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22 Venous Disease Management intheLimb Salvage Patient: Diagnostics, Compression, andAblation
303
16. Wittens C, Davies AH, Baekgaard N, Broholm R,
Cavezzi A, Chastanet S, et al. Editor’s choice—
management of chronic venous disease: clinical
practice guidelines of the European Society for
Vascular Surgery (ESVS). Eur J Vasc Endovasc Surg.
2015;49(6):678–737.
17. Gloviczki P, Comerota AJ, Dalsing MC, Eklof BG,
Gillespie DL, Gloviczki ML, etal. The care of patients
with varicose veins and associated chronic venous
diseases: clinical practice guidelines of the Society for
Vascular Surgery and the American Venous Forum. J
Vasc Surg. 2011;53(5 Suppl):2S–48S.
18. Lurie F, Passman M, Meisner M, Dalsing M, Masuda
E, Welch H, etal. The 2020 update of the CEAP classication system and reporting standards. J Vasc Surg
Venous Lymphat Disord. 2020;8(3):342–52.
19. Killewich LA, Bedford GR, Beach KW, Strandness
DE Jr. Spontaneous lysis of deep venous thrombi: rate
and outcome. J Vasc Surg. 1989;9(1):89–97.
20. Saha P, Humphries J, Modarai B, Mattock K,
Waltham M, Evans CE, etal. Leukocytes and the natural history of deep vein thrombosis: current concepts
and future directions. Arterioscler Thromb Vasc Biol.
2011;31(3):506–12.
21. Ismail L, Normahani P, Standeld NJ, Jaffer U.A systematic review and meta-analysis of the risk for development of varicose veins in women with a history
of pregnancy. J Vasc Surg Venous Lymphat Disord.
2016;4(4):518–24 e1.
22. Willenberg T, Schumacher A, Amann-Vesti B,
Jacomella V, Thalhammer C, Diehm N, etal. Impact
of obesity on venous hemodynamics of the lower
limbs. J Vasc Surg. 2010;52(3):664–8.
23. Dua A, Desai SS, Heller JA.The impact of race on
advanced chronic venous insufciency. Ann Vasc
Surg. 2016;34:152–6.
24. Natour AK, Rteil A, Corcoran P, Weaver M, Ahsan S,
Kabbani L. Socioeconomic status and clinical stage
of patients presenting for treatment of chronic venous
disease. Ann Vasc Surg. 2022;83:305–12.
25. Schleimer K, Barbati ME, Grommes J, Hoeft K,
Toonder IM, Wittens CHA, et al. Update on diagnosis and treatment strategies in patients with postthrombotic syndrome due to chronic venous obstruction
and role of endovenous recanalization. J Vasc Surg
Venous Lymphat Disord. 2019;7(4):592–600.
26. Tan MKH, Sutanto SA, Onida S, Davies AH. The
relationship between vein diameters, clinical severity,
and quality of life: a systematic review. Eur J Vasc
Endovasc Surg. 2019;57(6):851–7.
27. Nicolaides AN, Labropoulos N.Burden and suffering
in chronic venous disease. Adv Ther. 2019;36(Suppl
1):1–4.
28. Passman MA, McLafferty RB, Lentz MF, Nagre SB,
Iafrati MD, Bohannon WT, etal. Validation of venous
clinical severity score (VCSS) with other venous
severity assessment tools from the American Venous
Forum, National Venous Screening Program. J Vasc
Surg. 2011;54(6 Suppl):2S–9S.
29. Raju S, Knight A, Lamanilao L, Pace N, Jones
T.Peripheral venous hypertension in chronic venous
disease. J Vasc Surg Venous Lymphat Disord.
2019;7(5):706–14.
30. Meissner MH, Moneta G, Burnand K, Gloviczki P,
Lohr JM, Lurie F, etal. The hemodynamics and diagnosis of venous disease. J Vasc Surg. 2007;46 Suppl
S:4S–24S.
