Operative Technique in Plastic Surgery – Kevin C.Chung

muscle rotation flaps, posterior thigh V-Y advancement flap (hamstring
muscles may be included if nonambulatory), or gracilis musculocutaneous flap.
■ Sacral pressure injuries: Common reconstruction includes bilateral V-to-Y
gluteus advancement, gluteus maximus myocutaneous flap, and superior
gluteal artery perforator flap.8
■ Coccygeal pressure injuries can be treated with coccygectomy.
■ Trochanteric pressure injuries are typically reconstructed with tensor fascia
lata flap.
Preoperative Planning
■ Identify and address causes of the pressure injury.
■ Control comorbidities.
■ Optimize nutritional status, including serum albumin and hemoglobin.
■ Consider diverting colostomy and catheterization to minimize urinary and
fecal soiling.
■ Careful consideration of future pressure sores in planning of operative
technique
Positioning
■ The patient is positioned prone on the operating table with pressure points well
padded.
■ General anesthesia is administered.
T E C H N I Q U E S
■ Debridement
■ Completely excise injured area, bursa, scar, and all necrotic tissue.
■ Debride all nonviable bone and calcifications.
■ Bony debridement should continue until healthy bleeding bone is apparent.
■ Biopsy of underlying bone should be sent for culture and pathology.
■ Reconstruct by filling dead space with well-vascularized muscle or fascial
flaps inset without tension.
■ Pressure injury recurrence or formation in new locations should be carefully
considered in reconstructive planning.

■ Drains should be placed under the flap.
■ V-Y Advancement Flap for Ischial Pressure
Injuries
■ V-Y biceps femoris musculocutaneous advancement flap design for ischial
pressure injury (TECH FIG 1A).
■ Reconstructed ischial pressure injury with V-Y biceps femoris flap (TECH
FIG 1B).
TECH FIG 1 • A. V-Y biceps femoris
musculocutaneous advancement flap design for
ischial pressure injury. B. Reconstructed ischial
pressure injury with V-Y biceps femoris flap.
■ Gluteus Maximus Myocutaneous Flap
■ Unstageable right ischial pressure injury prior to debridement (TECH FIG
2A)
■ Following debridement, a gluteal rotation flap design is outlined (TECH
FIG 2B).
■ The defect from the pressure injury is triangulated with the apex toward the
flap pedicle.
■ Rotation flap is outlined approximately 5 times the length of the defect base.
■ Gluteal skin and muscle are incised, and the flap is elevated until it can be
mobilized into the defect (TECH FIG 2C).
■ A small back cut can be performed at the end of the rotation flap.
■ Flap should be closed in layers over suction drains (TECH FIG 2D).

TECH FIG 2 • A. Ischial defect following debridement
with gluteal rotation flap design outlined. B. Gluteal
skin and muscle are incised and the flap elevated until
it can be mobilized into the defect. C. Flap should be
closed in layers over suction drains.
■ Bilateral V-to-Y Advancement of Gluteal Muscles
■ Following debridement of sacral pressure injury, bilateral V-Y gluteal flaps
are marked extending from the edges of the debrided pressure injury at the
sacrum medially and including the entire gluteal region (TECH FIG 3A).
■ Skin incisions are performed, and the gluteus maximus muscle is identified.
■ It is detached from sacral attachments medially and iliac crest attachments
superiorly.
■ Superior and inferior gluteal vessels must be preserved.
■ The lateral and inferior aspects of the myocutaneous flap are incised and
elevated at the edges to allow for advancement.
■ Gluteus myocutaneous flaps are then advanced to the midline.
■ Closure is performed in a V-to-Y fashion (TECH FIG 3B).
■ Suction drains are placed under each flap.
■ Large absorbable sutures such as 2-0 Vicryl or PDS should be used for deep
tissue approximation.
■ Deep dermal and subcuticular layers should then be closed.

TECH FIG 3 • A. Bilateral V-Y gluteal myocutaneous
flaps extend from the edges of the sacral pressure
injury at the sacrum medially and include the entire
gluteal region. B. Closure is performed in a V-to-Y
fashion.
PEARLS AND PITFALLS
General
■ Ensure the underlying etiology of the pressure injury is
corrected prior to surgical reconstruction.
■ Comorbidities, nutritional deficiencies, fecal/urinary
contamination, infection/osteomyelitis, and postoperative
pressure relief plan must be addressed prior to reconstruction.
■ Plan flap reconstruction accounting for possible recurrence of
the pressure injury and new pressure injury.
Debridement
■ Adequate debridement for the pressure injury is critical to a
successful outcome.

■ Complete excision of the bursa as well as any nonviable tissue
is essential.
■ Failure to adequately debride bone or bursa may lead to failure
of the reconstruction.
■ Consider staging the reconstruction if there are uncertainties
regarding infection or tissue/bone viability.
Ischial, sacral,
trochanteric
pressure
injuries
■ Ambulatory status of the patient must be determined if
considering use of gluteal or hamstring muscles in flap
reconstruction.
■ Gluteal rotation, posterior thigh, and TFL flaps must be
designed with adequate dimensions to fill the defect.
■ Ensure the vascular pedicle is preserved in design and
dissection of flap.
■ Ensure the flap is not inset under tension.
■ Do not excise dog ears or extra tissue.
■ Always close flaps over a drain.
POSTOPERATIVE CARE
■ Patients should be non–weight bearing on the operative site for up to 6 weeks
postoperatively.
■ Prone or lateral decubitus positioning should be maintained to avoid pressure
on the site.
■ Pressure relief adjuncts such as low air loss beds should be used to prevent
development of additional pressure injuries.
■ Nutrition status should be closely monitored in the postoperative period to
promote good wound healing.
■ After wounds are healed, sitting protocols should be used to gradually increase
the amount of time spent sitting.
■ Pressure relief should be performed every 15 minutes when in the seated
position.9
OUTCOMES
■ Pressure injuries represent a major burden of illness, affecting the quality of
life of patients and their families.10
■ For patients at high risk for pressure injuries, it is critical that pressure relief
measures—such as specialized support surfaces, frequent repositioning, and
efforts to minimize shear, moisture, and spasticity—are adhered to.
■ Optimizing nutrition and limiting medical comorbidities are also essential in

avoiding a high likelihood of recurrence.
■ High-risk patients should be followed regularly by a physiatrist for evaluation
and care.
■ Education on prevention and treatment of pressure injuries is critical to
successful outcomes.
COMPLICATIONS
■ Hematoma
■ Seroma—important to maintain suction drain beneath reconstruction until
minimal output
■ Wound dehiscence—if small, may heal with local wound care and offloading
pressure
■ Wound infection
■ Recurrence is high if patients who are noncompliant or do not have medical
management optimized preoperatively are at high risk of postoperative
recurrence.
REFERENCES
1. Okamoto GA, Lamers JV, Shurtleff DB. Skin breakdown in patients with
myelomeningocele. Arch Phys Med Rehabil. 1983;64(1):20-23.
2. Crenshaw RP, Vistnes LM. A decade of pressure sore research: 1977-1987. J
Rehabil Res Dev. 1989;26:63.
3. Enis J, Sarmiento A. The pathophysiology and management of pressure sores.
Orthop Rev. 1973;2:26.
4. Maklebust J. Pressure ulcers: etiology and prevention. Nurs Clin North Am.
1987;22:359.
5. Bouten CV, Oomens CW, Baaijens FP, Bader DL. The etiology of pressure
ulcers: skin deep or muscle bound? Arch Phys Med Rehabil. 2003;84:616.
6. Pallija G, Mondozzi M, Webb AA. Skin care of the pediatric patient. J Pediatr
Nurs. 1999;14(2):80-87.
7. Edberg EL, Cerny K, Stauffer ES. Prevention and treatment of pressure sores.
Phys Ther. 1973;53:246.
8. National Pressure Ulcer Advisory Panel (NPUAP). NPUAP Pressure injury
stages. NPUAP website.
clinical-resources/npuap-pressure-injury-stages/. Published April 13, 2016;
accessed October 18, 2017.
9. Kierney PC, Engrav LH, Isik FF, et al. Results of 268 pressure sores in 158

patients managed jointly by plastic surgery and rehabilitation medicine. Plast
Reconstr Surg. 1998;102:765.
10. Franks PJ, Morfatt CJ. Focus on wound management: quality of life issue in
chronic wound management. Br J Community Nurs. 1999;4(6):283-284.

