Phẫu Thuật Tạo Hình Grabb & Smith’s (Bản Cập Nhật – Kevin C. Chung)

compartment tendon.
As in the hand, reconstruction of the foot must take into place the soft tissue, tendon, joint, and bony
abnormalities. Severe toe contractures cause considerable functional morbidity and often involve deeper
structures, such as shortening of the tendons and fibrosis of the interphalangeal or metatarsophalangeal
joint capsules; thus, preoperative X-rays should be obtained. Similar to hand, burns on the dorsal skin
cause tissue shortening, hyperextension of the toes, and subluxation and dislocation of the
metatarsophalangeal joints. These contractures should be released aggressively. Depending on the
involvement of the deeper structures, we recommend the following additional steps: a thick STSG or an
FTSG for the skin, tendon lengthening, open capsulotomy, and pin fixation for several weeks to maintain
the integrity of the reconstruction. If exposed white structures exist, a thick fasciocutaneous flap should
be used. Webspaces are handled like the hand with five-flap jumping man Z-plasties.
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Hand Reconstruction
The complex anatomy of the hand must be analyzed when preparing for reconstruction of the burned
hand. Even small scar bands can result in significant functional impairment. Immediate splinting is
important to prevent debilitating contractures. The shoulder should be abducted at 90°, the elbow should
be extended at 180°, the wrist slightly extended, and the hand in intrinsic plus position. Early aggressive
debridement and grafting for the dorsum of the hand is recommended, whereas more conservative
treatment and possible staging with Integra is recommended for the palm. The dorsum of the hand is
especially susceptible to hypertrophic scar formation owing to the thin and pliable nature of the skin in
this area, which requires less thermal force to induce burn to the deeper dermal tissues and hypertrophic
scarring. Dorsal scarring may not only inhibit passive flexion but severe burns can result in
hyperextension and subluxation of the joints in severe cases. 48 On the volar surface, hypertrophic scar
formation of the palm can result in a cupping deformity, which is characterized by convex warping of the
longitudinal and horizontal palmar arches. 49 Acute burns to the palm should give more time to heal
secondarily because grafts to the palm will impair sensation for the remainder of the patient’s life.
Additionally, the palmar skin is more durable than any skin graft. If a graft is needed, a thick split- or
full-thickness graft is best used. Palmar burn scars commonly involve a large surface and can therefore
result in tight contractures. Mild forms can be addressed with a sequence of Z-plasties. If the contracture
is severe, release of the scar may be required which leaves a large defect. This defect can be filled with an
FTSG if no crucial structures are exposed. 50 FTSGs are preferred over split-thickness graft to decrease
secondary contraction and to minimize scarring. If the contracture release leads to exposed tendon or
bone, local or distant flaps may be required. 51 The extensor tendons dorsally often benefit from a fascia-
only reverse radial forearm flap with a skin graft for coverage or a reverse dorsal interosseous flap.
Alternatives include free fascia-only or fasciocutaneous flaps, although bulky flaps should be avoided if
possible. 52 Severe burns on the dorsal and volar surfaces of the hand often benefit from K-wire placement
to keep the digits in an intrinsic plus position to prevent deforming contractures. Thermal injury
involving opposing surfaces of border digits can result in a scar band reducing the interdigital space and
limiting abduction. Furthermore, if the first webspace is involved, thumb abduction is affected causing
adduction contractures, reducing grip strength and function (Table 22.3).
TABLE 22.3
ALGORITHM FOR HAND CONTRACTURE REPAIR
Region
Reconstruction
Webspace
Five-flap jumping man
MCP and PIP
Z-plasty
Nail bed and DIP
Release and FTSG
DIP, distal interphalangeal joint; FTSG, full-thickness skin graft; MCP, metacarpophalangeal joint; PIP, proximal interphalangeal joint.
Flexion contracture of the small finger is one of the most difficult reconstructive challenges for surgeons
because contracture of the collateral ligaments, flexor tendons, and skin results in shortening of the
vessels and nerves. For these patients, preoperative X-rays and analysis of the level of contracture of the
joint are crucial to a successful outcome. If severe joint contracture is present or the patient has a
boutonnière deformity from previous debridement or injury to the extensor tendon, the finger will not be
improved by an operation addressing the skin contracture alone. The surgeon should also avoid the urge
to straighten the small finger in one operation, as this will often lead to venous congestion or ischemia
due to the shortening of the vessels from the contracture. If the skin is the only area causing the
contracture then a Z-plasty or series of Z-plasties can be used. In more severe contractures, a release and
full-thickness hypothenar flap can be used. Finally, in cases with joint and skin contracture, a Digit
Widget can be used for slow distraction and stretching of the contracture. This device places two K-wires
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in the middle phalanx and has a series of bands that connect to the wrist slowly stretching the contracture
(Figure 22.10). 53
FIGURE 22.10 Digit Widget reconstruction of small finger proximal interphalangeal joint contracture. Preoperative (A),
postoperative digit widget placement (B), and postoperative digit widget removal (C).
(Courtesy of Steve Haase, MD, University of Michigan)
Another common and stigmatic deformity of the burned hand is the finger nail. Burn injury to the
dorsum of the digit can result in retraction of the soft tissue proximal to the nail fold leading to exposure
of the germinal matrix and alterations in nail growth. 54 This is caused by excess vertical tension across
the dorsal digit, which often restricts distal interphalangeal joint (DIP) flexion. To treat the contracture
and eponychial fold deformity, we use a technique of release and full-thickness graft proximal to the DIP.
This involves a distally based bipedicled flap, which is designed to release the proximal nail fold
contracture. This is accompanied by an extensive release of the dorsal soft tissues and resurfacing of the
resulting defect with an FTSG. Restoration of normal anatomy can thus be achieved and results in
normalized nail growth and improved DIP flexion 54 (Figure 22.11).
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FIGURE 22.11 Preoperative (A), intraoperative (B), and postoperative (C) photos of nail bed reconstruction with release and
full-thickness skin graft to restore eponychial fold and distal interphalangeal joint tightness.
Webspace contractures should be treated with modifications of Z-plasties. 55,56 The five-flap jumping man
Z-plasty (two Z-plasties with an intervening Y-to-V) is frequently used and is effective in creating a
concavity and lengthening within the webspace because of its geometric design. The Y-to-V region of this
flap should be placed in the region of desired deepening. Other options include V-Y advancement flaps,
which apply the supple dorsal tissue that is advanced into the web space. These flaps can be combined
with forms of Z-plasties. 2
Axillary scar contractures are the second most common contractures behind neck contractures and are
difficult to improve. Small linear bands can be released with Z-plasties (Figure 22.12). Z-plasties in this
region should be designed large, and flaps should be kept thick with subcutaneous fat. A five-flap
jumping man offers a useful reconstruction as in the webspace because it deepens the axilla. Care must be
taken during these tissue rearrangements not to move too much hair-bearing skin onto non–hair-bearing
skin. Larger more restrictive contractures can be treated with release and apply thick STSG or FTSG.
Others have described treatment of severe contractures with pedicled flaps or with regional and free
tissue transfer. 57 As in the neck, a thin fasciocutaneous flap will provide the optimal result.
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FIGURE 22.12 Preoperative (A) and postoperative (B) photos of Z-plasty reconstruction of the axilla.
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Questions
1. What flap is ideal to improve a webspace contracture between the ring and middle fingers?
a. Z-plasty
b. Five-flap jumping man flap
c. Kite flap
d. Littler flap
2. What laser modality would best treat an erythematous burn scar that is not hypertrophic?
a. Pulse dye
b. Alexandrite
c. CO2 laser
d. Erbium-yttrium aluminum garnet
3. What is the proper degree to splint the shoulder, elbow, and hand after a burned upper extremity
injury?
a. 120°; 120°; extrinsic plus
b. 90°; 180°; intrinsic plus
c. 45°; 90°; intrinsic plus
d. 90°; 90°; intrinsic plus
4. How can recurrent postoperative ectropion be avoided?
a. Bolster
b. Tarsorrhaphy
c. Meshed skin grafting
d. Laser
5. What percentage gain is provided by a Z-plasty that is 60°?
a. 50%
b. 75%
c. 100%
d. 125%
1. Answer: b. Many different local flaps can be used to fix webspace contractures. A five-flap
jumping man allows for both release of the contracture as well as webspace deepening. This
webspace deepening comes from the Y-to-V advancement flap. Z-plasties are useful for linear
contractures along fingers.
2. Answer: a. PDL targets chromophores at a wavelength that will heat up red tissues. Thus, the PDL
is the optimal laser to treat a burn scar that is only erythematous. For scars that are erythematous and
hypertrophic, the CO2 laser with or without the PDL is often the appropriate modality. The
Alexandrite laser is best used for hair removal.
3. Answer: b. Postoperative splinting is crucial to maintaining any releases that are performed for
burn patients. For the upper extremity, the shoulder should be maintained at 90°, the elbow should
be maintained at 180°, and the hand should be placed in intrinsic plus.
4. Answer: b. Acute burn ectropion and recurrent postoperative ectropion can be avoided with
tarsorrhaphy. These can be temporary or permanent depending on the extent of the ectropion and
the release. These can be placed medially, laterally, or both also depending on the location and extent
of the ectropion. Once ectropion forms, a release and FTSG is often necessary. Sometimes concurrent
midface lift, canthoplasty, and palatal grafts (to inner lamellae) are necessary. Meshed grafts should
never be used on the face.
5. Answer: b.
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References
Grishkevich, VM. Flexion contractures of fingers: contracture elimination with trapeze-flap plasty. Burns. 2011;37(1):126-133.
Peker, F, Celebiler, O. Y-V advancement with Z-plasty: an effective combined model for the release of post-burn flexion contractures of the
fingers. Burns. 2003;29(5):479-482.
Reish, RG, Eriksson, E. Scar treatments: preclinical and clinical studies. J Am Coll Surg. 2008;206:719-730.
Chan, RK, Bojovic, B, Talbot, SG, et al. Lower lip suspension using bilateral temporalis muscle flaps and fascia lata grafts. Plast Reconstr Surg.
2012;129(1):119-122.
Hove, CR, Williams, EF, Rodgers, BJ. Z-plasty: a concise review. Facial Plast Surg. 2001;17(4):289-294.
Furnas, DW, Fischer, GW. The Z-plasty: biomechanics and mathematics. Br J Plast Surg. 1971;24:144.This classic article discusses the power of the
Z-plasty to gain scar length by increasing scar width.
McGregor, IA. The Z-plasty. Br J Plast Surg. 1966;19(1):82-87.
Fraulin, FO, Thomson, HG. First webspace deepening: comparing the four-flap an five-flap Z-plasty : which gives the most gain? Plast
Reconstr Surg. 1999;104(1):120-128.
Chen, B, Song, H. The modification of five-flap Z-plasty for web contracture. Aesthet Plast Surg. 2015;39(6):922-926.
Shockley, WW. Scar revision techniques: Z-plasty, W-plasty, and geometric broken line closure. Facial Plast Surg. 2011;19(3):455-463.
Sokolowich, D, Zimman, O. W-plasty: make it easy. Plast Reconstr Surg. 1989;83(5):928-929.
