can easily be performed in an office setting when
vascular insufficiency is suspected.18,34,56–58
Transcutaneous oxygen tension is a measurement of the meta­
bolic state of the target tissues. Because transcutaneous oxygen
tension is not affected by arterial calcification, it is a useful measure­
ment for patients with diabetes since their ankle-brachial index
may be unreliable due to medial vessel calcifications. Although it
is possible to heal with lower transcutaneous oxygen tensions, a
transcutaneous oxygen tension of >40 mmHg predicts greater graft
survival.18,34,56–58
Skin graft survival is greatly enhanced if the appropriate parameters
are identified prior to surgery.18,34 Complete resolution of periwound
erythema and edema and a pH of 7.4 are optimal for survival. Granu­
lation tissue is a marker for skin graft readiness but should be thor­
oughly debrided before application, in order to reduce the number of
organisms per gram of tissue (<105).7,18,34,59–62
Weight-bearing surfaces are subjected to higher shear forces and
are fraught with complications with respect to skin grafting. The

212
Lower Extremity Soft Tissue & Cutaneous Plastic Surgery
PREOPERATIVE PREPARATION
OF THE RECIPIENT BED
Preparation of the recipient bed is an integral part of skin grafting.
The bacterial count should be <105 organisms per gram of granulation
tissue.60,74 Wound examination and quantitative bacterial counts are
helpful in determining bacterial growth.74 A technique called the rapid
slide method, which takes about 15 min to complete, is a helpful
diagnostic modality. The difference between the traditional quantita­
tive bacteria count and the rapid slide technique is that the former
involves a long process of serial tube dilutions over a 24–36 h period,
Donor-recipient site skin color match is preferable and is dependent
upon the donor site which maintains the epidermal specificity.
Instrumentations for split-thickness
skin graft harvesting
Harvesting a split-thickness skin graft has traditionally been accom­
plished the following ways: free-hand cutting, drum dermatomes and
power dermatomes. In general, free-hand knives and air-electric
powered dermatomes are used to cut lengthwise on the extremity and
drum dermatomes are used to cut transverse across the body.12
Free-hand cutting was exclusively used before the invention of the
power-driven and drum dermatomes. The skin is sliced in a similar
motion to that of cutting bread. Free-hand cutting is rarely used today
because of the unpredictable margin and depth created. Large Humby-
type knives are used less today, but the smaller Goulian-type knives
or razor blades are still useful in an outpatient setting where the power
dermatome may not be readily available.2,43,73 Many emergency depart­
ments use small disposable plastic battery-run dermatomes approxi­
mately the size of a razor blade.
There are two major types of drum dermatomes, the Reese® and the
Padgett-Hood® (Padgett Instruments, Kansas City, MO). The Reese®
drum dermatome is heavier and requires adhesive tape applied to the
drum and a glue applied to the skin. The major disadvantages of the
Reese drum is the calibration cannot be adjusted in the middle of
skin graft removal. The Reese drum is limited to a 7 × 4-inch graft.2,12
The Padgett-Hood® drum dermatome is lighter and easier to handle
and uses just tissue glue applied to both the drum and the skin
surface. It can be recalibrated during mid-harvest if the graft is too
thin or thick and can graft skin 8 inches by 3-, 4- or 5-inches wide.
The Padgett-Hood® drum dermatome may accidentally change
graft thickness during mid-harvest which makes it somewhat
unreliable.12
Most split-thickness skin grafts in the USA are harvested using either
the electrically driven Padgett-Hood® dermatome, or the air powered
or electrically powered Zimmer® (Zimmer Patient Care, Dover, OH)
dermatome because they are reliable and easy to use (Fig. 19.3A).
These dermatomes have a width setting of 2.5, 5.0, 7.5 and 10.0 cm
(Fig. 19.3B). The average intermediate split-thickness skin graft is
0.015 inches.
Figure 19.3  (A) Zimmer dermatome (Zimmer Patient Care, Dover, OH)
pneumatic dermatome. (B) Zimmer dermatome width setting 10, 7.5, 5,
2.5 cm and dermatome blade.
A
B
Figure 19.2  Thigh donor site. Split-thickness skin graft lateral thigh
donor site with petechial hemorrhages.

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Technique of split-thickness skin graft
donor site harvesting with power
instrumentation
The donor site should be chosen and measured preoperatively allow­
ing the patient to be properly positioned for the harvest. The donor
region is shaved preoperatively and prepped in the usual manner.
General, spinal, monitored anesthesia care, or local anesthesia can be
used. The donor site can be infiltrated with local anesthesia with or
without epinephrine.79,82,83
Povidone–iodine (Betadine, Purdue Frederick, Norwalk, CT) can be
used to surgically prep the donor site, but should be washed off prior
to harvesting. The povidone–iodine may cause the dermatome to stick
to the skin. Sterile mineral oil has been traditionally applied to the
site to allow the dermatome to slide easier during the harvest. Zimmer
while the latter uses one 0.02 mL aliquot of the suspension which is
Gram stained. If one organism is isolated on the slide, a reading of
>105 organisms per gram of tissue is noted. In addition to a bacterial
count of <105, a recipient wound bed ready for skin grafting should
have a red robust granular base, with increased skin lines and neoepi­
thelialization at the wound edges. Skin lines should be noted adjacent
to the wound signifying decreased edema. Periwound erythema
should be absent. Wound conversion from chronic to acute is para­
mount to a successful take.18,34,75
Wound debridement is accomplished with the following tech­
niques: (1) topical treatment; (2) serial debridement and (3) trial
porcine skin grafting or use of another biologic wound dressing.76
Topical treatment with silver sulfadiazine three times a day after
serial debridements will often decrease the bacterial count. Silver
sulfadiazine may actually stimulate epithelialization.77–79 Other
agents, such as 3% hydrogen peroxide, 1% povidone–iodine, 0.25%
acetic acid and 0.5% hypochlorite are acceptable as a one time use
in order to decrease bacterial load. These agents should not be
used daily due to their cytotoxic effects on epithelial migration.28 The
cytotoxicity of these agents is based on the particular agent’s concen­
tration. The typical concentrations previously mentioned are cyto­
toxic. Less potent concentrations of these agents are not toxic and may
render them non-antibacterial; the converse is true for more potent
concentrations.80
Porcine xenografting can be helpful in determining the potential
viability of a split-thickness skin graft. Advantages of xenografts
include the lack of donor site morbidity. The recipient bed is pre­
wounded, which allows for conversion to the proliferative phase,
which may decrease time to graft take when the permanent graft is
applied.3 Porcine grafts can be used to clean a wound unless the
wound is infected with Gram-negative bacteria.31 Gram-negative bac­
teria thrive in the porcine graft and the wound actually worsens. If the
porcine graft shows signs of take by days 7–10, then the wound is
clean enough to accept the autograft.18 Within granulation tissue,
many crevices exist in which bacteria may colonize. The wound bed
including all crevices should be fully debrided prior to graft applica­
tion.18,34 The presence of granulation tissue indicates conversion has
occurred and a split-thickness skin graft will most likely sustain itself.
Hemostasis is important in preventing hematoma and serum forma­
tion. Topical thrombin, cautery and ligation may be considered prior
to graft application.17,18,34
INTRAOPERATIVE PREPARATION
OF THE RECIPIENT BED
Skin graft failure is often a result of inappropriate preparation of the
recipient bed, therefore, careful attention is placed upon debridement
techniques. Intraoperative preparation of the recipient bed begins
with excision of the wound edges and curettage of the granulation
tissue from the base of the wound creating a clean, healthy bed for
skin graft application. Granulation tissue has many small crevices
which allow for bacterial colonization.81 Debridement of these areas
is important. Sharp debridement utilizing curettes and blades is
crucial (Figs 19.4, 19.5). The wound bed is then pulse-lavaged with
3–6 L of saline or lactated ringers. Protocol includes a plastic bowel
bag, suction tip and irrigant. The velocity and quantity of the fluid
that is used for lavaging the tissue, referred to as detergent action, is
important in cleansing the wound. Antibiotic-containing fluids are
not necessary in the pulse-lavage. Once the irrigation is complete,
gloves, gowns and light handles are changed. The surgical site is
re-draped, and a separate sterile closure table is used for the remainder
of the procedure.
Figure 19.4  (A) Wound prior to debridement. (B) Recipient bed after
debridement.
A
B

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Lower Extremity Soft Tissue & Cutaneous Plastic Surgery
during removal, allowing a more accurate cut. Another assistant can
then grasp the skin, with pick-ups, as the dermatome slices through
the skin, to allow the thickness of the graft to be judged. Thicker grafts
are opaque, while thinner grafts are more translucent.
A useful tool to evaluate the relative thickness of the graft is to
observe the bleeding pattern from the harvest site. Deeper cut split-
thickness skin grafts leave fewer bleeding points and petechial hemor­
rhages in the wound. More superficial grafts leave multiple smaller
bleeding points more consistent with the superficial vascular plexus
being transected.
Once the graft is harvested, the graft should be placed on a sterile
saline-soaked sponge until it is to be used. The graft can be meshed
or pie-crusted at this time. If bleeding is a problem, the donor site
may be sprayed with topical thrombin or 1 : 200 000 dilute epine­
phrine. Intraoperatively, the donor site may be temporarily covered
with saline-soaked gauze or a sheet of Xeroform® (Sherwood Medical
Industries, St Paul, MN) until the surgeon is ready to dress the site.
now recommends using sterile saline while harvesting the skin graft
to increase the life of the instruments. Alternatively, sterile HIBI­
CLENS® antimicrobial, antiseptic skin cleanser acts as an excellent
lubricant applied to the harvest site resulting in a smooth harvest of
the skin graft.
Before initiating the graft harvest, the dermatome thickness can be
checked at 0.015 in by introducing a No. 15 Bard-Parker scalpel blade
between the cutting blade and the base. The dermatome blade can be
dulled with continuous passes of the No. 15 blade between the der­
matome blade and base.12,18,34
The cutting of the graft requires the dermatome, with power running,
be set flat on the skin. The dermatome is then advanced along the
skin surface with sustained downward pressure. It is useful to visualize
the dermatome as an airplane landing on an aircraft carrier, moving
along the runway, and taking off again. Having an assistant apply
pressure to the skin ahead of the dermatome with a tongue depressor
can facilitate the process by creating uniform tension on the skin
Figure 19.5  (A) Wound prior to debridement. (B) Wound prior to debridement. (C) Recipient bed after debridement with curette.
A
B
C

Chapter
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(Fig. 19.6).85–87 Meshed grafts should not exceed a ratio of 1.0 to 1.5.
A ratio >1.0 to 1.5 leaves a criss-cross pattern on the skin because of
the inability of the larger spaces to fill in by epithelial migration from
the surrounding graft. Another reason not to over expand the mesh
graft is that it allows the recipient bed to contract more than smaller
meshed grafts. Meshing has three distinct advantages. First, it is a way
MESHING AND PIE-CRUSTING
A split-thickness skin graft can be used whole, meshed, or pie crusted.84
The technique of meshing involves placing the graft on a plastic
carrier and hand-cranking the tissue through the meshing machine
Figure 19.6  (A) Harvest of split thickness skin graft with Zimmer dermatome (Zimmer Patient Care, Dover, OH) (B) Mesh preparation. (C) Mesher.
(D) Split thickness skin graft meshing 1 : 1.5. (E) 1–1.5 meshed split-thickness skin graft.
A
B
C
D
E

