Molecular and cellular basis of hypertrophic scarring
505
Leask A, Abraham DJ. TGF-beta signaling and the fibrotic response.
FASEB J. 2004;18(7):816-827.
Tredget EE, Yang L, Delehanty M, et al. Polarized Th2 cytokine
production in patients with hypertrophic scar following thermal
injury. J Interferon Cytokine Res. 2006;26(3):179-189.
Wang J, Dodd C, Shankowsky HA, et al. Deep dermal fibroblasts
contribute to hypertrophic scarring. Lab Invest. 2008;88(12):
1278-1290.
Further reading
Desmoulière A, Chaponnier C, Gabbiani G. Tissue repair, contraction,
and the myofibroblast. Wound Repair Regen. 2005 Jan-Feb;13(1):
7-12.
Dunkin CSJ, Pleat JM, Gillespie PH, et al. Scarring occurs at a critical
depth of skin injury: precise measurement in a graduated dermal
scratch in human volunteers. Plast Reconstr Surg. 2007;119(6):
1722-1732.
Figure 45.9 Cytokine production in burn patients. Cytokine production by lymphocytes from burn patients as a function of time after injury. The
percentages of lymphocytes producing IFN-γ (A) or IL-4 (C) were estimated by flow cytometry analysis of cells stained for intracellular cytokines using
fluorescent-labeled antibodies (n = 22). Panels B and D show the time course of IL-12 (B) and IL-10 (D) production by peripheral blood mononuclear cells
(PBMC) cultured from burn patients who developed hypertrophic scar (HSc) and those who did not (noHSc), measured by ELISA (n=16). The values measured
for cells from normal human volunteers are shown in the shaded boxes (mean ± SD). (From Tredget EE, Nedelec B, Ghahary A. Hypertrophic scar, keloids and contracture:
The cellular and molecular basis for therapy. WB Saunders Co, A Barbul (editor), Surgical Clinics of North America, 77(3): 701-730, 1997).
IL-4 percent positive cells
Time postburn (months)
HSc
noHSc
0.25
0.50
0.75
1
2
6
12
12+
2
6
12
12+
0
20
15
10
5
IFN-γ percent positive
Time postburn (months)
0.25
0.50
0.75
1
2
6
12
12+
0
20
15
10
5
IL-10 (pg/mL)
IL-12 (pg/mL)
Time postburn (months)
1
0
16
12
8
4
0
16
12
8
4
2
6
12
12+
Time postburn (months)
1
C
D
A
B
Access the complete reference list online at
Molecular and cellular basis of hypertrophic scarring
505.e1
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References
1. Niessen FB, Spauwen PH, Schalkwijk J, et al. On the nature of
hypertrophic scars and keloids: a review. Plast Reconstr Surg.
1999;104(5):1435-1458.
2. Wynn TA. Cellular and molecular mechanisms of fibrosis.
J Pathol. 2008;214(2):199-210.
3. Scott PG, Dodd CM, Tredget EE, et al. Chemical characterization
and quantification of proteoglycans in human post-burn
hypertrophic and mature scars. Clin Sci (Lond). 1996;90(5):
417-425.
4. Wang H, Pieper J, Peters F, et al. Synthetic scaffold morphology
controls human dermal connective tissue formation. J Biomed
Mater Res A. Sep 15 2005;74(4):523-532.
5. Scott PG, Ghahary A, Tredget EE. Molecular and cellular aspects
of fibrosis following thermal injury. Hand Clin. 2000;16(2):
271-287.
6. Linares HA, Kischer CW, Dobrkovsky M, et al. The histiotypic
organization of the hypertrophic scar in humans. J Invest
Dermatol. 1972;59(4):323-331.
7. Bailey AJ, Bazin S, Sims TJ, et al. Characterization of the collagen
of human hypertrophic and normal scars. Biochim Biophys Acta.
1975;405(2):412-421.
8. Ehrlich HP, White BS. The identification of alpha A and alpha B
collagen chains in hypertrophic scar. Exp Mol Pathol. 1981;34(1):
1-8.
9. Hayakawa T, Hashimoto Y, Myokei Y, et al. Changes in type
of collagen during the development of human post-burn
hypertrophic scars. Clin Chim Acta. 1979;93(1):119-125.
10. Gay S, Vijanto J, Raekallio J, et al. Collagen types in early phases
of wound healing in children. Acta Chir Scand. 1978;144(4):
205-211.
11. Zhang LQ, Laato M, Muona P, et al. Normal and hypertrophic
scars: quantification and localization of messenger RNAs for
type I, III and VI collagens. Br J Dermatol. Apr 1994;130(4):
453-459.
12. Kischer CW. Collagen and dermal patterns in the hypertrophic
scar. Anat Rec. 1974;179(1):137-145.
13. Iozzo RV, Murdoch AD. Proteoglycans of the extracellular
environment: clues from the gene and protein side offer novel
perspectives in molecular diversity and function. FASEB J. Apr
1996;10(5):598-614.
14. Hardingham TE, Fosang AJ. Proteoglycans: many forms and
many functions. FASEB J. Feb 1 1992;6(3):861-870.
15. Shetlar MR, Dobrkovsky M, Linares H, et al. The hypertrophic
scar. Glycoprotein and collagen components of burn scars. Proc
Soc Exp Biol Med. Oct 1971;138(1):298-300.
16. Zhang G, Ezura Y, Chervoneva I, et al. Decorin regulates
assembly of collagen fibrils and acquisition of biomechanical
properties during tendon development. J Cell Biochem.
2006;98(6):1436-1449.
17. Orgel JP, Eid A, Antipova O, et al. Decorin core protein
(decoron) shape complements collagen fibril surface structure
and mediates its binding. PLoS One. 2009;4(9):e7028.
18. Danielson KG, Baribault H, Holmes DF, et al. Targeted
disruption of decorin leads to abnormal collagen fibril
morphology and skin fragility. J Cell Biol. Feb 10 1997;136(3):
729-743.
19. Zhang Z, Li X-J, Liu Y, et al. Recombinant human decorin
inhibits cell proliferation and downregulates TGF-beta1
production in hypertrophic scar fibroblasts. Burns. 2007;33(5):
634-641.
20. Nili N, Cheema AN, Giordano FJ, et al. Decorin inhibition
of PDGF-stimulated vascular smooth muscle cell function:
potential mechanism for inhibition of intimal hyperplasia after
balloon angioplasty. Am J Pathol. Sep 2003;163(3):869-878.
21. Bittner K, Liszio C, Blumberg P, et al. Modulation of collagen gel
contraction by decorin. Biochem J. 1996;314(Pt 1):159-166.
22. Zhang Z, Garron TM, Li XJ, et al. Recombinant human decorin
inhibits TGF-beta1-induced contraction of collagen lattice by
hypertrophic scar fibroblasts. Burns. Jun 2009;35(4):527-537.
23. Zhu JX, Goldoni S, Bix G, et al. Decorin evokes protracted
internalization and degradation of the epidermal growth factor
receptor via caveolar endocytosis. J Biol Chem. Sep 16
2005;280(37):32468-32479.
24. Goldoni S, Humphries A, Nystrom A, et al. Decorin is a novel
antagonistic ligand of the Met receptor. J Cell Biol. May 18
2009;185(4):743-754.
25. Schonherr E, Sunderkotter C, Iozzo RV, et al. Decorin, a novel
player in the insulin-like growth factor system. J Biol Chem. Apr
22 2005;280(16):15767-15772.
26. Sayani K, Dodd CM, Nedelec B, et al. Delayed appearance of
decorin in healing burn scars. Histopathology. Mar 2000;36(3):
262-272.
27. Williams KJ, Qiu G, Usui HK, et al. Decorin deficiency enhances
progressive nephropathy in diabetic mice. Am J Pathol. Nov
2007;171(5):1441-1450.
28. Kolb M, Margetts PJ, Galt T, et al. Transient transgene expression
of decorin in the lung reduces the fibrotic response to
bleomycin. Am J Respir Crit Care Med. 2001;163(3 Pt 1):770-777.
29. Ameye L, Young MF. Mice deficient in small leucine-rich
proteoglycans: novel in vivo models for osteoporosis,
osteoarthritis, Ehlers-Danlos syndrome, muscular dystrophy, and
corneal diseases. Glycobiology. Sep 2002;12(9):107R-116R.
30. Jarvelainen H, Puolakkainen P, Pakkanen S, et al. A role for
decorin in cutaneous wound healing and angiogenesis. Wound
Repair Regen. Jul-Aug 2006;14(4):443-452.
31. Zimmermann DR, Dours-Zimmermann MT, Schubert M, et al.
Versican is expressed in the proliferating zone in the epidermis
and in association with the elastic network of the dermis. J Cell
Biol. Mar 1994;124(5):817-825.
32. Kischer CW, Hendrix MJ. Fibronectin (FN) in hypertrophic scars
and keloids. Cell Tissue Res. 1983;231(1):29-37.
33. Leiss M, Beckmann K, Giros A, et al. The role of integrin binding
sites in fibronectin matrix assembly in vivo. Curr Opin Cell Biol.
Oct 2008;20(5):502-507.
34. Sorrell JM, Baber MA, Caplan AI. Human dermal fibroblast
subpopulations; differential interactions with vascular
endothelial cells in coculture: nonsoluble factors in the
extracellular matrix influence interactions. Wound Repair Regen.
2008;16(2):300-309.
35. Sorrell JM, Caplan AI. Fibroblast heterogeneity: more than skin
deep. J Cell Sci. 2004;117(Pt 5):667-675.
36. Wang J, Dodd C, Shankowsky HA, et al. Deep dermal fibroblasts
contribute to hypertrophic scarring. Lab Invest. 2008;88(12):
1278-1290.
37. Dunkin CSJ, Pleat JM, Gillespie PH, et al. Scarring Occurs at a
Critical Depth of Skin Injury: Precise Measurement in a
Graduated Dermal Scratch in Human Volunteers. Plast Reconstr
Surg. 2007;119(6):1722-1732.
38. Kwan P, Hori K, Ding J, et al. Scar and contracture: biological
principles. Hand Clin. Nov 2009;25(4):511-528.
39. Rossio-Pasquier P, Casanova D, Jomard A, et al. Wound healing
of human skin transplanted onto the nude mouse after a
superficial excisional injury: human dermal reconstruction
is achieved in several steps by two different fibroblast
subpopulations. Arch Dermatol Res. 1999;291(11):591-599.
40. Tomasek JJ, Gabbiani G, Hinz B, et al. Myofibroblasts and
mechano-regulation of connective tissue remodelling. Nat Rev
Mol Cell Biol. May 2002;3(5):349-363.
41. Hinz B, Celetta G, Tomasek JJ, et al. Alpha-smooth muscle actin
expression upregulates fibroblast contractile activity. Mol Biol
Cell. Sep 2001;12(9):2730-2741.
42. Hinz B, Mastrangelo D, Iselin CE, et al. Mechanical tension
controls granulation tissue contractile activity and myofibroblast
differentiation. Am J Pathol. Sep 2001;159(3):1009-1020.
Total Burn Care
45
505.e2
© Copyright 2012 Elsevier, Inc. All rights reserved.
43. Bergers G, Song S. The role of pericytes in blood-vessel
formation and maintenance. Neuro Oncol. Oct 2005;7(4):
452-464.
44. Desmouliere A, Redard M, Darby I, et al. Apoptosis mediates the
decrease in cellularity during the transition between granulation
tissue and scar. Am J Pathol. 1995;146(1):56-66.
45. Werner S, Grose R. Regulation of wound healing by growth
factors and cytokines. Physiol Rev. 2003;83(3):835-870.
46. Desmouliere A, Geinoz A, Gabbiani F, et al. Transforming
growth factor-beta 1 induces alpha-smooth muscle actin
expression in granulation tissue myofibroblasts and in quiescent
and growing cultured fibroblasts. J Cell Biol. Jul 1993;122(1):
103-111.
47. Ignotz RA, Massague J. Transforming growth factor-beta
stimulates the expression of fibronectin and collagen and their
incorporation into the extracellular matrix. J Biol Chem.
1986;261(9):4337-4345.
48. Serini G, Bochaton-Piallat ML, Ropraz P, et al. The fibronectin
domain ED-A is crucial for myofibroblastic phenotype induction
by transforming growth factor-beta1. J Cell Biol. Aug 10
1998;142(3):873-881.
49. Rubbia-Brandt L, Sappino AP, Gabbiani G. Locally applied
GM-CSF induces the accumulation of alpha-smooth muscle
actin containing myofibroblasts. Virchows Arch B Cell Pathol Incl
Mol Pathol. 1991;60(2):73-82.
50. Vyalov S, Desmouliere A, Gabbiani G. GM-CSF-induced
granulation tissue formation: relationships between macrophage
and myofibroblast accumulation. Virchows Arch B Cell Pathol Incl
Mol Pathol. 1993;63(4):231-239.
51. Appleton I, Tomlinson A, Chander CL, et al. Effect of
endothelin-1 on croton oil-induced granulation tissue in the rat.
A pharmacologic and immunohistochemical study. Lab Invest.
Dec 1992;67(6):703-710.
52. Souza BR, Cardoso JF, Amadeu TP, et al. Sympathetic
denervation accelerates wound contraction but delays
reepithelialization in rats. Wound Repair Regen. Sep-Oct
2005;13(5):498-505.
53. Dubuisson L, Desmouliere A, Decourt B, et al. Inhibition of rat
liver fibrogenesis through noradrenergic antagonism. Hepatology.
Feb 2002;35(2):325-331.
54. Arora PD, Narani N, McCulloch CA. The compliance of collagen
gels regulates transforming growth factor-beta induction of
alpha-smooth muscle actin in fibroblasts. Am J Pathol. Mar
1999;154(3):871-882.
55. Wells RG. The role of matrix stiffness in hepatic stellate cell
activation and liver fibrosis. J Clin Gastroenterol. Apr 2005;
39(4 suppl 2):S158-161.
56. Yeung T, Georges PC, Flanagan LA, et al. Effects of substrate
stiffness on cell morphology, cytoskeletal structure, and
adhesion. Cell Motil Cytoskeleton. Jan 2005;60(1):24-34.
57. Ng CP, Hinz B, Swartz MA. Interstitial fluid flow induces
myofibroblast differentiation and collagen alignment in vitro.
J Cell Sci. Oct 15 2005;118(Pt 20):4731-4739.
58. Hinz B, Pittet P, Smith-Clerc J, et al. Myofibroblast development
is characterized by specific cell-cell adherens junctions. Mol Biol
Cell. Sep 2004;15(9):4310-4320.
59. Follonier L, Schaub S, Meister JJ, et al. Myofibroblast
communication is controlled by intercellular mechanical
coupling. J Cell Sci. Oct 15 2008;121(Pt 20):3305-3316.
60. Follonier Castella L, Gabbiani G, McCulloch CA, et al.
Regulation of myofibroblast activities: calcium pulls some strings
behind the scene. Exp Cell Res. Sep 10 2010;316(15):2390-2401.
61. Ehrlich HP, Desmouliere A, Diegelmann RF, et al. Morphological
and immunochemical differences between keloid and
hypertrophic scar. Am J Pathol. 1994;145(1):105-113.
62. Lee JY, Yang CC, Chao SC, et al. Histopathological differential
diagnosis of keloid and hypertrophic scar. Am J Dermatopathol.
Oct 2004;26(5):379-384.
63. Verhaegen PD, van Zuijlen PP, Pennings NM, et al. Differences
in collagen architecture between keloid, hypertrophic scar,
normotrophic scar, and normal skin: An objective
histopathological analysis. Wound Repair Regen. Sep-Oct
2009;17(5):649-656.
64. van der Slot AJ, Zuurmond AM, van den Bogaerdt AJ, et al.
Increased formation of pyridinoline cross-links due to higher
telopeptide lysyl hydroxylase levels is a general fibrotic
phenomenon. Matrix Biol. Jul 2004;23(4):251-257.
65. Ulrich MM, Verkerk M, Reijnen L, et al. Expression profile of
proteins involved in scar formation in the healing process of
full-thickness excisional wounds in the porcine model. Wound
Repair Regen. Jul-Aug 2007;15(4):482-490.
66. Xi-Qiao W, Ying-Kai L, Chun Q, et al. Hyperactivity of
fibroblasts and functional regression of endothelial cells
contribute to microvessel occlusion in hypertrophic scarring.
Microvasc Res. Mar 2009;77(2):204-211.
67. Darby IA, Bisucci T, Pittet B, et al. Skin flap-induced regression
of granulation tissue correlates with reduced growth factor
and increased metalloproteinase expression. J Pathol. May
2002;197(1):117-127.
68. Costa AM, Peyrol S, Porto LC, et al. Mechanical forces induce
scar remodeling. Study in non-pressure-treated versus pressure-
treated hypertrophic scars. Am J Pathol. Nov 1999;155(5):
1671-1679.
69. Aarabi S, Bhatt KA, Shi Y, et al. Mechanical load initiates
hypertrophic scar formation through decreased cellular
apoptosis. FASEB J. Oct 2007;21(12):3250-3261.
70. Modarressi A, Pietramaggiori G, Godbout C, et al. Hypoxia
Impairs Skin Myofibroblast Differentiation and Function. J Invest
Dermatol. Aug 5 2010.
71. Menezes GC, Miron-Mendoza M, Ho CH, et al. Oncogenic
Ras-transformed human fibroblasts exhibit differential changes
in contraction and migration in 3D collagen matrices. Exp Cell
Res. Oct 1 2008;314(16):3081-3091.
72. Georges PC, Hui JJ, Gombos Z, et al. Increased stiffness of the
rat liver precedes matrix deposition: implications for fibrosis. Am
J Physiol Gastrointest Liver Physiol. Dec 2007;293(6):G1147-G1154.
73. Bellemare J, Roberge CJ, Bergeron D, et al. Epidermis promotes
dermal fibrosis: role in the pathogenesis of hypertrophic scars.
J Pathol. 2005;206(1):1-8.
74. Hakvoort TE, Altun V, Ramrattan RS, et al. Epidermal
participation in post-burn hypertrophic scar development.
Virchows Arch. Mar 1999;434(3):221-226.
75. Akaishi S, Ogawa R, Hyakusoku H. Keloid and hypertrophic
scar: neurogenic inflammation hypotheses. Med Hypotheses.
2008;71(1):32-38.
76. Ross R, Everett NB, Tyler R. Wound healing and collagen
formation. VI. The origin of the wound fibroblast studied in
parabiosis. J Cell Biol. Mar 1970;44(3):645-654.
77. Wang J, Dodd C, Shankowsky HA, et al. Deep dermal fibroblasts
contribute to hypertrophic scarring. Lab Invest. Dec 2008;88(12):
1278-1290.
78. Rajkumar VS, Howell K, Csiszar K, et al. Shared expression of
phenotypic markers in systemic sclerosis indicates a convergence
of pericytes and fibroblasts to a myofibroblast lineage in fibrosis.
Arthritis Res Ther. 2005;7(5):R1113-R1123.
79. Reeves HL, Friedman SL. Activation of hepatic stellate cells—a
key issue in liver fibrosis. Front Biosci. Apr 1 2002;7:d808-d826.
80. Guyot C, Lepreux S, Combe C, et al. Hepatic fibrosis and
cirrhosis: the (myo)fibroblastic cell subpopulations involved.
Int J Biochem Cell Biol. Feb 2006;38(2):135-151.
81. Andrade ZA, Guerret S, Fernandes AL. Myofibroblasts in
schistosomal portal fibrosis of man. Mem Inst Oswaldo Cruz.
Jan-Feb 1999;94(1):87-93.
82. Hewitson TD. Renal tubulointerstitial fibrosis: common but
never simple. Am J Physiol Renal Physiol. Jun 2009;296(6):
F1239-F1244.
Molecular and cellular basis of hypertrophic scarring
505.e3
© Copyright 2012 Elsevier, Inc. All rights reserved.
83. Pozzi A, Voziyan PA, Hudson BG, et al. Regulation of matrix
synthesis, remodeling and accumulation in glomerulosclerosis.
Curr Pharm Des. 2009;15(12):1318-1333.
84. Jahoda CA, Reynolds AJ. Hair follicle dermal sheath cells:
unsung participants in wound healing. Lancet. Oct 27
2001;358(9291):1445-1448.
85. Theise ND, Saxena R, Portmann BC, et al. The canals of Hering
and hepatic stem cells in humans. Hepatology. Dec 1999;30(6):
1425-1433.
86. Saxena R, Theise N. Canals of Hering: recent insights and current
knowledge. Semin Liver Dis. Feb 2004;24(1):43-48.
87. Abe R, Donnelly SC, Peng T, et al. Peripheral blood fibrocytes:
differentiation pathway and migration to wound sites.
J Immunol. 2001;166(12):7556-7562.
88. Yang L, Scott PG, Dodd C, et al. Identification of fibrocytes in
postburn hypertrophic scar. Wound Repair Regen. 2005;13(4):
398-404.
89. Schmidt M, Sun G, Stacey MA, et al. Identification of circulating
fibrocytes as precursors of bronchial myofibroblasts in asthma.
J Immunol. Jul 1 2003;171(1):380-389.
90. Okada H, Kalluri R. Cellular and molecular pathways that lead
to progression and regression of renal fibrogenesis. Curr Mol
Med. Aug 2005;5(5):467-474.
91. Prockop DJ. Marrow stromal cells as stem cells for
nonhematopoietic tissues. Science. Apr 4 1997;276(5309):71-74.
92. Pittenger MF, Mackay AM, Beck SC, et al. Multilineage potential
of adult human mesenchymal stem cells. Science. Apr 2
1999;284(5411):143-147.
93. Barisic-Dujmovic T, Boban I, Clark SH. Fibroblasts/
myofibroblasts that participate in cutaneous wound healing are
not derived from circulating progenitor cells. J Cell Physiol. Mar
2010;222(3):703-712.
94. Liu Y. New insights into epithelial-mesenchymal transition in
kidney fibrosis. J Am Soc Nephrol. Feb 2010;21(2):212-222.
95. Hinz B, Phan SH, Thannickal VJ, et al. The myofibroblast:
one function, multiple origins. Am J Pathol. Jun 2007;170(6):
1807-1816.
96. Watsky MA, Weber KT, Sun Y, et al. New insights into the
mechanism of fibroblast to myofibroblast transformation and
associated pathologies. Int Rev Cell Mol Biol. 2010;282:165-192.
97. Bucala R, Spiegel LA, Chesney J, et al. Circulating fibrocytes
define a new leukocyte subpopulation that mediates tissue
repair. Mol Med. 1994;1(1):71-81.
98. Pilling D, Fan T, Huang D, et al. Identification of markers that
distinguish monocyte-derived fibrocytes from monocytes,
macrophages, and fibroblasts. PLoS One. 2009;4(10):e7475.
99. Andersson-Sjoland A, de Alba CG, Nihlberg K, et al. Fibrocytes
are a potential source of lung fibroblasts in idiopathic
pulmonary fibrosis. Int J Biochem Cell Biol. 2008;40(10):
2129-2140.
100. Sakai N, Wada T, Matsushima K, et al. The renin-angiotensin
system contributes to renal fibrosis through regulation of
fibrocytes. J Hypertens. Apr 2008;26(4):780-790.
101. Wang J, Jiao H, Stewart TL, et al. Increased TGF-beta-producing
CD4+ T lymphocytes in postburn patients and their potential
interaction with dermal fibroblasts in hypertrophic scarring.
Wound Repair Regen. 2007;15(4):530-539.
102. Yang L, Scott PG, Giuffre J, et al. Peripheral blood fibrocytes
from burn patients: identification and quantification of
fibrocytes in adherent cells cultured from peripheral blood
mononuclear cells. Lab Invest. 2002;82(9):1183-1192.
103. Pilling D, Roife D, Wang M, et al. Reduction of bleomycin-
induced pulmonary fibrosis by serum amyloid P. J Immunol.
2007;179(6):4035-4044.
104. Hong KM, Belperio JA, Keane MP, et al. Differentiation of
human circulating fibrocytes as mediated by transforming
growth factor-beta and peroxisome proliferator-activated receptor
gamma. J Biol Chem. 2007;282(31):22910-22920.
105. Wang JF, Jiao H, Stewart TL, et al. Fibrocytes from burn patients
regulate the activities of fibroblasts. Wound Repair Regen.
2007;15(1):113-121.
106. Chesney J, Bacher M, Bender A, et al. The peripheral blood
fibrocyte is a potent antigen-presenting cell capable of priming
naive T cells in situ. Proc Natl Acad Sci USA. 1997;94(12):
6307-6312.
107. Balmelli C, Alves MP, Steiner E, et al. Responsiveness of
fibrocytes to toll-like receptor danger signals. Immunobiology.
2007;212(9–10):693-699.
108. Hartlapp I, Abe R, Saeed RW, et al. Fibrocytes induce an
angiogenic phenotype in cultured endothelial cells and promote
angiogenesis in vivo. FASEB J. 2001;15(12):2215-2224.
109. Curnow SJ, Fairclough M, Schmutz C, et al. Distinct types of
fibrocyte can differentiate from mononuclear cells in the
presence and absence of serum. PLoS One. 2010;5(3):e9730.
110. Medina A, Ghahary A. Fibrocytes can be reprogrammed to
promote tissue remodeling capacity of dermal fibroblasts.
Mol Cell Biochem. Jun 20 2010.
111. Werner S, Krieg T, Smola H. Keratinocyte–Fibroblast
Interactions in Wound Healing. J Investig Dermatol. 2007;127(5):
998-1008.
112. Deitch EA, Wheelahan TM, Rose MP, et al. Hypertrophic burn
scars: analysis of variables. J Trauma. 1983;23(10):895-898.
113. Ghahary A, Ghaffari A. Role of keratinocyte-fibroblast cross-talk
in development of hypertrophic scar. Wound Repair Regen.
2007;15(suppl 1):S46-53.
114. Amjad SB, Carachi R, Edward M. Keratinocyte regulation of
TGF-beta and connective tissue growth factor expression: a role
in suppression of scar tissue formation. Wound Repair Regen.
2007;15(5):748-755.
115. Harrison CA, Gossiel F, Bullock AJ, et al. Investigation of
keratinocyte regulation of collagen I synthesis by dermal
fibroblasts in a simple in vitro model. Br J Dermatol. Mar
2006;154(3):401-410.
116. Ghahary A, Marcoux Y, Karimi-Busheri F, et al. Differentiated
keratinocyte-releasable stratifin (14–3-3 sigma) stimulates
MMP-1 expression in dermal fibroblasts. J Invest Dermatol.
2005;124(1):170-177.
117. Machesney M, Tidman N, Waseem A, et al. Activated
keratinocytes in the epidermis of hypertrophic scars. Am J Pathol.
May 1998;152(5):1133-1141.
118. Andriessen MP, Niessen FB, Van de Kerkhof PC, et al.
Hypertrophic scarring is associated with epidermal
abnormalities: an immunohistochemical study. J Pathol.
Oct 1998;186(2):192-200.
119. Niessen FB, Andriessen MP, Schalkwijk J, et al. Keratinocyte-
derived growth factors play a role in the formation of
hypertrophic scars. J Pathol. Jun 2001;194(2):207-216.
120. Leask A, Abraham DJ. TGF-beta signaling and the fibrotic
response. FASEB J. 2004;18(7):816-827.
