Добавил:
Sekretar
kiopkiopkiop18@yandex.ru
t.me/Prokururor I Вовсе не секретарь, но почту проверяю
Опубликованный материал нарушает ваши авторские права? Сообщите нам.
Вуз:
Предмет:
Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_4581_Библиотеки_им_академика_М_И_Перельмана
.pdf
References
149
11.12 Long-Term Sequelae
ofBurns
Burn injury is often a devastating event with
long-term physical and psychosocial effects.
Many burn victims are being tormented even
decades after the event. Few studies have examined the impacts of burn injuries on long-term
health and function, life satisfaction, and community integration beyond 5 years post-injury.
Results on the above issues, 20years after burn
injury, were recently reported by Abouzeid etal.
(2022). These authors reviewed patient-reported
outcome measures of 421 adult burn survivors 5,
10, 15, and 20years after injury. Lower Physical
Component Summaries (PCS) scores (worse
health) were associated with longer hospital stay,
older age at injury, and greater time since injury.
Similarly, lower Mental Component Summaries
(MCS) scores were associated with long length
of hospital stay, female sex, and greater time
since injury. Female sex and pre-burn depression
have already been identied as risk factors for
lower MCS scores (Van Loey and Van Son 2003).
Satisfaction with Life Scale scores was reported
to decrease negatively over time (Abouzeid etal.
2022).
Not all burn patients show the same trajectory
regarding psychologic problems and posttraumatic stress syndrome. Sveen etal. (2011), in
a study of 95 adults with burns, identied four
clusters: (1) resilient, with low levels of posttraumatic stress disorder (PTSD) that decreased
over time; (2) recovery, with high levels of symptoms that gradually decreased; (3) delayed, with
moderate symptoms that increased over time; and
(4) chronic, with high levels of symptoms over
time. Several risk factors were reported: life
events, premorbid psychiatric morbidity, personality traits, avoidant coping, in-hospital psychologic symptoms, and social support. The resilient
trajectory consistently had fewer of the risk factors and differed most from the chronic trajectory
(Sveen etal. 2011).
Patients with head and neck (H&N) burns are
particularly affected regarding their social functioning, quality of life, physical health, and satisfaction with appearance. Sinha et al. (2019)
compared the above parameters in patients with
H&N burns and patients with burns to other areas
of the body. In the mixed model regression analyses, satisfaction with appearance and short form12 mental component score were signicantly
worse for adults with H&N burns compared to
those with non-H&N burns (p<0.01). The same
group compared the long-term outcomes of H&N
burns vs. non-H&N burns in adolescents (14–
17.9 years of age). The H&N group had more
extensive burns, had longer hospital stay, and
showed signicantly worse satisfaction with
appearance at 12months after injury (Wang etal.
2022). These results suggest that future research
should focus on improving strategies (reconstructive surgery, cognitive behavioral therapy,
social skill training), which in turn will provide
new means and improve satisfaction with appearance of adolescents as well as adult burn patients
mitigating their long-term suffering.
References
Abdi S, Zhou Y. Management of pain after burn injury.
Curr Opin Anaesthesiol. 2002;15:563–7.
Abouzeid CA, Wolfe AE, Ni P, etal. Are burns a chronic
condition? Examining patient reported outcomes up
to 20 years after burn injury– a burn model system
National Database Investigation. J Trauma Acute Care
Surg. 2022;92(6):1066–74. https://doi.org/10.1097/
TA.0000000000003547.
Adant JP, Bluth F, Jacquemin D.Reconstruction of neck
burns. A long-term comparative study between skin
grafts, skin expansion and free aps. Acta Chir Belg.
1998;98:5–9.
Adouani K, Zitouni K, Yacoub K, etal. Les sequelles de
brûlures cervicofaciales: Classication anatomoclinique et consequences therapeutiques. Ann Burns Fire
Disasters. 1997;10:166–70.
Akin S. Burned ear reconstruction using a prefabri-
cated free radial forearm ap. J Reconstr Microsurg.
2001;17:233–6.
Al-Zacko SM, Al-Kazzaz DA. Initial release of severe
post-burn contracture scar of the neck for intubation under ketamine. Ann Burns Fire Disasters.
2009;22:196–9.
American Burn Association. Hospital and prehospital
resources for optimal care of patients with burn injury:
guidelines for development and operation of burn centers. J Burn Care Rehabil. 1990;11:98–104.
American Burn Association. Advanced burn life sup-
port providers’ manual. Chicago, IL: American Burn
Association; 2005.
150
Данная книга находится в списке для перевода на русский язык сайта https://meduniver.com/
11 Burns oftheScalp, Face, andNeck
American Burn Association. 2015. www.ameriburn.org/
resources_factsheet.php- AmericanBurnAssociation.
Accessed 19 Nov 2015.
Antia NH.Organisation of plastic surgery in developing
countries. Br J Plast Surg. 1985;38:24–9.
Ariani N, Visser A, van Oort RP, etal. Current state of cra-
niofacial prosthetic rehabilitation. Int J Prosthodont.
2013;26:57–67.
Babar TF, Khan MT, Marwat MZ, etal. Patterns of ocular
trauma. J Coll Physicians Surg Pak. 2007;17:148–53.
Barrera A. The use of micrografts and minigrafts for
the treatment of burn alopecia. Plast Reconstr Surg.
1999;103:581–9.
Barret JP, Dziewulski P, Ramy PI, et al. Biobrane ver-
sus 1% silver sulfadiazine in second-degree pediatric
burns. Plast Reconstr Surg. 2000;105:62–5.
Barrow RE, Jeschke MG, Herndon DN.Early release of
third-degree eyelid burns prevents eye injury. Plast
Reconstr Surg. 2000;105:860–3.
Benmeir P, Neuman A, Weinberg A, etal. Reconstruction
of a completely burned nose by a free dorsalis pedis
ap. Br J Plast Surg. 1991;44:570–1.
Bernard SL.Reconstruction of the burned nose and ear.
Clin Plast Surg. 2000;27:97–112.
Bharadia D, Sinha I, Pomabac B. Role of facial vascu-
larized composite allotransplantation in burn patients.
Clin Plast Surg. 2017;44:857–64.