Grishkevich, VM. Trapeze-flap plasty: effective method for postburn neck contracture elimination. Burns. 2010;36(3):383-388.
Hultman, CS, Friedstat, JS, Edkins, RE, et al. Laser resurfacing and remodeling of hypertrophic burn scars: the results of a large, prospective,
before-after cohort study, with long-term follow-up. Ann Surg. 2014;260(3):519-529.This article demonstrates the benefit of laser treatment to
improve scar outcomes in burn patients.
Cho, SB, Lee, SJ, Chung, WS, et al. Treatment of burn scar using a carbon dioxide fractional laser. J Drugs Dermatol. 2010;9:173-175.
Klein, M. Skin grafting. In: Color Atlas of Burn Reconstructive Surgery. New York, NY: Springer-Verlag; 2010:132-138.
Pribaz, JJ, Pelham, FR. Use of previously burned skin in local fasciocutaneous flaps for upper extremity reconstruction. Ann Plast Surg.
1994;33:272-280.
Tolhurst, D, Haeseker, B, Zeeman, R. The development of the fasciocutaneous flap. Plast Reconstr Surg. 1983;71:597-605.
Cherup, LL, Zachary, LS, Gottlieb, LJ, Petti, C. The radial forearm skin graft-fascial flap. Plast Reconstr Surg. 1990;85:898-902.
Barret, J HD, McCauley, R. Use of previously burned skin as random cutaneous local flaps in pediatric burn reconstruction. Burns.
2002;28:500-502.
Wainwright, DJ. Burn reconstruction: the problems, the techniques, and the applications. Clin Plast Surg. 2009;36(4):687-700.
Menick, FJ. Reconstruction of the cheek. Plast Reconstr Surg. 2001;108(2):496-505.
Rose, EH. Aesthetic restoration of the severely disfigured face in burn victims: a comprehensive strategy. Plast Reconstr Surg. 1995;96(7):1573-
1585.
Levi, B, Ibrahim, A, Mathews, K, et al. The use of CO2 fractional photothermolysis for the treatment of burn scars. J Burn Care Res.
2016;37(2):106-114.
Anderson, RR, Donelan, MB, Hivnor, C, et al. Laser treatment of traumatic scars with an emphasis on ablative fractional laser resurfacing:
consensus report. JAMA Dermatol. 2014;150(2):187-193.This is the first article to provide a pathway for laser treatment of burn patients who would
benefit from fractional CO 2 laser.
Wong, S, Melin, A, Reilly, D. Head and neck reconstruction. Clin Plast Surg. 2017;44(4):845-856.
Egeland, B, More, S, Buchman, SR, Cederna, PS. Management of difficult pediatric facial burns: reconstruction of burn-related lower eyelid
ectropion and perioral contractures. J Craniofac Surg. 2008;19(4):960-969.
Manders, EK, Graham, WP, Schenden, MJ, Davis, TS. Skin expansion to eliminate large scalp defects. Ann Plast Surg. 1984;12(4):305-312.
Leedy, JE, Janis, JE, Rohrich, RJ. Reconstruction of acquired scalp defects: an algorithmic approach. Plast Reconstr Surg. 2005;116(4):54e-72e.
Daya, M. Nostril stenosis corrected by release and serial stenting. J Plast Reconstr Aesthet Surg. 2009;62(8):1012-1019.
Daines, SM, Hamilton, GS, Mobley, SR. A graded approach to repairing the stenotic nasal vestibule. Arch Facial Plast Surg. 2010;12(5):332-338.
Salvado, AR, Wang, MB. Treatment of complete nasal vestibule stenosis with vestibular stents and mitomycin C. Otolaryngol Head Neck Surg.
2008;138(6):795-796.
Copcu, E. Reconstruction of total and near-total nostril stenosis in the burned nose with gingivo-mucosal flap. Burns. 2005;31(6):802-803.
Taylor, HO, Carty, M, Driscoll, D, et al. Nasal reconstruction after severe facial burns using a local turndown flap. Ann Plast Surg.
2009;62(2):175-179.
Pribaz, JJ, Falco, N. Nasal reconstruction with auricular microvascular transplant. Ann Plast Surg. 1993;31(4):289-297.
Ashab Yamin, MR, Mozafari, N, Razi, Z. Reconstructive surgery of extensive face and neck burn scars using tissue expanders. World J Plast
Surg. 2015;4(1):40-49.
Chung, JE, Yen, MT. Midface lifting as an adjunct procedure in ectropion repair. Ann Plast Surg. 2007;59(6):635-640.
Karacaoglan, N, Uysal, A. Reconstruction of postburn scar contracture of the neck by expanded skin flaps. Burns. 1994;20(6):547-550.
Yang, JY, Tsai, FC, Chana, JS, et al. Use of free thin anterolateral thigh flaps combined with cervicoplasty for reconstruction of postburn
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anterior cervical contractures. Plast Reconstr Surg. 2002;110(1):39-46.
Akita, S, Hayashida, K, Takaki, S, et al. The neck burn scar contracture: a concept of effective treatment. Burns Trauma. 2017;5:22.
Inigo, F, Jimenez-Murat, Y, Arroyo, O, et al. Free flaps for head and neck reconstruction in non-oncological patients: experience of 200 cases.
Microsurgery. 2000;20(4):186-192.
Xu, J, Li, SK, Li, YQ, et al. Superior extension of the parascapular free flap for cervical burn scar contracture. Plast Reconstr Surg. 1995;96(1):58-
62.
Kunert, P, Schneider, W, Flory, J. Principles and procedures in female breast reconstruction in the young child’s burn injury. Aesthet Plast
Surg. 1988;12(2):101-106.
MacLennan, SE, Wells, MD, Neale, HW. Reconstruction of the burned breast. Clin Plast Surg. 2000;27(1):113-119.
Neale, HW, Smith, GL, Gregory, RO, MacMillan, BG. Breast reconstruction in the burned adolescent female (an 11-year, 157 patient
experience). Plast Reconstr Surg. 1982;70(6):718-724.
Guan, WX, Jin, YT, Cao, HP. Reconstruction of postburn female breast deformity. Ann Plast Surg. 1988;21(1):65-69.
Levi, B, Brown, DL, Cederna, PS. A comparative analysis of tissue expander reconstruction of burned and unburned chest and breasts using
endoscopic and open techniques. Plast Reconstr Surg. 2010;125(2):547-556.
Little, JW. Nipple-areola reconstruction. Clin Plast Surg. 1984;11(2):351-364.
Graham, TJ, Stern, PJ, True, MS. Classification and treatment of postburn metacarpophalangeal joint extension contractures in children. J
Hand Surg Am. 1990;15(3):450-456.
Cartotto, R, Cicuto, BJ, Kiwanuka, HN, et al. Common postburn deformities and their management. Surg Clin North Am. 2014;94(4):817-837.
Yotsuyanagi, T, Yamashita, K, Gonda, A, et al. Double combined Z-plasty for wide-scar contracture release. J Plast Reconstr Aesthet Surg.
2013;66(5):629-633.
Karanas, YL, Buntic, RF. Microsurgical reconstruction of the burned hand. Hand Clin. 2009;25(4):551-556.
Jones, NF, Jarrahy, R, Kaufman, MR. Pedicled and free radial forearm flaps for reconstruction of the elbow, wrist, and hand. Plast Reconstr
Surg. 2008;121(3):887-898.
Houshian, S, Gynning, B, Schroder, HA. Chronic flexion contracture of proximal interphalangeal joint treated with the compass hinge
external fixator: a consecutive series of 27 cases. J Hand Surg Br. 2002;27(4):356-358.
Donelan, MB, Garcia, JA. Nailfold reconstruction for correction of burn fingernail deformity. Plast Reconstr Surg. 2006;117(7):2303-2308.
Sari, E, Tellioglu, AT, Altuntas, N, et al. Combination of rhomboid flap and double Z-plasty technique for reconstruction of palmar and
dorsal web space burn contractures. Burns. 2015;41(2):408-412.
Grishkevich, VM. First web space post-burn contracture types: contracture elimination methods. Burns. 2011;37(2):338-347.
Ogawa, R, Hyakusoku, H, Murakami, M, Koike, S. Reconstruction of axillary scar contractures: retrospective study of 124 cases over 25
years. Br J Plast Surg. 2003;56(2):100-105.
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C H A P T E R 2 3
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Radiation and Radiation Injury
Natalia Fullerton and Christine Hsu Rohde
Key Points
Radiation therapy uses ionizing radiation for the treatment of various conditions, primarily as a
cancer therapy.
Improvements in radiation therapy are aimed at increasing the radiation to the site of therapy and
decreasing the radiation to surrounding tissue to reduce the injury to normal tissue through
improved therapy planning and more precise therapy delivery.
Radiation injury can be classified as acute toxicity or late toxicity.
Acute toxicity is reversible, beginning a few weeks after the start of therapy and resolving a few
weeks after the end of the therapy.
Late toxicity is permanent, occurring 6 months after the completion of therapy, and is characterized
by fibrosis.
Primary treatment for complications of late toxicity radiation therapy is reconstruction with well-
vascularized nonirradiated tissue.
The antecedent of the medical field of radiology was born in 1895, with Wilhelm Conrad von Roentgen’s
discovery of a new type of ray emitted from electrons in a Hittorf-Crookes tube. These rays could
penetrate tissues differentially, creating an image of the structures inside the body. Given the mysterious
nature of the rays, it was termed the X-ray. Following his discovery, the X-ray was developed for
diagnostic application, and by World War I, radiology became an established discipline. Soon after
Roentgen’s discovery, Pierre and Marie Sklodowska Curie isolated and reported on the radioactivity of
the radioactive element radium in 1889. A year later, the application of radiation to cure cancer was
reported in Sweden. Brachytherapy, utilizing radium, expanded in the 1900s and had become the
standard of care in oncology. 1,2
Externally administered radiation therapy (RT) was also successfully developed in the 1920s, after the
formulation of fractionated dosages, understanding of the relative sensitivity of different tissue to
radiation, and the development of normal and neoplastic tissue response to radiation as a response to
dose. Treatment was employed with peak voltage of 250 kV or less, limiting practice to superficial uses.
The next great development in external beam radiation came with the advent of the megavoltage (MV)
unit. In 1951, the cobalt-60 unit was developed in Canada, allowing for greater penetration of tissue, skin-
sparing capability, and improved homogeneity of dosage. This technology was followed by the MV linear
accelerators, or Linac systems, developed simultaneously at Stanford and Great Malvern, England. This
technology has supplanted the cobalt units in more affluent countries, although the cobalt-60 units
continue to be the mainstay of second and third world countries owing to ease of availability. 1,3
Presently, RT innovations are aimed at increasing radiation dose to the site of therapy, while decreasing
the radiation dose to surrounding normal tissue. This is being accomplished with improved treatment
planning utilizing simulation, computed tomography, and magnetic resonance imaging; enhanced
delivery of radiation to the target tissue with the use of multileaf collimators (MLC), allowing for
blocking or shielding of radiation from critical structures; and the use of intensity-modulated radiation
therapy (IMRT) and image-guided radiation therapy (IGRT) to more precisely deliver radiation to desired
locations. 1
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Basics of Radiation Therapy
Radiation therapy (RT) utilizes ionizing radiation for the treatment of various lesions. Radiation oncology
is the discipline in medicine that specializes in the treatment of cancer and other benign processes with
the use of ionizing radiation. In 2016, it was reported that a significant number of cancers were being
treated with some form of RT, either as a single modality or in combination with surgery and/or
chemotherapy. To demonstrate a few concrete examples, in stage I and II breast cancer treatment, 59% of
patients underwent some form of radiation schedule, with this number increasing to 73% of patients with
stage III breast cancer; 50% of patients with stage III and IV non–small cell lung cancer undergo RT; and
32% of patients with muscle invasive bladder cancer undergo RT. 4 Given the plastic surgeon’s close
relationship with surgical oncologists and their role in reconstruction after tumor extirpation, it is
important to be more cognizant of the management of certain cancers with RT, as well as the risks and
toxicities that may result from this particular treatment.