121. Roberts AB. Molecular and cell biology of TGF-beta. Miner
Electrolyte Metab. 1998;24(2–3):111-119.
122. Cutroneo KR. TGF-beta-induced fibrosis and SMAD signaling:
oligo decoys as natural therapeutics for inhibition of tissue
fibrosis and scarring. Wound Repair Regen. 2007;15(suppl 1):
S54-S60.
123. Tredget EE, Shankowsky HA, Pannu R, et al. Transforming
growth factor-beta in thermally injured patients with
hypertrophic scars: effects of interferon alpha-2b. Plast Reconstr
Surg. 1998;102(5):1317-1328; discussion 1329-1330.
124. Wang R, Ghahary A, Shen Q, et al. Hypertrophic scar tissues and
fibroblasts produce more transforming growth factor-beta1
mRNA and protein than normal skin and cells. Wound Repair
Regen. 2000;8(2):128-137.
125. Lanning DA, Nwomeh BC, Montante SJ, et al. TGF-beta1 alters
the healing of cutaneous fetal excisional wounds. J Pediatr Surg.
1999;34(5):695-700.
Total Burn Care
45
505.e4
© Copyright 2012 Elsevier, Inc. All rights reserved.
126. Grotendorst GR. Connective tissue growth factor: a mediator of
TGF-beta action on fibroblasts. Cytokine Growth Factor Rev.
1997;8(3):171-179.
127. Scott PG, Dodd CM, Ghahary A, et al. Fibroblasts from
post-burn hypertrophic scar tissue synthesize less decorin than
normal dermal fibroblasts. Clin Sci (Lond). May 1998;94(5):
541-547.
128. Yamaguchi Y, Mann DM, Ruoslahti E. Negative regulation of
transforming growth factor-beta by the proteoglycan decorin.
Nature. 1990;346(6281):281-284.
129. Willis BC, Liebler JM, Luby-Phelps K, et al. Induction of
epithelial-mesenchymal transition in alveolar epithelial cells by
transforming growth factor-beta1: potential role in idiopathic
pulmonary fibrosis. Am J Pathol. May 2005;166(5):1321-1332.
130. Arora PD, McCulloch CA. The deletion of transforming growth
factor-beta-induced myofibroblasts depends on growth
conditions and actin organization. Am J Pathol. Dec 1999;
155(6):2087-2099.
131. Occleston NL, Laverty HG, O’Kane S, et al. Prevention and
reduction of scarring in the skin by Transforming Growth Factor
beta 3 (TGFbeta3): from laboratory discovery to clinical
pharmaceutical. J Biomater Sci Polym Ed. 2008;19(8):1047-1063.
132. Bock O, Yu H, Zitron S, et al. Studies of transforming growth
factors beta 1–3 and their receptors I and II in fibroblast of
keloids and hypertrophic scars. Acta Derm Venereol.
2005;85(3):216-220.
133. Leask A, Abraham DJ. All in the CCN family: essential
matricellular signaling modulators emerge from the bunker.
J Cell Sci. Dec 1 2006;119(Pt 23):4803-4810.
134. Chen CC, Lau LF. Functions and mechanisms of action of
CCN matricellular proteins. Int J Biochem Cell Biol. Apr 2009;
41(4):771-783.
135. Mori T, Kawara S, Shinozaki M, et al. Role and interaction of
connective tissue growth factor with transforming growth
factor-beta in persistent fibrosis: a mouse fibrosis model.
J Cell Physiol. 1999;181(1):153-159.
136. Leask A, Abraham DJ. The role of connective tissue growth
factor, a multifunctional matricellular protein, in fibroblast
biology. Biochem Cell Biol. 2003;81(6):355-363.
137. Colwell AS, Phan T-T, Kong W, et al. Hypertrophic scar
fibroblasts have increased connective tissue growth factor
expression after transforming growth factor-beta stimulation.
Plast Reconstr Surg. 2005;116(5):1387-1390; discussion
1391-1382.
138. Shi-Wen X, Leask A, Abraham D. Regulation and function of
connective tissue growth factor/CCN2 in tissue repair, scarring
and fibrosis. Cytokine Growth Factor Rev. 2008;19(2):133-144.
139. Stratton R, Shiwen X, Martini G, et al. Iloprost suppresses
connective tissue growth factor production in fibroblasts and in
the skin of scleroderma patients. J Clin Invest. 2001;108(2):
241-250.
140. Abraham D. Connective tissue growth factor: growth factor,
matricellular organizer, fibrotic biomarker or molecular target
for anti-fibrotic therapy in SSc? Rheumatology (Oxford).
2008;47(suppl 5):v8-9.
141. Trojanowska M. Role of PDGF in fibrotic diseases and systemic
sclerosis. Rheumatology (Oxford). 2008;47(suppl 5):v2-4.
142. Andrae J, Gallini R, Betsholtz C. Role of platelet-derived growth
factors in physiology and medicine. Genes Dev. 2008;22(10):
1276-1312.
143. Powell DW, Mifflin RC, Valentich JD, et al. Myofibroblasts. I.
Paracrine cells important in health and disease. Am J Physiol.
Jul 1999;277(1 Pt 1):C1-9.
144. Bonner JC. Regulation of PDGF and its receptors in fibrotic
diseases. Cytokine Growth Factor Rev. 2004;15(4):255-273.
145. Younai S, Venters G, Vu S, et al. Role of growth factors in scar
contraction: an in vitro analysis. Ann Plast Surg. 1996;36(5):
495-501.
146. Bhagavathula N, Dame MK, Dasilva M, et al. Fibroblast
Response to Gadolinium: Role for Platelet-Derived Growth
Factor Receptor. Invest Radiol. Aug 13.
147. Abdollahi A, Li M, Ping G, et al. Inhibition of platelet-derived
growth factor signaling attenuates pulmonary fibrosis. J Exp Med.
2005;201(6):925-935.
148. Distler JHW, Jungel A, Huber LC, et al. Imatinib mesylate
reduces production of extracellular matrix and prevents
development of experimental dermal fibrosis. Arthritis Rheum.
2007;56(1):311-322.
149. Makower AM, Wroblewski J, Pawlowski A. Effects of IGF-I,
EGF, and FGF on proteoglycans synthesized by fractionated
chondrocytes of rat rib growth plate. Exp Cell Res. Dec
1988;179(2):498-506.
150. Rolfe KJ, Cambrey AD, Richardson J, et al. Dermal fibroblasts
derived from fetal and postnatal humans exhibit distinct
responses to insulin like growth factors. BMC Dev Biol. 2007;7:
124.
151. Miele C, Rochford JJ, Filippa N, et al. Insulin and insulin-like
growth factor-I induce vascular endothelial growth factor mRNA
expression via different signaling pathways. J Biol Chem.
2000;275(28):21695-21702.
152. Goldstein RH, Poliks CF, Pilch PF, et al. Stimulation of collagen
formation by insulin and insulin-like growth factor I in cultures
of human lung fibroblasts. Endocrinology. 1989;124(2):964-970.
153. Ghahary A, Shen Q, Shen YJ, et al. Induction of transforming
growth factor beta 1 by insulin-like growth factor-1 in dermal
fibroblasts. J Cell Physiol. 1998;174(3):301-309.
154. Ghahary A, Shen YJ, Nedelec B, et al. Collagenase production is
lower in post-burn hypertrophic scar fibroblasts than in normal
fibroblasts and is reduced by insulin-like growth factor-1. J Invest
Dermatol. 1996;106(3):476-481.
155. Ghahary A, Shen YJ, Wang R, et al. Expression and localization
of insulin-like growth factor-1 in normal and post-burn
hypertrophic scar tissue in human. Mol Cell Biochem. 1998;
183(1–2):1-9.
156. Pestka S, Krause CD, Walter MR. Interferons, interferon-like
cytokines, and their receptors. Immunol Rev. Dec 2004;202:8-32.
157. Tredget EE, Shen YJ, Liu G, et al. Regulation of collagen synthesis
and messenger RNA levels in normal and hypertrophic scar
fibroblasts in vitro by interferon alfa-2b. Wound Repair Regen.
Jul 1993;1(3):156-165.
158. Ghahary A, Shen YJ, Nedelec B, et al. Interferons gamma and
alpha-2b differentially regulate the expression of collagenase and
tissue inhibitor of metalloproteinase-1 messenger RNA in
human hypertrophic and normal dermal fibroblasts. Wound
Repair Regen. 1995;3(2):176-184.
159. Dans MJ, Isseroff R. Inhibition of collagen lattice contraction by
pentoxifylline and interferon-alpha, -beta, and -gamma. J Invest
Dermatol. Jan 1994;102(1):118-121.
160. Nedelec B, Dodd CM, Scott PG, et al. Effect of interferon-
alpha2b on guinea pig wound closure and the expression of
cytoskeletal proteins in vivo. Wound Repair Regen. 1998;6(3):
202-212.
161. Dao T, Ariyasu T, Holan V, et al. Natural human interferon-alpha
augments apoptosis in activated T cell line. Cell Immunol. May
1994;155(2):304-311.
162. Rodriguez-Villanueva J, McDonnell TJ. Induction of apoptotic
cell death in non-melanoma skin cancer by interferon-alpha. Int
J Cancer. Mar 29 1995;61(1):110-114.
163. McCauley RL, Chopra V, Li YY, et al. Altered cytokine production
in black patients with keloids. J Clin Immunol. Jul 1992;12(4):
300-308.
164. van der Veer WM, Bloemen MCT, Ulrich MMW, et al. Potential
cellular and molecular causes of hypertrophic scar formation.
Burns. 2009;35(1):15-29.
165. Sunderkotter C, Steinbrink K, Goebeler M, et al. Macrophages
and angiogenesis. J Leukoc Biol. 1994;55(3):410-422.
Molecular and cellular basis of hypertrophic scarring
505.e5
© Copyright 2012 Elsevier, Inc. All rights reserved.
166. Huber JP, Ramos HJ, Gill MA, et al. Cutting edge: Type I IFN
reverses human Th2 commitment and stability by suppressing
GATA3. J Immunol. Jul 15 2010;185(2):813-817.
167. Mosmann TR, Coffman RL. TH1 and TH2 cells: different
patterns of lymphokine secretion lead to different functional
properties. Annu Rev Immunol. 1989;7:145-173.
168. Wynn TA. Fibrotic disease and the T(H)1/T(H)2 paradigm. Nat
Rev Immunol. 2004;4(8):583-594.
169. Seder RA, Marth T, Sieve MC, et al. Factors involved in the
differentiation of TGF-beta-producing cells from naive CD4+ T
cells: IL-4 and IFN-gamma have opposing effects, while TGF-beta
positively regulates its own production. J Immunol. Jun 15
1998;160(12):5719-5728.
170. Hunt JP, Hunter CT, Brownstein MR, et al. The effector
component of the cytotoxic T-lymphocyte response has a
biphasic pattern after burn injury. J Surg Res. Dec 1998;80(2):
243-251.
171. Horgan AF, Mendez MV, O’Riordain DS, et al. Altered gene
transcription after burn injury results in depressed T-lymphocyte
activation. Ann Surg. Sep 1994;220(3):342-351; discussion
351-352.
172. O’Sullivan ST, Lederer JA, Horgan AF, et al. Major injury leads to
predominance of the T helper-2 lymphocyte phenotype and
diminished interleukin-12 production associated with decreased
resistance to infection. Ann Surg. Oct 1995;222(4):482-490;
discussion 490-492.
173. Shi Z, Wakil AE, Rockey DC. Strain-specific differences in mouse
hepatic wound healing are mediated by divergent T helper
cytokine responses. Proc Natl Acad Sci U S A. Sep 30
1997;94(20):10663-10668.
174. Tredget EE, Yang L, Delehanty M, et al. Polarized Th2 cytokine
production in patients with hypertrophic scar following thermal
injury. J Interferon Cytokine Res. 2006;26(3):179-189.
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Pathophysiology of the burn scar
Hal K. Hawkins, Celeste C. Finnerty
Introduction
This chapter reviews current knowledge of the process of
wound healing in humans and animals, with special empha
sis on abnormal long-term responses to thermal injury.
Prehistoric and historic perspectives
Wounds due to combat, hunting injuries, accidents and
thermal injuries have been the leading causes of death in
humans for millennia. On the other hand, prolonged sur
vival of large full-thickness wounds is a recent phenomenon.
Several complex biological responses to injury to the skin
have evolved over time, but there has been no evolutionary
pressure to evolve appropriate responses to very large
wounds. There are records of human attempts to improve
wound healing in the most ancient texts from Mesopotamia
and Egypt. Guido Majno has explored what can be learned
from archeology and paleontology regarding wounds and
their treatment in ancient times.1 He also provides a very
accurate brief description of the process of wound healing
in lay terms. In the development of modern medicine, the
advances in wound treatment advocated by Ambroise Pare
(1520–1590) stand out, together with the campaign for anti
sepsis of Joseph Lister (1827–1912), and the development
of antibiotics as well as the development of the modern
methods of treatment described in this book.
Incisional wounds with primary closure
The essential components of wound healing are easily
understood. They are: (1) activation in the wound of tissue
repair by phenotypic fibroblasts and small blood vessels, and
an inflammatory response initiated by vascular leakage and
(2) entry into the wound of circulating polymorphonuclear
neutrophils, lymphocytes and macrophages.2 When a sharp
incision is closed while still sterile, only minimal vascular
leakage and inflammation occur, and the predominant reac
tion to injury occurs in the fibroblasts present in the dermis
and subcutaneous tissue. These resting connective tissue cells
are rapidly activated to secrete collagen, which quickly
bridges the small remaining gap to restore the resistance
of the skin to tearing. Vascular continuity is restored by
budding and remodeling of blood vessels, and the basal
keratinocytes of the epidermis divide briefly to restore the
complete structure of the epidermal barrier. All that remains
to indicate the site of injury is a linear ribbon of dense col
lagen with little flexibility that marks the site of the incision,
as well as some small scars that mark the sites where sutures
were inserted. This process of incisional wound healing was
well described in humans by Russell Ross and his colleagues
in Seattle.3,4
Delayed wound closure ‘by second intention’
and wound contraction
If the epidermis and dermis are incised or removed and the
edges of the wound remain separated, much more promi
nent inflammatory and reparative events occur. Extensive
leakage of blood plasma by damaged small blood vessels
maintains an outward flow that serves to keep the wound
clean, but causes deposition of coagulated fibrin and other
desiccated proteins on the wound surface. Conversion of
fibrinogen into fibrin fills the gap in the epidermis and pro
vides a gelatinous matrix capable of sustaining migrating
cells. Thrombin stimulates expression of interleukin-6 in
connective tissue cells.5 Degranulation of platelets releases
platelet-derived growth factor (PDGF) as well as several
other proinflammatory cytokines.6 Degradation of fibrin
releases peptides that stimulate fibroblast proliferation and
secretion and division of vascular endothelial cells, and pro
duction of cytokines by other cells.7–9 The resting fibroblasts
of the dermis, together with circulating stem cells, divide
rapidly in the wound bed and secrete large quantities of col
lagen and proteoglycans, particularly those typically present
in skin during fetal life, with predominance of type III
collagen.10,11 Simultaneously, the endothelial cells of small
blood vessels proliferate rapidly and form numerous small
capillary loops that extend upwards toward the surface.
Together, these cells form a mass of granulation tissue that
covers the wound. All these activities of fibroblasts and
endothelial cells are stimulated by cytokines and other pep
tides, largely secreted by monocytes and lymphoid cells
that infiltrate the wound bed. Certain proteins and peptides
that are normally present in blood plasma also stimulate
and enable formation of the wound matrix, notably fibro
nectin and vitronectin.12–14 Polymorphonuclear neutrophils
also enter the wound bed in large numbers, where they
phagocytize and kill bacteria and fungi, which are always
present in the outside world and gain entry to the dermis
©2012 Elsevier Ltd, Inc, BV
DOI: 10.1016/B978-1-4377-2786-9.00046-1
CHAPTER 46
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can generate cells that can multiply, migrate and regenerate
the surface epidermis.24 The stem cell population that was
first identified is slowly cycling, expresses the conventional
stem cell surface marker CD34, and resides in the bulge
region of the follicle near the attachment of the arrector pili
muscle.25,26 More recently, additional stem cell populations
have been identified that reside in the isthmus region and
the hair germ region of the follicle and express distinct
markers.27–29 Much is being learned about the function of
these various groups of stem cells by studying knockout and
overexpressing mice. The changes in follicular stem cells
during healing of burn wounds, however, remain to be
described.
One new aspect of hair follicle biology that is of great
interest for burn surgeons is the delineation of the role of
the dermal papilla, the tiny cluster of mesenchymal cells
within the hair bulb.30 Fetal development of hair follicles
apparently depends upon interaction between epithelial
cells of the epidermis and mesenchymal cells. The mesen
chymal cells of the dermal papilla, which can be amplified
in culture using keratinocyte conditioned medium, can
induce formation of hair follicles from interfollicular skin.
Experiments have even been described, in which formation
of new hair follicles, complete with hair, was induced in
hairless nipple skin of the mouse, and in the renal capsule.31,32
Since one of the major problems in long-term care of
burn patients is alopecia, the possibility that hair follicles
could be caused to regenerate where there are none is very
appealing.33
Third degree or full thickness injury
In full thickness burns, thermal injury extends deep enough
to destroy all of the hair follicle that has the capacity to
regenerate the epidermis, and some of the upper subcutan
eous tissue may also become necrotic. In this case regenera
tion of the epidermis from hair follicles is not possible, and
the wound can develop an epidermal covering only slowly,
as the epidermis lateral to the wound spreads out over the
entire wound surface.2 During this time, the necrotic tissue
in the wound bed is at risk of infection, and extensive activity
of tissue macrophages is required to eventually remove it.
Biology of wound healing
Changes in vascular permeability
In order to review current understanding of the processes
important in wound healing, each will be considered sepa
rately. Changes in local blood vessels are the earliest com
ponent of the response of the wound to injury, and are
essential for the succeeding steps. Plasma exudation is due
to increased permeability of venules to proteins, largely due
to local release of histamine from mast cells and substance
P from local sensory nerve endings. In burn injury, there is
an added component of plasma leakage that occurs for a few
hours throughout the body in response to unknown stimuli.
Of course, both plasma and red blood cells enter the wound
through broken or necrotic blood vessels. Infection triggers
further plasma exudation by constantly stimulating and
prolonging the vascular phase of acute inflammation. In
and subcutis through the open wound. Next, the fibroblasts
develop interconnections among themselves and produce
and assemble the contractile machinery of actin and myosin
within the cytoplasm of each cell.15 These interconnected
myofibroblasts contract to shrink the size of the open
wound, pulling adjacent intact skin to cover the wound bed.
This process of wound contraction is more dramatic in
experimental wounds of rodents than in human wounds.
The effects of wound contracture in applying tension to
surrounding tissues, however, are sometimes very clear in
humans as well. Simultaneously with these processes, the
basal keratinocytes of the cut edges of the epidermis change
to a migratory and secretory phenotype, and begin to invade
the wound bed between the granulation tissue layer and the
scab of dried proteins on the surface.16 Cell division of kerati
nocytes occurs near the cut edge of the wound to supply cells
for this migration. Once they make contact to seal the center
of the wound, the migrating keratinocytes change their phe
notype again and restore the normal laminated structure of
the epidermis and produce a new basal lamina.17,18 Melano
cytes also develop migratory properties during healing of
large wounds, since they establish a degree of pigmentation
in the healed wound that approximates the pigmentation of
the uninjured skin. It should be noted that only the epider
mis regenerates to resemble the normal epidermis. Hair fol
licles, sweat glands and other epidermal appendages do not
regenerate. Thus, the part of the wound that was not closed
by contracture remains dry, hairless and flat. Furthermore,
the restored dermis in a fully healed scar is composed of
collagen type I fibers running in straight lines adjacent to
one another parallel to the surface, providing good strength
(though somewhat less than the native skin) but far less
elasticity and flexibility than the connective tissue of the
normal dermis.
First degree or superficial injury of skin
Superficial burn wounds are those in which part or all of the
epidermis is lost, but the epidermal basal lamina remains
intact and the dermis is uninjured. In these areas, only epi
dermal regeneration is required, hair follicles and sweat
glands remain intact, and healing can occur with little or no
disfigurement.19
Second degree or partial thickness injury
In partial thickness wounds, the entire epidermis and the
upper part of the dermis become necrotic. If left intact, the
presence of a large quantity of devitalized tissue requires
prolonged activity of macrophages to clear the necrotic
debris. Granulation tissue forms underneath the necrotic
dermal tissue, and epidermal migration occurs under the
eschar formed by dead tissue, leading to restoration of the
epidermis, and production of dermal connective tissue in
the form of a thin scar. The deep portions of the hair follicles
remain viable, and the keratinocytes lining the hair follicles
become migratory and undergo mitosis behind the migrat
ing cells, eventually covering the surface with new epidermis
derived from the hair follicle.16,20 In severe cases, loss of hair
follicles may lead to insufficient regenerative activity to cover
the surface.21–23 Recently, hair follicles have been found to
contain several populations of multipotent stem cells that
Pathophysiology of the burn scar
509
in the residual epidermis. Similar processes stimulate migra
tion and replacement of epithelial cells from hair follicles in
partial thickness wounds. After a sheet of epithelial cells is
established over the entire wound surface, they begin to
divide and eventually create a multilayered stratified squa
mous epithelium with a granular layer and keratinization.
Epidermal cells secrete substantial quantities of interleukin-
1β and other cytokines.51,52 The new proliferative epidermal
basal cells also secrete a new basal lamina composed of
laminin, type IV collagen and bullous pemphigoid antigen,
adhere tightly to that basal lamina, and develop attachments
of type VII collagen between the basal lamina and the under
lying fibers of type I collagen in the scarred dermis. Also, just
after the newly formed epithelial layer completely covers the
wound, the phenotype of the connective tissue cells in the
matrix undergoes a series of changes, and much less fibro
nectin is found in the wound matrix.17 As noted above, in
second-degree burns, epidermal cells from the hair follicles
regenerate the epidermis on the surface.
Collagen matrix formation and maturation
Scars gradually increase in their strength, as measured by
their resistance to tearing, but never reach the strength of
normal dermis. During this process, the delicate fibers of
newly secreted collagens I and III are replaced by large col
lagen I fibers that are oriented parallel to each other and to
the skin surface (Figs 46.1, 46.2). Maturation of collagen
fibers is largely a chemical process of remodeling that
involves covalent crosslinking of adjacent polypeptide
chains. Collagen fibers normally form and are degraded con
tinuously in normal skin as well as in scars, but the processes
that control the rates of formation and degradation and the
orientation of the mature fibers are not fully understood.
Cytokines and growth factors
Many short polypeptides, mostly cytokines and growth
factors, are responsible for the changes in cells that lead to
wound healing and the termination of wound healing pro
cesses, and the formation and organization of a scar. Among
the most important are the transforming growth factor
beta family (TGFβ), basic fibroblast growth factor (bFGF
or FGF2), platelet-derived growth factor (PDGF), and
vascular endothelial growth factor (VEGF).53–60 Frequently,
the response of a particular cell type to a particular peptide
depends not only upon binding of cell surface receptors by
the right peptide, but also upon simultaneous signals from
other cellular receptors. Thus the network of peptide signal
ing is complex, and the range of possible cellular responses
is large enough to allow generation of complex structures
and considerable fine-tuning.56,61 There are also many oppor
tunities for reparative processes to go wrong, to proceed in
an unbalanced fashion, or to fail to complete an appropriate
cycle of activation and regression. This complex area has
been well reviewed.62–64
Biophysics of thermal injury
Cells of the human skin are susceptible to killing when their
temperature is increased, largely because of the sensitivity
of the cell surface membrane to disruption outside fairly
addition, the newly formed capillaries of granulation tissue
allow passage of plasma proteins and fluid until they mature.
Certain plasma proteins, notably fibronectin and vitronec
tin, are important in stimulating reparative responses in the
wound.
Granulation tissue and the proliferative phase
of wound healing
Massive proliferation of fibroblasts and vascular endothelial
cells is characteristic of the early phase of wound healing.
These cells, and the fine fibrils of collagen and the gel pro
vided by multiple mucopolysaccharides and proteoglycans,
make up the granulation tissue that is a major feature of all
wounds that remain open. The most important of many
peptides that stimulate fibroblast growth appear to be TGFβ
and basic FGF, while the most important peptide that stimu
lates growth of endothelial cells appears to be VEGF.34–39 In
order for wound contraction to occur, it is important for
fibroblasts to form networks within the dermis that allow
the wound to contract. As Donald Ingber has pointed out,
interactions between the extracellular matrix and the cellular
cytoskeleton are important in controlling cellular differen
tiation and function.40–42 Apparently, when wound healing
is abnormal and hypertrophic scars develop, this process of
interlinking of fibroblasts to form a meshwork that supports
tension parallel to the surface is disrupted, since nodules of
collagen result that do not flatten out normally.
Influx of circulating cells
Many circulating cells actively migrate into wound beds and
play roles in defense against bacteria and fungi, clearance of
devitalized tissue components, and stimulation of later
phases of healing of the dermis and epidermis. Based on
experiments with partially selective ablation of individual
cell types, the cells most important in stimulating and
maintaining tissue repair appear to be the T lymphocytes
and monocytes.43 Monocytes, which differentiate into tissue
macrophages, are responsible for synthesis and release of
many of the cytokines important in wound healing, as are
connective tissue cells and epithelial cells. In addition, recent
research has clearly shown that circulating stem cells enter
healing wounds, where they can differentiate to form fibro
blasts and other connective tissue cells needed to restore
tissue integrity.44,45
Migration of keratinocytes to cover
the wound (epiboly)
When the epidermis is transected, changes take place rapidly
in the basal cells of the epidermis adjacent to the wound.
The process of epidermal regeneration has been well studied
by Stenn and his colleagues.16,46,47 Altered basal keratinocytes
send out thin sheets and undergo ameboid motion over the
wound bed, but under the nonviable eschar and/or scab,
secreting a provisional matrix as they go.48,49 Development
of this migratory phenotype is stimulated by the plasma
protein vitronectin, and requires the presence of albumin as
a cofactor.16,47,50 Cell division occurs to support this migra
tion, not among migratory cells, but among their precursors
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510
narrow limits of temperature. Of course flame burns, as well
as electrical and contact burns, often lead to pyrolysis and
disruption and oxidation of some tissues as well. Among
the various cell types present in the skin, some are likely to
be more sensitive to killing by elevated temperature than
others. The degree of temperature elevation at a given site
in the skin also depends on the rate of heat transfer within
the tissue. The thermal conductivity of the dermis is much
greater than that of the subcutis, since fat is a good insula
tor. Perhaps for this reason, thermal injury often leads to
necrosis of the entire dermis with little cell death in the
subcutis, as seen in wound biopsies. Hair follicles in some
sites typically extend well beyond the dermis into the
adipose tissue of the upper subcutis, and eccrine sweat
glands are also often present in the subcutaneous fat.