Bosse GM, Wadia SA, Padmanabhan P.Hot asphalt burns:
a review of injuries and management options. Am J
Emerg Med. 2014;32(820):e1–3.
Boykin JV, Eriksson E, Pittman RN.In vivo microcircula-
tion of a scald burn and the progression of postburn
dermal ischemia. Plast Reconstr Surg. 1980;66:191–8.
Brigham PA, McLoughlin E. Burn incidence and medi-
cal care use in the United States: estimates, trends and
data sources. J Burn Care Rehabil. 1996;17:95–107.
Brusselaers N, Monstrey S, Vogelaers D, et al. Severe
burn injury in Europe: a systematic review of the inci-
dence, etiology, morbidity and mortality. Crit Care.
2010;14:R188.
Buckley NA, Juurlink DN, Isbister G, etal. Hyperbaric
oxygen for carbon monoxide poisoning. Cochrane
Database Syst Rev. 2011;2011:CD002041.
Cai Z, Pan B, Jiang H, etal. Chondrogenesis of human
adipose-derived stem cells by in vivo co-graft with
auricular chondrocytes from microtia. Aesthet Plast
Surg. 2015;39:431–9.
Caputo G, Monese C, Governa M, et al. Conservative
treatment in auricle burns. (Lett.). Ann Burns Fire
Disasters. 2005;18:217–8.
Carr JA, Crowley N. Prophylactic sequential bronchos-
copy after inhalation injury: results from a three-year
prospective randomized trial. Eur J Trauma Emerg
Surg. 2013;39:177–83.
Charles WN, Collins D, Mandalia S, et al. Impact of
inhalation injury on outcomes in critically ill burns
patients: 12-year experience at a regional burns centre.
Burns. 2021;S0305-4179(21):0037–5.
Chen J, Qian Y, Wang D, et al. Expanded scarred or
skin-grafted forehead ap for nasal reconstruction
in severe postburn facial deformity. Ann Plast Surg.
2008;61:447–51.
Cherry GW, Austed GD, Pasyk KA, etal. Increased sur-
vival and vascularity of random pattern skin aps
elevated in controlled, expanded skin. Plast Reconstr
Surg. 1983;72:680–5.
Ching JA, Shah JL, Doran CJ, et al. The evaluation
of physical exam ndings in patients assessed for
suspected burn inhalation injury. J Burn Care Res.
2015;36:197–202.
Ching JA, Ching YH, Shivers SC, et al. An analysis of
inhalation injury diagnostic methods and patient outcomes. J Burn Care Res. 2016;37:e27–32.
Choi YC, Kim JC. Single hair transplantation using
Choi hair transplanter. J Dermatol Surg Oncol.
1992;18:945–8.
Claassen K, Dos Anjos DR, Broding HC.Current status of
emergency treatment of chemical eye burns in workplaces. Int J Ophthalmol. 2021;14:306–9.
Clayton NA, Ward EC, Maitz PK. Orofacial contracture
management outcomes following partial thickness
facial burns. Burns. 2015a;41:1291–7.
Clayton NA, Ward EC, Maitz PK. Full thickness facial
burns: outcomes following orofacial rehabilitation.
Burns. 2015b;41:1599–606.
Cronin T. The use of a molded splint to prevent con-
tracture after split-skin grafting on the neck. Plast
Reconstr Surg. 1961;27:7–18.
D’ Souza AL, Nelson NG, McKenzie LB.Pediatric burn
injuries treated in US emergency departments between
1990 and 2006. Pediatrics. 2009;124:1424–30.
Daya M. Nostril stenosis corrected by release and
serial stenting. J Plast Reconstr Aesthet Surg.
2009;62:1012–9.
Donelan MB. Reconstruction of the head and neck. In:
Herndon DN, editor. Total burn care. Edinburgh:
Saunders–Elsevier; 2007. p.701–18.
Dougherty ME, Warden GD. A thirty-year review of
oral appliances used to manage microstomia, 1972 to
2002. J Burn Care Rehabil. 2003;24:418–31.
Dries DJ, Endorf FW. Inhalation injury: epidemiol-
ogy pathology, treatment strategies. Scand J Trauma
Resusc Emerg Med. 2013;21:31–48.
Dries DJ, Marini JJ.Airway pressure release ventilation. J
Burn Care Res. 2009;30:929–36.
Echinard C, Dantzer E. Reconstruction of the nose in
deep extensive facial burns. Ann Chir Plast Esthet.
1995;40:238–50.
Elamrani D, Zahid A, Aboujaafr N, et al. Les retrac-
tions cervicales post-brûlure-a propos de 49 cas et
revue de la literature. Ann Burns Fire Disasters.
2011;24:149–56.
Endorf FW, Dries DJ. Noninvasive ventilation in the
burned patient. J Burn Care Res. 2010;31:217–28.
Endorf FW, Gamelli RL. Inhalation injury, pulmonary
perturbations, and uid resuscitation. J Burn Care Res.
2007;28:80–3.
Erol OO.Prefabricated vertical myocutaneous ap of the
nose in facially burned patients. Plast Reconstr Surg.
1995;96:341–5.
References
151
Fagan SP, Bilodeau ML, Goverman J.Burn intensive care.
Surg Clin North Am. 2014;94:765–79.
Feldman AE, MacMillan BG. Burn injury in children:
declining need for reconstructive surgery as related
to use of neck orthoses. Arch Phys Med Rehabil.
1980;61:441–9.
Fochtman A, Keck M, Mittlböck M, etal. Tissue expan-
sion for correction of scars due to burn and other
causes: a retrospective comparative study of various
complications. Burns. 2013;39:984–9.
Foster MA, Moledina J, Jeffery SL.Epidemiology of U.K.
military burns. J Burn Care Res. 2011;32:415–20.
Frank DH, Wachtel T, Frank HA. The early treat-
ment and reconstruction of eyelid burns. J Trauma.
1983;23:874–7.
Fraulin FO, Illmayer SJ, Tredget EE.Assessment of cos-
metic and functional results of conservative versus
surgical management of facial burns. J Burn Care
Rehabil. 1996;17:19–29.
Gangemi EN, Gregori D, Berchialla P, etal. Epidemiology
and risk factors for pathologic scarring after burn
wounds. Arch Facial Plast Surg. 2008;10:93–102.
