T h e Ph y s i o l o g y a n d

Biomechanics of Skin
Flaps
James B. Lucas, MDa,b,*

KEYWORDS
 Cutaneous vascular anatomy  Skin physiology  Local skin flaps  Cutaneous flap physiology
 Vascular delay  Skin flap biomechanics  Mohs reconstruction

KEY POINTS
 The skin is an incredibly complex organ system responsible for the 3 main functions of protection,
thermoregulation, and sensation.
 The vascular anatomy of the skin comprises an intricate network of vascular plexuses that are
responsible for maintaining the vitality of the cutaneous structures and facilitating the use of local
skin flaps in Mohs reconstruction.
 Local skin flaps are categorized based on their vascular supply and include random cutaneous
flaps, axial or direct cutaneous flaps, and fasciocutaneous flaps.
 Significant physiologic changes occur within the skin during flap elevation and transfer, enhancing
and promoting flap survival. These changes can be further leveraged using the concepts of vascular
delay.
 An understanding of the biomechanical properties of nonlinearity, anisotropy, and viscoelasticity is
critical in the design and execution of local skin flap reconstruction.

INTRODUCTION survivability to the flap when correctly designed.

A full understanding of the physiology of integu-
The closure of skin defects created by Mohs mi- mentary structures and the biomechanics involved
crographic surgery routinely requires the use of in tissue transfer results in improved flap survival
cutaneous flaps borrowed from the surrounding and outcomes.
skin to produce an aesthetically pleasing result.
Flap creation results in tissue stresses that can VASCULAR ANATOMY AND PHYSIOLOGY OF
have a significant impact on survival of the flap THE SKIN
by potentially compromising the neurovascular
supply to the cutaneous structures. With these The skin is a complex organ system comprising
stresses in mind, cutaneous surgeons must com- the epidermis, the dermis, and the subcutaneous
mand a full knowledge and understanding of the tissues. It is the body’s largest organ system,
vascular patterns, physiology, and biomechanics responsible for 3 main functions: sensation, pro-
of skin flaps. That a skin flap is able to survive tection, and thermoregulation. The thermoregula-
such insults is a direct result of these redundant tory function and nutritional support of the
and complex systems providing vitality and integument result from the unique configuration
facialplastic.theclinics.com

Disclosure Statement: The author has nothing to disclose.

a
Facial Plastic and Reconstructive Surgery, Carl R. Darnall Army Medical Center, 36065 Santa Fe Avenue, Fort
Hood, TX 76544, USA; b Department of Surgery, Uniformed Services University of Health Sciences, 4301 Jones
Bridge Road #A3007, Bethesda, MD 20814, USA
* 36065 Santa Fe Avenue, Fort Hood, TX 76544.
E-mail address: [email protected]

Facial Plast Surg Clin N Am - (2017) -–-

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1064-7406/17/Ó 2017 Elsevier Inc. All rights reserved.
2 Lucas

