Key Notes on Plastic Surgery

Foreword

This second edition of Key Notes on Plastic Surgery distills the breadth and depth of the entire specialty into a compact format. Clear, concise, accurate and accessible—that is what the trainee desires when refreshing their memory of conditions during clinic, of reconstructive algorithms before operating, and of the entire syllabus when preparing for plastic surgery board examinations. Key Notes on Plastic Surgery fulfils this niche admirably.

A consistent balance has been struck between prose and bullet points throughout the book. Key Notes on Plastic Surgery fosters understanding, facilitates the commitment of information to memory, and provides structure to ease the recall of facts and principles. One can rapidly glean key information with a glance at the page and yet solidify an understanding with a few minutes' read. The textual formatting and presentation of information is where this book particularly shines.

Key Notes on Plastic Surgery will be embraced as a trusted companion by trainees all over the world as they progress through training and sit for their board examinations. And when they become established plastic surgeons, Key Notes on Plastic Surgery will take pride of place on their bookshelves as a reliable quick reference handbook for teaching the next generation.

I highly recommend Key Notes on Plastic Surgery to all aspiring, training and established plastic surgeons worldwide.

Fu-Chan Wei, MD, FACS

Distinguished Chair Professor

Chang Gung University

Medical College

Taipei, Taiwan

Academician

Academia Sinica

Taiwan

Preface

Hywel Dafydd has updated and improved the first edition of Key Notes on Plastic Surgery. He has worked tirelessly to include new and better diagrams and improve the content whilst maintaining the book's ethos—to succinctly communicate the essentials of Plastic Surgery.

We hope you enjoy the book and find it helpful in making you a better Plastic Surgeon.

Adrian Richards

The first edition of Key Notes has proved to be exceptionally popular for over a decade. Accessible, informative and succinct, it became the preferred handbook for innumerable plastic surgery trainees. It was typeset with enough ‘white space’ to accommodate trainees' notes and sketches as they approached their final plastic surgery examination.

Nevertheless, an update was much-needed: the field of plastic surgery has moved on apace and a detailed British plastic surgery syllabus was introduced. The material of the first edition has been updated, rewritten and expanded with several new sections to reflect this. In addition, a new chapter is provided: ‘Ethics and the law’. The number of diagrams has more than doubled, which should help with learning the ‘essentials’, such as cleft lip repair and eyelid anatomy. Key Notes is now more complete and, although necessarily larger, remains true to the format and style of the first edition. We hope that Key Notes continues to be useful to plastic surgeons worldwide.

Hywel Dafydd

Dedications

AR—To my Family, Helena, Josie, Ciara, Alfie and Ned.

HD—For Jenny and Ioan.

Acknowledgements

As any Plastic Surgeon will tell you, the training and practice of the speciality takes dedication and hard work. Writing a book in your free time adds to this and requires patience and support from your family. For this reason I would like to thank my family Helena, Josie, Ciara, Alfie and Ned for their constant support. I would also like to thank my surgical mentors of whom there were many—in particular Brent Tanner and Michael Klaassen.

Adrian Richards

I would like to thank my wife Jenny and my son Ioan for their love and patience. Jenny also helped edit final drafts for brevity. Thank you Per Hall for inspiring me to become a plastic surgeon. Thanks to those who have trained me over the years in Cambridge, Wellington, Leicester, Birmingham, Coventry, Swansea, Taipei, and Auckland. Special thanks to Sarah Hemington-Gorse, Ian Josty, Dai Nguyen, Nick Wilson Jones, Tom Potokar, Peter Drew, Leong Hiew, Hamish Laing, Dean Boyce, Max Murison and Ian Pallister, who spent hours proofreading early drafts. I am also grateful to Rhidian Dafydd LLB, Karen Wong and Chris Wallace, who checked much of the text for accuracy. Tom Macleod has been a constant source of support and encouragement, and did a great deal of preparatory work on many of the chapters. The book could not have been written without the staff of Morriston Hospital's library. They sourced over 600 references from three centuries without as much as a grumble: thank you Anne, Sue, Rita and Lisa.

Hywel Dafydd

Abbreviations

Chapter 1

General Principles

Embryology, structure and function of the skin

Blood supply to the skin

Classification of flaps

Geometry of local flaps

Wound healing and skin grafts

Bone healing and bone grafts

Cartilage healing and cartilage grafts

Nerve healing and nerve grafts

Tendon healing

Transplantation

Tissue engineering

Alloplastic implantation

Wound dressings

Sutures and suturing

Tissue expansion

Lasers

Local anaesthesia

Microsurgery

Haemostasis and thrombosis

Further reading

Embryology, structure and function of the skin

Skin differentiates from ectoderm and mesoderm during the 4th week.

Skin gives rise to:

Teeth and hair follicles, derived from epidermis and dermis

Fingernails and toenails, derived from epidermis only.

Hair follicles, sebaceous glands, sweat glands, apocrine glands and mammary glands are ‘epidermal appendages’ because they develop as ingrowths of epidermis into dermis.

Functions of skin:

Physical protection

Protection against UV light

Protection against microbiological invasion

Prevention of fluid loss

Regulation of body temperature

Sensation

Immunological surveillance.