Despite the presence of adipose tissue around follicles, in
Figure 46.2 (a) In a normal flat scar, the epidermis is flat and does not
have any rete ridges, and the dermis is replaced by collagen fibers that are
oriented parallel to the skin surface. (b) A Movat pentachrome stain of a
normal scar shows mature collagen fibers stained yellow-orange, and does
not demonstrate any elastin fibers.
aA
bB
Figure 46.1 Photomicrographs of normal skin, stained with hematoxylin
and eosin. (a) The hair follicles often extend through the dermis into the
subcutaneous adipose tissue. The epidermis forms irregular rete ridges at
its base. (b) The reticular dermis of normal skin has an orderly arrangement
of collagen fibers with no preferred orientation. (c) With the Movat
pentachrome stain, normal collagen fibers stain yellow-orange, and delicate
interconnecting black elastin fibers are present between collagen fibers.
aA
bB
cC
Pathophysiology of the burn scar
511
excision which removes the entire subcutis. The wound is
initially covered with meshed cadaver skin from the skin
bank. Within a few days autografting is done using meshed
partial-thickness grafts from unburned regions. Over the face
and the hands, unmeshed sheet autografts are often used to
obtain the best cosmetic result. The epidermis of the cadav
eric homograft slowly degenerates, but the dermal matrix
often is incorporated into the healing wound. The interstices
of the autograft fill with granulation tissue derived partly
from the underlying fibrous or adipose tissue, and partly by
migration of fibroblasts from the strands of autograft. The
epidermis of the autograft migrates over the granulation
tissue matrix, under the fibrin layer, and reconstitutes the
epidermis, though without any follicles or other epidermal
appendages. The pattern of the meshed grafts is usually
visible in the healed wound. The incorporation of dermal
connective tissue elements from the donor site may enhance
the pliability of the final scar. Occasionally, epidermal inclu
sion cysts develop within grafted burn wounds, and they
may rupture. These cysts could develop from residual hair
roots that had lost their connection to the surface, from
aberrant migration of epidermal cells during wound resur
facing, or from trapping of epidermis by expanding connec
tive tissue. In addition, tiny bits of hair shaft are sometimes
encountered in healing wounds, associated with a giant cell
foreign body reaction, perhaps representing hairs left behind
after necrosis of the hair follicles that originally produced
them.
Wound infection
Bacterial infection frequently complicates wound healing.
The risk is increased in burn patients, since large amounts
of necrotic cells and tissue are present in the wound, provid
ing a good culture medium for bacteria. When infection
occurs, the inflammatory component of wound healing is
greatly amplified, and the processes of conversion of granu
lation tissue to a dense scaffolding of collagen, wound con
traction, and regeneration of the epidermis are all delayed.
Frequently, the wound suppurates. Some bacteria cause
additional tissue necrosis, and some bacteria can invade into
normal tissues, leading to hyperemia around the original
wound and/or enlargement and deepening of the original
wound. In response to the bacterial infection and the
enhanced inflammatory reaction, the cytokine milieu of the
wound is altered.69–71 Grafts placed over wounds with resid
ual infected tissue typically do not take, and when large
numbers of bacteria are present deep in the wound bed there
is always the hazard that the bacteria may enter the blood
stream, incite septicemia and invade remote tissues. These
processes, which were common in the era before antibiotics
and before the practice of early wound excision became
common, are now being seen again due to infection with
highly antibiotic-resistant strains of bacteria, particularly
Pseudomonas and Acinetobacter.
Hypertrophic wound healing
In most patients with large burns treated in our institution,
healing of the burn wounds is complicated by development
of elevated, thick, firm, reddish scars that itch constantly.
many cases their capacity to regenerate is entirely destroyed
by burns even though there is little or no apparent necrosis
in the upper subcutis. In the most severe burns, however,
the entire subcutis may become necrotic, and cell death may
occur in the underlying fascia and skeletal muscle or even
in underlying internal organs.
Factors that alter wound healing
Changes in blood supply and perfusion
Development of methods to study local blood supply by
ultrasonic measurement has led to the discovery that there
is usually a zone of greatly increased blood flow below a
burn wound, which is not surprising as part of a local
inflammatory response to tissue injury. Above this zone of
hyperemia is a zone of tissue ischemia, in which blood flow
is less than normal. Remarkably, during the first 24 h after
a burn wound, the zone of ischemia typically becomes sig
nificantly deeper, indicating that ischemic injury of dermal
tissues actually leads to a depth of tissue necrosis greater
than that produced by the immediate thermal injury.65
Experiments in animals have shown that neutrophils are
involved in this progressive ischemic cell death in injured
but viable tissue deep to a burn wound.66 Altered blood
flow may lead to vascular thrombosis in a burn wound, also
contributing to the risk of ischemic tissue injury. In normal
skin, there is a plexus of arteries and veins immediately
below the dermis in the upper layer of subcutaneous adipose
tissue. This subdermal plexus is at risk of thrombosis in
deep partial-thickness burns and in full-thickness burns,
and it is vulnerable to damage in the process of tangential
wound excision, with further loss of blood supply to the
wound.
Compromised wound healing – requirements
for optimal wound healing
Long clinical experience has demonstrated clearly that
wound healing is greatly slowed and impaired when there is
deficiency of essential ingredients for construction of the
scar, or of an adequate energy supply. Vitamin C deficiency
and protein-calorie malnutrition are characterized by defi
cient wound healing, and provision of sufficient calories and
reversal of the usual protein catabolism are major goals of
general burn care. Diabetic vasculopathy is associated with
deficient wound healing, demonstrating the importance of
an adequate microcirculation. Heart failure similarly com
promises wound healing. Radiation, cigarette smoking, and
hypoxemia also have been associated with delayed wound
healing.67 Advanced age is associated with increased mortal
ity from large burns, but does not in itself prevent good
wound healing.19,68
Biologic responses to wound excision
and grafting
The current standard of treatment in our institution is early
excision of the burn wound, normally within 24 h of admis
sion, with removal of all necrotic tissue, using either tangen
tial excision to leave most of the subcutaneous fat, or fascial
Total Burn Care
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512
These occur more commonly in wounds that had become
infected or took longer than usual to become fully covered.
They may cover large areas, but do not usually extend
beyond the original burn wound. These abnormal wounds
also are associated with more severe wound contraction. In
the great majority of affected cases, these hypertrophic scars
enlarge for a period of months, and then gradually regress
over a period of a few years, eventually becoming flat scars
with no further symptoms. There are often abnormalities of
skin pigmentation, either depigmentation or hyperpigmen
tation, in wounds that have developed hypertrophic scars,
and these abnormalities evolve over time (Fig. 46.3). The
largest hypertrophic scars are surgically excised, often with
creation of Z-plasties or sheet grafting to release scar con
tractures. Generally, new hypertrophic scars do not follow.
Many of the patients at our institution are Mexican nation
als with predominantly Native American ethnicity. However,
this type of hypertrophic scarring occurs in about 75% of
Caucasian patients as well as in black and Hispanic
patients.72
Clearly, this experience is quite different from that
described in the literature with keloids, which frequently
occur spontaneously or in response to puncture wounds or
clean incisions that were closed primarily.73–75 They extend
beyond the initial site of injury, respond poorly to medical
therapy, persist for many years, and usually recur after surgi
cal excision. There is often a positive family history of keloi
dal scarring, and keloids are 10–15 times more common in
dark-skinned people of African ancestry than in northern
Europeans and their descendants. Elaborate patterns of
raised scars are a symbol of status in many African tribes,
leading one to wonder whether this practice may have
exerted selective pressure during human evolution.
Histologic features of hypertrophic scars
Numerous hypertrophic scars have been examined histologi
cally in our laboratory, those removed both during plastic
surgical procedures to treat release wound contractures and
in samples taken for research purposes. The abnormal ele
vated scars consistently show several distinct differences
from uncomplicated flat scars. The most striking is the pres
ence of rounded whorls of immature collagen that consist
of delicate collagen fibrils, mostly of type III collagen, small
blood vessels, and plentiful acid mucopolysaccharide. These
nodules are very sharply demarcated from the surrounding
scar tissue, which may be composed of similar material or
may be composed of mature thick collagen fibers that are
oriented parallel to each other and to the wound surface,
typical of mature scars. Although they are clearly visible with
routine H&E staining, they are most distinctly seen with the
Movat stain, which stains mucopolysaccharides blue-green
and mature collagen fibers yellow-orange. The nodules of
hypertrophic scars vary from 0.5 mm to more than 1 cm in
diameter, and appear to be sometimes spherical and some
times ovoid or cylindrical in shape. The abnormal dermal
tissue is very firm, and may reach a thickness of several cen
timeters. Both normal and hypertrophic scars are character
ized by lack of elastin, which is also visible using the Movat
stain. However, there are often residual elastin fibers in
the deepest part of the dermis below zones of hypertrophic
Figure 46.3 Typical appearances of hypertrophic scars of burn patients.
(a) The hypertrophic scar is raised above the surrounding normal skin, has
sharp borders, and is very firm to the touch. This scar recurred after
complete excision. (b) Hypertrophic scars often have patterns corresponding
to meshed grafts, and often are hyperpigmented, as shown here, or
hypopigmented. (c) This round firm lesion developed from a minor burn on
the patient’s ear. It did not recur after excision.
aA
bB
cC
Pathophysiology of the burn scar
513
hypertrophic scars. These features are illustrated in Figure
46.6. These are the features that have been described as
typical of the histology of keloids. However, in our patient
population, typical keloids are distinctly unusual, and there
is no evidence to suggest that the patients with these thick,
eosinophilic collagen fibers have a worse prognosis or a
more delayed course of scar maturation than other patients
with hypertrophic scars. Thus in our extensive experience
with the histology of scars from large burns in children, the
histologic features typical of keloids are seen as part of the
spectrum of hypertrophic scarring.
The distinction between hypertrophic scars and keloids
was first made by Mancini and Quaife in 1962.76–79 The fea
tures typical of hypertrophic scars were further described
by Linares, Kischer and others.80–83 The literature on
scarring, and sometimes there is a narrow zone of normal
elastin fibers above the hypertrophic scar, perhaps derived
from the applied skin grafts. Occasionally, small rounded
nodules of hypertrophic scar tissue are seen scattered between
intact hair follicles. It is not unusual to see residual eccrine
sweat glands in the adipose tissue beneath a large hyper
trophic scar, suggesting that these scars may originate in deep
partial-thickness burns. These features are illustrated in
Figures 46.4 and 46.5. In addition, in a minority of hyper
trophic scars, an additional histologic feature is seen, con
sisting of very broad, hypereosinophilic collagen fibers
oriented parallel to each other, but at varying angles with
the skin surface. In some cases such broad, dense fibers
dominate the wound. Generally, they are surrounded by
whorls of circularly oriented, immature collagen typical of
Figure 46.4 Photomicrographs of hypertrophic scars. (a) Within the dermis
there is a rounded nodule of collagen that has a sharp border and is distinct
from the surrounding scar tissue. (b) The border of a collagenous nodule
in a hypertrophic scar. In the surrounding scar tissue, collagen fibers are
oriented parallel to the skin surface. Within the nodule, collagen fibers are
very thin and are oriented circumferentially.
aA
bB
Figure 46.5 (a) This Movat-stained slide shows a minimal hypertrophic scar
consisting of a single round nodule between hair follicles. The nodule stains
light green, in contrast to the yellow-orange color of the surrounding
mature collagen fibers. The greenish color reflects a larger quantity of
sulfated proteoglycans within the collagen nodule. (b) At higher
magnification, numerous small blood vessels can be seen within a large,
green-staining nodule from a hypertrophic scar.
aA
B
Total Burn Care
46
514
indeed a clinical history of atopy and higher levels of circu
lating IgE have been found in patients with hypertrophic
scars. Recently, much larger numbers of epidermal Langer
hans cells have been identified in association with hyper
trophic scars.85,86
Immunohistochemical staining has demonstrated addi
tional striking differences between hypertrophic scars and
normal scars. Staining for alpha-smooth-muscle actin has
consistently demonstrated this contractile protein within
spindle cells in the characteristic collagen nodules of hyper
trophic scars. The sulfated proteoglycans of hypertrophic
scars are quite different from those of normal scars, in that
much less decorin is present, and versican is predominant
in the rounded nodules. More immunostaining for VEGF is
seen in hypertrophic scars. Larger numbers of small nerve
fibers have been identified by immunostaining in hyper
trophic scars. These consistent findings may be providing
important clues as to the pathogenesis of hypertrophic scar
ring, but at this time they are difficult to incorporate into a
single hypothesis. The study of the biology of hypertrophic
scars has been complicated by the lack of a suitable animal
model, and by the scarcity of relevant material from human
scars, as well as by confusion as to the proper identification
of cases of hypertrophic scarring. However, study of cell
culture models has yielded important information on
biologic processes that may be important in human
hypertrophic scars, and potential animal models are being
developed.
Experimental models of hypertrophic healing
The first animal model of keloids was described in 1959,
based on immunization of experimental animals with auto
logous skin, followed by induction of wounds.87 Extensive
work has been done in which normal and abnormal human
scar tissue has been implanted into the athymic nude mouse,
which allows testing of potential therapies and modification
of the biological milieu in vivo.88–91 In this model, it is even
possible to irradiate the mouse and transplant human bone
marrow to study interactions between immune reactions
involving human cells and the human skin grafts. Engrav
and his colleagues in Seattle developed a model in the
female red Duroc pig that apparently mimics many of the
features of human hypertrophic scarring.92–100 It will be of
great interest to test interventions that might modify the
development of hypertrophic scars in that model.
Phenotypic abnormalities of hypertrophic
scar fibroblasts
There have been many studies of the functions and
molecular biology of fibroblasts derived from hypertrophic
scars and keloids in tissue culture. It does appear from
these studies that there is a significantly different phenotype
of fibroblasts from hypertrophic scars that persists in
culture. Hypertrophic scar fibroblasts have been found con
sistently to secrete collagen more rapidly than fibroblasts
derived from normal skin or normal scars. More secretion
of TGFβ has also been described.101 Several groups have
described abnormal control of proliferation, collagen secre
tion or peptide secretion in fibroblasts derived from keloids
hypertrophic scars and keloids was thoroughly reviewed in
1999 by Niessen.84
Multiple concepts have been proposed to explain the
origin and development of hypertrophic scars and keloids.
For purposes of this discussion, it may be best to assume that
the etiology and pathogenesis of hypertrophic scars is differ
ent from that of keloids, and to limit our discussion to
hypertrophic scars.
A number of differences have been described between
normal scars and hypertrophic scars. Hypertrophic scars
contain more type III collagen, more fibronectin, and more
hyaluronic acid, all characteristic of the early phases of
wound repair, than normal flat scars. They appear more
vascular, and studies of cutaneous blood flow by Doppler
sonography have shown consistently higher flows in hyper
trophic scars. Hypertrophic scars contain significantly more
T cells and macrophages than normal scars. Larger numbers
of mast cells have been found in hypertrophic scars, and
Figure 46.6 (a) Some otherwise typical dermal nodules in hypertrophic
scars contain very broad, hypereosinophilic collagen fibers similar to those
typical of keloids. This specimen is from the patient shown in Figure 46.3c.
(b) The typical appearance of the thick, dense collagen fibers that stain
intensely with eosin can be seen at higher magnification.
A
B
Pathophysiology of the burn scar
515
Pathogenic concepts
Development of understanding of the biology of hyper
trophic scarring has been hampered by multiple factors,
including problems in gaining consensus on the definition
of the lesion, the lack of a suitable animal model, and the
consequent inability to test hypotheses by altering the
course of the disease. Multiple concepts of pathogenesis
have been proposed. None has yet gained wide acceptance,
and none has been experimentally excluded. It does seem
clear that development of a hypertrophic scar represents an
abnormality in control of the normal processes of wound
healing, which may occur early, as Linares and Larson
suggested.72 Failure of the normal processes limiting colla
gen secretion and matrix formation is apparent in hyper
trophic scars. One might suppose that the normal processes
by which tensions in the matrix signal cellular responses
have become defective in hypertrophic scars.40,42 Myofibro
blasts are more prominent in hypertrophic scars than in
normal or mature scars, and are thought to play a role in
excessive wound contraction. These myofibroblasts may
derive from resting dermal fibroblasts, or they might
arise from pre-existing pericytes, as suggested by Kischer.115
They also might represent bone marrow derived fibrocytes
in increased numbers.45 The fibrous nodules of hypertrophic
scars might represent persistence and uncontrolled growth
of a separate population of connective tissue cells, perhaps
related to the perifollicular cells that normally express
versican. Since burn patients have higher circulating levels
of glucocorticoids and interleukin-6 than normal individu
als, a selection process might operate that would tend to
allow proliferation of cells resistant to the usual effects of
these agents to suppress fibroblast proliferation. A recent
suggestion was made that less vitamin D-3 is made in
patients with strongly pigmented skin.116 Finally, abnormal
macromolecular expression by the covering epithelium may
lead to abnormal development of the dermal scar, or fail
to suppress inappropriate fibroblast functions.117 Clearly, it
continues to be important to develop and test many hypo
theses until the problem of hypertrophic scarring is finally
solved.
Summary
Healing of burn wounds requires activation of several host
processes, including fibrin clotting and lysis, deposition of
an immature connective tissue matrix and its reorganization
into a mature scar, and epithelial outgrowth and interaction
between the epidermis and the dermal matrix. In many burn
patients, excessive scar tissue forms, with adverse conse
quences. Continued study of this problem will continue to
be important until more effective modes of treatment are
developed.
Further reading
Clark RA. Basics of cutaneous wound repair. J Dermatol Surg Oncol.
1993;19:693-706.
Ingber DE. Mechanical control of tissue growth: function follows
form. Proc Natl Acad Sci USA. 2005;102:11571-11572.
in response to cytokine stimulation or treatment with
glucocorticoids. However, in most of these studies the
regulatory responses of hypertrophic scar fibroblasts were
similar to those of fibroblasts from normal skin. Genomic
analysis has been done in several laboratories on hyper
trophic scar fibroblasts, with identification of numerous
differences in gene expression. In a genomic study from
our institution, cultured fibroblasts from hypertrophic scars
showed a reduced response to IL-6 as compared to fibro
blasts from adjacent normal skin, suggesting that decreased
receptor activation might be a factor in hypertrophic
scarring.102
Gene expression in hypertrophic scars
Studies of gene expression and its regulatory pathways in
hypertrophic scar tissue have begun to illuminate the biology
of normal wound healing. This is an active area of research
that promises to provide much better understanding and
potential control of both normal and hypertrophic wound
healing. Initial studies of hypertrophic scars using microar
ray analysis of gene expression have shown consistent differ
ences in expression of genes for multiple collagen isoforms,
growth factors and metalloproteinases.103 Similar analyses
have been reported recently for the porcine model of hyper
trophic scarring.104 In several experimental studies in animals,
interventions have been applied that alter wound expression
of important genes or signaling pathways, with substantial
change in size of the resulting wound.105–110 Although much
more research is needed, such studies promise to allow ther
apeutic intervention in the processes that lead to hyper
trophic scarring.
Interplay of systemic and local inflammatory
responses
Recent studies have revealed that both local cytokine expres
sion and signaling and also systemic inflammatory processes
impact the development of hypertrophic scarring. In burned
children who do not develop hypertrophic scars, active and
total TGFβ1 levels in plasma increased during the first 2
weeks following the burn injury before dropping to levels
below those found in non-burned patients. In burned chil
dren who later developed hypertrophic scars, however, active
and total TGFβ1 levels in plasma were diminished from the
day of burn until at least 180 days later.111 Augmented levels
of systemic TGFβ1 have been correlated with increased cir
culating fibrocytes.112 Although elevated systemic levels of
TGFβ1 may be beneficial following a burn injury, prolonged
expression locally within the burn wound may lead to hyper
trophic scarring with increased fibrosis, downregulation of
decorin, upregulation of versican, increased neovasculariza
tion and decreased collagenase113 The type of inflammatory
response also appears to play a role in hypertrophic scarring,
not only the magnitude and location of inflammation. Char
acterization of CD4+ T-helper cells revealed that following a
burn, polarization of lymphocyte populations leads to a
shift from a Th1/anti-fibrotic phenotype to a Th2/pro-fibrotic
response.114 Decreased systemic expression of IFN-γ and IL-4
and increased IL-4 producing lymphocytes apparently persist
for a year following a burn injury.
Total Burn Care
46
516
Tredget EE. Pathophysiology and treatment of fibroproliferative
disorders following thermal injury. Ann NY Acad Sci.
1999;888:165-182.
Zhu KQ, Engrav LH, Armendariz R, et al. Changes in VEGF and nitric
oxide after deep dermal injury in the female, red Duroc pig –
further similarities between female, Duroc scar and human
hypertrophic scar. Burns. 2005;31:5-10.
Niessen FB, Andriessen MP, Schalkwijk J, et al. Keratinocyte-derived
growth factors play a role in the formation of hypertrophic scar.
J Pathol. 2001;194:207-216.
Tran KT, Griffith L, Wells A. Extracellular matrix signaling through
growth factor receptors during wound healing. Wound Repair Regen.
2004;12:262-268.
Access the complete reference list online at
Pathophysiology of the burn scar
516.e1
© Copyright 2012 Elsevier, Inc. All rights reserved.
References
1. Majno G. The healing hand – man and wound in the ancient world.
Cambridge: Harvard University Press; 1975.
2. Clark RA. Basics of cutaneous wound repair. J Dermatol Surg
Oncol. 1993;19(8):693-706.
3. Ross R. Wound healing. Sci Am. 1969;220(6):40-50.
4. Ross R, Odland G. Human wound repair. II. Inflammatory cells,
epithelial-mesenchymal interrelations, and fibrogenesis. J Cell
Biol. 1968;39(1):152-168.
5. Sower LE, Froelich CJ, Carney DH, et al. Thrombin induces IL-6
production in fibroblasts and epithelial cells. Evidence for the
involvement of the seven-transmembrane domain (STD)
receptor for alpha-thrombin. J Immunol. 1995;155(2):895-901.
6. Ross R, Bowen-Pope DF, Raines EW. Platelet-derived growth
factor: its potential roles in wound healing, atherosclerosis,
neoplasia, and growth and development. Ciba Found Symp.
1985;116:98-112.
7. Naldini A, Pucci A, Carney DH, et al. Thrombin enhancement of
interleukin-1 expression in mononuclear cells: involvement of
proteinase-activated receptor-1. Cytokine. 2002;20(5):191-199.
8. Naldini A, Carney DH, Bocci V, et al. Thrombin enhances T cell
proliferative responses and cytokine production. Cell Immunol.
1993;147(2):367-377.
9. Carney DH, Mann R, Redin WR, et al. Enhancement of
incisional wound healing and neovascularization in normal rats
by thrombin and synthetic thrombin receptor-activating
peptides. J Clin Invest. 1992;89(5):1469-1477.
10. Clark RA. Biology of dermal wound repair. Dermatol Clin.
1993;11(4):647-666.
11. Clark RA. Fibrin and wound healing. Ann N Y Acad Sci.
2001;936:355-367.
12. Grinnell F. Fibronectin and wound healing. Am J Dermatopathol.
1982;4:185-188.
13. Greiling D, Clark RA. Fibronectin provides a conduit for
fibroblast transmigration from collagenous stroma into fibrin
clot provisional matrix. J Cell Sci. 1997;110 ( Pt 7):861-870.
14. Swerlick RA, Brown EJ, Xu J, et al. Expression and modulation
of the vitronectin receptor on human dermal microvascular
endothelial cells. J Invest Dermatol. 1992;99(6):715-722.
15. Gabbiani G, Ryan GD, Majno G. Presence of modified
fibroblasts in granulation tissue and their possible role in
wound contraction. Experientia. 1971;27:549-553.
16. Stenn KS, Depalma L. Re-epithelialization. In: Clark RA, ed. The
molecular and cellular biology of wound repair. 2nd ed. New York:
Plenum Press; 1996:321-335.
17. Clark RA. Fibronectin matrix deposition and fibronectin receptor
expression in healing and normal skin. J Invest Dermatol.
1990;94(6 Suppl):128S-134S.
18. Staiano-Coico L, Carano K, Allan VM, et al. PAI-1 gene
expression is growth state-regulated in cultured human
epidermal keratinocytes during progression to confluence and
postwounding. Exp Cell Res. 1996;227(1):123-134.
19. Gamelli RL, He LK. Incisional wound healing. Model and
analysis of wound breaking strength. Methods Mol Med.
2003;78:37-54.
20. Daly TJ. The repair phase of wound healing – re-epithelialization
and contraction. In: Kloth LC, McCullough J, Feedar JA, eds.
Wound healing. Philadelphia: FA Davis; 1990:14-30.
21. Barret JP, Dziewulski P, Wolf SE, et al. Outcome of scalp donor
sites in 450 consecutive pediatric burn patients. Plast Reconstr
Surg. 1999;103(4):1139-1142.
22. Chang LY, Yang JY, Chuang SS, et al. Use of the scalp as a donor
site for large burn wound coverage: review of 150 patients. World
J Surg. 1998;22(3):296-299.
23. McCauley RL, Oliphant JR, Robson MC. Tissue expansion in the
correction of burn alopecia: classification and methods of
correction. Ann Plast Surg. 1990;25(2):103-115.
24. Levy V, Lindon C, Zheng Y, et al. Epidermal stem cells arise from
the hair follicle after wounding. FASEB J. 2007;21(7):1358-1366.
25. Oshima H, Rochat A, Kedzia C, et al. Morphogenesis and
renewal of hair follicles from adult multipotent stem cells. Cell.
2001;104(2):233-245.
26. Morris RJ, Liu Y, Marles L, et al. Capturing and profiling adult
hair follicle stem cells. Nat Biotechnol. 2004;22(4):411-417.
27. Jensen UB, Yan X, Triel C, et al. A distinct population of
clonogenic and multipotent murine follicular keratinocytes
residing in the upper isthmus. J Cell Sci. 2008;121(Pt 5):609-617.
28. Blanpain C. Stem cells: Skin regeneration and repair. Nature.
2010;464(7289):686-687.
29. Jaks V, Kasper M, Toftgard R. The hair follicle-a stem cell zoo.
Exp Cell Res. 2010;316(8):1422-1428.
30. Yang CC, Cotsarelis G. Review of hair follicle dermal cells.
J Dermatol Sci. 2010;57(1):2-11.
31. Inamatsu M, Matsuzaki T, Iwanari H, et al. Establishment of rat
dermal papilla cell lines that sustain the potency to induce hair
follicles from afollicular skin. J Invest Dermatol. 1998;111(5):
767-775.
32. Mayer JA, Foley J, De La CD, et al. Conversion of the nipple to
hair-bearing epithelia by lowering bone morphogenetic protein
pathway activity at the dermal-epidermal interface. Am J Pathol.
2008;173(5):1339-1348.
33. Stenn K, Parimoo S, Zheng Y, et al. Bioengineering the hair
follicle. Organogenesis. 2007;3(1):6-13.
34. Spindler KP, Murray MM, Detwiler KB, et al. The biomechanical
response to doses of TGF-beta 2 in the healing rabbit medial
collateral ligament. J Orthop Res. 2003;21(2):245-249.
35. Broadley KN, Aquino AM, Hicks B, et al. Growth factors bFGF
and TGF beta accelerate the rate of wound repair in normal and
in diabetic rats. Int J Tissue React. 1988;10(6):345-353.
36. Bennett NT, Schultz GS. Growth factors and wound healing:
Part II. Role in normal and chronic wound healing. Am J Surg.
1993;166:74-81.