29
CHAPTERPressure Injuries
Lawrence J. Gottlieb and Maureen Beederman
DEFINITION
■ A pressure injury is a soft tissue injury due to the complex interplay of tissue
deformation, stress, strain and ischemia from unrelieved pressure, shear, and
friction typically overlying bony prominence.1
■ The standard for classifying pressure injuries is based on the four grades
originally described by Shea in 1975.2
■ Grades I and II have potentially reversible acute inflammatory reactions
involving all soft tissue layers; grade III has full-thickness tissue loss,
extending to fascia; and grade IV extends through the deep fascia to bone.
■ Skin loss in grades I and II is thought to be more likely due to shear, friction,
and maceration rather than pressure per se.
■ Over time, refinements have been made to this classification with the most
recent being a six-stage classification by The National Pressure Ulcer Advisory
Panel during their 2016 Staging Consensus Conference.3
ANATOMY
■ Pressure injuries typically occur over bony prominences and are dependent on
patient positioning.
■ Supine: greatest pressure overlying heels, sacrum, occiput, and scapula
■ Sitting: greatest pressure at ischial tuberosities, elbows
■ Lateral decubitus: greatest pressure over greater trochanters (often
accompanied by hip flexion contractures), fibular head, and malleoli
■ Pressure injuries also occur due to inadvertent pressure from external objects
pressing on the skin (ie, IV connectors, side rail of bed pressing on the skin or
small object in shoe of the patient with neuropathy) or securing devices too

tight (ie, nasal tubes, CPAP devices).
■ Extrusion of internal objects (ie, hardware or internal prosthetic or tubing) is
generally caused by the same pathophysiology of classic pressure injuries over
bony prominences.
PATHOGENESIS
■ Unrelieved pressure
■ External pressure greater than capillary pressure leads to decreased blood
flow and tissue ischemia, eventually causing tissue necrosis.
■ Pounds-per-square-inch pressure highest in thin patients over bony
prominences. Obese patients are able to distribute pressure better.4
■ Reperfusion injury
■ Tissue loss after restoration of blood flow and generation of oxygen free
radicals after relief of pressure
■ Deformation injury of cells
■ Local cell damage and death
■ Tissue breakdown may also occur due to
■ Friction
■ Shearing forces
■ Moisture/maceration
■ Tissue breakdown is more likely with circulatory disturbances.
■ The presence of infection and edema can influence the wound environment
and ultimately the extent of necrosis.
NATURAL HISTORY
■ Pressure injuries are “inside-out” injuries caused by soft tissue damage from
unrelieved pressure on the skin, typically overlying bony prominences.
■ Tissues most sensitive to pressure die first.
■ Nerve and muscle are the most sensitive to ischemia from pressure, which is
why there is no muscle or major nerves between the skin and bony
prominences in any area of the body.
■ Subcutaneous fat dies first in the typical pressure injury occurring over bony
prominences.
■ Skin is one of the most resistant tissues to pressure. The earliest changes seen
in the skin (ie, swelling and erythema of stage 1 pressure injuries) generally
reflect injury to the tissues beneath.
■ Skin breakdown without underlying tissue loss (stage II) is generally due to

shearing, friction, and maceration and not pressure per se.
■ The tissue type most resistant to pressure is fascia, which has very low
metabolic demands.
■ “Iceberg effect”: by the time that there is any evidence of pressure injury in the
skin, there is significant tissue destruction beneath; the skin findings are only
the “tip of the iceberg.”
■ Although pressure injuries are typical in debilitated, immobile, and/or
insensate patients, they are not inevitable and indeed should be preventable in
most situations.
■ Prevention is directly related to educating and motivating patients and or
caregivers in
■ Recognizing risks in various situations
■ Pressure-relief training
• Relieving pressure every 15 minutes when seated or for 5 minutes every 2
hours when in decubitus position will generally prevent pressure injuries.
■ Providing resources (eg, cushions for seats)
■ Compliance
■ Change in caregivers and/or intermittent psychological disturbance (such as
depression) correlate with pressure injury development and recurrence.
■ Evaluation and coordination with a rehabilitative team preoperatively leads to
the least incidence of recidivism.5,6
PATIENT HISTORY AND PHYSICAL FINDINGS
■ Patients at risk
■ Patients with diminished mobility
• Paralyzed patients
• Spinal cord injury, disease, or dysfunction
• Patients under anesthesia or deep sedation during surgery or undergoing
procedure or treatment requiring prolonged immobilization (eg, ECMO)
• Patients requiring others to move them
• Patients with quadriplegia
• Patients who are debilitated due to cerebral dysfunction (stroke,
intoxication, infection)
■ Debilitated patients in acute care and long-term care facilities
■ Patients with diminished sensation
• Spinal cord injury, disease, or dysfunction

• Peripheral neuropathy
■ Assess for muscle spasticity, which increases the risk of shearing forces and
friction and postoperative healing issues if not controlled.
■ Assess for joint contractures, which make avoiding pressure on bony
prominences very difficult for health care providers.
■ Assess for tunneling and pseudobursa formation.
■ Assess for involvement of joint spaces and other adjacent structures.
■ Assess for bone exposure.
■ Assess for infection: soft tissue and bone.
■ Assess for urinary tract infections, in patients with spinal cord dysfunction.
■ Assess patient and caregiver knowledge, home resources, likelihood of being
compliant, and potential social/psychological issues, all of which can affect
incidence of recurrence.
IMAGING
■ X-rays are helpful for assessment of osteoporosis, fractures, and heterotopic
ossification.
■ Radionuclide bone scans are helpful in assessing activity of heterotopic
ossification.
■ MRI is the best diagnostic imaging to evaluate for acute osteomyelitis;
however, bone biopsy remains gold standard for the diagnosis of osteomyelitis.
■ CT scan or MRI and sinograms are helpful to evaluate for sinus tracts, fluid
collections, and tunneling in the pelvis or possible involvement of rectum.
NONOPERATIVE MANAGEMENT
■ Nonoperative management of pressure injuries is appropriate in patients who
■ Are prohibitive surgical risk due to comorbidities
■ Demonstrate that they would not be compliant with postoperative regimens
■ Need to be prepared for possible operative management in the future
■ Optimize nutrition (sufficient protein, vitamins/minerals).
■ Monitor prealbumin levels.
■ Check vitamin D levels.
■ Promote optimization of general medical care.
■ Evaluate cardiovascular, pulmonary, and genitourinary systems.
■ Promote smoking, alcohol, and drug cessation.
■ Promote treatment of depression.

■ Optimize wound conditions.
■ Quantitative bacteriologic assessment of wound with wound tissue biopsy
■ Pathologic assessment of long-standing (more than 5 years) wounds with
wound tissue biopsy
■ Offloading/frequent turning for pressure relief
• Air mattresses/cushioning
■ Provide patient and caregiver education.
■ Prevent spasticity.
■ Medical management: baclofen, dantrolene, diazepam, botulinum toxin
■ Surgical management: rhizotomy, baclofen pump, peripheral nerve blocks
■ Infection control
■ Assess colonization vs infection of wound using quantitative cultures.
• If quantitative culture shows greater than 105 organisms per gram, use a
topical antimicrobial (eg, silver sulfadiazine, mafenide acetate, dilute
hypochlorite solution).
• If unable to control bacteria with topical, it may need surgical debridement.
■ Systemic antibiotics used for treatment of cellulitis, osteomyelitis, or joint
space infections as well as for any distant infection of genitourinary or
respiratory tracts
• If repeat quantitative culture shows greater than 105 organisms per gram,
consider additional debridement and/or change in topical antibiotic
treatment prior to definitive closure.
SURGICAL MANAGEMENT
■ All patients are candidates for surgical debridement, but not all patients are
candidates for surgical closure.
■ Candidates for closure should demonstrate (along with their caregivers) an
understanding, commitment, and motivation to prevent future injuries.
■ In addition, they must demonstrate compliance with nonoperative
management (including nutrition, pressure relief, and wound care) and have
the necessary resources available prior to definitive surgical closure.
■ Evidence of improvement of wounds with nonoperative management is a
good indicator that patient/family are motivated, have the appropriate
resources, and will likely abide by postoperative protocols.
■ Surgical options for pediatric patients and adult patients are similar.
■ Consider whether child (or adult) has the potential to become ambulatory in