The epidermis

Composed of stratified squamous epithelium.

Derived from ectoderm.

Epidermal cells undergo keratinisation—their cytoplasm is replaced with keratin as the cell dies and becomes more superficial.

Rete ridges are epidermal thickenings that extend downward between dermal papillae.

Epidermis is composed of these five layers, from deep to superficial:

Stratum germinativum

Also known as the basal layer.

Cells within this layer have cytoplasmic projections (hemidesmosomes), which firmly link them to the underlying basal lamina.

The only actively proliferating layer of skin.

Stratum germinativum also contains melanocytes.

Stratum spinosum

Also known as the prickle cell layer.

Contains large keratinocytes, which synthesise cytokeratin.

Cytokeratin accumulates in aggregates called tonofibrils.

Bundles of tonofibrils converge into numerous desmosomes (prickles), forming strong intercellular contacts.

Stratum granulosum

Contains mature keratinocytes, with cytoplasmic granules of keratohyalin.

The predominant site of protein synthesis.

Combination of cytokeratin tonofibrils with keratohyalin produces keratin.

Stratum lucidum

A clear layer, only present in the thick glabrous skin of palms and feet.

Stratum corneum

Contains non-viable keratinised cells, having lost their nuclei and cytoplasm.

Protects against trauma.

Insulates against fluid loss.

Protects against bacterial invasion and mechanical stress.

Cellular composition of the epidermis

Keratinocytes—the predominant cell type in the epidermis.

Langerhans cells—antigen-presenting cells (APCs) of the immune system.

Merkel cells—mechanoreceptors of neural crest origin.

Melanocytes—neural crest derivatives:

Usually located in the stratum germinativum.

Produce melanin packaged in melanosomes, which is delivered along dendrites to surrounding keratinocytes.

Melanosomes form a cap over the nucleus of keratinocytes, protecting DNA from UV light.

The dermis

Accounts for 95% of the skin's thickness.

Derived from mesoderm.

Papillary dermis is superficial; contains more cells and finer collagen fibres.

Reticular dermis is deeper; contains fewer cells and coarser collagen fibres.

It sustains and supports the epidermis.

Dermis is composed of:

Collagen fibres

Produced by fibroblasts.

Through cross-linking, are responsible for much of the skin's strength.

The normal ratio of type 1 to type 3 collagen is 5:1.

Elastin fibres

Secreted by fibroblasts.

Responsible for elastic recoil of skin.

Ground substance

Consists of glycosaminoglycans (GAGs): hyaluronic acid, dermatan sulphate, chondroitin sulphate.

GAGs are secreted by fibroblasts and become ground substance when hydrated.

Vascular plexus

Separates the denser reticular dermis from the overlying papillary dermis.

Skin appendages

Hair follicles

Each hair is composed of a medulla, a cortex and an outer cuticle.

Hair follicles consist of an inner root sheath (derived from epidermis), and an outer root sheath (derived from dermis).

Several sebaceous glands drain into each follicle.

Drainage of the glands is aided by contraction of arrector pili muscles.

Vellus hairs are fine and downy; terminal hairs are coarse.

Hairs are either in anagen (growth), catagen (regressing), or telogen (resting) phase.

<90% are in anagen, 1–2% in catagen and 10–14% in telogen at any one time.

Eccrine glands

These sweat glands secrete odourless hypotonic fluid.

Present in almost all sites of the body.

Occur more frequently in the palm, sole and axilla.

Apocrine glands

Located in axilla and groin.

Emit a thicker secretion than eccrine glands.

Responsible for body odour; do not function before puberty.

Modified apocrine glands are found in the external ear (ceruminous glands) and eyelid (Moll glands).

The mammary gland is a modified apocrine gland specialised for manufacture of colostrum and milk.

Hidradenitis suppurativa is a disease of apocrine glands.

Sebaceous glands

Holocrine glands that drain into the pilosebaceous unit in hair-bearing skin.

They drain directly onto skin in the labia minora, penis and tarsus (meibomian glands).

Most prevalent on forehead, nose and cheek; absent from palms and soles.

Produce sebum, which contains fats and their breakdown products, wax esters and debris of dead fat-producing cells.

Sebum is bactericidal to staphylococci and streptococci.

Sebaceous glands are not the sole cause of so-called sebaceous cysts.

These cysts are in fact of epidermal origin and contain all substances secreted by skin (predominantly keratin).

Some maintain they should therefore be called epidermoid cysts.

Types of secretion from glands

Eccrine or merocrine glands secrete opened vesicles via exocytosis.

Apocrine glands secrete by ‘membrane budding’—pinching off part of the cytoplasm in vesicles bound by the cell's own plasma membrane.

Holocrine gland secretions are produced within the cell, followed by rupture of the cell's plasma membrane.

Histological terms

Acanthosis: epidermal hyperplasia.

Papillomatosis: increased depth of corrugations at the dermoepidermal junction.

Hyperkeratosis: increased thickness of the keratin layer.

Parakeratosis: presence of nucleated cells at the skin surface.

Pagetoid: when cells invade the upper epidermis from below.