37. Broadley KN, Aquino AM, Woodward SC, et al. Monospecific
antibodies implicate basic fibroblast growth factor in normal
wound repair. Lab Invest. 1989;61(5):571-575.
38. Davidson JM, Broadley KN. Manipulation of the wound-healing
process with basic fibroblast growth factor. Ann N Y Acad Sci.
1991;638:306-315.
39. Falanga V. Growth factors and wound healing. J Dermatol Surg
Oncol. 1993;19(8):711-714.
40. Ingber DE. Cellular tensegrity: defining new rules of biological
design that govern the cytoskeleton. J Cell Sci. 1993;104:
613-627.
41. Ingber DE. Mechanical control of tissue growth: function follows
form. Proc Natl Acad Sci U S A. 2005;102(33):11571-11572.
42. Huang S, Ingber DE. The structural and mechanical complexity
of cell-growth control. Nat Cell Biol. 1999;1(5):E131-E138.
43. Barbul A, Breslin RJ, Woodyard JP, et al. The effect of in vivo
T helper and T suppressor lymphocyte depletion on wound
healing. Ann Surg. 1989;209(4):479-483.
44. Quan TE, Cowper S, Wu SP, et al. Circulating fibrocytes:
collagen-secreting cells of the peripheral blood. Int J Biochem Cell
Biol. 2004;36(4):598-606.
45. Mori L, Bellini A, Stacey MA, et al. Fibrocytes contribute to the
myofibroblast population in wounded skin and originate from
the bone marrow. Exp Cell Res. 2005;304(1):81-90.
46. Stenn KS. The role of serum in the epithelial outgrowth of
mouse skin explants. Br J Dermatol. 1978;98(4):411-416.
47. Stenn KS. Epibolin: a protein of human plasma that supports
epithelial cell movement. Proc Natl Acad Sci U S A. 1981;78(11):
6907-6911.
48. Kubo M, Van de WL, Plantefaber LC, et al. Fibrinogen and fibrin
are anti-adhesive for keratinocytes: a mechanism for fibrin
eschar slough during wound repair. J Invest Dermatol.
2001;117(6):1369-1381.
Total Burn Care
46
516.e2
© Copyright 2012 Elsevier, Inc. All rights reserved.
49. Stenn KS, Madri JA, Roll FJ. Migrating epidermis produces AB2
collagen and requires continued collagen synthesis for
movement. Nature. 1979;277:229-232.
50. Stenn KS. Coepibolin, the activity of human serum that
enhances the cell spreading properties of epibolin, associates
with albumin. J Invest Dermatol. 1987;89(1):59-63.
51. Qwarnstrom EE, Jarvelainen HT, Kinsella MG, et al. Interleukin-
1β regulation of fibroblast proteoglycan synthesis involves a
decrease in versican steady state mRNA levels. Biochem J.
1993;294:613-620.
52. Niessen FB, Andriessen MP, Schalkwijk J, et al. Keratinocyte-
derived growth factors play a role in the formation of
hypertrophic scars. J Pathol. 2001;194(2):207-216.
53. Karr BP, Bubak PJ, Sprugel KH, et al. Platelet-derived growth
factor and wound contraction in the rat. J Surg Res.
1995;59(6):739-742.
54. Savage K, Siebert E, Swann D. The effect of platelet-derived
growth factor on cell division and glycosaminoglycan synthesis
by human skin and scar fibroblasts. J Invest Dermatol.
1987;89(1):93-99.
55. Tredget EE. Pathophysiology and treatment of fibroproliferative
disorders following thermal injury. Ann N Y Acad Sci.
1999;888:165-182.
56. Scott PG, Ghahary A, Tredget EE. Molecular and cellular aspects
of fibrosis following thermal injury. Hand Clin. 2000;16(2):
271-287.
57. Tran KT, Griffith L, Wells A. Extracellular matrix signaling
through growth factor receptors during wound healing. Wound
Repair Regen. 2004;12(3):262-268.
58. Younai S, Venters G, Vu S, et al. Role of growth factors in scar
contraction: an in vitro analysis. Ann Plast Surg. 1996;36(5):
495-501.
59. Tonnesen MG, Feng X, Clark RA. Angiogenesis in wound
healing. J Invest Dermatol Symp Proc. 2000;5(1):40-46.
60. Grinnell F. Fibroblasts, myofibroblasts, and wound contraction.
J Cell Biol. 1994;124(4):401-404.
61. Roberts AB. The ever-increasing complexity of TGF-beta
signaling. Cytokine Growth Factor Rev. 2002;13(1):3-5.
62. Barrientos S, Stojadinovic O, Golinko MS, et al. Growth factors
and cytokines in wound healing. Wound Repair Regen.
2008;16(5):585-601.
63. Kondo T, Ishida Y. Molecular pathology of wound healing.
Forensic Sci Int. 2010;203:93-98.
64. Kwan P, Hori K, Ding J, et al. Scar and contracture: biological
principles. Hand Clin. 2009;25(4):511-528.
65. Burns JL, Mancoll JS, Phillips LG. Impairments to wound
healing. Clin Plast Surg. 2003;30(1):47-56.
66. Mileski WJ, Borgstrom D, Lightfoot E, et al. Inhibition of
leukocyte-endothelial adherence following thermal injury. J Surg
Res. 1992;52:334-339.
67. Burns JL, Mancoll JS, Phillips LG. Impairments to wound
healing. Clin Plast Surg. 2003;30(1):47-56.
68. Ono I. The effects of basic fibroblast growth factor (bFGF) on
the breaking strength of acute incisional wounds. J Dermatol Sci.
2002;29(2):104-113.
69. Hunt TK, Hopf H, Hussain Z. Physiology of wound healing. Adv
Skin Wound Care. 2000;13(2 Suppl):6-11.
70. Thornton FJ, Schaffer MR, Barbul A. Wound healing in sepsis
and trauma. Shock. 1997;8(6):391-401.
71. van den BR, Wilmink JM, O’Kane S, et al. Transforming growth
factor-beta levels during second-intention healing are related to
the different course of wound contraction in horses and ponies.
Wound Repair Regen. 2002;10(3):188-194.
72. Linares HA, Larson DL. Early differential diagnosis between
hypertrophic and nonhypertrophic healing. J Invest Dermatol.
1974;62(5):514-516.
73. Burd A, Huang L. Hypertrophic response and keloid diathesis:
two very different forms of scar. Plast Reconstr Surg. 2005;116(7):
150e-157e.
74. Ketchum LD, Cohen IK, Masters FW. Hypertrophic scars and
keloids. A collective review. Plast Reconstr Surg. 1974;53(2):
140-154.
75. Murray JC, Pollack SV, Pinnell SR. Keloids: a review. J Am Acad
Dermatol. 1981;4(4):461-470.
76. Mancini Re, Quaife JV. Histogenesis of experimentally produced
keloids. J Invest Dermatol. 1962;38:143-181.
77. Peacock Jr EE, Madden JW, Trier WC. Biologic basis for the
treatment of keloids and hypertrophic scars. South Med J.
1970;63(7):755-760.
78. Blackburn WR, Cosman B. Histologic basis of keloid and
hypertrophic scar differentiation. Arch Pathol. 1966;82:
65-71.
79. Ehrlich HP, Desmouliere A, Diegelmann RF, et al. Morphological
and immunochemical differences between keloid and
hypertrophic scar. Am J Pathol. 1994;145(1):105-113.
80. Linares HA, Kischer CW, Dobrkovsky M, et al. On the origin of
the hypertrophic scar. J Trauma. 1973;13(1):70-75.
81. Linares HA, Kischer CW, Dobrkovsky M, et al. The histiotypic
organization of the hypertrophic scar in humans. J Invest
Dermatol. 1972;59(4):323-331.
82. Kischer CW. Collagen and dermal patterns in the hypertrophic
scar. Anat Rec. 1974;179(1):137-145.
83. Kischer CW, Shetlar MR, Chvapil M. Hypertrophic scars and
keloids: a review and new concept concerning their origin. Scan
Electron Microsc. 1982; (Pt 4):1699-1713.
84. Niessen FB, Spauwen PH, Schalkwijk J, et al. On the nature of
hypertrophic scars and keloids: a review. Plast Reconstr Surg.
1999;104(5):1435-1458.
85. Niessen FB, Schalkwijk J, Vos H, et al. Hypertrophic scar
formation is associated with an increased number of epidermal
Langerhans cells. J Pathol. 2004;202(1):121-129.
86. Cracco C, Stella M, Teich AS, et al. Comparative study of
Langerhans cells in normal and pathological human scars. II.
Hypertrophic scars. Eur J Histochem. 1992;36(1):53-65.
87. Chytilova M, Kulhankek V, Horn V. Experimental production of
keloids after immunization with autologous skin. Acta Chir Plast.
1959;1:72-79.
88. Shetlar MR, Shetlar CL, Hendricks L, et al. The use of athymic
nude mice for the study of human keloids. Proc Soc Exp Biol
Med. 1985;179(4):549-552.
89. Kischer CW, Sheridan D, Pindur J. Use of nude (athymic) mice
for the study of hypertrophic scars and keloids: vascular
continuity between mouse and implants. Anat Rec.
1989;225(3):189-196.
90. Kischer CW, Pindur J, Shetlar MR, et al. Implants of hypertrophic
scars and keloids into the nude (athymic) mouse: viability and
morphology. J Trauma. 1989;29(5):672-677.
91. Barbul A, Shawe T, Rotter SM, et al. Wound healing in nude
mice: a study on the regulatory role of lymphocytes in
fibroplasia. Surgery. 1989;105(6):764-769.
92. Zhu KQ, Engrav LH, Armendariz R, et al. Changes in VEGF and
nitric oxide after deep dermal injury in the female, red Duroc
pig—further similarities between female, Duroc scar and human
hypertrophic scar. Burns. 2005;31(1):5-10.
93. Zhu KQ, Engrav LH, Tamura RN, et al. Further similarities
between cutaneous scarring in the female, red Duroc pig and
human hypertrophic scarring. Burns. 2004;30(6):518-530.
94. Liang Z, Engrav LH, Muangman P, et al. Nerve quantification in
female red Duroc pig (FRDP) scar compared to human
hypertrophic scar. Burns. 2004;30(1):57-64.
95. Zhu KQ, Engrav LH, Gibran NS, et al. The female, red Duroc pig
as an animal model of hypertrophic scarring and the potential
role of the cones of skin. Burns. 2003;29(7):649-664.
96. de Hemptinne I, Gallant-Behm CL, et al. Dermal fibroblasts
from red Duroc and Yorkshire pigs exhibit intrinsic differences
in the contraction of collagen gels. Wound Repair Regen.
2008;16(1):132-142.
Pathophysiology of the burn scar
516.e3
© Copyright 2012 Elsevier, Inc. All rights reserved.
97. Xie Y, Zhu KQ, Deubner H, et al. The microvasculature in
cutaneous wound healing in the female red Duroc pig is similar
to that in human hypertrophic scars and different from that in
the female Yorkshire pig. J Burn Care Res. 2007;28(3):500-506.
98. Harunari N, Zhu KQ, Armendariz RT, et al. Histology of the
thick scar on the female, red Duroc pig: final similarities to
human hypertrophic scar. Burns. 2006;32(6):669-677.
99. Zhu KQ, Carrougher GJ, Gibran NS, et al. Review of the female
Duroc/Yorkshire pig model of human fibroproliferative scarring.
Wound Repair Regen. 2007;15(Suppl 1):S32-S39.
100. Gallant-Behm CL, Olson ME, Hart DA. Cytokine and growth
factor mRNA expression patterns associated with the
hypercontracted, hyperpigmented healing phenotype of red
Duroc pigs: a model of abnormal human scar development?
J Cutan Med Surg. 2005;9(4):165-177.
101. Xue H, McCauley RL, Zhang W, et al. Altered interleukin-6
expression in fibroblasts from hypertrophic burn scars. J Burn
Care Rehabil. 2000;21(2):142-146.
102. Dasu MR, Hawkins HK, Barrow RE, et al. Gene expression
profiles from hypertrophic scar fibroblasts before and after IL-6
stimulation. J Pathol. 2004;202(4):476-485.
103. Tsou R, Cole JK, Nathens AB, et al. Analysis of hypertrophic and
normal scar gene expression with cDNA microarrays. J Burn Care
Rehabil. 2000;21(6):541-550.
104. Zhu KQ, Carrougher GJ, Couture OP, et al. Expression of
collagen genes in the cones of skin in the Duroc/Yorkshire
porcine model of fibroproliferative scarring. J Burn Care Res.
2008;29(5):815-827.
105. Sisco M, Kryger ZB, O’Shaughnessy KD, et al. Antisense
inhibition of connective tissue growth factor (CTGF/CCN2)
mRNA limits hypertrophic scarring without affecting wound
healing in vivo. Wound Repair Regen. 2008;16(5):661-673.
106. Song B, Zhang W, Guo S, et al. Adenovirus-mediated METH1
gene expression inhibits hypertrophic scarring in a rabbit ear
model. Wound Repair Regen. 2009;17(4):559-568.
107. Tan J, Peng X, Luo G, et al. Investigating the role of P311 in the
hypertrophic scar. PLoS ONE. 2010;5(4):e9995.
108. Reid RR, Roy N, Mogford JE, et al. Reduction of hypertrophic
scar via retroviral delivery of a dominant negative TGF-beta
receptor II. J Plast Reconstr Aesthet Surg. 2007;60(1):64-72.
109. Dabiri G, Tumbarello DA, Turner CE, et al. TGF-beta1 slows the
growth of pathogenic myofibroblasts through a mechanism
requiring the focal adhesion protein, Hic-5. J Invest Dermatol.
2008;128(2):280-291.
110. Hakkinen L, Koivisto L, Gardner H, et al. Increased expression
of beta6-integrin in skin leads to spontaneous development
of chronic wounds. Am J Pathol. 2004;164(1):229-242.
111. Rorison P, Thomlinson A, Hassan Z, et al. Longitudinal changes
in plasma transforming growth factor beta-1 and post-burn
scarring in children. Burns. 2010;36(1):89-96.
112. Yang L, Scott PG, Giuffre J, et al. Peripheral blood fibrocytes
from burn patients: identification and quantification of
fibrocytes in adherent cells cultured from peripheral blood
mononuclear cells. Lab Invest. 2002;82(9):1183-1192.
113. Ladak A, Tredget EE. Pathophysiology and management of the
burn scar. Clin Plast Surg. 2009;36(4):661-674.
114. Tredget EE, Yang L, Delehanty M, et al. Polarized Th2 cytokine
production in patients with hypertrophic scar following thermal
injury. J Interferon Cytokine Res. 2006;26(3):179-189.
115. Kischer CW, Thies AC, Chvapil M. Perivascular myofibroblasts
and microvascular occlusion in hypertrophic scars and keloids.
Hum Pathol. 1982;13(9):819-824.
116. Cooke GL, Chien A, Brodsky A, et al. Incidence of hypertrophic
scars among African Americans linked to vitamin D-3
metabolism? J Natl Med Assoc. 2005;97(7):1004-1009.
117. Andriessen MP, Niessen FB, Van de Kerkhof PC, et al.
Hypertrophic scarring is associated with epidermal
abnormalities: an immunohistochemical study. J Pathol.
1998;186(2):192-200.
Introduction
The physical rehabilitation of patients who have sustained a
burn injury is a serious undertaking and requires, among
other disciplines, the involvement of physical therapy, occu
pational therapy and exercise physiology, in order to produce
the most functional and cosmetic outcomes. Recent advances
in medicine have significantly contributed to increased
patient survival rates necessitating faster, more comprehen
sive and prolonged burn rehabilitation. With severe burn
injuries, as perhaps with any other order of trauma, there is
an urgent need for immediate and aggressive initiation of
patient-specific rehabilitation programs. The distribution
and depth of the burn injury clearly predict the patterns of
deformity and joint contractures and mandate the establish
ment of therapeutic goals and the initiation of treatment as
soon as possible. As stated previously, the more extensive the
burn injury, the greater the rehabilitation challenge becomes.
A seriously burned extremity in an otherwise modestly
burned patient is much easier to restore to function than an
extremity similarly burned in a patient with full-thickness
burns involving multiple anatomical surfaces. In the case of
seriously burned patients, the immediate and primary focus
will always be preservation of life and wound coverage. Now
adays, burn rehabilitation specialists intervene early on in
the patient recovery process through the development and
implementation of rehabilitation programs intended to
maximize the potential of functional and cosmetic patient
recovery.
The primary short-term rehabilitation goal is to preserve
the patient’s range of motion and functional ability. Long-
term rehabilitation goals include the return of the patient to
independent living and to train patients on how to com
pensate for any functional loss suffered as a result of the
burn injury and contribute toward acceptable cosmetic
outcomes.
This chapter addresses the evaluation, positioning,
splinting/orthotics, casting, skeletal suspension, prosthetics,
scar management, exercise, performance of activities of daily
living (ADL) and patient and caregiver education utilized in
burn rehabilitation along the continuum of care.
Evaluation of the burn patient
Upon admission to the burn center, patients undergo a
comprehensive evaluation by burn rehabilitation therapists
(physical or occupational therapists) in order to assess their
medical status and formulate a plan of care. It is crucial that
therapists document the findings of their evaluation in the
patients’ medical record as they will serve as the baseline
upon which progress will be determined. A good burn evalu
ation should include: (1) the history of how the accident
occurred; (2) an interview with the patients’ caregiver in
order to gather information regarding the patients’ pre-
injury functional status and activity level; (3) documenta
tion of the etiology, classification and total body surface area
(TBSA) of the burn injury; (4) documentation of associated
injuries such as fractures, smoke inhalation injury, exposed
tendons and bone; (5) measurement of edema, range of
motion (ROM), strength and sensation if appropriate; (6)
assessment of activities of daily living (ADLs) performance;
(7) development of short- and long-term treatment goals
and (8) development and documentation of a treatment
plan. The patients’ status should be reassessed on a regular
basis and after each surgical procedure in order to update
the plan of care as needed. Therapists should communicate
the results of their evaluation and the treatment plan to the
burn team, to the patients and their families.
Positioning and splinting of the burn patient
Positioning of the burned patient is vital in bringing about
the best functional outcomes in burn rehabilitation. Posi
tioning programs should begin immediately upon admis
sion to the burn center and continue throughout the
rehabilitative process. The role of the burn therapist is inval
uable in designing a positioning program, which counteracts
all contractile forces without compromising function. In
planning and implementing an effective patient-specific
positioning program, the therapist should be aware of the
patient’s total body surface area (TBSA) of burns, the depth
of all injuries, respiratory status and associated injuries such
©2012 Elsevier Ltd, Inc, BV
DOI: 10.1016/B978-1-4377-2786-9.00047-3
Comprehensive rehabilitation
of the burn patient
Michael A. Serghiou, Sheila Ott, Christopher Whitehead, April Cowan,
Serina McEntire, Oscar E. Suman
CHAPTER 47
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IN THIS CHAPTER
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Total Burn Care
47
518
modified to maximize surface area while protecting bony
prominences.
Side-lying may be used on a rotating basis for patients at
risk for sacral or scapular skin breakdown. In a preventive
program, the rotation is right side to supine to left side. The
order is then reversed on a 1- to 2-h schedule. Full side-lying
at 90° from supine should not be allowed for any significant
length of time due to excessive pressure over the greater
trochanter. A more appropriate position for side-lying is
approximately 30–40° from the supine position, which dis
tributes pressure more evenly between the head of the femur
and the lateral portion of the sacrum.
The mechanics of a side-lying position can be accom
plished using pillows or wedges made of foam or wood. The
advantage of foam or wooden wedges is that they can be
placed directly under the mattress with less manipulation of
the patient. As the rotation schedule is completed the wedge
can either be removed for the supine position or transferred
to the opposite side of the mattress to achieve side-lying on
the opposite surface.
Prone positioning systems are usually the position of last
resort (Fig. 47.1). They are reserved for patients who are not
successfully being managed in supine or side-lying. There
may be non-healing grafts or wounds in the rectal region
that increase the risk of sepsis due to the introduction of
fecal matter. Other common candidates for this protocol
include those with sacral pressure ulcers or posterior trunk
grafts that are not healing.
There are a host of issues that must be considered when
instituting a prone program. Airway is always the first issue
that must be considered when designing a prone positioning
mattress. The supporting surface is cut from a solid open-cell
foam mattress that is placed on a wire mesh bed frame.
Airway concerns are addressed first and the patient is evalu
ated for mode of respiration. Nasal and tracheal intubation
are issues to consider, but are not contraindications for the
prone position. A trough should be provided so that direct
access can be obtained for routine airway care and if breaths
are needed using an Ambu-bag. If the airway becomes com
promised the prone position should be abandoned imme
diately until proper respiration is established.
as exposed tendons/joints or fractures. Individualized posi
tioning programs are monitored closely for any necessary
adjustments depending on the patient’s medical status. The
quote that ‘the position of comfort is the position of deform
ity’ applies to every burned patient who sustained a serious
injury.
Anti-deformity positioning can be achieved through
multiple means: splinting, mechanical traction, cut-out
foam troughs and mattresses, pillows, strapping mecha
nisms, serial casting and in some cases, through surgical
application of pins. The burn therapist needs to be aware of
physician-specific protocols and work closely with the entire
burn team to design the most effective positioning program.
Orthotics and splinting devices are vital in burn rehabilita
tion as they are utilized extensively to obtain appropriate
positioning of the entire body and to counteract the contrac
tile forces that lead to deformity. No matter how the burn
therapist approaches splinting (material choice, design, and
application schedules) the goal is to achieve the best func
tional outcome at the completion of rehabilitation. When
fabricating a splint or an orthosis the burn therapist must be
aware of the anatomy and kinesiology of the body surface
to be splinted. Also, the therapist should be well aware of
all mechanical principles of splinting as they relate to pres
sure, mechanical advantage, torque, rotational forces, first-
class levers, friction, reciprocal parallel forces and material
strength.1
Positioning and splinting must be designed in a way to:
•
Allow for edema reduction
•
Maintain joint alignment
•
Support, protect and immobilize joints
•
Maintain and/or increase range of motion
•
Maintain tissues elongated
•
Remodel joint and tendon adhesions
•
Promote wound healing
•
Relieve pressure points
•
Protect newly operated sites (grafts/flaps)
•
Stabilize and/or position one or more joints, enabling
other joints to function correctly
•
Assist weak muscles to counteract the effects of gravity
and assist in functional activity
•
Strengthen weak muscles by exercising against springs
or rubber bands.1
Devices should:
•
Not cause pain
•
Be designed with function in mind
•
Be cosmetically appealing
•
Be easy to apply and remove
•
Be lightweight and low profile
•
Be constructed out of appropriate materials
•
Allow for ventilation in preventing skin/wound
maceration.1
Typical burn care positioning protocols describe the
supine position in great detail. More emphasis is now being
placed on the use of side-lying and prone positioning for
patients with large burns who must be immobilized
for extended periods of time due to newer grafting tech
niques that cover larger areas with fragile skin substitutes.
When designing a positioning program the traditional joint
angles are maintained, and the supporting surfaces are
Figure 47.1 Patients may be positioned prone in order to protect posterior
grafts from shearing.
Comprehensive rehabilitation of the burn patient
519
are custom-made by the therapist or they may be obtained
commercially. Mouth splints may be fabricated static or
dynamic for the horizontal or vertical opening of the
mouth.3–6 In cases of severe microstomia where compliance
is an issue, an orthodontic commissure appliance which
attaches to the teeth may be fabricated by an orthodontist.7
The use of stacked tongue blades is an acceptable technique
to aid in reversing oral microstomia. Ongoing research looks
at the development of a microstomia device that circumfer
entially opens the mouth according to its anatomy (Fig.
47.3). Facial scar hypertrophy may require fabricating a high
thermoplastic transparent mask such as the Uvex™ and
W-clear™ masks or a silicone elastomer facemask.8–10 A semi-
rigid low thermoplastic opaque mask may also be fabricated
depending on the state of scar maturation.
Neck
The neck is positioned in neutral or in slight extension of
approximately 15° without any rotation. The amount of
neck extension must not be so great that traction on the chin
causes the mouth to open. Positioning may be achieved with
a short mattress supine, a rolled towel or foam cushion
placed behind the upper back on the scapular line. Pillows
should be avoided in the cases of anterior neck burns as they
may lead to flexion contractures. In the case of anterior neck
burns a conforming custom thermoplastic collar may be
fabricated (Fig. 47.4).11 For long-term needs, a soft neck
collar or a Watusi-type collar may also be fabricated as the
patient’s wounds heal and contractures or scars develop. The
Watusi-type collar allows for isolated, direct pressure to a
thicker scar band.10,12,13 It has been observed that in some
cases, acute patients rotate or laterally flex their neck on one
side, which may lead to a lateral neck contracture (torticol
lis). If the patient is to remain in bed for a while, a dynamic
head strap mechanism may be fabricated to counteract the
lateral neck contractile forces and bring the neck in the
neutral position. For the prevention of torticollis the thera
pist may fabricate a lateral neck splint which conforms to
the head of the patient, the lateral neck and anterior/
posterior shoulder (Fig. 47.5).
The facial opening should be cut in a manner that maxi
mizes weight distribution without allowing the head to enter
into the opening. Using this protocol places direct weight-
bearing pressure on the brow ridge, zygomatic arches, and
the anterior mandible. These structures should be monitored
closely and the patient should be educated that breakdown
is likely to occur due to the limited subcutaneous tissue
protecting the face. If burn scars are encroaching on the
eyelids, then the corneas should be evaluated as well. Corneal
abrasion can be avoided with due diligence and prevention
of the foam from contacting the unprotected eye. Counter
sinking a gel cushion into the upper portion of the foam
mattress can protect the forehead and brow-ridge.
The sternum, pelvic region, and patellae are protected with
the use of an air-cell mattress that is inserted into the mat
tress in a length-wise manner. The air-cell segments are typi
cally supplied in standard lengths and may not reach from
the sternum to the ankles. If there is an unsupported area
between the distal portion of the air-cell mattress and the
dorsum of the foot, then the area can be supported with
open cell egg-crate type foam. The feet are supported at the
distal end of the mattress with a foam footboard. Extra pre
cautions should be taken to evaluate the elevation of the
great toe from the supporting bed frame.
In the prone position, all of the traditional joint alignment
suggestions are maintained with the possible exception of
the elbows. Shoulder mobility dictates the style of mattress
that can be made for the individual burn patient. If the
patient has >115° of abduction, then the mattress is modi
fied to horizontally adduct and externally rotate the shoulder
while flexing the elbow to allow for elevation of the hands.
This minimizes edema in the hands and allows for greater
function once the prone position is no longer needed. If the
shoulders have limited abduction then a ‘butterfly’ cut is
used to allow for horizontal adduction of the shoulder to
protect the brachial plexus with the hands remaining slightly
dependent. This will result in some hand edema, which can
be addressed with pressure wrapping (Coban™ glove) and
active exercise.