Genuino GA, Baluyut-Angeles KV, Espiritu AP, et al.
Topical petrolatum gel alone versus topical sil-
ver sulfadiazine with standard gauze dressings for
the treatment of supercial partial thickness burns
in adults: a randomized controlled trial. Burns.
2014;40:1267–73.
Goldenheim PD. An appraisal of povidone iodine and
wound healing. Postgrad Med. 1993;69(Suppl
3):S97–105.
Governa M, Bortolani A, Beghini D, etal. Skin expansion
in burn sequelae: results and complications. Acta Chir
Plast. 1996;38:147–53.
Greenhalgh DG, Hinchcliff K, Sen S, et al. A ten-year
experience with pediatric face grafts. J Burn Care Res.
2013;34:576–84.
Grifths RW. Management of multiple casualties with
burns. Br Med J. 1985;291:917–8.
Grishkevich VM. Post-burn microstomia: anatomy
and elimination with trapeze-ap plasty. Burns.
2011;37:484–9.
Haik J, Liran A, Tessone A, etal. Burns in Israel: demo-
graphic, etiologic and clinical trends, 1997-2003. Isr
Med Assoc J. 2007;9:659–62.
Hall C, Hardin C, Corkins CJ, et al. Pathophysiologic
mechanisms and current treatments for cutane-
ous sequelae of burn wounds. Compr Physiol.
2017;8:371–405.
Han TH, Teissler H, Han RJ, et al. Managing dif-
cult airway in patients with post-burn mentosternal
and circumoral contractures. Int J Burns Trauma.
2012;2:80–5.
Hartford CE, Kealy GP. Care of outpatient burns. In:
Herndon DN, editor. Total burn care. Saunders-
Elsevier; 2007. p.67–80.
Heilbronn CM, Srider PF, Folbe AJ, etal. Burns in the
head and neck: a national representative analy-
sis of emergency department visits. Laryngoscope.
2015;125:1573–8.
Heinrich JJ, Brand DA, Cuono CB.The role of topical
treatment as a determinant of infection in outpatient
burns. J Burn Care Rehabil. 1988;9:253–7.
Herndon DN, Thompson PB, Traber DL.Pulmonary injury
in burned patients. Crit Care Clin. 1985;1:79–96.
Herndon DN, Rutan R, Rutan T. The management of
burned children. J Burn Care Rehabil. 1993;14:3–8.
Hlava P, Moserova J, Konigova R. Validity of clinical
assessment of the depth of a thermal injury. Acta Chir
Plast. 1983;25:202–8.
Holley AD, Reade MC, Lipman J, et al. There is no
re without smoke! Pathophysiology and treatment
of inhalational injury in burns: a narrative review.
Anaesth Intensive Care. 2020;48:114–22.
Hoogewerf CJ, van Baar ME, Hop MJ, etal. Burns to the
head and neck: epidemiology and predictors of surgery. Burns. 2013a;39:1184–92.
Hoogewerf CJ, Van Baar ME, Hop MJ, etal. Topical treat-
ment for facial burns. Cochrane Database Syst Rev.
2013b;1:CD008058.
Hoogewerf CJ, Hop MJ, Nieuwenhuis MK, etal. Topical
treatment for facial burns. Cochrane Database Syst
Rev. 2020;7:CD008058.
Hu J, Liu T, Zhou X, etal. Treatment of post burn ear defect
with expanded upper arm ap and consequent expansion
without skin grafting. Ann Plast Surg. 2014;72:398–401.
Huang TT, Larson DL, Lewis SR. Burn alopecia. Plast
Reconstr Surg. 1977;60:763–7.
Hudson DA, Grob M. Optimizing results with tis-
sue expansion: 10 simple rules for successful tissue
expander insertion. Burns. 2005;31:1–4.
Ioannides C, Fossion E, McGrouther AD.Reconstruction
for large defects of the scalp and cranium. J
Craniomaxillofac Surg. 1999;27:145–52.
Ivy RH. Who originated the Z-plasty? Plast Reconstr
Surg. 1971;47:67–72.
Jandera V, Hudson DA, de Wet PM, et al. Cooling the
burn wound: evaluation of different modalities. Burns.
2000;26:256–70.
Janis JE, Khausa I, Lehrman CR, et al. Reconstructive
management of devastating electrical injuries to the
face. Plast Reconstr Surg. 2015;136:839–47.
Jaskille AD, Ramella-Roman JC, Shupp JW, etal. Critical
review of burn depth assessment techniques: part
II.Review of laser Doppler technology. J Burn Care
Res. 2010;31:151–7.
Jin X, Teng L, Zhao M, etal. Reconstruction of cicatricial
microstomia and lower facial deformity by windowed,
bipedicled deep inferior epigastric perforator ap. Ann
Plast Surg. 2009;63:616–20.
Kalantar Motamedi MH, Heydari M, et al. Prevalence
and pattern of facial burns: a 5-year assessment of 808
patients. J Oral Maxillofac Surg. 2015;73:676–82.
Kauvar DS, Cancio LC, Wolf SE, et al. Comparison of
combat and non-combat burns from ongoing U.S. military operations. J Surg Res. 2006;132:195–200.
Khatib M, Jabir S, Fitzgerald O’ Connor E, etal. A sys-
tematic review of the evolution of laser Doppler
techniques in burn depth assessment. Plast Surg Int.
2014;2014:621792.
152
Данная книга находится в списке для перевода на русский язык сайта https://meduniver.com/
11 Burns oftheScalp, Face, andNeck
Kraenzlin FS, Mushin OP, Ayazi S, et al. Epidemiology
and outcomes of auricular burn injuries. J Burn Care
Res. 2018;39:326–31.
Kumar P, Shah PL.Preauricular ap for post burn ear lobe
reconstruction– a case report. Burns. 2000;26:571–4.
Larkin JM, Moylan JA.Tetanus following a minor burn. J
Trauma. 1975;15:546–8.
Lazzeri D, Su W, Qian Y, et al. Prefabricated neck
expanded skin ap with the supercial temporal ves-
sels for facial resurfacing. J Reconstr Microsurg.
2013;29:255–62.
Lee JW, Jang YC, Oh SJ.Esthetic and functional recon-
struction for burn deformities of the lower lip and
chin with free radial forearm ap. Ann Plast Surg.
2006;56:384–6.
Li Q, Zan T, Gu B, et al. Face resurfacing using a cer-
vicothoracic skin ap prefabricated by lateral thigh
fascial ap and tissue expander. Microsurgery.
2009;29:515–23.
Longacre J, Berry HK, Bosom CR, etal. The effects of
Z-plasty on hypertrophic scars. Scand J Plast Reconstr
Surg. 1976;10:113–28.
Lund CC, Browder NC.The estimation of areas of burns.
Surg Gynecol Obstet. 1944;79:352–8.
Luo X, Liu F, Wang X, etal. Region –oriented and staged
treatment strategy in reconstruction of severe cervical
contracture. PLoS One. 2015;10:e 0122669.
Mabrouk A, Boughdadi NS, Helal HA, etal. Moist occlu-
sive dressing (Aquacel® Ag) versus moist open dress-
ing (MEBO®) in the management of partial-thickness
facial burns: a comparative study in Ain Shams
University. Burns. 2012;38:396–403.
Mackie DP, van Dehn F, Knape P, etal. Increase in early
mechanical ventilation of burn patients: an effect of
current emergency trauma management. J Trauma.
2011;70:611–5.
MacLennan SE, Corcoran JF, Neale HW.Tissue expan-
sion in head and neck burn reconstruction. Clin Plast
Surg. 2000;27:121–32.
Makiguchi T, Yokoo S, Koitabashi A, etal. Treatment of
microstomia caused by burn with a nasolabial ap– an
ingenious approach for tugging and xation of the oral
commissure. J Craniofac Surg. 2014;25:568–70.
Malhotra R, Sheikh I, Dheansa B. The management of
eyelid burns. Surv Ophthalmol. 2009;54:356–71.
Manders EK, Graham WP, Schendon MT, et al. Skin
expansion to eliminate large scalp defects. Ann Plast
Surg. 1984;12:305–12.
McCall JE, Cahill TJ.Respiratory care of the burn patient.
J Burn Care Rehabil. 2005;26:200–6.
McCauley RL, Oliphant JR, Robson MC.Tissue expan-
sion in the correction of burn alopecia: classica-
tion and methods of correction. Ann Plast Surg.
1990;25:103–15.
McCrory MC, Woodruff AG, Saha AK, et al.
Characteristics of burn-injured children in 117
U.S.PICUs (2009-2017): a retrospective virtual pedi-
atric systems database study. Pediatr Crit Care Med.
2021;22:616–28.
Menon S, Jacques M, Harvey JG, etal. Pediatric scalp
burns: hair today, gone tomorrow? J Burn Care Res.
2015;236:e18–22.
Middle KK, Batchinsky A, Cancio LC, etal. Wood bark
smoke induces lung and pleural plasminogen activator
inhibitor 1 and stabilizes its mRNA in porcine lung
cells. Shock. 2011;36:128–37.
Miller TA. The Tagliacozzi ap as a method of nasal
and palatal reconstruction. Plast Reconstr Surg.
1985;76:870–5.
Miller AC, Ferrada PA, Kadri SS, etal. High-frequency
ventilation modalities as salvage therapy for smoke
inhalation-associated acute lung injury: a systematic
review. J Intensive Care Med. 2018;33:335–45.
Mills DC 2nd, Roberts LW, Mason AD Jr, etal. Suppurative
chondritis: its incidence, prevention, and treatment in
burn patients. Plast Reconstr Surg. 1988;82:267–76.
Mlcak RP, Buffalo MC.Pre-hospital management, trans-
portation, and emergency care. In: Herndon DN,
editor. Total burn care. Saunders- Elsevier; 2007.
p.81–92.
Mlcak RP, Suman OE, Herndon DN.Respiratory manage-
ment of inhalation injury. Burns. 2007;33:2–13.
Morgan ED, Bledsoe SC, Barker J.Ambulatory manage-
ment of burns. Am Fam Physician. 2000;62:2015–26.
Motamed S, Davami B.Eyebrow reconstruction follow-
ing burn injury. Burns. 2005;31:495–9.
Moylan JA Jr, Wilmore DW, Mouton DE, et al. Early
diagnosis of inhalation injury using 133 xenon lung
scan. Ann Surg. 1972;176:477–84.
Muller M, Gahankari D, Herndon DN.Operative wound
management. In: Herndon DN, editor. Total burn care.
Saunders-Elsevier; 2007. p.192.
Mun GH, Jeon BJ, Lim SY, et al. Reconstruction of
postburn neck contracture using free thin thoracodorsal artery perforator aps with cervicoplasty. Plast
Reconstr Surg. 2007;120:1524–32.
Murakami K, Traber DL. Pathophysiological basis
of smoke inhalation injury. News Physiol Sci.
2003;18:125–9.
Mustardé JC. Repair and reconstruction in the orbital
region. Churchill Livingstone; 1991. p.34–51.
Neale HW, High RM, Billmon DA, etal. Complications
of controlled tissue expansion in the pediatric burn
patient. Plast Reconstr Surg. 1988;82:840–5.
Ngim RC.The burned ear (II): a prospective clinical study
of 100 patients with 150 ear burns. Ann Acad Med
Singap. 1992;21:605–11.
Nielson CB, Duethman NC, Howard JM, et al. Burns:
pathophysiology of systemic complications and current management. J Burn Care Res. 2017;38:e469–81.
Norman G, Christie J, Liu Z, etal. Antiseptics for burns.
Cochrane Database Syst Rev. 2017;7:CD011821.
https://doi.org/10.1002/14651858.
Nugent N, Herndon DN.Diagnosis and treatment of inha-
lation injury. In: Herndon DN, editor. Total burn care.
Saunders/Elsevier; 2007. p.262–72.
Ojo P, Palmer J, Garvey R, etal. Patterns of burns in child
abuse. Am Surg. 2007;73:253–5.
References
153
Onah II.A classication of post-burn mentosternal con-
tractures. Arch Surg. 2005;140:671–5.
Pallua N, Wolter TP. Moving forwards: the anterior
supraclavicular artery perforator (a-SAP) ap: a new
pedicled or free perforator ap based on the anterior
supraclavicular vessels. J Plast Reconstr Aesthet Surg.
2013;66:489–96.