Ionizing radiation is the propagation of energy necessary to displace one or more orbital electrons. This
can result in direct ionization, wherein the charged particle of sufficient energy can directly disrupt the
atomic structure of the absorbing material, such as DNA. The energy can also produce indirect ionization,
in which there is ionization of an intermediary, commonly water (H2O), producing free radicals, such as a
hydroxyl radical (OH−), which can then interact and damage DNA, cell membranes, or other critical
structures, resulting in cell injury or death.
It is estimated that two-thirds of radiation from X-rays and gamma photons produce DNA damage
through indirect ionization and free radicals. The exact mechanism of radiation-induced cell death is not
well characterized, although it is believed to be due to damage to DNA causing apoptosis or reproductive
death, in which the cell is unable to divide in an unlimited fashion. 5
As radiation can affect both tumor and normal tissue, it is important to find ways to increase the tumor
control and decrease the normal tissue complication. This dose-response relationship between tumor
control and normal tissue complication is known as the therapeutic ratio (Figure 23.1). In an ideal
situation, there would be no overlap between the tumor control and normal tissue complication curves.
However, more frequently, there is a degree of overlap. Traditionally, it is accepted that normal tissue
will have a 5% risk of complication, represented by a 5% overlap of the two curves. 5-7 A significant
portion of technological advances in RT are focused at increasing the tumor control and decreasing the
normal tissue complication probability, improving the therapeutic ratio.
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FIGURE 23.1 Therapeutic ratio. A. Ideal situation—no overlap between the tumor control and normal tissue complication
curves. B. Accepted 5% risk of complication to normal tissue, represented by a 5% overlap of the two curves. C. Significant
overlap between the tumor control curve and normal tissue complication, resulting in a significant level of normal tissue toxicity.
The energy required for radiation to be ionizing is quantified in electron volts (eV). The energy used in
therapeutic X-rays begins at the kilovoltage (kV) unit. This energy was the first available modality for
cancer therapy. Today, therapy with these units can be subdivided into superficial therapy using 50 to
150 kV, which is suitable for lesions up to 5 mm in depth, with the delivery of 90% of the dose to the
surface of the skin. These units are particularly useful for skin cancers, as the majority of the radiation
does not penetrate deep and the radiation is tightly focused to the treatment zone. 8 Deep therapy, also
known as orthovoltage therapy, is categorized by energies of 150 to 500 kV. The therapy has a penetration
depth of 4 to 6 cm, a steep drop-off of dose with depth of penetration, and a tight penumbra of dose
dispersion. 8,9 For increased penetration, MV therapy is used for improved skin sparing and dose
homogeneity. The two main modalities that operate at the MV energy level are the cobalt-60 units, which
generate gamma rays with an average energy of 1.3 MV and the linear accelerator units (Linac), with
photon energies of 4 to 18 MV. As elucidated earlier, cobalt-60 units are the most widely used therapy
modality in the world. However, Linac units are replacing this older technology owing to its deeper
penetration, tighter penumbra, and more a uniform dose. The Linac functions by producing high-

frequency electromagnetic waves that accelerate electrons, which then pass through a beamline,
eventually colliding with a high-density target, emitting an MV X-ray beam. The Linac system can also
emit electrons to treat superficial lesions. 3,5
A newer system of external beam radiation utilizes particle therapy, rather than X-ray and gamma
photon radiation. This group of particles is usually grouped as heavy particle therapy, as it encompasses
protons, neutrons, or other positive ions such as carbon. Electron therapy is generally not classified in this
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subgroup, as they have a shallow depth of penetration. The slow implementation of proton therapy in the
realm of RT is associated with the high start-up cost in building a large infrastructure dedicated for its
use. The benefit of heavy particle therapy is the maximal deposition of energy at the end of their intended
path, with minimal dose deposition along the path. This phenomenon is called the Bragg peak. After the
Bragg peak, the dose falls off considerably. This advantage allows for less toxicity to surrounding normal
tissue with greater effect on the target tissue. This also allows for a sharp penumbra within shallow or
moderately deep tissue. 10,11 There is concern for some effect on the particle by the heterogeneity of tissue,
resulting in an unknown change in effect on the target tissue. 12 This concern for variability in effect is
especially prominent in tissue fields where the particle must traverse multiple organ types, such as the
lung, head and neck, prostate, etc. 10,11 However, the advantage of this treatment modality is especially
prominent in the pediatric population, particularly craniospinal tumors, rhabdomyosarcoma, and
retinoblastoma, where salvage of radiation toxicity to normal tissue has shown to decrease secondary
malignancies and decrease effects on organ growth and function. 10,13
Similar to proton therapy, carbon therapy also portrays a Bragg peak effect, sparing radiation toxicity to
normal surrounding tissue. The heavier charged carbon particle produces radiation damage within the
cell nuclei, leading to increased relative biologic effectiveness compared with proton therapy. However,
this technology is still in its infancy, and studies on superiority are in progress. 11
Brachytherapy offers an additional source of RT to local tissue. As the name implies, brachy, the Greek
root for short, is the use of a radioactive source placed in close proximity to the target tissue. 1 The close
proximity of the radiation source to the target tissue imparts a high radiation dose to the target tissue
with a rapid dose falloff to the surrounding tissue. 14 The main methods of brachytherapy delivery
include interstitial, when the source is directly implanted into the target tissue, intracavitary, when a
sealed source is inserted into the cavity of an organ (e.g., a cylindrical rod inserted into the cervix), or
surface application, in which an applicator can be used to directly deliver a radiation dose to the surface
of a tumor (e.g., eye plaque for uveal melanoma). 14,15 Major advances in the realm of brachytherapy
include the use of newer imaging modalities to aid in the planning and positioning of brachytherapy
treatments, planning algorithms to more precisely deliver appropriate doses to the tumor and avoid
surrounding normal tissue, and newer delivery techniques such as high and pulsed dose rate therapies,
which deliver higher dose rates through a previously placed catheter. 16-18
Another modality of radiotherapy is intraoperative RT, whereby radiation is delivered to the tumor bed
during surgical resection. This technique is typically used in combination with other modalities in a
multidisciplinary approach to cancer therapy and has been shown to have efficacy in locally advanced
and recurrent rectal cancer, retroperitoneal sarcomas, pancreatic cancers, early breast cancers, and some
gynecological and genitourinary cancers. The advantage of this technology is that it gives precise and
high-dose radiation delivery to the tumor bed while sparing local normal tissue, improving the
therapeutic ratio of radiation delivery. It also delivers dose escalation or reirradiation of patients who
would otherwise not be candidates with the conventional external beam radiation. 19
Advances in RT are now aimed at improving RT delivery accuracy and the planning and verification of
radiation, all to improve the accuracy of radiation dose to the affected tissue while decreasing the dose
received by normal tissue. Conventionally, RT is delivered in a uniform field. With the use of special
shields, wedges, compensators, or blocks, the beam can be modified to deliver differential doses to
different tissues. Current technology makes use of a MLC, which utilizes narrow strips of metal mounted
on the head of Linac machine. The MLC can be programmed to statically or dynamically conform the
aperture of the radiation to adjust to differentially delivery of radiation to the various tissues, with the
goal of excluding a significant amount of radiation to normal tissue. This technology is supplemented
with the implementation of IMRT, a three-dimensional treatment planning, and computer-controlled RT
delivery system. The system utilizes computed tomography images to specify the dose-based or dose
volume–based parameters of radiation to the target tissue (tumor and margin for uncertainty) as well as
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the surrounding normal tissue to plan an optimized nonuniform radiation beam intensity to different
tissue (Figure 23.2) This is then calculated into an algorithm for controlling the MLC to deliver the
appropriate dose to the target tissue. 20 Different structures will receive varying doses of radiation during
the therapy treatment. With the advent of IGRT, the therapy sessions are further tailored to the changing
evolution of the tumor by evaluating alterations to the initial plan with serial imaging throughout the
treatment processes. The changes in tumor size or anatomical changes facilitate adapting the treatment
plan. This can further reduce the radiation exposure to surrounding structures by decreasing the margin
of uncertainty that is generally applied when making the dose-based parameters in the initial planning of
the therapy. 21
FIGURE 23.2 Intensity-modulated radiotherapy. Preoperative radiation plan for a patient with a right thigh sarcoma. A. Color
wash of low-dose radiation, sparing a skin strip and vital midline structures. B. Color wash of high-dose radiation, sparing the
adjacent femur.
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Radiation Toxicity
As described earlier, RT affects cells through molecular injury either by direct disruption of the DNA
structure or through ionization of an intermediary, producing free radicals to interact and damage DNA.
5 This damage affects both the target tissue and the normal surrounding tissue, resulting in radiation
toxicity of the normal tissue. Radiation toxicity can be classified as either acute, delayed acute, or late
toxicities to tissue.
DNA damage preferentially affects cells during the proliferative phase of the cell cycle, therefore
primarily affecting cells with rapid turnover such as oral mucosa and epithelium. Injury to these cells
causes an acute toxicity. The pathophysiology of the acute toxicity is from free radicals and irreversible
breaks in DNA leading to a local inflammatory cascade of cytokines (IL-1, IL-3, IL-5, IL-6, TNF-α),
chemokines (IL-8, eotaxin, CCR receptor), receptor tyrosine kinase, and adhesion molecules (ICAM-1,
VCAM, E-selectin), which recruit an eosinophil and neutrophil response, driving a self-perpetuating
tissue damage. In the skin, injury can also affect the epidermal permeability barrier, facilitating increased
entrance of toxins and antigens to aggravate dermal inflammation, and can predispose the epidermis to
infections. 22 This form of injury presents 2 to 4 weeks after the initiation of therapy, is dependent on the
dose of radiation, volume of tissue irradiated, or concurrent chemotherapeutic drug use, and is generally
reversible with healing beginning at about 2 weeks after the completion of therapy owing to the slow
turnover of progenitor stem cells. Acute toxicity typically presents with skin erythema, edema,
pigmentary changes, depilation, wet and dry desquamation, mucositis, and esophagitis (Figure 23.3). The
exception to the reversibility of this injury is a result from injury to the progenitor stem cells that can
occur with high doses of radiation. This is termed consequential damage and can present as ulceration or
necrosis to the site of radiation toxicity. 5,23
FIGURE 23.3 Acute radiation toxicity. A. Hyperpigmentation of left chest 1 week following completion of radiation therapy. B.
