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What is the intervention or a problematic in antile hemangioma that is too large to inject with corticosteroid?
Oral pharmacotherapy with either prednisolone (3 mg/kg) or propranolol (2 mg/kg).

What are the advantages and disadvantages o prednisone therapy?
~100% response rate (10% will stop growing and 90% will become smaller), sa e, minimal monitoring, and no
long-term side e ects.

What are the advantages and disadvantages o propranolol therapy?
10% nonresponse rate, long duration o treatment, may have greater initial shrinkage o the tumor compared to
prednisone, more complicated monitoring or bradycardia, hypotension, hyperkalemia, and hypoglycemia.

Is resection o a problematic in antile hemangioma generally recommended in in ancy?
No. Operative morbidity is high while the tumor is vascular and rapidly growing.

What is the ideal time or operative intervention?
Between 3 and 4 years o age. At this time the tumor has completed involution, become less vascular, and
decreased in size. Resection is still per ormed be ore long-term memory and sel -esteem begin.

What are the indications or operative intervention?
Damaged or excess skin, injured anatomic structures, bro atty residuum, and residual telangiectasias.

Should laser therapy be used to treat a cutaneous in antile hemangioma during in ancy?
No, laser does not stop the growth o the tumor and increases the risk o ulceration.

Should laser be used to treat an in antile hemangioma a ter it has involuted?
Yes, pulse-dye laser can e ectively eliminate residual telangiectasias in childhood.

What is a congenital hemangioma?
A hemangioma that is ully grown at birth and does not enlarge postnatally.

How many types o congenital hemangiomas exist?
wo; rapidly involuting congenital hemangioma (RICH) and noninvoluting congenital hemangioma (NICH).

How common are they?
Rare. T ey comprise less than 1% o all hemangiomas.

Do congenital hemangiomas look like in antile hemangioma?
No, they are reddish purple, have coarse telangiectasias, and a peripheral halo.

What other eatures dif erentiate congenital hemangiomas rom in antile hemangioma?
Congenital hemangiomas have an equal sex distribution, are solitary, most commonly a ect the extremities,
average 5 cm in diameter, and do not stain positive or the immunohistochemical marker GLU 1.

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How is RICH managed?
Observation. It undergoes complete involution by 14 months o age.

How is NICH managed?
NICH may be observed or resected. Unlike RICH or in antile hemangioma, it does not regress.

What is kaposi orm hemangioendothelioma?
A benign tumor that can cause Kasabach–Merritt phenomenon (thrombocytopenia, petechiae, and bleeding).

How is kaposi orm hemangioendothelioma treated?
Vincristine or rapamycin.

What is a pyogenic granuloma?
Pyogenic granuloma is a common pedunculated red lesion that presents at an average age o 6 years, is small
(mean diameter 6 mm), and requently bleeds.

How is pyogenic granuloma treated?
De nitive treatment is resection. Other methods such as cautery, cryotherapy, or laser have a 50% recurrence rate.

How do vascular mal ormations dif er rom vascular tumors?
Unlike vascular tumors (hemangiomas, kaposi orm hemangioendothelioma, pyogenic granuloma), vascular
mal ormations are errors in embryogenesis, and do not have rapidly proli erating endothelium. Although vascular
mal ormations are present at birth, they may not be diagnosed until childhood or adolescence a ter they have
enlarged and/or become symptomatic (Figs. 70-1 and 70-2).
A

B
Figure 70-1 Vascular tumors. A: In antile hemangioma. B: Congenital hemangioma.

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A

B
C

D
Figure 70-2 Vascular mal ormations. A: Capillary mal ormation. B: Lymphatic mal ormation. C: Venous mal ormation. D: Arteriovenous
mal ormation.
C

D
Figure 70-1 (Continued) C: Kaposi orm hemangioendothelioma. D: Pyogenic granuloma.

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How common are vascular mal ormations?
Vascular mal ormations are much less common than vascular tumors, a ecting 0.5% o the population.

What is a capillary mal ormation?
T e lesion used to be called “port-wine stain.” It is an anomaly o dermal capillaries that results in a pink area o
skin. Recently, the causative mutation or the lesion has been identi ed (GNAQ).

How is capillary mal ormation diagnosed?
T e lesion is noted at birth and is diagnosed by history and physical examination.

What is the natural history o capillary mal ormation?
T e stain darkens and becomes purple. T e skin thickens, pyogenic granulomas may develop, and the tissues
underneath the stain can become overgrown.

What is the treatment or capillary mal ormation?
First-line management is pulse-dye laser to lighten the color o the lesion. Resection is required to improve
overgrown tissues.

What is a lymphatic mal ormation?
An error in lymphatic development due to a mutation in PIK3CA.

How is lymphatic mal ormation classi ed?
Lesions can be macrocystic (> 5 mm), microcystic (< 5 mm), or combined.

How is lymphatic mal ormation diagnosed?
Most lesions can be diagnosed by history and physical examination. However, subcutaneous lymphatic
mal ormations may require ultrasound or diagnosis. Patients requently undergo MRI to con rm the diagnosis
and determine the extent o disease.

What is the morbidity o lymphatic mal ormation?
Psychosocial distress, bleeding, leakage o lymph uid (lymphorrhea), in ection, and overgrowth o tissues.

How is lymphatic mal ormation treated?
First-line intervention or symptomatic macrocystic lesions is sclerotherapy. Because microcystic lesions have cystic
spaces that are too small to sclerose, management is either resection or carbon dioxide laser.

What is sclerotherapy?
Sclerotherapy involves injecting a scleroscent into a space (e.g., lymphatic cyst, vein). Commonly used scleroscents
include doxycycline, sodium tetradecyl sul ate, and ethanol. T e scleroscent causes shrinkage o the space, scarring,
and improvement in symptoms.

What is a venous mal ormation?
An error in venous development, most commonly due to a mutation in TIE2.

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What are subtypes o venous mal ormation?
Glomuvenous mal ormation is an autosomal dominant lesion that is o ten small and multiple (due to a mutation
in Glomulin). Verrucous venous mal ormation is a hyperkeratotic lesion that typically a ects the lower extremity
and is caused by a mutation in MAP3K3.

How are venous mal ormations diagnosed?
Most are diagnosed by history and physical examination. However, subcutaneous venous mal ormations may
require ultrasound or diagnosis. Patients requently undergo MRI to con rm the diagnosis and determine the
extent o disease.

What is the morbidity o venous mal ormation?
Lowered sel -esteem, pain rom phlebothrombosis, and overgrowth o tissues.

How is venous mal ormation treated?
First-line therapy is sclerotherapy. Resection is reserved or small lesions or or symptomatic venous mal ormations
that are no longer able to be sclerosed.

What is an arteriovenous mal ormation?
An abnormal connection o arteries to veins without an intervening capillary bed.

What are subtypes o arteriovenous mal ormation?
Capillary mal ormation—arteriovenous mal ormation is an autosomal dominant condition caused by a mutation
in RASA1; patients typically have circular cutaneous lesions associated with deeper arteriovenous mal ormations.
Patients with a PTEN mutation can have arteriovenous mal ormations.

What is the natural history o arteriovenous mal ormation?
T e lesion is present at birth and then progresses through our stages: 1 (quiescence), 2 (expansion), 3
(destruction), and 4 (decompensation).

What is the morbidity o arteriovenous mal ormation?
Psychosocial distress, pain, ulceration, bleeding, and destruction o tissues.

How is arteriovenous mal ormation treated?
First-line management is embolization. Resection is reserved or small lesions or or symptomatic arteriovenous
mal ormations that have ailed embolization.

What is embolization?
Embolization is the delivery o a substance to the nidus o the lesion, causing lesion ischemia, scarring, and
improvement in symptoms. ypically, a catheter is inserted into the emoral artery and then is advanced to the
nidus o the arteriovenous mal ormation.

What are the most common vascular mal ormation overgrowth syndromes?
CLOVES, Klippel– renaunay, Parkes Weber, and Sturge–Weber.

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What is CLOVES syndrome?
Congenital lipomatosis, overgrowth, vascular mal ormations, epidermal nevi, and scoliosis/skeletal/spinal
anomalies. T e lesion results rom a mutation in PIK3CA.

What is Klippel–Trenaunay syndrome?
Capillary–lymphatic–venous mal ormation typically o the lower extremity causing overgrowth. T e causative
mutation is PIK3CA.

What is Parkes Weber syndrome?
Di use arteriovenous mal ormation o the leg causing overgrowth. Patients o ten have a RASA1 mutation.

What is Sturge–Weber syndrome?
Capillary mal ormation in the V1 trigeminal nerve distribution with either ocular abnormalities and/or
leptomeningeal vascular mal ormation. T e condition is due to a mutation in GNAQ.
REFERENCES
Boon LM, Enjolras O, Mulliken JB. Congenital hemangioma: evidence o accelerated involution. J Pediatr. 1996;128:329–335.
Chang LC, Haggstrom AN, Drolet BA, et al. Hemangioma Investigator Group. Growth characteristics o in antile hemangiomas:
implications or management. Pediatrics. 2008;122:360–367.
Couto JA, Greene AK. Management o problematic in antile hemangioma using intralesional triamcinolone: ef cacy and sa ety in 100
in ants. J Plast Reconstr Aesthet Surg. 2014;67:1469–1474.
Couto JA, Maclellan RA, Greene AK. In antile hemangioma: treatment rate during the proli erating phase. J Craniofac Surg. 2014;25:
1933–1934.
Couto RA, Maclellan RA, Zurakowski D, Greene AK. In antile hemangioma: clinical assessment o the involuting phase and implications
or management. Plast Reconstr Surg. 2012;130:619–624.
Enjolras O, Mulliken JB, Boon LM, Wasse M, Kozakewich HP, Burrows PE. Noninvoluting congenital hemangioma: a rare cutaneous
vascular anomaly. Plast Reconstr Surg. 2001;107:1647–1654.
Greene AK. Current concepts o vascular anomalies. J Craniofac Surg. 2012;23:220–224.
Greene AK. Management o hemangiomas and other vascular tumors. Clin Plast Surg. 2011;38:45–63.
Greene AK, Alomari AI. Management o venous mal ormations. Clin Plast Surg. 2011;38:83–93.
Greene AK, Couto RA. Oral prednisolone or in antile hemangioma: ef cacy and sa ety using a standardized treatment protocol. Plast
Reconstr Surg. 2011;128:743–752.
Greene AK, Liu AS, Mulliken JB, Chalache K, Fishman SJ. Vascular anomalies in 5,621 patients: guidelines or re erral. J Pediatr Surg.
2011;46:1784–1789.
Greene AK, Orbach DB. Management o arteriovenous mal ormations. Clin Plast Surg. 2011;38:95–106.
Greene AK, Perlyn CA, Alomari AI. Management o lymphatic mal ormations. Clin Plast Surg. 2011;38:75–82.
Hassanein AH, Mulliken JB, Fishman SJ, Greene AK. Evaluation o terminology or vascular anomalies in current literature. Plast
Reconstr Surg. 2011;127:347–351.
Maguiness SM, Liang MG. Management o capillary mal ormations. Clin Plast Surg. 2011;38:65–73.
Mulliken JB, Glowacki J. Hemangiomas and vascular mal ormations in in ants and children: a classi cation based on endothelial
characteristics. Plast Reconstr Surg. 1982;69:412–422.
Sarkar M, Mulliken JB, Kozakewich HP, Robertson RL, Burrows PE. T rombocytopenic coagulopathy (Kasabach-Merritt
phenomenon) is associated with kaposi orm hemangioendothelioma and not with common in antile hemangioma. Plast Reconstr
Surg. 1997;100:1377–1386.