Head
Acutely, in aiding with facial edema reduction, the head
should be positioned by placing in midline and elevating
the head of the bed at 30–45° if the patient’s hips are not
involved. In cases where the hips are burned, the entire bed
may be elevated at the head of the bed with the use of shock
blocks (wooden blocks 12–16 inches high with recessed
slots for bed legs). This will avoid positioning the hips in
the flexion contracture position (Fig. 47.2). In the cases
where the ears are burned they may be protected by strap
ping ear cups made of thermoplastic materials or foam.2 An
ear conformer may be constructed to prevent the rim of the
ear from contracting toward the head. Internal ear canal
splints may also be fabricated and serially adjusted as the
circumference of the canal increases. In addition, if the ear
is affected, a soft circular foam can be positioned posteriorly
to the head to elevate the ears of the surface of the bed. A
nasal obturator may be required to maintain the nostrils
open. These obturators may be serially adjusted as the cir
cumference of the nostril increases. Mouth splints are uti
lized for the prevention of oral microstomia. These devices
Figure 47.2 Wooden blocks are utilized to place the bed on an incline to
help with edema reduction and prevent hip contractures.
Total Burn Care
47
520
Figure 47.4 An anterior neck conformer helps prevent neck flexion
contractures.
Figure 47.5 (a) A dynamic head strap mechanism aids in positioning the
neck in neutral position during a prolonged ICU bed confinement. (b) A
lateral neck splint is utilized to prevent lateral neck flexion contractures
(torticollis).
A
B
Figure 47.3 Horizontal, vertical and circumferential mouth-opening devices are utilized to correct oral microstomia.
Comprehensive rehabilitation of the burn patient
521
nerve compression. The glenohumeral joint is externally
rotated in order to counteract anticipated deformities of
internal rotation and adduction and to maintain balance of
the soft tissues of the shoulder complex.
Positioning of the shoulder may be achieved with splints,
silicone-filled pillows, bedside tables, foam arm troughs,
metal abduction troughs, and thermoplastic slings sus
pended from a trapeze mechanism (Fig. 47.7). Splinting of
the shoulder joint becomes more intensive as scar matura
tion heightens the risk of contracture development. Airplane
splints are used for the resolution of axillary contractures
and post-operatively to protect reconstructive procedures. To
accommodate wound dressings and promote healing, a
three-piece airplane splint may be fabricated (Fig. 47.8).
Other adaptations may be required in the presence of
amputations. Pre-fabricated airplane splints come equipped
with mechanisms that allow for adjustments depending
upon available shoulder range of motion.10,11,13 A figure-of-
eight axillary wrap may be utilized in conjunction with an
Figure 47.6 Scoliosis resulting from a left chest, abdomen and left lateral
trunk injury.
Figure 47.7 Foam arm troughs are utilized for positioning the shoulders in
bed.
Figure 47.8 A three-piece airplane splint may be fabricated to
accommodate wound dressings and promote healing while maintaining
the shoulder abducted.
Spine
Contracture resulting from unilateral or asymmetric burns
of the neck, axilla, trunk and groin will cause lateral curva
ture of the spine (scoliosis). The level and amplitude of
curvature will vary with the site and severity of the contrac
ture. In addition, pelvic obliquity accompanying asymmetric
hip or knee flexion contracture will impose a lateral lumbar
curve. As long as the patient is recumbent, lateral curvature
can be prevented by maintaining straight alignment of the
trunk and neck (Fig. 47.6). However, the curve is often insid
ious in onset and will not be recognized until the patient
begins to walk. Trunk list observed early in the ambulation
period can be simply a transient accommodation to pain
and wound tightness, but a persistent list may herald the
development of scoliosis. Other subtle signs of spinal curva
ture are asymmetry of shoulder levels, scapular asymmetry,
asymmetry of dependent upper extremity alignment to the
trunk and asymmetry of pelvic rim levels. A spinal mobiliza
tion exercise program is established with a patient once a
curvature is identified, however once there is an established
asymmetric contracture it is difficult by therapeutic means
to stretch it out, so it is probably better to deal surgically
with a deforming scar early than to permit even minor sco
liosis to persist.
Shoulder girdle/axilla
Acutely, the upper extremity positioning program focuses on
reducing edema through elevation. Failure to reduce edema
in the first 48–72 h can promote the development of a fixed
deformity. Additionally, improper elevation techniques for
the upper extremity may lead to soft tissue calcification,
increased bone density, and compressive neuropathies. The
recommended position for the burned shoulder and axillary
complex is 90° abduction, 15–20° horizontal adduction
and external rotation towards maximal. Abduction alone
places the glenohumeral joint at risk for anterior subluxation
if the position is maintained for an extended period of time.
Placement in horizontal adduction anatomically reduces the
potential for tractioning of the brachial plexus or peripheral
Total Burn Care
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522
to intrinsic muscle ischemia and a resultant ‘intrinsic-minus’
posture. The unsupported burned hand postures in wrist
flexion, metacarpophalangeal (MCP) hyperextension, inter
phalangeal (IP) flexion, thumb adduction, and thumb IP
flexion. The overall appearance is that of a claw deformity
(Fig. 47.10a) Edema following a full-thickness burn to the
dorsal hand imposes MCP hyperextension and IP flexion
(Fig. 47.10b). Persistence of this position results in a claw
deformity). The claw hand posture is primarily due to post
burn edema, but may persist throughout the course of treat
ment due to scar contracture. Among the digits, the second
and fifth most easily drift into MCP hyperextension because
each has a proper extensor tendon.
While superficial burns result in minor, transient edema,
full thickness injuries exhibit more severe and prolonged
postburn edema. Superficial hand burns should not be
splinted in order to allow for frequent movement and
the freedom to function independently. In cases of severe
thermal injury it is important to monitor for signs and
symptoms of vascular insufficiency or compartment syn
drome. In treating the edematous, burned hand, it is impor
tant to position the hand above the level of the heart at all
times, without compromising the neurovascular supply to
the hand.10,11,13
airplane splint to provide compression for axillary contour
and elongation of skin surfaces (Fig. 47.9). For successful
contracture management to the shoulder, the positioning
program must be supplemented by exercise routines for
range of motion and strengthening.
Elbow/forearm
Acutely, elevation and extension is the desired position of
the elbow. Severe burns involving the elbow may result in
flexion contracture and threaten posterior exposure of the
joint. Full extension is the protecting position for the elbow.
If the joint is exposed posteriorly, extension may need to
be rigidly maintained for several weeks. If the joint is
not exposed, mobilization into increasing flexion range can
begin very soon after the burn. The elbow is integral to the
so-called delivery system for the hand, and elbow range to
full or near-full flexion is more important for overall func
tion than range to full or near-full extension.
Radial head rotation for pronation and supination is less
often affected by the burn injury than flexion and extension.
The pronators and supinators are frequently injured in elec
trical accidents where bone, being a poor conductor, heats
destroying the muscles closest to it. Forearm rotation is
essential for accurate hand placement and the rehabilitative
program must seriously address that function. Depending
on the location and severity of the injury the forearm may
be positioned in neutral or in slight supination. Static elbow
splints may be soft or custom-fabricated of thermoplastic
materials. An anterior elbow conformer may be fabricated
over the burn dressing. Dynamic elbow extension or flexion
splints may be utilized to provide prolonged gentle sus
tained stretch and aid in the correction of contractures.14
Forearm dynamic pronation/supination splints may be
custom-fabricated or obtained commercially for the correc
tion of contractures.10,11,13
Wrist/hand
Treating therapists must have a thorough understanding of
the effects of thermal injury on the anatomical structures of
the wrist and hand. The presence of dorsal hand edema leads
Figure 47.10 (a) Edema following a full-thickness burn of the dorsum of
the hand – imposed metacarpophalangeal extension and interphalangeal
flexion. (b) The deformity resulting from the persistence of this position is
that of a claw hand.
A
B
Figure 47.9 A figure-of-eight axillary wrap provides a constant stretch of
the axillary skin surfaces.
Comprehensive rehabilitation of the burn patient
523
proximal IP flexion.16 The claw hand deformity is function
ally detrimental because it makes it impossible to smoothly
reach around objects (Fig. 47.12).
Burns to the volar surface of the forearm will predispose
the patient to wrist flexion contracture, while burns to the
dorsal surface will likely result in a wrist extension contrac
ture. If the wrist ROM becomes limited in a specific direc
tion, splinting the wrist in the opposite direction is indicated.
The fifth digit is occasionally pulled into extreme abduction
and hyperextension by scar contracture, muscle imbalance,
or ulnar neuropathy. The thumb may become similarly dis
placed into adduction and retroposition. It is important to
remember that the likelihood for MCP joint problems exists
throughout scar maturation. Palmar hand burns are prone
to MCP flexion and thumb opposition contractures and
should be splinted into palmar extension and thumb radial
abduction.
Static positioning with custom thermoplastic splints can
be relatively efficient. However, two common faults are seen
in custom splints that are designed to gain MCP flexion and
to position the thumb in MCP flexion/radial abduction. If
the distal transverse fold of the splint is not proximal to the
MCPs of digits 2–5, the splint will impede rather than favor
MCP flexion. If the thumb component of the splint applies
volar pressure rather than medial pressure, the MCP will
extend and the first metacarpal will become correspondingly
more adducted. The first MCP joint should be maintained
in slight flexion and pressure from the splint should be
applied just to the medial surface. Any degree of first meta
carpal adduction contracture increases the likelihood that
the proximal phalanx will be pushed into hyperextension
and eventually into subluxation.
In the case of circumferential hand burns, a palmar exten
sion splint is fabricated to prevent flexion contractures and
a cupping deformity of the palm (Fig. 47.13). The burn hand
splint and an extension splint may be alternated. A ‘sand
wich’ splint may be fabricated which includes a burn hand
splint with a dorsal shell over the IP joints to prevent flexion
of the digits. All splints may be secured with elastic bandage
or with Velcro® strapping components (Fig. 47.14).17 Indi
vidual gutter splints are used to prevent flexion contractures,
to restrict boutonnière and mallet finger deformities, and for
Figure 47.11 The intrinsic plus position hand splint (burn hand splint)
positions the hand appropriately to prevent contractures and preserve
function.
Figure 47.12 The claw hand deformity limits both grasp and functional
dexterity.
Acute positioning of the wrist and hand after burn injury
is for edema control, immobilization/protection of tendons,
joint structures, and/or skin grafts, and optimal positioning
to maintain soft tissue lengths and functional abilities.
Within the first 24–72 h it is recommended that the wrist be
splinted into extension, allowing the MCP joints of digits 1
through 5 to fall into flexion due to the normal tenodesis
action of the wrist and hand. Wrist extension is essential in
order to control digital position and prevention of a claw
hand deformity. The recommended functional position of
the wrist is from 0–30° of extension.
The burned wrist and hand should be positioned to
oppose impending wound contracture. The optimal position
for the burned hand is wrist 0–30° extension, 70–80° MCP
flexion and IP joints in full extension (although some burn
centers may advocate a slight amount of IP flexion deeming
the position to be ‘safe.’). The thumb should be positioned
in a combination of palmar and radial abduction with the
MCP/IP joints slightly flexed. This position resembles the
‘intrinsic-plus’ position and is achieved through fabrication/
fitting of a burn hand splint by a rehabilitation therapist
(Fig. 47.11; The burn hand splint positions the hand appro
priately to minimize soft tissue contractures and preserve
functional mobility). Involvement of the extensor tendon
apparatus should be assumed and protected until viability
of the system is known.15 Continuous splinting is recom
mended to manage edema, exposed tendons, peripheral
neuropathies, and uncooperative/unresponsive patients.
In the intermediate phase, positioning and splinting is
used to prevent/correct deformities and protection of surgi
cal reconstructed sites. Splints may be fabricated dorsal,
volar or on the medial/lateral aspects. Contractures are a
major complication of hand burns as they affect one’s ability
to perform activities of daily living. Dorsal hand burns are
prone to contract into MCP hyperextension, IP flexion, and
thumb adduction and should be splinted into MCP flexion,
IP extension, and thumb palmar abduction. The most
common post-burn upper extremity contractures are: wrist
flexion, index finger MCP hyperextension, index finger pro
ximal IP flexion, and small finger MCP hyperextension/
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524
symmetric contractures impose increased lumbar lordosis or
knee flexion or both. Asymmetric contracture will cause
pelvic obliquity and scoliosis. In adults and older children
thighs are more likely to be held in adduction than in abduc
tion, whereas in pre-ambulatory infants the secondary com
ponent of the contracture is abduction. Thus, for the hips
the preventive position is full extension, 0° rotation and
symmetric abduction of 15–20°. If elevation of the upper
body is needed for edema reduction then the entire frame
of the bed is elevated with the use of wooden shock blocks
placed at the head of the bed. Soft mattresses should be
avoided as they may promote hip flexion. Hip positioning
is accomplished with the use of abduction pillows and other
strapping mechanisms eliminating hip rotation. If the
patient wears bilateral foot splints then connector bars may
be utilized on the splints to bring about the desired bilateral
hip positioning stated above. Hip flexion contractures may
be serially corrected with an anterior hip spica or with a
3-point hip extension splint (Fig. 47.16).10,11,13 Subtle hip
flexion contractures can be easily overlooked when the
patient stands, there being only a slight increase in lumbar
lordosis or forward or lateral shift of the trunk. If established
hip flexion contractures are not surgically corrected, body
posture is likely to be permanently altered with scoliosis or
exaggerated lordosis.
Knee
Burn injury to the anterior or posterior surface of the lower
extremity that crosses over the knee joint may result in knee
flexion. Deep anterior burns may expose the joint, occasion
ally destroying the patellar tendon. Deep posterior burns
result in bridging scar formation. The appropriate position
for the knee is full extension to be maintained by splint or
in severe cases skeletal traction until there is efficient quad
riceps function and the patient is ambulatory. Thereafter,
night splints must be used until scar contracture is no longer
a threat. Knee splints may include a posterior custom-made
thermoplastic knee conformer or a soft knee immobilizer.
Persisting bilateral knee flexion contractures will impose
hip flexion. Persisting unilateral contractures may impose
pelvic obliquity and scoliosis. As with the hip, posture
Figure 47.14 The ‘sandwich’ hand splint prevents PIP flexion contractures.
Figure 47.15 A dynamic MCP extension splint promotes functional use of
the hand.
Figure 47.13 An example of a palmar extension splint to stretch a palmar
contracture.
protection of exposed extensor tendons until wound closure
C-bar splints are used to prevent adduction contracture of
the first web space. Figure-of-eight splints are fit to correct or
restrict swan neck deformities.
Dynamic splints are utilized to provide low-load pro
longed stretch to counteract contractile forces. Dynamic
splinting of the hand will focus on MCP extension/flexion
splints, IP flexion/extension splints, thumb abduction, and
may include pre-fabricated or spring-loaded splints (Fig.
47.15). Patients may require dynamic splinting to assist
muscles weakened by peripheral neuropathy. The therapist
monitors dynamic splinting closely and makes frequent
adjustments in order to provide effective tissue mobilization.
Additionally, the fit of dynamic splints is checked frequently
to insure that the anatomical structures remain properly
aligned.
Hip
When anterior burns extend from the abdomen to the thigh,
hip flexion is the position of comfort. If the hip is fixed in
any degree of flexion, posture will be modified. Bilateral
Comprehensive rehabilitation of the burn patient
525
support the foot at neutral if the traction pin is placed in the
calcaneus well behind the axis of ankle motion. A balanced
traction system demands that the knees be supported in
flexion with tibial pins at the level of the tibial tubercle.
Calcaneal pins will not prevent forefoot equinus. If traction
must be employed for several weeks, proximal pull dorsal
pins in the first or first and second metatarsals may be
required for support of the forefoot. Transmetatarsal pins are
useful as well when calcaneal traction alone is not sufficient
to correct equinus.
Minor established equinus deformity can be corrected
with a standing and walking program. At the outset gradu
ated heel lifts may be used to accommodate to the deformity.
If the patient must be bed-confined, skeletal traction through
the calcaneus may be the quickest and most efficient way to
correct the deformity. Traction is effective even if scar con
tracture contributes to the deformity. Serial corrective casts
or posterior splints alone are useful mainly for minor con
tractures. For the treatment of circumferential foot/ankle
burns anterior foot splints are also fabricated and their appli
cation is alternated with the posterior foot splints in prevent
ing plantar or dorsal foot contractures.10,11,13 The Multi
Podus® System foot splints may be utilized for the position
ing of the burn foot/ankle as they relieve heel pressure in
preventing pressure ulcers (Fig. 47.17). For fixed, unyielding
deformity, scar release combined with tendo-Achillis length
ening with or without posterior capsulotomy is a standard
surgical procedure that yields inconsistent results. The cor
rection achieved is often just to neutral or to slight dorsiflex
ion. The Ilizarov technique has been used with generally
satisfactory immediate results in severe cases.18 No matter
how correction is achieved, if there are no dorsiflexion
motors and if the range of ankle motion is only a few degrees,
ankle fusion may in the end yield the best functional result.
The most common intrinsic deformity of the foot is
extreme extension of the toes due to dorsal scar contracture.
This deformity is insidious in onset and is difficult to prevent
as there is no type of non-skeletal splinting that will hold
the toes flexed. In its extreme, the deformity includes dorsal
metatarsophalangeal (MTP) subluxation which may involve
one or all toes depending on the location of the scar. The
alteration may be so subtle as to be overlooked. Correction
of even a slight contracture should be a surgical priority as
should elimination of a soft bridging scar band that does
not prevent complete willful knee extension but causes the
patient habitually to hold the knee in slight flexion.
Foot/ankle
Ankle equinus is the most frequently occurring deformity
involving the foot. Initially, it is related more to gravity and
failure to support the foot at neutral at the talotibial joint
than to the early effect of the burn. Loss of deep and super
ficial peroneal nerve function will compound the problem
by encouraging the foot to drift into inversion as well as
equinus because of loss of dorsiflexion and eversion motors.
In the end, the total deformity for the unsupported foot may
be ankle equinus, hind-foot inversion, and forefoot varus
and equinus. Ankle equinus quickly becomes a resistant
deformity so that within a few days or even hours the
foot can no longer be positioned at 90° of dorsiflexion in
the neutral ankle position. Eventually the contractures of
scar, muscle and capsular structures combine to fix the
deformity.
Equinus deformity and the attending inversion and fore
foot varus can be prevented by accurate and unyielding
support of the foot in neutral alignment or slight dorsiflex
ion. If the patient must be nursed prone, the feet must be
allowed to fall free from the mattress. Static splinting if not
performed correctly by an experienced therapist is often
unsuccessful because of the patient’s desire and tendency to
plantarflex strongly, displacing the splint and leading to
ulcers of the heel, malleoli, toes and where the splint edges
touch the skin. A stable footboard may be effective if the feet
are kept securely and totally against it. For large burns and
particularly for circumferential burns of the lower extremi
ties, skeletal suspension incorporating calcaneal traction will
Figure 47.16 An anterior hip spica splint is utilized to prevent anterior hip
flexion contractures.
Figure 47.17 The Multi Podus splint is utilized to position the burned feet
appropriately and prevent heel and malleoli skin breakdown.
Total Burn Care
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526
foot. Such systems may include a metal ankle–foot orthosis
(AFO), polypropylene plastic posterior AFO (solid ankle or
with an articulation), an AFO with stirrup attachment, an
AFO with stirrups and patellar tendon support. A dorsiflex
ion spring assist may be incorporated in the AFO to aid weak
ankle motion. Different straps such as a valgus correction
strap may be attached to the AFO for the correction of spe
cific problems. Interface materials, such as silicone, Plasti
zote® and Aliplast®, can be incorporated into an AFO to
provide protection of the soft tissue, provide for total surface
weight-bearing, and to accommodate any anatomical anom
alies that may be present (Fig. 47.18). In the event that a
return of range of motion is anticipated, an AFO could be
fabricated that can be modified as the patient progresses. The
ankle joints can be incorporated into the AFO, however, left
solid and articulated at a later date.
During more complicated cases, and depending on the
anatomy and function of the lower extremities, a knee–
ankle–foot orthosis, hip–knee–ankle–foot orthosis or a
trunk–knee–ankle–foot orthosis may also be designed for
the best functional outcome.19
Serial casting
Casting has been used in patients with burns for postopera
tive immobilization to promote graft adherence and to
minimize scar contracture during the remodeling phase of
healing.20 Circumferential casting after skin grafting to the
lower extremity is an effective means of providing protection
to the grafted area.21 Serial casting has been used successfully
on outpatients with burns when active range of motion is
limited due to scar tissue formation.22 The goal of serial
casting is gradual realignment of the collagen in a parallel
and lengthened state by constant circumferential pressure.23
Prolonged gentle sustained stretch provided by the cast aids
in tissue elongation for the correction of contractures (Fig.
47.19). Burn scar under constant traction shows collagen
formation in parallel alignment along the forces of stress.24
Low intensity force with prolonged duration for stretching
metatarsal heads become prominent on the plantar surface
and walking may be painful. Correction of the deformity
requires dorsal surgical release of the contracture, manual
correction of the deformity and in severe cases intrinsic or
extrinsic pinning of the digit or digits in an overcorrected
position, i.e. MTP and interphalangeal flexion. The deform
ity will commonly if not inevitably recur to some degree,
unless the patient, after the operation, is able to achieve in
all digits active MTP flexion.
Dorsal scar contractures extending from leg to foot to toes
may pull the foot into marked inversion if the scar is medial
or into eversion if the scar is lateral. The fifth and first toes
may be separately displaced by the same scar bands. These
contractures must always be surgically corrected. Their per
sistence will lead to bone deformity in a growing child and
will permanently adversely affect foot and ankle function.
Even slight inversion, whether imposed by scar contracture
or motor weakness, will increase pressure on the lateral
border of the foot, leading to callus formation and a painful
inefficient gait. Occasionally, the base of the fifth metatarsal
is so offensive as to require partial surgical osteotomy.
When there is both anterior and posterior scar contracture,
the talus will remain aligned with the calcaneus in a rela
tively plantar flexed position as the midfoot and forefoot are
pulled into dorsiflexion. The result is so-called rocker bottom
foot with the head of the talus being the principal weight-
bearing feature. This deformity once established defies cor
rection by usual surgical means because of the shortage of
soft tissue and because vessels and nerves cannot be stretched
to accommodate to the corrected position. The Ilizarov tech
nique may offer a partial solution to the problem. Removal
of the head of the talus may give a reasonable weight-bearing
surface. With chronic painful ulceration, amputation is the
best treatment.18
Orthotic treatment of the lower extremity
The approach of the orthotist in treating the injured foot
depends on the extent of the burn injury. Orthotic shoes,
which are the fundamental component of most lower
extremity orthotics, may be utilized with some modifications
in correcting deformities of the burned foot. Modifications
of these shoes may include arch pads, molded foot thermo
plastics, tongue pads, and metatarsal bars. The orthotic shoes
should distribute all forces to the foot appropriately and
should reduce pressure on sensitive or deformed structures
and encourage total surface weight-bearing along the plantar
aspect of the foot. Inserts for plantar foot support such as
the University of California Biomechanical Laboratory
(UCBL) type may be utilized as indicated.
During the preambulation stage the patient may be fitted
with those orthoses; if properly utilized, they can position
the ankle joint appropriately, and assist in preventing or cor
recting plantar/dorsal contractures and inversion/eversion of
the foot.
Leg length discrepancies are seen frequently in the cases of
severe lower extremity burn injuries and they should be
addressed with a shoe lift. The ankle–foot complex is diffi
cult to address, especially in the case of a severe thermal
injury. In most cases, the resultant deformity is the equino
varus foot. Both conventional and thermoplastic systems
may be designed to treat the equinovarus or equinovalgus
Figure 47.18 Specialized materials may be required to accommodate
anatomical anomalies that may be present. Standard ankle–foot orthoses
can be fabricated utilizing silicone materials to accommodate excessive
scarring and limb loss.
Comprehensive rehabilitation of the burn patient
527
Other disadvantages of this technique include a decreased
water resistance and breakage if not constructed strongly
enough. Plaster casts may be removed with a cast saw or
moistened and removed with scissors.
Fiberglass casting material is an alternative to Plaster-of-
Paris. Fiberglass casting tape is fast setting when reacting
with cool water. Fiberglass materials require a shorter drying
time (15–30 min), are lighter weight and more durable, and
offer resistance to dirt and water. Fiberglass casting methods
are more costly than plaster. Because of fiberglass’s abrasive
properties, therapists must wear gloves for handling the
materials during cast fabrication and removal. The patient’s
skin and clothing should be protected from contact with the
fiberglass casting tape, as well as to fiberglass fibers during
cast removal. Fiberglass casts require use of the cast saw for
removal.
Recently, non-latex polyester materials such as Delta-Cast™
are utilized as alternatives to plaster and fiberglass. These
materials, which resemble fiberglass, are very lightweight,
flexible, and because of their elastic properties conform very
well. These casts may be cut in a bivalve fashion so that they
can be removed and reapplied after wound care, hygiene,
and exercise.27
After cast fabrication is complete, the clinician should
check the following: firmness of the cast, neurovascular
status of the extremity, sharpness of cast edges, and any signs
of the cast rubbing adjacent structures. When casting is com
pleted, the patient should feel a gentle, but not painful
stretch. The first cast should be removed at approximately
24 h and thereafter, depending on the patient’s tolerance, it
could be applied for up to 1 week at a time. In cases of
casting over open wounds, the cast should be removed every
1–2 days in order to avoid complications in wound
healing.21,23 The use of insert material for scar management
under casts has been documented and found to be useful.23
Serial casting is terminated when either normal range of
motion has been restored or no further functional gains are
achieved.
Skeletal suspension and traction
Skeletal suspension and traction systems have been used to
a limited extent in burn management for a number of years.
The early reports of Larson28 and Evans29–31 described the use
of skeletal suspension for positioning and for extremity ele
vation for open wound management and of skeletal traction
for prevention and correction of contractures. The later
reports of Harnar32 and Youel33 deal mainly with the man
agement of hand burns with the skeletally anchored digital
traction splints bearing the names banjo, halo, and hay rake
(Fig. 47.20).
The adaptation of skeletal suspension and traction systems
to burn management grew out of earlier experience with
traction to correct the elbow and knee contractures of
patients with rheumatoid disease, and out of traction and
suspension as definitive means for treating certain extremity
fractures. In its earliest application to burn management,
skeletal suspension was used for extremity elevation only to
facilitate wound care. From this experience evolved better-
defined traction systems, including those expressly designed
for hands and feet. Rehabilitation therapists may remove the
can be applied to connective tissue whether it is scarred,
contracted or surgically shortened.25 Casting is a relatively
simple, fast and painless intervention and provides an alter
native to dynamic splinting but is not feasible when patient
compliance is an issue (e.g. pediatrics).
A pre-casting assessment should include the following:
ROM measurements, end-feel assessment of the involved
joint, duration of limitation, skin or wound status, neurov
ascular status, functional needs, and cognition of all involved
parties. The patient is educated on the position in which
the cast will be applied, the expected duration of casting and
any restricted activities. Ridgway (1991) described the serial
casting technique: (1) skin hygiene; (2) scar massage with
moisturizer; (3) ROM exercises and assessment; (4) wound
dressings; (5) application of a silicone insert; 6) extremity in
figure-of-eight wrap or tubular bandage; (7) padding over
bony prominences; (8) one therapist to position and one
therapist to fabricate cast. Serial casting may be supple
mented with splinting of adjacent joints. There should
be a minimal time lapse between cast removal and
reapplication.