Dry desquamation and hyperpigmentation of inframammary fold following radiation therapy.
Similar to acute toxicity, there can be a delayed acute toxicity in certain tissues. Examples include acute
radiation pneumonitis, which occurs 8 to 16 weeks following the initiation of radiation to the lung and is
due to endothelial and epithelial cells death, microvascular thrombosis, and type II pneumocyte
desquamation. 5 Lhermitte syndrome is a temporary demyelination of the posterior columns during
spinal irradiation, presenting 2 to 6 months following RT. 5
Late or chronic toxicity can be seen about 6 months to years following the completion of RT and is
generally not reversible. The main characteristic is stromal tissue fibrosis but can also present as
parenchymal tissue atrophy, as a result of cell apoptosis, necrosis, or senescence. 5 Damage can be
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predominantly seen in vessel endothelium, particularly capillaries, resulting in telangiectasia and tissue
ischemia. Owing to poor vascularity, the tissue becomes fragile and susceptible to breakdown and poor
wound healing with minor trauma. Injury can also be caused by damage to parenchymal cells with slow
cell regeneration and poor repopulation from a stem cell population (Figure 23.4).
FIGURE 23.4 Chronic radiation toxicity. A. Telangiectasia of left chest mastectomy scar. B. Fibrosis of right neck. C. Chronic
nonhealing wound for 8 months, 7 years after completion of radiation therapy.
The pathophysiology behind the fibrosis response to RT is thought to be activated by cyclin-dependent
kinase inhibitors p21, p27, and p16 which coordinate cell cycle arrest, ensuing in a predominantly TGF-β1
self-perpetuating expression, mediating terminal differentiation of progenitor fibroblasts into postmitotic
fibroblasts, leading to an upregulation of collagen production with resultant fibrosis. 24,25
The effect of radiation toxicity is dependent on the dose of radiation given, with more severe injury
occurring with higher doses of radiation, the volume of tissue being irradiated, and the time frame at
which the dose is given or the fractions. 5,23 Fractions of radiation doses are aimed at delivering lower
daily doses of radiation over a prolonged period of time, so that the tumor is given high doses, while
allowing normal tissue to heal, therefore decreasing the toxicity to this tissue. The biologic effects
depending on the four R’s of radiation biology: repopulation, redistribution, repair, and reoxygenation. 25
Various factors can additionally exacerbate the radiation effects. These include patient related factors,
including smoking, obesity, overlapping skin folds (in skin toxicity), poor nutrition, and preexisting
trauma to the tissue; genetic disorders including ataxia telangiectasia, Gorlin syndrome, Fanconi anemia,
Bloom syndrome, xeroderma pigmentosum, familial polyposis, Gardner syndrome, hereditary malignant
melanoma, and dysplastic nevus 
 syndrome; systemic diseases such as scleroderma, systemic lupus
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erythematosus, rheumatoid arthritis, hyperthyroidism, and diabetes mellitus; and certain therapeutic
agents, particularly chemotherapeutic agents including doxorubicin, tamoxifen, methotrexate, bleomycin,
5-fluorouracil, and actinomycin D. 22,23,26
Given the complexity of timing of radiation injury, it has been proposed to delay RT at least seven or
more days after surgery to allow adequate time for healing. Similarly, surgery should be delayed 3 to
10 weeks after completion of RT for optimal wound healing after the effects of acute radiation toxicity has
resolved but before the onset of the deleterious effects of delayed tissue toxicity. Additionally, given the
relative hypoxia and hypovascularity of radiated tissue, improving blood supply through the recruitment
of healthy, nonirradiated tissue to the site of radiation has been shown to decrease wound complication
and breakdown. 25
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Specific Therapies and Toxicities
Breast Cancer
RT in breast cancer serves as an adjunct in eradicating microscopic disease after surgical excision of gross
tumor, leading to a reduction in local recurrence and increasing breast cancer–specific survival.
Guidelines for its use have been set in breast conservation therapy (BCT) and in certain postmastectomy
patients.
Several randomized control trials (RCTs) have demonstrated the benefit of RT in decreasing local
recurrence rates in BCT for early-stage invasive breast cancer and ductal carcinoma in situ. NSABP B-06,
the largest trial, which included 1851 patients with tumors of 4 cm or less, demonstrated a local
recurrence rate of 14.8% in the mastectomy group, 17.5% in the lumpectomy group compared with 8.1%
in the lumpectomy and RT group at 20 years. There was no significant difference in disease-free or overall
survival among the three groups. This study was substantiated by additional RCTs and a meta-analysis
by the EBCTCG group that demonstrated similar results.
Absolute contraindications to RT in BCT include pregnancy, positive margins, multicentric cancer, or
diffuse malignant-appearing calcifications. Relative contraindications to RT include a history of prior RT
to the chest and patients with collagen vascular disease, most prominently in patients with scleroderma.
In patients over the age of 70 years who are undergoing BCT for small, node-negative, estrogen receptor–
positive breast cancer, who plan on receiving hormonal therapy, local recurrence rates have been
demonstrated to be sufficiently low that RT may be omitted in their cancer therapy plan.
Although specific regimens for breast RT vary among institutions, the standard course of RT for whole
breast radiation consists of 50 to 50.4 grays (Gy), delivered in 25 to 26 fractions, followed by a 10 to 16 Gy
boost, which is additional radiation aimed specifically at the tumor bed. Various alternative methods of
treatment have been developed to improve breast RT. Hypofractionation, in which larger than standard
doses of radiation over fewer fraction doses, has been devised to decrease treatment length of time. This
treatment has been found to have compatible aesthetic outcome and recurrence rates compared with
standard RT regimens. Currently, hypofractionation is considered appropriate in all patients, with any
stage disease, provided that the intent is to treat the whole breast without an additional field to cover
regional lymph nodes, with any chemotherapy, and a radiation plan with any volume of the breast
receiving >105% of the prescription dose should be minimized regardless of the dose fractionation. 27
Additional alternatives include prone breast irradiation and accelerated partial breast irradiation,
wherein larger doses are delivered to the postsurgical cavity with a specified surrounding margin, over 1
to 2 weeks, in order to decrease the RT dose to the normal tissue. Methods of RT delivery include
multicatheter brachytherapy, intracavitary balloon brachytherapy, intraoperative RT, and external beam
conformal therapy. The use of accelerated partial breast irradiation is still in clinical trials but may be
acceptable in patients over the age of 50 years with negative margins by ≥2 mm, Tis or T1 stage, and
ductal carcinoma in situ.
RT for postmastectomy patients is recommended in patients with four or more positive axillary lymph
nodes, primary tumors greater than 5 cm with any number of positive nodes, or any T4 tumors.
Postmastectomy radiation therapy (PMRT) is controversial for patients with one to three positive lymph
nodes, with research still in progress to determine its efficacy. 28-30
In plastic surgery, we are asked to perform breast reconstruction after the patient has undergone RT,
either after failed BCT or as a delayed reconstruction after PMRT, or prior to radiation as in immediate
breast reconstruction after mastectomy in patients who have a high likelihood of requiring PMRT. In
patients with previous breast RT, studies have shown an increased incidence of implant-based
reconstructive failure (14% pooled analysis) and complication rate, including capsular contracture risk,
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infection, mastectomy flap necrosis, and seroma. 31,32 Traditionally, it is recommended that patients with
previous RT undergo autologous tissue reconstruction with either a latissimus dorsi myocutaneous flap
with or without implant reconstruction, decreasing the incidence of reconstructive failure by 72%, or by
means of other autologous reconstruction. 31 However, in patients who have undergone RT, the dissection
for free flap reconstruction can have increased fibrosis. These patients have shown to have an in increase
in intraoperative microvascular complications as well as postoperative minor complications, without an
increased risk of flap loss. 33,34 In patients who are to undergo PMRT, institutional protocols differ with
regard to radiation after tissue expansion or after the final implant reconstruction, depending on
surgeon’s or radiation oncologist’s preference for improved RT to the internal mammary lymph nodes.
Various systemic reviews have been conducted on the subject without clear consensus as to which, RT to
tissue expander (TE) or to the permanent implant, has superior results in reconstruction. Many meta-
analyses show an increased rate of reconstructive failure when RT is applied to the TE with an increased
rate of capsular contracture when RT is applied to the final implant; however, there are systemic reviews
that show contradictory results. 34-36 When considering autologous breast reconstruction in the setting of
PMRT, there has been a move toward delayed immediate reconstruction to avoid direct radiation of the
free flap, which can result in increased flap fat necrosis. The idea behind this technique is to place a TE at
the time of mastectomy to act as a placeholder if RT were to be necessary to preserve the breast pocket. If
radiation is not required or following radiation, the expander is removed and autologous reconstruction
can proceed. 34,37
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Head and Neck Cancer
Head and neck cancers (HNC) are a group of cancers primarily involving the hypopharynx, oropharynx,
lip, oral cavity, nasopharynx, or larynx, with the majority of the cancers being squamous cell carcinomas.
RT plays an integral role as the primary modality in many early-stage diseases, as well as part of a
multimodality treatment for the more common presentation of locally advanced HNC, which may
include chemoradiation therapy, induction chemotherapy followed by cetuximab and RT or
chemoradiation therapy with surgery.
The standard of RT care in HNC is the use of IMRT or other three-dimensional conformal techniques,
including IGRT and proton beam therapy, to reduce the radiation dose to closely located organs,
including the parotid and other salivary glands, temporal lobes, and auditory optic or intracranial
structures. Additionally, various fractionation treatments exist in HNC RT. The commonly used
simultaneous integrated boost technique uses differential dose painting of 66 to 74 Gy to gross disease and
50 to 60 Gy to subclinical disease, administered in various fractionation/hyperfractionation schedules.
Given the complex interplay between various radiation technologies, fractionation regimens, and
chemotherapy options, there is a large combination of therapies available that can affect local toxicity as
well as tumor control. 38
Acute radiation toxicities in HNC include mucositis, xerostomia, mucosal infection including candidiasis,
pain, and sensory disturbances. Mucositis affects the majority of HNC patients undergoing RT and
presents with significant pain that can result in decreased nutritional status requiring gastric tubes or
other forms of nutritional supplementation. Presentation includes erythema beginning at 2 to 3 weeks
after the start of RT followed by progression to ulceration and pseudomembranes, peaking at the end of
RT, and continuing for 2 to 4 weeks after the end of RT. Concurrent chemotherapy or targeted therapies
can prolong or amplify mucositis. Treatment is aimed at alleviating symptoms and includes oral care,
pain control with morphine and doxepin mouthwashes and oral analgesics, wound healing promotion
with the use of zinc, and photomodulation therapy. 39
Xerostomia results from damage to the acinar cells of salivary glands. The damage can be transient,
beginning after the first week of RT and terminating 3 months after completion of treatment. However,
when the dose exceeds 52 Gy, the damage can become permanent. Changes in salivary production can
have an effect on oral lubrication, oral pH (resulting in a more acidic environment),
demineralization/remineralization of tooth surfaces, and oral flora equilibrium, which can cause difficulty
in chewing and swallowing, periodontal disease, halitosis, pain, and contribute to changes in taste.