and rheology of the blood supply to the skin. more than one source of blood supply to a partic-
Although the sensory and barrier functions of the ular area of the skin,3 which contributes signifi-
skin are of obvious and of vital importance, the cantly to the hardiness of the cutaneous flaps
main focus of this discussion is on the blood sup- commonly used in facial reconstruction.
ply and thermoregulatory function of the skin. As many as 5 different vascular plexuses within
the skin and superficial soft tissues have been
described in the literature, including the dermal,
Vascular Anatomy
subdermal, subcutaneous, prefascial, and subfas-
The vascular supply to the skin is extraordinarily cial networks.3 The dermal and subdermal net-
complex. It receives contributions from a variety works are sometimes considered a single unit,
of sources, coupled with a dizzying network of referred to as the dermal-subdermal plexus. The
anastomosing vessels that forms several exten- prefascial and subfascial networks are formed
sive and highly interconnected vascular plexuses from the fasciocutaneous system off the septocu-
at differing levels within the architecture of the taneous arteries. The subcutaneous plexus is
skin. A fair degree of variance exists in the litera- probably the least consistent and least described
ture when describing the vascular anatomy, with of the skin plexuses. Fig. 1 represents the manner
certain terms used interchangeably by different in- in which all these vascular webs are extensively
vestigators. To help alleviate any confusion, an interconnected, creating a vast and elaborate sys-
attempt is made to simplify the anatomic descrip- tem of collateral blood flow. This rich collateral
tions and maintain consistency in the application blood flow, facilitated by the various plexuses,
of this terminology. provides an impressive breadth of vascular redun-
There are 3 main locoregional conduits of blood dancy to the cutaneous structures. It is this redun-
flow to the skin: musculocutaneous arteries, direct dancy of flow that provides not only the
cutaneous arteries, and septocutaneous arteries. mechanism for the thermoregulatory function of
Musculocutaneous arteries are perforators from the skin but also the critical nutrient flow, allowing
deeper muscular arteries that pass through their for cutaneous flap survival and optimal healing.
corresponding muscle tissue and enter the subcu- These robust vascular networks form the founda-
taneous fat to ultimately drain into the subdermal tion for the complex circulatory physiology of the
and dermal plexuses. Less common than their skin.
musculocutaneous counterparts, direct cuta-
neous arteries are generally specific, named ar- Physiology of the Skin
teries or branches of named arteries that run
through the subcutaneous tissues in a plane paral- Due to the important role of the integument in corpo-
lel to the skin. They have been described as real thermoregulation and homeostasis, the skin
confined to specific areas of the body1 and are has a remarkable hemodynamic ability to vary
generally accompanied by veins known as venae the rate and quantity of flow through its vascular
comitantes. Although they may branch off septo- plexuses. Even under normal circumstances, the
cutaneous arteries, they are generally named
branches of larger arteries. Examples include the
parietal and frontal branches of the superficial
temporal artery, the posterior auricular artery, the
occipital artery, the supratrochlear artery, and the
supraorbital artery.1 Septocutaneous arteries
course through the fascial septa dividing the indi-
vidual muscle segments to provide blood flow to
the skin. The fasciocutaneous component of these
arteries runs parallel to the skin surface atop and/
or deep to the superficial muscular fascia, and they
are also generally accompanied by a pair of veins.2
The direct cutaneous and septocutaneous arteries
are responsible for supplying larger, more diffuse
Fig. 1. Graphic representation of the cutaneous
regions of skin, whereas the areas supplied by
vascular plexuses as an extension of the musculocuta-
musculocutaneous arteries are generally smaller neous and septocutaneous perforating arteries.
and more discrete in distribution. All 3 arterial sour- (From Larrabee WF, Makielski KH, Henderson JL.
ces drain into components of the rich network of Surgical anatomy of the face. Second edition. Phila-
plexuses that exist within the superficial soft tis- delphia: Lippincott Williams & Wilkins; 2004; p. 97;
sues. It is particularly relevant that there is often with permission.)
 The Physiology and Biomechanics of Skin Flaps 3

blood supply provided to the skin is far greater than or increase flow through the papillary network in
that needed for its nutrient support. It has been esti- response to the thermal or systemic pressure
mated that the rate of flow through the skin at changes affecting the skin locally or the body glob-
normal temperatures is approximately 10 times ally. Other factors, such as inflammation, cyto-
greater than the minimal requirement for adequate kines, nitric oxide, free radicals, tissue edema,
tissue nutrition.4 As the body is heated, cutaneous and toxins, such as tobacco smoke, can also
vasodilatation increases to such an extent that the have a profound impact on cutaneous blood
flow through the cutaneous plexuses can elevate flow. Several of these factors are discussed in
as high as 6 L/min to 8 L/min during periods of hy- more detail, as the discussion broadens to include
perthermia.5 Likewise, hypothermia or extreme cutaneous flap physiology.
local skin cooling can induce a thermoregulatory
vasoconstriction in skin that can reduce blood LOCAL CUTANEOUS FLAPS
flow rates to levels that are barely adequate to
completely inadequate for cutaneous cellular nutri- Cutaneous flaps of the head and neck region are
tion. These autonomic vasoconstrictive and vasodi- generally broken down into 2 categories: random
latory mechanisms also significantly contribute to pattern flaps and axial pattern flaps. A third cate-
reflex control of systemic blood pressure.5 gory considered is the fasciocutaneous flap, which
The variability of blood flow to and through the also has relevant applications in facial reconstruc-
skin is the result of arterioles that serve as regula- tion. Fig. 3 illustrates the anatomic differences be-
tory sphincters under conditions of adequate sys- tween the differing flaps.
temic pressure, controlling flow through the
cutaneous subdermal and dermal networks. The Random Flaps
dermal networks are divided into 2 main segments Random pattern flaps, also known as local cuta-
that are responsible for the primary functions of neous or random cutaneous flaps, are frequently
the integumentary circulation. The reticular dermis
contains a capillary network that is responsible for
nutrient flow to the skin. The arterioles serving as
precapillary sphincters control flow through this
intricate endothelial web and are chiefly respon-
sive to conditions of hypoxemia and increased
metabolic demand, resulting in sphincter dilation
to increase local blood flow.2 Conversely, the
papillary dermis contains a network of looping
arteriovenous shunts (Fig. 2) that allow for the ther-
moregulatory and hemodynamic functions of the
skin. The arterioles serving as preshunt sphincters
respond primarily to local autonomic release of
norepinephrine or acetylcholine to either decrease