Palmieri TL. Inhalation injury: research progress and
needs. J Burn Care Res. 2007;28:549–54.
Parihar A, Parihar MS, Milner S, et al. Oxidative stress
and anti-oxidative mobilization in burn injury. Burns.
2008;34:6–17.
Park C, Suk Roh T.Total ear reconstruction in the devas-
cularized temporoparietal region: I.Use of the contra-
lateral temporoparietal fascial free ap. Plast Reconstr
Surg. 2001;108:1145–53.
Parrett BM, Pomahac B, Orgill D, etal. The role of free-
tissue transfer for head and neck burn reconstruction.
Plast Reconstr Surg. 2007;120:1871–8.
Patel KH, Nayyer L, Seifalian AM.Chondrogenic poten-
tial of bone narrow-derived mesenchymal stem cells
on a novel auricular-shaped, nanocomposite scaffold.
J Tissue Eng. 2013;4:2041731413516782.
Pearl R, Sabbagh W. Reconstruction following traumatic
partial amputation of the ear. Plast Reconstr Surg.
2011;127:621–9.
Philp L, Umraw N, Cartotto R.Late outcomes after graft-
ing of the severely burned face: a quality improvement
initiative. J Burn Care Res. 2012;33:45–56.
Planas J, Cervelli V, Planas G.The retraction of the oral
opening in burned patients. Plast Reconstr Surg.
1999;103:1082–6.
Prakash S, Mullick P.Airway management in patients with
burn contractures of the neck. Burns. 2015;41:1627–35.
Pruitt BA, Wolf SE, Mason AD Jr. Epidemiological,
demographic and outcome characteristics of burn
injury. In: Herndon DN, editor. Total burn care.
Saunders-Elsevier; 2007. p.14–32.
Purdue GF, Hunt JL. Chondritis of the burned
ear: a preventable complication. Am J Surg.
1986;152:257–9.
Ray E, Wu T, Nazarian Mobin SS, etal. Review of options
for burned ear reconstruction. J Craniofac Surg.
2010;21:1165–9.
Rak A, Chabak H, Diouri M, et al Cervical burns
sequelae: epidemiological, clinical and therapeuti-
caspects in Morocco. Pan Afr Med J. 2015;20:413.
Rhee P, Nunley MK, Demetriades D, etal. Tetanus and
trauma: a review and recommendations. J Trauma.
2005;58:1082–8.
Richardson C, Upton D, Rippon M. Treatment for
wound pruritus following burns. J Wound Care.
2014;23:227–8.
Romanowski KS, Palmieri TL, Sen S, etal. More than one
third of intubations in patients transferred to burn cen-
ters are unnecessary: proposed guidelines for appro-
priate intubation of the burn patient. J Burn Care Res.
2016;37:e409–14.
Rose GK, Mason JD, Varma SK.Effect of facial burns on
the nasal mucosa. Burns. 1996;22:631–2.
Rubino C, Farace F, Puddu A, etal. Total upper and lower
eyelid replacement following thermal burn using an
ALT ap – a case report. J Plast Reconstr Aesthet
Surg. 2008;61:578–81.
Ruth GD, Smith S, Bronson M, etal. Outcomes related
to burn-related child abuse: a case series. J Burn Care
Rehabil. 2003;24:318–21.
Sakurai H, Soejima K, Takeuchi M, etal. Reconstruction
of perioral burn deformities in male patients by using
the expanded frontal scalp. Burns. 2007;33:1059–64.
Schmid E. The use of auricular cartilage and compos-
ite grafts in reconstruction of the upper lip, with
special reference to reconstruction of the philtrum.
In: Broadbent TR, editor. Transactions of the Third
International Congress of Plastic Surgery. Amsterdam:
Excerpta Medica; 1964. p.306.
Schrage NF, Struck HG, Gerard M.Recommendations for
acute treatment for chemical and thermal burns of eyes
and lids. Ophthalmologe. 2011;108:916–20.
Serghiou MA, McLaughlin A, Herndon DN.Alternative
splinting methods for the prevention and correction of burn scar torticollis. J Burn Care Rehabil.
2003;24:336–40.
Shavit I, Knaani-Levinz H.Images in emergency medi-
cine. Child abuse caused by cigarette burns. Ann
Emerg Med. 2008;51:579–82.
Shen W, Cui J, Chen J, et al. Inversion of the ap at the
lower ear and restoration of the ap at postauricular
skin for reconstruction of the earlobe. J Craniofac
Surg. 2012;23:560–2.
Sheridan RL.Airway management and respiratory care of
the burn patient. Int Anesthesiol Clin. 2000;38:129–45.
Shirani KZ, Pruitt BA Jr, Mason AD Jr. The inuence of
inhalation injury and pneumonia on burn mortality.
Ann Surg. 1987;205:82–7.
Sinha M, Scott JR, Watson SB.Prelaminated free radial
forearm ap for a total nasal reconstruction. J Plast
Reconstr Aesthet Surg. 2008;61:953–7.
Sinha I, Nabi M, Simko LC, etal. Head and neck burns are
associated with long-term patient-reported dissatisfaction with appearance: a burn model system National
Database study. Burns. 2019;45:293–302.
Slaviero L, Avruscio G, Vindigni V, et al. Antiseptics
for burns: a review of the evidence. Ann Burns Fire
Disasters. 2018;31:198–203.
Solanki NS, Middleton S, Quinn L, etal. Audit of teta-
nus immunization status in pediatric burn patients. J
Paediatr Child Health. 2014;50:495–6.
Song B, Xiao B, Liu C, et al. Neck burn reconstruc-
tion with pre-expanded scapular free aps. Burns.
2015;41:624–30.
Sousse LE, Herndon DN, Andersen CR, etal. High tidal
volume decreases adult respiratory distress syndrome,
atelectasis, and ventilator days compared with low
tidal volume in pediatric burned patients with inhalation injury. J Am Coll Surg. 2015;220:570–8.
Spence RJ. An algorithm for total and subtotal facial
reconstruction using an expanded transposition
ap: a 20-year experience. Plast Reconstr Surg.
2008;121:795–805.
154
Данная книга находится в списке для перевода на русский язык сайта https://meduniver.com/
11 Burns oftheScalp, Face, andNeck
Spencer T, Hall AJ, Stawell RJ.Ophthalmologic sequelae
of thermal burns over ten years at the Alfred Hospital.