Treatment includes saliva substitutes, saliva-stimulating medications, including parasympathomimetic
medications that stimulate cholinergic receptors, including pilocarpine or cevimeline, as well as good oral
hygiene. 40
Chronic radiation toxicities include tissue fibrosis, permanent salivary gland dysfunction as previously
discussed, and osteoradionecrosis (ORN) which will be discussed separately. Fibrosis can affect any
number of tissues in the radiated field. Radiation can affect muscular function as with the muscles of
mastication, muscles of the pharynx, and lingual muscles, which can result in trismus, dysphagia, and
poor tongue function, respectively. Of note, radiation to the neck can result in fibrosis of the nerves and
vessels in the neck, making microvascular anastomoses more challenging. 39
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Nonmelanoma Skin Cancers
Nonmelanoma skin cancers are the most common malignancies in the world, with basal cell cancer (BCC)
and squamous cell cancer (SCC) accounting for 99% of these cancers. Other nonmelanoma skin cancers
include Merkel cell carcinoma (MCC), dermatofibrosarcoma, primary cutaneous B cell lymphoma, Kaposi
sarcoma, and carcinosarcoma.
RT has had a long history in the treatment of many of these malignancies. Given better-quality evidence
on treatment efficacy and changing radiation technologies, the role of RT for these cancers continues to
evolve. Current guidelines for RT use are delineated at the National Comprehensive Cancer Network and
the American Joint Committee on Cancer. For BCC and SCC, the primary treatment remains Mohs
micrographic surgery or surgical excision. However, if the patient is not a surgical candidate or has a
preference for RT, then RT may be the primary therapy for low- or high-grade BCC and SCC. RT should
not be chosen as a first-line agent owing to the higher recurrence rate compared with surgical excision,
7.5% versus 0.7% for BCC and between 4% and 7% for SCC. Additionally, this therapy is generally
reserved for patients older than 60 years owing to concerns over long-term sequela, has been found to
have poorer appearance, and has more posttreatment complications. RT is advocated as adjuvant RT for
BCC with perineural involvement or positive tissue margins. It is also useful in SCC with perineural
involvement, positive margins that are not candidates for re-excision, or for regional therapy after lymph
node dissection.
Therapy modality varies depending on institutional preferences. Given the superficial nature of the
malignancy, therapy options that deliver the majority of their energy at the surface of the skin, including
kilovoltage and electron therapy, are the mainstay of treatment. Although not sanctioned by the National
Comprehensive Cancer Network due to insufficient data on long-term efficacy, brachytherapy may have
a role owing to its shorter treatment course, shallow dose deposition, and ability to conform to irregular
surfaces. 41-43
Unlike SCC and BCC, MCC is a neuroendocrine tumor of the skin with a highly aggressive nature and
rate of local recurrence, regional, and distant metastatic rates (25%–30%, 52%–59%, and 34%–36%,
respectively). RT is advocated as a primary therapy in patients who are not candidates for surgical
excision and as an adjuvant therapy to surgical excision in all instances of MCC except when the tumor is
less than 1 cm after undergoing wide local excision and is without lymphovascular invasion or
immunosuppression of the patient. RT is also recommended for the draining nodal basin when there is a
positive sentinel lymph node with or without lymph node dissection.
RT toxicities for the treatment of skin cancers have been listed previously and include erythema,
hyperpigmentation, dry and moist desquamation, acute ulceration, chronic wounds and skin necrosis as
consequential damage, and fibrosis, atrophy, hypo-/hyperpigmentation, and telangiectasias. 23
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Sarcoma
Malignancies of mesenchymal cell origin are classified as sarcomas. This category of cancers is a
heterogeneous group of rare solid tumors that account for approximately 1% of all adult malignancies
and about 15% of all pediatric malignancies. Sarcomas are subclassified into two distinct groups,
including soft tissue sarcomas, which include malignancy of fat, muscle, nerve, nerve sheath, blood
vessels, and other connective tissues, and malignancy of bone. The most common subtype of soft tissue
sarcoma in adults is undifferentiated pleomorphic sarcoma, while the most common subtype in children
is rhabdomyosarcoma. The most common location of disease is the extremity (43%) with the most
common location of metastasis being the lung. One of the main risk factors for developing sarcomas
includes prior RT.
Treatment of sarcoma with adjuvant RT should be considered for all adult patients, unless they present
with stage I disease with negative margins after resection. There continues to be a debate of whether RT
should be administered prior to surgical excision or after surgical excision. The advantages of
preoperative RT include possible regression of the tumor size prior to excision, formation of a
pseudocapsule to ease excision of tumor, decrease seeding of cancer during the tumor manipulation
during surgery, and reduction of late toxicities when treated with IGRT. However, preoperative RT has
been shown to decrease wound healing after surgery and requires the surgical team to wait 3 to 6 weeks
until they can excise the tumor. For this reason, plastic surgeons are often called to aid with closure and
reconstruction to improve soft tissue wound healing.
Postoperative RT facilitates excision of the tumor without delaying therapy. It has also been shown to
improve local tumor control when positive surgical margins are present. The disadvantage of using this
regimen, however, is its association with higher rates of long-term treatment related side effects. Despite
the differences in timing, there has been no evidence to suggest differences in disease outcomes between
the two regimens. 44,45
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Additional Toxicities
Osteoradionecrosis
Late radiation toxicity to bone may manifest as ORN. It is defined as chronically exposed devitalized
irradiated bone for 3 to 6 months without the recurrence of tumor. About 70% to 94% of cases are seen in
the first 3 years following RT but can occur at any point after RT. ORN can occur at multiple sites,
including the maxilla, sternum, pelvis, temporal bone, and vertebrae, but is generally seen in the
mandible after irradiation of HNC. The pathophysiology of ORN suggests that the mechanism for its
development may be due to microvascular thrombosis and decreased vascularity, abnormal fibroblastic
activity, and fibroblastic remodeling leading to bone fibrosis and loss of osteocytes in the bone. 39,46
Risk factors for developing ORN include hyperfractionated irradiation regimens, with a higher total dose
to the bone exceeding 6000 cGy, concomitant chemotherapy, pre- or postirradiation dental extraction or
trauma to the irradiated bone (preirradiation extraction with irradiation occurring before the bone has
been given time to heal), poor oral hygiene and periodontal disease contributing to local infection, and
alcohol and tobacco use. 46
Treatment of ORN includes prevention with dental care before the initiation of RT. Early-stage disease is
treated with conservative management with improved oral hygiene, saline irrigation, antibiotic therapy,
hyperbaric oxygen therapy, and newer medical modalities including pentoxifylline and tocopherol, with
resolution in about 8%–33% of patients after 1 year. It should be noted that therapy with hyperbaric
oxygen therapy is controversial with some data reporting a lack of efficacy. Later-stage ORN can be
treated with wound debridement, sequestrectomy, decortication and resection of necrotic bone, and free
flap reconstruction. 39,46
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Lymphedema
In the United States, the leading cause of lymphedema comes from lymph node dissection for cancer
therapy. Given the prevalence of breast cancer with the primary source of metastasis to axillary lymph
nodes resulting in lymph node dissection, it has become the most common cause of lymphedema in the
Western countries. RT has been identified as a major risk factor for lymphedema after lymph node
dissection for breast cancer as well as other malignancies. 29,47,48 In a study by Chandra et al., the 2-year
incidence of lymphedema in breast cancer patients treated with RT who had undergone regional lymph
node dissection ranged between 20% and 22% depending on the type of RT administered to the axilla.
Risk factors for the development of lymphedema in the setting of axillary RT included axillary node
dissection compared with sentinel lymph node dissection and increased body mass index. 48 The
mechanism by which radiation results in lymphedema can be attributed to depletion of lymphatic vessels
and endothelial cells as well as increased fibrosis. 47
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Radiation-Induced Malignancies
Radiation may cause mutations in normal tissue resulting in various other malignancies. Cahan criteria to
define radiation-induced malignancies (RIMs) include: a malignancy arising in an irradiated field,
sufficient latency between the initial RT and new malignancy (generally longer than 4 years), a new
malignancy of different histology to the primary cancer, and tissue of the new malignancy that is
genetically and metabolically normal prior to the radiation exposure. For this reason, RIM is a
complication that affects cancer survivors. Histologically, sarcomas are most common RIM in tissues
receiving high-dose RT. Patients who undergo RT for HNC are at increased risk of developing SCC
followed by sarcoma RIM. Patients who undergo RT for breast cancer are at increased risk for developing
carcinoma of the lung, contralateral breast, esophagus, and sarcoma RIM. Those patients who underwent
mantle field RT for Hodgkin disease are at increased risk of developing breast, lung, and thyroid RIM.
Patients who undergo craniospinal RT and total body irradiation are at increased risk of meningioma,
glioma, leukemia, and lymphomas. Risk factors for developing a RIM include higher radiation doses,
chemotherapy, environmental exposures such as smoking, hereditary predisposition (familial
retinoblastoma, Li-Fraumeni syndrome, tuberous sclerosis, and neurofibromatosis I), and age of RT, with
a significant increase in RIM in pediatric patients undergoing RT. The increased risk of RIM with age is
thought to be multifactorial with genotoxic injury to stem cells and longer survival of childhood
malignancies both contributing to RIM. 49
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General Considerations in Treatment of Cutaneous Radiation
Toxicities
Acute Toxicities
Management of acute cutaneous toxicities (ACT) can be divided into preventive and treatment therapies.
Currently, there are no standardized guidelines in the management of ACT. It is up to the discretion of
the treating institution to decide on best practices. A recent meta-analysis of RCTs may be able to better
direct treating physicians on best practices, although further research is still warranted (Table 23.1).
TABLE 23.1
Radiation Toxicity Treatments
Acute Cutaneous Toxicities
Preventive Treatment
Pharmacotherapy
Wobe-Mugos®
Lifestyle
modification
Hygiene with mild soap and water
Water-based lanolin-free moisturizer
Avoidance of metallic-based deodorants
Wearing loose fitting clothing
Avoidance of sun exposure
Active Treatment
Lifestyle
modification
Hygiene with soap and water
Pharmacotherapy
Wobe-Mugos®
Zinc supplementation
Erythema and dry
desquamation
Pharmacotherapy
0.1% betamethasone cream or 0.1% methylprednisolone cream
Conflicting data exist on efficacy of hyaluronic acid
Moist desquamation
Dressings
Treatment with hydrogel, silver nylon, or Mepilex Lite® dressing
Full-thickness
necrosis/ulceration
Treatment with discontinuation of radiation therapy, debridement, and wound
care
Late Cutaneous Toxicities
Telangiectasia
Pulsed dye laser therapy
Ulceration and necrosis
Lifestyle
modification
Local wound care
Pharmacotherapy
Hydrophilic or lipophilic barrier cream
Dressings
Hydrogel dressing to increase moisture to wound
Hydrocolloid dressing to decrease moisture to exudative wounds
Infected wounds
Dressings
Antibacterial agents with or without silver-based dressings
Severe ulceration
Surgical management with flap reconstruction
Rule out radiation-induced malignancies
Fibrosis
Rehabilitative
therapy
Physical therapy or massage therapy
Pharmacotherapy
Pentoxifylline and tocopherol with long-term therapy
Superoxide dismutase may be useful, but larger trials are warranted to determine
efficacy
Severe fibrosis
Excision of fibrosis with healthy tissue interposition
For preventive management of ACT, oral Wobe-Mugos® (proteolytic enzyme containing 100 mg papain,
40 mg trypsin, 40 mg chymotrypsin) was found to decrease the risk of developing an ACT by 87%. It is
generally recommended that patients practice good hygiene with mild soaps and water, followed by
water-based lanolin-free moisturizers, and avoiding metallic-based deodorants. However, no RCT
validated these practices. Additional common recommendations, not covered by the meta-analysis,
include wearing loose fitting clothing and avoiding sun exposure to areas of RT.