31. Lurie F, Lal BK, Antignani PL, Blebea J, Bush R,
Caprini J, et al. Compression therapy after invasive
treatment of supercial veins of the lower extremities:
clinical practice guidelines of the American Venous
Forum, Society for Vascular Surgery, American
College of Phlebology, Society for Vascular Medicine,
and International Union of Phlebology. J Vasc Surg
Venous Lymphat Disord. 2019;7(1):17–28.
32. Barnes M, Mani R, Barret D, White JE.Changes in
skin microcirculation at periulcerous sites in patients
with chronic venous ulcers during leg elevation.
Phlebology. 1992;7(1):36–9.
33. Dix F, Reilly B, David M, Simon D, Dowding E, Ivers
L, et al. Effect of leg elevation on healing, venous
velocity and ambulatory venous pressure in venous
ulceration. Phlebology. 2005;20(2):87–94.
34. Xie T, Ye J, Rerkasem K, Mani R.The venous ulcer
continues to be a clinical challenge: an update. Burns
Trauma. 2018;6:18.
35. Dezotti NRA, Dalio MB, Ribeiro MS, Piccinato CE,
Joviliano EE.The clinical importance of air plethysmography in the assessment of chronic venous disease. J Vasc Bras. 2016;15(4):287–92.
36. Ibegbuna V, Delis KT, Nicolaides AN, Aina
O. Effect of elastic compression stockings on
venous hemodynamics during walking. J Vasc Surg.
2003;37(2):420–5.
37. Mosti G, Partsch H. Compression stockings with a
negative pressure gradient have a more pronounced
effect on venous pumping function than graduated
elastic compression stockings. Eur J Vasc Endovasc
Surg. 2011;42(2):261–6.
38. Lim CS, Davies AH.Graduated compression stockings. CMAJ. 2014;186(10):E391–8.
39. Spreaco G, Kabnick L, Berland TL, Cayne NS,
Maldonado TS, Jacobowitz GS, et al. Laser saphenous ablations in more than 1,000 limbs with longterm duplex examination follow-up. Ann Vasc Surg.
2011;25(1):71–8.
40. Goode SD, Chowdhury A, Crockett M, Beech A,
Simpson R, Richards T, et al. Laser and radiofrequency ablation study (LARA study): a randomised
study comparing radiofrequency ablation and endovenous laser ablation (810 nm). Eur J Vasc Endovasc
Surg. 2010;40(2):246–53.
41. Lurie F, Creton D, Eklof B, Kabnick LS, Kistner
RL, Pichot O, et al. Prospective randomized study
of endovenous radiofrequency obliteration (closure
procedure) versus ligation and stripping in a selected
patient population (EVOLVeS Study). J Vasc Surg.
2003;38(2):207–14.
304
Данная книга находится в списке для перевода на русский язык сайта https://meduniver.com/
B. Cutler et al.
42. Nordon IM, Hinchliffe RJ, Brar R, Moxey P, Black
SA, Thompson MM, etal. A prospective double-blind
randomized controlled trial of radiofrequency versus
laser treatment of the great saphenous vein in patients
with varicose veins. Ann Surg. 2011;254(6):876–81.
43. Subramonia S, Lees T. Radiofrequency ablation vs
conventional surgery for varicose veins—a comparison of treatment costs in a randomised trial. Eur J
Vasc Endovasc Surg. 2010;39(1):104–11.
44. Rautio T, Ohinmaa A, Perala J, Ohtonen P, Heikkinen T,
Wiik H, etal. Endovenous obliteration versus conventional stripping operation in the treatment of primary
varicose veins: a randomized controlled trial with comparison of the costs. J Vasc Surg. 2002;35(5):958–65.
45. Van Den Bos RR, Neumann M, De Roos KP, Nijsten
T.Endovenous laser ablation-induced complications:
review of the literature and new cases. Dermatol Surg.
2009;35(8):1206–14.
46. Rasmussen LH, Lawaetz M, Bjoern L, Vennits B,
Blemings A, Eklof B.Randomized clinical trial comparing endovenous laser ablation, radiofrequency ablation,
foam sclerotherapy and surgical stripping for great saphenous varicose veins. Br J Surg. 2011;98(8):1079–87.