Ophthal Plast Reconstr Surg. 2002;18:196–201.
Stern JD, Goldfarb IW, Slater H.Ophthalmological com-
plications as a manifestation of burn injury. Burns.
1996;22:135–6.
Still JM Jr, Law EJ, Belcher KE, etal. Experience with
burns of the eyes and lids in a regional burn unit. J
Burn Care Rehabil. 1995;16:248–52.
Stratta RJ, Safe JR, Kravitz M, etal. Management of tar
and asphalt injuries. Am J Surg. 1983;146:766–9.
Sveen J, Ekselius L, Gerdin B, etal. A prospective lon-
gitudinal study of posttraumatic stress disorder
symptom trajectories after burn injury. J Trauma.
2011;71:1808–15.
Taylor LB, Walker J. A review of selected microstomia
prevention appliances. Pediatr Dent. 1997;19:413–8.
Taylor HO, Carty M, Driscoll D, etal. Nasal reconstruc-
tion after severe facial burns using a local turn-down
ap. Ann Plast Surg. 2009;62:175–9.
Tayyaba FU, Amin MM, Attaur-Rasool S, et al.
Reconstruction of post burn scalp alopecia by using
expanded hair-bearing scalp aps. Pak J Med Sci.
2015;31:1405–10.
Thai KN, Billmire DA, Yakuboff KP.Total eyelid recon-
struction with free dorsalis pedis ap after deep facial
burn. Plast Reconstr Surg. 1999;104:1048–51.
Tsai FC, Yang JY, Mardini S, etal. Free split- cutaneous
perforator aps procured using a three-dimensional
harvest technique for the reconstruction of post-
burn contracture defects. Plast Reconstr Surg.
2004;113:185–93.
Van Loey NE, Van Son MJ. Psychopathology and psy-
chological problems in patients with burn scars: epi-
demiology and management. Am J Clin Dermatol.
2003;4:245–72.
Varkey M, Ding J, Tredget EE. Advances in skin
substitutes- potential of tissue engineered skin for
facilitating anti-brotic healing. J Funct Biomater.
2015;6:547–63.
Walker PF, Buehner MF, Wood LA, etal. Diagnosis and
management of inhalation injury: an updated review.
Crit Care. 2015;19:351–67.
Wallace AB. The exposure treatment of burns. Lancet.
1951;1:501–4.
Wang J, Fan J. Cicatricial eyebrow reconstruction with
a dense-packing one- to two-hair grafting technique.
Plast Reconstr Surg. 2004;114:1420–6.
Wang XK, Zhai QK, Xue L, etal. Treatment of postburn
anteriorly located neck contractures with local aps. J
Craniofac Surg. 2012;23:e387–90.
Wang BB, Patel KF, Wolfe AE, et al. Adolescents with
and without head and neck burns: comparison of longterm outcomes in the burn model system National
Database. Burns. 2022;48:40–50.
Wasiak J, Cleland H, Campbell F, et al. Dressings for
supercial and partial thickness burns. Cochrane
Database Syst Rev. 2013;3:CD 002106.
Watanabe T, Furuta S, Hataya Y, etal. Reconstruction of
the eyelids and nose after a burn injury using a radial
forearm ap. Burns. 1997;23:360–5.
WHO. 2014. www.who.int/entity/mediacentre/factsheets/
fs365/en/- WHO/Burns. Accessed 19 Nov 2015.
Wiesner N, Dutescu RM, Uthoff D, etal. First aid therapy
for corrosive chemical eye burns: results of a 30-year
longitudinal study with two different decontamination concepts. Graefes Arch Clin Exp Ophthalmol.
2019;257:1795–803.
Wilkes GH, Wolfaardt JF.Osseointegrated alloplastic ver-
sus autogenous ear reconstruction: criteria for treatment selection. Plast Reconstr Surg. 1994;93:967–79.
Yamamura H, Kaga S, Kaneda K, etal. Chest computed
tomography performed on admission helps predict
the severity of smoke inhalation injury. Crit Care.
2013;17:R95.
Yang JY, Tsai FC, Chana JS, etal. Use of free thin antero-
lateral thigh aps combined with cervicoplasty for
reconstruction of postburn anterior cervical contractures. Plast Reconstr Surg. 2002;100:39–46.
Yeong EK, Mann R, Goldberg M, etal. Improved accu-
racy of burn wound assessment using laser Doppler. J
Trauma. 1996;40:956–61.
Yeung JK, Leung LT, Papp A.A survey of current prac-
tices in the diagnosis of and interventions for inhalational injuries in Canadian burn centres. Can J Plastic
Surg. 2013;21:221–5.
Yu JA, Lin HZ, Jin ZH, etal. Free anterolateral thigh ap
for coverage of large scalp defects in pediatric burn
population. J Burn Care Res. 2012;33:e180–5.
Zan T, Li H, Gu B, etal. Surgical treatment of facial soft-
tissue deformities in postburn patients: a proposed
classication based on a retrospective study. Plast
Reconstr Surg. 2013;132:1001e–14e.
Zweifel CJ, Guggenheim M, Jandali AR, etal. Management
of microstomia in adult burn patients revisited. J Plast
Reconstr Aesthet Surg. 2010;63:a351–7.
Wound Healing Disturbances:
TheUnfavorable Result
12
12.1 Phases ofWound Healing
There are four distinct but overlapping phases of
wound healing (hemostasis, inammation, proliferation, and remodeling). During wound healing, highly specialized cells interact with an
extracellular matrix to lay down a new framework for tissue growth and repair (Diegelmann
and Evans 2004). The whole process is inuenced by various cellular interactions, and the
various steps are regulated by the local release of
cytokines, chemokines, growth factors, and
inhibitors (Goldberg and Diegelmann 2010).
12.1.1 Hemostasis
Hemostasis aims at reducing and nally stopping
hemorrhage. Vasoconstriction; activation of
platelets which release bronectin, thrombospondin, sphingosine-1-phosphate, and von
Willebrand factor resulting in further activation
and aggregation of platelets; and formation of a
brin matrix in which platelets are trapped lead
to the formation of a stable clot within the provisional matrix. Platelets further release plateletderived growth factor (PDGF) and transforming
growth factor-β (TGF-β), which recruit additional cells such as neutrophils, macrophages,
and broblasts and activate the production of collagen and glycosaminoglycans by broblasts,
which are important for the repair of extracellular
matrix (Rumalla and Borah 2001).