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For treatment of ACT, oral Wobe-Mugos® as well as 25 mg of zinc supplementation was found to be
effective at reducing the severity of ACT. Small studies have shown that 0.1% betamethasone cream and
0.1% methylprednisolone were effective at reducing the severity of ACT. There are conflicting results on
whether the use of topical hyaluronic acid is effective at reducing ACT severity. When dressings are
required for treatment of moist desquamation, hydrogel, silver nylon, and Mepilex Lite® dressings may
be more effective at decreasing time to healing compared with other dressings. Finally, washing with
soap compared with no washing or washing with only water was found to be more effective at
decreasing desquamation and severity of erythema. Of note, in severe ACT when full-thickness skin
necrosis and ulceration occur, the treatment should include discontinuation of RT, debridement, and
advanced wound care management. 23,50
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Late Toxicities
Unlike ACT, late cutaneous toxicities are not transient and may require intervention for resolution. For
the treatment of telangiectasias associated with late cutaneous toxicities, pulsed dye laser therapy has
been shown to have satisfactory results on physical appearance of the skin. Patients who present with
chronic ulcerations and necrosis may be treated with local wound care with hydrophilic or lipophilic
barrier creams and hydrogel or hydrocolloid dressings depending on amount of wound exudate. Infected
wounds benefit from antibacterial agents with or without silver-based dressings. Finally, severe
ulcerations may require surgical management with flap reconstruction. It is important to rule out
secondary skin malignancies in refractory ulcers, as they can have a similar presentation. 23
RT-induced fibrosis may be more difficult to manage with therapies consisting of rehabilitative care
including several massage techniques as well as physical therapy to reduce contraction and improve
movement. Pharmacotherapy with pentoxifylline, a methylated xanthine derivative, with concurrent
tocopherol (vitamin E), shows promise at reducing superficial fibrosis with long-term therapy. Small
trials with superoxide dismutase, an antioxidant enzyme may also be useful at decreasing fibrosis, but
larger studies are required before asserting its efficacy. In severe cases of fibrosis, where there is poor
quality of life, very limited mobility, and pain, surgery to remove the area of fibrosis with interposition of
healthy vascularized tissue may be considered. Clinical suspicion should be heightened in these patients,
as they may be at risk for tumor recurrence or an RIM. It is important to weigh the risk and benefits of
such intervention, as there can exacerbate fibrosis and patients are at increased risk for wound healing. 23
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Conclusion
There have been great advancements in the management of malignancies with the use of RT as a primary
or multidisciplinary mode of therapy. With the advent of IMRT and IGRT in radiation planning and
delivery to the site of interest, ionizing radiation can more accurately be directed at the tumor while
minimizing the toxicity to the surrounding normal tissue, improving the therapeutic ratio.
Despite these improvements, radiation is still responsible for local tissue injury, both acute and late
toxicities. Although acute local tissue toxicities are reversible and can be managed with proper wound
care, late toxicities may require further and more drastic interventions for resolution. Key plastic surgery
concepts can be employed to improve the detrimental effects of fibrosis, including decreased mobility,
pain, or chronic wounds. For areas with contracture bands, Z-plasties can be used to improve joint range
of motion or tissue pliability. Healthy, nonradiated tissue should be brought into the areas of radiation
injury, as they can provide vascularized tissue to areas with contracture and poor tissue perfusion. These
can include pedicled muscle flaps like a latissimus dorsi, vertical rectus myocutaneous flap or transverse
myocutaneous flap, or fasciocutaneous flaps. If no local, unirradiated tissue is available, free flaps should
be used for reconstruction.
Given the tremendous improvement in cancer survival with the use of RT, more patients will be
requiring reconstruction of difficult-to-manage resection defects and late local toxicity injuries. It is
important for the plastic surgeon to understand the pathophysiology behind radiation injury to more
properly treat this patient population.
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Questions
1. A 55-year-old woman with a history of a 6 cm mass of the left breast, found to be invasive ductal
carcinoma with positive regional lymph node, who underwent left mastectomy and RT to the breast
15 years prior, now presents with a 1 cm nonhealing wound on the superior medial border of the
chest wall. What should the next step be?
a. Local wound care and antibiotic therapy
b. Local tissue rearrangement for reconstruction
c. Pectoralis major turnover flap
d. Free transverse rectus abdominis myocutaneous flap with microvascular anastomosis to the
thoracodorsal vessels for coverage of the sinus as well as breast reconstruction
e. Biopsy and culture of wound
2. When performing autologous breast reconstruction of a previously irradiated breast, there is an
increased risk of
a. Mastectomy flap loss compared with implant-based reconstruction
b. Implant loss with latissimus dorsi reconstruction
c. Free flap necrosis compared with nonirradiated tissue
d. Microvascular complication compared with nonirradiated tissue
e. None of the above; there is no increased complication risk when using autologous
reconstruction in an irradiated field
3. Risk factors for developing ORN of the mandible include all of the following except
a. Radiation at doses higher than 30 Gy
b. Extraction of tooth to the area of radiated bone after RT
c. Tobacco use
d. Poor oral hygiene
e. Alcohol use
4. A 40-year-old man with an undifferentiated pleomorphic sarcoma of the right lower extremity,
who underwent preoperative RT 3 weeks prior to tumor excision. The sarcoma now measures
5 × 5 cm and is located on the medial lower extremity 2 cm below the knee. What is the optimal
reconstructive option?
a. Lateral gastrocnemius flap
b. Medial gastrocnemius flap
c. Local random rotational flap
d. Right anterior lateral thigh flap
e. Deep inferior epigastric perforator flap
5. Fibrosis following RT is associated with all of the following except
a. Differentiation of fibroblasts to postmitotic fibroblasts resulting in the upregulation of
collagen
b. Upregulation of TGF-β1 expression
c. Dose dependent
d. Usually presents 2 to 3 weeks after the completion of RT
e. Potentiated by concurrent chemotherapeutic agents including doxorubicin, tamoxifen,
methotrexate, bleomycin, 5-fluorouracil, and actinomycin D
1. Answer: e. A patient with a history of cancer and RT 15 years prior with a new wound should be
worked up for an RIM. Radiation-induced, nonbreast cancer malignancies have a 23% higher
incidence in irradiated breast cancer patients compared with the general female population. This
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population has a higher risk of second cancer of the lung, esophagus, thyroid, and sarcoma that
increases over time, peaking at 10 to 15 years after initial cancer diagnosis. The standardized
incidence ratio of sarcoma is 6.54 in irradiated patients compared with 1.42 in nonirradiated patients.
2. Answer: d. Microvascular arterial complications are significantly more common in a radiated field
compared with a nonirradiated field. Radiation, however, did not have an impact on outcomes,
including fat necrosis or flap loss. There is no difference in breast-related complications when
comparing implant-based or autologous reconstruction in a radiated breast. Furthermore, there is a
decrease in implant loss when reconstructed with a latissimus dorsi flap compared with no
autologous reconstruction.
3. Answer: a. Risk factors for developing ORN of the mandible include radiation at doses higher than
60 Gy, trauma or surgery to the radiated field including tooth extraction, social habits including
tobacco and alcohol use, and poor oral hygiene leading to periodontal disease and caries.
4. Answer: d. After RT, tissue to the irradiated field has poor wound healing capabilities due to the
slow turnover of progenitor cells. Chronically, there is damage to vessel endothelium, predisposing
radiated tissue to poor wound healing with minor trauma. For this reason, reconstruction should
recruit nonradiated tissue to improve wound healing after tumor excision. A right anterior lateral
thigh flap would offer nonradiated tissue with less donor site morbidity compared with a deep
inferior epigastric perforator flap.
5. Answer: d. Fibrosis following RT is associated with the upregulation of TGF-β1 expression,
resulting in the differentiation of postmitotic fibroblasts and subsequent upregulation of collagen
formation. It is dose dependent, with increased risk of fibrosis with higher doses of radiation. Many
factors can exacerbate fibrosis, including smoking, obesity, overlapping skin folds, poor nutrition,
preexisting trauma to the tissue, genetic disorders, systemic diseases, and chemotherapeutic agents
including doxorubicin, tamoxifen, methotrexate, bleomycin, 5-fluorouracil, 
 and actinomycin D.
Fibrosis is a manifestation of late radiation toxicity, appearing about 6 months to years following the
completion of RT.
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References
Laughlin, JS. Development of the technology of radiation therapy. Radiographics. 1989;9(6):1245-1266.
Timins, JK. Communication of benefits and risks of medical radiation: a historical perspective. Health Phys. 2011;101(5):562-565.
Kaplan, HS. Basic principles in radiation oncology. Cancer. 1977;39(2 suppl):689-693.
Miller, KD, Siegel, RL, Lin, CC, et al. Cancer treatment and survivorship statistics, 2016. CA Cancer J Clin. 2016;66(4):271-289.A collaborative
effort between the American Cancer Society and the National Cancer Institute estimating cancer survivorship as well as treatment patterns and
treatment-related side effects in an attempt to raise awareness of survivorship issues.
Fajardo, LF, Berthrong, M, Anderson, RE, Meyer, JL. Radiation Pathology. Oxford University Press; 2001.
Chargari, C, Magne, N, Guy, JB, et al. Optimize and refine therapeutic index in radiation therapy: overview of a century. Cancer Treat Rev.
2016;45:58-67.
Bloomer, WD, Hellman, S. Normal tissue responses to radiation therapy. N Engl J Med. 1975;293(2):80-83.A description of the normal tissue
response curve to radiation therapy in comparison to the tumor response curve, resulting in the understanding of the therapeutic index.
Wolstenholme, V, Glees, JP. The role of kilovoltage X-rays in the treatment of skin cancers. Eur Oncol Haematol. 2006;1(1):32.
Hill, R, Healy, B, Holloway, L, et al. Advances in kilovoltage x-ray beam dosimetry. Phys Med Biol. 2014;59(6): R183-R231.
Mitin, T, Zietman, AL. Promise and pitfalls of heavy-particles therapy. J Clin Oncol. 2014;32(26):2855-2863.
Combs, SE, Debus, J. Treatment with heavy charged particles: systematic review of clinical data and current clinical (comparative) trials. Acta
Oncol. 2013;52(7):1272-1286.
Urie, MM, Sisterson, JM, Koehler, AM, Goitein, M, Zoesman, J. Proton beam penumbra: effects of separation between patient and beam
modifying devices. Med Phys. 1986;13(5):734-741.
Bassal, M, Mertens, AC, Taylor, L, et al. Risk of selected subsequent carcinomas in survivors of childhood cancer: a report from the
Childhood Cancer Survivor Study. J Clin Oncol. 2006;24(3):476-483.