the future when deciding best reconstructive option.
■ Optimize nutrition, minimize muscle spasms, and obtain bacteriologic balance
in the wound prior to definitive surgical closure.
■ Ensure that adequate debridement is performed prior to definitive closure.
Preoperative Planning
■ Preoperative evaluation and coordinating with the multidisciplinary
rehabilitative team that will care for patient postoperatively has been shown to
minimize recurrence.5,6
■ Assess location, size, and depth of wound.
■ Is there a pseudobursa that needs resection?
■ Is there a bony prominence that needs to be flattened?
■ Is their evidence of osteomyelitis?
• Does it need to be resected?
■ Is there heterotopic ossification?
• Does it need to be resected?
■ Review previous surgical interventions and incisions.
■ Consider ambulatory status of the patient.
■ Plan closure with skin graft or flap depending on location of wound and goal.
■ If the wound is amenable to closure with a graft, is it the best technique to
use or would a flap give a better result?7
■ If a flap is chosen; determine whether it should be a muscle,
musculocutaneous, fasciocutaneous, cutaneous, or perforator flap.
■ Plan obliteration of anticipated dead space.
■ Plan flaps with the understanding that recurrence of pressure injuries is
frequent and the ability to reuse a flap is frequently helpful.
Positioning
■ Need to ensure that all bony prominences and pressure points are protected
and padded to avoid creating new pressure injuries during surgery.
■ Posterior wounds are generally best positioned prone but may be put in lateral
decubitus position if needed.
■ Airway needs to be secured well.
■ The hips should be flexed for insetting of thigh-based flaps.
■ Ischial injuries may be addressed in lithotomy position.

Approach
■ Adequate debridement includes removal of the pseudobursa and all necrotic,
devitalized, and infected tissue as well as removal of all scars if possible.
■ Preliminary bedside debridement can be helpful to obtain tissue cultures and
decrease the wound burden of nonviable tissue.
■ Long-standing (greater than 5 years) wounds should be biopsied to rule out
Marjolin ulcer.
■ Bedside debridement is rarely adequate because of inability to remove all dead
tissue without too much bleeding or pain in patients with sensation.
■ The use of methylene blue dye during operative debridement will assist in
removing pseudobursa and ensuring all surface tissue is removed, especially in
irregular wounds with tracts and tunneling.
■ Bony prominences should be flattened.
■ All nonbleeding infected bone should be removed.
■ Pre- and postdebridement tissue cultures should be obtained of soft tissue and
bone.
■ Many patients require more than one operative debridement to optimize the
wound or allow for optimization of a systemic condition prior to definitive
surgical closure.
■ Once a wound is adequately debrided, determine if the next goal is to close the
wound or to reconstruct the part.
T E C H N I Q U E S
■ Closure should be preceded by adequate debridement.
■ The techniques below describe typical debridement techniques and examples
of closure or reconstructive options utilizing standard principles and
concepts.
■ Surgical Debridement
■ Paint the wound (and/or inject sinuses) with methylene blue dye to stain the
pseudobursa, granulation tissue, and other surface tissue to ensure complete
removal (TECH FIG 1A,B).
■ This is particularly important in irregular wounds with tracts and tunneling.
■ An incision should be made through normal skin circumferentially around

the wound (TECH FIG 1C).
■ Incision should be carried down through normal subcutaneous tissue,
beneath all blue-stained as well as indurated tissue and scar converging on
any bony prominences if present.
■ Wounds that have bony prominences such as ischial and trochanteric
pressure injuries should have these prominences flattened, typically with an
osteotome.
■ Pre- and postdebridement samples of soft tissue and bone should be sent for
quantitative bacteriologic assessment.
■ Postdebridement bone biopsy samples should be sent for pathologic
assessment to rule out osteomyelitis.
■ The entire debrided wound should be sent for pathologic assessment,
especially in long-standing chronic ulcers (TECH FIG 1D).
TECH FIG 1 • Debridement. A. Sacral and
trochanteric pressure injuries after bedside

debridement. B. After application of methylene blue to
help guide debridement. C. Immediately after
excisional debridement of sacral and trochanteric
pressure injuries. D. Five weeks later after nutritional
repletion.
■ Sacral Pressure Sore Closure
■ Sharp surgical redebridement into normal tissue as described above.
■ Determine location of perforator vessels with handheld Doppler.
■ Large left-sided inferiorly based rotation perforator flap is designed (TECH
FIG 2A).
■ Incisions are made and the flap is elevated above the muscle to large medial
perforator (TECH FIG 2B,C).
■ Skin overlying the left gluteal muscle rotated clockwise to close most of the
wound and contralateral skin overlying the right inferior gluteal muscle
rotated to close the rest without tension (TECH FIG 2D).

TECH FIG 2 • Sacral and trochanteric pressure
injuries. A. Design of the left superior gluteal
perforator fasciocutaneous rotation flap. B. Flap
elevated. Arrow points to perforator. C. Design of the
right inferior gluteal myocutaneous flap. D. Sacral and
right trochanteric pressure injuries closed. Arrows
demonstrate direction of skin rotation.
■ Ischial Pressure Sore Closure
■ Sharp surgical debridement into normal tissue as described above.
■ Previously used left posterior thigh flap, based on the descending branch of
the inferior gluteal artery, was re-elevated and transposed, and along with a
gluteal perforator rotation flap, the left ischial pressure sore was able to be
closed.
■ Right ischial pressure sore closed with a crescent VY inferior gluteal

myocutaneous flap with distal muscle extension to be “tucked” underneath to
fill dead space (TECH FIG 3).

TECH FIG 3 • Bilateral ischial pressure injuries. A. Left
side recurrent, note design of previous posterior thigh
flap. B. After debridement. C. Design of right ischial
closure with inferior gluteal myocutaneous flap with
the skin designed to be moved as a V-Y and muscle
extension to be folded under to fill dead space. D.
Inferior gluteal muscle before it is folded under to fill

dead space. E. V-Y closure of cutaneous portion of
flap. F. Six-month follow-up of left ischial closure by
transposing previous posterior thigh flap and right with
inferior gluteal myocutaneous flap.
■ Medial Inframalleolar Perforator Flap
■ After determining location of perforator vessels and direction of venous
flow, the flap can be designed with the anticipated pivot point centered over
perforator vessels.
■ Incision is made and carried down through the subcutaneous tissue.
■ The flap is elevated toward the perforator.
■ Transposition of flap is less than 90 degrees, so the perforator vessels do
not need to be skeletonized.
■ The flap is transposed and inset.
■ Donor site is closed with a split-thickness skin graft (TECH FIG 4).

TECH FIG 4 • Pressure injury of left medial heel. A.
Initial eschar. B. After debridement. C. Design of
medial inferior malleolar perforator flap. D. Elevation
of flap (arrow points to perforator). E. Flap transposed
and donor site closed with a skin graft. F. Stable
closure demonstrated 6 months later.