12.1.2 Inammation
This is the second phase of wound healing, which
begins within the rst 24h after an injury and can
last up to 2weeks in a normally healing wound.
Clinically, it is characterized by rubor (redness),
calor (heat), tumor (swelling), and dolor (pain),
all of which result from the release of vasoactive
amines and histamine-rich granules from mast
cells. These mast cell mediators alter vascular
permeability and allow the passage of neutrophils from the vasculature through the vascular
wall to the site of injury together with uid,
which causes the swelling and pressure-causing
pain (Ali Komi etal. 2020).
The neutrophils are attracted to the site of
injury by a process called chemotaxis and are
drawn there by soluble mediators, such as a
breakdown of complement called C5a that is a
waste product produced by bacteria and the
potent chemokine interleukin (IL)-8 (Guo and
Ward 2005; Goldberg and Diegelmann 2010).
The neutrophils move through the extracellular matrix by releasing matrix-degrading enzymes
such as elastase and matrix metalloproteinase
(MMP)-8. On their arrival at the wound site, they
begin to aggressively phagocytize any foreign
© The Author(s), under exclusive license to Springer Nature Switzerland AG 2023
C. A. Ioannidis, Soft Tissue Injuries of the Head and Neck,
https://doi.org/10.1007/978-3-031-14915-3_12
155
156
Данная книга находится в списке для перевода на русский язык сайта https://meduniver.com/
12 Wound Healing Disturbances: TheUnfavorable Result
materials and kill bacteria by the enzymes and
reactive oxygen species, which they generate.
They also release IL-1 and tumor necrosis factor
(TNF)-a to begin the activation of broblasts and
epithelial cells, thus initiating the proliferative
phase.
Macrophages also play a key role during the
inammatory phase. Wound macrophages are
derived from xed tissue monocytes and are activated by chemokines, cytokines, growth factors,
and soluble fragments of extracellular matrix
components produced by proteolytic degradation
of collagen and bronectin (Diegelmann et al.
1981). The function of the macrophages is to
remove any residual bacteria, foreign bodies, and
remaining necrotic tissue. It is similar to that of
neutrophils, but macrophages better regulate proteolytic destruction of wound tissue by secreting
protease inhibitors. Macrophages also ingest the
bacteria-laden neutrophils and mediate progression of the wound from the inammatory to the
proliferative phase (Goldberg and Diegelmann
2010). They secrete a number of growth factors
and cytokines (PDGF, TGF-β, TNF-α, broblast
growth factor, insulin-like growth factor 1, and
IL-6), which recruit broblasts and endothelial
cells to the wound site for matrix deposition and
neovascularization.
12.1.3 Proliferation
The proliferative phase is characterized by broblast proliferation and neoangiogenesis.
Granulation tissue formation and process of epithelization also occur.
Mast cells stimulate broblast proliferation
during the proliferative phase via IL-4, vascular
endothelial growth factor (VEGF), and basic
broblast growth factor (bFGF) to produce a new
extracellular matrix (Ali Komi et al. 2020).
Fibroblasts migrate into the wound in response to
mediators released from macrophages and platelets. They move through the extracellular matrix
by binding bronectin, vitronectin, and brin and
by secreting MMPs, which facilitate their movement. Once the broblasts have entered the
wound, they produce collagen, proteoglycans,
and other components to replace the provisional
matrix and to provide a stable extracellular
matrix. Fibroblast activity is mainly regulated by
PDGF and TGF-β. PDGF secreted by platelets
and macrophages stimulates broblast proliferation, chemotaxis, and collagenase expression.
Angiogenesis is initiated by the activation of
endothelial cells by TNF-a and basic FGF
(βFGF). The new blood vessels promote blood
ow to support the high metabolic needs of the
newly formed tissue. Local stimulatory factors
(VEGF, angiostatin, endostatin, pigment
endothelium- derived growth factor, thrombospondin) regulate angiogenesis (Tahergorabi and
Khazaei 2012). Oxygen tension, low pH, and
high lactate levels stimulate angiogenesis (Hunt
etal. 2007).
In the course of wound healing, the granulation tissue forms. It provides the transitional
replacement for normal dermis and ultimately
evolves into scar. Granulation tissue is rich in
blood vessels, broblasts, macrophages, and randomly organized collagen bers. The metabolic
rate for this tissue is higher compared with normal dermis, which reects the activity required
for cellular migration, division, and protein synthesis and thus the importance of adequate nutrition and oxygen to properly heal the wound
(Goldberg and Diegelmann 2010).
Contraction is an important part of wound
healing, as it enables wound closure. It occurs
during the proliferative phase. The traction forces
of broblasts and myobroblasts are believed to
be responsible for wound contraction and closure
(Tomasek etal. 2002). However, excessive myobroblast activity, accompanied by elevated levels of mechanical stress in the healing region,
often causes scar tissue formation and, in the
worst case, contracture of tissues, leading to local
immobilization and loss of function (Li and Wang
2011).
12.1.4 Remodeling
This is the last phase of wound healing, and it is
characterized by maturation of granulation tissue
into a scar. Metabolic activity, cell density, and
12.2 Mechanisms ofWound Healing
157
water content of the wound decrease. The most
dramatic change, however, occurs in the overall
type, amount, and organization of collagen bers,
resulting in increased tensile strength of the
wound. Initially, there is increased deposition of
type III collagen that is gradually replaced by
type I collagen, the dominant brillar collagen in
skin (Clore etal. 1979). Collagen bers are crosslinked by the enzyme lysyl oxidase, which is
secreted by broblasts in the extracellular matrix
(Smith-Mungo and Kagan 1998). Overexpression
of lysyl oxidase seems to increase cross-linking
and improve tissue strength in dermal wound
healing (Lau et al. 2006). The degradation of
extracellular matrix components to facilitate epithelial cell migration into the wound, angiogenesis, and overall tissue remodeling is controlled by
matrix metalloproteinases (MMPs). Matrix adhesion and signaling are regulated by integrins.