Sadeghi, M, Enferadi, M, Shirazi, A. External and internal radiation therapy: past and future directions. J Cancer Res Ther. 2010;6(3):239.
Jang, B-S, Chang, JH, Oh, S, Lim, YJ, Kim, IH. Surgery vs. radiotherapy in patients with uveal melanoma. Strahlenther Onkol. 2017;193(11):931-
942.
Lee, CD. Recent developments and best practice in brachytherapy treatment planning. Br J Radiol. 2014;87(1041):20140146.
Nicholas Lukens, J, Gamez, M, Hu, K, Harrison, LB. Modern brachytherapy. Semin Oncol. 2014;41(6):831-847.
Thomadsen, BR, Erickson, BA, Eifel, PJ, et al. A review of safety, quality management, and practice guidelines for high-dose-rate
brachytherapy: executive summary. Pract Radiat Oncol. 2014;4(2):65-70.
Pilar, A, Gupta, M, Laskar, SG, Laskar, S. Intraoperative radiotherapy: review of techniques and results. Ecancermedicalscience. 2017;11:1-33.
Boyer, A, Butler, B, DiPetrillo, T, et al. Intensity modulated radiotherapy: current status and issues of interest. Intensity modulated radiation
therapy collaborative working group. Int J Radiat Oncol Biol Phys. 2001;51(4):880-914.An overview, description, guidelines, and
recommendations for implementation of intensity-modulated radiation therapy by a Collaberative Working Group of experts in IMRT, formed by the
National Cancer Institute.
Goyal, S, Kataria, T. Image guidance in radiation therapy: techniques and applications. Radiol Res Pract. 2014;2014:1-10.
Jaschke, W, Schmuth, M, Trianni, A, Bartal, G. Radiation-induced skin injuries to patients: what the interventional radiologist needs to know.
Cardiovasc Intervent Radiol. 2017;40(8):1131-1140.
Bray, FN, Simmons, BJ, Wolfson, AH, Nouri, K. Acute and chronic cutaneous reactions to ionizing radiation therapy. Dermatol Ther.
2016;6(2):185-206.A review of the clinical manifestations, pathophysiology, epidemiology, risk factors, prevention, and treatment of both acute and
chronic cutaneous radiation toxicities.
Hill, RP, Rodemann, HP, Hendry, JH, et al. Normal tissue radiobiology: from the laboratory to the clinic. Int J Radiat Oncol Biol Phys.
2001;49(2):353-365.
Devalia, HL, Mansfield, L. Radiotherapy and wound healing. Int Wound J. 2008;5(1):40-44.
Wunderle, K, Gill, AS. Radiation-related injuries and their management: an update. Semin Intervent Radiol. 2015;32(2):156-162.
Smith, BD, Bellon, JR, Blitzblau, R, et al. Radiation therapy for the whole breast: executive summary of an American Society for Radiation
Oncology (ASTRO) evidence-based guideline. Pract Radiat Oncol. 2018;8(3):145-152.
Jonathan Yang, T, Ho, AY. Radiation therapy in the management of breast cancer. Surg Clin North Am. 2013;93(2):455-471.
Castaneda, SA, Strasser, J. Updates in the treatment of breast cancer with radiotherapy. Surg Oncol Clin North Am. 2017;26(3):371-382.
Recht, A, Comen, EA, Fine, RE, et al. Postmastectomy radiotherapy: an American Society of Clinical Oncology, American Society for
Radiation Oncology, and Society of Surgical Oncology focused guideline update. Pract Radiat Oncol. 2016;6(6):e219-e234.
Lee, KT, Mun, GH. Prosthetic breast reconstruction in previously irradiated breasts: a meta-analysis. J Surg Oncol. 2015;112(5):468-475.
Ascherman, JA, Hanasono, MM, Newman, MI, Hughes, DB. Implant reconstruction in breast cancer patients treated with radiation therapy.
Plast Reconstr Surg. 2006;117(2):359-365.
Fracol, ME, Basta, MN, Nelson, JA, et al. Bilateral free flap breast reconstruction after unilateral radiation: comparing intraoperative vascular
complications and postoperative outcomes in radiated versus nonradiated breasts. Ann Plast Surg. 2016;76(3):311-314.
Nelson, JA, Disa, JJ. Breast reconstruction and radiation therapy: an update. Plast Reconstr Surg. 2017;140(5):60S-68S.A review of the current
understanding and treatment options for the management of surgical reconstruction of breast cancer patients who have undergone or are to undergo
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radiation therapy.
El-Sabawi, B, Carey, JN, Hagopian, TM, et al. Radiation and breast reconstruction: algorithmic approach and evidence-based outcomes. J
Surg Oncol. 2016;113(8):906-912.
Cordeiro, PG, Albornoz, CR, McCormick, B, et al. What is the optimum timing of postmastectomy radiotherapy in two-stage prosthetic
reconstruction: radiation to the tissue expander or permanent implant? Plast Reconstr Surg. 2015;135(6):1509-1517.
Kronowitz, SJ, Hunt, KK, Kuerer, HM, et al. Delayed-immediate breast reconstruction. Plast Reconstr Surg. 2004;113(6):1617-1628.
Head and neck cancers. National Cancer Institute Website. Reviewed
Mar 29, 2017.
Sroussi, HY, Epstein, JB, Bensadoun, RJ, et al. Common oral complications of head and neck cancer radiation therapy: mucositis, infections,
saliva change, fibrosis, sensory dysfunctions, dental caries, periodontal disease, and osteoradionecrosis. Cancer Med. 2017;6(12):2918-
2931.A description of the common complications of radiation therapy in head and neck cancer, including complication grading scales, clinical
manifestations, and treatment recommendations.
Pinna, R, Campus, G, Cumbo, E, et al. Xerostomia induced by radiotherapy: an overview of the physiopathology, clinical evidence, and
management of the oral damage. Ther Clin Risk Manag. 2015;11:171-188.
Fahradyan, A, Howell, A, Wolfswinkel, E, et al. Updates on the management of non-melanoma skin cancer (NMSC). Healthcare. 2017;5(4):82.
Squamous cell skin cancer. Medline Plus. Updated August 14, 2018.
Bichakjian, CK, Olencki, T, Aasi, SZ, et al. Basal Cell Skin Cancer, Version 1.2016, NCCN Clinical Practice Guidelines in Oncology. J Natl
Compr Canc Netw. 2016;14(5):574-597.
Eastley, N, Green, PN, Ashford, RU. Soft tissue sarcoma. BMJ. 2016;352:i436.
Wang, D, Zhang, Q, Eisenberg, BL, et al. Significant reduction of late toxicities in patients with extremity sarcoma treated with image-guided
radiation therapy to a reduced target volume: results of radiation therapy oncology group RTOG-0630 trial. J Clin Oncol. 2015;33(20):2231-
2238.
Rivero, JA, Shamji, O, Kolokythas, A. Osteoradionecrosis: a review of pathophysiology, prevention and pharmacologic management using
pentoxifylline, α-tocopherol, and clodronate. Oral Surg Oral Med Oral Pathol Oral Radiol. 2017;124(5):464-471.
Avraham, T, Yan, A, Zampell, JC, et al. Radiation therapy causes loss of dermal lymphatic vessels and interferes with lymphatic function by
TGF- 1-mediated tissue fibrosis. AJP Cell Physiol. 2010;299(3):C589-C605.
Chandra, RA, Miller, CL, Skolny, MN, et al. Radiation therapy risk factors for development of lymphedema in patients treated with regional
lymph node irradiation for breast cancer. Int J Radiat Oncol Biol Phys. 2015;91(4):760-764.
Kumar, G, Yadav, V, Singh, P, Bhowmik, KT. Radiation-induced malignancies making radiotherapy a “ two-edged sword ”: a review
literature. World J Oncol. 2017;8(1):1-6.
Chan, RJ, Webster, J, Chung, B, et al. Prevention and treatment of acute radiation-induced skin reactions: a systematic review and meta-
analysis of randomized controlled trials. BMC Cancer. 2014;14:53.A meta-analysis looking at the efficacy of various interventions directed at
preventing and treating both acute and late radiation induced skin toxicities.
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C H A P T E R 2 4
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Lasers in Plastic Surgery
Nathanial R. Miletta and R. Rox Anderson, and Matthias B. Donelan
Key Points
Modern advances in laser surgery have contributed to a paradigm shift in reconstructive and
aesthetic medicine, necessitating a familiarity with this valuable modality.
Lasers generate spatially and temporally coherent electromagnetic radiation allowing the generation
of very bright and focused laser beams with medium-specific, fixed wavelengths.
Chromophores within the skin absorb specific wavelengths of light and subsequently respond with
thermal, mechanical, or chemical reactions.
The unique characteristics of lasers can be leveraged to create tools of remarkable therapeutic and
diagnostic precision in order to better optimize patient outcomes.
A conceptual overview will be presented along with representative clinical cases to better develop
the physician’s comfort level in utilizing laser surgery.
Modern advances in laser surgery have contributed to a paradigm shift in reconstructive and cosmetic
surgery that favors minimally invasive procedures, necessitating a familiarity with this valuable
modality. Laser surgery is utilized in a number of conditions germane to the plastic surgeon and may
serve as a definitive treatment of choice or as an adjuvant therapy to best optimize patient outcomes. In
the reconstructive realm, laser therapy for hypertrophic burn and trauma scars has led to significant
improvements in scar aesthetics, functioning, and symptoms often obviating the need for more extensive
surgical procedures. 1-4 Aggregated laser surgery ranks only behind botulinum toxin injections and soft
tissue fillers in cosmetic procedures performed annually and has contributed to the trend of patients
seeking aesthetic treatments earlier in life and with a more equal gender distribution. 5
Most laser platforms are now equipped with manufacturer-
 recommended starting settings that are
target and Fitzpatrick skin type (FST) specific. Although generally considered safe, the surgeon will find
that a better understanding of laser surgery will allow therapeutic customization resulting in better
patient outcomes. This chapter will highlight key concepts in laser surgery complete with representative
case examples in order to better inform the clinical decision making of the laser surgeon.
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Basic Science
Laser Light
Laser is an acronym for light-amplified stimulated emission of radiation. Lasers generate spatially and
temporally coherent electromagnetic radiation of a fixed wavelength focused into a precise beam of
energy (Figure 24.1). Lasers consist of an energy source and a medium housed within an optical cavity
(Figure 24.2). The electrons of the atoms within the medium are excited upon exposure to the energy
source, commonly a flash lamp. The medium may be a solid, liquid, or gas. As the electrons
spontaneously fall from the excited to resting state, photons with medium-specific wavelengths are
emitted. 6 Using a system of reflective and semireflective mirrors, the emitted photons are redirected back
into the medium allowing for (1) excitement of additional electrons within the medium (amplification)
and (2) coherence and collimation due to constructive and destructive interference. 7,8 Once a sufficient
amount of energy is generated, the laser beam will be allowed to exit the optical cavity. The laser light
may be delivered to the tissue by a series of mirrors within an articulating arm or transported along a
fiber optic cable.
FIGURE 24.1 Electromagnetic spectrum.
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FIGURE 24.2 Basic components of a laser.