Patients may require premedication and may also benefit
from soft tissue preconditioning (heating) for stretch prior
to cast application. Precautions should be taken to ensure
proper and evenly applied padding, including extra layers at
the proximal and distal ends of the cast. The casting material
should be rolled out and handled with an open hand as
much as possible. Aggressive molding or over tight applica
tions are to be avoided and can lead to compression
neuropathies or vascular compromise. When cast materials
harden an exothermic reaction occurs, causing the tempera
ture within and beneath the cast material to rise, which leads
to elevated temperatures and burns. The greatest risk of
thermal injury occurs when a thick cast using warm dip
water is allowed to mature while resting on a pillow.26 A
variety of materials are available for the fabrication of casts.
The most widely known would probably be Plaster-of-Paris.
Plaster is fast setting when reacting with lukewarm water.
Plaster casts are inexpensive, stronger, and easy to fabricate.
However, they require longer drying times (24–48 h), are
prone to indentations and skin irritations, and are heavier.
Figure 47.19 Serial casting provides prolonged gentle sustained stretch
and aids in tissue elongation and correction of contractures without pain.
Total Burn Care
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528
insults, but can also result from more severe thermal injuries
as well. Prosthetics are designed, fabricated, and fit by a
certified prosthetist. Each device is individualized based
upon the needs of the patient. But, in general, the
prosthesis should be comfortable to wear, easy to don/doff,
lightweight, of durable construction, and be cosmetically
appealing. The prosthetist and rehabilitation professional
will consider the following when designing the prosthesis
and its components: level of amputation, shape and contour
of the residual limb, functional expectations, cognitive abili
ties, vocational requirements, hobbies/leisure pursuits, and
financial resources. Standard prosthetic texts are useful in
providing broad basic information and explanation of the
many components available and their use.34,35
Patients who have sustained severe burns and subsequent
amputations have complex, long-term impairments and face
considerable functional deficits.
Severely burned patients tend to have sensorimotor limita
tions in the intact extremities, which may affect their ability
to utilize a prosthesis. Their limitations and strengths are
important considerations when planning treatment. These
patients may exhibit muscle weakness not usually seen at
the same amputation levels in the non-burn patient. Areas
of weakness should be noted and compensation such as
increasing joint stability through alignment or componentry
should be provided. Burned individuals may use their
remaining functioning extremities differently than patients
without total body involvement. Prosthetic rehabilitation
should enhance adaptations and necessary compensatory
methods. The challenge to the prosthetist is to design a
device which is maximally useful to a person who may have
multiple limitations. To be useful, a device must be as easy
to use as possible. Simplicity often determines whether the
device is successful or discarded.
Prostheses may be preparatory or definitive. Preparatory
devices are ones fitted while the residual limb is still matur
ing. A preparatory prosthesis is provided when reduction of
patient from the traction apparatus as indicated for exercises
and ambulation and reapply the traction at the completion
of treatment. Positioning within the traction is often changed
by nurses and therapists by altering the amount of the trac
tion weights, thus preventing the affected joints from being
locked into one position over time (Fig. 47.21).
Prosthetic interventions
A prosthesis is a device used to replicate the function and
appearance of a missing limb. Amputations among the burn
patient population most often occur as a result of electrical
Figure 47.21 Skeletal traction is utilized for positioning of extensive burns
and for the protection of delicate grafts through suspension. Rehabilitation
therapists may remove the traction and ambulate or exercise patients as
needed. Traction weights may be changed to achieve different positions
within the traction system and help shift the weight of patients in bed.
Figure 47.20 (a) Banjo external fixator.
(b) Functional position external fixator.
A
B
Comprehensive rehabilitation of the burn patient
529
Table 47.1 Prosthetic components
Upper extremity
Functions
Lower extremity
Socket
Interface between prosthesis and residual limb
Socket
Selective loading/pressure relief
Suspension
Holds prosthesis to residual limb
Suspension
Force transmission for function
Control system – Usually movement
of the shoulder or chest
Links movement of a body part to the prosthesis
Control system – usually movement
of the hip or knee
Interposed elbow joint
Performance of hand to midline
Interposed knee joint
Provides support during stance phase, smooth swing phase and
motion for sitting and kneeling
Interposed wrist joint
Attaches socket to terminal device; orients terminal device in space
Shank (pylon)
Terminal device
Restores cosmetic appearance
Prosthetic foot
Replicates anatomic joints
Replaces hand/ankle function
Stable, weight bearing surface
Shock absorption
stump volume is anticipated or when fitting over a bulky
dressing is necessary. These devices are usually simple,
passive devices that allow for early motion skills and weight-
bearing through the affected limb. Some patients will con
tinue to use their preparatory prosthesis for extended periods
of time while other areas of the body are treated. Prior to
definitive fitting, body weight, residual limb volume, wear
and use patterns should be stable in order to optimize the
long-term result with the definitive prosthesis. The definitive
prosthesis is fit when the residual limb is fully mature. The
use of a preparatory prosthesis is not mandatory, but the use
of one will improve the fit and control of the definitive
prosthesis; and may, secondarily, reduce the amount of time
needed for rehabilitation post-burn injury.
Prosthetic preparation in burn rehabilitation begins in the
post-surgical phase. Early prosthetic treatment of an amputee
includes splinting for the prevention of contracture. An upper
extremity splint may extend past the distal end of the residual
limb to match the length of the whole limb, thus assisting a
patient in retaining the concept of length. Initially, therapists
must address: promotion of wound healing; pain manage
ment; residual limb shaping; prevention of contractures; skin
desensitization techniques (tapping, massage, scar mobi
lization, pressure application); edema control, and coping
mechanisms for adjustment and grief. With early socket
fitting, some skin problems will be encountered, but these
are not usually of major significance. Silicone gel or urethane
socket inserts have been used successfully for pressure relief
to burn-scarred skin. As wound healing progresses, prosthetic
training will begin to focus on care of the prosthetic device,
don/doff methods, skin inspection routines, weight-bearing
with the device, and progressive functional skills.
Just as upper extremities are different from lower extremi
ties; so, too are upper and lower extremity prostheses. The
minimum requirements for successful use of an upper
extremity prosthesis are: trunk control to support an upright
posture, sufficient upper body strength to selectively activate
the control devices, and static and dynamic balance
skills. The patient will need to be trained on specific body
movements to develop control of the upper extremity pros
thesis. Glenohumeral flexion provides excellent power and
reach for functional routines. It can be used to flex the elbow,
activate the terminal device, and for activities away from
the midline of the body. Scapular protraction is also trained
for activation of the terminal device and facilitation of
fine motor tasks at midline or close to the body. The other
motions of glenohumeral depression/elevation, extension,
and abduction are most frequently used to lock or unlock
an elbow joint.
Different types of upper extremity prostheses are available
along a continuum from mostly passive or cosmetic to pri
marily functional. Most devices fall somewhere in the middle
range between cosmesis and function. Cosmetic prostheses
are difficult to keep clean, expensive, and ultimately sacrifice
function for appearance. Functional prostheses fall into two
categories. They can be designed to be body-powered (using
cables) or externally powered (myoelectric or switch control).
Body-powered prostheses are moderate in cost and weight,
more durable, and offer higher sensory feedback. However,
they require more gross limb movement and can be
less cosmetically appealing. Externally powered prosthetic
devices allow for more proximal function, greater strength
for grasp/prehension, and improved cosmesis. Additionally,
they may be heavy and expensive, offer less sensory feed
back, and require more regular maintenance. Regardless of
the type of prosthesis planned for, fitting of an upper extrem
ity body powered prosthesis within 7–30 days correlates
with higher acceptance and success rates.36 Body-powered
prostheses are most commonly used in burn rehabilitation
and Table 47.1 describes the components of upper extremity
prosthetic devices.37,38
The rehabilitation upper extremity prosthetic goals should
include: stability of shoulder girdle to allow prehension,
overall ease of movement of the entire limb, energy efficient
use of the device, and the appearance of a normal upper
extremity. Table 47.2 describes upper extremity amputations
by level and identifies the appropriate prosthetic device to
address the patient’s functional needs.37,38
Total Burn Care
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530
The overall process of prosthetic evaluation and fitting is
described in Figure 47.22. Satisfactory use of a prosthetic
device in burn rehabilitation requires continuous dialogue
between the patient, therapist, prosthetist, and surgeon.
Return clinic visits should include consistent prosthetic
re-evaluation. However, ultimately, the use of a prosthetic
device depends largely upon patient motivation.37 Most
prostheses can be expected to last at least 3–5 years with
standard daily use. Children will need more frequent
modifications or adjustments as they grow and develop.40
In general, the simplest system which provides the most
functional–cosmetic level is accepted by the amputee as the
best choice.
Burn scar management
History
The burn wound, like any other wound, heals by the forma
tion of scar at the injured site in order to replace the destroyed
tissues. Scar is defined as the fibrous tissue replacing normal
tissues destroyed by injury or disease.41 In the case of a burn
injury, the scars, if not managed appropriately, have the
potential of becoming thick and raised, resulting in scar
hypertrophy. Hypertrophic scars are not cosmetically appeal
ing and if they cross any joints they may restrict function.
Pressure therapy for scar management is a very old and estab
lished component of a recovering burn patient’s continuing
rehabilitation program. Extensive historical notes on the ear
liest references to scarring are provided by Linares and col
leagues who attribute the first full medical description of
scars to Petz in 1790.42 They also state that the first medical
reference to the use of pressure for treatment was written by
Johnson in 1678 referring to the work of Ambroise Paré in
the 16th century.42 Other historical events noted by Linares
et al. are: first known accounts of the use of pressure for treat
The rehabilitation program for successful use of lower
extremity prosthetics begins with donning/doffing of the
device, transfer skills, activities to build wearing tolerance,
practice to reinforce balance reactions, and pre-ambulation
skills. Preparatory weight-bearing treatment for use of a
lower extremity prosthesis usually begins on a tilt table,
progressing to standing and then ambulation in the parallel
bars. The rehabilitation goals should address stability, ease
of movement, energy efficiency, and the appearance of
natural gait.39 Table 47.1 outlines the common components
of lower extremity prostheses and their functions.
Lower limb prosthetics require the following minimum
requirements for successful use: upright trunk control, suf
ficient upper body strength, adequate lower body stability
and control, static and dynamic balance skills, and good
postural alignment. Lower extremity prosthetic fitting begins
when the patient’s wounds are well-healed and will tolerate
pressure and weight-bearing. Lower limb devices may be
either preparatory or definitive. Table 47.2 details types of
lower extremity amputations by level and identifies the
appropriate prosthetic and components.37,38
Two common sequelae of traumatic amputations are
phantom sensation and phantom pain. Phantom sensation
is the perceived sense that the amputated limb is still present.
It is not typically characterized as painful by the patient. The
patient may report feeling that the amputated limb has
shrunk (telescoping). In contrast, phantom pain is the sensa
tion of pain originating in the amputated part. Upon assess
ment the pain may or may not be dermatomal in presentation.
The patient may report constant burning, stinging, cramp
ing, or a feeling of awkward positioning. Phantom pain is
most intense acutely, gradually becomes intermittent, is
worse at night, and is often exacerbated by stress/anxiety.
From a therapy standpoint, phantom sensation may be
managed by desensitization techniques, while phantom
pain may be responsive to transcutaneous electrical nerve
stimulation.
Table 47.2 Types of amputations and prosthetic needs
Types of amputations
Prosthetic needs
Upper extremity
Transphalangeal
Passive for cosmesis
Transmetacarpal
Oppositional devices
Transcarpal
Body-powered hand or hook
Wrist disarticulation
Transradial
Forearm socket, wrist component, and terminal device
Elbow disarticulation
Transhumeral
Proximal arm socket, elbow hinge (passive, active, or externally powered), forearm lever arm,
wrist component, and terminal device
Shoulder disarticulation
Harness system and transhumeral components
Interscapulothoracic disarticulation
Harness system, shoulder socket and transhumeral components
Lower
extremity
Transphalangeal
Toe disarticulation
Ray amputation
Transmetatarsal
Transtarsal
Toe-filler
Foot plate
Partial foot to tibial height prosthesis
Syme
Socket to knee, low-profile foot
Transtibial
Knee disarticulation
Socket with foot and ankle
Transfemoral
Socket, knee joint, and ankle/foot complex
Hip disarticulation
Hemipelvectomy
Socket is total contact shell, hip/knee joints, and ankle/foot complex
Comprehensive rehabilitation of the burn patient
531
Figure 47.22 Algorithm showing the process of prosthetic evaluation and fitting.
Preprosthetics
Prosthetics
Preop consultation
Postop consultation
Upper extremity
Lower extremity
Splinting
Initial stance/
ambulation
Air bag
system
Provision of
preparatory prosthesis
Additions to
Ilizarov
device for
ambulation
Ischial weight-
bearing
prosthesis-
orthosis
Cast &
measurement
Fabrication of
prosthesis
Early fitting
Postponement
factors
Limited
range of
motion
Increasing
functional
demands
Prosthetic
use/therapy
Adjustment
prosthetic
Cast &
measurement;
fabrication of
prosthesis
Contracture
prevention
Concept
of length
Definitive
prosthesis
Contralateral
U/E involvement
Bilateral
considerations
Due to increasing
range of motion
Preparatory
prosthesis
Adjustment
for growth
Finalize prosthetic
for home use
Follow-up
Adjust or replace,
improve function
RX change
Skin tolerance
Initial fitting
of prosthesis
Prosthetic use
and therapy
Adjustment of
prosthesis
Increasing
weight
bearing
Adjustment
for growth
Adjustment or replace,
improve function,
definitive prosthesis
Rx change
Increasing
range
of motion
Completion of
preparatory prosthesis
for home use
Follow-up until
definitive fitting
Skin
tolerance
Total Burn Care
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532
normal versus injured skin. In his study, Bartell showed that
scars, if left untreated, will show improvement over time.58
Hosoda utilized laser flowmetry to determine the perfusion
of hypertrophic scars versus non-hypertrophic scars.59 Other
studies suggest that laser Doppler flowmetry and monitoring
of transcutaneous oxygen tension may in the future be ways
of determining scar maturation.60
Treatment of hypertrophic scars
To this date, hypertrophic scars remain very problematic and
difficult to manage. Even though the mechanism of scar
maturation is not yet well understood, clinically the accepted
protocol to treat hypertrophic scars includes the use of pres
sure therapy, which should be instituted early on in the
maturation process of the burn scar. Means of pressure
therapy include pressure garments, inserts, and conforming
orthotics. Once the skin has healed enough to withstand
sheering, massage and heat modalities may be utilized as an
adjunct in scar management. The use of pressure in effec
tively depressing scars was well documented by Silverstein
and Larson in the 1970s; their observations and studies
sparked the near-universal use of pressure garments. When
an active scar is compressed, it blanches, which indicates
decreased blood flow in the area.61 Less blood leads to
decreased oxygen in the tissues, which in turns leads
into decreased collagen production, which brings a balance
between collagen synthesis and collagen breakdown (lysis).
When a balance in the production and breakdown of col
lagen is established, the resultant scar appears flatter.62 Kealey
et al. conducted a prospective randomized study to compare
efficacy of pressure garment therapy in patients with burns.
Patients were randomly assigned to receive either pressure
garment therapy or no pressure garment therapy. Assessment
of the maturity of scar included use of the Vancouver Burn
Scar Assessment Scale. The results on 113 patients studied in
the follow-up revealed no significant differences between
groups when age, body surface area burned, length of hos
pital stay or time to wound maturation were compared.63 In
addition to this study, other studies have reported problems
related to lack of adherence and discomfort, blistering, ulcer
ation or scar breakdown, swelling of extremities and skeletal
and dental deformity due to excessive pressures, which often
leads to stoppage of treatment, significant side-effects and
deformity.63–69
On the other hand, studies have also reported benefits of
pressure garments.70–72 The reader is referred to various recent
excellent review articles on the efficacy or lack of efficacy of
pressure garments in the management of hypertrophic burn
scars.73,74 Reasons for the absence of unequivocal evidence is
that garments must be worn continuously for a least 23 h a
day, making compliance or adherence difficult.66,75,74 In addi
tion, the optimal pressure that must be applied to the scar
for treatment is not known.66,76–78 Thus, the studies and
debates continue, and, at least until more evidence is gath
ered, pressure therapy with the familiar elastic garments
is still prescribed. Patients and families would no doubt
feel relieved if the data eventually show that pressure does
not make a significant difference in long-term outcomes.
However, it should be noted that the studies thus far include
neither the examination of burns over joints nor do they
include burns of the hands, neck and face. In addition, none
ment of children in 1859; use of elastic bandages in 1860;
adhesive plaster for pressure in 1881, and use of traction to
treat scars in 1902. Linares’ review includes descriptions of
Nason’s work in 1942, in which he noted that ischemia
produced by pressure arrests the overproduction of scar
tissue, ‘where the imprint of the elastic of an undergarment
or a belt may be seen – no keloid is present.42 Another histori
cal review by Ward43 reveals that Blair in 1924 reported the
positive influence of pressure on healing wounds. Nason’s
application of the ‘constant pressure’ principle included
developing a type of neck splint made of a piece of dental
impression compound or a piece of heavy felt strapped
tightly over the scar for 6–8 weeks and possibly longer. Later,
various splints were developed utilizing pressure and immo
bilization.44 In the 1960s Silverstein and Larson observed the
influence of pressure on healing burns. Their observations
led to the manufacture of customized pressure garments that
revolutionized scar management in the 1970s, which contin
ues to-date, with some modifications.42,43
The scar
As the burn wound progresses toward healing, or after skin
grafting operations take place, scars begin to form. Generally,
the deeper the burns are, the higher the risk is for the devel
opment of hypertrophic scars. Also, the longer a wound
remains open, the higher the chances for hypertrophic scar
formation.44,45 As the wound begins the healing process, col
lagen fibers develop to bridge the wound, forming an imma
ture (active) scar, which appears as a red, raised and rigid
mass.46–49 Abston reported that pressure therapy during mat
uration led to a flatter, softer and a more devascularized
scar.50 Burn scars may take up to 2 years or longer to mature.
Factors contributing to the formation of hypertrophic scars
may include: wound infection, genetics, immunological
factors, repeated harvesting of donor sites, altered ground
substance, age, chronic inflammatory process, location of the
injury, and tension.51 Scar hypertrophy may be evident at
8–12 weeks after wound closure.52
Scar assessment
Devoting clinical time to evaluate burn scars can be time
consuming, but is imperative to our practice for efficiency in
the remodeling and overall function of the burn scar. In
order to better study the process of scar maturation, ongoing
research is looking at alternative techniques in assessing the
state of scars. The Vancouver Burn Scar Assessment devel
oped by Sullivan and colleagues is a subjective way of rating
the burn scar pigmentation, vascularity, pliability and height,
and is widely used amongst clinicians.53,54 Hambleton and
colleagues studied the thickness of scars with ultrasonic
scanning. This method, which is completely non-invasive,
allows for a comparison of the thickness of dermal tissue in
the traumatized area with that in the normal skin at regular
intervals following initial healing.55 Darvey et al. described
a technique for the objective assessment of scars utilizing a
video camera image on a computer and quantitatively ana
lyzing the color of the scars using a custom-written computer
program.56 Esposito used a modified tonometer to measure
skin tone which correlates to skin pliability and tension.57
Bartell and co-workers used the elastometer properties of
Comprehensive rehabilitation of the burn patient
533
elastic by cutting holes into it will alter the pressure gradient
provided by these materials. The tubular elastic bandages
should be doubled over the skin surface area treated in order
to provide adequate pressure.83 Early pressure application
over the hand and digits can be accomplished by the use of
thin, elastic and self-adherent wraps such as Coban™ (Fig.
47.23). This form of pressure is excellent for adult and pedi
atric patients for controlling edema and aids in the early scar
management of hands when the shearing forces of a glove
cannot be tolerated. Small children are excellent candidates
for Coban™ gloves versus a garment glove because of compli
ance issues, comprehension of instructions in assisting with
the application of a custom glove and difficulties in obtain
ing accurate measurements for a custom glove. Coban™ may
be applied over the burn dressings or directly onto the
healed digits. The burn therapist needs to be aware that if
Coban™ is wrapped too tight it may deform the interosseous
structures of the healing hand. However, if Coban™ is
wrapped too loose it may encourage swelling of the hands
when used in combination with arm elastic garments.
Coban™ strips are pre-cut approximately twice the length of
the digits to be wrapped. Each strip is wrapped in a spiral
fashion beginning at the nail bed of each digit, overlapping
half of the Coban™ width and ending in the adjacent web
space. Each fingertip needs to be exposed so that blood cir
culation can be monitored at all times. The Coban™ is
stretched from 0–25% of the entire elasticity of each strip.
Once all web spaces are covered, the rest of the hand is
wrapped with Coban™, extending approximately 1 inch past
the wrist joint. No skin areas should be visible once the
Coban™ glove is completed. If small hand areas remain
uncovered, a small piece of Coban™ is stretched over the area
and adheres to the rest of the Coban™. When the glove is
completed, the therapist should very superficially lubricate
the entire glove with lotion in order to eliminate the adher
ent effect of the Coban™ and allow for the functional use of
the hand. Coban™ should be removed on a daily basis by
the therapist or the caregiver. Removal of Coban™ should be
done carefully by cutting off or unwrapping each digit strip
individually to avoid disturbing any small wound healing.
The use of prefabricated interim pressure garments is widely
of the studies to date address the use of pressure in the form
of splints, another source of discomfort and tension for
burned children and their families.
None of the known studies yet have broached the face with
an attempt to determine the efficacy of pressure versus no
pressure. Facial pressure garments in children may pose
problems due to interference with growth.79,80 We recom
mend that these patients should be closely monitored for
normal facial and dental development by physicians includ
ing dental specialists. The elastic hood and underlying sili
cone face pad present special problems for patients, and
some extreme challenges for the adults trying to assist a
burned child or adolescent. The elastic mask and hood,
covering head, face, and hair, effectively hides the identity of
the person wearing it. It is perceived by children as sinister,
associated with ‘bad men’ or monsters, and most children
who have worn this garment can relay stories of being ridi
culed by strangers who did not know the purpose of the
garment. Emotional expressiveness, usually apparent in
facial movements, is hidden by the hood. More than one
child has explained non-adherence with the prescribed
wearing of the elastic mask with a statement similar to ‘I
want my friends to see me laugh.’ A study by Groce et al.
compared the elastic mask and hood with silicone pad to
the transparent silicone face mask and found no significant
differences between the amount of pressure applied by each
to the forehead, cheeks, and chin.81 Many children have
expressed a preference for, and seem to wear more readily,
the transparent mask. This study should make it easier for
them to be granted their choice – an important event during
a time when so much is happening to them outside of their
control.
Pressure therapy
As long as the scars are active, they may be influenced by
pressure therapy. However, not all burn scars require pres
sure. Patients with burn wounds which heal within 7–14
days do not need pressure therapy. Those patients whose
wounds heal within 14–21 days are closely monitored for
pressure therapy needs and may be generally advised to use
pressure garments prophylactically. A wound that heals after
21 days will require the use of pressure garments.62 The
correct amount of pressure in suppressing the hypertrophic
scar has not yet been determined. Pressure of as little as
10 mmHg may be effective in remodeling the scar tissue over
time. Pressures over 40 mmHg, however, may be destructive
to tissues and cause paresthesias.52 Early forms of pressure
therapy include the use of elastic bandages directly applied
on the newly healed skin or on top of the burn dressings.
The use of conforming thermoplastics along with elastic
bandages may also be utilized as means of early pressure
therapy.82 Once the wounds are almost or completely closed,
tubular elastic bandages such as Tubigrip™ may be utilized.
These tubular bandages are offered in different sizes and
accommodate all anatomical circumferences. Care should be
taken in applying these tubular bandages so that the fragile
skin or the freshly applied skin grafts do not shear, or the
minimal dressing underneath is not disturbed. The burn
therapist should be aware that these tubular bandages are
materials made of a single elastic thread spiraling through
the weave of the fabric, and disturbance of the continuous
Figure 47.23 A Coban™ wrap can be used to decrease edema and aid in
the effective management of hand scar hypertrophy.
Total Burn Care
47
534
should choose a reputable company that provides excellent
service and support for the patient and the therapist. The
company’s willingness and flexibility to manufacture non-
standard garments, availability of special options, cost and
turnaround time should be taken into consideration when
selecting the burn center’s pressure garment provider.86
Inserts
Inserts are widely utilized in burn rehabilitation as an
adjunct to achieving effective pressure over certain anatomi
cal locations where pressure garments do not provide ade
quate pressure. These locations include concave body areas
such as the face, neck, antecubital fossae, sternum, palm of
the hands, web spaces, upper back and arches of the feet.
These materials come commercially prefabricated or may be
custom-made by the burn therapist or the medical sculpture
technician. Inserts come in different forms such as silicone
gels, elastomers, putties mixed with a silicone catalyst, skin
care silastic pads, foam and even in the form of hard ther
moplastic materials contouring to different anatomical loca
tions. The experienced burn therapist chooses the appropriate
insert material best suitable for the patient according to the
stage of scar maturation and skin sensitivity. Generally, pres
sure therapy begins with a soft, thin and elastic insert and
progresses to a more rigid insert in depressing the more
unyielding burn scar. Inserts need to be worn underneath
pressure garments, starting with a few hours of application
and progressing as tolerated, toward a 24-hour application.
They should be removed frequently for cleaning (warm
water and soap), drying and application of cornstarch to
avoid scar maceration and skin breakdown. Patients may be
allergic to certain insert materials so the burn therapist may
try different inserts until one is found to be best tolerated by
the patient’s skin. In cases of scar maceration, blisters, skin
breakdown, contact dermatitis and a rash or an allergic reac
tion, inserts should be removed until healing occurs. Sili
cone, a polymer, based on the element silicon, appears to be
the trend in the treatment of hypertrophic scars. To date, the
mechanism of how silicone affects the burn scar is not
known. Clinically, silicone has been observed to depress the
height of hypertrophic scars, prevent shrinking of fresh skin
grafts (hard elastomer silicone pads versus silicone gel pads),
and increase the pliability of a scar, thus allowing for increase
in the range of motion of affected joints. Patients report that
silicone is soothing to the skin and aids in decreasing pain.
Silicone, being occlusive, may cause the collection of exces
sive moisture and cause skin maceration if not removed
frequently for cleaning and drying. Its disadvantages are that
it is very expensive and short-lived.87–89 The therapist should
look for silicone gel pads with a non-shearing protective
medium on the non-skin surface in order for the gel to last
longer. Also, buying larger-size gel pads and cutting them to
fit the patient’s need may be a cost-effective method for
today’s shrinking clinic budgets.
Other insert materials include liquid silicone elastomer,
which when mixed with a catalyst form a solid but elastic
insert (Fig. 47.25). The experienced therapist could create
custom inserts for difficult anatomical locations such as the
face and web spaces using this technique. Prosthetic Foam™
is a liquid-based silicone elastomer which, when mixed with
a catalyst, solidifies in the form of a very pliable foam insert
accepted and utilized in burn rehabilitation. These garments
are available commercially by different companies and they
include pieces for the entire body. Interim garments which
are made of softer materials introduce the burn patient to
circumferential pressure and protect the newly healed skin.