RECONSTRUCTION
Section VII

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Christian Kirman, MD, FACS
PRINCIPLES OF WOUND HEALING

What are the layers o the epidermis and dermis?
Epidermis (super cial to deep):
1. stratum corneum
2. stratum lucidum
3. stratum granulosum
4. stratum spinosum
5. stratum basalis
Dermis—contains adnexal structures and vasculature
Papillary dermis—super cial, contains vascular tissue
Reticular dermis—deep, contains denser tissue

What are the steps involved in wound healing?
1. Coagulation: Minutes to hours.
2. In ammation: 1 to 2 days.
3. Proli eration: 3 to 30 days (depends on bacterial load).
4. Remodeling/di erentiation: up to 1 year.

What are the cell types primarily responsible or each o these stages?
1. Coagulation: platelets.
2. In ammation: PMNs, macrophages.
3. Proli eration: macrophages, broblasts.
4. Remodeling: myo broblasts (wound contraction), epithelial cells (reepithelialization).

What are the steps involved in epithelialization across a wound?
Mobilization, migration, mitosis, and di erentiation o epithelial cells. T e loss and reestablishment o contact
inhibition initiate and terminate the process.
Wound Healing/Keloids
and Negative Pressure
Wound Therapy
CHAPTER 71

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In a healthy individual, how long does it take or a surgical incision to reepithelialize a ter closure?
A ter a surgical incision is primarily closed, it takes approximately 24 hours or the wound to reepithelialize. A ter
this point, it is not necessary to keep the surgical area dry with an occlusive dressing.

What is the key cell involved in wound remodeling?
Macrophage. T e macrophage is probably the most critical cell in wound healing in general—it initiates the
growth actor cascade that results in broblast proli eration and thus collagen production.

Which cells are responsible or wound contracture?
Myo broblasts: broblasts that contain myo brils permitting contractile activity similar to muscle.

What provides tensile strength to a healing wound?
Collagen.

Which cells produce collagen in the healing wound, and when does production peak?
Fibroblasts produce collagen; maximal net collagen production occurs at about 1 to 2 weeks.

How does platelet-derived growth actor (PGDF) a ect wound healing?
PGDF is released by platelets in the in ammatory phase, and attracts macrophages.

How does trans orming growth actor-beta ( GF-β) a ect wound healing?
GF-β is released primarily by macrophages which attracts broblasts and is involved with collagen production.

What isomers mediate the pro brotic phenotype o GF-β?
GF-b has three isomers. GF-β1 and GF-β2 are pro brotic. GF-β3 is anti brotic.
Various brotic diseases (such as keloids) might result rom aberrant ratios o GF-β isomers (i.e., increased
GF-β1 and GF-β2 and decreased GF-β3).

What is the role o broblast growth actor (FGF) in wound healing?
• FGF-1 and FGF-2 (acidic and basic FGF) are the major proteins in this amily and drive rapid proli eration o
broblasts, epithelial cells, and endothelial cells.
• FGF-7 (keratinocyte growth actor) is a major epidermal growth actor and is involved in dermal–epidermal
signaling.
• T e sequence o events in wound healing is largely mediated by orchestration o intra- and extracellular
regulation o FGF proteins in a de ned pattern.

What are the biologic e ects o FGF?
• Fibroblast and epithelial proli eration.
• Collagen production.
• Potent angiogenic actor.

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When is a scar ully matured, and how much tensile strength does it achieve?
Skin incisions have gained approximately 80% o their nal strength by 6 weeks, and a scar has its ull tensile
strength at 12 weeks, at which point it has gained approximately 80% to 90% o its initial tensile strength. ensile
strength doubles approximately every week over the rst 4 weeks, secondary to collagen cross-linking.

What de nes a chronic wound?
Wounds that ail to heal in 3 months are classi ed as “chronic wounds.”

How does the metalloproteinase level in chronic wounds compare to that in acute wounds?
In chronic wounds, the metalloproteinase level is increased as compared to that o an acute wound resulting in
increased ECM degradation.

What are the di erent types o collagen?
T ere are many types o collagen (more than 10). Critical to wound healing are:
• ype I: most common; in skin, bone, and tendon/ligament.
• ype II: hyaline cartilage.
• ype III: vessel walls; intestine; skin; early scar ormation.
• ype IV: basement membrane.
• ype V: etal and placental tissue.

What is the ratio o type I to type III collagen in normal skin and scars?
1. Normal skin: 4:1 (i.e., predominantly type I collagen).
2. Immature scar: 2:1.
3. Hypertrophic scar: 2:1.
4. Keloid: 3:1 (varies).
5. Fetal skin: predominantly type III collagen.

Which conditions adversely a ect key steps in collagen synthesis?
1. Vitamin C de ciency (scurvy): inhibits hydroxylation o proline and lysine (required or collagen
cross-linking).
2. Colchicine: inhibits secretion o tropocollagen rom the cell.
3. Copper de ciency and penicillamine: prevent lysine oxidation (which is necessary or intra- and intermolecular
bonding).

What are the detrimental e ects o corticosteroids on wound healing?
Corticosteroids inhibit macrophages, resulting in poor broblast stimulation and wound contraction.

What strategy can overcome the e ects o steroids?
Vitamin A (25,000 IU by mouth daily or 3 to 5 days, alternatively 200,000 IU topically three times a day).

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How long should you wait be ore revising a scar?
One year to allow scar remodeling to complete.

What actors impair wound healing?
1. Foreign bodies.
2. In ection.
3. Radiated tissue—decreases blood supply.
4. Inadequate blood supply—any cause.
5. Local trauma.
6. Systemic actors (steroid use, obesity, edema, smoking, comorbidities, malnutrition).

What are the escalating strategies that can be used to close a de ect (the “reconstructive ladder”)?
• Secondary sintent
• Primary intent
• Skin gra t
• Local tissue rearrangement
• ransposition ap
• Free tissue trans er

How do the ollowing tissues di er in healing?
Bone, endon, Nerve, Liver.
Bone healing is accomplished via osteoinduction, osteoconduction, or osteogenesis. Osteoinduction re ers
to precursor cells in the bony tissue being induced to become osteoblasts, o ten by demineralized bone or bone
morphogenic protein (BMP). Osteoconduction re ers to osteoblasts entering the site, along a nonviable bony
sca old such as cortical gra ts or cadaveric bone which is replaced by new bone, by “creeping substitution.”
Osteogenesis re ers to healing with vascularized bone gra ts or cancellous bone, where osteoblasts survive the
transplantation and produce new bone.
endons heal by intrinsic (minimal in ammation with epitenon cells producing collagen) and extrinsic
(in ammation, proli eration, remodeling) healing. Extrinsic healing produces adhesions and is increased with
immobilization.
Peripheral nerves heal by a combination o degeneration and regeneration. T e degenerative process is called
Wallerian degeneration and occurs distal to the site o nerve injury.
Hepatic tissue undergoes regeneration.

What adult tissues are able to heal without scarring?
Bone and liver are the only adult tissues that are able to heal without scar ormation. Chronic damage can cause
hepatic scarring (cirrhosis).

How are operative wounds classi ed?
Class I: Clean—atraumatic, unin ected, no entry into GI/GU/respiratory tract.
Class II: Clean-contaminated—entry into GI/GU/respiratory tract.
Class III: Contaminated—traumatic wounds or gross spillage o enteric contents.
Class IV: Dirty—drainage o abscess or so t tissue in ection.

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TYPES OF WOUNDS

What organisms are associated with bite wounds?
Cat and dog bites are associated with Pasteurella multocida as well as Staphylococcus and Streptococcus species.
Human bites are associated with Eikenella corrodens as well as Staphylococcus and Streptococcus species and
Bacteroides.
Bite wounds are typically treated with Augmentin or prophylaxis.

What is the staging o pressure ulcers?
Stage 1: Skin intact; nonblanching erythema.
Stage 2: Partial-thickness skin loss, abrasions, and blisters included (so into epidermis or dermis).
Stage 3: Full-thickness skin loss with extension into subcutaneous tissue but not through the underlying ascia.
Stage 4: Full-thickness skin loss with extension into muscle, bone, joint, or tendon.

How long does it take or pressure ulcers to arise?
Early (stage I, nonblanching erythema) pressure ulcer ormation can occur within 30 minutes o unrelieved
pressure. Partial-thickness skin loss (stage II) can be seen in as little as 2 to 6 hours.

How much pressure is required to cause a pressure sore?
Unrelieved pressure above 32 mm Hg (capillary arterial pressure) can lead to tissue ischemia and pressure sores.

What are the principles o sacral wound management?
1. Remove pressure.
2. Maintain hygiene in region (diverting colostomy i needed).
3. Optimize medical issues.
4. Serial wound debridements.
5. Dressing changes (wet-to-dry; enzymatic therapy i necrotic tissue or dilute acetic acid i in ected, especially
with pseudomonas).
6. Repair with excision and choice o ap once above actors addressed.

In the evaluation o a pressure ulcer, what is the imaging modality o choice or diagnosis o osteomyelitis?
MRI is the current imaging modality o choice.
Bone biopsy is the gold standard to con rm osteomyelitis.

Where can pressure ulcers occur?
Anywhere bony prominences exist. In order o prevalence:
1. ischial tuberosity
2. trochanter
3. sacrum
4. calcaneus
5. occiput
6. scapula

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What type o f ap reconstruction or pressure ulcers is best or ambulatory patients?
Fasciocutaneous aps preserve muscle and do not a ect ambulation.

What is rostbite, and how is it classi ed?
Frostbite occurs with extremely cold temperatures that cause tissue reezing and ormation o intracellular ice
crystals and microvascular occlusion. A ter thawing, tissue in ammation and coagulation lead to cell death. It is
classi ed similarly to burns:
First degree: involves epidermis only with hyperemia.
Second degree: involves dermis with blister ormation.
T ird degree: ull-thickness skin and subcutaneous tissue involvement.
Fourth degree: necrosis o deeper tissues such as muscle and bone.

What are the steps o rostbite management?
1. Resuscitation
2. Rapid rewarming
3. T rombolytic therapy
4. Watch ul waiting

Which animals can potentially transmit rabies?
Carnivores: dog, cat, raccoon, bat, ox, skunk, coyote. Incidence o rabies rom cats is increasing. Exposure alone
without a bite can transmit rabies and is an indication or prophylaxis (entering a cave harboring rabid bats).
Rodents do not carry rabies.

How is a rabies exposure managed?
1. Wash the wound in virucidal agent (dilute Betadine).
2. Rabies immune globulin: give single dose o 20 IU/kg around the wound.
3. Rabies vaccine (human diploid cell vaccine): give ve 1-cc doses over a 28-day period (days 0, 3, 7, 14, and
28); intramuscular injection in the deltoid.
4. Give both rabies immune globulin and vaccine to all patients, except or patients with a documented antibody
titer, who do not need immune globulin.

Which wounds are “tetanus prone”?
1. Wounds that are contaminated.
2. Contain devitalized tissue.
3. Are open or more than 6 hours.
4. Are deeper than 1 cm.

What tetanus measures are required or a wound in a “ ully immunized” patient?
A ully immunized patient is one who has received complete tetanus toxoid immunization (3 to 5 doses) with
a booster within 5 years o the current injury. I the wound is “tetanus prone,” give tetanus toxoid (0.5 mL o
adsorbed toxoid intramuscularly). I the wound is not “tetanus prone,” do nothing.

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What tetanus measures are required or a wound in a patient o unknown or inadequate immunization
status?
T ese patients need to receive tetanus toxoid or all wounds. In addition, i the patient has received less than two
injections o immunization, also give immune globulin (250 units o human tetanus immune globulin).

What organisms are typically associated with necrotizing asciitis?
Necrotizing asciitis is a severe in ection that leads to lique action necrosis along ascial planes. Beta-hemolytic
streptococci are commonly associated with this devastating process; however, mixed aerobes and anaerobes can also
be ound.

What organism is responsible or “gas gangrene”?
T e Clostridia species (typically Clostridium perfringens) cause gas gangrene. T ey are obligate anaerobes and so
in addition to radical debridement, hyperbaric oxygen has been shown to be bene cial in the treatment o gas
gangrene.
KELOIDS

What is the di erence between keloids and hypertrophic scars?
1. Keloids extend beyond the margin o the initial scar, whereas hypertrophic scars do not.
2. Keloids have an increased ratio o types I/III collagen unlike hypertrophic scars.
3. Keloids have larger, thicker, and more irregular collagen bers than hypertrophic scars.
4. Keloids are commonly ound on the ace, earlobes, chest, and upper back, whereas hypertrophic scars are
commonly ound across exor sur aces.
5. Keloids appear late a ter initial injury, and can grow inde nitely. Hypertrophic scars arise over the rst ew
weeks, quickly grow, and then regress.

What are the chemical and histological di erences between keloids and normal scar tissue?
Keloids contain elevated levels o GF-β. In addition, they have increased collagen (especially type III) and
vascularity compared with normal tissue. Fibroblasts proli erate aster in keloids than normal tissue.

What are the principles o keloid and hypertrophic scar management?
1. Excision plus adjuvant therapy (intradermal steroids, silicone gel, radiation therapy).
2. Meticulous tissue handling and closure with intradermal sutures.
3. Pressure earrings/garments.

What are the contraindications to radiation therapy or keloids?
1. Pediatric patients.
2. Pregnant women.
3. issue with underlying visceral structures.
Despite the theoretical risk o neoplastic trans ormation, ewer than 10 cases o cancer due to radiation therapy or
keloids have been reported.

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What are the potential side e ects o radiation therapy or keloids?
1. Hypo- or hyperpigmentation.
2. elangiectasias.
3. Acute skin desquamation.

What is the mechanism o intralesional steroid (triamcinolone acetonide) therapy or keloids?
1. Inhibits broblast proli eration and collagen production by gene inhibition.
2. Stimulates collagenase production.
3. Normalizes collagen ultrastructural organization that is disrupted in keloid nodules.

What is the optimal treatment or earlobe keloids?
Surgical excision with or without steroid injection, ollowed by wearing o magnetic pressure earrings.

Where does scarless wound healing occur?
Wound healing occurs without scar in the early mammalian etus (including human). Levels o hyaluronic acid are
signi cantly higher in etal skin and appear to correlate with scarless wound healing.
WOUND THERAPY/TREATMENT

What diagnosis should be considered in a chronic nonhealing lower extremity wound despite adequate
wound care?
A Marjolin’s ulcer is malignant degeneration o a chronic wound such as a burn or venous stasis ulcer. A biopsy
should be per ormed or diagnosis.

Can a partial-thickness burn scar be le t to heal by secondary intention?
Generally, partial-thickness burn scars can be given up to 3 weeks to close by secondary intent. I not closed by
3 weeks, they need to be gra ted to avoid hypertrophic scar ormation.

How is burn scar hypertrophy best managed?
Pressure garments decrease blood ow to active scars, and decrease collagen ber production.

During wound therapy with leeches, which bacteria grow in the leech gut?
Aeromonas hydrophila. Cipro oxacin, bactrim, or tetracycline can be used or prophylaxis.

What is the antibacterial mechanism o Acticoat?
Acticoat contains silver ions that are directly bactericidal. It needs to be moistened with distilled water prior
to application (ions in normal saline will negate the antibacterial e ect o Acticoat). It is e cacious against
Pseudomonas, MRSA, VRE, and some species o yeast.

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What are the associated side e ects o topical antimicrobial agents?
Silvadene (silver sul adiazine)—leukopenia.
Sul amylon (ma enide acetate)—acidosis (secondary to carbonic anhydrase inhibition).
Silver nitrate—hyponatremia.
Bacitracin—vesicular rash.

What are the clinical indications or Regranex gel (becaplermin, PDGF)?
Regranex is indicated or lower extremity ulcers:
• o diabetic neuropathy.
• that extend into the subcutaneous tissue.
• that have a good vascular supply.
• that are not in ected.
Regranex is not FDA approved or use in ischemic, in ected, or super cial wounds, or those that are being closed
primarily.

Which biologic dressings contain cultured cells?
1. ransCyte: a dermal substitute that is composed o cultured neonatal dermal broblasts seeded on a silicone/
collagen matrix, covered with a nylon sheet.
2. Dermagra t: contains neonatal broblasts on a sheet o dexon (polyglycolic acid) or vicryl.
3. Epicyte: a matrix o cultured autologous keratinocytes (i.e., rom the same patient).
4. Apligra : contains both neonatal keratinocytes and broblasts; these cells are seeded onto a collagen matrix.

Which other biologic dressings contain dermal matrix?
1. Biobrane: a nylon sheet covering a silicone layer containing dermal collagen.
2. Integra: a silicone sheet coated with collagen and glycosaminoglycan obtained rom bone tendon cartilage.
3. AlloDerm: cadaveric acellular dermis that has been deepithelialized.

Which biologic dressings contain ECM or basement membrane?
1. Gra x: cryopreserved placental membrane.
2. ACELL: porcine bladder ECM and basement membrane.
3. OASIS: porcine small intestine ECM.

Which wounds are best treated with alginates?
Highly exudative wounds. Calcium alginate gels are made rom seaweed and are hydrophilic, so they can absorb
signi cant amounts o uid. Alginates prevent tissue maceration, trap bacteria, and can be rinsed o .

How does a split-thickness skin gra t initially receive nutrition?
Plasma imbibition or the rst 48 hours until an adequate vascular supply is established. Inosculation:
Connection o recipient and donor vessels in the gra t and recipient bed. Neovascularization: Sprouting o new
blood vessels.

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What are the steps in adherence o a skin gra t?
Phase 1: brin phase ( rst 72 hours).
Phase 2: brovascular phase (a ter 72 hours)—vascular ingrowth and anastomosis.

What dressing is ideal to bolster a split-thickness skin gra t?
A VAC dressing con orms to the wound, holds the skin gra t in place or rapid revascularization, and prevents
shearing.

What are the causes o skin gra t ailure?
1. Hematoma
2. Seroma
3. In ection
4. Shearing orces disrupting skin gra t adherence and thus nutrition

What bacterial load is required to cause clinical in ection in a split-thickness skin gra t?
105 bacteria per cm3 o tissue.

Which f ap type o ers the greatest resistance to bacterial in ection?
Musculocutaneous aps bring in a large proportion o blood supply that best wards o bacterial in ection.

What histologic layer mediates skin gra t contraction?
Elastin within the dermis—thicker skin gra ts mean more dermis, which means more elastin, and which means
more primary or immediate contraction.
Conversely, elastin inhibits delayed (secondary) gra t contraction so those gra ts without dermis, such as cultured
epithelial cells, demonstrate the most delayed contraction.

Hyperbaric oxygen therapy might be bene cial in which clinical situations?
• Osteomyelitis
• Necrotizing in ections
• Ischemia-reper usion injury
• Diabetic lower extremity wounds
TISSUE EXPANSION

What are the e ects o tissue expansion on f ap properties?
1. Increased tissue sur ace area, collagen, and ground substance content.
2. Increased vascularity (similar to ap delay).
3. Decreased tensile strength and elasticity (since thinner dermis).
4. Markedly increased sensitivity to epinephrine-induced necrosis.
issue expansion results in a net gain o tissue that is due to both stretching o existing tissue and de novo tissue
generation.

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What growth actor is responsible or increased vascularity in expanded tissue?
Vascular endothelial growth actor (VEGF) is responsible or angiogenesis by increasing endothelial cell growth
and migration.

What are the histologic changes seen ollowing tissue expansion?
1. Subcutaneous at atrophies.
2. Dermis becomes thinner.
3. Epidermis becomes thicker, particularly the stratum spinosum (increased mitotic activity).
4. Rete ridges become atter.

What are the tissue zones that result rom tissue expansion?
issue expansion results in ormation o a capsule surrounding the expander, which is essentially a oreign body
reaction. T ese zones are, rom inside to outside, as ollows:
Zone A: inner zone, cellular (predominantly macrophages).
Zone B: central zone, brous, with broblasts and myo broblasts.
Zone C: transitional zone, with loose collagen.
Zone D: vascular zone.

What is mechanical creep?
1. A response to constant mechanical orce.
2. Collagen realigns and results in a change in tissue elasticity.
3. Interstitial uid and ground substance are displaced.
4. Depends on viscoelastic properties o skin.

What is stress relaxation?
Less orce is needed to keep tissue stretched to a given length the longer it is held at that length.

Which tissue expansion protocol results in maximal tissue recruitment?
Cyclic loading: repeated cycles o stretching ollowed by relaxation.

How can extra tissue be recruited intraoperatively?
Approximately, 15% to 20% tissue expansion can be gained with a brie 1- to 2-hour session (acute tissue
expansion). Clinical studies suggest acute tissue expansion provides tissue o comparable quality to that expanded
over a much longer time rame (weeks).

What are the concerns with lower extremity tissue expansion, especially below the knee?
1. Extensive tissue expansion can cause sural nerve neuropraxia.
2. T e region below the knee has relatively limited lymphatic out ow (compared with the trunk), and a tissue
expander is at increased risk or cellulitis.
3. issue expansion in the lower extremity is particularly problematic in the pediatric population.

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What e ect does tissue expansion have on hair growth?
issue expansion, such as in the scalp, decreases the telogen, or growth-arrest phase.

How does irradiated tissue di er rom normal during tissue expansion?
Irradiated tissue does not undergo the histologic changes that are seen with normal tissue during tissue expansion.
Previous irradiation decreases the net tissue gain rom expansion by approximately 25%.

How long do sutures retain tensile strength?
Catgut—1 week or less.
Monocryl (poliglecaprone 25)—7 to 10 days.
Chromic gut—1 week.
Vicryl, dexon—2 to 4 weeks.
PDS—4 to 6 weeks.

Which conditions associated with impaired wound healing preclude elective rejuvenation surgery?
• Ehlers–Danlos syndrome: inherited disorder o collagen polymerization, characterized by joint laxity,
hyperextensible skin, and poor wound healing.
• Progeria: autosomal recessive disorder (rare) o premature aging, characterized by premature aging, loss o
subcutaneous at, poor wound healing, atherosclerosis.

In which inherited skin disorders is it possible to per orm rejuvenation surgery?
• Cutis laxa: have non unctioning elastase inhibitor characterized by coarsely textured drooping skin due to
degeneration o dermal elastic bers.
• Pseudoxanthoma elasticum: associated with increased collagen degradation and deposition o calcium in elastic
bers.
BASICS OF NEGATIVE PRESSURE WOUND THERAPY

What is Negative Pressure Wound T erapy (NPW )?
NPW is a device or wound care apparatus that applies vacuum to a wound sur ace. It includes a wound–
inter ace material, an adhesive lm or drape, and tubing connected to a vacuum source.

When was NPW rst introduced?
Closed suction drainage has been a long recognized principle o surgery that predates NPW . However,
Morykwas and Argenta rst introduced the concept o NPW in the early 1990s.

What are the indications o NPW ?
NPW is indicated in acute, chronic, traumatic, and dehisced wounds; partial-thickness burns; diabetic, pressure,
and venous ulcers; aps and gra ts.

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What are contraindications to NPW ?
NPW is contraindicated in wounds with exposed vasculature, nerves, anastomotic sites and solid organs,
malignancy in the wound, untreated osteomyelitis, necrotic tissue present in the wound, and nonenteric or
unexplored stulas.

What is the basic principle o NPW ?
T e exact mechanism o action o NPW is multi actorial and includes accelerated wound healing by increasing
granulation tissue ormation, removal o wound uid, maintenance o moist wound environment, and contracting
the wound edges together.

What actors do NPW e ect to increase blood f ow in the wound?
Blood ow is dependent on the pressure applied, distance rom the edge, and the tissue type. Blood ow decreases
at the wound edge, but immediately increases with vacuum release suggesting that intermittent NPW may
urther increase blood ow.

How does NPW e ect wet or draining wounds?
In patients with large open wounds, serous uid may accumulate in the wound bed and be e ciently removed by
NPW leading to accelerated wound healing.

What e ect does NPW have on skin surrounding the wound?
In wounds where the surrounding skin is de ormable, such as the abdomen or thigh, it is commonly observed that
the wound shrinks considerably when using an NPW device.

How does NPW maintain wound homeostasis?
Covering the wound with a semiocclusive dressing and using oam with insulation qualities minimize evaporation,
desiccation, and heat loss.

What complications can occur rom NPW ?
Bleeding and in ection have been reported by the FDA in a small number o patients.
In addition, retained oam dressing pieces have also been reported.

Can NPW be used in patients on anticoagulants or platelet aggregation inhibitors?
Yes, but extreme caution should be used with patients at higher risk o bleeding or hemorrhage, such as those on
anticoagulants or platelet aggregation inhibitors.
CLINICAL USES OF NPWT

How is NPW applied to wounds?
An inter ace material is tted to the size o the wound and placed on or into the wound bed. T e adhesive dressing
is placed over the wound. ubing is connected to the wound through a hole in the adhesive drape and connected
to a collection canister and a vacuum source.

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What is used or the wound–inter ace material?
Many materials can be used including open pore oam, gauze, polyvinyl alcohol sponges, and corrugated
polymers. Open pore sponges are most commonly used.

How does the wound–inter ace material act on the wound?
T e inter ace material distributes the vacuum throughout the wound and allows or uid removal. In addition,
the wound–inter ace material causes microde ormations at the wound sur ace and draws the surrounding skin
together.

Can the wound–inter ace material be hemostatic on the wound?
T e wound–inter ace materials used in NPW are not hemostatic and should not be applied to wounds that are
bleeding or have a potential to bleed.

Does the wound–inter ace material have antibacterial properties?
T e commonly used wound–inter ace materials are inert substances that have no inherent antibacterial properties
and should not be applied to grossly in ected wounds. T ere is a silver-impregnated oam that can be used with
certain NPW devices and there are also antibacterial gauze products that can be used with the device.

What happens to the wound i there is no adequate seal to maintain continuous suction on the wound bed?
T ere must be an adequate seal to maintain the vacuum or air will leak into the wound causing desiccation.

What pressure is commonly used or NPW ?
T ere are no established guidelines on the amount o pressure applied in NPW . Applying a pressure o 125 mm
Hg is most commonly used, but pressures between 60 and 150 mm Hg have also been applied.

What wave orms are commonly used?
T e original work by Morykwas and Argenta showed increased granulation tissue ormation with cycling
wave orms; however, varying the level o suction can cause pain and may not be well tolerated by patients. Instead,
continuous suction is most commonly used.

When is a wound ready or NPW ?
Wounds may be ready or NPW a ter complete debridement o in ected and necrotic tissue.

Does NPW debride wounds?
NPW does not debride or remove devitalized tissue in wounds but rather aids to accelerate wound healing.

How o ten does the wound–inter ace material need to be changed?
T ere are no speci c recommendations or changing the wound–inter ace material. In heavily colonized wounds,
the dressing should be changed every 12 to 24 hours, or several days to make sure the wound is clean. A terward,
the dressings are generally changed every 2 to 3 days.

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When changing the NPW dressing, what should be assessed?
T e wound should be assessed or in ection, odor, and need or urther debridement. In addition, the wound
bed should be assessed requently or duskiness, bruising, and bleeding. T e surrounding skin integrity should
be monitored or skin breakdown rom the adhesive drape and rash secondary to contact dermatitis or ungal
in ection. Devitalized tissue should be removed as indicated with each dressing change. I the wound is
malodorous, the treatment should be stopped or 24 to 48 hours and replaced with saline dressings until the odor
has subsided. T en NPW treatment can be resumed.

How long can NPW be used on a wound?
Prolonged use o NPW beyond 3 months may not be o bene t unless the wound sur ace area continues to
signi cantly decrease.

When should NPW be discontinued?
NPW should be discontinued i the patient does not tolerate dressing changes or i the wound needs to be
requently assessed or in ection. I the wound bed is dusky, bruised, or bleeding, the wound becomes grossly
in ected, or there is persistent devitalized tissue present, the therapy should be discontinued. T e therapy should
also be immediately stopped i blood or purulent exudate is noted in the suction canister.

Can NPW be used in dirty or grossly contaminated wounds?
NPW devices should be used with extreme caution in in ected wounds. Some clinicians use NPW devices on
in ected wounds, and i used, the device should be changed every 12 to 24 hours to avoid worsening in ection or
sepsis.

Can NPW be applied to diabetic wounds?
NPW has been used as a wound healing therapy a ter debridement o diabetic oot ulcers. Most o the ew
randomized diabetic oot ulcer trials compare NPW to hydrogel, alginate, or gauze—all indicating better wound
healing with NPW .

How does NPW prepare a wound or surgical closure?
NPW prepares the wound bed or surgical closure with skin gra ts or tissue substitutes by increasing granulation
tissue ormation, decreasing the sur ace area, and possibly increasing blood ow to the wound bed.

What e ect does NPW have on lower extremity wounds?
NPW can be used in patients with lower extremity stasis ulcers. In studies o patients with lower extremity
ulcers, there was a trend toward less secondary amputations with NPW applied to the wounds compared to
nontreated controls. Patients with lower extremity traumatic injuries, speci cally tibia– bula ractures, treated
with NPW were less likely to require ree ap closure o their wounds and were more likely to be closed
primarily or with simple skin gra ts.

How is NPW used in the treatment o an open abdomen?
When the abdominal ascia is le t open a ter a laparotomy, NPW can be applied in the wound to control
in ection, manage exudate, and reduce visceral edema. Any exposed viscera should be covered with a nonadherent
dressing prior to placement o the NPW wound–inter ace material.

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How can NPW be applied to enterocutaneous stulae?
T e stula can be isolated and controlled rom the surrounding tissues by placing wound–inter ace material over
the stula. T e ef uent can be controlled, while the surrounding tissues are protected, the tissues can granulate
and the wound can contract around the stula. Additional therapy must be directed at the underlining cause and
control o the stula.

Can NPW prevent burn wound progression?
Early work by Morykwas showed that NPW prevents tissue injury progression in swine a ter partial-thickness
burns. T ere have been several small studies since, but no robust clinical trial has been per ormed to assess the
theoretical edema reduction, improved tissue per usion, or less scarring with NPW .

Can NPW be used in chest wall wounds ollowing median sternotomies?
NPW allows or wound drainage, chest wall stabilization, and isolation o the chest cavity to prevent
contamination, maintenance o a moist environment, granulation stimulation, and increased blood ow to the
tissues. A ter NPW is used or several days in a deep sternal wound, de nitive closure is usually per ormed with
so t-tissue aps.

How is NPW used as a bolster or skin gra ts?
T e use o NPW as a bolster or skin gra ts has been shown to increase gra t take compared with oam bolsters
without vacuum. NPW is generally used or 48 to 72 hours and then removed. A nonadherent material should
be applied between the skin gra t and wound–inter ace material.

How is NPW used to treat lower extremity compartment syndrome?
NPW can be applied to open asciotomy wounds, which decreases the edema and promotes granulation tissue
ormation allowing these wounds to either completely close in an accelerated manner or contract enough to accept
a skin gra t.

What role does NPW have in controlling lymphatic injuries?
NPW is e ective in controlling lymphocele or lymphatic stula with complete resolution o the drainage in a
mean o 1 to 2 weeks.
REFERENCES
Argenta LC, Morykwas MJ. Vacuum-assisted closure: a new method or wound control and treatment: clinical experience. Ann Plast
Surg. 1997;38:563–577.
Attinger CE, Janis JE, Steinberg JS, Schwartz J, Al-Attar A, Couch K. Clinical approach to wounds: debridement and wound bed
preparation including the use o dressings and wound-healing adjuvants. Plast Reconstr Surg. 2006;117:72S–109S.
Blume PA, Walters J, Payne W, Ayala J, Lantis J. Comparison o negative pressure wound therapy using vacuum assisted closure with
advanced moist wound therapy in the treatment o diabetic oot ulcers: a multicenter randomized controlled trial. Diabetes Care.
2008;31(4):631–636.
Cothren CC, Moore EE, Johnson JL, Moore JB, Burch JM. One hundred percent ascial approximation with sequential abdominal
closure o the open abdomen. Am J Surg. 2006;192:238–242.
Fitzpatrick B. T e validity and practicality o sun reactive skin types I–VI. Arch Dermatol. 1988;124:869–871.
Goldman R. Growth actors and chronic wound healing: past, present, and uture. Adv Skin Wound Care. 2004;17:24–35.

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Hamed O, Muck PE, Smith JM, Krallman K, Gri th NM. Use o vacuum-assisted closure (VAC) therapy in treating lymphatic
complications a ter vascular procedures: new approach or lymphoceles. J Vasc Surg. 2008;48:1520–1523.
Liu W, Wang DR, Cao YL. GF-beta: a brotic actor in wound scarring and a potential target or anti-scarring gene therapy. Curr
Gene T er. 2004;4:123–136.
Morkywas MJ, Argenta LC, Shelton-Brown EI, McGuirt W. Vacuum-assisted closure: a new method or wound control and treatment:
animal studies and basic oundation. Ann Plast Surg. 1997;38:553–562.
Pandya AN, Vadodaria S, Coleman DJ. issue expansion in the limbs: a comparative analysis o limb and nonlimb sites. Br J Plast Surg.
2002;55:302–306.
Powers CJ, McLeskey SW, Wellstein A. Fibroblast growth actors, their receptors and signaling. Endocr Relat Cancer. 2000;7:165–197.
Ratner D. Skin gra ting. Semin Cutan Med Surg. 2003;22:295–305.
Rumalla VK, Borah GL. Cytokines, growth actors, and plastic surgery. Plast Reconstr Surg. 2001;108:719–733.
Saxena V, Hwang CW, Huang S, Eichbaum Q, Ingber D, Orgill DP. Vacuum-assisted closure: microde ormations o wounds and cell
proli eration. Plast Reconstr Surg. 2004;114:1086–1096.
Sood A, Granick MS, omaselli NL. Wound dressings and comparative e ectiveness data. Adv Wound Care. 2014;3(8):511–529.
Zeng YJ, Xu CQ, Yang J, Sun GC, Xu XH. Biomechanical comparison between conventional and rapid expansion o skin. Br J Plast
Surg. 2003;56:660–666.

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693
Douglas M. Sammer, MD

What are the two main types o skin gra t?
Split-thickness skin gra t (S SG) and ull-thickness skin gra t (F SG).

Which parts o skin are included in skin gra ts?
T e epidermis and part (S SG) or all (F SG) o the dermis.

What structures are included with the dermis in both split-thickness and ull-thickness skin gra ts?
Adnexal structures including sebaceous glands, hair ollicles, sweat glands, and capillaries.

How thick is a “thin” STSG?
0.005 to 0.012 in.

How thick is an “intermediate” STSG?
0.012 to 0.018 in.

How thick is a “thick” STSG?
0.018 to 0.028 in.

What are the advantages o meshing a partial-thickness skin gra t?
Expansion o gra t sur ace area up to six times, better contouring, decreased seroma or hematoma ormation
beneath the gra t.

How does the mesher ratio a ect the gra t sur ace area?
A mesher expansion ratio o 1:1.5 (most commonly used) increases sur ace area by 50%, a ratio o 1:2 increases
sur ace area by 100%, etc.

What are the disadvantages o meshing?
Wa ed appearance, increased gra t contraction (may be an advantage in some situations).
Principles of Skin
Grafting
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Where should meshing be avoided?
On the ace, hand, or orearm (cosmetically sensitive areas), and over joints, where contracture becomes a problem.

What is the postoperative bolster made o ?
Xero orm, cotton balls, or batting moistened in saline/mineral oil, secured with tie-over sutures or a stapled-on
oam dressing.

How long should the bolster stay on postoperatively?
Five to seven days. wo to three days i the recipient site is contaminated.

What are typical donor sites or STSGs?
Anterior or lateral thigh in adults, buttock in children ( or concealment o scar). T e abdomen, back, chest, and
scalp are o ten used i other donor sites are limited.

What is an appropriate donor-site dressing?
Xero orm gauze dried with a hair-dryer or heat lamp is the traditional dressing. An occlusive semipermeable
dressing, such as Opsite or egaderm may be used.

What is the advantage o Tegaderm or Opsite or the donor-site dressing?
Faster healing and pain reduction.

Do the dermis and epidermis regenerate in split-thickness donor sites?
T e donor site epidermis regenerates rom the periphery and rom adnexal structures, but the dermis does not
regenerate. T e donor site can be reharvested a ter it is well healed, i the underlying dermis is thick enough.

How long does a split-thickness donor site take to heal?
A thin S SG donor site will heal within 1 week, whereas thicker S SG donor sites will take 2 to 3 weeks to heal.

What are the advantages o ull-thickness skin gra ts?
Better color, thickness, and texture match with recipient site, decreased contraction.

What are the disadvantages o FTSG?
Donor site must be closed primarily, limited donor sites, more di cult take compared to split-thickness skin gra ts.

What are typical FTSG donor sites?
Supraclavicular, preauricular, postauricular, volar orearm, and inguinal region.

Why should an FTSG be de atted a ter harvesting?
F SG should be aggressively de atted to improve imbibition and take.

What is a composite gra t?
A gra t that includes at, muscle, or cartilage in addition to skin.

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What is the maximum size o a composite gra t?
Variable, but composite gra ts that contain cartilage will not take i greater than 1 to 1.5 cm in diameter.

What is the di erence between an isogra t/autogra t, an allogra t/homogra t, and a xenogra t/heterogra t?
Autogra t or isogra t: rom same person, or an identical twin.
Allogra t or homogra t: rom same species.
Xenogra t or heterogra t: rom di erent species.

What is the purpose o allogra t or xenogra t?
Used or temporary coverage o wounds until they are suitable or autogra ting. Cadaver allogra t or more rarely
porcine xenogra ts can be used. Cadaveric allogra ts do take initially, but are rejected a ter 10 days. Xenogra ts are
more quickly rejected.

What is the di erence between the primary and secondary skin gra t contraction?
Primary contraction is the immediate shrinkage o a skin gra t a ter harvesting, which is due to dermal elastin.
Secondary contraction is the contracture that occurs with healing, and is due to myof broblast activity.

Do split-thickness or ull-thickness skin gra ts contract more?
Primary contraction is greater with thicker skin gra ts, whereas secondary contraction is greater with thinner skin
gra ts.

How does gra t thickness a ect the ability o the gra t to sweat?
T icker gra ts contain more dermis, and there ore more sweat glands, and will have a greater potential to sweat.

How does gra t thickness a ect the ability o the gra t to grow hair?
More hair ollicles are harvested with thicker gra ts, and these will have greater hair growth.

How does gra t thickness a ect the ability o the gra t to develop sensation?
T icker gra ts contain more neurilemmal sheaths, allowing greater ingrowth o nerve f bers, and greater potential
or sensation over time. T in gra ts have less potential or sensation, but may develop sensation more quickly.

What type o sensation develops f rst in a healing skin gra t?
Pain returns f rst, then light touch, then hot/cold sensation.

What are the phases o skin gra t take?
Imbibition, inosculation, and revascularization.

What is imbibition?
T e f rst phase o take, involving the uptake o nutrients rom serum in the wound bed by capillary action, lasting
48 to 72 hours.

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What is inosculation?
T e second phase o take, involving donor and recipient capillary alignment.

What is revascularization?
T e third phase o take, revascularization occurs through the aligned capillaries, complete at 7 days.

How does revascularization occur?
Controversial; new recipient site vessels may grow into the gra t along the path o gra t vessels, new ingrowth may
occur randomly, recipient and donor vessels may anastomose, or a combination o the above.

To what type o tissue will a skin gra t not take?
Exposed bone, cartilage, or tendon (unless there is overlying periosteum, perichondrium, or paratenon).

What are the most common causes o ailure o skin gra t take?
Hematoma or seroma, poorly debrided or poorly vascularized wound, shearing o the gra t, and in ection. T e
most common is hematoma or seroma beneath the gra t.

What level o bacterial load in the recipient site precludes skin gra t take?
Skin gra ts will not take in wounds with bacterial loads o 105 per gram or greater.

What are the two phases o gra t adherence?
T e f rst phase is due to f brin deposition between the gra t and the wound bed, lasting 72 hours. T e second
phase involves ingrowth o vessels into the gra t and production o f brous tissue.

Once a skin gra t is well healed, how should it be taken care o ?
Hand-lotion or cream should be used to prevent desiccation. Skin gra ts have decreased sweat and sebaceous
glands.
Sweat glands do not unction until innervated. Sebaceous gland unction is also delayed, although innervation is
not required or unction.
REFERENCES
Chang E. Gra ts. In: Brown DL, Borschel GH, eds. Michigan Manual of Plastic Surgery. Philadelphia, PA: Lippincott Williams &
Wilkins; 2004:16–21.
Place MJ, Herber SC, Hardesty RA. Basic techniques and principles in plastic surgery. In: Aston SJ, Beasley RW, T orne CHM, eds.
Grabb and Smith’s Plastic Surgery. 5th ed. Philadelphia, PA: Lippincott-Raven; 1997:13–26.
Preuss S, Breuing KH, Eriksson E. Plastic surgery techniques. In: Achauer BM, Eriksson E, eds. Plastic Surgery Indications, Operations,
and Outcomes. St Louis, MO: Mosby; 2000:147–162.
Vasconez HC. Skin gra ts. In: Cohen M, ed. Mastery of Plastic and Reconstructive Surgery. Boston, MA: Little, Brown and Company;
1994:45–55.
Wol SE, Herndon DN. Burns and radiation injuries. In: Mattox K, Feliciano D, Moore E, eds. Trauma. 4th ed. New York, NY:
McGraw-Hill; 2000:1137–1152.

697
Matthew M. Hanasono, MD

What is a ap?
issue that is either trans erred or transplanted with intact circulation.

How are muscle aps classi ed by Mathes and Nahai?
ype I: single vascular pedicle.
ype II: dominant vascular pedicle(s) and minor vascular pedicle(s).
ype III: two dominant pedicles.
ype IV: segmental vascular pedicles.
ype V: dominant vascular pedicle and secondary segmental vascular pedicles.

What is the average tissue survival rate or a microvascular ree ap?
95% or better.

What type o ultrasonography will most reliably image and locate vascular per orators preoperatively?
Duplex ultrasonography.

What is most likely to improve the survival o the distal portion o a random pattern cutaneous ap?
Surgical delay prior to ap elevation.

What is the reexploration rate or ap compromise?
Approximately 10%.

What is the salvage rate or microvascular ree aps that require reexploration or ap ischemia?
50 to 85%.

What is the maximum warm ischemia time tolerated by muscle aps?
Less than 3 hours.
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What is the maximum warm ischemia time tolerated by bone aps?
Less than 3 hours.

What is the maximum warm ischemia time tolerated by skin and asciocutaneous aps?
Approximately 4 to 6 hours.

What is the warm ischemia time tolerated by jejunal aps?
Less than 2 hours.

How can the maximum tolerated ischemia time be increased?
Cooling o tissues: up to 12 hours o ischemia tolerated or asciocutaneous tissues, 8 hours or muscle, and
24 hours or bone.

Which results higher ap survival rates, end-to-end or end-to-side anastomoses?
Most studies demonstrate similar patencies.

Which type o arteriotomy, slit or circular/oval, is more success ul?
Most studies demonstrate similar patencies.

Under what circumstances might an end-to-side anastomosis be advantageous?
Vessel size discrepancy (larger donor vessel), only one artery or vein available and needed or distal organ/tissue
per usion, limited exposure/availability o similar size donor vessels.

What anastomotic angles are thought to be the most desirable and result in the greatest amount o blood
ow to the recipient vessel in an end-to-side anastomosis?
Based on technical actors and blood ow rates, angles o 45 to 90 degrees result in greater arterial ow than
obtuse angles up to 135 degrees.

What methods relieve vasospasm?
opical anesthetics (e.g., lidocaine), topical papaverine, topical calcium channel blockers (e.g., verapamil),
vessel dilation, adventitial stripping, and sympathetic nerve block (e.g., epidural anesthesia or lower extremity
reconstruction).

What is the reason or adventitial stripping?
o relieve vasospasm and to prevent loose adventitia rom being caught in the vessel lumen, a potential trigger or
thrombosis.

Which method o adventitial stripping is pre erred, blunt or sharp?
Sharp adventitial stripping is associated with less vessel trauma resulting less vasospasm and improved blood ow
to the ap.

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What is papaverine?
Papaverine is an opium alkaloid antispasmodic drug used in the treatment o visceral spasm, vasospasm, and
ormerly in the treatment o erectile dys unction. In microvascular surgery, it is applied topically to relieve
vasospasm. T e mechanism o action is not entirely clear, but it is believed to involve inhibition o the enzyme
phosphodiesterase leading to increased levels o cyclic AMP, ultimately leading to vascular smooth muscle
relaxation.

What are the characteristics o a viable ap?
Warmth, pink/per used color, so tness, capillary re ll, and detectable pulse (e.g., Doppler).

What are signs o inadequate arterial ow?
Pale, cool ap with slow (> 2 seconds) capillary re ll and decreased tissue turgor.

What are signs o inadequate venous ow?
Cyanotic or dusky ap with ast (< 1 second) capillary re ll and increased tissue turgor.

What are the most reliable methods o ree ap monitoring?
Clinical observation, Doppler ultrasound owmetry, pinprick or scratch testing, near-in rared spectroscopy, pulse
oximetry, quantitative uorometry, sur ace temperature probing.

Besides cost, what is the main disadvantage o using an implantable Doppler probe or ree ap monitoring?
T e risk o alse positives (loss o Doppler signal when microvascular anastomosis is patent and ree ap is viable)
due to accidental detachment o the Doppler probe, loosening o the implantable Doppler cu around the blood
vessel, or equipment mal unction. In one study o 20 buried aps, the implantable Doppler had 100% sensitivity
and an 88% alse-positive rate. However, other studies have suggested the alse-positive rate or the implantable
Doppler system is no higher than clinical monitoring.

How is near-in rared spectroscopy used in ree ap monitoring?
In near-in rared spectroscopy monitoring, ree ap tissues are exposed to near-in rared light. For each type o
tissue, a portion o this light is absorbed and some is re ected back. T e detector senses the re ected light and
the device uses the ratio o oxyhemoglobin (HgbO2) to deoxyhemoglobin (Hgb) to provide noninvasive real-time
measurement o tissue oxygenation. Changes in tissue oxygenation suggest decreased blood ow to the ap and
may be secondary to thrombosis o the vascular pedicle. T ere is some clinical evidence in the literature that a
decrease in tissue oxygenation is detected prior to clinical signs that the ap is compromised and may acilitate
early reoperation and higher ap salvage rates.

How can buried aps, such as those used or pharyngeal reconstruction, be monitored?
A segment o the ap can be pedicled on separate per orating blood vessels and exteriorized. Alternately, an
implantable Doppler can be placed on the vein or artery or both, distal to the anastomosis.

How long be ore a pseudointima orms at the anastomotic site?
Approximately 5 days.

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How long be ore a new intima orms at the anastomotic site?
Approximately 1 to 2 weeks.

What types o sutures are typically used or microvascular surgery?
Nylon or polypropylene sutures ranging rom 8-0 to 12-0.

How is the microvascular suture selected?
T icker sutures with larger needles are indicated or larger vessels. T inner sutures with ner needles are indicated
or smaller vessels. In general, 9-0 sutures are used or vessels o 2 mm or more in diameter and 10-0 sutures are
used or vessels o 1 to 2 mm.

Describe the halving (or “0–180 degrees”) technique o microvascular anastomosis.
T e halving technique is probably the most common method o suturing end-to-end anastomoses. T e halving
technique involves placing the rst two sutures 180 degrees apart at 3 and 9 o’clock (or alternately at 6 and
12 o’clock) and adding the intervening sutures using the principle o halves (Fig. 73-1A). T e advantage o this
technique is that it makes it easy to visualize how to evenly space sutures, making it use ul when there is a vessel
size mismatch.

Describe the triangulation technique o microvascular anastomosis.
T e triangulation technique, rst described by Alexis Carrel, involves placing the rst three sutures 120 degrees
apart (Fig. 73-1B). T is technique decreases the risk o inadvertent inclusion o the opposite wall o the vessel
during subsequent sutures placement by retraction o the three initial stay sutures.

Describe the “back wall up” technique o microvascular anastomosis.
T e back wall up technique involves placing the rst suture in the middle o the back wall and progressively
suturing orward rom this point on either side (Fig. 73-1C). It is used or vessels that are especially delicate or that
cannot be rotated very much due to short length, but is technically more challenging to take even bites o both
vessels so as not to end up with a discrepancy on the ront wall.
Figure 73-1 Halving (A), triangulation (B), and “back wall up” (C) suture placement techniques or microvascular anastomosis. Numbers
indicated the order o suture placement.

In an end-to-end anastomosis, what is the maximum size discrepancy between vessels that can be
accommodated?
Between 2:1 and 3:1.

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What are some strategies or per orming an anastomosis between vessels with a size mismatch?
Other than placing sutures arther apart on the larger vessel, strategies include beveling or spatulating the smaller
vessel, partially closing or narrowing the larger vessel lumen with sutures, or using an interposition gra t that is
intermediate in diameter between the two vessels (Fig. 73-2). When the recipient vessel is larger, an end-to-side
anastomosis into the recipient vessel can be per ormed.
Figure 73-2 Strategies or dealing with a vessel size mismatch include narrowing the larger vessel with sutures, beveling the smaller vessel,
using an interposition gra t o intermediate diameter, and per orming an end-to-side anastomosis when the recipient vessel is larger.

What is “supermicrosurgery”?
Supermicrosurgery is de ned as the microsurgical anastomosis o vessels with a diameter o < 0.8 mm.

What are the indications or supermicrosurgery?
Supermicrosurgical technique is used or lymphovenous bypass in the treatment o lymphedema as well as or ree
ap trans er based on per orator level microvascular anastomoses (per orator-to-per orator anastomoses).

Under what circumstances can microvascular coupling anastomotic devices generally be used?
Coupling devices are usually used or minimally discrepant, so t, pliable venous microvascular anastomoses.

Which has superior patency rates, coupled or hand-sewn anastomoses?
T ey are similar when used appropriately.

Can coupling devices be used on arteries?
Yes, but they generally do not work well on thick-walled or inelastic, atherosclerotic vessels.

What is the maximum closing pressure o vascular clips that should be used to minimize damage to vessels?
30 g/mm2.

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What are some key points when per orming an anastomosis or preventing exposure o subendothelium and
thereby inducing platelet aggregation?
Use small needles, avoid repeated needle punctures, equal placement o sutures, avoid tying sutures too loose or
too tight, avoid use o too many sutures, which can cause endothelial slough.

How does heparin prevent coagulation?
Primarily by increasing the action o antithrombin-3, which inactivates thrombin. It also decreases platelet
adhesion and inhibits the conversion o brinogen to brin.

What risks are associated with heparin use?
In addition to bleeding and hematoma ormation, heparin can cause thrombocytopenia. Heparin-induced
thrombocytopenia is thought to be caused by antibodies to the complex ormed by heparin and platelet actor 4.

How does aspirin unction to prevent platelet aggregation?
Aspirin blocks the endothelial cyclooxygenase pathway with subsequent blockage o thromboxane A2 preventing
vasoconstriction and thrombus ormation.

Is high-dose aspirin more ef ective than low-dose aspirin to prevent platelet aggregation?
No. At low doses, aspirin selectively inhibits thromboxane A2, a platelet aggregator and vasoconstrictor. At
high doses, prostaglandin I2, a vasodilator and inhibitor o platelet aggregation are also inhibited. For example,
aspirin in doses o 81 and 325 mg has been shown to be more e ective in preventing cerebrovascular accidents,
myocardial in arction, and death a ter carotid endarterectomy than doses o 650 and 1,300 mg.

How does dextran work to prevent clotting?
Dextran is a volume expander that prevents platelet adhesion by increasing the negative electric charge o platelets,
erythrocytes, and endothelial cells, resulting in a destabilization o brin polymerization. Dextran is also an
inactivator o von Willebrand actor, a major contributor to platelet aggregation and adhesion to vessel wall
collagen.

What are some possible complications associated with the use o low–molecular-weight dextran?
Bleeding, pulmonary edema, and allergic reaction including anaphylaxis.

What is the mechanism o the no-re ow phenomenon?
Ischemia results in cellular swelling in the vascular endothelium with subsequent intravascular platelet aggregation
and leakage o intravascular uid into the interstitial space.

What pharmacologic agents can be used to rescue some ree aps in which anastomotic revision ails to
restore ap per usion or is associated with recurrent thrombosis?
T rombolytic agents such as streptokinase, urokinase, tissue plasminogen activator.

How do thrombolytic agents work?
T rombolytic agents, such as streptokinase, urokinase, and tissue plasminogen activator, unction by directly
or indirectly activating plasminogen to orm plasmin, which cleaves brin in clots as well as brinogen and
coagulation actors V, VIII, IX, XI, and XII.

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What are the risks associated with using streptokinase?
In addition to bleeding and hematoma ormation, streptokinase is antigenic and can result in an allergic response
(6% incidence) with a 0.1% incidence o anaphylactic reaction. Streptokinase can also result in a “lytic state,”
causing di use bleeding when administered in high doses. Unlike streptokinase, urokinase and tissue plasminogen
activator do not appear to be antigenic.

What is the mechanism o thrombosis in microvascular anastomosis?
Exposure o subendothelial collagen-containing sur aces to which platelets adhere eventually leading to brin
deposition, vasospasm, stenosis, and thrombosis, causing loss o blood ow.

What is Virchow’s triad?
Virchow’s triad re ers to risk actors or thrombosis and includes stasis, intimal injury, and hypercoagulability.

Besides a technical error in the microvascular anastomosis, what are other causes o ree ap vascular
thrombosis?
Causes o ree ap thrombosis include: in ection, pedicle compression, kinking, or twisting, thermal or traction
injury during ap harvest or to the recipient blood vessel, hypercoagulable disorder, and, possibly, hypotension or
vasospasm.

Can a microvascular ree ap be success ul in a hypercoagulable patient?
Yes, patients with inherited hypercoagulable disorders (thrombophilias) can success ully undergo microvascular
ree ap surgery, though probably with lower success rates and need or prophylactic anticoagulation. In one series
o 58 patients with various thrombophilias, the ree ap success rate was 80%.

Why is bipolar electrocautery pre erable to monopolar electrocautery in the control o bleeding rom or
around a recipient or donor blood vessel used in microvascular ree tissue trans er?
Bipolar cautery damages tissue, including endothelium and media, over a much more limited distance
(approximately 1–2 mm) compared to unipolar cautery.

Why is the number o sutures placed in an anastomosis critical?
oo ew sutures result in excessive bleeding and thrombus ormation; too many result in increased damage to the
endothelium and thrombus ormation.

Which anastomotic technique demonstrates greater success rates, interrupted suture placement or
continuous sutures?
In experienced hands, similar success rates are observed.

What is the Acland (vessel strip) test?
T e Acland test is used to con rm antegrade vascular ow through the venous anastomosis. wo jeweler orceps
are used to gently occlude the vessel distal to the venous anastomosis. Blood is milked out o the vessel between
the orceps by gently sliding the distal orceps along the vessel without injuring in, resulting in a segment o
collapsed vessel between the proximal and distal orceps. Releasing the proximal orceps should result in lling o
the collapsed vessel segment i the anastomosis is patent.

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Does smoking tobacco increase ree ap ailure rate?
In nondigital aps, most retrospective studies demonstrate similar (nondigital) ap survival and thrombosis rates
between smokers and nonsmokers, although smokers have a higher incidence o healing complications at the ap
inter ace and at the donor site.

What happens to vein gra ts when they are used to bridge intra-arterial gaps?
T ere is ingrowth o smooth muscle cells and creation o a neointima that results in signi cant thickening o the
vein wall. Also, gra t length decreases by 26% to 30% when used as an intra-arterial or intravenous gra t.

In addition to excellent vascular and neural anastomoses what other actor determines the success o
unctional ree skeletal muscle trans er?
Reestablishment o the correct resting tension since very small decreases in resting tension can markedly reduce the
power and amplitude o muscle contraction.

Name some commonly used donor sites or ree osseous and osseocutaneous aps.
Rib, bula, iliac crest, second metatarsal, radius, calvarium, scapula.

In what ways are vascularized bone trans ers superior to nonvascularized bone gra ts?
Vascularized bone gra ts demonstrate earlier incorporation, bone hypertrophy, mechanical strength to ailure,
osseous mass retention, and resistance to local in ection.

What techniques can be used to prolong ischemia time in limb replantation?
Cooling and AV shunting.

What are the major contraindications to replantation?
Concomitant li e-threatening injury, multiple segmental injuries to the amputated part, severe crushing or
avulsion o the tissues, extreme contamination, inhibiting systemic illness (small vessel disease, diabetes mellitus,
etc.), prior surgery or trauma to the amputated part precluding replantation.

How do leeches unction to relieve venous congestion?
By secreting hirudin, a selective thrombin inhibitor that is injected into the hosts tissue as they eed on host blood.

What pathogenic bacterium do leeches commonly transmit?
Aeromonas hydrophila.

What antibiotics should be used in the prophylaxis or treatment o bacterial in ections associated with the
use o leeches?
Cipro oxacin, tetracycline, trimethoprim-sul amethoxazole, or second- and third-generation cephalosporins.

Does the order o anastomosis and microvascular clamp removal af ect the survival o ree aps?
T ere are no signi cant di erences in ap survival based on the order o anastomosis or microvascular clamp
removal seen in an animal model, although early, transient venous congestion does develop i the artery is
anastomosed rst and the clamp on the artery is removed prior to venous anastomosis and clamp removal.

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Can loupe magni cation be sa ely used or microvascular anastomoses?
High-power loupes have been used or anastomosing vessels greater than 1 mm in diameter with success rates
comparable to those achieved using a microscope.

Can microvascular surgery be success ully per ormed in children?
Yes. A success rate o 93% has been observed in children younger than 15 years, despite smaller blood vessel size.

Can microvascular surgery be success ully per ormed in the elderly?
Yes. Age has not been ound to be an independent predictor o ap loss in several studies. However, older age
is requently associated with medical comorbidities, including cardiac and peripheral vascular disease, as well as
development o other complications related to long surgeries.

What is the role o computed tomography angiography (C A) in ree ap surgery?
C A can be used to visualize asciocutaneous and myocutaneous per orators, which can be help ul in ap design,
minimizing the incision length and allowing the surgeon to more precisely center the ap skin paddle to ensure
adequate per usion. C A may also be use ul in selecting a speci c per orator to supply blood to the ap skin
paddle, allowing the surgeon to ligate other per orators and pedicle side branches knowing that the ap will
remain well per used. C A has been most commonly used or deep in erior epigastric per orator aps, but has also
been described in anterolateral thigh and bula ree aps.
FLAPS

What is the vascular supply and classi cation o the sartorius muscle?
Super cial emoral artery and vein, type IV—segmental.

What is the vascular supply o the gastrocnemius muscle?
Sural vessels.

T e lateral arm ap is supplied by what artery?
Posterior radial collateral artery.

T e arterial pedicle to the radial orearm ap arises between what two muscles?
Brachioradialis and exor carpi radialis.

What are the indications o leech therapy?
Venous congestion.

What method o ap monitoring is most reliable?
Clinical observation.

What ap receives its motor innervation rom the obturator nerve?
Gracilis.

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What is the dominant vascular supply o the gracilis ap?
Ascending branch o the medial circum ex artery.

T e rectus emoris receives its blood supply rom what source?
Lateral circum ex emoral artery.

What organism is associated with medicinal leeches?
Aeromonas hydrophila (Gram-negative rod).

What artery provides the primary blood supply to a groin ap?
Super cial circum ex iliac artery.

T e gluteal thigh ap is supplied by what vessel?
In erior gluteal artery.

T e periosteal per orators o the peroneal artery will be ound bordering what aspect o the bula.
Posteromedial.

T e parascapular ap is based on what vessel?
Circum ex scapular artery.

Which nerve provides sensation to the lateral arm ap?
Posterior brachial cutaneous nerve (C5–6).

T e venous out ow o the reverse radial orearm ap depends on what vessel?
Radial venae comitantes.

T e bula ap is based on what vessel?
Peroneal vessels.

T e bula and radial orearm osteocutaneous ap can provide up to what length o bone?
25 and 10 cm, respectively.

What is the dominant vascular supply to the vastus lateralis muscle?
Descending branch o the lateral emoral circum ex artery.

Which muscles comprise the borders o the triangular space?
riceps (lateral), teres major (in erior border), and teres minor (superior).

What vessel traverses the triangular space?
Circum ex scapular artery.

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T e gracilis muscle is immediately posterior to what muscle?
Adductor longus muscle.

Name the three subtypes o asciocutaneous aps according to Cormack–Lamberty.
ype A: Multiple per orators
ype B: Solitary per orator
ype C: Segmental per orator

Name the three subtypes o asciocutaneous aps according to Nahai–Mathes.
ype A: Direct cutaneous per orator
ype B: Septocutaneous per orator
ype C: Musculocutaneous per orator

Describe the arc o rotation o a ap.
T e range o reach o the ap when transposed at its point o rotation (usually the vascular pedicle).

What is the vascular supply o the temporoparietal ascia ap?
Super cial temporal artery and vein.

T e saphenous artery originates rom what artery?
Genicular.

What is the secondary vascular supply o the gracilis ap?
Super cial emoral artery and vein.

T e paramedian orehead ap is based on what vessel?
Supratrochlear.

What is the source o ree radicals in the ischemic ap?
Xanthine oxidase.

What is the blood supply o the deltopectoral ap?
First, second, and third per orating branches o the internal mammary artery.

T e posterior thigh ap involves trans er o what three muscles?
Biceps emoris, semimembranosus, and semitendinosus muscles.

What are the main unctions o the gluteus maximus muscle?
Extension o the hip joint and adductor o the thigh.

T e deep in erior epigastric artery arises rom what artery?
External iliac.

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What is the dominant pedicle to the latissimus dorsi muscle?
T oracodorsal.

Where does the gluteus maximus muscle insert?
Greater trochanter o the emur.

What is the blood supply to the trapezius ap?
ransverse cervical artery.

What is an angiosome?
Composite area o tissue supplied by the same source artery.

Which gastrocnemius muscle has a longer reach?
Medial head.

What is the blood supply to the soleus muscle?
Popliteal.

T e radial orearm neurosensory ap is innervated by what nerve(s)?
Lateral and medial antebrachial cutaneous nerves.

T e great toe ap and second toe ap are based on what vessel?
First dorsal metacarpal artery and venae comitantes.

What is the blood supply o the external oblique?
Lateral cutaneous branches o the in erior eight posterior intercostal arteries.

What are the muscles that de ne the boundaries o the quadrangular (quadrilateral) space?
Long head o the triceps (medial), teres major (in erior), and teres minor (in erior), humerus (lateral).

What structures traverse the quadrangular (quadrilateral) space?
Posterior circum ex humeral vessels and axillary nerve.

Which is more lateral, the quadrangular space or the triangular space?
T e quadrangular space is more lateral (makes sense since the humerus is one o its borders).

What are the two dominant pedicles o the omental ap?
T e right and le t gastroepiploic artery and vein.

Can the anterolateral thigh ap be neurotized?
Yes, rom the lateral emoral cutaneous nerve.

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What is the origin and insertion o the gracilis muscle?
T e pubic symphysis and the medial tibial condyle.

T e orehead ap is based on what vessel?
Super cial temporal artery and vein.

T e random pattern ap is based on what blood supply?
Subdermal plexus.

What is the appropriate length-to-width design ratio o a random pattern ap?
2 to 1.5.

What is the blood supply o the nasolabial ap?
Angular artery ( rom acial artery).

What is the dominant vascular pedicle to the pectoralis major ap?
Pectoral branch o the thoracoacromial artery and venae comitantes.

What is the origin o the pectoralis major muscle?
T e medial hal o the clavicle, the anterior sur ace o the sternum, the cartilaginous portions o the upper seven
ribs, and the aponeurosis o the external oblique muscle.

T e vascular pedicle to the anterolateral thigh ap traverses what muscles?
Vastus lateralis and rectus emoris muscles.

What is the unction o the rectus emoris muscle?
Hip exion and knee extension.

What is the blood supply o the abductor digiti minimi ap?
Deep palmar artery ( rom ulnar artery) and venae comitantes.

T e reverse sural ap depends on what blood supply?
T e median super cial sural artery.

What is the origin o the tensor ascia lata ap?
Anterior 5 cm o the outer portion o the iliac crest and ASIS.

What is the blood supply o the tensor ascia lata ap?
Ascending branch o the lateral circum ex emoral artery.

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What is the course o the radial collateral artery to the lateral arm ap?
Courses through the lateral intermuscular septum between the brachialis and lateral head o the triceps muscle.

What is the innervation o the trapezius muscle?
Spinal accessory nerve (XI).
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713
Ming-Huei Cheng, MD, MBA, FACS and
Jung-Ju Huang, MD

What is the arterial source o a per orator ap?
Either septocutaneous branch or musculocutaneous branch passing through muscle to nourish the asciocutaneous
ap rom its mother vessel.

What is an angiosome?
T e angiosomes o the body are distinct vascular territories that are composed o muscle and the overlying skin and
the adipose tissues. T e angiosomes de ne the anatomical borders rom which tissues are available or composite
trans er.

How are the cutaneous vessels def ned according to their course?
T ey are de ned as septocutaneous and myocutaneous vessels. Septocutaneous vessels course either between the
tendons or muscles ollowing the intermuscular septa. Myocutaneous per orators penetrate through the muscle to
nourish the subcutaneous tissue.

What is the anatomical basis or per orator-based skin ap design and harvest?
T e size, length, direction, and connections o the cutaneous per orators provide basis o ap design. At least one
adjacent anatomical cutaneous vascular territory can be captured with sa ety when based on a particular per orator.

What is the contribution o Taylor and Daniel to the evolution o the per orator ap surgery?
T ese authors were the rst who attempted to harvest skin aps on the septocutaneous and myocutaneous
per orators that they had identi ed during their vascular anatomy studies on cadavers. T ey mapped the vascular
anatomy o the skin and identi ed an average o 374 dominant cutaneous vessels o 0.5 mm or greater in diameter,
and introduced the angiosome concept or urther per orator ap surgery.

What is a true per orator ap?
A “true” per orator ap relies on per orator vessels rom a given source vessel that must rst penetrate a muscle
be ore piercing the deep ascia to reach the skin.
Perforator Flaps
CHAPTER 74

714
Plastic & Reconstructive Surgery Board Review

What are the advantages o the per orator aps?
1. Less donor site morbidity.
2. Muscle sparing and allows thin ap harvesting.
3. Versatility in design to include as little or as much tissue as required.
4. Improved postoperative recovery o the patient.
5. Increased versatility in ap design and more economic ap application, including chimeric ap design or
harvesting more than one ap basing on the same mother vessel.

What is the def nition o a reliable per orator vessel?
T e reliable per orator is de ned as a per orator that sprouts rom the carrier muscle with a “visible” pulsation,
usually greater than 1 mm in diameter. A reliable per orator is believed to have the ability to expand its per usion
over its territory a ter the per orator ap elevation.

How are the per orator vessels identif ed?
Currently, the most practical, simple, sa e, speedy, and inexpensive method is the use o handheld Doppler
ultrasound probe. Other techniques include computed tomographic angiography, magnetic resonance imaging
angiography, and color- ow duplex scanning.

How are the axial artery and per orators discriminated with the Doppler probe?
T e axial artery has a unidirectional pulsating course whereas there is no evident pulsating sound around the
per orator.

What are the available preoperative tools to identi y the exact location o the per orators?
T e available and reliable image studies include multidetector-row helicon computed tomography angiography
and magnetic resonance imaging.

What is the most common consequence when a tiny per orator is selected?
Marginal ap necrosis beyond the territory o the per orators.

What are the requirements or an acceptable per orator ap donor site?
1. Predictable and consistent blood supply;
2. At least one large per orator with the diameter greater than 1 mm;
3. Su cient pedicle length;
4. Primary closure o the donor site with the absence o excessive wound tension.
5. Provision o similar so t-tissue volume that matches the recipient de ect
6. Donor site with well-hidden scar is more avorable

What are the most commonly used per orator aps?
Anterolateral thigh per orator ap, deep in erior epigastric per orator (DIEP) ap, super gluteal artery per orator
ap, in erior gluteal artery per orator ap, thoracodorsal per orator ap, tensor ascia lata per orator ap, medial
plantar per orator ap, deep circum ex iliac per orator ap, super cial circum ex iliac artery per orator ap,
medial sural artery per orator ap, transverse gracilis per orator ap, internal mammary artery per orator ap,
pro unda artery per orator ap, anterior obturator artery per orator ap, lumbar artery per orator ap, intercostal
artery per orator ap, and submental artery per orator ap.

CHAPTER 74 Per orator Flaps
715

What is a ree-style ree ap?
An anatomic region that is not the traditional ap territory with the appropriate size, color, and pliability is
selected, and the skin per orators in that region are mapped using a Doppler probe. Mapped per orators are
dissected toward source vessels to provide adequate vessel length and size. By applying the concept o ree-style ree
ap, small- or moderate-sized ap can be designed and harvested rom almost any part o the body as long as the
donor site appearance is acceptable to the patient.

What is the main advantage o a ree-style ree ap?
T e advantage o this concept is that it provides the surgeon an extra sense o reedom and variability when
approaching a ap harvest and choosing the recipient site. Once per orators can be identi ed, any area o the
body can serve as donor site or ap harvesting. T ere is no limitation on the ap selection and more aps can be
harvested or reconstruction, even in areas that had been used as ap donor site be ore.

What are the most common causes o the per orator thrombosis?
Stretching, twisting, drying, compression o the per orator and technical error.

What are the strategies to reexplore a thrombosed per orator ap?
1. Explore early.
2. Resect the thrombosed vessel segment and reanastomose with or without vein gra t. Vessels with damaged
intima should be resected as much as possible.
3. Open the vessels and squeeze the proximal vessel to evacuate the thrombus. T rombus can also be suctioned
out gently with smooth needle and manually applied suction orce with syringe.
4. Do not inject any solution rom the cut end since this maneuver may cause migration and plugging o
thrombus into the smaller per orators.
5. Relieve the tension rom the ap.
6. Inject ew thrombolytic agents, such as urokinase, streptokinase rom the donor artery and drain it out rom
the donor vein in an attempt o thrombolysis.
7. Systemic in usion o low-dose heparin 2,500 to −5,000 units/day.
8. I the ap remained unper used, the whole pedicle should be checked under microscope.
9. Inappropriate ap inset can cause twist o the pedicle and subsequent thrombus ormation. All the stitches can
be released to make sure the ap is inset in appropriate manner.

What are the principles in “thinning” o a per orator ap?
1. Preserve the at and the ascia within a circle o 1 cm diameter around the per orator;
2. Use loupes or microscope to per orm the procedure;
3. Per orm thinning when there is circulation in the ap, either be ore division o pedicle or a ter restoration o
blood circulation.

What is “supermicrosurgery” as a technique?
Supermicrosurgery technique involves division o the per orator ap pedicle above the deep ascia and
anastomosing small vessels that are less than 1 mm (0.5–0.7 mm) using 12-0 nylon with a greater magni cation
microscope. It allows ree trans er o aps on vessels harvested without breaching deep ascia, the so-called
“per orator-to-per orator” ree ap trans er. T e technique o supermicrosurgery has also been expanded in
lymphatic surgeries, such as lymphatico-lymphatical anastomosis or lymphaticovenous anastomosis with various
anastomosis techniques or lymphedema treatment.