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Laser-Tissue Interactions
Laser light may be reflected, transmitted, scattered, or absorbed by tissue. The molecules that absorb light
are known as chromophores and include hemoglobin, melanin, tattoo pigment, and water. After
absorption, chromophores may reemit photons or undergo photothermal, photomechanical, or
photochemical reactions. 9 Photothermal events represent the majority of medical laser reactions and
result from an increase of local kinetic energy and the generation of localized heat. 7 Photomechanical
reactions result in structural degradation of the chromophore through vibrations following
photoexcitation of the chromophore. 9 Photochemical reactions occur when the excited state of the
chromophore has markedly different physical or chemical properties than the resting state. 9
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Laser Variables
When choosing a laser, it is critical to consider the absorption spectrum of the chromophore and its
location within the skin. These two factors will determine the wavelength of the laser medium chosen,
both for absorption and depth of laser penetration (Table 24.1 and Figure 24.3). Laser wavelength and
depth are directly proportional until water begins to serve as the primary chromophore, at which point,
laser penetration decreases owing to the ubiquity and highly absorptive nature of water. The amount of
physiologic melanin present must be considered, and the wavelength selected should minimize collateral
injury that could result in dyspigmentation. The pulse width of the laser may vary by several orders of
magnitude and should be carefully titrated based upon the thermal relaxation time (TRT) of the target,
which corresponds to its size (Table 24.2). 7 The pulse width should not exceed the TRT, as this can lead to
collateral injury within the skin and a loss of selectivity. 7
TABLE 24.1
Medical Lasers
Medium
Spectrum
ʎ (nm)
Chromophore
Argon
Visible light
488, 514
Oxyhemoglobin, melanin
Intense pulsed light a
515, 560, 650
Oxyhemoglobin, melanin
Potassium titanyl phosphate (KTP)
532
Oxyhemoglobin, melanin, tattoo pigment
Yellow dye
595
Oxyhemoglobin
Ruby
694
Melanin, tattoo pigment
Alexandrite
Near infrared
755
Melanin, tattoo pigment, deoxyhemoglobin
Titanium sapphire
785
Tattoo pigment
Diode
800
Melanin, deoxyhemoglobin
Neodymium:yttrium aluminum garnet (Nd:YAG)
1064
Melanin, tattoo pigment, deoxyhemoglobin
Erbium-doped glass (Er:glass)
Mid infrared
1550
Water
Thulium-doped glass (Th:Glass)
1927
Water
Erbium:yttrium aluminum garnet (Er:YAG)
Far infrared
2940
Water
Carbon dioxide (CO2)
10,600
Water
aIntense pulsed light (IPL) is filtered light.
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FIGURE 24.3 Penetration depth of common laser mediums.
TABLE 24.2
Pulse Width Domains
Domain
Range
Continuous wave
Seconds (s)
Long pulsed
Milliseconds (ms)
Short pulsed
Nanoseconds (ns)
Ultrashort pulsed
Picoseconds (ps)
Femtoseconds (fs)
Once an appropriate wavelength and pulse width have been selected, the laser surgeon must choose a
starting fluence, which is measured in energy/treatment area. Most laser platforms recommend starting
settings from which the laser surgeon may titrate upward to the desired therapeutic end point, which is
specific to each target. Increasing the laser spot size allows for more rapid treatment sessions and a
decrease in the relative scatter of light. 
 Of note, if the spot size is increased, the fluence will likely need
to be decreased to prevent excessive energy delivery. Epidermal cooling mechanisms must be also
considered in order to prevent damage to the superficial layer of the skin and can be achieved by contact
or noncontact (spray) cooling. Hertz (Hz), or the rate in which pulses are delivered, is also important to
consider in order to avoid excessive bulk heating.
As we discuss the conditions that can be treated with lasers, we will review approaches and tips for
selecting appropriate settings, as well as, the desired therapeutic end points of the common targets within
the skin.
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Chromophores
The chromophores in the skin include oxyhemoglobin, deoxyhemoglobin, melanin, water, and tattoo
pigment (Figure 24.4). Chromophore-wavelength selectivity allows the laser surgeon to generate
photothermal, photomechanical, or photochemistry reactions limited to discrete structures or in a
spatially selective manner within the skin optimizing clinical outcomes. 7
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SKIN COMPONENT-SELECTIVE PHOTOREACTIONS
FIGURE 24.4 Chromophore absorption spectrum with common laser mediums noted.
(Courtesy of Lumenis Ltd.)
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Hemoglobin
The treatment of cutaneous vasculature relies upon the selective absorption of laser light by
oxyhemoglobin and deoxyhemoglobin and the photothermal reaction that ensues. 7 The focal heating of
intravascular hemoglobin damages vessel endothelium resulting in coagulation and vessel elimination
while sparing local tissue. 7 Oxyhemoglobin displays an absorption band from 400 to 1200 nm, with major
peaks at 418, 542, and 577 nm and a minor peak that encompasses 1064 nm (see Figure 24.4). 7
Deoxyhemoglobin demonstrates an absorption peak that includes the 755 and 800 nm wavelengths.
When treating vasculature, it is important to remember physiologic melanin absorbs laser light
particularly well at lower wavelengths. For patients with higher FSTs, longer wavelength lasers should be
utilized. When selecting a pulse width, titrate to the target (blood vessel) and not the chromophore
(hemoglobin). Epidermal cooling is important to prevent damage to the epidermis. Devices commonly
used to treat vasculature include the 532 nm potassium titanyl phosphate (KTP), 560 nm intense pulsed
light (IPL), 595 nm pulsed dye laser (PDL), 755 nm alexandrite, 810 nm diode, and 1064 nm neodymium-
doped:yttrium aluminum garnet (Nd:YAG) (Table 24.1). All of the lasers above fall in the long-pulsed
domain (Table 24.2). Fully ablative lasers targeting water as a chromophore may also be used to
nonselectively destroy vasculature in the treatment area. Many vascular conditions can be treated by
targeting hemoglobin to include capillary vascular malformations; telangiectasias; erythema; angiomas;
infantile hemangiomas; postprocedural purpura; spider veins; reticular veins; and erythematous scars.
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Capillary Vascular Malformations (Port Wine Stains)
The treatment of capillary vascular malformations, or port wine stains (PWSs), illustrates the therapeutic
rationale for treating vascular conditions. With one million patients in the United States and 22 million
affected globally, PWSs represent a common cause of presentation to the laser surgeon. 10 Without
treatment, 65% of PWSs become hypertrophic, often leading to bleeding, aesthetic deformation, and
psychological stress. 11-17 Although the etiology is unclear, the clinical phenotype results from ectatic
capillaries and postcapillary venules with varying degrees of oxygenation and dilatation within the
superficial and deep dermis. 18,19 In infants and young children, PWSs are erythematous with increased
oxyhemoglobin and respond well to shorter wavelength lasers. PWSs in adult patients are often more
violaceous owing to deoxyhemoglobin and demonstrate increased thickness necessitating use of the
longer wavelength lasers. Initiating treatment as early as possible is critical for minimizing laser light
scatter due to dermal collagen and acquired tanning melanin (Figure 24.5). 20-25
FIGURE 24.5 A. A 26-year-old, Fitzpatrick skin type (FST) II patient with an isolated facial port wine stain (PWS) presented
with concern for its color and thickness. Anesthesia was achieved with topical anesthetic. The erythematous and violaceous
nature of the PWS demonstrated the presence of both oxyhemoglobin and deoxyhemoglobin. Given the relative paucity of
melanin in FST II patients, a shorter wavelength is appropriate to target the oxyhemoglobin. The most extensively studied
device in this range for PWS and treatment of choice is the pulsed dye laser (PDL). 20,21 The long-pulsed potassium titanyl
phosphate (KTP) laser, intense pulsed light (IPL), and alexandrite laser have also demonstrated efficacy in the treatment of
PWS. 20,21 Given the various sizes of the vessels within the PWS, PDL was chosen with a short pulse width of 0.45 ms, fluence
of 8 J/cm2, spot size of 7 mm, and dynamic cooling device (DCD) engaged to achieve the treatment end point of durable
purpura. 22 The pulse width was chosen to eliminate very fine vessels. A longer pulse width would have exceeded the TRT of
the narrow diameter vessels, which could have resulted in sclerotic white patches within the PWS. At subsequent treatment
sessions, the pulse width was increased to 1.5 and 3 ms with the fluence titrated to the same end point to target the larger
vessels. Future visits were scheduled every 3 weeks. 23 At the fourth visit, the alexandrite laser was used prior to the PDL to
better target deoxyhemoglobin in the postcapillary venules. Using a pulse width of 3 ms, an 8 mm spot size, and the DCD
engaged, a fluence of 35 J/cm2 was selected and titrated upward to 85 J/cm2 to the end point of transient, bluish purpura. 22
Caution was used, as the risk of scarring is much greater with the infrared lasers in PWS. 24,25 An additional five treatments were
performed using the principles above to achieve a desired outcome. Additional treatments could have been performed but the
patient became pregnant and opted to halt therapy until after the delivery of the baby. B. Final result.
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Infantile Hemangiomas
The serendipitous discovery of propranolol as a safe, effective treatment of infantile hemangiomas
drastically changed the management of superficial, deep, and mixed infantile hemangiomas. 26 However,
selective photothermolysis of the vasculature continues to play a role in the treatment of superficial or
ulcerated infantile hemangiomas, as well as resolved hemangiomas with residual vasculature. 27-29
Adjuvant treatment with topical timolol 0.5% solution may help expedite resolution, but early studies
have not demonstrated a cumulative benefit. 30
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Varicose Veins and Spider Veins
Endovenous laser ablation represents the gold standard in the management of larger varicosities
achieving a 90% to 100% success rate in improving cosmesis and symptoms. 31 Access to the vascular
lumen is achieved with a fiber optic laser percutaneously under ultrasound guidance. Superficial spider
veins are common in patients with underlying venous insufficiency. After successful endovenous laser
ablation, spider veins may be treated with sclerotherapy or vascular laser treatment. 32
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Telangiectasias and Erythema
Telangiectasias (broken blood vessels) result from photodamage, inflammatory skin disease, radiation, or
underlying systemic disease. 33 Optimal treatment includes longer pulse widths and the end point of
durable purpura; however, patients are often willing to sacrifice clinical efficacy to minimize downtime
achieved with subpurpuric settings. 34 Facial erythema represents a similar process to telangiectasia but is
composed of fine dilated vessels that require magnification to be appreciated. Shorter pulse widths and
subpurpuric fluences have been shown to achieve ideal outcomes in generalized erythema. 34
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Angiomas (Cherry and Spider)
Cherry angiomas represent capillary proliferations that commonly arise on the trunk of middle-aged
patients. These growths can easily be treated with lasers that target hemoglobin. As they arise from
capillaries, short millisecond pulse widths may be used with purpuric fluences. Spider angiomas
represent a similar process and are treated in a similar fashion.
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Verruca Vulgaris
Treatment of warts using laser therapy has demonstrated equivocal outcomes to cryotherapy or
electrodessication. 35 Paring must be performed to eliminate keratinization, but once complete, vascular
lasers are capable of destroying wart vasculature. 35 Purpuric settings should be used without epidermal
cooling.
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