Another reason for using these garments prior to ordering
custom-made garments is to allow for the patient’s weight
to stabilize (post-acute hospitalization) and any remaining
edema to subside. In some cases where obtaining custom-
made garments on regular intervals (approximately 12
weeks) is not an option the recommendation should be that
interim garments should be the choice for long-term pres
sure therapy. Once the patient’s weight has stabilized, edema
has subsided and the skin is able to withstand some shearing
(approx. 3–4 weeks post-wound closure), measurements are
taken for the fabrication of custom-made pressure garments
(Fig. 47.24). Today several companies specialize in the fab
rication of these garments. Clinically, custom therapeutic
pressure for the prevention, control and correction of scar
hypertrophy averages 24–28 mmHg, which is approximately
equal and opposing to the capillary pressure (25 mmHg). At
this pressure level, many researchers believe that scars may
be altered.84 In order for pressure therapy to be effective,
pressure garments need to be worn at all times, day and
night. They should only be removed for bathing and on
occasion during exercises should they interfere with move
ments. Each order is duplicated so one set of garments can
be worn while the other is being washed. Today, pressure
garment companies offer multiple colors of materials and
for the pediatric population cartoon characters may be
sewed on the garments to make them cosmetically appealing
and improve the patients’ compliance.85 The burn therapist
Figure 47.24 Custom-made pressure garments may be fabricated for the
entire body.
Comprehensive rehabilitation of the burn patient
535
A silicone elastomer facemask may be created utilizing the
existing positive facial mold and is worn under facial pres
sure garments (Fig. 47.26b). The use of the clear and silastic
masks is preferred over the use of just a facial garment as
they provide conforming pressure around facial openings
(eyes, nose, and mouth). Frequently, the burn therapist
manufactures the clear mask to be worn during the day and
the silastic mask along with the facial garment to be worn
at night.42,90–92
Burn scar massage
Once the burn scars have matured enough to tolerate shear
ing forces, massage may be incorporated into the scar man
agement regimen. Scar massage is an effective modality for
maintaining joint mobility in the case of contractures. It aids
in softening or remodeling the scar tissues by freeing
adhering fibrous bands, allowing the scars to become more
elastic and stretchy, thus improving joint mobility. Initially,
the therapist may utilize a non-frictional massage applying
mostly stationary pressure to skin blanching and mobilizing
the skin surface without friction. Utilization of lubricants
during this massage technique should be avoided. As the
skin begins to tolerate frictional massage, the scar tissue is
manipulated in rotary, parallel and perpendicular motions,
using a lubricant and pressing the skin to blanching. Clini
cally, massage is found to alleviate itching. It is also used for
desensitization purposes. An electrical massager with a heat
attachment may be used along with lubrication, as heat and
massage in combination may increase scar pliability. Massage
should be performed at least twice daily (3–5 times pre
ferred) for 5–10 min on each treated body surface. The burn
therapist should frequently assess the skin condition in
avoiding further injuries. The patient and/or family are
instructed on home massage techniques and electrical mas
sagers may be issued for home use. In order to combat the
effects of scar tissue, a burn therapist must utilize all options
to achieve a functional outcome. Even though under-
utilized, therapeutic modalities should be employed in
a rehabilitation therapist’s treatment plan for scar
that works best for the palm of the hands where function
needs to be preserved while pressure is applied. These foam
inserts also work best for applying pressure to contour sur
faces on the face (around eyes, mouth, and nose), while
protecting these sensitive areas from excess and rigid pres
sure. Elastomer putties such as Otoform K™ or Rolyan
Ezemix® form semi-rigid but still elastic inserts for different
areas of the body where the scar can tolerate more pressure
such as in the web spaces to prevent syndactyly.88 Early on
in scar management, a soft foam such as Plastizote®,
Velfoam™ or Betapile™ may be utilized to apply gentle pres
sure to the very fragile and sensitive scar.
High thermoplastic transparent masks were developed in
1968 by Padewski to be applied directly to the face to
prevent, control and reverse scar hypertrophy. These masks
require the moulaging of the patient in creating a negative
facial mold. A positive mold of the face is fabricated with
the use of plaster. The patient’s positive facial mold is then
‘sculptured’ in an attempt to recreate the patient’s non-
burned face. A high thermoplastic material such as Uvex™ or
W-Clear™ is then pulled over the positive mold in order to
create the hard plastic mask (Fig. 47.26a). Holes for the eyes,
nose and mouth are cut. The mask is worn under pressure
garments or with a head strapping mechanism. The use of
three dimensional scanners can also be used to replace the
traditional methods of face mask fabrication. Using a scanner
greatly reduces patient anxiety by achieving the same accu
racy as moulaging in a fraction of the time without physi
cally touching the patient’s face. The scan is ‘sculptured’ on
a computer and a positive tool is manufactured out of foam
off site. The positive tool is then sent to the facility for mask
fabrication. In the past, scanners were so large that facilities
had to have an entire room dedicated to its use, whereas
scanners now are small enough to fit in a portable case and
are run by laptops. These newer portable scanners enable a
therapist the freedom to scan patients in any setting in the
hospital including intraoperatively. In cases of significant
scar hypertrophy on the face, the positive mold is ‘sculp
tured’ sequentially over a period of time in order to avoid
excessive pressure over facial scar leading to skin breakdown.
Figure 47.25 Silicone elastomer inserts for the dorsum of the hand and
web spaces are utilized for the prevention of syndactyly and depression in
scar tissue.
Figure 47.26 (a) A Uvex™ clear face mask provides pressure to the face so
as to prevent scar hypertrophy and to preserve facial features. (b) A silicone
elastomer face mask provides pressure to the face in preventing facial scar
hypertrophy and preserving facial features.
A
B
Total Burn Care
47
536
lubrication and other therapeutic scar management proce
dures to be performed by the patients and their caregivers.
Lubricants, which do not contain perfume and other skin
irritants should be selected and applied (at least 2–3 times
daily) to the healing skin. Lubricants with sun protection
factor (SPF) of at least 15 are recommended.101 Written
instructions with pictures and diagrams along with videos
addressing scar management should accompany the patient
home upon discharge from the hospital. Follow-up visits to
the burn or rehabilitation clinic for the assessment of overall
recovery to include garments, inserts and other home thera
peutic interventions are needed for the patient to success
fully complete his/her burn rehabilitation. The therapists’
knowledge, creativity and continuing research in improving
the currently existing scar management techniques may be
the key to positive outcomes in pressure therapy.
Therapeutic exercise
Burns often result in devastating injuries that severely impact
a person’s ability to perform functional activities through
severe deconditioning, range of motion limitations, weak
ness, and fatigue.102,103 Therapeutic exercise is one of the
central interventions used by physical and occupational
therapists to combat the multitude of problems associated
with burn injuries. Therapeutic exercise is defined as scien
tific supervision of bodily movement with or without appa
ratus, for purpose of restoring normal function to diseased
or injured tissues.104 The use of therapeutic exercise in con
junction with a comprehensive rehabilitation plan helps to
prevent deforming contractures and to maintain strength in
both the involved and uninvolved extremities.105
Even though painful and extensive therapy is required
during the long rehabilitation process, the results are for the
most part dependent on the patients’ and families under
standing, involvement and dedication to the treatment.94
The goals of therapeutic exercise in burn rehabilitation
are to:
•
reduce the effects of edema and immobilization;
•
maintain functional joint motion and muscle strength;
•
stretch the scar tissue;
•
return the patient to optimal level of function.
Exercise prescription is an ongoing process which is altered
according to the patient’s medical status and changing
needs.106 In the conservative treatment of burn wounds, a
vigorous physical therapy program is instituted immediately
so as to maintain function.107 Postoperatively, exercises
involving autografted skin over joints are usually discontin
ued for 4–5 days. Escharotomies, fasciotomies, heterografts,
and synthetic dressings are not contraindications for exer
cise.108 Early mobilization to decrease edema, proper exercise
techniques, and accurate documentation of function are
more important than the type of wound closure.107
One of the most common and clinically significant com
plications after severe burn injuries are burn scar contrac
tures which lead to decreased range of motion and joint
deformities.103 Scar contracture and joint mobility limita
tions are the result of the shortening of immature connective
tissue. Therapy aims to prevent deformity and the
subsequent limitation of movement. In circumferential
burns, both the flexor and extensor surfaces are at risk of
management. Therapeutic heat is the most common modal
ity used in burn scar management. Application of heat may
permit easier elongation of scar tissue through increased
extensibility of connective tissue.93 Heat relaxes tissues and
makes them pliable in preparation for mobilization. Heat
modalities may include hot packs, paraffin wax, fluidother
apy and ultrasound. Even though the use of therapeutic heat
as an adjunct to rehabilitation is well documented, thera
peutic heat modalities are infrequently being utilized in
burn rehabilitation.94,95
Caution should be used in the application of heat modali
ties on patients who have sustained a burn injury. Patients
may not be able to tolerate heat over areas of healed or
grafted burns due to hypersensitivity. Conversely, patients
with diminished sensation are unable to determine if the
temperature is appropriate and are at risk for further injury.
Although caution needs to be taken, the use of therapeutic
heat in burn patients can provide an effective method of
increasing burn scar extensibility.
The use of passive stretch in conjunction with therapeutic
heat greatly increases the effectiveness of the treatment.
Studies have shown that the use of therapeutic heat during
a slow load prolonged stretch is an effective method
for attaining rapid and lasting increases in range of
motion when compared to low load prolonged stretch
alone.96 Warren et al. reported that low loads for prolonged
periods of time were found to produce significantly greater
residual length in rat tail tendon, especially at elevated
temperatures.97
Hot packs can provide superficial heat to burn scars and
assist with stretching contractures. Common treatments in
burn rehabilitation include using hot packs alone before
treatment or in conjunction with therapeutic exercise such
as active range of motion or prolonged stretch. Because of
the shallow depth of heat penetration, hot packs may have
little effect on deeper layers of scar tissue.93
Ultrasound has been used by rehabilitation therapists to
increase temperatures deep within the tissue. Reported ben
efits of ultrasound in the treatment of burn scar include
increased extensibility of collagen tissue, increased blood
flow, and elevation of pain thresholds.93 Application of
topical therapeutic ultrasound to scar tissue has been
reported to produce a tissue temperature rise, which leads to
an increase in the extensibility of collagen.98 The combina
tion of ultrasound and passive stretch was found to further
increase tissue elongation.93
Paraffin is an effective heat modality used most commonly
for the hands or feet. Paraffin provides extensibility on col
lagen produced by the heat and may also be beneficial
because of the softening of the scar by the mineral oil in the
paraffin.93 The use of passive stretch in conjunction with
paraffin has been shown to increase joint range of motion
and was found to make patient’s skin noticeably softer and
more pliable after the use of paraffin.99 Similar to other
heating modalities, paraffin has been found to increase
range of motion in conjunction with stretching compared to
stretching alone.100
Burn scar management is a complicated and lengthy
process and for it to be successfully completed the patient
and caregivers should be committed to follow the therapist’s
recommendations. Extensive training should take place
addressing the use and care of pressure garments, inserts,
Comprehensive rehabilitation of the burn patient
537
physiological and psychological needs, rather than passive
range of motion.112 Although active range of motion may be
a superior form of exercise for a burn patient, its use during
the acute burn phase may be somewhat limited. Medical
status, intubation, as well as fear and anxiety may all make
active range of motion exercises difficult to carry out.
If a patient can actively participate in movement but
cannot move actively through their full range of motion,
active-assistive range of motion is appropriate. Active-
assistive range of motion exercises utilize the same principles
as active; however, a patient is ‘assisted’ by an outside force
(therapist or assistive device) to achieve the full range of
motion. A patient will achieve improvements in strength and
range of motion, but not equal to those provided by active
exercise. Therapists should use their judgment in letting the
patient perform as much of the exercise as possible actively
and only assisting when needed.
While active range may be the most beneficial, it can
be difficult to initiate after admission due to the patient’s
medical status and level of responsiveness. Critically ill,
septic, and heavily medicated patients are often unable to
cooperate in active exercises.106 In these conditions, passive
exercise is used to maintain range of motion, assess joint
motion, and elongate tissue.113 Passive range of motion exer
cises are an important factor in preventing contractures and
maintaining range of motion when a patient cannot or does
not willing actively move through their available range of
motion. Although passive range of motion requires less
energy expenditure, it does not fulfill as many of the patient’s
needs as active exercise.112 The use of a continuous passive
motion (CPM) device has been documented to be an effec
tive modality for improving joint range of motion.108 Reha
bilitation advances have shown CPM treatment to be a viable
option because of its benefits to soft tissue remodeling, joint
nutrition, wound healing, and venous dynamics.114,115
Strengthening exercises are of great importance through
out the continuum of burn rehabilitation to combat muscle
atrophy and can begin during the acute rehabilitation phase.
Resistive exercises are used to maintain or increase strength,
range of motion, proprioception, and coordination.116 Due
to patients’ level of consciousness and comprehension
during the acute rehabilitation phase strengthening exercises
may be difficult to institute and should start with simple
exercises progressing as the patient’s status improves. Isomet
ric exercises are beneficial to maintain muscle strength when
a patient is on bed rest and is comfortable for the patient
to perform while requiring a minimal amount of energy
expenditure.113 The benefit of isometric exercise is that a
patient does not ‘forget’ how to contract the muscle, a
common phenomenon with periods of prolonged immobi
lization. Isometric exercise also helps in maintaining muscle
strength. Manual resistance can also be applied gently by the
therapist as the patient contracts his muscles and attempts
motion against the resistance, or the patient is asked to
maintain a position then resistance is applied.106
Another important aspect of a patient’s recovery is the
ability to ambulate. Ambulation can begin as soon as pos
sible after admission as long as the patient is medically
stable.116 Severe weakness, impaired motor control, decreased
cognitive status, pain, risk of graft shearing are all factors that
can make a ambulation a difficult task.117 An Unna boot may
be applied at time of skin grafting to the lower extremity and
contracture. Therapeutic exercise in conjunction with
splinting should promote agonist and antagonist move
ments around those joints in order to maintain mobility.109
Treatments are tailored to each individual patient, with inde
pendent living being the ultimate goal throughout the reha
bilitation continuum.
Therapeutic exercise begins immediately after the burn.
For a patient being treated conservatively, movement helps
maintain strength and range of motion, and aids in circula
tion and healing. Exercise is initially painful and the very
first repetition is often the most difficult. Discomfort is
due to stretching skin which has lost its natural lubricating
mechanism and has become dry and tight. Movement
itself decreases pain. Each subsequent repetition will be
easier as the skin stretches, and the muscle pumping action
of active movement helps resolve edema, thus significantly
reducing pain.
To show the progression of exercise throughout a patient’s
stay after a burn injury, exercise will be discussed in terms
of the rehabilitation phases as described by Richard.110
Exercise during the acute rehabilitation phase
The acute rehabilitation phase is defined as the time from
admission until about the time that a patient’s wounds are
50% closed or skin grafting for wound closure has begun.110
Early therapeutic intervention on the burn unit has long
term implications for restoration of function.102 Early initia
tion of burn rehabilitation with an emphasis on several
factors including early ambulation and a focus on preventing
joint contracture through stretching exercise has been shown
to be effective in reducing contractures.111
During the early part of the acute rehabilitation phase,
exercise goals are resolution of edema, maintenance of joint
mobility, and prevention of respiratory complications which
can often be performed without interfering with life saving
measures.106
During this phase, patients spend long periods of time
without getting out of bed due either to their medical status
or postoperative immobilization after skin grafting. Results
of patient immobilization due to burn injury include
decreased
cardiovascular
fitness,
disuse
osteoporosis,
increased risk of thromboemboli, pulmonary complications,
decubiti, and muscle atrophy.106 Due to the patient’s medical
status during the acute rehabilitation phase, patients may
not be able to tolerate vigorous exercise. It is therefore rec
ommended that exercise programs focus on increased fre
quency of treatment sessions that are shorter in duration.
Active range of motion exercises are significant in the
reduction of edema in the extremities and can begin within
24–72 h after burn injury.106 Active range of motion exercise
is performed independently by a patient. This is the form of
exercise most recommended because it stretches healing skin
and provides strength-inducing benefits. Frequent exercise
performed actively (with voluntary muscle contribution) by
a patient promotes the greatest increase in movement. Active
range of motion exercises are vital during burn rehabilitation
to counteract the effects of prolonged bed rest and muscle
atrophy as well as maintain range of motion and prevent
contractures. The best exercise for a joint affected by
burns is complete active range of motion.105 Active range of
motion more adequately addresses the patient’s functional
Total Burn Care
47
538
certain place. Children do well when provided with a desired
incentive such as a toy or a game. Frequent rest periods
may be necessary secondary to decreased endurance levels
or pain.
Exercise during the intermediate
rehabilitation phase
The intermediate phase is the time surrounding closure of
the wound and extending up until the time of complete
wound closure.110 The prevention of functional impairments
becomes the focus of therapeutic exercise as patients begin
to achieve wound coverage. The goals of exercise during
this timeframe include the stretching of healing skin,
maintaining full joint range of motion, preserving motor
skill coordination, promoting functional independence, and
maintaining strength and endurance to minimize muscle
atrophy.106
As wounds close, scar formation begins which leads to
contractures that limit range of motion and impede function
which makes exercise become even more important. As a
patient’s medical status continues to improve and operations
become less frequent, more time can be allotted to
spend with rehabilitation. Increased alertness and improved
medical status also lead to increased involvement of the
patient in rehabilitation. As the patient advances medically,
the therapeutic course should become more challenging.
While pure passive range of motion should be utilized
less during the intermediate phase of rehabilitation due to
increased ability of the patient to move actively, it still serves
an important purpose. Passive range of motion provides an
opportunity to assess joint movement and determine if the
patient can attain as much movement actively as the thera
pist can passively.116
Another form of passive movement that can be utilized by
a rehabilitation therapist is the sustained stretch. Sustained
contribute to early patient ambulation. The Unna boot is a
bandage impregnated with calamine lotion and zinc oxide
which, when applied over the grafted lower extremity (six
layers), hardens to a semi-rigid dressing resembling a plaster
cast. This cast-like total contact dressing provides uniform
support to the fresh skin graft and when reinforced with a
thermoplastic or plaster splint facilitates early ambulation.
An Unna boot may be applied for up to 7 days post-grafting,
though it could be removed earlier for the inspection of the
skin graft. If removed, a new Unna boot needs to be fabri
cated depending on the burn center’s lower extremity post
operative immobilization protocol.118
Primary goals of ambulation include maintaining lower
extremity range of motion, reducing the risk of throm
bophlebitis, preventing decubiti, providing mild cardio
vascular conditioning, and maintaining or increasing
strength and endurance.106 Ambulation exercises may also
help prevent decubiti, provide mild, cardiovascular condi
tioning, and increase appetite. In addition, ambulatory
patients have fewer problems with lower extremity contrac
tures and physical endurance.108
All wounds must have the proper dressings prior to ambu
lation. Lower extremity burn wounds should be wrapped
with elastic bandages in order to facilitate capillary support.
Wrapping which incorporates the figure-of-eight pattern has
been reported to provide better pressure than the spiral
wrap, perhaps due to increased vascular support.119
As with other exercise, proper positioning facilitates proper
gait.109 The patient who has been allowed to assume a posi
tion of comfort will have difficulty extending the hips and
knees during ambulation. The ankle may be tight, limiting
plantigrade position when in the upright position. If the
joints are in the normal alignment, the amount of pain and
energy are greatly reduced.
In the past, it was common practice to have patients placed
on bed rest for long periods of time after autograft applica
tion to the lower extremities, approximately 5–10 days after
autograft application.120–122 More recently however, there
have been several studies that have shown the benefits of
earlier postoperative ambulation.121,123–126
The proposed benefits of early ambulation include:
decrease in the incidence of pulmonary embolism, deep vein
thrombosis, and joint stiffness, as well as a shorter hospital
length of stay.123 Other benefits include maintaining strength
and endurance, increased independence, a decrease in fear,
and fewer complaints of pain.125
In preparing for ambulation, therapists may use a tilt table
with patients who lack the capacity to stand and mobilize
their lower extremities (Fig. 47.27).119,127,117,128 Tilt tables pro
vided passive weight-bearing with no active muscle contrac
tion needed. Tilt tables provide gradual weight-bearing
through the lower extremities and is also an effective treat
ment for orthostatic hypotension.117 However, therapists
should keep in mind that a tilt table represents a mostly
passive introduction of gravity to the body and does not
promote proper alignment of the musculoskeletal system.
Creative efforts and aggressive techniques are sometimes
necessary to encourage ambulation in patients that first
appear incapable or unprepared to begin erect weight-
bearing exercise.
Patients tend to perform much better when given an
achievable goal such as walking a specific distance or to a
Figure 47.27 The tilt table may be utilized prior to ambulation for those
patients who may have difficulty assuming the upright position.
Comprehensive rehabilitation of the burn patient
539
rather than strengthening the patient as normal healthy
muscle is unable to generate the force required to elongate
burn scar tissue.113
The role of exercise physiology
in burn rehabilitation
Exercise for the outpatient
This section describes methodology used in designing an
exercise-training program for persons with severe burns that
have been discharged from the hospital. Exercise training is
defined here as ‘a planned, structured and repetitive body
movement done to improve or maintain one or more com
ponents of physical fitness.132,133 The evidence for the use of
exercise in the outpatient setting and the methodology pre
sented here is based primarily on the outpatient exercise
program that is implemented in severely burned children
at Shriners Hospitals for Children in Galveston, Texas and
in some severely burned adults.134 This exercise program
is supplemented by physical and occupational therapy.
The program has proven beneficial in children 7–18 years of
age.134,135 Recently, effects of a music- and movement-based
exercise program on children younger than 7 years of age
has been assessed in a pilot study at Shriners Burns Hospital
in Galveston, Texas. The effects include increases, as well as
maintenance, of range of motion in children that partici
pated in a movement and music program versus those that
did not. The principles in designing an exercise program in
children and adults with severe burns is based largely on
guidelines offered to healthy, non-burned children and
adults (Fig. 47.28).132,133,136–139
Exercise evaluation
It is important to perform an initial evaluation of risks
factors and/or symptoms for various chronic conditions con
comitant to the burn. These include pre-existing conditions
stretch becomes an important intervention as the formation
of burn scars lead to contractures.
Sustained stretching exercises are performed with a slow,
prolonged force. Gentle, sustained stretch is more effective
than multiple repetitive movements in gaining length of
burned tissues. Slow sustained stretch is considered to be
one of the most effective methods to combat the strong
destructive forces that lead to contracture formation.129 Con
nective tissue has the characteristic of plastic elongation
under constant tension. Therefore, correction of contractures
around joints can be accomplished most effectively by the
application of prolonged stretching to the shortened connec
tive tissues.130 When applying a sustained stretch, two factors
may be considered when applying pressure to an extremity:
blanching of the scar tissue and the patient’s response.116
While this is an effective treatment for range of motion limi
tations, it can be uncomfortable or painful for patients. It is
important to impart enough force on the affected extremity
to produce plastic elongation without causing trauma to the
tissues or to the patient
Strengthening exercises move from manual resistance
towards the use of weights and resistive tubing. Areas to be
concentrated on should include areas of weakness found
during strength assessments as well as muscles opposing scar
tissue contractures.113
Concerning ambulation it is important that the therapist
set goals daily for the patient to achieve and to progress the
patient to walk further while providing the least amount of
support needed. As the patient begins to ambulate more, it
is important that the rehabilitation therapist frequently
assess the patient’s gait. Any gait deviations must be identi
fied and corrected before they become lasting habits.
As the patient begins to ambulate further with less assist
ance, they become more confident in their abilities. Increased
independence provides the patient with a sense of functional
independence.112
Long-term rehabilitation phase
The long-term phase occupies the timeframe from wound
closure or discharge from the acute hospital setting until
such time that a patient has received maximal benefit from
rehabilitation services.110
As the patient nears discharge from the acute hospital
setting, the patient will be given more responsibility over
their exercise program. As the patient progresses, they will
be expected to perform beyond their daily rehabilitation
treatment sessions. Patient compliance with home exercise
programs is vital to increasing functional independence.
During the long-term rehabilitation phase, patients should
progress to ambulating independently community distances.
Gait pattern should be refined to become more efficient
without any gait deviations. If the patient is able to progress
further, rehabilitation therapists can challenge the patient by
having them ambulate on uneven surfaces, navigate around
various obstacles, and climb stairs. It is important that the
patient be able to ambulate in their normal surroundings,
not just in the confines of the rehabilitation department.
Most burn rehabilitation programs emphasize functional
gains and prevention of contractures with only modest atten
tion to aerobic conditioning.131 If ROM is lacking, the thera
pist’s priority should be to treat the limitation in motion
Figure 47.28 Basic diagram depicting various components involved in the
design of an exercise program.
History of medical problems
History of physical activity (pre-burn)
Present medications
Exercise evaluations
Generate problems and realistic objectives
Formulation of a plan: safe, fun
and effective
• Intensity: 45% to 95% of HRR
• Duration: 20 to 60 minutes
• Frequency: 3-5 days per week
• Mode: Involves large muscle groups, rhythmic, sustained
• Progression: Variable, based on goals, pain tolerance
Assessment
Interpretation
Prescription
Total Burn Care
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540
tests such as gait analysis, balance time or reaction time.
Finally, assessment of functional performance can also be
done such as sit-and-stand scores, timed walk/jog and or
lifting. The results of these evaluations will be used to iden
tify major problem areas, to write an exercise prescription or
to design the exercise program, and to assess progress during
and after an exercise program.
Exercise testing
The objectives for exercise testing involve many factors. The
primary objectives during cardiopulmonary testing are to
evaluate physical work capacity and cardiorespiratory or
aerobic fitness, observe cardiorespiratory and metabolic
responses, establish bases for an appropriate exercise pre
scription, and assess changes in fitness due to exercise train
ing. The primary objectives during muscular function and
testing include measuring muscle strength (absolute and
relative to body weight), measuring antagonist/agonist
muscle ratios, assessing changes in body composition (lean
mass, fat mass, and bone density), and providing a basis
for the progressive resistance exercise prescription. Exercise
testing should be conducted prior to the start of any exercise
rehabilitation program and again at the end to evaluate its
efficacy. Sometimes, if the program is of long duration, a
mid-point evaluation can be done. It is important to con
sider the patient’s developmental maturity when performing
exercise testing and training. We recommend a chronological
age of ≥7 years, although children as young as 3–4 years of
age have been tested.147
Peak Oxygen Consumption or Aerobic Exercise Capacity. All
patients should undergo a standardized exercise test for
objectively evaluating peak aerobic exercise capacity. We
use the treadmill exercise test and the modified Bruce tread
mill protocol. We must note that other treadmill protocols
such as the ‘Ramp Protocol’, can also be used.148,149 In addi
tion, if it is not possible for the patient to be tested on a
treadmill, a cycle ergometer or arm ergometer can also be
used to evaluate or assess the physical conditioning of the
patient, before starting exercise rehabilitation or a training
program. In addition, estimation of aerobic capacity is also
possible with exercise field tests such as the Cooper 12-min
test or the 1.5 mile run test. Heart rate can be easily obtained
with monitors. Oxygen consumption (VO2) should be meas
ured if possible, but requires more expensive equipment
that can perform continuous breath-by-breath analysis of
inspired and expired gases, flow, and volume. For the Bruce
protocol, speed and grade begin at 1.7 mph and 0%,
respectively. Thereafter, the speed and level of incline are
increased every 3 min. Patients are constantly encouraged to
complete 3 min stages and the test is terminated when peak
volitional effort is achieved. Additional variables that can
be collected during the test include blood pressure, Borg’s
rated perceived exertion (RPE),150,151 basic electrocardiogram
(ECG), and spirometry. The peak VO2 and peak heart rate
can then be used to establish the intensity at which patients
will exercise during the exercise program.
