Plastic surgery
Definition: is branch of surgery that is concerned with remold, repair and restore body parts especially
by transfer tissues.
Plastic as adjective mean capable of being shaped or formed.
Divided into 2 parts:
1. Aesthetic or cosmetic surgery: which performed to reshape normal structure of body to
improve the patient appearance e.g. rhinoplasty, face lift?
2. Reconstructive surgery: which is done for these who have congenital deformities e.g. cleft lip
and palate, or those who have acquired deformities as result f infection, accident, burn?
Anatomy of skin: skin is largest organ in body ranging from 0.22 m² in new born to more than 2m² in
the adult.
It provided barrier to invasion by microorganism, regulate the exchange of heat with environment,
provided surface for vitamin D synthesis by U.V. light.
It consists of epidermis and dermis.
Epidermis: is the outer layer composed of keratinized stratified squamous epithelium, it divided into:
Stratum germinatirum: which rest on dermis and generate the cell of stratum corneum.
Stratum corneum: This is the desquamating dead superficial layer.
selected part in our body still has this ability e.g. liver, intestinal mucosa.
Dermis: which is 20 times thicker than epidermis, it consists of non-cellular connective tissues
(collagen and elastic fibers) and ground substances. It divided into:
Upper papillary dermis (thin).
Lower reticular dermis (thick) which extended form papillary dermis to subcutaneous tissue
Dermis contained sweat gland, blood vessels, lymphatic and pilosebaceous units.
Subcutaneous layer: the skin is connected to the underlying bone and deep fascia by layer of areolar
tissues that varies in thickness, it prominent in palm and sole, and absent in eyelid.
Blood supply:
1.
2.
Major vessels: deep to muscle (musculocutaneous) perforators which pass perpendicular
through the muscle and deep fascia dermosubdermal plexus which supply the skin.
Direct cutaneous artery: superficial to muscles then dermo-subdermal plexus.
WOUNDS
A wound can be defined as a disruption of the normal anatomical relationships of
tissues as a result of injury. The injury may be intentional such as a surgical incision or
accidental following trauma. Immediately following wounding, the healing process
begins.
Phases of wound healing
Wound healing consists of four phases: (i) haemostasis; (ii) inflammation; (iii) proliferation;
and (iv) remodelling.
1.Haemostasis
• The vessels vasoconstrict immediately after division.
• A platelet plug is then formed.
• The platelets degranulate; platelet-derived growth factor (PDGF) and thromboxanes
stimulate the conversion of fibrinogen to fibrin. This stimulates propagation
of the thrombus.
• The thrombus is initially pale when it contains platelets alone (white thrombus).
• As red blood cells are trapped within it the thrombus becomes darker (red
thrombus).
2.Inflammation
• This phase occurs in the first 2–3 days after injury.
• Its stimulus may be:
• Physical injury
• Antigen–antibody reaction
• Infection.
• The thrombus releases growth factors such as PDGF.
• Endothelial cells swell, allowing the egress of polymorphonuclear lymphocytes
(polymorphs or PMNs) and mononuclear cells (monocytes and macrophages)
into the surrounding tissue.
3.Proliferation
• The proliferative phase of wound healing is generally accepted as occurring from days 4 to 21
following injury.
• Macrophages within the tissue release growth factors which are chemoattractant
to fibroblasts.
• Fibroblasts which are usually located in perivascular tissue migrate along networks
of fibrin fibres into the wound.
Certain facets of the proliferative phase, such as re-epithelialization, probably begin almost
immediately following injury.
Epithelialization results in the formation of a barrier between the internal and external
environments. Within hours of the injury, migration of epithelial cells across the
wound (i.e., reepithelialization) begins. The cells at the leading edge begin to lose their
basement membrane adhesion, flatten, send out cytoplasmic projections, secrete
proteases, and phagocytize a path for the impending keratinocyte migration. One to 2
days after injury, epithelial cells at the wound edges begin to proliferate behind the
migrating epithelium.
4.Remodelling
• The remodeling phase is the longest part of wound healing and in humans is believed to last
from 21 days up to 1 year. Once the wound has been “filled in” with granulation tissue and after
keratinocyte migration has re-epithelialized it, the process of wound remodeling occurs. Again,
these processes overlap, and the remodeling phase likely begins with the programmed
regression of blood vessels and granulation tissue described above. In humans, remodeling is
characterized by both the processes
of wound contraction and collagen remodeling . The process of wound contraction is produced
by wound myofibroblasts, which are fibroblasts with intracellular actinmicrofilaments capable
of force generation and matrix contraction.It remains unclear whether the myofibroblast is a
separate cell from the fibroblast or whether all fibroblasts retain the capacity to “trans
differentiate” to myofibroblasts underthe right environmental conditions. Myofibroblasts
contact the wound through specific integrin interactions with the collagen
matrix.Collagen remodeling is also characteristic of this phase.Type III collagen is initially laid
down by fibroblasts during the proliferative phase, but over the next few months this will
be replaced by type I collagen.
*Function of the macrophage in wound healing
• Macrophages are derived from mononuclear leucocytes.
• They debride tissue and remove micro-organisms.
• They co-ordinate the activity of fibroblasts by releasing growth factors.
• These include interleukin 1 (IL-1), tumour necrosis factor alpha (TNF-alpha)
and transforming growth factor beta (TGF-beta).
• Macrophages are essential for normal wound healing.
• Wounds depleted of macrophages heal slowly.
*Principles of wound closure
1. When the wound is clean, incised wound as seen in surgical wound or clear cut
wound, direct closure achieved y approximation its edge without tension.
2. When the wound is lacerated, with irregular edge and contaminated, direct
approximation should not done unless the wound is irrigated and debrided.
Debridment: involves the excision of all devitalized, contaminated tissues and
foreign body.
Irrigation: involves washing the wound by copious amount of saline and ringer
lactate.
Method of debridment:


Mechanical: This involved sharp or blunt excision of dead tissues.
Gauze: repetitive application of moistened gauze which desiccates and
gradually removed necrotic debris from the wound.
 Chemical: topical enzyme application which digests devitalized tissues.
3. When handling the tissues during closure we should avoiding excessive
retraction and pressure on wound, irrigation and moist pack should be used to
prevent wound desiccation.
4. aseptic technique: by strict using aseptic measurement such as hand scrubbing,
using of sterile instrument, and clean operative site, and hair shaving
5. hemostasis: as bleeding can cause ischemia and hematoma formation which
can lead to infection which affect normal wound healing.hemostasis can
achieved by:
 Topical application of adrenaline.
 Electrocautery.
 Large vessels can be clamped or suture.
 Topical hemostatic e.g. fibrin glue.
6. antibiotics: which indicated for the fallowing:
 Acute wound with surrounding cellulitis with gross contaminated.
 Human or animal bit.
 Immunosuppressed or diabetic patient.
 Vulvular heart disease to prevent endocarditis.
Most soft tissues infection caused by gram (+) organism e.g. (staph., strept.).Usually
we begin with broad spectrum antibiotics such as cephalosporin, and more specific
therapy directed by bacterial culture and sensivity.
* Timing of wound healing
.A
Primary intention occurs when the wound is closed by direct approximation of the
wound margins or by placement of a graft or flap. Direct approximation of the edges of
a wound provides the optimal treatment provided that the wound is clean, the closure
can be done without undo tension, and the closure can occur in a timely fashion.
Wounds that are less than 6 hours old are considered in the “golden period” and are less
likely to develop into a chronic wound-healing state. At times, rearrangement of tissues
is required to achieve this goal. Directly approximated wounds typically heal as outlined
above provided that there is adequate perfusion of the tissues and no infection. Primary
intention also describes the healing of wounds created in the operating room that are
.closed at the end of the operative period
.B
Secondary intention, or spontaneous healing, occurs when a wound is left open and is
allowed to close by epithelialization and contraction. Contraction is a myofibroblast
(modified fibroblasts that have smooth-muscle cell–like contractile properties)–
mediated process that aids in wound closure by decreasing the circumference of the
wound. This method is commonly used in the management of wounds that are treated
beyond the “golden period” (initial 6 hours) or the contaminated infected wounds with a
bacterial count greater than 105/g tissue. These wounds are characterized by prolonged
inflammatory and proliferative phases of healing that continue until the wound has
.completely epithelialized or been closed by other means
.C
Tertiary intention, or delayed primary closure, is a useful option for managing wounds
that are too heavily contaminated for primary closure but appear clean and well
vascularized after 4–5 days of open observation so that the cutaneous edges can be
approximated at that time. During this period, the normally low PaO2 at the wound
surface rises, and the inflammatory process in the wound bed leads to a minimized
bacterial concentration, thus allowing a safer closure than could be achieved with
primary closure and a more rapid closure than could be achieved with secondary wound
healing.
D.
Healing of Partial-Thickness Wounds
1. In this type of wound, only the epithelium and the superficial portion of the dermis is
injured. Epithelial cells that remain within the dermal appendages, hair follicles, and
sebaceous glands proliferate to close the wound.
2. Thus, epithelialization is the main process by which the exposed dermis is covered in
partial thickness wounds, with minimal collagen deposition and wound contraction.
*SYSTEMIC FACTORS ASSOCIATED WITH DELAYED
WOUND HEALING
The surgeon must be aware of the factors that can impair healing before implementing a
proper prevention and treatment plan.
A. Diabetes— Wound healing is impaired in diabetic patients by unknown
mechanisms, although recent studies have implicated a lack
of KGF and PDGF function in the wound.60,61 Many of these
patients have microvascular occlusive disease that may cause
ischemia and impaired repair. Healing is enhanced if glucose
levels are well controlled.
B. Malnutrition—25–50% of all acute care patients are malnourished. Poor caloric
intake can cause malnutrition, and it can also occur with normal caloric intake if the
patient is cachectic. Cachexia results from malabsorption or increased metabolism
secondary to a systemic illness. There is no distinct cut-off point of any single
parameter that defines malnutrition. Current guidelines indicate that malnutrition is
likely present if serum albumin is <3.5 mg/dL, total lymphocytes (TLC) are
<1800/mm3, or body weight has decreased >15%. Increased dietary protein has
been associated with improved wound healing.
• Specific nutrient deficiencies have been identified. These include: arginine
(Tlymphocyte
function), linoleic acid (precursor for prostanoids and inflammation),
cystine (collagen formation), glutamine, vitamin A (retinal, retinol, retinoic acid,
epithelial tissue maintenance), vitamin E, vitamin C (collagen synthesis), ferrous
iron (hydroxylation of lysine and proline), calcium (cleavage of procollagen),
cuprous ion (lysine metabolism), and zinc (cell replication).
• Trace elements should be supplemented, as should vitamin B6 in alcoholics and
vitamin A with steroid use. Vitamin C stores are quickly depleted, and most
severely ill patients will benefit from daily supplements. Unlike vitamin C, the
human body has a 4-year store of vitamin E. Despite its popularity, there is no
evidence that topical or systemic supplementation of vitamin E improves wound
healing or scar formation.
C. Marked obesity—A well-known risk factor for wound complications of dehiscence,
infection, and delayed healing.
D. Age—Some studies have shown that wounds heal less effectively with increasing
age.
E. Tobacco—Nicotine constricts vessels and carbon monoxide decreases oxygen
delivery. These short-term effects last for several hours. Respiratory tract changes
persist for weeks. Peripheral vascular disease is usually a permanent effect.
F. Corticosteroids—Vitamin A can partially counteract the effects of steroids.
G. Immunosuppression—Congenital disorders, steroids, malnutrition, diabetes, and
malignancies result in immunosuppression. AIDS slightly impairs healing.
H. Genetic disorders—Ehlers-Danlos and Marfan’s syndromes have various
deficiencies in collagen synthesis. Many other genetic disorders are known to have an
effect on wound healing.
I. Chemotherapy—The evidence is contradictory. Chemotherapy, particularly
adriamycin and 5-FU, might slightly impair healing. A several-week postoperative
delay, when possible, is recommended.
J. Renal or liver failure—Some evidence suggests a slight impairing effect, but
comorbidities such as diabetes confuse interpretation of the studies.
K. Massive or metastatic cancer—Directly impairs healing in addition to the effects of
chemotherapy or radiation therapy. Smaller localized tumors are not thought to
significantly impair healing.
*LOCAL FACTORS CAUSING DELAYED WOUND HEALING
A. Necrotic tissue is probably the single most detrimental factor to wound healing, and
also the factor that surgeons are most equipped to correct.
B. Wound contamination is ubiquitous and simply refers to colonized organisms on the
surface. Wound infection denotes a deeper penetration of the wound by bacteria that
induce an inflammatory response. Foul smell indicates anaerobes. The overall
bioburden is greater in undermined or necrotic wounds. Bacterial loads greater than
105 bacteria per gram of tissue or greater impair healing.
Diagnoses are primarily made from clinical signs such as erythema, pain, odor, and
drainage. Wound swab cultures are unreliable and should rarely be used.
Quantitative biopsy cultures are the gold standard, but cost limitations prevent their
routine use in most medical centers. Multiple needle-stick aspiration of a wound is a
slightly less specific test compared to the tissue biopsy gold standard. Culture of pus
or necrotic tissue is seldom reliable, as it will infrequently represent the same
organisms infecting the viable tissue. β-Hemolytic streptococci are particularly
detrimental to healing.
Systemic antibiotics are of limited use in wound infection treatment unless
administered within 4 h of wounding. Adequate tissue levels are usually not achieved.
Topical antibacterial such as silver sulfadiazine (Silvadene®), mafenide acetate
(Sulfamylon®), and gentamycin reach adequate tissue levels but are also injurious to
tissue cells. Mafenide 5% solution appears to be able to fight infection without
causing tissue damage.
C. Osteomyelitis. Diabetic wounds that can be probed down to bone have a 90% chance
of having osteomyelitis. Sensitive physical exam signs are crepitance or a spongy bone
consistency. The presence of osteomyelitis in pressure ulcers is less certain and may
warrant radiological workup. MRI and nuclear medicine scans can be useful for ruling
out (false-positive rates are too high to reliably rule in) osteomyelitis and therefore
reducing the length of antibiotic therapy.
D. Arterial ischemia or venous insufficiency
E. Edema decreases oxygen diffusion to cells. Edema is a very potent inhibitor to
healing, particularly in the lower extremity. Elevation of the wound and/or
compression garments should be emphasized.
F. Radiation exposure
G. Foreign bodies
H. Tension
I. Pressure and shear forces
J. Dry environment inhibits epithelialization and healing.
K. Urinary or fecal incontinence may contaminate the wound and impair healing. In
addition, these are important risk factors to the development of skin ulcers.
Basic Surgical Techniques
Sutures and Suturing
ANESTHESIA
•ı inject anesthetic before debridement and irrigation
•ı lidocaine ± epinephrine (vasoconstrictor, limits bleeding)
• toxic limit and duration of action (1 cc of 1% solution contains 10 mg lidocaine):
•ı without epinephrine: 5 mglkg, lasts 46-60 min
•ı with epinephrine: 7 mglkg, lasts 1.5-2 hrs
• signs of toxicity: CNS excitation followed by CNS, respiratory, and
cardiovascular depression
IRRIGATION
AND DEBRIDEMENT
• clean surrounding skin, do not use antiseptic solutions in the wound as they are toxic
this to exposed tissue
• irrigate copiously with a physiologic solution - forceful ejection of Ringer's lactate or
normal saline removes surface clots, foreign material, and bacteria
• debride all obviously devitalized tissue, irregular or ragged wounds may be excised to produce
sharp wound edges that will reduce scarring when approximated
SUTURES
•ı use of a particular suture material is highly dependent on surgeon preference
•ı subsequent bacterial infection: monofilament < multifilament (braided)
•ı tissue reaction: synthetic < natural
•ı dehiscence of tissue under stress: nonabsorbable < absorbable
SUTURE MATERIALS
Other Skin Closure Materials
• tapes sterile adhesive tape (e.g. Steri-Strips) is the skin closure of choice for clean or
contaminated wounds, as they minimize infection by separating skin surface from
wound dead space. Tape cannot be used on actively bleeding wounds, or wounds with
complex surfaces. Placed across the incision; will prevent surface marks and can be
used primarily or after surface sutures have been removed. Tape bums may occur if
there is excessive tension or swelling around the incision
• skin adhesives e.g. 2-octyleyanoacrylate (e.g. Dermabond) works well on small areas
without much tension or shearing. Advisable in children
• staples - steel-titanium alloys that incite minimal tissue reaction. Healing is
comparable for wounds closed by suture or staples
Dressings
• goals: protection, environment for healing (absorption), immobilization, cosmesis,
compression
• "wet-to-dry" dressing (for dirty or infected wounds): dressing cleans wound and
prevents build-up of exudates. Exudates, debris and nonviable tissue adhere to
gauze and are removed with dressing change
• wet dressing: for healing uninfectcd wounds; doesn't debride wound
• 1st layer (contact layer)
• clean wounds (heal by re-epithelialization)
• protect new epithelium
• use "wet-to-wet" dressing, non-adherent (e.g. Mepitel) impregnatedˇ
gauze (e.g. Jelonet, Bactigras™) or antibiotic ointmentˇ
** chronic/contaminated wounds:
• mechanically debride nonviable tissue
• use "wet-to-dry" dressing (e.g. adherent saline or betadine soaked gauze)
• 2nd layer (absorbent layer): saline soaked gauze, to encourage exudate into dressing by
"wick" effect
• 3rd layer (protective layer): dry gauze held in place with roller gauze or tape
ABNORMAL HEALING
Hypertrophic Scar
•ı scar remains roughly within boundaries of original injury
•ı red, raised, widened, frequently pruritic
•ı common sites: back, shoulder, sternum
•ı treatment: conservative, improves with time, rarely improved by surgical revision
Keloid Scar
•ı scar extends beyond boundaries of original injury
•ı frequently pruritic, often painful; collagen in whorls rather than bundles
•ı common sites: sternum, deltoid, earlobe; more common in darker skinned people
•ı treatment: pressure dressings, silicone sheets, topical steroids, intralesional steroid
injection, radiation therapy, surgical resection (intralesional excision ± steroids used
as it may recur/become worse with surgical revision)
Chronic Wound
•ı fails to heal within 3 months (e.g. diabetic, pressure and venous stasis ulcers)
•ı treatment: may heal with meticulous wound care; many require surgical intervention
•ı Marjolin's ulcer: squamous cell carcinoma arising in a chronic wound (e.g. chronic
bum scars and pressure sores) secondary to genetic changes caused by chronic
inflammation → consider biopsy of chronic wound)
Contaminated Wounds
• a contaminated wound contains>100,000 bacteria/gram
Acute Contaminated Wound «24 hr)
• cleanse and irrigate open wound with physiologic solution (NS or RL) - don't use
irritants (soap, alcohol, etc.)
• debridement: removal of foreign material, devitalized tissue, old blood
• surgical debridement: blade or irrigation
• gauze debridement: wet to dry dressings
• evaluate for injury to underlying structures (vessels, nerve, tendon and bone)
• control active bleeding
• systemic antibiotics: wound older than 8 hours, severely contaminated,
immunocompromised, involvement of deeper structures (e.g. joints, fracture), obvious
infection
• ± tetanus toxoid (Td) 0.5 mlIM ± tetanus immunoglobulin 250 U deep 1M
• ±postexposure treatment of:
• hepatitis B, hepatitis C, HIV
• re-evaluate in 24-48 hours for signs of deep infection
• open infected portion of wound by removing sutures
Chronic Contaminated Wounds (e.g. lacerations >24 hours, ulcers)
•ı irrigation and debridement: surgical or mechanical (e.g. wet-to-dry dressings)
•ı topical antibacterial creams (e.g. bacitracin, Neosporin™) - avoid inhibitors of
epithelialization
•ı systemic antibiotics are not useful- no penetration into the bed of granulation tissue
•ı closure: final closure via secondary intention (most common), delayed wound closure
(tertiary closure), skin graft or flap; successful closure depends on -↓,. bacteria count to
Less than 100,000/gram prior to closure and frequent dressing changes
Fetal wound healing
Tissue healing during the first 3 months of fetal life occurs by regeneration
rather than by scarring.
• Regenerative healing is characterized by the absence of scarring.
• Regenerative wound healing differs from normal adult healing in the following
ways.
• Inflammation is reduced.
• Epithelialization is more rapid.
• Angiogenesis is reduced.
• Collagen deposition is rapid, not excessive and organized.
• More type 3 rather than type 1 collagen is laid down.
• The wound contains a greater proportion of water and hyaluronic acid.
•
• The
lack of TGF-in fetal wounds may be responsible for some of these
differences.