47. van Eekeren RR, Boersma D, Holewijn S, Vahl A, de
Vries JP, Zeebregts CJ, etal. Mechanochemical endovenous Ablation versus RADiOfrequeNcy Ablation
in the treatment of primary great saphenous vein
incompetence (MARADONA): study protocol for a
randomized controlled trial. Trials. 2014;15:121.
48. van Eekeren RR, Boersma D, Konijn V, de Vries JP,
Reijnen MM.Postoperative pain and early quality of
life after radiofrequency ablation and mechanochemical endovenous ablation of incompetent great saphenous veins. J Vasc Surg. 2013;57(2):445–50.
49. Holewijn S, van Eekeren R, Vahl A, de Vries J, Reijnen
M, group Ms. Two-year results of a multicenter randomized controlled trial comparing Mechanochemical
endovenous Ablation to RADiOfrequeNcy Ablation
in the treatment of primary great saphenous vein
incompetence (MARADONA trial). J Vasc Surg
Venous Lymphat Disord. 2019;7(3):364–74.
50. Leung CC, Carradice D, Wallace T, Chetter
IC. Endovenous laser ablation versus mechanochemical
ablation with ClariVein((R)) in the management of supercial venous insufciency (LAMA trial): study protocol
for a randomised controlled trial. Trials. 2016;17(1):421.
51. Mohamed AH, Leung C, Wallace T, Smith G,
Carradice D, Chetter I.A randomized controlled trial
of endovenous laser ablation versus mechanochemical ablation with ClariVein in the management of
supercial venous incompetence (LAMA trial). Ann
Surg. 2021;273(6):e188–95.
52. Almeida JI, Javier JJ, Mackay E, Bautista C, Proebstle
TM. First human use of cyanoacrylate adhesive for
treatment of saphenous vein incompetence. J Vasc
Surg Venous Lymphat Disord. 2013;1(2):174–80.
53. Proebstle TM, Alm J, Dimitri S, Rasmussen L,
Whiteley M, Lawson J, et al. The European multicenter cohort study on cyanoacrylate embolization of
reuxing great saphenous veins. J Vasc Surg Venous
Lymphat Disord. 2015;3(1):2–7.
54. Morrison N, Gibson K, Vasquez M, Weiss R, Cher D,
Madsen M, etal. VeClose trial 12-month outcomes of
cyanoacrylate closure versus radiofrequency ablation
for incompetent great saphenous veins. J Vasc Surg
Venous Lymphat Disord. 2017;5(3):321–30.
55. Gibson K, Ferris B.Cyanoacrylate closure of incompetent great, small and accessory saphenous veins
without the use of post-procedure compression:
initial outcomes of a post-market evaluation of the
VenaSeal System (the WAVES Study). Vascular.
2017;25(2):149–56.
56. Morrison N, Gibson K, McEnroe S, Goldman M,
King T, Weiss R, et al. Randomized trial comparing
cyanoacrylate embolization and radiofrequency ablation for incompetent great saphenous veins (VeClose).
J Vasc Surg. 2015;61(4):985–94.
57. Kabnick LS, Sadek M, Bjarnason H, Coleman DM,
Dillavou ED, Hingorani AP, et al. Classication and
treatment of endothermal heat-induced thrombosis:
recommendations from the American Venous Forum
and the Society for Vascular Surgery. J Vasc Surg
Venous Lymphat Disord. 2021;9(1):6–22.
58. Dermody M, O’Donnell TF, Balk EM.Complications
of endovenous ablation in randomized controlled trials. J Vasc Surg Venous Lymphat Disord.
2013;1(4):427–36 e1.
59. Ceulen RP, Sommer A, Vernooy K. Microembolism
during foam sclerotherapy of varicose veins. N Engl J
Med. 2008;358(14):1525–6.
60. Cho S, Gibson K, Lee SH, Kim SY, Joh JH.Incidence,
classication, and risk factors of endovenous glueinduced thrombosis after cyanoacrylate closure of
the incompetent saphenous vein. J Vasc Surg Venous
Lymphat Disord. 2020;8(6):991–8.
61. Creager MA, Creager MA, Beckman JA, Loscalzo
J, ScienceDirect. Vascular medicine: a companion to
Braunwald’s heart disease. 2nd ed. Philadelphia, PA:
Elsevier/Saunders; 2013.