Fig. 3. Illustration of the various types of flaps. (A)

Local cutaneous (random) flap. (B) Direct cutaneous
Fig. 2. Illustrated cross-section of skin demonstrating (axial) flap. (C) Fasciocutaneous flap. (D) Musculocuta-
the papillary loops of the dermal plexus. (From Honrado neous flap. (From Honrado CP, Murakami CS. Wound
CP, Murakami CS. Wound healing and physiology of skin healing and physiology of skin flaps. Facial Plast
flaps. Facial Plast Surg Clin North Am 2005;13(2):211; Surg Clin North Am 2005;13(2):212; Figure 10; with
Figure 9; with permission.) permission.)
4 Lucas

used in reconstruction of facial skin defects.

Dissection of these flaps occurs in the subcutane-
ous tissue plane, and they can be classified into
advancement, transposition, and rotation flaps
based on their geometric design. The vascular
supply to random cutaneous flaps is through
musculocutaneous perforators located near the
base of the flap. Blood flow to the body, margins,
and tip of the flap are supplied via the dermal-
subdermal plexus. The maximal survival length
of these flaps is reliant on the vascular perfusion
pressure. In the past, a length-to-width ratio no
greater than 3:1 had been advocated for random
cutaneous flaps. This rule of thumb is now gener-
ally regarded as inaccurate. The vascular perfu-
sion pressure of a random flap can be
unpredictable based on several variables. Ulti-
mately, if the perfusion pressure at any portion
of the flap falls below the arteriole closing pres-
sure, the distal soft tissues becomes ischemic
and ultimately results in necrosis of that portion
of the flap. Recruiting more vessels into the
base of the flap does not change the perfusion
pressure of those vessels, thus providing no
Fig. 4. Distal flap perfusion depends on capillary
change in the maximal survival length of the perfusion pressure as opposed to flap width. Flaps A
flap2 (Fig. 4). and B represent flaps of equal length but differing
base width. (From Gaboriau HP, Murakami CS. Skin
anatomy and flap physiology. In: Baker SR, editor.
Axial Flaps
Local flaps in facial reconstruction. Philadelphia:
Axial pattern flaps (also known as direct cuta- Mosby; 1995. p. 19; with permission.)
neous or arterial cutaneous flaps) in the head
and neck differ from random flaps in that their
arterial supply is based off a direct cutaneous ar-
Fasciocutaneous Flaps
tery that is located beneath the long axis of the
flap, thus providing a more definitive and easily The third type of flap is the fasciocutaneous flap.
described blood supply. Survival lengths of the These flaps are based on the fasciocutaneous sys-
flap are directly related to the length of the cuta- tem of vessels branching off the septocutaneous
neous artery supplying the flap. Skin extending arteries running in the fascia between muscle
beyond the arterial component of these flaps is bellies. This system forms the subfascial and pre-
the essential equivalent of a random pattern fascial plexuses (discussed previously). Branches
flap, with perfusion of the distal soft tissues pro- and perforators off of these networks connect
vided solely via the dermal-subdermal plexus.2 with the dermal-subdermal plexus to supply the
Although these flaps are not as common as skin and subcutaneous tissues. These fascial plex-
random pattern flaps in facial reconstruction, uses typically have an element of directionality,3
they are advantageous because of the longer so flap orientation is important and is generally
flap lengths that can be achieved without axial in nature. There seems some debate within
compromising survival. The paramedian forehead the literature1,2,6 over whether the paramedian
flap is an axial pattern flap that is frequently used forehead flap is best categorized as a direct cuta-
in nasal reconstruction. Based off the supratro- neous flap or a fasciocutaneous flap, owing to the
chlear artery and vein(s), the axial arterial supply supratrochlear artery described as both a direct
of this flap allows for flap lengths that can be cutaneous artery and a fasciocutaneous artery. A
rotated from the upper limits of the forehead dilemma in flap nomenclature occurs when a flap
down to the nasal tip and columella. The axial is based on a vessel that feeds a fascial plexus
configuration also facilitates rotation of the para- with a predominant directionality, such as the
median flap by minimizing pedicle width while supratrochlear artery and its accompanying fascial
maintaining adequate perfusion to the distal tip plexus.1 Although the paramedian flap might be
of the flap. more aptly considered an axial fasciocutaneous
 The Physiology and Biomechanics of Skin Flaps 5

flap, the confusion seems mostly a matter of se- was reduced rather than eliminated. Fortunately,
mantics with little to no practical impact. When extensive collateral flow through the intercon-
designed with a skin component, the temporopar- nected vascular networks within the cutaneous
ietal flap is also properly classified as a fasciocuta- structures provides adequate support from adja-
neous flap. A versatile flap, it can be used for cent tissues to the more poorly perfused areas.
coverage of auricular, orbital, and other defects This allows the majority of flaps the ability to sur-
of the upper two-thirds of the face. vive until more complete vascular flow can be re-
established to the transposed tissues. An addi-
BASIC CUTANEOUS FLAP PHYSIOLOGY tional factor to consider as it pertains to vascular
compromise is the interruption of venous outflow.
What are the physiologic changes that occur Although complete venous occlusion of a flap has
within the skin and surrounding soft tissue when the potential to be more damaging than inade-
flap elevation occurs? What effect do these phys- quate arterial perfusion, the subdermal plexus
iologic changes have on the potential for flap sur- alone is usually adequate for venous outflow.2
vival or demise? Without question, the most
obvious and profound physiologic insult to occur
Vascular Delay
with elevation of a cutaneous flap is the significant
reduction in blood flow to the involved skin due to When discussing the subject of vascular compro-
the partial transection of the vascular supply. The mise, it is also important to address the topic of
ability of a properly designed flap to survive in light vascular delay, also known as the delay phenom-
of the resulting ischemia serves as a testament not enon. Briefly, vascular delay occurs when a
only to the low nutrient requirements of the skin portion of the vascular supply to a flap is divided
but also to the importance of collateral flow pro- before it is definitively elevated and transferred.
vided by the intricate vascular networks within Surgical delay can be accomplished in several
the skin. This collateral flow can be further ways, including
augmented by applying the concepts of vascular
delay when appropriate. Additional factors to  Making only the incisions needed to create
consider in blood flow alterations to the skin flap the flap without elevating any tissues
include the effects of sympathetic denervation,  Initially elevating a bipedicled flap
local inflammatory changes, and the neovasculari-  Elevating only a portion of a planned single
zation of the flap within its recipient bed. pedicle flap
After the delay procedure, the flap is then fully
Vascular Compromise
elevated and transferred at a later time, typically
When a cutaneous flap is elevated, the most direct within 5 days to 14 days. Holzbach and col-
blood flow to that segment of skin is interrupted. leagues10 demonstrated an ideal delay time of
The disruption of flow results in a drop in the perfu- 5 days in an exquisitely designed rat model;
sion pressure to the involved skin. In random conversely, numerous investigators11–15 have
pattern flaps, the elevated skin is reliant on the advocated for a delay of 2 weeks, allowing for
vascular supply from the base of the flap. Perfu- full development of neovascular channels within
sion pressures are further diminished as the dis- the flap. Although it is difficult to draw definitive
tance from the base of the flap increases.2 conclusions based on the disparate nature of
Widening the base may recruit more feeding ar- these findings, it indicates that there is likely a fairly
teries into a random flap; however, the perfusion broad sweet spot as it applies to the timing of flap
pressures at the base of the flap remain un- elevation and transfer after a delay procedure.
changed.7,8 As discussed previously, once the It is well known that delay results in improved
perfusion pressure falls below critical closing pres- viability and survival of skin flaps. What is less
sures of the arterioles within the dermal- well known are the exact mechanisms responsible
subdermal plexus, nutrient flow to the distal tis- for the beneficial effect on flap viability. Several
sues ceases. This ultimately results in necrosis to mechanisms that are generally agreed on include
the distal portion of the flap unless flow can be the loss of sympathetic tone (with the ultimate
re-established to the critically ischemic areas. Ker- depletion of vasoconstrictive substances) and
rigan and Daniel9 used a porcine model to demon- the axial reorientation and dilation of vascular
strate that arterial (axial) and random flaps tolerate channels and choke vessels within the flap.16
an average of 13 hours of complete avascularity The existence of choke vessels arose from the
before tissue viability is irreversibly compromised. concept of angiosomes first described by Taylor
It can be logically extrapolated that this viability and Palmer17 and further refined by Taylor and
would be significantly lengthened if perfusion others in later research.18–21 In short, choke
6 Lucas