Palisading: when cells are oriented perpendicular to a surface.

Blood supply to the skin

Epidermis contains no blood vessels.

It is dependent on dermis for nutrients, supplied by diffusion.

Anatomy of the circulation

Blood reaching the skin originates from named deep vessels.

These feed interconnecting vessels, which supply the vascular plexuses of fascia, subcutaneous tissue and skin.

Deep vessels

Arise from the aorta and divide to form the main arterial supply to head, neck, trunk and limbs.

Interconnecting vessels

The interconnecting system is composed of:

Fasciocutaneous (or septocutaneous) vessels

Reach the skin directly by traversing fascial septa.

Provide the main arterial supply to skin in the limbs.

Musculocutaneous vessels

Reach the skin indirectly via muscular branches from the deep system.

These branches enter muscle bellies and divide into multiple perforating branches, which travel up to the skin.

Provide the main arterial supply to skin of the torso.

Vascular plexuses of fascia, subcutaneous tissue and skin

Subfascial plexus

Small plexus lying on the undersurface of deep fascia.

Prefascial plexus

Larger plexus superficial to deep fascia; prominent on the limbs.

Predominantly supplied by fasciocutaneous vessels.

Subcutaneous plexus

At the level of superficial fascia.

Mainly supplied by musculocutaneous vessels.

Predominant on the torso.

Subdermal plexus

Receives blood from the underlying plexuses.

The main plexus supplying blood to skin.

Accounts for dermal bleeding observed in incised skin.

Dermal plexus

Mainly composed of arterioles.

Plays an important role in thermoregulation.

Subepidermal plexus

Contains small vessels without muscle in their walls.

Predominantly nutritive and thermoregulatory function.

Angiosomes

An angiosome is a three-dimensional composite block of tissue supplied by a named artery.

The area of skin supplied by an artery was first studied by Manchot in 1889.

His work was expanded by Salmon in the 1930s, and more recently by Taylor and Palmer.

The anatomical territory of an artery is the area into which the vessel ramifies before anastomosing with adjacent vessels.

The dynamic territory of an artery is the area into which staining extends after intravascular infusion of fluorescein.

The potential territory of an artery is the area that can be included in a flap if it is delayed.

Vessels that pass between anatomical territories are called choke vessels.

The transverse rectus abdominis myocutaneous (TRAM) flap illustrates the angiosome concept well:

Zone 1

Receives musculocutaneous perforators from the deep inferior epigastric artery (DIEA) and is therefore in its anatomical territory.

Zones 2 and 3

There is controversy as to which of the following zones is 2 and which is 3.

Hartrampf's 1982 description has zone 2 across the midline and zone 3 lateral to zone 1.

Holm's 2006 study shows the opposite to be true.

Skin lateral to zone 1 is in the anatomical territory of the superficial circumflex iliac artery (SCIA).

Blood has to travel through a set of choke vessels to reach it from the ipsilateral DIEA.

Skin on the contralateral side of the linea alba is in the anatomical area of the ipsilateral DIEA.

It is also within the dynamic territory of the contralateral DIEA.

This allows a TRAM flap to be reliably perfused based on either DIEA.

Zone 4

This lies furthest from the pedicle and is in the anatomical territory of the contralateral SCIA.

Blood passing from the pedicle to zone 4 has to cross two sets of choke vessels.

This portion of the TRAM flap has the worst blood supply and is often discarded.

Arterial characteristics

Taylor made the following observations from his detailed anatomical dissections:

Vessels usually travel with nerves.

Vessels obey the law of equilibrium—if one is small, its neighbour will tend to be large.

Vessels travel from fixed to mobile tissue.

Vessels have a fixed destination but varied origin.

Vessel size and orientation is a product of growth.

Venous characteristics

Venous networks consist of linked valvular and avalvular channels that allow equilibrium of flow and pressure.

Directional veins are valved; typically found in subcutaneous tissues of limbs or as a stellate pattern of collecting veins.

Oscillating avalvular veins allow free flow between valved channels of adjacent venous territories.

They mirror and accompany choke arteries.

They define the perimeter of venous territories in the same way choke arteries define arterial territories.

Superficial veins follow nerves; perforating veins follow perforating arteries.

The microcirculation

Terminal arterioles are found in reticular dermis.

They terminate as they enter the capillary network.

The precapillary sphincter is the last part of the arterial tree containing muscle within its wall.

It is under neural control and regulates blood flow into the capillary network.

The skin's blood supply far exceeds its nutritive requirements.

It bypasses capillary beds via arteriovenous anastomoses (AVAs) and has a primarily thermoregulatory function.

AVAs connect arterioles to efferent veins.

AVAs are of two types:

Indirect AVAs—convoluted structures known as glomera (sing. glomus)

Densely innervated by autonomic nerves.

Direct AVAs—less convoluted with sparser autonomic supply.

Control of blood flow

The muscular tone of vessels is controlled by:

Pressure of the blood within vessels (myogenic theory)

Originally described by Bayliss, states that:

Increased intraluminal pressure results in constriction of vessels.

Decreased intraluminal pressure results in their dilatation.

Helps keep blood flow constant; accounts for hyperaemia on release of a tourniquet.