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Lower Extremity Soft Tissue & Cutaneous Plastic Surgery
to expand the skin graft to cover larger areas (Fig. 19.7). Second, it
adheres better to irregular surfaces versus non-meshed skin. Third, it
allows fluid to drain from the recipient bed and thereby prevents
hematoma or seroma formation beneath the graft.12,18,34
Pie-crusting is the practice of placing the split-thickness onto a hard
surface, dermis side up and using a scalpel to create a variable number
of small cuts or slits into the graft (Fig. 19.8).88,89 Pie crusting, like
meshing, allows for drainage decreasing the likelihood of hematoma
or seroma formation beneath the graft. Pie-crusting does not have the
criss-cross pattern in the healed skin like meshed skin grafts, but has
the disadvantage of not allowing the same degree of subgraft
hematoma or seroma drainage or expansion.
Figure 19.7  (A) Granular leg wound prior to split thickness skin graft application. (B) Application of meshed split-thickness skin graft. (C) Final
application of meshed split-thickness skin graft.
A
B
C
Figure 19.8  Pie-crusted split thickness graft on partial 1st ray
amputation site.
APPLICATION OF THE SPLIT-THICKNESS
SKIN GRAFT
Split-thickness skin grafts, especially if meshed, have a tendency to
fold back on themselves. Patience and a steady hand are required for
insetting the graft. Either the meshing plate, saline-soaked gauze, or
Telfa® (Kendall Co, Boston, MA), with the shiny dermis side up and
pick-ups, are used to transport the graft into place on the recipient
bed. There are basically four ways of adhering the graft to the recipient
site: (1) skin staples (Fig. 19.9); (2) simple interrupted suture tech­
nique with 4.0 or 5.0 monofilament nylon; (3) running 5.0 polygly­
colic acid, polyglactin, chromic, or plain gut stitch and (4) topical skin
adhesive or (5) nothing at all. Care should be taken neither to stretch
the graft out too vigorously nor to let it fold back upon itself. Trim­
ming of the excess skin graft is completed once inset is finalized.
DRESSING THE SKIN GRAFT
Once the graft is in place on the recipient bed, a stent dressing of two
varieties can be placed. The graft can be covered with a traditional
bolster stent type dressing using Xeroform® (Sherwood Medical Indus­
tries, St Paul, MN) placed directly on the graft followed by saline
soaked cotton balls. This stent or bolster dressing applies pressure to
the graft over the recipient bed preventing hematoma and seroma
formation beneath the graft and reducing mechanical shear forces by
adhering the graft over irregular surfaces.
Bolster dressings are then wrapped, with some combination of 4 × 4
gauze, gauze roll, cast padding, Red Cross cotton rolls, elastic band­
ages (ACE, Becton, Dickinson, and Co, Franklin Lakes, NJ) and Coban
(3M Health Care, Tustin, CA). An alternative method of dressing the
graft is to apply a dome-paste bandage (Unna Boots, Miles, West
Haven, CT) over a bolster dressing.84,90–93

Chapter
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Negative pressure wound therapy (NPWT) (Vacuum-Assisted
Closure, V.A.C.®, Kinetic Concepts Inc., San Antonio, TX) is an alterna­
tive dressing to apply as a bolster dressing for skin grafts (Fig. 19.10).94
NPWT has been shown to accelerate wound healing possibly due to
removal of interstitial fluids, which increases oxygen and nutrient
delivery to tissues leading to increased vascularity and granulation
tissue, decreased bacterial colonization and removal of inhibitory
factors from chronic wounds.95 The NPWT has been shown to result
in less wound edema, faster narrowing of the separation plane between
the graft and the recipient wound bed, and earlier termination of
the acute inflammatory reaction in a pig model with a split thickness
skin graft.96
In the application of the VAC as a bolster dressing, a non-adhering
dressing is applied between the skin graft and VAC sponge. Non-
adhering dressing options include, but are not limited to, Xeroform
(Sherwood Medical Industries, St Paul, MN), Mepitel (Mölnlycke
Health Care Norcross, GA) or Adaptic (Johnson and Johnson, New
Brunswick, NJ) The non-adhering dressing is cut to the dimensions
of the wound, as is the VAC sponge prior to application. The
VAC is maintained for a period of 4–5 days under a continuous pres­
sure of 120 mmHg and is not changed during this time period
postoperatively.
POSTOPERATIVE CARE
Postoperative care of the limb is critical to the prevention of potential
complications. The limb should be placed on strict elevation for 5
days allowing graft-host circulation to develop. A sequential dangling
regimen is undertaken, 5 min/h on day 7; 10 min/h on day 8;
Figure 19.9  (A) Application of split thickness skin graft status post-rotational heel flap. (B) Application of split thickness skin graft with skin staples.
(C) 5 days status post-application of graft.
A
B
C
15 min/h on day 9, allowing the skin graft to become re-accustomed
to venous gravitational force without excessive edema.12,18,28,34
The patient may begin physical therapy at around the third postopera­
tive week to increase the range of motion. By 4–6 weeks postopera­
tively, the patient may progress to guarded weight-bearing, with
an appropriate assistance device. The foot should remain wrapped
with an ACE bandage whenever it is in a dependent position. By 6–8
weeks postoperatively, the patient may progress to full weight-bearing
with decreasing assistance as tolerated. Preoperative physical therapy
and gait training is often beneficial. This schedule may be altered
depending upon the percentage of graft take, location of the recipient
site, adjunctive procedures performed and the patient’s medical
history.
FULL-THICKNESS SKIN GRAFTS
Split-thickness skin grafts have a higher percentage of take and a
greater rate of success than full-thickness because of decreased vascular
framework through which the recipient bed site capillaries can enter
the full-thickness skin graft dermis. Full-thickness skin grafts are more
durable than split-thickness skin grafts and usually regain use of their
sweat glands. These qualities make full-thickness skin grafts more
desirable and viable, once they have taken. Full-thickness skin grafts
are harvested by elliptical excision at a ratio of length to width of
3–4 : 1, with subsequent primary closure of the donor site as opposed
to a split-thickness skin graft, which is harvested with a dermatome.
In general, full-thickness skin grafts in the foot and ankle are small
pinch grafts used for covering limited areas like in avulsive-type inju­
ries or desyndactylizations.

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Lower Extremity Soft Tissue & Cutaneous Plastic Surgery
crease, popliteal fossa, or antecubital fossa make for the best full-
thickness skin grafts.12,18 In the foot, the area above the sinus tarsi is
ideal for donation of a 3–4 : 1 full-thickness ellipse to fill small deficits
(Fig. 19.11) (see Ch. 25).97 Traumatically amputated digits may be
debrided of fat and used as full-thickness skin grafts.98 By appropri­
ately selecting the location of the donor site, later hair growth can be
avoided. This is particularly important in children. Donor site selec­
tion becomes especially important when grafting from the groin area
with the possibility of pubic hair growth.
A particularly useful area of the foot to harvest a full-thickness skin
graft is from the sinus tarsi.97 The technique called pinch grafting is
used because of the favorable extensibility of the tissue making for
ease of closure of the donor site. In order to assure appropriate closure
of the donor site, the clinician must take a 3–4 : 1 length-to-width ratio
of tissue (4 : 1 is preferred). Minor undermining of the skin may be
necessary to obtain adequate skin closure with no tension.
Full-thickness skin graft harvesting
Harvesting of the full-thickness skin graft is initiated by tracing out the
dimensions of the defect to be filled. The tracing is then cut out, with
its long axis along the flexor crease and placed onto the donor site.
Next, an ellipse with a 3–4 : 1 length to width ratio is drawn to encom­
pass the traced area in an area of maximal extensibility. An ellipse is
then excised at a 90° angle to the dermis, such that as little fat as pos­
sible is harvested. The fat which accompanies the full-thickness skin
graft must be trimmed away from the dermis. The full-thickness skin
graft is matched to the defect and trimmed to be properly inset. Note
that the recipient site is prepared in the same meticulous manner that
a recipient site for split-thickness skin graft is prepared. The recipient
bed must not be infected or graft failure is imminent.
The full-thickness skin graft is then either stapled or sutured into
place typically with monofilament nylon because of its low reactiv­
ity.99 Pie-crusting the graft prevents drainage from accumulating
beneath the graft, thus, necessary to help prevent hematoma or seroma
formation beneath the graft.
The perimeter of the donor site is then undermined and primarily
closed. This site is then dressed in the typical surgical fashion.76
Xeroform® and a fluffy compressive dressing is applied over the inci­
sion site.
Full-thickness skin graft dressing
A stent dressing is applied in the same manner used for split-thickness
skin grafts, to maximize the full-thickness skin graft-recipient bed
contact to prevent hematoma or seroma formation beneath the graft.
Again, a protective dressing and a posterior splint or Unna® boot are
applied.
Postoperative care
Based on the physiology of skin grafting, the limb should be elevated
for at least 5 days. Then, a dangling regimen, similar to the one for
split-thickness skin grafts can be used. Full-thickness skin grafts need
to be stress protected for a total of 3–4 weeks.
Donor site healing
The majority of full-thickness skin graft donor sites are closed prima­
rily after undermining the wound margins. On the other hand, split-
thickness skin graft donor sites were historically covered with
Xeroform® gauze covered by a layer of Telfa® and a bulky gauze dress­
ing. One day postoperatively, the Telfa® would be removed and the
Xeroform® allowed to air dry. Then, heat lamp application or
Donor site locations: full-thickness
skin grafts
Full-thickness skin grafts are almost always harvested from regions
where the skin is thin because the thicker the skin, the higher rate of
necrosis and graft failure. As a rule, flexor creases like the inguinal
A
B
Figure 19.10  (A) Anterior ankle split thickness skin graft status
post-burn injury. (B) VAC application to act as stent dressing. (C) Anterior
ankle graft 100% healed.
C

Chapter
Skin grafts
219
| 19 |
Figure 19.11  (A) Syndactyly preoperatively. (B) Pinch graft/full-thickness donor site in sinus tarsi. (C) Status post-full-thickness harvest with preservation
of superficial veins. (D) Application of full-thickness skin-graft status post desyndactylization. (E) Close-up of final graft position.
A
B
C
D
E

