Добавил:
Sekretar
kiopkiopkiop18@yandex.ru
t.me/Prokururor I Вовсе не секретарь, но почту проверяю
Опубликованный материал нарушает ваши авторские права? Сообщите нам.
Вуз:
Предмет:
Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_531_Библиотеки_им_академика_М_И_Перельмана
.pdf
of the lower leg: the cause of lipodermatosclerosis and venous ulceration. Br Med J (Clin
Res Ed) 1982;285:1071–2.
patients with lipodermatosclerosis and venous ulceration. Arch Dermatol
1990;126:1195–7. doi:10.1001/archderm.1990.01670330075010
patients with lipodermatosclerosis and venous ulceration. Arch Dermatol
1991;127:75–8.
biosynthesis by broblasts in vitro. Haemostasis 1989;19:274–83.
Hemorheol 1987;7:119–22.
patients with venous hypertension: a possible mechanism for trophic changes in the
skin. Br Med J (Clin Res Ed) 1988;296:1693–5.
1997;48:71–5. doi:10.1177/000331979704800112
1993;341:1006–8.
possible trapping of transforming growth factor‐β in venous ulceration. Br J Dermatol
1995;132:79–85. doi:10.1111/j.1365‐2133.1995.tb08629.x
1999;38:161–72. doi:10.1046/j.1365‐4362.1999.00581.x
rosis. J Am Acad Dermatol 1993;28:623–7.
carcinoma: a large scale epidemiological study. Br J Dermatol 1995;133:571–4. doi:
10.1111/j.1365‐2133.1995.tb02707.x
clinical practice guidelines of the Society for Vascular Surgery®and the American
Venous Forum. J Vasc Surg 2014;60:3S–59S. doi:10.1016/j.jvs.2014.04.049
raphy in the investigation of venous insuciency. Aust N Z J Surg 1992;62:270–5. doi:
10.1111/j.1445‐2197.1992.tb07554.x
http://dx.doi.org/10.5772/63962
Venous Leg Ulceration
305
venous valvular function of the lower limb. Br J Surg 1994;81:1591–5. doi:10.1002/bjs.
1800811108
diagnosis of chronic venous insuciency. J Vasc Surg 1998;27:660–70. doi:10.1016/
S0741‐5214(98)70231‐9
(plethysmography). In: Gloviczki P, editor. Handbook of venous disorders: Guidelines
of the American Venous Forum. 3rd ed. London: Hodder Arnold; 2009. p. 156–9. doi:
10.1201/b13654‐17
lation 1991;83:120–7.
Disease. Reporting standards in venous disease: an update. J Vasc Surg
1995;21:635–45.
venous disorders. Consensus statement. J Vasc Surg 2004;40:1248–52. doi:10.1016/j.jvs.
2004.09.027
and reproducibility of the revised venous clinical severity score (rVCSS). J Vasc Surg
Venous Lymphat Disord 2013;1:219–24. doi:10.1016/j.jvsv.2012.10.059
D, Kane D, editors. Chronic wound care. 2nd ed. Wayne (PA): Health Management
Publications; 1997. p. 165–71.
Ges 2006;4:627–34. doi:10.1111/j.1610‐0387.2006.06052.x
Dermatol Ges 2011;9:1035–51. doi:10.1111/j.1610‐0387.2011.07814.x
Dermatol 2015;173:379–90. doi:10.1111/bjd.13953
Therap 2013;26:181–6. doi:10.1111/dth.12054
10.1016/0738‐081X(90)90050‐B
10.1016/j.jtv.2013.04.003
Wound Healing: New insights into Ancient Challenges306
a prospective study of aeitology, wound healing, and pain reduction after pinch
grafting. Rheumatology (Oxford) 2001;40:816–20. doi:10.1093/rheumatology/40.7.816
or systemic sclerosis: the importance of concomitant arterial and venous disease. J Vasc
Surg 2000;32:322–9. doi:10.1067/mva.2000.106942
features and response to therapy. Int J Rheumatol 2010:8, article ID 747946, doi:
10.1155/2010/747946
Clin Rheumatol 2007;26:1173–5. doi:10.1007/s10067‐006‐0306‐2
Care Res (Hoboken) 2010;62:1040–6. doi:10.1002/acr.20181
legs in a patient with mixed connective tissue disease. J Dermatol 2011;38:791–3. doi:
10.1111/j.1346‐8138.2010.01177.x
connective tissue disease. J Med 2006;64:91–4.
leg ulceration. Br J Dermatol 2003;148:388–401. doi:10.1046/j.1365‐2133.2003.05222.x
the literature. J Am Acad Dermatol 2011;64:405–12. doi:10.1016/j.jaad.2009.12.007
Intern Med 1997;12:374–83. doi:10.1046/j.1525‐1497.1997.00063.x
circulation in chronic venous insuciency. J Vasc Surg 1994;20:705–10.
Surgery 1961;49:48–58.
1999;9:36–43.
to the wound. Wounds 1989;1:35–51.
Dermatol 1984;120:1329–31.
http://dx.doi.org/10.5772/63962
Venous Leg Ulceration
307
and new. Postgrad Med 1999;105:159–79.
proteolytic enzyme composition suitable for the debridement of burn wound eschar. J
Burn Care Rehabil 1993;14:544–51.
1988;124:544–51.
debridement. Australas J Dermatol 1994;35:35–41. doi:10.1111/j.1440‐
0960.1994.tb01799.x
1989;39:61–9.
venous ulcers. Dermatol Surg 1996;22:643–4. doi:10.1111/j.1524‐4725.1996.tb00611.x
of the therapeutic agents. Wounds 2002;14:47–57.
using a decision analysis methodology. Adv Wound Care 1999;12:81–8.
care. 2nd ed. Wayne (PA): Health Management Publications; 1997. p. 227–34.
Westerhof W, Vanscheidt W, editors. Proteolytic enzymes and wound healing. New
York: SpringerVerlag; 1994. p. 38–9. doi:10.1007/978‐3‐642‐78891‐8_4
venous ulceration. J Vasc Surg 1994;19:525–31.
venous ulcer. Ann Plast Surg 1997;38:611–9.
17.
treatment guidelines: what's new in ve years? Wound Rep Reg 2012;20:619–37. doi:
10.1111/j.1524‐475X.2012.00815.x
sidered in wound management? A report of a consensus meeting on the use of iodine
in wound care. J Wound Care 1997;6:148–50.
Wound Healing: New insights into Ancient Challenges308
Phlebology 2016;31:63–7. doi:10.1177/0268355516633383
a review. J Pharm Sciences 2015;104:3653–80.
wound dressings on healing of chronic wounds: systematic review and meta‐analysis.
Dermatology 2013;226:172–84. doi:10.1159/000348331
on non‐healing wounds: recommendations to improve the quality of evidence
in wound management. J Woundcare 2010;19:239–68. doi:10.12968/jowc.
2010.19.6.48471
program: the role of chronic venous insuciency and patient compliance. J Vasc Surg
1995;22:629–36. doi:10.1016/S0741‐5214(95)70051‐X
1991;17:799–808.
Surg Oncol 1997;23:955–9. doi:10.1111/j.1524‐4725.1997.tb00759.x
particularly with compression stockings. Dermatologist 1980;31:355–65.
61.
Intern Med 1997;12:374–83. doi:10.1046/j.1525‐1497.1997.00063.x
compression therapy and its impact on healing and prevention of recurrence. Int
Wound J 2009;6:386–93. doi:10.1111/j.1742‐481X.2009.00634.x
closure of hard‐to‐heal venous ulcers. Wound Rep Reg 1999;7:201–7.
morphonuclear cell adhesion to cultured endothelial cells. In: Mandell GL, Novicl WJ,
editors. Pentoxifylline and leukocyte function. Sommerville (NJ): Hoechst Roussel
Pharmaceuticals; 1988. p. 68–74.
1998;2:1474–7. doi:10.1016/S0140‐6736(89)92929‐2
http://dx.doi.org/10.5772/63962
Venous Leg Ulceration
309
[92] Falanga V, For the Trental Collaborative Group: Pentoxifylline (Trental) accelerates the
healing of venous ulcers in a double blind randomised study. In: Proceedings from the
European Tissue Repair Society, Cologne, Germany, Aug 25, 1997.
[93] Jull AB, Arroll B, Parag V, et al. Pentoxifylline for treating venous leg ulcers. Cochrane
Database Syst Rev 2012;12:CD001733. doi:10.1002/14651858.CD001733.pub3
[94] de Oliveira Carvalho P, Magolbo NG, De Aquino RF, et al. Oral aspirin for venous leg
ulcers. Cochrane Database Syst Rev 2016 Feb 18;2:CD009432. doi:
10.1002/14651858.CD009432.pub2
[95] Cyrus T, Sung S, Zhao L, et al. Eect of low‐dose aspirin on vascular inammation,
plaque stability, and atherogenesis in low‐density lipoprotein receptor‐decient mice.
Circulation 2002;106:1282–7. doi:10.1161/01.CIR.0000027816.54430.96
[96] Serra R, Rizzuto A, Rossi A, et al. Skin grafting for the treatment of chronic leg ulcers―a
systematic review in evidence‐based medicine. Int Wound J 2016 Mar 4. doi:10.1111/
iwj.12575.
[97] Serra R, Buone G, De Franciscis A, et al. Skin grafting followed by low‐molecular‐
weight heparin long‐term therapy in chronic venous leg ulcers. Ann Vasc Surg
2012;26:190–7. doi:10.1016/j.avsg.2011.04.008
[98] Richmond NA, Maderal AD, Vivas AC. Evidence‐based management of common
chronic lower extremity ulcers. Dermatol Ther 2013;26:187–96. doi:10.1111/dth.12051
[99] Dumville JC, Land L, Evans D, et al. Negative pressure wound therapy for treating leg
ulcers. Cochrane Database Syst Rev 2015 Jul 14;7:CD011354. doi:
10.1002/14651858.CD011354.pub2
[100] Mostow EN, Haraway GD, Dalsing M, et al. OASIS Venus Ulcer Study Group.
Eectiveness of an extracellular matrix graft (OASIS Wound Matrix) in the treatment
of chronic leg ulcers: a randomized clinical trial. J Vasc Surg 2005;41:837–43.
[101] Ehrenreich M, Ruszczak Z. Update on tissue‐engineered biological dressings. Tissue
Eng 2006;12:2407–24. doi:10.1089/ten.2006.12.2407
[102] Cavorsi J, Vicari F, Wirthlin DJ, et al. Best‐practice algorithms for the use of a bilayered
living cell therapy (Apligraf) in the treatment of lower‐extremity ulcers. Wound Repair
Regen 2006;14:102–9. doi:10.1111/j.1743‐6109.2006.00098.x
[103] Fivenson D, Scherschun L. Clinical and economic impact of Apligraf for the treatment
of nonhealing venous leg ulcers. Int J Dermatol 2003;42:960–5. doi:10.1111/j.1365‐
4632.2003.02039.x
[104] Purdue GF. Dermagraft‐tc pivotal ecacy and safety study. J Burn Care Rehabil
1997;18:13–4.
Wound Healing: New insights into Ancient Challenges310
[105] Marston WA. Dermagraft, a bioengineered human dermal equivalent for the treatment
of chronic nonhealing diabetic foot ulcer. Expert Rev Med Devices 2004;1:21–31. doi:
10.1586/17434440.1.1.21
[106] Marston WA, