PLASTIC SURGERY schwartz  Align skin incisions along lines of minimal

 plastikos = to mold tension (relaxed skin tension lines)

 predicated on the fundamentals of wound healing &  Soft tissue Reconstruction
tissue regeneration  Skin Grafts
 Primary wound healing  Mainstays for reconstruction of superficial
 Mechanical apposition of wound edges defects or adjuncts to more complex
 cascade of inflammatory cell activation reconstructions
 allow reepithelialization & collagen  “graft”  all vessels nourishing the graft are
strengthening harvested ; donor tissue
 Delayed primary wound healing  wound bed  recipient site
 Healing process is compromised by incipient
infection Split thickness Full thickness
 Mx: leave tissue unapposed & allow native Portion of dermis + Whole dermis +
inflam & external debridement to cleanse the epidermis epidermis
wound (then after a few days can be closed) Reliable take Secondary contracture
 Secondary healing Available donor sites Mechanical durability
 Wound that doesn’t show potential for early Primary contracture Ability to grow hair,
closure secrete sweat & sebum
 Mx: allow to close over time by inflam, Pigmentary changes
contraction (myofibroblast), &
reepithelialization  Events in vascular independence
 serum imbibition  direct absorption of
 Impt corollary to timely & robust wound healing = nutrients from capillary beds ; 24 hrs
appropriate interaction among inflammatory cells  inosculation  connecting of donor &
 Critical to the overarching success of inflam & wound recipient vesells ; 24-72hrs
healing = angiogenesis  angiogenesis  vascular ingrowth of
 Fundamental limiting step to both wound healing & vessels from the recipient bed into the
tissue reconstruction = presence of adequate graft; after 72 hrs
vascularity  Factors that interrupt the processes
mentioned:
 Impaired wound healing  Fluid collection under the graft
 Compromised blood supply  Mechanical shear forces
 Radiation  microangiopathic damage  local  Both can be prevented (and the
ischemic conditions grafts fixed in place) by compressive
 Paucity of basic constituents of inflammatory dressing for 5 days (for vascular
cytokines or matrix components (vitamins, zinc, ingrowth)
copper, iron)  Split thickness: occlusive or
 Diabetic px  glucose metabolism & insulin moist antibiotic impregnated
regulation gauze
 12/1000 inch skin graft can reepithelialize in 7-14
 Manifests as scars (altered collagen deposition & days
breakdown)
 Hypertrophic scars  Thicker grafts  more difficulty w/ definitive
 Raised, collagen-rich adherance & survival (greater demand on
 Do NOT go beyond initial boundaries of vascular ingrowth)
the insult  Greater proportion of dermis = greater
 Keloids inhibition of the myofibroblasts that
 Progressed beyond boundaries cause secondary contracture
 Thicker collagen fibers  Full thickness are taken from areas where
 Greater degree of hyaluronic acid @ primary closure can be accomplished:
epidermis  Groin
 Mx (intractable): radiation therapy +  Redundant skin folds
surgical incision  Meshed grafts (split)
 Tx of scars:  Drawbacks: 
 Pressure  Suboptimal appearance
 Silicone sheet & gels  Tendency to contract
 Intralesional corticosteroids  Use: 
 Topical Vitamin A & E *  Large area burn reconstruction
(paucity of donor sites)
 Suture Closure  most common & durable technique of
creating precise skin closures  Skin Flap
 Impt!  MINIMiZING TENSION to maintain wound  Volume of tissue that can be transferred &
closure & prevent excess scar formation survive in it’s new location baased on an
 Accomplished by  independent blood supply
 Dermal & Subdermal sutures  to diffuse
the tension among multiple layers

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  “flap”  some aspect of the blood supply to
the segment of tissue has remained intact
during transfer
 Skin flap  skin + subcutaneous tissue
 Myocutaneous flap  skin + subcutaneous +
muscle
 Random flap   vessels w/ nourish the
tissue; smaller & less defined (axial); used for
smaller, full thickness defects; flap is supplied
by the subdermal plexus
 Axial pattern flap  tissue has an anatomically
defined configuration of vessels; direct
cutaneous, the flap is nourised by a definite
cutaneous artery & vein
 May have varying vessel configurations
 Dermal subdermal plexus is impt
 Supplying vessels may directly approach
the skin or traverse through muscle or
fascial septae between muscle territories
 Island flap  vessel is isolated from the
surrounding tissue over an intervening segment
 Free flap  the vascular supply & flap proper
is severed to be reattached via microvascular
techniques
 Z-plasty  the tension of the scar/incision is
reoriented from a transverse direction to a
vertical direction; create 2 identical triangles
and interchanging the flaps
 W-plasty  way of breaking up the continuity
of a linear scar in a manner that can
camouflage scar
 V-Y advancement flap  recruiting tissue from
a region of excess to a defect
 Rotational advancement flap  around a pivot
point
 Burow’s triangle  used if the tension is
to great
 Rectangular advancement flap
 2 Burow’s triangle
 Rhomboid flap
 Transposition flap  primary & secondary
defect
 Bilobed flap  loose skin is transposed in
sequence via two flaps, the most distal flap
being closed primarily
 Muscle based flap
 Angiosome  actual anatomic territory that a
given vessel supplies
 Defines the potential flaps that can be
constructed for a given defect
 Delay Phenomenon  the vascularity of
flaps can be rendered more robust by
temporarily interrupting the normal
inflow of blood
 Allows metabolic conditioning of the
flap to ischemia
 Allows new channels to form
 Example:
 Transverse rectus abdominis
myocutaneous flap
 Deep inferior epigastric artery –
interrupted major supply
 Choke vessels  vessels w/c connect
adjacent angiosomes; opens up during
“delay phenomenon”
 Tissue will be ischemically preconditioned
to rely upon the secondary vessel
(superior epigastric artery)
 10-14 days later  flap can be safely
transferred & theres less chance of the
distal vessels becoming ischemic &
potentially necrotic
 For wounds that are prone to
infection/irradiated  muscle flap better if
highly vascular soft tissue
 Tissue Expansion
 Quantity & quality may exceed supply
 Creep  a chronic, appropriately applied
stretch can generate & recruit new tissue
formation
 The epidermis thickens concomitantl to a
relative thinning of the dermis
 Microsurgery
 Technique employed to reconstruct the critical
vascular elements of tissue to be transferred
(free flaps)
 complication:
 Vessel thrombosis  flap necrosis
 Clearing periadventitia  stripping
vasavasorum
 Venous congestion > arterial occlusion
 Screen:
 Thromboembolic phenomena (Protein C &
S deficieny)
 Hypovolemia, etc
 Smoking  no difference in
thromboembolic problem BUT  in wound
healing complications
 Caffeine & other vasoactive agents
 Atherosclerosis
 Tensionless, kink-free vessel anastomoses are
critical!
 Intraoperative monitoring of blood pressure to
ensure constant flap perfusion!
 Prolonged exposure to cold may aggravate
vasospasm!
 Mainstays of flap care:
 Examine color, temp, undue swelling,
mottled pattern
 Doppler assessment of arterial & venous
signals
 Anticoagulants:
 Dextran & rheologic agents – limited by
adverse rxns
 Systemic heparin – excessive bleeding
 ASA -  prostacyclin
 Fibrinolytic agents – systemic hemorrhage
& rebound thrombosis
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  Leeches  must have prophylaxis against  Submucous cleft palate  most common
Aeromonas hydrophilia  Bifid uvula
 There is NO reflow phenomenon bec:  Thin membranous central portion
 Endothelial cell inflammation  VC,  Posterior palpable notch
(possible) thrombosis
 Persistent flap ischemia  Hard palate  static partition between oral &
 Free radicals, LT, oxidases nasal chambers
 Craniofacial surgeries  Soft palate  dynamic barrier; elevates &
 Amalgamation of soft tissue & skeletal moves posteriorly during velopharyngeal
reconstruction closure (facilitating swallowing & speech
production)
 CLEFT LIP & PALATE  In cleft 
 Primary palate  lip, alveolus, hard palate to   velopharyngeal valving = hypernasal
the incisive foramen speech / velopharyngeal insufficiency
 Secondary palate  hard & soft palate  nasal & oral continuity = negative
posterior to the incisor foramen intraoral pressure cannot be sustained =
ineffective sucking & feeding
 Classic Theory  failure of fusion of the  Ear disease
maxillary processes & frontonasal processess =
cleft of the primary palate  Timing:
 Mesodermal penetration theory  palate  Early – affords advantage of improved
closure is predicated on mesodermal speech, but exacerbates midface
penetration, w/o this migration & retrusion
reinforcement, epithelial breakdown &  Before 12 months
separation ensues = cleft  Additional procedures after 4 y/o if
did not respond well
 Cleft lip
 Complete – extends to nostril
 Incomplete – a tissue bridge unites the
lateral & central lip
 Cleft lip 
 ill defined philtral ridge on the cleft side,
 vertical shortness,
 vermillion thinning,
 obfuscated white roll,
 hypoplastic musculature
 abn muscle insertions
 concatenated w/ nasal deformity
 tilted platform
 unilateral shortness of columella
height
 nasal floor deficiency
 outward flaring of alar base
 malpositioned lower cartilages
 Bilateral
 More challenge
 Nasal & osseous deformities

 Timing: Rule of tens

 10 wks of age
 10 lbs
 10 mg/dL Hgb
 Presurgical: orthodontics
 Facilitate alveolar segment alignment 
more symmetrical platform

 CLEFT PALATE
 Swellings of the medial maxillary prominences
 palatal shelves  downward growth
adjacent to the tongue  become horizontal
 fuse
 Complete closure = 12 wks

 Complete  extension into the nose

 Incomplete  existing midline attachment

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