62. Bergan JJ, Murray J, Greason K. Subfascial endoscopic perforator vein surgery: a preliminary report.
Ann Vasc Surg. 1996;10(3):211–9.
63. Lawrence PF, Alktai A, Rigberg D, DeRubertis
B, Gelabert H, Jimenez JC. Endovenous ablation
of incompetent perforating veins is effective treatment for recalcitrant venous ulcers. J Vasc Surg.
2011;54(3):737–42.
64. Shamimi-Noori SM, Clark TWI.Venous stents: current status and future directions. Tech Vasc Interv
Radiol. 2018;21(2):113–6.
65. Neglen P, Hollis KC, Olivier J, Raju S.Stenting of the
venous outow in chronic venous disease: long-term
stent-related outcome, clinical, and hemodynamic
result. J Vasc Surg. 2007;46(5):979–90.
66. George R, Verma H, Ram B, Tripathi R.The effect of
deep venous stenting on healing of lower limb venous
ulcers. Eur J Vasc Endovasc Surg. 2014;48(3):
330–6.
Science andPracticality ofTissue
Products inLimb Salvage
AlexandraN.Verzella, AllysonR.Alfonso,
andErnestChiu
23
Introduction
In 2017, the CDC estimated that the total direct
and indirect expenditure on diagnosed diabetes
in the USA was $327 billion, an increase of $56
billion dollars since 2012 [1]. Globally, the estimated cost in 2019 was 760 billion, and that is
projected to reach 825 billion in 2030 [2]. The
crude estimate of Americans with diabetes in
2018 was 34.1 million or 13.0%, and 7.3 million
(21.4%) of whom were not aware of the diagnosis, with diabetic complications being the greatest contributor to healthcare expenditure in these
patients [3, 4]. Some of these diabetes-related
complications include kidney disease, ocular disease, death, and hospitalizations secondary to
major cardiovascular disease, hyperglycemia,
hypoglycemia, and diabetic ulcers. Foot ulcers
develop in up to 34% of patients with diabetes,
and failure of these ulcers to heal can lead to limb
amputation [3, 4]. In fact, up to 5.6 out of 1000
adults with diabetes underwent a lower-extremity
amputation for a total of 130,000 people in 2016
alone, underlining the importance of nding a
A. N. Verzella · A. R. Alfonso · E. Chiu (*)
Hansjörg Wyss Department of Plastic Surgery, New
York University Grossman School of Medicine,
New York, NY, USA
e-mail: Alexandra.verzella@nyulangone.org;
Allyson.alfonso@nyulangone.org;
Ernest.chiu@nyulangone.org
way to better heal diabetic wounds and salvage
limbs in these individuals [4].
Current Treatments
Diabetic wounds are precipitated by motor, sensory, and autonomic neuropathy. Motor decits
include atrophy of intrinsic muscles of the foot
and dislocated metatarsophalangeal joints caused
by unopposed power of the long exors and
extensors of the foot [5]. Sensory neuropathy
decreases the protective ability to sense pain and
impairs proprioception, causing balancing decits. Autonomic system dysregulation then further contributes to the formation of diabetic foot
ulcers through decreased sweat and oil gland
secretions, which predisposes patients to cracks
and ssures in the skin barrier [5].
According to guidelines from the American
Diabetes Association, there are 6 vital components to the treatment algorithm for a diabetic
wound which include: wound off-loading, surgical debridement of the wound early and often,
maintenance of a moist wound bed, treatment of
active infections, vascular assessment with correction of ischemia, and strict glycemic control
[6–13]. Though there are a multitude of imperative components to healing a diabetic wound, the
standard of care (SOC) for these wounds is limited to saline washes and vaseline gauze [14].
© Springer Nature Switzerland AG 2023
C. E. Attinger, J. S. Steinberg (eds.), Functional Limb Salvage,
https://doi.org/10.1007/978-3-031-27725-2_23
305
306
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A. N. Verzella et al.
In addition to the standard practices of care,
the clinical practice guidelines published by the
Society for Vascular Surgery in collaboration
with the American Podiatric Medical Association
and the Society for Vascular Medicine also recommend negative pressure therapy, hyperbaric
oxygen therapy, and biologics as adjunctive therapy for wounds recalcitrant to current SOC alone
[15, 16]. However, before biologics like tissue
products can be considered for use, the wound
bed must be optimized through demonstrating
adequate perfusion, debridement, and edema
control.
Tissue Product Denition
In this chapter, tissue products are dened as
anything that substitutes for skin and incorporates into the healing wound. The ideal tissue
product for a diabetic foot ulcer should resist
infection, prevent water loss, withstand the
shearing forces endured by native skin, conform
to irregular wound surfaces, lack signicant antigenicity, and possess exible thickness. It should
also be cost- effective, widely available, easy to
apply, durable and stable, and easy to store with
a long shelf- life. Unfortunately, the ideal tissue
product with all of these qualities does not currently exist.
Several systems of classication for tissue
products have been proposed such as Kumar’s 3
classes that divide the products into temporary
impervious dressing materials, single-layer
durable substitutes, and composite skin substitutes or Dieckman etal.’s 2 classes of biomaterial or cellular products with allogenic,
xenogenic, and autologous subcategories [17,
18]. Because there is a lack of consensus in
these classication systems, in this chapter, biologic tissue products will be organized into their
individual brand product and will be placed into
4 broader categories: (1) allografts/xenografts,
(2) dermal substitutes, (3) biosynthetic dressings, and (4) cultured skin grafts. We will also
highlight some of the currently commercially
available products and do not endorse one over
another.
Science andPracticality
ofAllografts andXenografts
Allografts and xenografts are skin substitutes that
are harvested from human and animal sources,
respectively, that act as temporary skin grafts [19,
20].
Allografts can be either cellular or acellular
and are exclusively derived from human sources,
most commonly from neonatal foreskin. Cellular
allografts contain living cells like broblasts and
keratinocytes that encourage wound healing
through secretion of growth factors and cytokines
that promote the ingrowth of native host cells and
neovascularization. Because these grafts retain
non-autologous living cells, they can provoke an
immunologic response in the host.
Apligraf® (Organogenesis, Inc., Canton, MA),
previously called Graftskin, is a bilayer composite allograft that is indicated for full-thickness
neuropathic diabetic foot ulcers that have been
present for greater than 3 weeks and have not
responded to SOC [21, 22] (Fig.23.1a, Table23.1).
While Apligraf can be used in wounds that extend
through the dermis, it is not indicated for diabetic
ulcers that involve tendon, muscle, joint, or bone
[22]. Its epidermal layer is comprised of living
human neonatal foreskin- derived keratinocytes
and stratum corneum, and its dermal layer contains bovine type I collagen and neonatal broblasts that produce growth factors and cytokines
like VEGF, IL-6, and IL-8. These components
function to activate host keratinocytes at the edge
of the wound, regulate growth factors signals,
provide a barrier against further wound damage
and infection, control brosis and scar formation,
and revitalize broblasts in the base of the
wound—correcting ECM and matrix metalloproteinase balance. Because of the impact on brosis
and scar formation, Apligraf also has reports of
improved cosmesis and functional outcomes
when used in chronic wounds [21, 23]. While
Apligraf preserves many extracellular matrix
(ECM) proteins and cytokines native to human
skin, it does not contain Langerhans cells, melanocytes, macrophages, lymphocytes, blood vessels, or hair follicles [22]. In addition, Apligraf’s
allogenic cells are not able to survive long-term in
a Allografts
®i
Int J Mol Sci. 2017;18(4):789. Published 2017 Apr 7. doi:10.3390/ijms18040789
rcine collagen
23 Science andPracticality ofTissue Products inLimb Salvage
307
i) Apligraf
Keratinocytes
and stem cells
b
i) Integra® DRTii) Bibrane®
Fibroblasts
Collagen and growth factors
Biosynthetic Dressings
Silicon
Bovine collagen
Chondroitin-6-sulfate
glycosaminoglycans
i) Orcel®
Keratinocytes
Ty pe I Collagen
Sponge
Fibroblasts
Silicon
Nylon mesh
Po
c
i) MySkin® ii) Epicel®
Cultured Skin Grafts
Keratinocyte cell
suspension
d Dermal Substitutes
i) Promogran Prisma™ ii) GraftJacket®
Bovine collagen
Oxidized regenerated
cellulose
Silver ORC
Adapted from Vig K, Chaudhari A, Tripathi S, et al. Advances in Skin Regeneration Using Tissue Engineering.