■ Skin graft
■ Flaps are not required for all wounds.
■ A well-vascularized wound bed may be closed with skin grafts or allowed to
close by secondary intention (TECH FIG 5).
TECH FIG 5 • A. Right lateral malleolus and heel
pressure injuries. B. After debridement C. Five weeks
after wound care and nutritional repletion wound
closed with a skin graft. D. Six months stable
coverage of malleolus. Heel closed by secondary
intention.
■ Propeller flap

■ After debridement as described above make an incision to verify location of
the perforator.
■ Elevate the flap and skeletonize the perforator.
■ Turned 180 degrees and flap inset (TECH FIG 6).
TECH FIG 6 • A. Left elbow pressure sore. B. After
debridement and incision to verify location of

perforator. C. Propeller flap elevated. D. Propeller flap
turned 180 degrees. E. Flap inset. F. Stable closure
demonstrated 6 months later.
PEARLS AND PITFALLS
Debridement
■ All patients are candidates for surgical debridement, but not all
patients are candidates for surgical closure.
■ Wide local debridement prior to definitive surgical closure is
necessary for successful pressure ulcer coverage.
Methylene
blue
■ Paint wound and inject sinuses to help facilitate adequate
debridement.
Infection
■ Obtain bacteriologic balance prior to definitive closure.
■ Assess soft tissue and bone by tissue biopsy cultures.
Flaps
■ Flaps should be well vascularized, inset without tension, and able to
obliterate dead space.
■ Do not burn bridges with closure options; consider flaps that can be
reused if recurrence occurs.
Skin grafts
■ Skin grafts tolerate pressure but do not tolerate shear forces well.
POSTOPERATIVE CARE
■ Use perioperative antibiotics only, unless postdebridement cultures are
positive.
■ Closed suction drains should be used to help obliterate dead space, improve
tissue apposition, and minimize fluid collections.
■ Patients should be nursed on a specialized mattress, air fluidized bed, or in
prone position for 3 to 6 weeks postoperative.
■ Gradually progress advancement of activity.
■ Control/prevent spasticity.
■ Continue optimization of nutritional support.
OUTCOMES
■ Despite optimization, recurrence rate is high for many patients.

■ Minimize recurrence by working with multidisciplinary rehabilitative team
preoperatively and postoperatively.4,5
COMPLICATIONS
■ Acute wound breakdown is generally related to poor surgical planning, with
either ischemic flap edges or excess tension on suture lines or a complication
such as hematoma.
■ Hematomas are thought to be more common in patients with spinal cord
injury due to loss of sympathetic vascular tone and inability to vasoconstrict
blood vessels.
■ Subacute recurrence (wound breakdown) is generally related to failure to
obliterate dead space with fluid collection, which may subsequently get
infected.
■ Delayed recurrence is generally related to inadequate compliance with
pressure preventing protocol.
REFERENCES
1. Olesen CG, de Zee M, Rasmussen J. Missing links in pressure ulcer research
—an interdisciplinary overview. J Appl Physiol. 2010;108:1458-1464.
2. Shea JD. Pressure sores: classification and management. Clin Orthop Relat
Res. 1975;(112):89-100.
3.
pressure-injury-stages/
4. Lindon O, Greenway RM, Piazza JM. Pressure distribution on the surface of
the human body. I. Evaluation in lying and sitting positions using a “Bed of
Springs and Nails”. Arch Phys Med Rehabil. 1965;46:378-396.
5. Singh DJ, Bartlett SP, Low DW, Kirschner RE. Surgical reconstruction of
pediatric pressure sores: long-term outcome. Plast Reconstr Surg.
2002;109(1):265-269.
6. Kierney PC, Engrav LH, Isik FF, et al. Results of 268 pressure sores in 158
patients managed jointly by plastic surgery and rehabilitation medicine. Plast
Reconstr Surg. 1998;102:765.
7. Gottlieb LJ, Krieger LM. Editorial: From the reconstructive ladder to the
reconstructive elevator. Plast Reconstr Surg. 1994;93(7): 1503-1504.

30
CHAPTERVascular Lesions
Benjamin C. Garden and Jerome M. Garden
DEFINITION
■ Vascular lesions can be classified into two main categories: proliferative and
malformations.1
■ Vascular proliferative lesions are characterized by a proliferation of blood
vessels.
■ Infantile hemangiomas are the most common form of vascular proliferative
lesions.
■ Other vascular proliferative lesions include kaposiform
hemangioendotheliomas, tufted angiomas, and pyogenic granulomas.
■ Vascular malformations are characterized by vessels with abnormal structure
and normal endothelial cell turnover. Types of malformations include capillary,
venous, lymphatic, arterial, and arteriovenous malformations (AVMs).
■ Capillary malformations include nevus simplex (salmon patch) and nevus
flammeus (port-wine stain, PWS).
■ Venous malformations (VM) are a fairly common slow-flow type of vascular
malformation present at birth. Various names used to describe these lesions
include venous angioma and cavernous angioma.
■ Lymphatic malformations (LM) are composed of interconnected lymphatic
channels.2
• Older terminologies used include cavernous lymphangioma, lymphangioma
circumscriptum, and cystic hygroma.
• LM can be further differentiated into macrocystic and microcystic
depending on the size of the involved channels.
■ AVMs are rare vascular malformations consisting of both arterial and venous

components with AV shunting.2
ANATOMY
■ Vascular lesions may occur on any cutaneous surface but are most commonly
found on the head and neck.
■ Hemangiomas have been noted to have a nonrandom distribution, with the
majority of lesions occurring on the central face at sites of development
fusion.3
■ Capillary malformations are often, but not always, unilateral.
PATHOGENESIS
■ Hemangiomas are thought to occur due to a first-trimester developmental error
regarding angiogenesis or a result of embolized placental cells. There is a
suggested autosomal dominance inheritance.4
■ Although their exact cause is unknown, PWSs evolve due to a progressive
ectasia of the superficial vascular plexus. This progression is likely due to an
abnormal neural regulation of blood flow. PWSs have significantly less nerve
density and a higher vessel to nerve ratio.4
NATURAL HISTORY
■ Infantile hemangiomas become evident in the first weeks of life and exhibit a
proliferative phase, with continued growth, until around 8 to 12 months. This is
followed by a plateau phase, followed by a period of spontaneous regression as
the lesion involutes.
■ Initial involution is usually noted with a color change from the original bright
red to dull red or gray.
• It is estimated that completed involution occurs at a rate of 10% per year,
such that 30% have involuted by 3 years of age, 50% by 5 years of age, and
greater than 90% by 9 to 10 years of age.3
• These lesions occasionally have residual changes, including telangiectasias,
atrophy, scarring, or fibrofatty material.
■ Ulcerations occur in 5% to 13% of infantile hemangiomas.
• Most frequent locations include the lip, perineum, and intertriginous areas.
• Ulcerations are painful, increase the risk of infection, and can cause scarring
and textural changes.3
■ Vascular malformations tend to be present at birth and persist for a lifetime.
■ PWS may darken progressively over many years, and occasional lesions

develop secondary vascular blebs on their surface. They may also become
hypertrophic later in life.
■ VMs are present at birth but may not become obvious until later in life.
Occasionally, a patient first notices the lesion after trauma to the overlying
area. In those cases, the trauma may cause the underlying vessels to
temporally enlarge allowing the patient to notice it for the first time.
PATIENT HISTORY AND PHYSICAL FINDINGS
■ The preoperative evaluation for patients with vascular lesions includes a
detailed history and exam to determine the type of lesions and to assess the
risks of the patient having any associated complications or syndromes.
■ Infantile hemangiomas may occur as superficial, deep, or mixed lesions.
■ Superficial lesions tend to appear as bright red nodules or plaques (FIG 1A).
FIG 1 • A. Superficial infantile hemangioma. B. Port-
wine stain. C. Venous malformation. D. Mixed
microcystic lymphatic and venous malformation.
■ Deep hemangiomas are subcutaneous nodules, and usually present with an
overlying blue hue, venous network, or telangiectatic vessels.