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Lower Extremity Soft Tissue & Cutaneous Plastic Surgery
Mechanical shearing forces cause disruption of the delicate micro­
circulation of the recipient bed leading to the inability of the host bed
to revascularize the graft.34 This occurs when the patient prematurely
ambulates and stresses the graft site. A properly applied stent dressing
coupled with a bulky dressing over the extremity decrease mechanical
shearing forces. Of utmost importance is patient compliance to
remain strict nonweightbearing on the grafted extremity.
Inadequate recipient bed vascularity can be avoided by proper
patient selection elicited through a thorough physical exam and non-
invasive vascular exams as needed.7,57,58 If the patient has peripheral
vascular disease, then working closely with a vascular surgeon is
crucial. Often, patients with decreased perfusion will need a bypass
graft to reperfuse the affected area prior to skin graft application.
Seroma occurs in areas where a confluence of lymphatic channels
meet as in the groin.12,28,29 In split-thickness skin grafts, elevation by
seroma may allow epithelialization on the underside of the graft
preventing revascularization resulting in sloughing of the graft.
Long-term mechanical issues should be addressed before skin graft­
ing. Skin grafts should not be placed on weight-bearing surfaces of
the foot without significant consideration given to the pressures that
the graft will have to endure.88,105–107 Often, patients who need skin
grafts do not have normal feet with normal plantar force plate pressures.
Many patients have had previous foot reconstruction creating mechan­
ical and structural instability or have markedly deformed feet.105,108 A
patient with a Charcot foot with abnormal structural architecture may
have altered weight-bearing mechanics. Radiographs and a biome­
chanical examination are necessary prior to reconstruction with a skin
graft.
Non-weight-bearing surfaces are prone to break down with certain
shoe gear. The medial aspect of the first metatarsal-phalangeal joint
in a patient with a severe hallux abductovalgus deformity can be inap­
propriate for skin grafting if the deformity is not addressed. Knowl­
edge of the biomechanical profile of the patient is critical when
considering using a skin graft.
Other factors which may affect the take of the skin graft should be
elicited in a thorough history and physical. Of particular importance
are a bleeding history and anticoagulation use, such as aspirin and
non-steroidal antiinflammatory medications.7,99 These factors may
lead to clot formation beneath the graft. Many systemic medications,
such as corticosteroids, chemotherapeutic and immunosuppressive
drugs may interfere with wound healing and this should all be assessed
before surgery.7
After graft take has occurred, there are more factors that can lead to
decreased blood supply to the graft-recipient bed interface and even­
tual failure. Most notable of these is cigarette smoking, but diabetes
mellitus, malnutrition or use of medications which result in vitamin
trace element or protein deficiencies, also increase the risk of graft
failure.7,55,109 Donor site pain, infection or delayed healing can be a
difficult and protracted problem to deal with. The recipient site can
be plagued with hyperesthesia, hypoesthesia, paresthesia, skin color
changes, bullae and unwanted hair growth with skin grafting.16,18,34,74
SUMMARY
In this chapter, the authors have explored the anatomy, physiology,
mechanics and biology of skin grafts. Armed with this knowledge, one
can predict or anticipate potential complications and thereby avoid
them. The authors have emphasized the importance of converting
chronic infected wounds to acute sterile wounds prior to skin grafting
and have discussed the need to assess the patient’s vascular status. Skin
grafting, when properly used, can be a valuable tool – an adjunct for
wound closure and reconstruction (Fig. 19.12).
application of scarlet red was tried to speed up epithelialization.12,100
This is seldom used in today’s surgical arena. Currently, a Xeroform®
dressing continues to be used but it remains on the donor site until
it falls off. Also semi-occlusive dressings, such as BioBrane® (Dow B.
Heckman, Sugar Hill, TX), occlusive dressings, such as OpSite® (Smith
and Nephew Medical, Hull, England, UK) or Tegaderm® (3M Medical-
Surgical Division, St Paul, MN) have been shown to minimize the
donor site pain, increase epithelialization, and create a moist environ­
ment for wound healing.101 If fluid accumulates under the dressing, it
should be drained under sterile conditions. If the drainage is suspect,
the wound should be cultured and appropriate antibiotic therapy
initiated followed by daily silver sulfadiazine dressing changes.
The inflammatory phase represents the initial stage of healing fol­
lowed by blood clotting and fibrin formation on the wound surface.
Epithelialization occurs from the wound edges as well as the epithelial
appendages, such as hair follicles, sebaceous glands or sweat glands.
Evidence of these appendages laying down epithelial tissue is seen as
small, dark spots on the surface of the donor site.
GRAFT STORAGE
Autograft banking is the process of reapplying the graft to the donor
site, for use at a later date. The graft must be harvested for reapplica­
tion within 5 days after it was first severed from the donor site. This
has the added benefit of loading the graft with nutrient fluid before
placing it onto the recipient bed.27,102
Refrigeration of the skin graft is commonly employed and can
remain up to 21 days. Excess graft should be refrigerated. Freezing,
without using a protective agent, such as glycerol, which binds with
water, causes cell death.98
Autograft cadaver skin grafts are stored in banks after preservation
with glycerol and rapid freezing with liquid nitrogen. Porcine grafts
may also be used fresh or frozen to cover wounds. Lyophilized and
freeze-dried human and porcine grafts may be useful if allograft skin
is not available, although fresh allograft is definitely preferred.12,98
SKIN GRAFT COMPLICATIONS
Several factors may cause skin graft failure. The most common
complication is hematoma. Other complications include infection,
mechanical shearing forces, inadequate recipient bed vascularity,
seroma, poor selection of skin graft location and technical error.12,17,62
Hematoma prevents graft recipient bed contact increasing the
ischemic period and decreasing the chance of graft survival.18,80 If there
is 0.5 mm of fluid between the graft and the recipient bed, then revas­
cularization is delayed 12 h. If the amount of fluid is increased to
5.0 mm, then revascularization is delayed by 5 days if the graft sur­
vives at all.18 Hemostasis first and foremost prevents hematoma for­
mation. If excessive bleeding is noted intraoperatively, then graft
placement may need to be delayed by 24 h.
Infection is the second most common cause of graft failure. Sterili­
zation of the recipient bed prior to graft placement is imperative. Prior
to graft application, both the number of organisms (<105 organisms
per gram of granulation tissue) and the identification of specific
offending organisms are of importance.74 Organisms like Staphylococ­
cus aureus, Pseudomonas, and beta-hemolytica Streptococcus have been
implicated in graft failure more than other organisms.79,103 One study
revealed a 35% and 25% decrease in graft take in grafts infected with
S. aureus and Pseudomonas, respectively.104 Bacteria produce plasmin
and proteolytic enzymes which break down fibrin and decreases graft
adherence.

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| 19 |
Figure 19.12  (A) Wound status post-VAC therapy, partial 1st and 2nd ray amputation, serial debridement. (B) Application of split-thickness skin-graft
pie-crusted. (C) 1st postoperative dressing with 100% graft take. (D) Postoperative day 18. (E) Completely healed.
A
B
C
D
E

222
Lower Extremity Soft Tissue & Cutaneous Plastic Surgery
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split-skin grafts on their donor sites. Plast
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99. Craven, N.M., Telfer, N.R., 1999. An open
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skin grafting. J Am Acad Dermatol 40,
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100. Lawrence, J.E., Blake, G.B., 1991. A
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FURTHER READING
Blume, P.A., Key, J.J., Thakor, P., et al, 2010.
Retrospective evaluation of clinical
outcomes in subjects with split-thickness
skin graft: comparing V.A.C. therapy and
conventional therapy in foot and ankle
reconstructive surgeries. Int Wound J 7 (6),
480–487.
Boyce, S.T., Goretsky, M.J., Greenhalgh, D.G.,
et al., 1995. Comparative assessment
of cultured skin substitutes and native
skin autograft for treatment of full-
thickness burns. Ann Surg 222,
743–752.
Brongo, S., Pilegaard, J., Blomqvist, G., 1997.
Clinical experiences with the external tissue
extender. Scand J Plast Reconstr Hand Surg
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et al., A pilot study to evaluate porcine
small intestinal submucosa as a covering
for partial thickness wounds. Presented
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Falanga, V., 1999. Care of venous leg ulcers.
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Ramanujam, C.L., Stapleton, J.J., Kilpadi, K.L.,
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CHAPTER CONTENTS
Introduction
225
Skin autograft
225
Skin allograft and xenograft
226
Cultured cells and composite grafts
227
Conclusion
229
INTRODUCTION
In cutaneous surgery, there is a constant battle between the donor site
availability and morbidity, and the acceptance of the recipient site of
the donor tissue. There is a variety of tissue to select from, depending
on the needs of the patient and the tissue available. Understanding
the various characteristics of different tissues will assist the surgeon in
choosing the best material for each condition.
A graft is defined as a tissue separated from the donor vascular
bed that relies on the ingrowth of new vessels from the recipient bed
for survival. It provides no vascular elements of its own. In contrast,
a flap is tissue that is either still attached to the donor blood supply
or provides elements of its own vasculature to anastomose to the
recipient vessels. The survival rate of a graft is usually higher than a
flap, providing the vascular bed of the recipient site is properly pre­
pared with good granulation tissue present and devitalized tissue
removed.
Grafts may be classified further depending on the thickness and the
source of the graft. A split-thickness graft is the gold standard to resur­
face wounds and involves the harvest of the epidermis and varying
portions of the dermis. A full-thickness skin graft includes the entire
dermis with the epidermis and also provides for excellent coverage of
wounds. The advantage of the split-thickness graft over full-thickness
graft is better graft ‘take’ and large donor areas available for harvest,
but it has a greater risk of graft contraction and hypertrophic scar
formation. The full-thickness graft has very minimal graft contracture
and excellent cosmetic results, but has a less reliable ‘take’ of the graft
and limited tissue availability.
One difficulty with all grafts and flaps is the availability of donor
tissue. If there has been extensive skin loss, as seen in some burn
patients, there may not be adequate remaining tissue to provide cover­
age of the wounds. Even expansion of the split-thickness skin graft
with meshing of the graft from 1 : 1.5 up to 1 : 9 will provide some
additional coverage, but still may not be adequate. Alternative forms
of grafting can be considered for these more difficult conditions.
An autograft is defined as the transplantation of tissue from one
location to another in the same individual. This would include the
autologous split-thickness and full-thickness grafts just reviewed. An
isograft is the transplant of tissue from a genetically identical twin
donor to the recipient. An allograft involves the transplantation of
tissue between unrelated individuals of the same species and a
xenograft is the transplant of tissue between different species. Of the
graft types available, there are risks and benefits that should be con­
sidered for each patient and each graft type.
SKIN AUTOGRAFT
In the partial and full-thickness autologous skin grafts, the trans­
planted skin derives its initial nutrition from the serum of the recipi­
ent site. This is known as imbibition. Although the graft is sutured
around the recipient site, it is not anchored to the underlying vascular
bed and is highly susceptible to mechanical shearing, resulting in graft
loss. The formation of a seroma or hematoma during this early post­
operative period will also result in graft loss as the donor tissue is
raised from the nutrient layer below.
The ingrowth of blood vessels from the recipient bed, referred to as
inosculation, begins within approximately 48 h of transplant, during
which time the donor tissue is very vulnerable to external or internal
factors that may disrupt the tenuous blood supply. Meshing of the
graft can expand graft coverage and enhance graft ‘take’ by allowing
release of excess fluid that could otherwise build up under the graft
site (Fig. 20.1). Failures can and do occur due to the fragility of the
newly transplanted skin especially in patients with arteriopathies,
diabetes, debilitating diseases and when local conditions are not favo­
rable such as presence of infection or necrotic tissue, hematoma or
seroma formation or motion at the graft site. However, when sufficient
©2012 Elsevier Ltd.
Autografts, allografts and xenografts
in cutaneous surgery
Mary E. Crawford
Chapter
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either from immunologic rejection or as a result of damage to the
epidermal–dermal junction from cryopreservation leaving behind
the dermal components capable of supporting an autologous
skin graft. Widely meshed autologous split-thickness skin grafts
with meshed allograft overlay have also shown improved healing
compared with the autograft alone. Burn patients are frequently
immunocompromised for several weeks after a burn and, therefore,
the rejection of the allograft is usually delayed. Prolonged immuno­
suppression is required in order to maintain these grafts for any longer
duration due to the antigenicity. Allogeneic skin is becoming more
widely available with regional tissue banks capable of cryopreserving
or using glycerol to preserve the graft and storing the allograft for
protracted period of time. Widespread use of the allograft is still
limited by the risk of disease transmission, especially hepatitis and
human immunodeficiency virus, and the subsequent rejection seen
with its use.
The xenograft carries with it additional issues not seen with the
allograft. First of all, cells of one species may not function in the other
species environment. A more pressing issue, however, is the presence
of preexisting antibodies to the xenogeneic tissue in the recipient prior
to transplantation that results in a hyperacute rejection of the xenograft
within the first few minutes to hours after transplantation. The
volume of donor tissue is available for harvest and transplant, the
autograft has the highest rate of success with the fewest complications
compared with the other graft types available (Fig. 20.2).
SKIN ALLOGRAFT AND XENOGRAFT
When donor tissue availability is limited, other wound coverage
options are considered. The allogeneic or xenogeneic tissues may
provide the optimal option with no limit to the amount of tissue
available and no associated donor site morbidity, but these tissues can
be subject to immunologically mediated rejection and subsequent
graft loss. All grafts must ultimately be resurfaced with the patient’s
own epidermal cells. Rejection of the allogeneic tissue occurs through
both a cellular and humoral immunologic response. These responses
are generated when the host defence system detects certain antigens
expressed on the donor cell surface. Certain components of skin are
strongly antigenic, such as the keratinocytes, whereas the human
fibroblasts appear to be non-immunogenic.
Allogeneic skin graft can still be highly beneficial as a temporary
biologic coverage of extensive wounds, as the epidermis sloughs off
Figure 20.1  Split-thickness skin graft (STSG). (A) Extensive burn over dorsum of foot. (B) Following STSG over defect site. (C) Close-up showing effect
of meshing the graft to gain increased coverage.
A
B
C
Figure 20.2  Split-thickness skin graft (STSG). (A) Considerable tissue loss following a lawn mower accident. (B) Following a toe-fillet graft and STSG of
remaining defect. There was sufficient graft for coverage and meshing was not necessary. A few ‘pie-crust’ cuts were made into the graft to allow
drainage.
A
B

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transplantation. One example of this cultured epidermal autograft is
Epicel® (Genzyme Corporation, Cambridge, MA, USA).
Some of the disadvantages to cultured epithelial autografts are: that
there is a long delay between biopsy and transplantation of 3–4 weeks;
the technique is susceptible to bacterial contamination; the ‘take’ is
less reliable than the split-thickness graft and there is significant
expense associated with this process. The cultured epithelial autografts
also lack any dermal elements in the graft, which makes the final skin
look somewhat atrophic and accentuates contour defects under the
graft. With the absence of the dermis, there is also a delay in the for­
mation of anchoring fibrils and a poorly-defined dermal–epidermal
junction making the graft prone to shear injuries and spontaneous
blisters.
To counter the time disadvantage of the cultured epithelial autograft,
cultured allogeneic epithelial grafts are also available; however, due to
the antigenicity of the keratinocyte, there is still the possibility for
rejection of the graft and disease transmission with this cultured
process.
The lack of a dermal layer with the cultured epithelial grafts, either
autologous or allogenic, can be more of a frustration than the long
delay between procurement and transplantation. The lack of the
dermal layer leads to increased contraction of the graft, contour
defects and spontaneous blister formation. The solution lies in the
creation of an artificial dermis and a composite graft. The impetus
behind the development of a dermal component for full-thickness
defects lies in the knowledge that the human fibroblast is relatively
non-antigenic and is a crucial cell for the development of dermal
proteins and the collagen matrix.
A variety of dermal replacements are currently in use as reviewed in
Box 20.1. One method is the use of polyglycolic acid or polyglactin
membrane as a substrate and the injection of human dermal fibrob­
lasts isolated from neonatal foreskin after circumcision. These alloge­
neic fibroblasts are propagated in a culture medium and then seeded
into the polyglactin mesh. As the cells continue to proliferate, they
secrete multiple matrix proteins including collagen types 1, 2, 3, 6 and
elastin, fibronectin and other proteins. Once the dermal components
are in place, the polyglactin mesh or polyglycolic membrane is then
slowly degraded over time by hydrolysis (not enzymatic degradation),
resulting in very minimal inflammatory reaction and decreased
rejection.
Cultured autologous fibroblasts may also be injected into the acel­
lular membrane of bovine collagen and glycosaminoglycans creating
a synthetic dermis. The acellular dermal layer is eventually remodeled
with ingrowth of fibrovascular tissue from the autologous fibroblasts.
With the use of bovine collagen in the dermal component, there is a
risk of patient reaction to foreign proteins and possible rejection. The
cultured autologous fibroblasts can also be injected into the acellular
reticular dermis of cadaveric skin that has been sterilized to prevent
antigenicity and disease transmission. Again, the fibroblasts will pro­
liferate and create an adequate substrate capable of supporting overly­
ing keratinocytes.
In some preparations, the basement membrane has been retained,
which allows for rapid epithelial growth over the sterilized dermis.
These dermal substitutes can then be covered with a split-thickness
skin graft or a graft composed of cultured autologous keratinocytes.
The composite graft offers superior quality wound coverage with
diminished wound contraction, decreased contour defects or accen­
tuation and reduced shear injuries and blister formation. The primary
disadvantage of the composite graft is infection, as the cultured cells
require many weeks of laboratory preparation to expand to usable
numbers allowing ample time for bacterial growth. The overall take
of the graft is still only around 50%.
A true artificial acellular skin has also been developed, called a
bilayer matrix wound dressing, which incorporates a porous matrix of
presence of these antibodies precludes the use of the xenograft in
many patients unless extensive immunosuppressive therapy is uti­
lized. The porcine xenograft has been used with some limited success
as a temporary dressing in providing for wound coverage, while simul­
taneously preparing the underlying recipient bed for subsequent graft­
ing by stimulating granulation tissue formation (Fig. 20.3).
One area currently under study that may enhance the use of allo­
geneic and xenogeneic grafts is the induction of immunotolerance
to graft tissue rather than immunosuppression. Immunotolerance
refers to a state of immunologic acceptance or unresponsiveness
of the recipient to the donor allograft or xenograft. This would
allow for use of these materials without the need for prolonged
immunosuppression.
CULTURED CELLS AND COMPOSITE GRAFTS
The search for readily available wound coverage with reduced risk and
improved benefit for the patient continues. As autologous tissue has
the fewest complications associated with transplantation, the need to
increase the availability of this tissue is apparent, but not without its
own difficulties. Cultured epithelial autografts can expand the tissue
available for transplantation 10 000-fold. Small keratinocytic biopsies
are cultured in the laboratory for 3–4 weeks and are then ready for
Figure 20.3  Porcine skin graft. (A) A 4 × 4 cm mini-patch of irradiated
porcine skin can be cut to fit small areas of tissue loss. (B) Complete
coverage over extensive burn across dorsum of foot.
A
B

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Lower Extremity Soft Tissue & Cutaneous Plastic Surgery
Box 20.1  Currently available skin substitutes
AlloDerm®
AlloDerm® is an acellular dermal matrix (allograft) derived from
donated human skin tissue supplied by tissue banks using the
standards of the American Association of Tissue Banks (AATB) and US
Food and Drug Administration’s (FDA) guidelines. Since AlloDerm is
regarded as minimally processed and not significantly changed in
structure from the natural material, the FDA has classified it as
banked human tissue.
Apligraf®
Apligraf® is a living, bilayered skin construct. The epidermal layer is
formed by neonatal keratinocytes. The dermal layer is composed
of neonatal fibroblasts in a bovine Type 1 collagen web.
Dermagraft®
Dermagraft® is a single-layered cryopreserved dermal substitute
composed of neonatal fibroblasts, extracellular surrounding substance
and a bioabsorbable framework of polyglycolic or polygalactic suture.
The human fibroblasts are seeded into a framework and proliferate
to fill the spaces and secrete human dermal collagen, matrix proteins,
growth factors and cytokines, to create a three-dimensional human
dermal replacement.
Integra®
Integra® is a synthetic two-layer membrane system for skin
replacement. The dermal replacement layer is made of a porous
template of fibers of bovine tendon collagen and glycosaminoglycan
(chondroitin-6-sulfate). The epidermal substitute layer is made of
thin silicone to control moisture loss from the wound.
OASIS® Wound Matrix
The OASIS® Wound Matrix is a biologically derived extracellular
matrix-based wound product that is compatible with human tissue.
OASIS® Wound Matrix is a xenograft created from porcine-derived
acellular small intestine submucosal for use in wound management.
OrCel™
OrCel™ is a two-layer cellular template in which neonatal epidermal
keratinocytes and dermal neonatal fibroblasts are cultured in two
separate layers onto a bovine collagen sponge. When OrCel™ is
applied to a wound it serves as a protective dressing and provides
a favorable environment for the body’s cells to grow and secrete
various growth factors, aiding in wound healing. As healing occurs,
it is expected that OrCel™ will dissolve and the patient’s own skin
cells will replace it, creating a new skin surface.
TransCyte®
TransCyte® is a skin substitute consisting of a polymer nylon
membrane and collagen seeded neonatal fibroblast cells. It is
transparent due to the silicone outer layer and allows direct visual
monitoring of the wound bed.
Xenograft
Traditional xenograft is made from porcine skin and has been used
for several decades. Pigskin is anatomically close to human skin,
so this was one of the earliest dressing materials used to improve
healing of a number of different wounds. It is still available on the
market, but its role is becoming obsolete as better replacement
materials are developed.
A
B
Figure 20.4  Bilayer matrix wound dressing. (A) The wound after
debridement and application of a negative pressure wound therapy with
excellent granulation base. (B) The meshed wound graft after the silicone
layer has been removed. The staples may be removed at this time. (C) At
3 months after the procedure, showing excellent healing of the chronic
wound.
(Courtesy of Dr Stephen Schroeder.)
C

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Autografts, allografts and xenografts in cutaneous surgery
229
| 20 |
CONCLUSION
When possible, autologous skin grafts transplanted to a recipient bed
provide for the best wound coverage with the fewest complications.
In large wound defects without adequate donor tissue, consideration
of other wound-coverage materials must be given.
Allogeneic and xenogeneic tissues are readily available, but carry a
high risk of graft rejection and possible disease transmission. These
tissues can frequently be utilized as biologic dressings to cover a
wound while waiting for the more permanent cultured wound cover
to become available. The creation of the composite graft and bioen­
gineered skin substitutes hold much promise and might one day make
the split-thickness and full-thickness graft obsolete.
cross-linked bovine tendon collagen and chondroitin-6-sulfate
(glycosaminoglycan) with a semi-permeable polysiloxane (silicone)
elastomer epidermal component. This allows for rapid ingrowth of
fibrovascular tissue from the host, while allowing near-normal levels
of water flux across the silicone layer and protecting the wound from
mechanical trauma or microbial invasion. The patient is then returned
to the operating room and the silicone is peeled away leaving a
vascular bed for the application of a widely expanded thin-meshed
split-thickness skin graft. This is followed by epithelialization of
the autograft and wound closure (Fig. 20.4).
A composite graft that is cellular in origin incorporates neonatal
foreskin fibroblasts and keratinocytes in bovine collagen gel. This is
very effective in closure of chronic ulcerations but is very costly in
preparation and difficult to store.
FURTHER READING
Achauer, B.M., Hewitt, C.W., Black, K.S., et al.,
1986. Long term skin allograft survival after
short term cyclosporine treatment in a
patient with massive burns. Lancet 27,
14–15.
Alfrey, E.J., Wang, X., Lee, L., et al., 1995.
Tolerance induced by direct inoculation of
donor antigen into the thymus in low and
high responder rodents. Transplantation 59,
1171–1172.
Andreassi, A., Bilenchi, R., Biagioli, M., et al.,
2005. Classification and pathophysiology of
skin grafts. Clin Derm 23, 332–337.
Balasubramani, M., Kumar, T., Babu, M., 2001.
Skin substitutes: a review. Burns 27,
534–544.
Blome-Eberwein, S., Jester, A., Kuentscher, M.,
et al., 2002. Clinical practice of glycerol
preserved allograft skin coverage. Burns 28,
S10–S12.
Boyce, S.T., Christianson, D.J., Hansbrough,
J.F., 1988. Structure of a collagen-GAG
dermal skin substitute optimized for
cultured human epidermal keratinocytes.
J Biomed Mater Res 22, 939–957.
Burke, J.F., Yannas, I.V., Quinby Jr., W.C., et al.,
1981. Successful use of physiologically
acceptable artificial skin in the treatment
of extensive burn injury. Ann Surg 194,
413–414.
Clark, J.A., 1987. HIV transmission and skin
grafts. Lancet 1, 983–984.
Clugston, P.A., Snelling, D.F.T., Macdonald,
I.B., et al., 1991. Cultured epithelial
autografts: three years of clinical experience
with eighteen patients. J Burn Care Rehab
12, 533–534.
Compton, C.C., Gill, J.M., Bradford, D.A.,
et al., 1989. Skin regenerated 6 days to 5
years after grafting. A light, electron
microscopic and immunohistochemical
study. Lab Invest 60, 600–601.
Cooper, M., Hansbrough, J., Foreman, T.,
et al., 1990. Early formation of basement
membrane with an autologous dermal-
epidermal composite cultured skin
substitute: a clinical series. Proc Am Burn
Assoc 22, 1–6.
Cuono, C.B., Langdon, R., McGuire, J., 1986.
Use of cultured epidermal autografts and
dermal allografts as skin replacement after
burn injury. Lancet 112, 1123–1124.
Cuono, C.B., Langdon, R., Birchall, N., et al.,
1987. Composite autologous allogeneic
skin replacement: development and clinical
application. Plast Reconstr Surg 80,
628–635.
DeLuca, M., Albanese, E., Bondanza, S., et al.,
1989. Multicentre experience in the
treatment of burns with autologous and
allogenic cultured epithelium, fresh or
preserved in a frozen state. Burns 5,
303–305.
Epstein, A., Hendrick, S., Sanchez, R., et al.,
1988. Persistent dermal blistering in split
thickness skin graft sites. Arch Dermatol
124, 244–248.
Faure, M., Mauduit, G., Schmitt, D., et al.,
1987. Growth and differentiation of human
epidermal cultures used as auto- and
allografts in humans. Br J Dermatol 116,
161–170.
Gallico III, G.G., 1990. Biologic skin
substitutes. Clin Plast Surg 17, 519–526.
Hallock, G.C., Morris, S.F., 2011. Skin grafts
and local flaps. Plast Reconstr Surg 127 (1),
5e–22e.
Hammer, C., 1989. Preformed natural
antibodies and possibilities of modulation
of hyperacute xenogeneic rejection.
Transplant Proc 21, 522–523.
Hammond, J., Buck, B.E., Malinin, T., 1989.
Human immunodeficiency virus and
cadaver skin allografts: reducing the risk.
Proc Am Burn Assoc 21, 162–164.
Hanpanich, B.S., 2010. Tissue engineering of
skin and soft tissue augmentation, medical
view. J Med Assoc Thai 93 (suppl 7),
S332–S336.
Hansbrough, J.F., Boyce, St., Cooper, M.L.,
et al., 1989. Burn wound closure with
cultured autologous keratinocytes and
fibroblasts attached to a collagen-
glycosaminoglycan substrate. JAMA
262, 2125–2130.
Hansbrough, J.F., Franco, E.S., 2000. Skin
replacements. Clin Podiatr Med Surg 17,
239–265.
Hata, K., 2007. Current issues regarding skin
substitutes using living cells as industrial
materials. J Artif Organs 10, 129–132.
Heck, E.L., Bergstresser, P.R., Baxter, C.R., 1985.
Composite skin graft. Frozen dermal
allografts support the engraftment and
expansion of autologous epidermis. J
Trauma 25, 105–112.
Hefton, J.M., Finkelstein, J.L., 1983. Grafting
of burn patients with allografts of cultured
epidermal cells. Lancet 2, 428–430.
Heimbach, D., Luterman, A., Burke, J., et al.,
1988. Artificial dermis for major burns. A
multi-center randomized clinical trial. Ann
Surg 208, 313–320.
Hrabchak, C., Flynn, L., Woodhouse, K., 2006.
Biological skin substitutes for wound cover
and closure. Expert Rev Med Devices 3 (3),
373–385.
Isseroff, R.R., Missavage, A.E., 1994.
Autologous skin grafting. In: Wheeland,
R.G. (Ed.), Cutaneous surgery. WB
Saunders, Philadelphia, pp. 1077–1089.
Kahn, S.A., Beers, R.J., Lentz, C.W., 2010. Use
of acellular dermal replacement in
reconstruction of nonhealing lower
extremity wounds. J Burn Care Res 32 (1),
124–128.
Lee, W.P.A., Bulter, P.E.M., 1997. Transplant
biology. In: Aston, S.J., Beasley, R.W.,
Thorne, C.H.M. (Eds), Grabb and Smith’s
plastic surgery, 5th edn. Lippincott-Raven,
Philadelphia, pp. 27–37.
Lindford, A.J., Kaartinen, I.S., Virolainen, S.,
et al., 2011. The dermis graft: another
autologous option for acute burn wound
coverage. Burns Epub 2011, Sep 6.
Monami, M., Vivarelli, M., Desideri, C.M.,
et al., 2011. Autologous skin fibroblast and

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kertinocyte grafts in the treatment of
chronic foot ulcers in aging type 2 diabetic
patients. J Am Podiatr Med Assoc 101 (1),
55–58.
Nanchahal, J., Otto, W.R., Dover, R., et al.,
1989. Cultured composite skin grafts:
biological skin equivalents permitting
massive expansion. Lancet 22,
191–193.
O’Connor, N.E., Gallico, G.G., Compton, C.C.,
1990. Modification of hypertrophic scars
and keloids with cultured epithelial
autografts. Proc Am Burn Assoc 22,
7–8.
Pham, C., Greenwood, J., Cleland, H., et al.,
2007. Bioengineered skin substitutes for the
management of burns: a systematic review.
Burns 33, 946–957.
Regauer, S., Compton, C.C., 1990. Cultured
keratinocyte sheets enhance spontaneous
re-epithelialization in dermal explant
model of partial-thickness wound healing.
J Invest Dermatol 95, 341–346.
Rheinwald, J., Green, H., 1975. Serial
cultivation of strains of human
keratinocytes. Cell 6, 331–344.
Shores, J., Gabriel, A., Gupta, S., 2007.
Skin substitutes and alternatives: a
review. Adv Skin Wound Care 20 (9),
493–508.
Silverstein, G., 2006. Dermal regeneration
template in the surgical management of
diabetic foot ulcers: A series of five cases.
J Foot Ankle Surg 45 (1), 28–33.
Supp, D., Boyce, S., 2005. Engineered skin
substitutes: practices and potentials. Clin
Dermatol 23, 403–412.
Wooley, D.T., Peterson, H.D., Herzog, S.R.,
et al., 1988. Burn wounds resurfaced by
cultured epidermal autografts show
abnormal reconstitution of anchoring
fibrils. JAMA 259, 2566–2567.

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CHAPTER CONTENTS
Background
231
Basic principles of soft tissue reconstruction
232
Soft tissue of the sole
232
Principles of closure of partial-foot amputations
232
Debridement
232
Vascular assessment
233
Treatment of infection
233
Management of comorbidities
233
Vascular disease
233
Anemia
233
Wound closure
234
Closure of specific types of partial-foot amputations
234
Ungual tuft
234
Amputation of the toe
234
Toe fillet flaps
234
Resections of the first ray
235
Central ray resections
236
Fifth ray resections
236
Transmetatarsal amputations
238
Lisfranc disarticulation
239
Chopart’s disarticulation
240
Amputation of the heel
240
Conclusion
242
BACKGROUND
Amputations of the upper and lower extremities are ancient opera­
tions, performed even prior to recorded history. The frequency of
amputations traditionally increased during periods of armed conflict,
and with the introduction of firearms, the standard treatment for
gunshot wounds of the extremities was amputation. These were done
primarily because the frequency of sepsis from these contaminated
wounds was incredibly high. Amputations were the standard of care,
right up to the end of the nineteenth century. Although the develop­
ment of prosthetic limbs reduced the associated morbidity, major
amputations were still disabling.
By the beginning of the twentieth century, an understanding of the
effects of bacterial contamination of wounds led to an appreciation
of the importance of debridement and wound care in managing inju­
ries of the extremities. With Fleming’s discovery of penicillin and other
subsequent antibiotics, the fear of bacterial infection and sepsis was
significantly reduced and surgeons looked more to reconstructive
operations rather than ablative ones. With the introduction of insulin
therapy in the twentieth century, the life expectancy of patients with
diabetes increased dramatically, but as these patients lived longer, the
ravages of the disease and foot-related complications began to exact
a toll and the frequency of peacetime amputations began to climb.
Today, diabetics are 46 times more likely to undergo a major ampu­
tation of the lower extremity than non-diabetics.1 The majority of
these operations are performed because of ulceration, ischemia, infec­
tion and unmanageable deformities. With the advent of distal bypass
surgery, the frequency of major amputations has been significantly
reduced. As a result of preserving the knee and often the ankle, the
energy expenditures of these patients are less during periods of activ­
ity.2 Preservation of the leg and foot reduces the demand on the
patient’s cardiac reserve, which is often compromised in this popula­
tion. It is with an eye towards reducing energy expenditures that the
frequency of partial-foot amputations has increased.
With the introduction of managed care in US medicine, the finan­
cial considerations in treating the diabetic foot cannot be overlooked.
Patients, who are admitted to the hospital with diabetic foot infec­
tions, often require several trips to the operating room before the foot
is considered stable. However, discharging a patient with a primarily
closed foot is certainly preferable and, in the long term, more cost-
effective than discharging a patient with an open wound and relying
on local wound care for closure. The cost of daily dressing changes,
dressing materials, the services of a visiting nurse and weekly trips to
the surgeon are quite substantial. Although there is no argument that
there is a significant cost associated with outpatient treatment for
chronic open wounds, it has been shown that the mean cost of treat­
ing a patient with a major amputation (above knee or below knee)
©2012 Elsevier Ltd.
Soft tissue considerations in partial-foot amputations
Gary P. Jolly, Thomas Zgonis
Chapter
21

232
Lower Extremity Soft Tissue & Cutaneous Plastic Surgery
a radiologist, an infectious disease specialist, a nutritionist and an
orthotist/prosthetist.
Soft tissue of the sole
The plantar surface of the foot is covered by a unique envelope of soft
tissue, which resists penetration, diffuses the stress of shear and assists
in the process of shock absorption. The glabrous skin of the sole is
significantly thicker than the skin that covers the rest of the body. With
its thicker stratum corneum, penetrating injuries are largely avoided.
Connecting the dermis to the deep fascial layer is a number of struc­
tures called mooring ligaments. These serve to anchor the skin to the
fascia, thereby resisting shear and preventing avulsion during weight-
bearing activities. Interposed between the mooring ligaments are fat
bodies that are arranged in columns and absorb some of the energy
of axial loads, reducing the shock of heel strike and forefoot loading
(Fig. 21.1). The integration of the properties of the skin, mooring liga­
ments and the columnar fat bodies are what makes the soft tissue of
the sole so unique and also so difficult to replace.16
When a plantar defect is created by trauma or ulceration, closure by
secondary intention will occur partially by contraction of the sur­
rounding tissue and partially by the production of scar. Unfortunately,
scar is unable to tolerate shear and axial compression so that signifi­
cant friction develops on the scar, which results in marginal tears as
well as friction blisters over the scar. Making a bad situation worse is
the superimposition of insensitivity in these patients, which permits
them to walk beyond the tolerance of the plantar soft tissues. Because
of the chronic instability of full-thickness plantar scars, primary
closure of wounds should be the surgeon’s first choice. This is particu­
larly important in the patient who has undergone a partial-foot ampu­
tation and, as a result of that amputation, has a reduced surface area
for weight-bearing. It should also be noted that peak plantar pressures,
as well as the duration of those peak pressures are increased following
partial-foot amputations, so that the remaining soft tissue of the sole
must be made stable if the foot is to be preserved.1,17,18
Principles of closure of partial-foot
amputations
Debridement
When planning for closure of a wound, all devitalized tissue must
be debrided from the wound before beginning. It is not uncommon
for a patient who has undergone an emergent partial-foot amputation
during a 2-year period after amputation is also quite high and is often
over US$40 000. This number does not include the cost of rehabilita­
tion, the patient’s loss of future earnings, the earnings lost by the
family as the result of having to care for the family member affected,
nor does it even begin to measure the psychosocial costs associated
with the loss of a leg. The imperative for limb salvage, therefore, is
obviously justified.
To make limb preservation possible, a number of techniques for
soft tissue reconstruction of the foot have been developed. This is
especially important in patients whose protective threshold has been
compromised and where an unstable soft tissue envelope would be
at great risk for breakdown. Although partial-foot amputations are still
performed because of trauma, tumor and infection, the overwhelming
majority are performed in the diabetic population. It is to this sub­
group of patients that most of this chapter will focus.
BASIC PRINCIPLES OF SOFT
TISSUE RECONSTRUCTION
The success of any partial-foot amputation is dependent upon a
number of factors. These include the nutritional status of the patient,
the arterial perfusion of the leg and foot, the presence of infection,
the durability of the soft tissues of the foot, as well as the compliance
of the patient. It should be noted that a reconstructive foot surgeon’s
success is greatly dependent on the skills of the vascular surgeon with
whom he collaborates. Diabetic patients, with peripheral vascular
disease, typically present with obstructions of the superficial femoral
artery as well as lesions at or below the trifurcation of the popliteal
artery. Success in revascularization in these patients is only possible if
the vascular surgeon can revascularize successfully below the knee. It
is not uncommon for a bypass in a diabetic to jump to the dorsalis
pedis, peroneal or posterior tibial arteries in the foot.3–10
There are three major arteries that supply blood to the foot. Each
named artery supplies specific blocks of tissue, which are called angio­
somes. Some areas, such as the soft tissue of the heel, consist of two
angiosomes; one from the medial calcaneal artery and one from the
peroneal artery. In disease states, where one or more of the arteries to
the foot are compromised, collateral or choke vessels dilate in response
to lowered tissue PCO2, permitting blood to flow from one angiosome
to another. The soft tissues of the foot contain a rich subdermal and
subcutaneous plexus of vessels that permit perfusion of the entire foot
in the presence of profound occlusive disease of the infrapopliteal
vessels. Knowledge of these anatomic variants and the predominant
direction of flow are essential in planning any soft tissue reconstruc­
tion, particularly when that reconstruction is associated with a partial-
foot amputation.11,12
In order for distal amputations to remain viable, careful considera­
tion must be given to the integrity and durability of the soft tissue
cover, which must resist the mechanical stress of weight-bearing. Full-
thickness wounds on the foot that close by secondary intention
usually require constant attention and are prone to repeated break­
down. Because the modulus of plasticity and the modulus of elasticity
of scar and normal tissue are so fundamentally different, when exter­
nal stress is applied to scar, significant strain at the margins often leads
to tears at the interface with surrounding normal tissue.13,14
Surgery, in an inadequately nourished patient, is less likely to
succeed than when it is performed in a patient who is well nourished.
Similarly, a poorly-controlled diabetic faces a greater risk of wound
complication than a patient with well-controlled hemoglobin A1c.15
The successful management of the diabetic foot is only possible when
there is a well-coordinated team approach, which includes a recon­
structive foot and ankle surgeon, a vascular surgeon, an internist,
Figure 21.1  A magnetic resonance imaging cross-section through the
soft tissues of the heel of the foot. The mooring ligaments (black lines)
and longitudinally arrayed fat bodies are visible.

Chapter
Soft tissue considerations in partial-foot amputations
233
| 21 |
Management of comorbidities
The diabetic patient, who is facing a partial-foot amputation, generally
presents with multiple co-morbidities, not the least of which is sensory
neuropathy (Box 21.1). It is precisely this lack of protective threshold
that contributes to the development of ulcerations and infection that
all too often go unrecognized, until systemic signs appear. When treat­
ing any patient whose protective threshold has been altered, it is
essential to elevate the awareness of the patient and the patient’s
family of the effects of neuropathy.
The development of abnormal plantar pressures as a result of
Charcot neuroarthropathy is a frequent etiology of plantar ulceration
in the forefoot and/or midfoot joints.37–40 The synergy of Charcot
deformity and sensory neuropathy is not to be underestimated. There­
fore, it is essential to correct the underlying deformity, as well as any
secondary equinus when considering a patient for closure of a par­
tially amputated foot. It is not uncommon for a neuropathic patient
with a Charcot deformity to present with a digit or ray that will require
amputation or ray resection, as well as a midfoot ulceration associated
with a midfoot deformity. If one wound is going to be closed on a
foot, all wounds should be closed.
The effects of autonomic neuropathy are vast, and can produce
cardiac arrhythmias, significant variations in blood pressure, problems
with gastrointestinal motility as well as retard the production of sweat
from the glabrous skin of the foot. This can become problematic in a
patient who has undergone a partial-foot amputation and increases
the risk for irritation of the stump. Adequate moisturizing agents
should be employed to minimize this concern.
Vascular disease
Diabetes mellitus is associated with significant cardiovascular effects,
with the lower extremity seeing major involvement. In patients with
congestive heart failure (CHF) and/or end-stage renal disease (ESRD),
problematic edema in the foot can compromise the integrity of the
incision line in any lower extremity amputation and lead to delays in
wound healing. Reduction in a patient’s stroke volume, coupled
with occlusive peripheral vascular disease reduces the perfusion of
tissue in the lower extremity.41–44 The presence of an open wound in
a patient with occlusive lesions of the superficial femoral artery (SFA)
or the infra-geniculate vessels reduces the threshold for vascular
intervention.45
Anemia
Chronic anemia is often seen in patients with long-standing diabetes,
and is associated with chronic renal insufficiency. Many of these
patients live with hematocrit values between 26% and 30% and
remain asymptomatic as long as their activities are limited. The
to return to the operating room several times for debridement
before the wound is considered clean enough to close. Although
quantitative microbiology may be used to assist the surgeon in deter­
mining when the wound is clean enough to close, the clinical appear­
ance of the tissues is generally sufficient for the experienced surgeon
to make that determination. The presence of erythema at the wound
margins, edema of the wound edge or the presence of tissue that is
grey and non-granular, are all signs of inadequate debridement. A
wound that appears healthy and bleeds freely when curetted and is
free of fibrous or necrotic material is a wound that is ready for
closure.19–25
Vascular assessment
Open partial-foot amputations are often performed emergently or
urgently in the face of a severe infection, to prevent further soft tissue
loss, major foot or lower extremity amputation, septicemia and even
death. In this emergent or urgent setting, a thorough vascular assess­
ment is often recommended postoperatively. The surgeon also obtains
an intraoperative assessment of tissue perfusion and bleeding during
the initial debridement. However, before the wound is considered for
closure, an adequate vascular examination, including angiography if
necessary, should be obtained. If there is a significant vascular deficit,
then appropriate intervention is indicated before the open amputa­
tion may be considered for closure.
The appropriate level for amputation is found by assessing func­
tional considerations and perceived viability of the foot. Non-invasive
vascular testing, digital plethysmography, angiography and transcuta­
neous partial pressures of oxygen, are often helpful in deciding on the
level of amputation. The absence of palpable pedal pulses is a clear
indication of vascular insufficiency, and requires an evaluation by a
vascular surgeon. In the diabetic population, the presence of a palpa­
ble pulse does not always signify sufficient perfusion to the distal foot.
Calcification of the vessels, which reduces the compliance of the
vessels, can yield artificially elevated ankle pressures during non-
invasive vascular testing. Care should be taken not to rely too heavily
on this method in diabetic patients. Angiography is the most reliable
method of assessing vascular patency in the diabetic patient. In
patients with renal compromise, the use of carbon dioxide instead of
a radiopaque dye or magnetic resonance angiography may be used as
an alternative. Above all, the most reliable indicator of the ability of
an amputation to heal is active arterial bleeding at the time of debride­
ment or amputation.26–34
Treatment of infection
Because the majority of partial-foot amputations are performed in the
presence of infection or at least colonization, it is important at the
time of the initial debridement to obtain adequate deep cultures so
that the appropriate antibiotic(s) may be prescribed as expeditiously
as possible. In addition, if the presence of osteomyelitis is confirmed
histologically, then adequate resection of that bone is essential to
prevent a subsequent re-infection of the foot. If feasible, the entire
bone should be removed to affect a surgical cure. Cultures should
also be taken immediately before the wound is closed, so that if
it is colonized, appropriate changes in antibacterial therapy may be
instituted.
The duration of treatment for a soft tissue infection may vary,
although 2 weeks seems to be the prevailing conventional wisdom. In
patients with histologically confirmed osteomyelitis and incomplete
resection of the entire bone, 6 weeks of therapy on an appropriate
parenteral antibiotic followed by a period of oral therapy should be
considered.35,36
Box 21.1  Co-morbidities associated with partial foot
amputations in the diabetic patient
• Coronary artery disease
• Sensory neuropathy
• Congestive heart failure
• Charcot neuroarthropathy
• Hypertension
• Autonomic neuropathy
• Renal insufficiency
• Anemia of chronic disease

234
Lower Extremity Soft Tissue & Cutaneous Plastic Surgery
production of a wound in the foot increases the metabolic demands
on the body, and a reduced-oxygen carrying potential can severely
compromise wound healing, and may require the transfusion of
packed red blood cells. It is not uncommon after multiple foot deb­
ridements for patients to require the administration of several units.
In patients with well-documented coronary artery disease, the produc­
tion of an acute blood loss can precipitate an acute myocardial
infarction.46,47
Wound closure
When a wound is ready to be closed, the tissues should be handled
as atraumatically as possible. Skin margins should be manipulated
gently, avoiding any crushing instruments. Furthermore, wound
margins should not be made or forced to fit. Tension on the skin
margins, particularly in the diabetic patient, inevitably results
in dehiscence at that location. Following the recommendations
outlined for tissue handling and suturing from previous chapters, is
essential.
The closure of the soft tissue envelope over a partial-foot amputa­
tion can be accomplished in any number of ways. The simplest and
most desirable method is primary closure of the wound. Ideally, this
is facilitated by planning the amputation and allowing for adequate
length of the soft tissue flaps (Fig. 21.2). If there is insufficient tissue
to provide coverage and a more proximal level of amputation would
be ill advised, then delayed assisted primary closure, using a tension-
assisted device or negative pressure wound therapy (NPWT) may be
considered.48,49
Closure of specific types of
partial-foot amputations
It should be noted that many of the principles of soft tissue recon­
struction are non-specific to the great toe or to the lesser digits. There
are, however, some anatomical and functional factors that affect the
hallux and the first ray specifically, so that it is impossible to com­
pletely generalize and treat all digits as if they were the same. Where
appropriate, the differences between the first ray and the others will
be mentioned.
Figure 21.2  A primarily closed partial foot amputation. Note the
absence of tension from the incision line.
Ungual tuft
Amputations through the tip of the toe are usually performed because
of compromise of the ungual tuft of the toe. Amputations at this level
may also be performed because of persistent, chronic nail deformities
or because of traumatic soft tissue avulsions of the tip of the toe. The
blood supply to the tip of the toe is based on the vascular plexus that
is formed from the anastomosis of the terminal networks of the
medial and lateral axial arteries of the toe.50
If a guillotine amputation was performed, closure of the wound
may be facilitated by an advancement of the plantar pulp. The opera­
tion involves the development of a bipedicled flap, which is mobilized
from the toe at the level of the periosteum. It is typically designed in
a tear shape with the point proximal. Mobilization of the proximal
skin, proximal to the plexus, aids in the mobilization of the flap. The
flap is then rotated around the tip of the toe and the trailing edge of
the flap is sutured to the surrounding skin. The donor site is closed
primarily in a V–Y fashion (Fig. 21.3).
In diabetics with neuropathy, hallux tip ulcers are seen when there
is intrinsic wasting and clawing of the toes. This typically occurs
because of the unsupported pull of the flexor hallucis longus (FHL).
In these instances, a transfer of the insertion of the FHL to the base
of the proximal phalanx may be considered. This effectively plantar­
flexes the metatarsophalangeal joint (MTPJ) and may be combined
with a tenotomy of the EHL, distal to the transfer, and a plantar release
of the interphalangeal joint may also be necessary to release a fixed
contracture of the toe (Fig. 21.4).
Amputation of the toe
Toe amputations have been described at the levels of the interphalan­
geal joints (IPJ), the shaft of the proximal phalanx and at the MTPJ.
Attachment of the FHL tendon to the plantar cortex of the proximal
phalanx should be considered to replace the pull of the lost intrinsics.
Tenodesis of the extensor hallucis longus (EHL) to the dorsal cortex
of the proximal phalanx with the IPJ in neutral may be considered as
well, to prevent ‘drooping’ of the IPJ.50 Amputations through the IPJ
of a toe, particularly the hallux, does not provide a durable plantar
surface because the skin of the flexor crease is thin and does not stand
up well to the stress of weight-bearing, particularly during propulsion.
A more durable and stable coverage may be achieved by amputating
through the mid-shaft of the proximal phalanx.
In patients without intrinsic wasting, those muscles inserting into
the proximal phalanx, unopposed by the long extensor and unsup­
ported by the long flexor may pull the distal end of the phalanx
into plantar-flexion, sometimes producing a new ulcer. Although it is
often desirable, for psychologic or esthetic reasons to preserve a
portion of the toe, from a functional standpoint, a disarticulation at
the MTPJ with removal of all cartilage and sesamoids is often preferred
for the hallux or the lesser toes. However, one needs to be concerned
about the pressure distribution on the adjacent joints after a great toe
amputation. Studies have shown an increased development of
deformities on the second and third toes and lesser MTPJs after hallux
amputations.18,51,52
Toe fillet flaps
The soft tissue of the toe is an excellent source of coverage for defects
of the forefoot.53,54 Even in the presence of osteomyelitis of the
phalanges, the soft tissue of the toe can be spared and used for recon­
struction, providing that adequate antibiotic therapy has been insti­
tuted. An intact Doppler signal from at least one of the digital arteries
is a good indicator for a successful reconstruction. With both arteries
intact, the odds of survival are greatly improved.