Strength measurements. Isokinetic dynamometry strength
testing should be performed to assess muscle function and
to later on evaluate progress. If using the Biodex Isokinetic
dynamometer, the test can be done on the dominant leg
extensors and/or leg with burns. We recommend testing at
such as chronic cardiovascular, pulmonary and metabolic
diseases. The objective of the exercise evaluations is to obtain
information to optimize safety during exercise testing and
training and also to develop a sound and effective exercise
rehabilitation program.
Health screening before exercise evaluation should begin
with the collection of subjective data. This should include
evaluation of exercise or sports interests, objectives, level of
activity prior to burn, functional limitations (e.g. loss of
digits, lower body bilateral amputee), and other pertinent
information. To our knowledge, there are no burn-specific
physical activity questionnaires. However, simple question
naires for assessing pre-burn physical activity exist and can
be modified to fit a specific given population.140–142 This
evaluation can consist of muscle strength, cardiopulmonary,
and muscle/joint flexibility testing. The information gath
ered during the subjective and objective evaluations can then
be used to design a structured exercise program or plan to
be carried out at home or at an exercise facility. Finally, a
plan to periodically re-evaluate subjective and objective data,
and the exercise program itself should be incorporated.
Subjective data
Characterization of limitations or problems of a patient
should be done. Obtaining a history of pre-burn physical
activity or habits, present medical complaints, symptoms
and limitations is crucial to develop a sound exercise
program. Symptoms or limitations which may affect exercise
tolerance may include pain during ambulation, weakness in
ambulation, itching, joint contractures, amputations, short
ness of breath, or ease of fatigability. In addition, you should
note present medications and note possible effects of these.
Following the evaluation of subjective data, an exercise eval
uation to gather objective data on the patient’s exercise or
physical capacity should be performed.
Objective data
Assessment of objective data includes age, height and weight,
%TBSA burn, and percent full-thickness burn. Variables
before, during, and after a cardiopulmonary exercise test
(CPET) should be obtained if possible. These include
heart rate, blood pressure, Borg’s rated perceived exertion
(RPE), basic electrocardiogram (ECG), and spirometry.143,144
However, if a CPET is not possible, an exercise program that
is effective can also be designed. Assessment of upper and
lower body muscle strength should also be done. This
includes assessment of peak strength levels (if possible), as
well as determining the loads or weights that will be used
during the resistive component of the exercise program. The
assessment of peak muscle strength can be accomplished
during knee or elbow extension but can also be accom
plished during a handgrip.134,145,146 These tests involve peak-
to-maximal efforts, and good communication between
patient and tester must exist. In addition, there is a develop
mental mental maturity that must exist in order for many of
these objective data to be maximally helpful. We recom
mend a chronological age of ≥7 years, though children as
young as 3–4 have also been tested successfully.147 Finally,
major muscle/joint flexibility should be assessed using
measures such as sit-and-reach or goniometry for range of
motion. Other types of tests may include neuromuscular
Comprehensive rehabilitation of the burn patient
541
to measure body composition such as underwater weighing
or bio-impedance are applicable to patients with burns due
to the burn scars.
Additional testing can include major muscle and joint
flexibility using sit-and-reach or goniometry for ROM. Other
tests include gait analysis, balance, or reaction time. Sit-and-
stand scores, timed walk/jog, and/or lifting exercises may
also be used to assess functional performance. The results
of all evaluations should help in identifying problem
areas, writing an exercise prescription, designing an exercise
program, and assessing progress during and after an exercise
program.
Components of an exercise program
An exercise program typically consists of a warm-up phase,
an endurance phase, recreational activities (optional), and a
cool-down phase. While aerobic training activities should
be done 3–5 days per week, complementary flexibility and
resistance exercises may be performed at a lower frequency
(2–3 days per week).152 Flexibility exercises can be included
as part of the warm-up or cool-down, or done at a separate
time. Resistive training is often performed on alternate days
to aerobic training; however, both types of activities can
be combined into the same workout session. Typically,
the warm-up period will be of approximately 5–10 min,
though it can be longer. This will be followed by a stimulus
or endurance phase of 20–60 min, and a cool-down period
of approximately 5–10 min. Aerobic and resistance training
should be prescribed in specific terms of intensity, duration,
frequency, and mode of exercise. Each of these terms will be
discussed in greater detail later. An optional recreational
game may occasionally substitute the endurance phase.
However, because of potential difficulties in setting an
appropriate intensity for an appropriate length of time, it is
suggested that it be done as a complement to the endurance
phase. If a recreational activity is added to the endurance
phase, then the shortening of the endurance phase should
be carefully considered though maintaining a minimum of
20 min.
Warm-up stage
Prior to the endurance phase, a variety of very light exercises,
low-intensity calisthenics, should be done to improve the
transition from rest to the endurance phase of the exercise
session. The emphasis at the onset of an exercise session is
to gradually increase the level of activity until the proper
intensity is reached to begin the endurance phase. Stretching
exercises to increase the range of motion of the joints
involved in the activity were previously included in the
warm-up. However, recently, evidence has been introduced
to contraindicate the inclusion of stretching during the
warm-up period.153,154
In fact, evidence suggests that a pre-exercise warm-up that
consists of only light aerobic exercise to increase body tem
perature is adequate for increasing flexibility before an exer
cise session.133 For example, patients might walk moderately
fast during the endurance phase, but might conclude the
warm-up period with slow, easy walking. However, a moder
ate walk (e.g. 3.5 mph) can be a warm-up for a patient that
jogs at 5.5 mph during the endurance phase. Heart rate may
various angular velocities, such as 150°/s, 90°/s or 180°/s.
The patients are seated and their position stabilized with a
restraining strap over the mid-thigh, pelvis, and trunk. All
patients should be familiarized with the equipment before
the actual test starts. We recommend that first, the procedure
is demonstrated by the administrator of the test. Second, the
test procedure is explained to the patients, and then,
patients are allowed to practice the actual movement during
three submaximal repetitions without load as warm-up.
Third, after the three submaximal warm-up repetitions, 10
maximum voluntary muscle contractions (full extension and
flexion) can be performed consecutively without rest in
between. The amount of repetitions and the number of
times the sets of repetitions can be varied. For example, we
recommend 10 repetitions and two sets, with a 2 min rest
interval between sets. Values of peak torque, total work, and
average power are calculated by the Biodex software system,
and progress of muscle function can be monitored.
Three Repetition Maximum Test (3RM)
Typically, before starting a resistive training program, it is
useful to determine a safe and effective load for patients to
use during workouts. To determine the amount of weight
or load that can be used as baseline or starting loads, the
‘Repetition Maximum (RM)’ method can be used. We rec
ommend the 3-repetition maximum load (3RM), which is
determined as follows. After an instruction period on correct
weight-lifting technique, the patient warms up with lever
arm and bar (or wooden dowel) and is allowed to become
familiar with the movement. After this, the patient lifts a
weight that allows successful completion of 4 repetitions.
If the fourth repetition is achieved successfully and with
correct technique, a 1 min resting period should be allowed.
After the resting period, a progressively increased amount
of weight or load is instructed to be lifted at least four times.
If the patient lifts a weight that allows successful completion
of 3 repetitions, with the fourth repetition not being voli
tionally possible, due to fatigue or inability to maintain
correct technique, the test is terminated and the amount of
weight lifted from the successful set is recorded as their
individual 3RM. We recommend the order of exercises to
be from exercises that involve large muscle groups to
ones that involve smaller muscle groups: bench press, leg
press, shoulder press, leg extension, biceps curl, leg curl and
triceps curl.
Body composition measurement
Patients with severe burns lose a significant amount of lean
body mass (LBM). Therefore, assessment of LBM should be
made. Additionally, assessment of bone mass and fat mass
should also be made. We assess body composition using
dual-energy X-ray absorptiometry (DXA). DXA with pediat
ric software can measure the attenuation of two X-ray beams;
one which is high energy and one which is low energy. These
measurements are then compared with standard models of
thickness used for bone and soft tissue. Subsequently, the
calculated soft tissue is separated into LBM and fat mass. This
is a great measurement to also assess progress of the program
and if applicable, nutritional interventions. However, the
DXA machine is expensive. It is not known if other methods
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of specificity refers to the concept that the training effect is
specific to the muscle fibers involved in the activity. Specifi
city also refers to the types of training in a very specific
manner to produce a very specific adaptation or outcome. If
a muscle is engaged in endurance types of exercise, the
primary adaptations are in the capillary and mitochondrial
number, which increase the aerobic capacity of the muscle.
These principles are applicable to burned patients; however,
it must be noted that a high intensity of exercise is not
needed (low to moderate intensity) to achieve health-related
benefits. On the other hand, to achieve athletic performance
or competitive-related goals, moderate to high levels of
intensity will be required. Another consideration that should
be kept in mind when designing an exercise program is the
age of the population. Prepubescent children are very differ
ent in their physiological and mental response to exercise
training than postpubescent children. Older adults also have
different health and physical problems than younger adults.
It is for these reasons that medical exams, as well as exercise
evaluations, are strongly recommended prior to starting an
exercise program. It is beyond the scope of this chapter to
address these differences and/or problems. However, general
guidelines for both children and adults are offered and it is
suggested to the reader to seek additional information for
population-specific recommendations or position stands on
exercise and physical activity, from associations such as the
American College of Sports Medicine (
publications/positionStands.htm); the American Academy
of Pediatrics (); the American Medical
Association (), or the American
Heart Association ().
Aerobic training
Intensity
To improve aerobic fitness, generally the intensity of exercise
should be between 65% and 95% of the peak heart rate or
between 45% and 85% of the heart rate reserve (HRR).155
The heart rate reserve is the difference between peak heart
rate obtained during a CPET and resting heart rate. The range
of heart rate values associated with the exercise intensity
needed to induce an improvement in cardiovascular fitness
is termed the ‘target heart rate zone.’
The peak heart rate (HRpeak) is obtained from the CPET.
However, when this not possible, one simple method to
estimate HRpeak is to use the formula (220 minus age).132 This
formula may not be applicable to young children, so we
recommend that in children, rated perceived exertion (see
below), together with the heart rate obtained during a
maximal exercise capacity test, be used.
The rating of perceived exertion or (RPE) scale can also be
used as a guideline in setting the intensity of exercise.150 The
RPE is a valuable and reliable indicator of exercise tolerance,
but also intensity. This method of monitoring exercise inten
sity is useful when it is impossible to obtain a HRpeak or if
patients are on medications which affect heart rate such
as β-blockers. There are currently two RPE scales that are
commonly used: the original or category scale, which rates
exercise intensity on a scale of 6–20 and the revised or
category-ratio scale of 0–10. It is reported that the category-
ratio scale uses terminology better understood by the subject,
be monitored or assessed if needed to ensure that the
warm-up activity is not too strenuous.
Endurance stage
The endurance phase develops cardiorespiratory or aerobic
fitness and includes 20–60 min of continuous or intermit
tent (minimum of 10 min bouts accumulated throughout
the day) aerobic activity. Duration depends on the intensity
of the activity; thus, moderate-intensity activity should be
conducted over a longer period of time (≥30 min), and,
conversely, individuals training at higher levels of intensity
(i.e. vigorous exercise) should train for at least ≥20 min.152
The most effective exercises for the endurance phase employ
large muscle groups in activities that are rhythmic or dynamic
in nature. Sports such as soccer, basketball or tennis also
have aerobic conditioning potential if a sufficient amount
of time for inducing aerobic improvement is achieved
(minimum of 20 min total). On the other hand, activities
like golf and bowling are unlikely to elicit a cardiovascular
training effect, but are enjoyable and may yield health-
related, as well as psychosocial, benefits.
Recreational activities
The inclusion of enjoyable recreational activities during (or
immediately after) the endurance phase often enhances
compliance with the exercise program. Rules of the games
may need to be modified to adjust skill level requirements,
competition, and to ensure safety. The outcome of the game
(winning or losing) should be of lesser importance than the
safety, participation and enjoyment of the patient. It is
important to remember that recreational activities comple
ment the endurance phase and should not consistently
replace it. Recreational activities may also promote develop
ment or improvements in psychosocial health, by increasing
the amount of social interaction.
Cool-down stage
At the end of the activity session, about 2–5 min of cool-
down activities – slow walking and stretching exercises – are
recommended to gradually return HR and BP toward resting
levels. This period includes exercises of diminishing intensi
ties; e.g. slower walking or jogging, calisthenics and stretch
ing exercises. This part of the exercise session is viewed as
important in reducing the chance of a hypotensive episode
after the exercise session, as well as other cardiovascular
complications.
Exercise prescription
Some basic exercise physiology principles should be kept in
mind when designing an exercise program for burned
patients. Two such principles are: the progressive overload
and the specificity principles. The progressive overload prin
ciple refers to the observation that a body system must be
exercised at a level above that to which it is presently accus
tomed in order for a training effect to occur.132 The system
or tissue gradually adapts to this overload. The typical vari
ables that comprise the overload include the intensity, dura
tion and frequency (days per week) of exercise. The principle
Comprehensive rehabilitation of the burn patient
543
days per week) exercise sessions. Clearly, the number of
exercise sessions per week will vary depending on the
patient’s limitations, but also by the patient and caregiver’s
lifestyle.
Mode
The most important consideration in choosing the mode of
exercise for the endurance phase of the sessions is to engage
large muscle groups in activities that are rhythmic or dynamic.
The greatest improvements in aerobic fitness result when
exercise involves the use of large muscle groups over appro
priate periods of time (Fig. 47.29). The mode of exercises
includes treadmill walking/running, rowing or cycling. If no
treadmill is available, then walk/jog at a track or field is
appropriate. Swimming is also an appropriate mode of
exercise, though closure of burn wounds should be ensured
to minimize infection of wound or the contamination
of others. Endurance games are also appropriate modes of
exercise.
Progression of exercise
We recommend starting slowly and safely progressing in
duration and intensity, but also in transitioning from early
activities to activities that are more difficult to perform. This
method of progression decreases the potential for inducing
excessive muscle soreness, causing new injuries or aggravat
ing old injuries. The emphasis on slow-to-moderate walking
as the primary activity early in the fitness program is consist
ent with this recommendation, and the participant must be
educated to not move too quickly into the more demanding
activities. For example, if the individual can walk about
1–2 miles without fatigue, then the progression to a walk-jog
or jogging program is a reasonable recommendation.
The recommended rate of progression in an exercise con
ditioning program depends on the functional capacity,
medical and health status, pain tolerance, location of burns,
age, individual activity preferences and goals, and an indi
vidual’s tolerance to the current level of training. For burned
patients, the endurance aspect of the exercise prescription
can be divided into three stages of progression: initial,
improvement, and maintenance.133
Initial conditioning stage
The initial stage should include light and moderate muscular
endurance activities (e.g. 40–60% of HRR). These exercises
typically have a low potential for injury, and induce minimal
muscle soreness and pain. Exercise adherence may be com
promised if the level or intensity of exercises in the program
is initiated too aggressively. The amount of time spent in this
stage varies depending on the individual’s adaptation to the
exercise program. We recommend at least 4 weeks of initial
conditioning. The duration of the exercise session during the
initial stage may begin with approximately 15–20 min and
progress up to 30 min, at least 3 times per week. Decondi
tioned individuals should be allowed more time for adapta
tion at each stage of conditioning. Age of the individual
should also be taken into account when progressions are
recommended, as adaptation to conditioning likely takes
longer in older individuals, but also in extremely debilitated
individuals.152
thereby providing the tester with more valid information. It
has been found that an aerobic training effect and the thresh
old for the start of anaerobic training are achieved at a rating
of ‘somewhat hard’ to ‘hard,’ which approximates a rating of
12–16 on the category scale or 4–5 on the category-ratio
scale.156 Finally, if a patient cannot use the heart rate method
or the RPE method, the ‘Talk Test’ can also be used as a
highly consistent method to set and monitor intensity of
exercise.157
The ‘Talk Test’, or the point where speech first becomes
difficult, approximates exercise intensity almost exactly
equivalent to the ventilatory threshold. One could advise the
patient to exercise at an intensity where speech is comfort
able. When speech becomes uncomfortable, one can assume,
based on previous studies, that exercise intensity is consist
ently above ventilatory threshold or above the desired inten
sity of exercise needed for general improvements in fitness.157
It must be noted that when setting the exercise intensity,
safety and effectiveness are linked. An appropriate intensity
should also be well suited to result in a long-term, active
lifestyle.
Duration
The duration of an aerobic exercise session is closely linked
to the intensity of the activity, i.e. a longer duration of low-
intensity exercise can be accomplished than of high-intensity
exercise. In general, the duration of exercise for burned
patients once discharged, should be from 5 to 20 min the
first week. This will depend on the functional status of the
patient and also pain tolerance.
If the patient tolerates up to 20 min, then this duration is
appropriate. The objective should be to exercise 20–60 min
of aerobic activity. This can be accomplished continuously
or intermittently throughout the day, with a minimum of
10 min bouts. Typically a duration of 20–30 min at between
40% and 50%, up to 85% of the heart rate reserve (excluding
time for warm-up and cool-down) should induce health and
fitness improvements.152,158
In burned patients with extremely low aerobic capacity or
endurance, 4–6 5-min bouts with rest periods between bouts
would be a program that would induce benefits. The dura
tion of the exercise sessions (or bouts) can be progressively
increased over time. However, as mentioned before, a high
intensity of exercise or very long duration of exercise are not
needed to achieve health-related benefits, particularly during
the initial stages of outpatient exercise rehabilitation.
Frequency
It is reported that deconditioned persons may improve car
diorespiratory fitness with only twice-weekly exercise.152
However, it is generally agreed that optimal training fre
quency appears to be achieved with 3–5 workouts per week.
The additional benefits of more frequent training appear to
be minimal, whereas the incidence of lower extremity inju
ries increases abruptly. For those exercising at 60–80% HRR,
an exercise frequency of 3 days per week is sufficient to
improve or maintain VO2peak. When exercising at the lower
end of the intensity continuum, exercising more than 3 days
per week is not deleterious. Patients with extremely low
functional capacities may benefit from multiple, short (5
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longer be interested in continually increasing the condition
ing stimulus. Also, in this stage, further improvement may
be none to minimal, but continuing the same workout
routine enables individuals to maintain their fitness levels,
as well as develop the healthy exercise habit. At this point,
it is suggested that goals of the program be re-examined and
new goals or objectives set.
Resistive training
Strength is defined as the ability to produce force, and the
ability to produce force over an extended period of time is
referred to as muscular endurance. Both muscle strength
and endurance impact activities of daily living (ADL)
because ADL require a percentage of an individual’s muscu
lar capacity to perform these everyday tasks. Severe burns
result in extensive and prolonged loss of muscle mass;
therefore, resistance training, which increases LBM, should
be part of an exercise rehabilitation program for burned
individuals.134
Similarly to designing the aerobic portion of an exercise
program, the resistive training portion of an exercise program
follows similar principles of training. Both the overload prin
ciple and specificity principle are applicable. Strict rules of
proper technique and safety must be observed to reduce
Improvement stage
The goal of the improvement stage of training is to provide
a progressive increase in the overall exercise stimulus, which
will allow for significant improvements in aerobic fitness.
The improvement stage of the exercise-conditioning program
differs from the initial stage in that the participant is pro
gressed at a more rapid rate. This stage is reported to usually
last from 4 to 5 months, during which, intensity is progres
sively increased within the upper half of the target range of
50–85% of HRR. However, our experience in a 12-week
training program in children 7–18 years of age indicates that
after 3–4 weeks of initial conditioning, some patients are
able to start the improvement stage. In this stage, duration
may be increased consistently every 2–3 weeks until partici
pants are able to exercise at a moderate-to-vigorous intensity
for 20–30 min continuously. During this stage, interval
training may also be beneficial, provided the total time
engaged in moderate to vigorous exercise is at least 20 min.
Maintenance stage
The goal of this stage of training is the long-term mainte
nance of the cardiopulmonary fitness level developed during
the improvement stage. This stage of the exercise program
may begin at any time the participant has reached previously
agreed objectives. During this stage, the individual may no
Figure 47.29 Aerobic training should incorporate the use of large muscle groups over appropriate time periods.
Comprehensive rehabilitation of the burn patient
545
Type of contraction
Resistance exercise programs or exercises that emphasize
accentuated lengthening or contractions (eccentric) are not
recommended for severely burned individuals. These types
of contractions have a high potential for acute delayed onset
of muscle soreness, while having similar outcomes to con
centric or isometric muscle contractions. The muscle sore
ness if severe enough has the potential for discouraging
further participation in exercise activities. The movements
during weight-lifting should be rhythmic, done at moderate
repetition and duration.
Amount of load lifted
Commonly, a certain percentage of the 1RM or 3RM is used
as guideline for choosing a training load. The amount of
load lifted can be as much as 100% of 1RM or as little as
lifting no load. We recommend initially, during the first week
of training, allowing the individual to become familiarized
with the exercise equipment and to be instructed on proper
weight-lifting techniques. Initially, the weight or load the
subjects will lift should be set at 50–60% of their individual
3RM for 12–15 repetitions for the first 1–2 weeks. Thereafter,
the load lifted can be increased to 70–75% (8–10 repeti
tions) of their individual 3RM and continued for weeks 2 or
3, to week 6. After this, the training intensity can be increased
to 75–85% (8–12 repetitions) of the 3RM and implemented
from weeks 7–12 or longer. We must note that these are
guidelines to provide an estimate of training load and have
some limitations.160 Another method of determining train
ing load is to perform multiple RM based on the number of
repetitions planned for the specific exercise. For example,
if 8 repetitions were desired for biceps curl, then one
would test the individual by having him or her perform 8RM
testing sets.
Number of repetitions
It is believed that muscle strength and endurance can be
obtained simultaneously by performing a specific number of
repetitions within a certain range (e.g. 6–10 repetitions). The
number of repetitions will depend on load lifted (% of 1RM)
and also the objective or goals set at the start of the exercise
program. However, we recommend 8–12 repetitions, at a
moderate to high intensity to improve both muscle strength
and endurance.134
Number of sets
There are very limited data in children as to whether 3 sets
or 1 set is required to increase muscle strength and hyper
trophy. Much of the adult-based literature supports similar
responses of muscle strength, muscle endurance, hypertro
phy between single and multiple set resistance training pro
grams.152,161–164 Finally, it is important to stress two points:
(1) the difference in strength gains is typically more pro
nounced in trained individuals; and (2) both single and
multiple training increases strength. The first point is usually
not the case with burned patients, and the second point
stresses the fact that an increase in strength is expected with
resistance training compared to the standard of care in
burned individuals.
potential for injury or accidents. A normal breathing pattern
should be maintained, with breath holding avoided. Breath
holding during lifting can induce excessive increases in
blood pressure, which in individuals with hypertension, dia
betes or other medical risks can be dangerous.
Similarly to the aerobic exercise program, testing or evalu
ation of muscle function precedes the resistive exercise
program. This helps individuals identify problem areas,
areas in need of required improvement, goal setting and
tracking progress of individuals. In addition, muscle strength
tests have value in determining back to work status.159 Some
of these tests involve peak to maximal muscular efforts.
These tests can be done on weight machines or using
dumbbells.
Typically these tests are done at 100% of one-repetition
maximum (1RM), but can also be done at 3RM. For
extremely deconditioned individuals or for very young chil
dren, modification of these guidelines can involve testing
using 3RM up to 12RM if needed. An important point to
remember is that safety of the individual is crucial. There
fore, correct technique during all testing and training must
be observed. The order of exercises or muscle tested is also
important. It is recommended that large muscle groups are
tested first and alternate between upper body and lower
body. For example, a 3RM test may be done in the following
order of exercises: bench press, leg press (or squats), shoul
der press, leg extension, biceps curl, leg curl, and triceps
curl. The three repetitions maximum (3RM) load can be
determined as follows. After an instruction period on correct
weight-lifting technique, the patient or individual warms up
with lever arm and bar (or wooden dowel) and is allowed
to become familiar with the movement. After this, the
patient lifts a weight that allows successful completion of
four repetitions. If the fourth repetition is achieved success
fully and with correct technique, a 1 min resting period is
allowed. After the resting period, a progressively increased
amount of weight or load is instructed to be lifted at least
four times. If the patient lifts a weight that allows successful
completion of three repetitions, with the fourth repetition
not being volitionally possible, because of fatigue or inabil
ity to maintain correct technique, the test is terminated and
the amount of weight lifted from the successful set is
recorded as their individual 3RM. This weight is then used
to determine the amount of weight or load that will be used
during the first 1–2 weeks (of for example, a 12-week
program) as baseline loads.
Exercise type
There are many resistance-training exercises. However, these
can be divided into core exercises and assistance exercises.
Core exercises recruit one or more large muscle groups (e.g.
chest, shoulder and back). Assistance exercises typically
recruit smaller muscle groups such as biceps, triceps, calves.
A good program should typically involve both types of
exercises.
Training frequency
The number of days to train varies according to the indi
vidual’s training status. For severely burned individuals, we
recommend 2–3 days per week of resistance training.
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Progressive overload
In order for improvements to continue over time, it is impor
tant to carefully monitor and chart the individual’s workouts
or loads lifted. Progressive overload can be applied in a
variety of ways, such as increasing the weight lifted, increas
ing repetitions while keeping load constant, or decreasing
rest periods. A conservative method termed the ‘2-for-2 rule’
is suggested. This rule states ‘if an individual can perform
two or more repetitions above his or her assigned repetitions
goal in the last set, for two consecutive workouts for a spe
cific exercise, then weight or load should be added to that
specific exercise for the next training session.167 For example,
if the assigned number of sets and repetitions is 3 sets of
8–12 reps in the chest press machine, and if the individual
performs 12 reps in all 3 sets, after several workout sessions
(the specific number of sessions depends on many factors),
the individual is able to complete 12 reps in the third set
(i.e. the last set) for two consecutive workout sessions, then
in the following training session, the load for that exercise
should be increased. The amount of weight (load) that
should be added depends on factors such as the physical
condition of the individual (strong or weak) and the body
area (upper body or lower body). In general, an increase of
Exercise order
There are many methods of ordering resistance exercises.
One of these is to arrange core exercises, then assistance
exercises.164 Another method is to arrange large muscle
groups and then small muscle groups.165–167 Yet another
method, which allows the individual to recover more fully
between exercises, is to alternate upper body with lower
body exercises. This is especially well-suited for decondi
tioned individuals or untrained individuals.165,166 For
example, we have successfully implemented, in severely
burned children, the following order of resistive exercises:
bench press, leg press or squats, shoulder press, leg exten
sion, biceps curl, leg curl, triceps curl, and toe raises. These
exercises can be done on variable resistance machines or free
weights.134 Both free weights, bands or variable resistance
machines are appropriate for burned individuals wishing to
participate in an exercise program (Fig. 47.30).
Rest periods
As a general rule, it is important to allow enough time
between exercises to perform the next exercise in proper
form. The rest period also varies depending on the individ
ual’s training status and also specific training objectives.
Figure 47.30 Resistance training consists of exercises with free weights or variable resistance machines.