■ Hemangiomas in certain locations may suggest a higher probability of
complications or associated findings.3
■ With periorbital hemangiomas, an ophthalmologic examination is generally
recommended in many cases.
■ Larger lesions of the beard area require evaluation for potential airway
obstructions.
■ Hemangiomas on the tip of the nose, the lip, and the parotid areas can have
very slow involution periods.
■ PWSs are normally easy to recognize with their well-defined red macular
stains (FIG 1B). They do not proliferate, but will grow proportional to the
child’s growth. Patients with PWS should be assessed for any associated
syndromes that would necessitate additional referrals.
■ The most common syndrome is Sturge-Weber syndrome (SWS), which most
commonly occurs with a PWS occurring in the distribution of the ophthalmic
branch of the trigeminal nerve (V1).
■ PWS can be associated with many other syndromes including Klippel-
Trenaunay, Parkes-Weber, Proteus, Cobb, Rubinstein-Taybi, and Beckwith-
Wiedemann syndrome.
■ VMs usually present as blue to purple nodules in the skin (FIG 1C). They may
have prominent surrounding veins and calcified phleboliths within the lesion.
These lesions may expand with dependent drainage of venous blood; this may
be elicited by placing the patient in the Trendelenburg position or by
performing the Valsalva maneuver.2
■ Most VM are asymptomatic, although they may occasionally become painful
in association with their gradual enlargement and pressure on surrounding
structures.
■ They may be found in association with syndromes, including Maffucci and
blue rubber bleb nevus syndrome.
■ Macrocystic LMs, sometimes referred to as cystic hygromas, present as large,
translucent masses under normal-appearing skin. Microcystic LM usually
present as erythematous to flesh-colored papules, which may be somewhat
translucent, and have traditionally been compared to the appearance of frog
spawn (FIG 1D).
■ AVMs may be clinically pulsatile and warm and have a thrill. They present as
a vascular stain at birth, with increasing erythema and size with age. They can
spontaneously bleed.

IMAGING
■ One should strongly consider doing a liver MRI in those patients having five
or more hemangiomas due to the increased potential of having visceral
lesions.3
■ Large segmental facial hemangiomas should prompt imaging to assess
possible PHACES syndrome:
■ Posterior fossa malformations
■ Hemangiomas
■ Arterial anomalies
■ Coarctation of the aorta
■ Eye abnormalities
■ Sternal or supraumbilical raphe
■ Perineal hemangiomas should prompt evaluation for PELVIS syndrome:
■ Perineal hemangiomas
■ External genital malformations
■ Lipomyelomeningocele
■ Vesicorenal abnormalities
■ Imperforate anus
■ Skin tags
■ In patients with a PWS, imaging may be necessary if there is concern for a
related syndrome, such as SWS. MRI is the preferred screening modality of
SWS. Patients with a vascular malformation located in the midline lumbar
location may have an underlying AVM, as seen in Cobb syndrome, which
would be imaged by an MRI.
■ VM can be confirmed or the depth of involvement can be ascertained with
MRI with and without contrast.
NONOPERATIVE MANAGEMENT
■ Generally, appropriate treatment for infantile hemangiomas is
nonintervention.5 However, in those lesions where there is high visibility,
social concern or functional impairment, as well as complications such as
ulceration, infection or bleeding, therapy may be warranted.4,6
■ Topical timolol can be useful in the treatment of superficial hemangiomas.
■ Treatment using oral propranolol may be indicated for functional impairment,
significant ulceration, or lesions with potential for significant disfigurement.
■ Topical wound care is also necessary for ulcerated lesions.

SURGICAL MANAGEMENT
■ Lasers are designed to deliver energy precisely into the target chromophore
with minimal damage to surrounding tissue.
■ To keep the laser from causing widespread damage to other tissues, the laser
exposure should occur faster than the amount of time it takes for the heat to
extend significantly beyond the target.
■ Safe and effective heating occurs using a pulse duration equal to or less than
the target’s thermal relaxation time (TRT). TRT is the amount of time for the
tissue to lose half the heat gained from the laser.
• For PWS, the target venules have a TRT of tens of milliseconds.4
■ Surgical intervention with lasers for hemangiomas should be used cautiously
but can be very helpful, especially for lesions in areas of high visibility or areas
of high risk for ulcerations, such as the anogenital area.
■ Laser treatment of ulcerated hemangiomas can lead to decrease in pain and
more rapid healing. However, care must be taken because aggressive laser
treatment can occasionally induce ulcerations.
■ Lasers can also be used for the treatment of involuted lesions with residual
telangiectasis or residual dermal vascular involvement.7
■ Lasers can be used successfully in conjunction with propranolol.8
■ Excisional surgery of hemangiomas can lead to a more unsatisfactory result
than an untreated lesion, and therefore, the risks and merits of surgical
intervention should be discussed with the family and surgical removal
performed on a case-by-case basis.
■ PWS should be treated with laser surgery as early as possible with the natural
evolution of these lesions to become more hypertrophic over time.
Additionally, children younger than 1 year seem to have the most effective
lightening and require fewer treatments than older patients.4
■ One should note that laser surgery can be helpful in treating PWS, but some
PWSs can partially recur over an extended period of time with aging.
■ PWS lesions on the periorbital region, midforehead, lateral cheeks, chest and
proximal arms respond best to treatment, whereas the other areas are more
resistent.6
■ The superficial components of VMs may be treated with laser therapy.
However, more extensive malformations may be treated via sclerotherapy prior
to eventual surgical excision.2
■ Carbon dioxide lasers used in a nonfractional mode can be used to treat the

superficial blebs of lymphatic lesions, vaporizing the tissue nonselectively and
sealing the lymphatic channels.
■ Embolization and surgical resection are the mainstay of treatment of AVMs.
Preoperative Planning
■ A pretreatment consultation is advisable to discuss potential lesional response,
number of treatments, expected and potential adverse effects, and aftercare.
■ Visual examination of lesion and of patient skin type assists in planning of
laser treatment. Optimal coherence tomography, three-dimensional
photography, and reflectance spectrophotometry are newer technologies that
are being evaluated to assist in objective quantification of preprocedure and
postprocedure lesional depth, volume, and color.9
■ Patients should be advised to practice strict sun protection for at least 4 to 8
weeks prior to treatment. Treatment of a patient with a tan can result in
permanent hypopigmentation.
■ Patients with darker skin are at risk for hypopigmentation and
hyperpigmentation.
■ An assessment of the child’s ability to tolerate treatment should be made prior
to choosing an anesthesia option. Options include topical, intralesional, and
general anesthesia.
■ Although topical anesthetics such as topical liposomal lidocaine and a
eutectic mixture of local anesthetics (EMLA cream, 2.5% lidocaine/2.5%
prilocaine) have been used, topical anesthetics may cause significant
blanching of the vascular lesions, making them more difficult to be effectively
treated with the laser, as there is less hemoglobin to act as a target
chromophore.
• Special care should be used with prilocaine in infants as it is associated with
an increased risk of methemoglobinemia.
■ Most infants less than 1 year of age are restrained and treated without general
anesthesia.
■ General anesthesia is appropriate in older children. However, general
anesthesia also may be associated with blanching of the lesion. Care should
be taken to limit the use of the general anesthetic to as low a dose as safely
possible to reduce blanching.6,9
■ Photographs should always be taken before the initial treatment. Photographs
before subsequent treatment sessions to the same area are at the discretion of

the clinician.
■ Flammability is a risk when using lasers. Water or clear non–alcohol-based
viscous lubricants can be used to diminish singeing terminal hairs.
Positioning
■ The patient should be placed in a position that allows the clinician to
manipulate the laser handpiece without difficulty.
■ Infants and young children, who will be undergoing the treatment without
general anesthesia, are recommended to be held and restrained with a bear hug
by a parent or assistant. Placing an infant in a papoose may be of help in
addition to immobilization by an assistant.
FIG 2 • A. Overlapping white gauze held with a firm
hand should be used to cover the periorbital area in
young children in whom the protective eye glasses
would be too large. B. Globe eye shields should be
used when lasering close to the orbit. Note the
postoperative purpura from the pulsed dye laser.
■ Everyone present must use appropriate eye protection during laser treatment.