Neural innervation

Arterioles, AVAs and precapillary sphincters are sympathetically innervated.

Increased arteriolar tone results in decreased cutaneous blood flow.

Increased precapillary sphincter tone reduces blood flow into capillary networks.

Decreased AVA tone increases non-nutritive blood flow bypassing the capillary bed.

Humoral factors

Epinephrine, norepinephrine, serotonin, thromboxane A2 and prostaglandin F2α cause vasoconstriction.

Histamine, bradykinin and prostaglandin E1 cause vasodilatation.

Low O2 saturation, high CO2 saturation and acidosis also cause vasodilatation.

Temperature

Heat causes cutaneous vasodilatation and increased flow, which predominantly bypasses capillary beds via AVAs.

The delay phenomenon

Delay is any preoperative manoeuvre that results in increased flap survival.

Historical examples include Tagliacozzi's nasal reconstruction described in the 16th century.

Involves elevation of a bipedicled flap with length : breadth ratio of 2:1.

The flap can be considered as two 1:1 flaps.

Cotton lint is placed under the flap, preventing its reattachment.

Two weeks later, one end of the flap is detached from the arm and attached to the nose.

A flap of these dimensions transferred without a delay procedure would have a significant chance of distal necrosis.

Delay is occasionally used for pedicled TRAM breast reconstruction.

The DIEA is ligated two weeks prior to flap transfer.

The mechanism of delay remains incompletely understood.

These theories have been proposed to explain the delay phenomenon:

Increased axiality of blood flow

Removal of blood flow from the periphery of a random flap promotes development of an axial blood supply from its base.

Axial flaps have improved survival compared to random flaps.

Tolerance to ischaemia

Cells become accustomed to hypoxia after the initial delay procedure.

Less tissue necrosis therefore occurs after the second operation.

Sympathectomy vasodilatation theory

Dividing sympathetic fibres at the borders of a flap results in vasodilatation and improved blood supply.

But why, if sympathectomy is immediate, does the delay phenomenon only begin to appear at 48 hours, and why does it take 2 weeks for maximum effect?

Intraflap shunting hypothesis

Postulates that sympathectomy dilates AVAs, resulting in an increase in nonnutritive blood flow bypassing the capillary bed.

A greater length of flap will survive at the second stage as there are fewer sympathetic fibres to cut and therefore less of a reduction in nutritive blood flow.

Hyperadrenergic state

Surgery results in increased tissue concentrations of vasoconstrictors, such as epinephrine and norepinephrine.

After the initial delay procedure, the resultant reduction in blood supply is not sufficient to produce tissue necrosis.

The level of vasoconstrictor substances returns to normal before the second procedure.

The second procedure produces another rise in the concentration of vasoconstrictor substances.

This rise is said to be smaller than it would be if the flap were elevated without a prior delay.

The flap is therefore less likely to undergo distal necrosis after a delay procedure.

Unifying theory

Described by Pearl in 1981; incorporates elements of all these theories.

Classification of flaps

Flaps can be classified by the five ‘C’s:

Circulation

Composition

Contiguity

Contour

Conditioning.

Circulation

Can be further subcategorised into:

Random

Axial (direct, fasciocutaneous, musculocutaneous, or venous).

Random flaps

No directional blood supply; not based on a named vessel.

These include most local flaps on the face.

Should have a maximum length : breadth ratio of 1:1 in the lower extremity, as it has a relatively poor blood supply.

Can be up to 6:1 in the face, as it has a good blood supply.

Axial flaps

Direct

Contain a named artery running in subcutaneous tissue along the axis of the flap.

Examples include:

Groin flap, based on superficial circumflex iliac vessels.

Deltopectoral flap, based on perforating vessels of internal mammary artery.

Both flaps can include a random segment in their distal portions after the artery peters out.

Fasciocutaneous

Based on vessels running either within or near the fascia.

The fasciocutaneous system predominates on the limbs.

Fasciocutaneous flaps are classified by Cormack and Lamberty:

Type A

Dependent on multiple non-named fasciocutaneous vessels that enter the base of the flap.

Lower leg ‘super flaps’ described by Pontén are examples of type A flaps.

Their dimensions vastly exceed the 1:1 ratios recommended.

Type B

Based on a single fasciocutaneous vessel, which runs along the axis of the flap.

Examples include scapular/parascapular flap, and perforator-based fasciocutaneous flaps of the lower leg.

Type C

Supplied by multiple small perforating vessels, which reach the flap from a deep artery running along a fascial septum between muscles.

Examples include radial forearm flap (RFF) and lateral arm flap.

Type C flaps with bone

Osteofasciocutaneous flaps, originally classified as type D.

Examples include:

RFF raised with a segment of radius; lateral arm flap raised with a segment of humerus.

The Mathes and Nahai fasciocutaneous flap classification is slightly different:

Type A

Direct cutaneous pedicle.

Examples: groin, superficial inferior epigastric and dorsal metacarpal artery flaps.

Type B

Septocutaneous pedicle.

Examples: scapular and parascapular, lateral arm, posterior interosseous flap.

Type C

Musculocutaneous pedicle.

Examples: median forehead, nasolabial and (usually) anterolateral thigh flap.

Musculocutaneous

Flaps based on perforators that reach the skin through the muscle.

The musculocutaneous system predominates on the torso.

Muscle and musculocutaneous flaps were classified by Mathes and Nahai in 1981:

Type I

Single vascular pedicle.

Examples: gastrocnemius, tensor fasciae latae (TFL), abductor digiti minimi.

Good flaps for transfer—the whole muscle is supplied by a single pedicle.

Type II

Dominant pedicle(s) and other minor pedicle(s).

Examples: trapezius, soleus, gracilis.

Good flaps for transfer—can be based on the dominant pedicle after the minor pedicle(s) are ligated.

Circulation via minor pedicles alone is not reliable.

Type III

Two dominant pedicles, each arising from a separate regional artery or opposite sides of the muscle.

Examples: rectus abdominis, pectoralis minor, gluteus maximus.

Useful muscles for transfer—can be based on either pedicle.

Type IV

Multiple segmental pedicles.

Examples: sartorius, tibialis anterior, long flexors and extensors of the toes.

Seldom used for transfer—each pedicle supplies only a small portion of muscle.

Type V

One dominant pedicle and secondary segmental pedicles.

Examples: latissimus dorsi, pectoralis major.

Useful flaps—can be based on either the dominant pedicle or secondary segmental pedicles.

Venous

Based on venous, rather than arterial, pedicles.

In fact, many venous pedicles have small arteries running alongside them.

The mechanism of perfusion is not completely understood.

Example: saphenous flap, based on long saphenous vein.

Used to reconstruct defects around the knee.

Venous flaps are classified by Thatte and Thatte:

Type 1

Single venous pedicle.

Type 2

Venous flow-through flaps, supplied by a vein that enters one side of the flap and exits from the other.

Type 3

Arterialised through a proximal arteriovenous anastomosis and drained by distal veins.

Venous flaps tend to become congested post-operatively.

Survival is inconsistent; they have therefore not been universally accepted.

Modifying the type 3 arterialised venous flap by restricting direct arteriovenous shunting can improve survival rates by redistributing blood to the periphery of the flap.

Composition

Flaps can be classified by their composition as:

Cutaneous

Fasciocutaneous

Fascial

Musculocutaneous

Muscle only

Osseocutaneous

Osseous.

Contiguity

Flaps can be classified as:

Local flaps

Composed of tissue adjacent to the defect.

Regional flaps

Composed of tissue from the same region of the body as the defect, e.g. head and neck, upper limb.

Distant flaps

Pedicled distant flaps come from a distant part of the body to which they remain attached.

Free flaps are completely detached from the body and anastomosed to recipient vessels close to the defect.

Contour

Flaps can be classified by the way they are transferred into the defect:

Advancement

Stretching the flap

Excision of Burow triangles at the flap's base

V-Y advancement

Z-plasty at its base

Careful scoring of the undersurface

Combinations of the above.

Transposition

The flap is moved into an adjacent defect, leaving a secondary defect that must be closed by another method.

Rotation

The flap is rotated into the defect.

Classically, rotation flaps are designed to allow closure of the donor defect.

In reality, many flaps have elements of transposition and rotation, and may be best described as pivot flaps.

Interpolation

The flap is moved into a defect either under or above an intervening bridge of tissue.

Crane principle

This aims to transform an ungraftable bed into one that will accept a skin graft.

At the first stage, a flap is placed into the defect.

After sufficient time to allow vascular ingrowth into the flap from the recipient site, a superficial part of the flap is replaced in its original position.

This leaves a segment of subcutaneous tissue in the defect, which can now accept a skin graft.

Conditioning

This involves delaying the flap, discussed in ‘Blood supply to the skin’.

Geometry of local flaps

Orientation of elective incisions

In the 19th century, Langer showed that circular awl wounds produced elliptical defects in cadaver skin.

He believed this occurred because skin tension along the longitudinal axis of the ellipse exceeded that along the transverse axis.

Borges has provided over 36 descriptive terms for skin lines, including:

Relaxed skin tension lines (RSTLs)—these are parallel to natural skin wrinkles (rhytids) and tend to be perpendicular to the fibres of underlying muscles.

Lines of maximum extensibility (LME)—these lie perpendicular to RSTLs and parallel to the fibres of underlying muscles.

The best orientation of an incision can be judged by a number of methods:

Knowledge of the direction of pull of underlying muscles.

Making the incision parallel to any rhytids or RSTLs.

Making the incision perpendicular to LMEs.

Making the incision parallel to the direction of hair growth.

‘The pinch test’—if skin either side of the planned incision is pinched, it forms a transverse fold without distortion if it is orientated correctly; if a sigmoid-shaped fold forms, it is orientated incorrectly.

Plasty techniques

Z-plasty

Involves transposition of two adjacent triangular-shaped flaps.

Can be used to:

Increase the length of an area of tissue or scar

Break up a straight-line scar

Realign a scar.

The degree of elongation of the longitudinal axis of the Z-plasty is directly related to the angles of its constituent flaps.

30° → 25% elongation

45° → 50% elongation

60° → 75% elongation

75° → 100% elongation

90° → 125% elongation.

The amount of elongation can be worked out by starting at 30° and 25% and adding 15° and 25% to each of the figures.

Gains in length are estimates; true values depend on local tissue elasticity and tension.

Flaps with 60° angles are most commonly used as they lengthen without undue tension.

The angles of the two flaps need not be equal and can be designed to suit local tissue requirements.

However, all three limbs should be of the same length.

When designing a Z-plasty to realign a scar:

Mark the desired direction of the new scar.

Draw the central limb of the Z-plasty along the original scar.

Draw the lateral limbs of the Z-plasty from the ends of the central limb, to the line drawn in (1).

Two patterns will be available, one with a wide angle at the apex of the flaps, the other with a narrow angle.

Select the pattern with the narrower angle as these flaps transpose better.

The four-flap plasty

It is, in effect, two interdependent Z-plasties.

Can be designed with different angles.

The two outer flaps become the inner flaps after transposition.

The two inner flaps become the outer flaps after transposition.

The flaps, originally in an ‘ABCD’ configuration, end as ‘CADB’ (CADBury).

The five-flap plasty

Because of its appearance, this is also called a jumping-man flap.

Used to release first web space contractures and epicanthal folds.

It is, in effect, two opposing Z-plasties with a V-Y advancement in the center.

The flaps, originally in an ‘ABCDE’ configuration, end as ‘BACED’.

The W-plasty

Used to break up the line of a scar and improve its aesthetics.

Unlike the Z-plasty, it does not lengthen tissue.

If possible, one of the limbs of the W-plasty should lie parallel to the RSTLs so that half of the resultant scar will lie parallel to them.

Using a template helps ensure each wound edge interdigitates easily.

The technique discards normal tissue, which may be a disadvantage in certain areas.

Local flaps

Advancement flaps (simple, modified, V-Y, keystone, bipedicled).

Pivot flaps (transposition, interpolation, rotation, bilobed).

Advancement flaps

Simple

Rely on skin elasticity.

Modified

Incorporate one of the following at the flap's base to increase advancement:

Counter incision

Excision of Burow's triangle

Z-plasty.

V-Y

These are incised along their cutaneous borders.

Their blood supply comes from deep tissue through a subcutaneous pedicle.

Horn flaps and oblique V-Y flaps are modifications of the original V-Y.

Keystone

Trapezoidal flaps used to close elliptical defects.

Essentially two V-Y flaps end-to-side.

Designed to straddle longitudinal structures, e.g. superficial nerves and veins, which are incorporated into the flap.

Blunt dissection to deep fascia preserves perforators and subcutaneous veins.

The lateral deep fascial margin can be incised for increased mobilisation.

The extremes of the donor site are closed as V-Y advancements, which produces transverse laxity in the flap.

Bipedicled

Receive blood supply from both ends.

Less prone to necrosis than flaps of similar dimensions attached only at one end.

Example: von Langenbeck mucoperiosteal flap, used to repair cleft palates.

Bipedicled flaps are designed to curve parallel with the defect.

This permits flap transposition with less tension.

Pivot flaps

Transposition flaps

Transposed into the defect, leaving a donor site that is closed by some other means (often a skin graft).

Transposition flaps with direct closure of donor site

Include the rhomboid flap (Limberg flap) and Dufourmentel flap.

These are similar in concept but vary in geometry.

Both are designed to leave the donor site scar parallel to RSTLs.

The rhomboid flap

The Dufourmentel flap

Interpolation flaps

Flaps raised from local, but not adjacent, skin.

The pedicle is passed either over or under an intervening skin bridge.

Rotation flaps

These large flaps rotate tissue into the defect.

Tissue redistribution usually permits direct closure of the donor site.

Flap circumference should be 5–8 times the width of the defect.

These are used on the scalp for hair-bearing reconstruction.

The back cut at the flap's base can be directed towards or away from the defect.

The bilobed flap

Various designs have been described.

Consists of two transposition flaps.

The first flap is transposed into the original defect.

The second flap is transposed into the secondary defect—the donor site of the first flap.

The tertiary defect at the donor site of the second flap closes directly.

This suture line is designed to lie parallel to RSTLs.

Esser, who first described the flap, put the first flap at 90° to the defect and the second flap at 90° to the first flap.

Zitelli modified these angles to 45° each, resulting in smaller dog ears.

Wound healing and skin grafts

Healing by primary intention

Skin edges are directly opposed.

Healing is normally good, with minimal scar formation.

Healing by secondary intention

The wound is left open to heal by a combination of granulation tissue formation, contraction and epithelialisation.

More inflammation and proliferation occurs compared to primary healing.

Healing by tertiary intention

Wounds are initially left open, then closed as a secondary procedure.

Phases of wound healing

Haemostasis

Inflammation

Proliferation

Remodelling.

Haemostasis

Vasoconstriction occurs immediately after vessel division due to release of thromboxanes and prostaglandins from damaged cells.

Platelets bind to exposed collagen, forming a platelet plug.

Platelet degranulation activates more platelets and increases their affinity to bind fibrinogen.

Involves modification of membrane glycoprotein IIb/IIIa (blocked by clopidogrel).

Platelet activating factor (PAF), von Willebrand factor (vWF) and thromboxane A2 stimulate conversion of fibrinogen to fibrin.

This propagates formation of thrombus.

Thrombus is initially pale when it contains platelets alone (white thrombus).

As red blood cells are trapped, the thrombus becomes darker (red thrombus).

Inflammation

Occurs in the first 2–3 days after injury.

Stimulated by physical injury, antigen–antibody reaction or infection.

Platelets release growth factors, e.g. platelet-derived growth factor (PDGF).

Also release proinflammatory factors, e.g. serotonin, bradykinin, prostaglandins, thromboxanes and histamine.

These increase cell proliferation and migration.

Endothelial cells swell, causing vasodilatation and allowing egress of polymorphonuclear neutrophils (PMNs) and monocytes into the tissue.

T lymphocytes migrate into the wound under the influence of interleukin-1.

Lymphocytes secrete various cytokines, including epidermal growth factor and basic fibroblast growth factor (bFGF).

They also play a role in cellular immunity and antibody production.

Proliferation

Begins on the 2nd or 3rd day and lasts for 2–4 weeks.

Monocytes mature into macrophages that release PDGF and transforming growth factor-β (TGF-β), which are chemoattractant to fibroblasts.

Fibroblasts, usually located in perivascular tissue, migrate along fibrin networks into the wound.

Fibroblasts secrete GAGs to produce ground substance, and then produce collagen and elastin.

Initially, type III collagen is produced to increase the strength of the wound.

Some fibroblasts differentiate into myofibroblasts and effect wound contraction.

Angiogenesis occurs concurrently to supply oxygen and nutrients to the wound.

Endothelial stem cells from blood vessels migrate through extracellular matrix.

Attracted to the wound by angiogenic factors, thrombus and local hypoxia.

Zinc-dependent matrix metalloproteinases aid cell migration through tissues.

Remodelling

Begins 2–4 weeks after injury and can last a year or longer.

During remodelling there is no net increase in collagen (collagen homeostasis).

Type III collagen is replaced by the stronger type I collagen.

Collagen fibres, initially laid down haphazardly, are arranged in a more organised manner.

The wound's tensile strength approaches 50% of normal by 3 months; eventually becomes 80% as strong.

The extensive capillary network is no longer required and is removed by apoptosis, leaving a pale collagen scar.

Abnormal scars

Classified as either hypertrophic or keloid.

Keloids extend beyond the original wound margins.

Hypertrophic scars are limited to original wound margins; commoner than keloids.

Increased numbers of mast cells in abnormal scars may account for the pruritus experienced by some patients.

Hypertrophic scars

Usually occurs within 8 weeks of wounding.

Grow rapidly for up to 6 months before gradually regressing to a flat, asymptomatic scar.

This may take a few years.

Typically form at locations under tension, e.g. shoulders, neck, presternal area, knees, ankles.

Microscopy shows well-organised type III collagen bundles with nodules containing myofibroblasts.

Keloid scars

Dark-skinned individuals are more prone to keloid scars.

There is often a family history.

May develop at any point up to several years after minor injuries.

Typically persist for long periods of time and do not regress spontaneously.

Pain and hypersensitivity are associated more with keloids than hypertrophic scars.

Commonly form on anterior chest, shoulders, earlobes, upper arms and cheeks.

Excision typically results in recurrence.

Microscopy shows poorly organised type I and III collagen bundles with few myofibroblasts.

Expression of proliferating cell nuclear antigen (PCNA) and p53 is upregulated.

Epithelial repair

If the epidermal basement membrane is not breached, epithelial cells are replaced by upward migration of keratinocytes as in uninjured skin.

If the basement membrane is breached, re-epithelialisation must occur from the wound margins and, if present and intact, from epidermal appendages.

Re-establishing epithelial continuity consists of these four phases:

Mobilisation

Epithelial cells at the wound edges elongate, flatten and form pseudopodia.

They detach from neighbouring cells and basement membrane.

Migration

Decreased contact inhibition promotes cell migration.

Epithelial cells climb over one another to migrate.

As cells migrate, epithelial cells at the wound edge proliferate to replace them.

Cells migrate until they meet those from the opposite wound edge.

At this point, contact inhibition is reinstituted and migration ceases.

Mitosis

Epithelial cells proliferate once they have covered the wound.

They secrete proteins to form a new basement membrane.

Cells reverse the morphological changes required for migration.

Desmosomes and hemidesmosomes are re-established to anchor themselves to the basement membrane and to each other.

This new epithelial cell layer forms a stratum germinativum and undergoes mitosis as in normal skin.

Cellular differentiation

The normal structure of stratified squamous epithelium is re-established.

Collagen

Constitutes approximately 30% of total body protein.

Formed by hydroxylation of amino acids lysine and proline by enzymes that require vitamin C as a cofactor.

Procollagen is initially formed within the cell.

Procollagen is transformed into tropocollagen after it is excreted from the cell.

Fully formed collagen has a complex structure.

Consists of three polypeptide chains wound in a left-handed helix.

These three chains are further wound in a right-handed coil to form the basic tropocollagen unit.

Collagen formation is inhibited by colchicine, penicillamine, steroids and deficiencies of vitamin C and iron.

Cortisol stimulates degradation of skin collagen.

Thus far, 28 types of collagen have been identified.

Each type shares the same basic structure but differs in the relative composition of hydroxylysine and hydroxyproline, and in the degree of cross-linking between chains.

The five most common types are:

Type I: predominant in mature skin, bone and tendon.

Type II: present in hyaline cartilage and cornea.

Type III: present in healing tissue, particularly fetal wounds.

Type IV: predominant constituent of basement membranes.

Type V: similar to type IV. Also found in hair and placenta.

The ratio of type I collagen to type III collagen in normal skin is 5:1.

Hypertrophic and immature scars contain ratios of 2:1 or less.

90% of total body collagen is type I.

The macrophage

Derived from mononuclear leukocytes.

Debrides tissue and removes micro-organisms.

Co-ordinates angiogenesis and fibroblast activity by releasing growth factors:

PDGF, FGF 1 and 2, tumour necrosis factor alpha (TNF-α) and TGF-β.

Essential for normal wound healing.

Wounds depleted of macrophages heal slowly.

The myofibroblast

First identified by Gabbiani in 1971.

Differs from a fibroblast—contains cytoplasmic filaments of α-smooth muscle actin, which are also found in smooth muscle.

Actin fibres within myofibroblasts are thought to be responsible for wound contraction.

The number of myofibroblasts within a wound is proportional to its contraction.

Increased numbers have been found in the fascia of Dupuytren's disease.

Thought to be responsible for the abnormal contraction of this tissue.

TGF-β

Macrophages, fibroblasts, platelets, keratinocytes and endothelial cells secrete this growth factor.

Believed to play a central role in wound healing:

Chemoattraction of fibroblasts and macrophages

Induction of angiogenesis

Stimulation of extracellular matrix deposition

Keratinocyte proliferation.

Three isoforms have been identified:

Types 1 and 2 promote wound healing and scarring; upregulated in keloids.

Type 3 decreases wound healing and scarring—may have a role as an antiscarring agent.

Fetal wounds have higher levels of TGF-β3 than adult wounds.

TGF-β3 is thought to antagonise TGF-β1 and 2.

May be one factor responsible for decreased inflammation and improved scarring observed in fetal tissue.

Factors affecting healing

Systemic

Congenital

Acquired

Local.

Systemic factors: congenital

Pseudoxanthoma elasticum

Autosomal recessive.

Characterised by increased collagen degradation and mineralisation.

Skin is pebbled and extremely lax.

Most have premature arteriosclerosis in their 30s.

Ehlers–Danlos syndrome

Heterogeneous collection of connective tissue disorders.

Most are autosomal dominant.

Results from defects in synthesis, structure or cross-linking of collagen.

Clinical features:

Hypermobile fingers

Hyperextensible skin

Fragile connective tissues.

Surgery is avoided if possible—wound healing is poor.

Cutis laxa

Presents in the neonatal period.

Skin is abnormally lax.

Patients have inelastic, coarsely textured, drooping skin.

Progeria

Characterised by premature ageing.

Clinical features:

Growth retardation

Wrinkled skin

Baldness

Atherosclerosis.

Werner syndrome

Autosomal recessive.

Skin changes similar to scleroderma.

Elective surgery avoided whenever possible—healing is poor.

Epidermolysis bullosa

Heterogeneous collection of separate conditions.

Skin is very susceptible to mechanical stress.

Blistering may occur after minor trauma (Nikolsky sign).

The most severe subtype, dermolytic bullous dermatosis (DBD), results in hand fibrosis and syndactyly—the ‘mitten hand’ deformity.

Patients may develop squamous cell carcinoma in areas of chronic erosion.

Systemic factors: acquired

Nutrition

Vitamin A involved in collagen cross-linking; deficiency delays wound healing.

Vitamin C required for collagen synthesis.

Vitamin E acts as a membrane stabiliser; deficiency may inhibit healing.

Zinc, copper and selenium are important cofactors for many enzymes; administration accelerates healing in deficient states.

Hypoalbuminaemia is associated with poor healing.

Pharmacological

Steroids decrease inflammation and subsequent wound healing.

Cytotoxics damage basal keratinocytes.

Non-steroidal anti-inflammatory drugs (NSAIDs) decrease collagen synthesis.

Anti-TNF-α drugs used in rheumatoid may increase post-operative wound complications.

Endocrine abnormalities

Diabetics often have delayed wound healing; this is multifactorial.

Untreated hypothyroidism is associated with slow healing.

Age

Cell multiplication rates decrease with age.

All stages of healing are therefore protracted.

Healed wounds have decreased tensile strength in the elderly.

Smoking

Nicotine is a sympathomimetic that causes vasoconstriction and consequently decreases tissue perfusion.

Carbon monoxide in cigarette smoke decreases oxygen-carrying capacity of haemoglobin.

Hydrogen cyanide in cigarette smoke poisons intracellular oxidative metabolism pathways.

Local factors