vessels ordinarily regulate collateral blood flow be- few days as a result of neovascularization of the
tween neighboring vascular territories (angio- flap. This process begins at approximately days
somes). Vascular delay causes choke vessels 3 to 4 and is generally robust enough after day 7
along the longitudinal axis of the flap to irreversibly that the flap pedicle can be transected if appro-
dilate through a process of hypertrophy and hy- priate.2,25 The exact mechanisms through which
perplasia of the cells within the walls of the choke neovascularization occur are complex but likely
artery.18,21 This process seems maximal at 7 days. involve both angiogenic (new microvessels sprout-
A delay of 14 days allows for neovascularization to ing from a preexisting capillary network) and vas-
occur. Additionally, metabolic factors that have yet culogenic (new vessel formation from marrow-
to be well described are also likely factors in the derived endothelial progenitor cells) processes.15
enhanced viability of delayed flaps. In the presence of tissue ischemia, release of
growth factors, such as basic fibroblast growth
Sympathetic Denervation factor and vascular endothelial growth factor,
As discussed previously, flap creation results not stimulate endothelial cells and endothelial progen-
only in disruption of the cutaneous sensory inner- itor cells to proliferate and form new capillary
vation but also in the sympathetic innervation of channels.15 This capillary neovascularization is
the involved tissues. Sympathetic nerve division characterized by vessel ingrowth of the flap from
results in the release of catecholamines from the the surrounding tissues, down the ischemic
nerve terminal and impairs neurotransmitter reup- gradient, and toward the angiogenic source. New
take, resulting in a relative hyperadrenergic state capillary growth toward an angiogenic stimulus
and local vasoconstriction.22 This vasoconstriction occurs at rate of approximately 0.2 mm per day,
is clearly a part of the elaborate homeostatic ultimately spanning distances of 2 mm to 5 mm.2
mechanisms within the body, minimizing blood There are a significant number of additional fac-
loss after a penetrating injury. Unfortunately, it tors that can impede or enhance flap viability.
also contributes to diminished nutritive blood Some of the most commonly discussed and stud-
flow within the already flow-compromised skin ied include reperfusion/free radical injury, alter-
flap.23 Once the adrenergic neurotransmitter levels ations of rheology, increased nitric oxide
have diminished after 24 hours to 48 hours,24 the production, hyperbaric oxygen use, tissue irradia-
loss of sympathetic tone results in vasodilation of tion, and tobacco use. Although these factors are
the vascular networks supplying the flap. As dis- all notable for their potential effects on flap sur-
cussed previously, this rebound vasodilation after vival, further elaboration on these subjects is
sympathectomy is one of the mechanisms lever- beyond the scope of this discussion.
aged to enhance flap viability via the delay
phenomenon. SKIN FLAP BIOMECHANICS
Valued as a close companion to an understanding
Inflammatory Changes
of the vascular supply and physiology of the skin, a
When soft tissue is injured, as in skin flap elevation, thorough mastery of the biomechanics of soft tis-
an inflammatory response reliably ensues. This sue is a critical element in the proper design of
response is acutely mediated by the extracellular robust, viable skin flaps to repair facial defects. A
release of inflammatory mediators, such as hista- reconstructive surgeon must fully comprehend
mine, serotonin, and kinins. These substances the importance of the 3 main mechanical proper-
cause an increase in microvascular permeability, ties of the skin: nonlinearity, anisotropy, and visco-
with a subsequent elevation in the concentration elasticity. Consideration of these properties is
of inflammatory cells and proteins within the extra- imperative when designing a skin flap, because
cellular milieu.2 The resulting tissue edema can they have a profound impact on flap blood flow,
further reduce perfusion of the compromised flap viability, and aesthetic healing.
in the acute phase. The inflammatory response,
however, ultimately leads to the initiation of pros- Nonlinearity
taglandin synthesis which, among other functions, To adequately explain the concept of nonlinearity,
results in local vasodilation. Thus, the effects of a brief discussion of the mechanical quantities of
inflammation can have both positive and negative stress, strain, and the stress/strain ratio must be
effects on the overall viability of cutaneous flaps. undertaken. Stress is a measure of the force
applied to a material per unit of its cross-
Neovascularization
sectional area; strain is a measure of the change
After a flap is transposed to its recipient bed, blood in length of a material placed under stress, divided
flow reliably and gradually improves after the first by its original length. Accordingly, the stress/strain
 The Physiology and Biomechanics of Skin Flaps 7