■ Most glasses and goggles may be too large for small children.
■ Overlapping white gauze held with a firm hand should be used to cover the
periorbital area, as these will reflect laser light (FIG 2A). The gauze should
be moistened with water if used with general anesthesia. Pressure should be
placed on the orbital rim and not on the eye itself.
■ Globe eye shields must be used if lasering close to the eye (FIG 2B).
Approach
■ The most commonly used laser for superficial or ulcerated hemangiomas is the
pulsed dye laser (PDL). Suggested settings are dependent on the various
chosen parameters and may include wavelengths of 585 to 595 nm, fluences of
4 to 8.5 J/cm2, pulse durations between 0.45 to 3 ms, spot sizes of 5 to 10 mm,
and a concomitant cooling device.
■ Deeper parts of the lesion can respond to long-pulsed Nd-YAG or alexandrite
lasers, although there is a higher risk of scarring and pigmentary
complications.
■ The PDL is the most commonly used laser for PWS treatment. General
settings to be used could include 585 to 595 nm for wavelength, 5.5 to 11
J/cm2 for fluence, 0.45 to 3 ms for pulse duration, and 7 to 12 mm for spot size.
Lasering is most safely performed in combination with epidermal cooling
(Table 1).
■ A larger spot size allows the laser beam to penetrate deeper into the lesion.
However, lower fluences are used for larger spot sizes to maintain a high
safety profile.
■ Changing the pulse duration may allow targeting of different sized vessels.
Treatment often begins at 1.5 ms, and this can be adjusted down to 0.45 ms
and up to 3 ms. Lower fluences are required for shorter pulse durations.
■ PWS have a nonuniform response to laser surgery, likely due to variously
sized blood vessels, different flow rates, and different depths of involvement.
■ One should not use a cookbook approach to the settings used. Each lesion is
unique. It is strongly recommended that test sites be placed with each patient.
Or, if there are overriding reasons not to place test sites, initially use only very
low-energy parameters for the first treatment, especially in infants. If one is in
such a situation that limits the placement of test sites, one may treat a larger
area at a low-energy setting and place discreet test sites with slightly higher
settings during the first treatment session.

Table 1 General Settings Used With Pulsed-Dye Laser
Vascular
lesion
Wavelength
(nm)
Fluence
(J/cm2)
Pulse
Duration (ms)
Spot Size
(mm)
Hemangioma
585–595
4–8.5
0.45–3
5–10
Port-wine
stain
585–595
5.5–11
0.45–3
7–12
■ For older patients who prefer a treatment without purpura, one can use an
intense pulsed light (IPL) device (FIG 3). These systems are less safe around
the eyes and with higher skin types. Each IPL system is manufactured
differently and is applied in a unique approach appropriate to the particular
system. It is recommended to be very familiar with the device that is to be used
and always place test sites.
FIG 3 • Use of an intense pulsed light (IPL) device on a
partially treated port-wine stain.
T E C H N I Q U E S
■ Test Sites

■ One should perform test sites prior to treatment of the entire lesion. In larger
lesions, especially over multiple anatomical regions, test pulses should be
performed over the various regions and clinical lesional variations. Patients
are evaluated dependent on their age anywhere from 4 to 8 weeks after test
site placement to assess response of the test sites.
■ Laser Treatment of Vascular Lesion
■ Once the clinician has determined appropriate settings from the test pulses,
one can treat the entire lesion. If the test site outcomes were not decisive, one
should not hesitate to place additional test sites with even the same and other
parameters until one feels comfortable proceeding. One often treats different
anatomical regions with different parameters. Even the same anatomical
region may be treated with different parameters dependent on symmetry of
lesional involvement.
■ In those patients having ill-defined borders and especially for those patients
receiving general anesthesia that induces fading of the lesions, prior to
treatment, it may be helpful to outline the borders of the lesion. Place the
outline marker slightly beyond the margin of the lesion because the marker
material itself may absorb laser energy resulting in undesired damage to the
skin.
■ The laser handpiece should be pressed gently, perpendicularly, against the
skin (TECH FIG 1). Avoid aiming tangentially at the skin, as this may alter
the fluence and the cooling device effectiveness.
■ To regulate the amount of laser energy impacting the skin, thus reducing the
chance of undesired adverse effects, only single passes are generally placed
with pulsed dye laser and intense pulsed light (IPL) systems. Pulse overlap
should also be avoided or at least limited to less than 10% overlap.
■ Throughout the treatment, the clinician should always be monitoring the
tissue for the desired tissue changes such as tissue darkening or edema. When
there is any deviation, stop the procedure and check the laser and parameters
or reassess the lesional area being treated. In those patients who are not
anesthetized and are old enough to give reliable feedback, a change in pain
level is also an indicator that parameters should be reconsidered. Ask the
patient to inform the clinician if there is any change in baseline procedural
discomfort.

TECH FIG 1 • The laser handpiece should be pressed
gently, perpendicularly, against the skin. Note the
physician is protecting the patient’s eye with white
gauze.
PEARLS AND PITFALLS
Eye
protection
■ For children, cover the periorbital area using overlapping white
gauze held firmly.
■ Pressure should be placed on the orbital rim and not on the eye itself.
■ If there is use of inhalation anesthesia, the gauze should be
thoroughly wetted with water or saline. Tape or similar
nonflammable material may be placed on the closed eyelid to ensure
it remains closed.
■ With any lasering near or into the orbital rim, a full global eye shield
should be placed.
Clinical
endpoint
■ Always pay attention to tissue response to each pulse.
■ Any deviation from previous responses or blistering or vesiculation
is a cause of serious concern, mandating stopping the procedure and

reassessing the laser and parameters.
Therapeutic
outcome
■ Ideally, total lesional resolution is desired. With port-wine stain
vascular malformations, this is achieved only in a small minority of
cases after a series of many treatment sessions.
■ If after an initial trial no further lesional regression is accomplished,
it is probable that one has achieved the maximum lesional reduction
possible with the current therapeutic approach. Either another
approach should be tested or therapy should be suspended, and the
family should be informed of the ineffectiveness of further therapy
using the current approach.
Skin color
■ The higher the skin type the greater is the absorption of laser energy
by melanin in the epidermal layer and the increased chance of
cutaneous damage resulting in permanent hypopigmenation.
■ This concern is greatly enhanced if the patient has additional
coloring from the sun. Since even a modest amount of darkening
from the sun is associated with a significant increased risk, do not
treat patients who have any appreciable color from the sun. Wait for
it to fade.
POSTOPERATIVE CARE
■ After treatment, all patients experience local swelling and discomfort. The
discomfort is transient with the intensity dramatically reducing over the first 30
to 60 minutes. Ice packs, cooling gels, and nonsteroidal anti-inflammatory
medications may minimize discomfort.
■ Patients should practice proper sun protection for weeks after the treatment to
minimize risk of pigmentary changes.
■ Emollients should be applied routinely until clearing of the immediate
postlaser changes.
■ Topical antibiotics should be initiated if crusting or scabbing occurs, as these
can raise risks of secondary bacterial infection.
■ Postadjuvant antiangiogenesis therapy is currently being evaluated. Treatment
with topical imiquimod 5% and topical rapamycin in between laser treatments
has been shown to prevent reformation and reperfusion of blood vessels in
small trials.10,11
OUTCOMES
■ Approximately 20% of PWS can be lightened completely or almost
completely with the PDL. About 70% will lighten by more than 50% and about

10% to 20% of lesions will only respond minimally.12
■ For best results, vascular lesions will require multiple treatments. Very rarely
does a lesion clear after a few sessions. Typically, lesions would be treated for
at least 8 to 10 treatments at a minimum of 4- to 12-week intervals.
■ More resistant or hypertrophic PWSs may not respond to PDL and may be
better suited for treatment with longer wavelength lasers. Proven lasers include
the long-pulse alexandrite (755 nm), long-pulse 1064 nm Nd-YAG, and dual
595 nm/1064 nm lasers. These lasers are only recommended for skilled laser
surgeons, as there is a very small therapeutic window, and the risk of scarring
is higher.4,6,9
COMPLICATIONS
■ Skin darkening usually will develop immediately with PDL treatment and may
persist for 10 to 14 days.
■ Transient erythema and swelling typically persists for 4 to 8 days with the
PDL and less with the IPL.
■ Blistering and crusting can also develop, more commonly with higher fluences
or with overlapping pulses.
■ Transient or permanent hyper- and hypopigmentation can occur, especially in
darker-skinned patients and if one treats patients with a tan.
■ Pigmentary risks can be reduced in darker skin types with using appropriate
epidermal cooling, longer pulse durations and lower fluences. Treatment
efficacy is also likely to be reduced when using longer pulse durations and
lower fluences.
■ Alopecia can occur if using lasers in areas that have pigmented hairs. Care,
especially over the eyebrows, is necessary to prevent permanent hair loss.
■ The risk of scarring after PDL treatment of PWS is very low (less than 1%).
These risks can be minimized by using test sites.
REFERENCES
1. Mulliken JB, Glowacki J. Hemangiomas and vascular malformations in
infants and children: a classification based on endothelial characteristics. Plast
Reconstr Surg. 1982;69:412-422.
2. Hoff SR, Rastatter JC, Richter GT. Head and neck vascular lesions.
Otolaryngol Clin North Am. 2015;48(1):29-45.
3. Bruckner AL, Frieden IJ. Hemangiomas of infancy. J Am Acad Dermatol.
2003;48:477-493