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Fillet flaps of the toes are, by definition, peninsula flaps and they
are limited in their excursion by the tethering effects of the skin.
However, they also contain one or possibly two digital arteries that
may allow them to be converted to pedicle flaps or, in the case of two
patent arteries, bipedicle flaps. To convert the flap to an island, a
dorsal V–Y technique is employed, allowing the flap to be inset further
proximally on the bottom of the foot.55,56 It is important to remember
that these flaps contain glabrous skin, mooring ligaments and colum­
nar fat bodies and create a most serviceable surface on which to bear
weight (Figs 21.5, 21.6).
Resections of the first ray
The great toe and the first metatarsal bear approximately 60% of the
total forefoot load during stance. Therefore, the loss of the toe and,
more importantly, the metatarsal head, may result in a significant
disruption in foot mechanics.18,52 The first ray may be amputated at
any level, including disarticulation at the metatarsal-cuneiform joint,
but to prevent an overload of the lateral rays, a custom prosthetic filler
with a rocker bottom sole should be prescribed postoperatively.57
Overloading the lesser rays in an insensate foot can potentially be
disastrous. When the first ray requires amputation, because of com­
promise of the first metatarsal, and there is an associated soft tissue
loss, a fillet flap from the hallux may be used to close the defect
(Figs 21.7, 21.8).
It should be noted that disarticulation of the first metatarsal may
result in a loss of function of the tibialis anterior and peroneus longus.
To minimize the risk of this, the insertion of the tendon should be
secured to the first cuneiform. The loss of the first ray also means a
loss of the EHL as an ankle dorsiflexor. This increases the advantage
to the triceps surae and increases both the peak plantar pressures and
A
B
Figure 21.3  V–Y advancement flap (Atasoy). (A) A distal hallux ulcer.
(B) Resection of all necrotic tissue. (C) Distal advancement of the plantar
pulp. Atasoy E, Loakimidis E, Kasdan ML, et al. 1970. Reconstruction of
the amputated finger tip with a triangular volar flap. A new surgical
procedure. J Bone Joint Surg Am. 52(5):921–926.
C
Figure 21.4  A radiograph of a foot showing the presence of a bone
anchor in the proximal phalanx, which is attaching the flexor hallucis
longus tendon directly to the proximal phalanx.

236
Lower Extremity Soft Tissue & Cutaneous Plastic Surgery
metatarsal-cuneiform joint. In patients with confirmed osteomyelitis,
the complete resection of a bone including the corresponding digit
and soft tissue ensures a surgical cure and helps the patient avoid a
protracted course of antibiotics. As in the treatment of any infectious
process in the foot, an initial debridement that yields definitive cul­
tures and sensitivities may be followed by a delayed closure after
appropriate antibacterial therapy has been instituted. If there is a
significant plantar soft tissue defect, it may be closed by a fillet flap
from the toe or a flap may be rotated from the adjacent area on the
forefoot. These flaps are supplied by perforators arising from the
plantar metatarsal arteries, and arborize in the subcutaneous plexus.60
Reciprocal island advancement flaps or rotation flaps may be used to
close defects in this area (Figs 21.9, 21.10).61
Fifth ray resections
Partial fifth ray resections may be performed with relative impunity,
providing the other rays are intact. Associated soft tissue defects
may be addressed by fillet flap from the fifth toe, plantar rotation
flaps, advancement flaps, or if the defect is dorsal or lateral, with
the duration of those peaks in the forefoot. To offset this effect, a
lengthening of the triceps should be strongly considered.
Patients who develop plantar ulcers and associated osteomyelitis of
a lesser metatarsal head, who have already lost their first ray, should
not be considered candidates for an isolated metatarsal head resec­
tion. The distribution of weight in the forefoot with only three lesser
metatarsals usually results in overload, hyperkeratosis and eventual
breakdown. In this case, a resection of all of the remaining heads or
a trans-metatarsal amputation is preferable.1,2,58,59
As the effective surface area of the forefoot shrinks, it is impera­
tive that the remaining plantar soft tissue envelope is durable
and free of scar or keratosis. The presence of focal areas of dysfunc­
tional tissue requires meticulous attention and is at high risk for
ulceration.56
Central ray resections
Resections of a central ray have been described for a number of dif­
ferent conditions, including osteomyelitis of the metatarsal heads.
These may be performed at any level, as far proximal as the
Figure 21.6  A toe island fillet flap. (A) A fillet flap, which was converted to an island, was used to resurface the area where the first metatarsal had
been partially resected previously. Here it will be remobilized to replace an area of dysfunctional scar. (B) After resection of the scar. (C) The flap
was mobilized and inset.
A
B
C
Figure 21.5  Toe fillet flap. (A) A plantar ulcer after amputation of the second metatarsal. The area of excision has been marked. (B) The second toe
has been filleted. (C) The flap was trimmed to fit the defect and has been in-set.
A
B
C

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Soft tissue considerations in partial-foot amputations
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Figure 21.7  A fillet flap used to close a defect under the first metatarsal head. (A) A large plantar ulcer associated with osteomyelitis of the metatarsal
head and proximal phalanx. (B) The toe has been filleted and the first ray has been amputated through the midshaft of the metatarsal. (C) After
trimming and insetting of the flap.
A
B
C
Figure 21.8  (A) A preoperative partial first ray amputation. (B) Final closure after a revisional surgery and application of a split thickness skin graft.
A
B

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Lower Extremity Soft Tissue & Cutaneous Plastic Surgery
along the metatarsal shafts be done carefully to avoid damage to these
vessels. After removal of the osseous segment, the plantar plates and
deep transverse metatarsal ligaments, as well as any visible extensor
and flexor tendons, should be aggressively debrided. This tissue is
primarily fibrous and poorly vascularized. This will also serve to
debulk the flap and make it more manageable during closure.
Performing a TMA in the presence of a plantar forefoot ulcer is not
an absolute contraindication, unless there is associated vascular
embarrassment to the distal foot. The ulcer may be excised in a wedge
with a distal base and the tissue on either side rotated to closure. Since
there is generally a longer plantar wound margin, this also effectively
addresses any dog-ear that would ordinarily form. The actual level of
amputation may be dictated by the quality of the tissues and the
amount of active bleeding observed. The amputation may be carried
back as far as a disarticulation of the central metatarsal-cuneiform
joints, providing the attachments of the tibialis anterior and peroneus
brevis are preserved. A TMA results in the loss of extensor hallucis and
digitorum longus, and their effect on ankle dorsiflexion. In order to
restore a myogenic balance to the foot and ankle, a triceps surae
lengthening should be considered.65,66
The suture line of a TMA in a patient with diabetes and vascular
disease can be tenuous. To minimize the stress to this area, the patient
should be kept from bearing weight until the wound has healed. In
split-thickness skin grafts. In some patients whose defects are too large
for local rotation flaps or where a toe fillet flap was not an alternative,
a reverse flow island flap, taken from the instep and based on perfora­
tors from the medial plantar artery may be considered (Fig. 21.11).
Resection of the entire ray, including the styloid is often problematic
because of the loss of the peroneus brevis. A resultant varus deformity
typically leads to a lateral midfoot ulcer. If the styloid must be taken,
the insertion of the peroneus brevis should be moved to the dorsal
surface of the cuboid.
Transmetatarsal amputations
Transmetatarsal amputations (TMA) have proven to be a very service­
able level for partial ablation of the foot.62–64 The plantar forefoot pad
provides an excellent weight-bearing surface for the stump and when
it is brought dorsally to cover the distal surface of the amputation, it
functions well against prosthetic shoe filler (Fig. 21.12). When plan­
ning a TMA, preservation of a reasonable metatarsal parabola should
be of concern to the surgeon, since a protruding metatarsal in an
insensate foot is likely to lead to plantar ulceration.
Preservation of the plantar metatarsal arteries within the plantar
flap is probably the single most important technical consideration,
and one that will greatly aid flap survival. It is essential that dissection
Figure 21.9  Reciprocal rotation flaps for a plantar ulcer following resection of the fourth metatarsal. Note that the fourth toe was preserved. (A) The
appearance of the ulcer. (B) Planning the flaps. (C) After elevation and rotation of the flaps. (D) The final appearance.
A
B
C
D

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Soft tissue considerations in partial-foot amputations
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a tarsal-metatarsal disarticulation is being considered, a complete
triceps tenotomy should be performed at the same time in conjunc­
tion with a percutaneous posterior tibial tenotomy. This will aid in
offsetting the myogenic imbalance created by the loss of the peroneus
brevis and the extensors, and the unopposed supinatory effect of the
tibialis anterior (Fig. 21.13).
Unlike the TMA, a Lisfranc disarticulation should not be dependent
on a long plantar flap, as that may overtax the blood supply to the
distal edge. The dorsal and plantar flaps should be of approximately
the same length. Unfortunately, this will result in the incision line,
and the resultant scar, lying across the front of the stump. Special
considerations should be given to the surface of the prosthetic filler
to avoid secondary breakdown after the stump has healed. Because
the stump of a Lisfranc disarticulation is a difficult one to manage
addition, the use of a well-padded short-leg cast during the postopera­
tive period will also help to protect the stump. Because healing is
delayed in diabetics, particularly those with chronic renal insuffi­
ciency, sutures may remain in for 4 weeks or longer.
As an alternative to TMA, consideration should always be given to
a pan-metatarsal head resection, if the patient’s digits are well perfused
and not at risk for gangrene. Any soft tissue defects that may be present
are usually closed by simple transverse plantar elliptical excision.
Lisfranc disarticulation
Ablations at this level are not commonly performed. When Lisfranc
disarticulations are done, they often result in equinovarus deformities
of the stump with subsequent lateral column ulceration.67,68 When
Figure 21.10  Digital artery island flap to close a defect under the central forefoot. Because the ulcer involved two metatarsals, resection of the lesser
metatarsal heads was performed. This is preferable to a trans-metatarsal amputation. (A) The appearance of the foot before surgery. (B) After the
defect was debrided and the metatarsal heads were resected. The island flap from the lateral side of the great toe has been raised and placed in the
wound. (C) After the flap was sutured. (D) The final appearance.
B
A
C
D