ratio is a measurement of the dynamic relationship 3. A terminal stage where continuously increasing,
of an applied force and the resulting change in ma- maximal force results in little to no additional
terial length caused by that force for a given cross- lengthening of the skin
sectional area.26 Many of the common, more
homogeneous materials used in engineering appli- Histologic evaluation of these stages of stress/
cations have a linear stress/strain ratio. Simply strain on the skin renders a clear account of the
put, this means that the greater the force applied microanatomic changes that determine this
to the material, the greater the change in its length. nonlinear response to stress. When an initial stress
Skin, on the other hand, behaves differently from is applied, the haphazardly arranged collagen and
these uniform, linear materials. The construct of elastin fibers stretch along the vector of the
the integument is heterogeneous; its composition applied force with limited resistance to deforma-
includes collagen and elastic fibers, blood vessels, tion. This results in a stress/strain ratio (stage 1)
lymphatics, nerve fibers, and ground substance, all that is essentially linear and elastic.26 As the force
within the dermis. The collagen fibers are arranged and resulting deformation progress (stage 2), addi-
throughout the dermis in thick and thin bundles tional collagen fibers are recruited into a load-
that extend in multiple directions with numerous in- bearing role, causing rapid increases in resistance
terconnections. This complex mesh of collagen also to further deformation.1 Stage 2 is the strain at
has elastin fibers integrated throughout. These which many of the collagen fibers within the skin
elastin fibers provide memory to the bundles, allow- transition from a non–load-bearing role to one
ing collagen that is stretched to return to its original, that is wholly load bearing. Finally, as stress loads
relaxed state.26 Because of the heterogeneous rapidly increase to extremes (stage 3), essentially
construct of the skin, it behaves in a distinctly all the dermal collagen fibers are aligned in the di-
nonlinear manner when placed under stress. rection of the applied force. When collagen is fully
Fig. 5 demonstrates the nonlinear stress/strain oriented in one direction, it becomes inextensible
relationship of the skin.27 The graph demonstrates and resists further deformation. This allows for
that the mechanical response of skin to an applied preservation of the structural integrity of skin dur-
force can be broken down into 3 stages: ing unexpected, high-level stresses.26 Although
increasing tension on the skin may not cause
1. An initial flat stage showing a significant degree further deformation, it can have an extremely dele-
of strain (lengthening) in response to a minimal terious effect on the blood flow to the skin or skin
amount of stress (force) flap. At a certain point, increasing skin tension
2. An intermediate or transition stage, where a compromises the vascular supply to a skin flap, ul-
rapidly increasing amount of force is required timately resulting in necrosis of the involved
to achieve a smaller degree of lengthening portion of the flap.28

Anistropy
An understanding of the variations in extensibility
and tension of the skin is vitally important to the
concepts of skin biomechanics. Skin tension
varies significantly from one location on the body
to another. Each of these locations can display
significant variance in the directionality of cuta-
neous movement. The term, anisotropy, refers to
the directional qualities of the skin. Tension on
the skin exists in every direction in most locations
of the body; however, the greatest degree of skin
tension runs parallel to lines in the skin known as
relaxed skin tension lines (RSTLs).29,30 An incision
placed at a right angle to the RSTL results in a
widely gaping defect that commonly results in a
widened or hypertrophic scar.1,26 The lines of
maximal extensibility (LMEs) are imaginary lines
within the skin that run perpendicular to the
Fig. 5. The stress/strain curve. (From Honrado CP, Mur- RSTLs. Closure of skin defects in parallel with
akami CS. Wound healing and physiology of skin the LMEs produce the least amount of tension on
flaps. Facial Plast Surg Clin North Am 2005;13(2):213; the skin edges.31 Accordingly, every attempt
Figure 12; with permission.) should be made to place incisions parallel to
8 Lucas

RSTLs, whereas local skin flaps should be SUMMARY

designed to ensure that donor site closure is par-
allel to the LMEs.27 An intimate knowledge of the vascular anatomy
and basic physiology of skin allows the recon-
structive surgeon to accurately predict and
Viscoelasticity explain the physiologic changes that can affect
As discussed previously, skin behaves in an the viability of local skin flaps used to repair facial
essentially elastic manner in the earliest stage of defects created by Mohs surgery or other mech-
low-stress deformation. A material is considered anisms of trauma. The biomechanical properties
elastic when the stress/strain relationship does of skin are also vitally important to consider
not vary with time.26 Thus, at low stress levels, when designing skin flaps, because these prop-
the deformation of the skin is rapidly reversible erties also have an impact on the survivability
when the stress is removed. The same low-level and utility of the flap. Although an attempt is
stress repeated multiple times continues to result made to be as concise and consistent yet thor-
in the same degree of deformation followed by ough as possible in this brief review of the topic,
rapid return to the resting state. At higher stress readers are encouraged to further explore this
loads, however, skin assumes a more viscoelastic vast and fascinating subject to broaden and
property. Viscoelasticity results when strain refine their confidence in using many of the mo-
(lengthening) is a function of both stress and dalities of skin repair, as discussed in the
time. Due to the nonlinear nature of skin, further following articles of this review on facial recon-
lengthening at higher stress loads does not occur struction techniques.
acutely because of the load-bearing nature of
wholly aligned collagen bundles. When skin is REFERENCES
held under high stress for a period of time, howev-
er, additional lengthening ultimately occurs. This 1. Honrado CP, Murakami CS. Wound healing and the
time-dependent viscoelasticity is further defined physiology of skin flaps. Facial Plast Surg Clin North
by the properties of creep and stress relaxation. Am 2005;13:203–14.
The biomechanical property of creep occurs 2. Hom DB, Goding GS. Skin flap physiology. In:
when skin lengthens further than the original length Baker SR, editor. Local flaps in facial reconstruction.
observed when the skin is placed under a constant Philadelphia: Mosby Elsevier; 2007. p. 15–30.
tension or stress. A small degree of lengthening 3. Robertson K. Fasciocutaneous flaps. Medscape
can be rapidly achieved when the skin is placed 2015. Available at: http://emedicine.medscape.com/
under extremely high stress loads for a short article/1284631-overview. Accessed October 3, 2016.
period of time. This slight lengthening is a result 4. Hauben DJ, Zijlstra FJ. Prostacyclin formation in de-
of the displacement of interstitial fluids that are layed pig flank flaps. Ann Plast Surg 1984;13:304.
loosely bound to the extracellular matrix,26 and it 5. Charkoudian N. Skin blood flow in adult human ther-
is sometimes referred to as mechanical creep. It moregulation: how it works, when it does not, and
is the basis for the practice of rapid, intraoperative why. Mayo Clin Proc 2003;78(5):603–12.
tissue expansion. Further lengthening can be 6. Gaboriau HP, Murakami CS. Skin anatomy and flap
achieved in skin placed under constant load for physiology. Otolaryngol Clin North Am 2001;34(3):
longer periods of time. This lengthening is thought 555–69.
to be due to further histologic changes occurring 7. Cutting C. Critical closing and perfusion pressures
within the skin and is sometimes referred to as bio- in flap survival. Ann Plast Surg 1982;9(6):524.
logic creep. It is the basis for more conventional 8. Cutting C, Ballantyne D, Shaw W, et al. Critical clos-
tissue expansion techniques. ing pressure, local perfusion pressure, and the
The property of stress relaxation is closely failing skin flap. Ann Plast Surg 1982;8(6):504–9.
related to creep. It refers to the decline in stress 9. Kerrigan CL, Daniel RK. Critical ischemia time and
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