Adhesion by integrins regulates the expression of
MMPs. In addition, certain MMPs can bind to
integrins or other receptors on the cell surface
involved in enzyme activation, thereby providing
a mechanism for localized matrix degradation
(Steffensen etal. 2001).
MMP expression is regulated by TGF-β in
normal broblasts and keratinocytes. The three
mammalian isoforms (TGF-β 1, 2, and 3) have
been localized in healing wounds (O’Kane and
Ferguson 1997). Manipulation of the ratios of
TGF-β superfamily members, particularly the
ratio of TGF-β 1 relative to TGF-β 3, reduces
scarring and brosis (O’Kane and Ferguson
1997). TGF-β also minimizes matrix degradation
by downregulating protease secretion and stimulating synthesis of tissue inhibitors of metalloproteinases (TIMPs) (Goldberg and Diegelmann
2010).
Wound extracellular matrix remodeling continues as the matrix strives to achieve the highly
organized tissue structure, which was present
before the injury. The resulting scar tissue, however, can only achieve about 80% of the initial
tensile strength. When degradation maintains an
equilibrium, a ne line scar forms. If matrix synthesis is greater than degradation, the result is a
hypertrophic scar. If degradation is greater than
synthesis or if synthesis is inhibited (e.g., steroids, cancer chemotherapeutic agents), the scar
becomes weak and wound dehiscence may occur
(Goldberg and Diegelmann 2010).
12.2 Mechanisms ofWound
Healing
Dermal wounds heal by three main mechanisms:
connective tissue deposition, contraction, and
epithelialization. The latter is the process
whereby epithelial cells surrounding the wound
margin or in residual skin appendages (rete pegs,
hair follicles, sebaceous glands) migrate into the
wound because of the loss of contact inhibition of
cuboidal basal keratinocytes (O’Toole 2001).
These three processes come into play to varying
degrees, depending on the type of wound. Linear
wounds sutured together heal by what is termed
primary intention (per primam). The main mechanism necessary is connective tissue deposition.
There is also minimal epithelialization, which
occurs along the surface of the wound line.
Defect wounds heal by secondary intention (per
secundam). These open wounds heal mainly by
tissue contraction. An interaction between broblasts and the matrix generates a centripetal force
to advance the edges towards the center of the
wound. There is some connective tissue deposition, and this is nally covered by epithelialization. Abrasions (thickness <0.015mm) heal by
epithelialization. After an extensive multistep
process, the basal epithelial cells proliferate near
the wound margin, producing a monolayer that
covers the entire wound surface.
The restoration of the skin barrier is controlled
by several molecular mechanisms that synergistically regulate cell kinetics, enzymatic functions,
and neurovascular activation. These pathways
include genetic and epigenetic (DNA methylation, histone modication, and noncoding regulatory RNA editing) activation, which modulate
physiological wound healing. The DNA background modulating skin restoration could be used
to plan new diagnostics and therapeutics (Palmieri
etal. 2017).
158
Данная книга находится в списке для перевода на русский язык сайта https://meduniver.com/
12 Wound Healing Disturbances: TheUnfavorable Result
12.3 Pathologic Responses
toWound Healing
12.3.1 Hypo- andHyperpigmentation
Acute wounds progress through the healing
phases in an orderly fashion for normal healing to
occur. The early, immature scar is hard and raised
due to the bulk of excessive matrix (mostly collagen) deposited in the early healing stages. It is
also reddish due to the dense capillary network.
As wound maturity progresses, the broblasts
and capillaries recede, the collagen continues to
remodel, and the scar becomes at, soft, and usually pale to adjacent skin colored over a period of
6–12months.
Scar tissue contains no elastin, and the collagen bundles are oriented along stress lines; it
therefore lacks elasticity. Scar tissue contains no
sweat and sebaceous glands and is therefore dry.
Mature scar tissue typically lacks normal pigmentation and is usually pale. However, it can be
dark in patients with pigmented skin (Figs.12.1
and 12.2). Particularly in burns, a mixture of both
hypopigmentation and hyperpigmentation may
be encountered (Fig.12.3). A recent experimental study in a red Duroc pig model of hypertrophic scar formation showed that melanocyte
number was similar in hypopigmented and
hyperpigmented tissues. Hyperpigmented tissues, however, showed a greater amount of melanin and a-MSH, along with immunohistochemical
evidence of stimulated melanocytes. The authors’
observations encourage further investigation of
melanocyte stimulation and the inammatory
environment within a wound that may inuence
melanocyte activity (Travis etal. 2015). A change
of dendritic structure, reduced proliferation rate,
faulty melanin synthesis, and transfer of melanin
from melanocytes to keratinocytes in postburn
hypopigmented skin were considered potential
causes of hypopigmentation in burned patients
(Dutta etal. 2020).
Abnormal pigmentation renders scars more
noticeable with eventual serious adverse sequelae
for those affected. Furthermore, hypopigmented
scars lack melanin leaving them without protection against ultraviolet radiation.
Randomized animal studies as well as clinical
studies have shown that ultraviolet radiation
increases scar pigmentation and worsens a scar’s
clinical appearance (Haedersdal etal. 1998; Due
etal. 2007). Preventive measures include avoiding exposure to sunlight and use of sunscreens
with a high sun protection factor (SPF>50) until
the scar has matured.
Currently, there is a lack of proven treatment
options which effectively and permanently abolish this wound healing complication. Among
noninvasive treatments, makeup and skin tanning
(for hypo) and bleaching lotions (for hyper) can
offer some improvement. However, topical treatments carry risks (allergic reaction, skin irritation, infections, skin diseases, etc.). Laser has
been proven to be effective in hypo- (activates
melanosomes) and hyper- (destroys melanosomes) pigmented lesions. However, in cases of
hyperpigmentation, the possible worsening of the
problem through stimulating melanin production
should be considered. Furthermore, it can require
multiple treatments. Although laser therapy (e.g.,
picosecond and Q-switched lasers) is increasingly being utilized to treat dermal hyperpigmentation, the reported success rates have varied
Fig. 12.1 (a, b)
Hyperpigmented scar of
the left upper eyelid in a
patient with pigmented
skin. The notching of the
free lid margin is clearly
identiable
ab
Соседние файлы в папке Библиотека им академика М.И. Перельмана