240
Lower Extremity Soft Tissue & Cutaneous Plastic Surgery
from a standpoint of shoe accommodation, it is probably better suited
to a patient with extremely limited functional expectations.
Chopart’s disarticulation
Chopart’s (midtarsal) disarticulation has been controversial in the
literature and is not performed regularly in the diabetic patient. This
may be due in part to the frequent stump complications that have
been reported, which include equinus, varus and anterior dislocation
of the ankle.67,68 Even if a complete Achilles tenotomy is performed,
and disassociation of all the other extrinsic muscles exists, there is
still a tendency for the ankle to plantarflex in response to the forward
shear of the tibia during the stance phase of gait. In an attempt to
reduce this tendency, the tibialis anterior may be transferred to the
neck of the talus to reduce the plantarflexory moment of the advance­
ment of the center of gravity over the support limb during the
gait cycle.69,70
To assist in this, the extensor digitorum may be sutured to the distal
end of the plantar fascia, which also aids to prevent the soft tissue of
the plantar surface from migrating proximally. Postoperatively, a suc­
cessfully functioning stump is dependent on a prosthetic device that
will provide stability to the ankle, protect the soft tissue envelope by
reducing shear and allow for a normal heel-to-toe progression.71–73
One device that is currently in use is a two-part articulated prosthesis,
which consists of a socket that is moulded to the remainder of the
foot and a shoe insert into which the socket fits. Both pieces are made
from a thermally contoured plastic (Figs 21.14, 21.15).
Amputation of the heel
Calcanectomy has become a rather common operation that is usually
performed for posterior and plantar soft tissue defects (Fig. 21.16).
Although these defects are usually associated with an osteitis of the
heel, occasionally in the presence of a large ulcer, part of the calcaneal
tuberosity may be resected so that the margins of the wound may be
closed primarily. This seems a bit extreme, since there are a number
of alternatives to subtotal calcanectomy, such as instep flaps, island
pedicle flaps based on the medial plantar artery and reverse flow sural
artery flaps.74–80
Figure 21.11  Reverse flow pedicle flap from the instep to close a plantar
defect in a patient whose toes have already been amputated. (A) A
plantar ulcer following a fifth ray amputation. The area of the flap is
shown. (B) After skeletonizing the pedicle and insertion of the flap into
the defect.
A
B
Figure 21.12  An intraoperative photograph of a transmetatarsal
amputation. Note the extent of the plantar flap.
Figure 21.13  A postoperative photograph of percutaneous posterior
tibial tenotomy done in conjunction with a Lisfranc amputation and a
complete triceps tenotomy.

Chapter
Soft tissue considerations in partial-foot amputations
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| 21 |
literature. The pedicle for this flap is based on the sural artery, the
lacework of vessels that accompany the sural nerve and accompanying
arteries of the lesser saphenous vein and the lesser saphenous vein
itself. These flaps are supplied by septocutaneous perforators from the
peroneal artery (Fig. 21.19). Reverse-flow sural artery flaps may also
be used to provide soft tissue coverage to the plantar surface of the
heel (Fig. 21.20).82,83 Although the earlier reports on sural artery flaps
were for coverage of defects caused by trauma or tumor, some of the
The skin of the arch receives its blood supply from the medial and
lateral tarsal arteries, from perforators of the medial and lateral plantar
arteries, with collateralization occurring in the subcutaneous plexus.
Transposition flaps may be raised from the arch and moved proxi­
mally to cover plantar heel defects and, depending on the patency of
the perforators from the medial plantar arteries, may be raised as
islands (Fig. 21.17).
The posterior heel is a more problematic area to deal with than is
the plantar surface of the heel. The loss of soft tissue coverage from
decubitus ulcers is the most common cause of resection of the heel.
In order to avoid calcanectomy or below-the-knee amputation, several
techniques have been developed that can resurface this area and pre­
serve function of the triceps surae. A V–Y advancement flap has been
described, which relies on the cutaneous perforators from both the
posterior tibial and peroneal arteries for survival. Unfortunately,
this flap is limited to defects that are not larger than 2 cm in height
(Fig. 21.18).79
Free muscle flaps had been used exclusively to reconstruct the soft
tissues of the ankle and heel until the early 1990s. A pedicle flap based
on the sural artery was described by Masquelet et al.81 in 1992. Since
then, several hundred sural artery flaps have been reported in the
Figure 21.14  (A) A preoperative open Lisfranc’s amputation. (B) Final
closure after a revisional surgery and Chopart’s amputation with a double
local advancement flap.
A
B
A
B
Figure 21.15  A Chopart’s amputation. (A) The stump of the amputation.
(B) The components of the articulated prosthesis. (C) The device applied
to the extremity.
C

242
Lower Extremity Soft Tissue & Cutaneous Plastic Surgery
more recent works deal with diabetics and patients with vascular
disease.84–88
CONCLUSION
Partial-foot amputations have increased in number over the last 30
years, and with that increase, there has been an equal reduction in the
number of major (above-knee and below-knee) amputations. This
paradigm shift is due largely to advances in peripheral vascular surgery.
Partial-foot amputations should not be considered ablative proce­
dures so much as reconstructive ones.
A successful procedure is one in which the patient’s limb has been
preserved and the patient is able to remain community ambulatory.
In order to accomplish this, the foot and ankle surgeon must appreci­
ate the anatomy, physiology and biomechanics of the soft tissues of
the foot and be prepared to reconstruct those soft tissues to preserve
the function of a limb.
Figure 21.16  Amputation of the heel. (A) Osteomyelitis of the calcaneus
and a draining posterior sinus. (B) A subtotal calcanectomy utilizing an
anteriorly based flap for closure.
A
B
Figure 21.17  A full-thickness eschar of the heel covering osteomyelitis
of the calcaneus. (A) The preoperative appearance. (B) 3 days after
successful revascularization and emergent calcanectomy, a medially based
transposition flap from the instep was used to resurface the heel. A
split-thickness skin graft is covering the donor site.
A
B

Chapter
Soft tissue considerations in partial-foot amputations
243
| 21 |
Figure 21.18  A posterior defect of the heel
following partial amputation of the calcaneus.
Despite revascularization elevation of a posterior
V–Y advancement flap resulted in blanching of
the flap after movement. (A) The flaps (V–Y and
an instep transposition flap) were returned to
their donor site for 3 days to allow time for the
choke vessels to dilate. (B) Delayed transposition
of the flaps and application of a split-thickness
skin graft.
A
B
A
B
C
Figure 21.19  A reverse flow sural artery flap for coverage of a large heel defect. (A) The preoperative appearance after partial calcanectomy.
(B) Preliminary insertion of the flap. (C) The flap inset. A stint dressing is covering the donor site, which was resurfaced with a split-thickness
skin graft.

244
Lower Extremity Soft Tissue & Cutaneous Plastic Surgery
A
B
C
Figure 21.20  (A) The preoperative picture showing the open partial calcanectomy. (B) Harvesting of the sural pedicle flap. (C) Insetting into the
recipient heel area.

Chapter
Soft tissue considerations in partial-foot amputations
245
| 21 |
(D) Split thickness skin grafting at the proximal donor site. (E) Off-loading external fixation for daily monitoring of the
pedicle flap and better patient compliance.
D
E
Figure 21.20, Continued

246
Lower Extremity Soft Tissue & Cutaneous Plastic Surgery
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CHAPTER CONTENTS
Introduction
249
Microscope and microinstrumentation
249
History of microsurgery
252
Basic science concepts
252
Technical factors
253
Patient factors
255
Free flaps and free flap failure
256
Choices of flaps
256
Working with the vascular, orthopedic and
podiatric surgeons
263
Postoperative regimen
265
Revising free flaps
265
Future directions
265
Conclusion
266
INTRODUCTION
Now in its fourth decade, microsurgical-free tissue transfer has a well-
established role for the reconstruction of challenging soft tissue
defects, coverage of bone and tendons and the restoration of function
for complex wounds that previously would have resulted in amputa­
tion. Foremost, surgeons should adhere to the basic surgical principles
and concepts of reconstruction, the ‘reconstructive ladder’, and to
perform the simplest biomechanically sound procedure to correct
a particular condition. Despite its complexity however, the use of
microsurgical-free tissue transfer has become an almost routine soft
tissue reconstructive technique. The characteristics of the lower extrem­
ity such as bony prominences, gliding tendons, a reliance on protec­
tive sensation and the resilience of tissue to survive the constant
trauma of ambulation all present unique challenges to the reconstruc­
tive surgeon that are unlike any other part of the human body. The
last several decades have led to major developments and innovation
pushing the limits of free flap survival while at the same time
minimizing donor site morbidity. The original development of the
operating microscope, microsurgical instruments and microsuture
made microsurgery possible and led to a demand for a thorough
understanding of the vascular anatomy in different regions of the
body. Reconstructive surgeons rose to this challenge and began to
visualize the body as blocks of tissue supplied by individual vascular
pedicles that could be transplanted from one site to another. A better
understanding of the physiology of flap ischemia and other underly­
ing mechanisms of injury has led to a reduction in flap losses.
Refinements in flap preparation, surgical technique, and postopera­
tive regimen, as well as further understanding of flap physiology have
made the microsurgical transfer of tissue a very reliable procedure.
These advances have improved initial survival rates and allowed for
better detection of postoperative complications, thereby improving
long-term outcome and potentially challenging the notion of reserv­
ing free flap reconstruction to the top of the ‘reconstructive ladder’.
Free flap use in the foot and ankle is particularly applicable because
the local soft tissue may be vascularly compromised second to trauma,
chronic wounds or co-morbidities such as diabetes mellitus. Recent
interest in perforator flaps has allowed harvesting of flaps with
minimal donor site morbidity. The resulting myriad of available flap
choices allows for more anatomically appropriate tissue to close
wounds with excellent functional and aesthetic outcomes.
MICROSCOPE AND
MICROINSTRUMENTATION
The utility of the operating microscope is credited to Nylen1 in Sweden
for use in ear surgery and later adapted by Perrit2 in 1946 for use in
ophthalmic surgery. The 1960s were marked by a focus on the anas­
tomotic technique. Jacobson and Saurez3 described the use of the
microscope in anastomosing small blood vessels in 1960 and were
able to achieve a 100% patency rate in rabbit and dog carotid arteries
with diameters ranging from 1.4 to 3.2 mm. Green et al.4 were able
to achieve a 90% patency rate in rat aortas measuring between 0.8 and
1.5 mm in diameter. Even more remarkable was Acland,5 who was
able to obtain a 95% patency rate in 0.5 mm rat superficial epigastric
arteries.
©2012 Elsevier Ltd.
The role of microsurgical-free flaps
in foot and ankle surgery
Christopher E. Attinger, Mark W. Clemens, Ivica Ducic, Eric B. Unger, Lawrence B. Colen
Chapter
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