Fig. 23.1 Biologic skin substitutes. (a) Allografts: (i)
®
Apligraf
, (ii) Orcel®. (b) Biosynthetic dressings: (i)
Integra® DRT, (ii) Biobrane®. (c) Cultured skin grafts: (i)
MySkin®, (ii) Epicel®. (d) Dermal substitutes: (i)
Promogran Prisma™, (ii) GraftJacket
Petroleum
gauze
Keratinocytes
Murine
fibroblasts
Intact
basement
membrane
Ty pe I
collagen
Elastin and
aminoglycosides
®
308
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A. N. Verzella et al.
(1998)— Non-infected partial
a
Yes PMA
over SOC Indications
Difference
Storage
temperature
schedule Shelf-life
Application
Yes Weekly 10 days Room
cells
Intact
and full-thickness skin ulcers
secondary to venous insufciency >1
month resistant to standard therapies
PMA (2001)—full-thickness
neuropathic diabetic foot ulcers >3
weeks that have not responded to
SOC [95]
Off-label—epidermolysis bullosa
[96], recurrent hernia repair, pressure
sores, burn reconstruction [39]
temperature
(2001)—burns (partial and full
b
thickness) and recessive dystrophic
epidermolysis bullosa with hand
deformities
PMA—fresh, clean, split-thickness,
donor-site wounds in burn patients
No HDE
temperature
Yes One-time use 9 months Room
Off-label—chronic wounds (venous
and diabetic ulcers) [20, 95]
ulcers that have been present for >1
week and extend through the dermis
[95, 97]
Off-label—supercial wounds,
wounds with sinus tracts, and tendon
and osteal repairs [98]
wounds (diabetic and venous ulcers),
acute burns, breast reconstruction,
and other soft tissue trauma and can
be used on exposed joints, muscles,
bones, and tendons [97]
No PHS 361—full-thickness diabetic foot
temperature
No As needed 2 years Room
No PHS 361—chronic non-healing
temperature
No As needed 1.5–4 years Room
Neonatal foreskin-derived
keratinocytes with stratum
corneum (epidermis) and
bovine type-I collagen and
neonatal broblasts (dermis)
Manufacturer Source
Organogenesis,
Inc., Canton, MA
®
Allografts
Table 23.1 Biologic skin substitutes
Apligraf
Neonatal foreskin-derived
epidermal keratinocytes and
dermal broblasts cultured
on bovine type-I collagen
Forticell
Bioscience, Inc.,
NY, USA
®
Orcel
Cadaveric allogenic acellular
dermis with an intact
basement membrane and
dermal matrix with ECM
Wright Medical
Technologies,
Inc., Memphis,
TN
®
Dermal substitutes
GraftJacket
components
Decellularized cadaveric
LifeNet Health,
®
DermACELL
regenerative dermal matrix
Virginia Beach,
VA
23 Science andPracticality ofTissue Products inLimb Salvage
diabetic foot ulcers >6 weeks without
diabetic foot ulcers >6 weeks with no
capsule, tendon, or bone exposure
Internal and external tissue defects,
including acute, chronic, and surgical
wounds
ulcers, pressure ulcer, trauma wounds,
and surgical wounds
exposed tendon or bone [97]
including diabetic and other leg
ulcers; burns treatment and tendon
protection
chronic and acute wounds (diabetic
foot ulcers, venous stasis ulcers,
pressure ulcers), deep chronic
wounds, tendon repair, burns [97]
acute wounds, including diabetic and
venous/arterial ulcers, pressure ulcers,
trauma wounds, surgical wounds,
309
(continued)
burns, and wounds with exposed
muscle, tendon, bone and vital
structures
Yes Partial and full-thickness neuropathic
over SOC Indications
Difference
Storage
temperature
temperature
Yes Neuropathic ulcers, venous stasis
temperature
5 years Room
schedule Shelf-life
Application
cells
Intact
Weekly 3 years Room
Non-
viable
Minimal
disruption is
Non-
viable
ideal but
change as
– Partial and full-thickness neuropathic
needed
No Weekly 3 years Room
Yes Management of chronic and acute,
temperature
temperature
As needed 5 years Room
Non-
viable
No “Wound cover” for management of
−75 to
−85°C
Yes Weekly 3 years
No Management of complex chronic and
temperature
Weekly 5 years Room
Non-
viable
Dehydrated human amnion
and chorion allograft
Manufacturer Source
MFT Biologics,
Edison, NJ
®
Amnioband
Dehydrated human amnion
and chorion membrane with
epithelial cells, basement
membrane, and avascular
connective tissue
Acellular human reticular
dermal tissue
MiMedx,
Marietta, GA
®
Epix
MFT Biologics,
Edison, NJ
®
Allopatch
Pliable
Dehydrated human umbilical
cord allograft on an ECM of
hyaluronic acid and collagen
Cellular placental-based skin
substitute
MiMedx,
Marietta, GA
®
Epicord
Smith + Nephew
Osiris
Therapeutics, Inc.,
Columbia, MD
®
Grax
Trilayered human allograft
membrane
(chorion–amnion–chorion)
Integra
Lifesciences,
Plainsboro, NJ
®
AmnioExcel
310
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wounds including: partial and
full-thickness wounds; pressure
ulcers; venous ulcers; diabetic ulcers;
chronic vascular ulcers; tunneled,
undermined wounds; surgical wounds
(donor sites/grafts, post-Mohs
surgery, post-laser surgery, podiatric,
wound dehiscence); trauma wounds
(abrasions, lacerations, second-degree
burns, and skin tears); draining
wounds” [95]
management of exuding wounds
including: diabetic ulcers, venous
ulcers, pressure ulcers, ulcers caused
by mixed vascular etiologies, full
thickness and partial thickness
wounds, donor sites and other
bleeding surface wounds, abrasions,
traumatic wounds healing by
secondary intention, dehisced surgical
wounds” [95, 99]
partial and full-thickness wounds,
pressure ulcers, venous ulcers,
A. N. Verzella et al.
chronic vascular ulcers, diabetic
ulcers, trauma wounds, surgical
wounds, and draining wounds” [95,
100]
No 510(k) (2006)—“management of
over SOC Indications
Difference
Storage
temperature
temperature
schedule Shelf-life
Application
No Weekly 2 years Room
cells
Intact
<25°C No 510(k)—“intended for the
printed on
packaging
No Daily Use by date
– 510(k) (2013)—“management of
temperature
3 years Room
Kerecis is
absorbed and
no longer
visible
No When previous
Acellular ECM from porcine
jejunal submucosa
Manufacturer Source
Cook Biotech,
Lafayette, IN
®
Table 23.1 (continued)
Oasis
Collagen, oxidized
regenerated cellulose, and
silver on a sponge
3M, Saint Paul,
MN
®
Promogran
Prisma
Decellularized Icelandic
codsh skin that has been
Kerecis,
Arlington, VA
®
Kerecis
harvested, lyophilized, and
freeze-dried
23 Science andPracticality ofTissue Products inLimb Salvage
wounds, donor sites after hemostasis,
protective covering for meshed
autografts [95]
Off-label—dermabrasions, skin-graft
harvesting, laser resurfacing, chronic
wounds, venous ulcers [20, 101]
cover for surgically excised full-
thickness and deep partial-thickness
thermal burn wounds [21]
Off-label—chronic legs ulcers,
diabetic foot ulcers lasting >6 weeks,
wounds including: partial and
full-thickness wounds, pressure
venous ulcers, pressure ulcers [21]
ulcers, venous ulcers, diabetic ulcers,
chronic and vascular ulcers, surgical
wounds (donor sites/grafts, post-
Mohs surgery, post-laser surgery,
podiatric, wound dehiscence), trauma
wounds (abrasions, laceration,
second-degree burns, skin tears), and
diabetic foot ulcers >6 weeks’
duration which extend through the
dermis, but without tendon, muscle,
joint capsule, or bone exposure” [20,
21, 39, 91]
draining wounds” [95]
Off-label—chronic wounds,
311
(continued)
uninfected wounds, temporary or
permanent covering prior to STSG
graft on burn wounds [21, 75, 102]
– 510(k) (2009)—clean supercial burn
over SOC Indications
Difference
Storage
temperature
Room
~3 years (see
schedule Shelf-life
Application
No Typically one
cells
Intact
temperature
use by date
on
packaging)
time use
– PMA (1997)—temporary wound
−70 to
−20°C
18 months
time use
Yes Typically one
Yes 510(k) (2002)—“management of
temperature
6 months Room
disruption is
ideal but
change as
needed
No Minimal
Yes PMA (2001)—“full-thickness
−75°C
+/- 10
Yes Weekly 6 months
Manufacturer Source
Biosynthetic dressings
Porcine collagen in nylon
mesh with semipermeable
outer layer of silicone
Smith and
Nephew, St.
Petersburg, FL
®
Biobrane
Neonatal foreskin broblasts
seeded on bioabsorbable
nylon mesh and covered
Shire
®
Transcyte
Regenerative
with a layer of silicone
Medicine, San
Diego, CA
Bilayer of bovine collagen
cross-linked with
Integra
Lifesciences,
®
Integra
chondroitin-6-sulfate
glycosaminoglycans with a
semipermeable silicone
outer layer
Plainsboro, NJ
Cryopreserved neonatal
foreskin broblasts cultured
on a bioabsorbable
polyglactin polymer mesh
scaffold
Shire
Regenerative
Medicine, Inc.,
San Diego, CA
®
Dermagraft
312
Данная книга находится в списке для перевода на русский язык сайта https://meduniver.com/
A. N. Verzella et al.
over SOC Indications
Difference
Storage
temperature
Several days – No Non-infected chronic lower extremity
schedule Shelf-life
Application
Yes One-time
cells
Intact
ulcers (diabetic foot ulcers)
wounds in the granulation phase such
as pressure ulcers, venous and arterial
No Burns and non-healing wounds
−90°C
2–3 days
[103]
2 days – No 510(k) (2001)—“management of
application
application
Yes One-time
application
Yes One-time
ulcers, diabetic ulcers, surgical
incisions, second degree burns, skin
abrasions, lacerations, partial-
thickness grafts and skin tears,
wounds and burns treated with
meshed grafts. It is intended for use
as a temporary coverage for wounds
thickness burns comprising a total
body surface area of at least 30% for
use with split-thickness autografts or
alone; post nevus excision [95]
Off-label—diabetic and venous ulcers
[21]
and burns to aid in the natural healing
process” [95]
– HDE (2007)—deep dermal or full
13−23°C
1 day
application
Yes One-time
burns
No Non-infected diabetic foot ulcers and
−60°C
2 years
application
Yes One-time
Autologous broblasts
seeded on a 3D hyaluronic
matrix
Cell suspension of
autologous sub-conuent
keratinocytes
Autologous sub-conuent
keratinocytes and broblasts
biopsy on a biodegradable
benzyl esteried hyaluronic
acid matrix
Manufacturer Source
Fidia Advanced
Biopolymers,
Abano Terme,
Italy
CellTrain Ltd.,
UK
Fidia Advanced
Biopolymers,
Abano Terme,
Italy
MySkin
®
Laserskin
®
®
Cultured skin grafts
Hyalograft
Table 23.1 (continued)
3D
Autologous keratinocytes
and murine broblasts from
epidermal biopsy seeded on
petroleum gauze
Vericel Co.,
Cambridge, MA
®
Epicel
Allogenic keratinocytes
from neonatal foreskin
Tegoscience,
Seoul, Korea
®
Kaloderm
HDE humanitarian device exemption: regulatory pathway for products intended for use in rare/infrequent conditions
PMA-FDA premarket approval to evaluate the safety and effectiveness of products and devices that are integral in preventing serious illness or injury
a
b
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