4. Stier MF, Glick SA, Hirsch RJ. Laser treatment of pediatric vascular lesions:
port wine stains and hemangiomas. J Am Acad Dermatol. 2008;58(2):261-285.
5. Batta K, Goodyear HM, Moss C, et al. Randomized controlled study of early
pulsed dye laser treatment of uncomplicated childhood hemangiomas. Lancet.
2002;360:521-527.
6. Craig LM, Alster TS. Vascular skin lesions in children: a review of laser
surgical and medical treatments. Dermatol Surg. 2013;39(8):1137-1146.
7. Garden JM, Bakus AD, Paller AS. Treatment of cutaneous hemangiomas by
the flashlamp-pumped pulsed dye laser: prospective analysis. J Pediatr.
1992;120(4 Pt 1):555-560.
8. Reddy KK, Blei F, Brauer JA, et al. Retrospective study of the treatment of
infantile hemangiomas using a combination of propranolol and pulsed dye
laser. Dermatol Surg. 2013;39(6):923-933.
9. Brightman LA, Geronemus RG, Reddy KK. Laser treatment of port-wine
stains. Clin Cosmet Investig Dermatol. 2015;12;8:27-33.
10. Tremaine AM, Armstrong J, Huang YC, et al. Enhanced port-wine stain
lightening achieved with combined treatment of selective photothermolysis
and imiquimod. J Am Acad Dermatol. 2012;66(4):634-641.
11. Griffin TD Jr, Foshee JP, Finney R, Saedi N. Port wine stain treated with a
combination of pulsed dye laser and topical rapamycin ointment. Lasers Surg
Med. 2016;48(2):193-196.
12. Woo WK, Handley JM. Does fluence matter in the treatment of port-wine
stains. Clin Exp Dermatol. 2003;28:556-557.

31
CHAPTERLaser Burn Scar Revision
C. Scott Hultman and Yuen-Jong Liu
DEFINITION
■ Mortality from burn injury has markedly decreased in the second half of the
20th century as wound sepsis, wound coverage, kidney failure, and shock have
been largely overcome.
■ Burn injury is the result of high-energy transfer to a significant surface area of
the skin or soft tissues and can be categorized by the form of energy:
■ Contact with high temperature solids (contact), liquids (scald), or gases
(flame)
■ Contact with low temperatures (frostbite)
■ Exposure to chemicals (acids, alkalines, or other caustic reagents)
■ Electricity
■ Friction or abrasion
■ Burn wounds frequently heal in the form of hypertrophic scars, which hamper
functional and aesthetic outcomes.
■ Symptoms include pruritus, burning pain, and hyperesthesia, which may be
treated with antihistamines, narcotic analgesics, and non-narcotic analgesics.
■ Functional deficits may vary from tightness or tethering of the surrounding
skin to contractures that limit range of motion.
■ Hypertrophic burn scars may be erythematous due to hypervascularity.
■ Treatments include occupational therapy, physical therapy, compression
garments, moisturizing agents, sunblock, and scar massage.1,2
■ Evidence for the efficacy of laser therapy in the treatment of hypertrophic burn
scars is now well documented in individual cohort studies,3 review articles,4
and a rigorous meta-analysis of 28 well-designed clinical trials.5

■ The exact biologic mechanism for improvement has yet to be elucidated, but
pulsed dye laser (PDL) improves the inflammatory component of hypertrophic
burn scars, which have excess pathologic vascularity, whereas fractional
carbon dioxide (CO2) laser improves remodeling of dermal collagen, which is
disorganized and abnormal in hypertrophic burn scars.
■ Best practices involve six to eight laser sessions, performed every 4 to 6
weeks, using a combination of these two lasers, plus on occasion the
Alexandrite laser, to ablate hair follicles in cases of chronic folliculitis of the
burn scar.
■ Substantial, rapid improvement in hypertrophic burn scars is now observed
through objective measures, such as the Vancouver Scar Score (height,
erythema, pliability), as well as subjective reports, such as the UNC 4P Scar
Score (pruritus, paresthesias, pliability, and pain).6
■ A major benefit to both the patient and the payer is that multiple, minimally
invasive laser sessions may decrease or prevent the need for more complex and
more invasive surgical procedures, decreasing patient risk, reducing overall
cost, and potentially achieving outcomes not previously possible.
ANATOMY
■ Burn scars may affect any part of the body.
■ Hypertrophic scars across joints may cause contracture.
■ Contractures on the face may interfere with competence of the eyelids or the
mouth.
■ Burn scars are especially disfiguring on the face due to its high aesthetic
importance.
■ Neuropathic pain may be observed in burned areas, grafted regions, and even
donor sites.
PATHOGENESIS
■ The incidence of hypertrophic scarring after burn injury ranges from 5% to
40%, depending on anatomic location, depth of burn, method of closure, and
genomic response to healing.
■ Hypertrophic scarring and contractures can develop in burn scars that heal by
secondary intention or re-epithelialization, in split-thickness skin grafts over
excised burns, along the seams of full-thickness grafts, and in donor sites that
had delayed healing, due to infection of excessive depth of harvest.
■ Hypertrophic scars may be associated with an imbalance of collagen types 1

and 3, as well as TGF beta 1 and TGF beta 3.
■ Hypertrophic scarring can be viewed as an abnormal physiologic response
after wound closure, in which collagen deposition and angiogenesis continue
beyond their desired end points.
NATURAL HISTORY
■ Neuropathic symptoms, such as pruritus, searing pain, hyperesthesias, and
paresthesias, are a source of frustration for the patient, can limit quality of life,
and may prevent return to school, work, and social functions.
■ Hypertrophic scarring may cause disability ranging from minor discomfort to
joint contracture.
■ Hyper- or hypopigmentation, erythema, and abnormal texture may cause the
burn scars to be aesthetically unacceptable.
PATIENT HISTORY AND PHYSICAL FINDINGS
■ Complete patient history should be elicited, focusing on the type of energy
delivered: scald, electrical, flame, contact, chemical, cold, friction, abrasion, or
other.
■ Previous treatments and their effects should be noted, including skin grafting,
laser treatments, topical scar treatments, moisturizing agents, sunblock,
systemic medications, occupational therapy, physical therapy, compression
garments, and massage.
■ The patient should have had no significant improvement in symptoms for at
least 3 months on maximal medical therapy.
■ Relative contraindications to laser therapy include connective tissue disorders,
utilization of systemic steroids or immunosuppressive medications, and
chemotherapy or radiation therapy. Patients with moderate to severe
lymphedema should also be treated with caution, as healing from ablative
lasers may be delayed.
■ Complete physical exam should be performed, focusing on the burned area,
noting whether it is a native burn scar or burn scar after skin grafting.
■ The burned areas should be well healed without open wounds or evidence of
cellulitis.
■ Total body surface area of the burn injury should be noted, as extremely large
areas should be staged, in terms of laser treatment.
■ Functional deficits should be recorded, such as loss of range of motion or loss
of sensation.

■ Aesthetic concerns should also be considered, especially in burns of the face
and the hands.
■ The patient’s Fitzpatrick skin type should be documented, and this will advise
the initial energy settings for the laser.
■ Photographs are useful for insurance submission and to track progression of
the scar between laser treatments.
IMAGING
■ Imaging is not required. However, medical photography is often needed for
preauthorization from insurance companies.
■ For patients enrolled in a clinical trial, other imaging modalities might be
helpful to measure extent of hypertrophic scarring and quantify changes:
■ Ultrasound to measure thickness of scar
■ Chroma meter to measure light-dark axis and degree of redness from
erythema
■ Cutometer to measure elasticity of scar
SURGICAL MANAGEMENT
■ The patient is routinely consented for a series of laser treatments, involving
selective photothermolysis with the PDL, ablative resurfacing using the
fractional using CO2 laser, and either Alexandrite or diode lasers to rupture hair
follicles.
■ A series of 6 to 8 sessions is submitted for insurance coverage at a time,
though a patient may reach maximal benefit before 6 to 8 sessions or may
continue to experience symptomatic improvement beyond eight sessions.
■ We strongly recommend maintaining a burn scar registry, which includes
preoperative, operative, and postoperative data, which can be used for practice-
based learning, retrospective and prospective cohort analysis, insurance
preauthorization and payment, and medical-legal documentation.
■ We recommend working with a board-certified anesthesiologist who has
completed additional specialization in pediatric anesthesia or has significant
clinical experience with children and has expertise in ambulatory and office-
based anesthesia.
■ Multimodal anesthesia has been shown to significantly decrease patient pain,
need for intravenous opioids during recovery, and time to discharge from the
postanesthesia care unit.7
■ Patients must be treated in an accredited surgery facility, which can include a

hospital-based ambulatory surgery center and an office-based surgery facility.
■ Control of airway is paramount, even with mild sedation; burn patients may
have compromised airways from previous tracheostomy scars and/or
prolonged intubation and mechanical ventilation.
■ To maximize throughput with our practice, patients do not return until their
next laser session, which is typically 6 to 8 weeks later.
■ The next session serves as both the postoperative visit from the previous
treatment and the preoperative visit for that day’s session.
■ At that time, we ask the patient for feedback about their symptoms and tailor
the treatment for that day based on these observations, which can include
changing the energy levels as well as type of laser used.
Positioning and Preparation
■ Our burn patients usually receive a Propofol drip and boluses of fentanyl,
ketamine, and midazolam as appropriate.
■ The burn scar should be clean but sterile preparation is not necessary.
■ Sterile drapes are not necessary.
■ All operating room personnel must wear tinted eyewear for PDL or clear
eyewear for CO2 laser to protect against laser backscatter.
■ The patient’s eyes should be closed and covered with a saline-moistened
towel.
■ Fire prevention is of paramount concern for all laser cases, and patient safety
protocols for reducing the potential for an oxygen-enriched environment must
be followed.
■ This includes lower the inspired oxygen concentration to the lowest needed
FIO2, using room air only when discharging the laser in the head and neck
region, avoiding towels or drapes that can serve as a reservoir for oxygen, and
alerting all OR personnel when discharge of the laser commences.
■ The lasers must be calibrated and tested on the back table, before treating the
patient, to confirm that the appropriate amount of energy will be delivered.
T E C H N I Q U E S
■ Pulsed Dye Laser

Video p8-c031_02
Anesthesia
■ For small areas below the clavicles, as well as test areas, in adult patients
only, no anesthesia is necessary, except for the cooling of the cryogen jet,
which is administered milliseconds before the laser is discharged.
■ All children, adults with large surface areas, and patients with hypertrophic
scars on the face and neck require some type of anesthesia, which can range
from oral anxiolytics and narcotics to TIVA (total intravenous anesthesia);
general anesthesia with inhalation agents is rarely used, but patients will
often benefit from a LMA (laryngeal mask airway) to control the tongue and
epiglottis.
■ Of note, most topical anesthetics constrict the capillary targets in the dermis,
so we almost never utilize these agents, to ensure that the target receives and
absorbs adequate energy for selective photothermolysis.
Laser Application
■ We use a Candela V-Beam, 595-nm wavelength, PDL.
■ The laser is set to 1-cm diameter circular spot size, cryogen mix of 30/20,
and 1.5-ms pulse duration or pulse width (TECH FIG 1A).
■ The energy or fluence setting is titrated to mild bruising without blistering.
6.5 J/cm2 is a reasonable level for a patient’s first session for Fitzpatrick class
1 and 2 patients. For patients with Fitzpatrick grade 3 and 4 pigmentation,
acceptable starting energy settings are 4.5 to 5.0 J/cm2. Patients with
Fitzpatrick class 5 and 6 skin types must be counseled that they are at high
risk for mild blistering and hypopigmentation and should be treated with
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minimal fluence, such as 3.5 J/cm2.
■ The energy setting for subsequent sessions is increased if the patient
experiences minimal skin changes in the days following the procedure.
Conversely, the energy setting is decreased if the patient experiences severe
bruising, blistering, or epidermolysis in the days following the procedure.
■ As the operator fires the laser sequentially over the burn scar, there should be
mild overlap between successive bursts (TECH FIG 1B).
■ Each laser burst can be expected to sting as if struck by a drawn rubber band.
■ End points for titrating the fluence, in the OR, include slight ecchymosis of
the skin. Immediate blistering or purpura indicates that too much energy has
been applied and that reduction in fluence is required.
Wound Care
■ We use topical antimicrobial ointment for several days, until bruising begins
to resolve.
■ Oral antibiotics and antiviral agents are almost never given, except in cases
of recurrent cellulitis or frequent outbreaks of herpetic infection in the treated
areas.
TECH FIG 1 • A. We typically use these settings for a
patient’s first PDL treatment session on our Candela
V-Beam, 595 nm, PDL. The laser is set to 6.50-J/cm2
fluence, 1-cm diameter spot size, cryogen mix of
30/20, and 1.5 ms pulse duration. B. The PDL
handpiece is held so that the distance guide (purple
ring) is flat at skin level. The treatment area of
hyperemic autografted burn scar is encircled with
marked dots. There should be mild overlap between

successive bursts.
■ Fractional CO2 Laser
Video p8-c031_01
Anesthesia
■ Fractional CO2 laser ablation is extremely painful.
■ For small areas below the clavicle, in adults who have minimal baseline
neuropathic pain, topical anesthetics including lidocaine and bupivacaine
mixtures can be applied for 20 to 30 minutes, to create enough anesthesia that
the laser can be tolerated, when using 15 to 30 mJ/micropulse.
■ However, most burn patients already have neuropathic symptoms from their
hypertrophic scars, so most require at least intravenous sedation and
analgesia, but total intravenous anesthesia is usually employed.
Laser Application
■ We use a Lumenis UltraPulse fractional CO2 laser at wavelength of 10 600
nm.
■ The laser is set to 30 to 60 mJ/micropulse, 1- × 1-cm2 square spot size, 250
to 300 Hz for the micropulses, 0.3- to 0.5-second delay between sequential
firing, and 5% to 3% density in terms of tissue surface area (TECH FIG 2).
■ Higher energies of 60 to 90 mJ/micropulse can be delivered safely, provided
that density is dropped to 1%. We rarely use energy of this magnitude, expect
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in very thick hypertrophic scars that require a greater depth of penetration, to
yield fine, punctate, capillary bleeding. The efficacy of using such high
energies has not been rigorously studied, and we cannot recommend using
energy of this magnitude routinely.
TECH FIG 2 • A. On our Lumenis UltraPulse fractional
CO2 laser, initial settings consist of 30 to 60
mJ/micropulse, 1- × 1-cm2 square spot size, 0.5-
second delay between sequential spots, 300-Hz firing
rate, and 5% density. B. The CO2 laser handpiece is
held so that the distance guide (translucent grey ring)
is flat at skin level. The treatment area of indurated
autografted burn scar is outlined by skin marker.
There should be minimal or no overlap between
successive bursts. An assistant suctions vaporized
tissue smoke with the tip of the evacuator (purple end
of plastic tubing) held a few centimeters from the laser
spot to remove vaporized tissue smoke.
■ While some surgeons use very high energies to treat keloids, we prefer to
manage burn scar keloids by direct excision and fractionated, immediate
postoperative radiation. In children, patients with keloids of the neck (where
the thyroid and parathyroid glands could be in the field of irradiation), and
patients with a history of XRT, we instead close the wound through complex
repair, tissue rearrangement, or skin graft and then proceed with laser therapy
to reduce the incidence of recurrence.
■ The laser should be tested on a wooden tongue depressor, to confirm orderly
and consistent ablation, evidenced by a regular pattern of burn marks on the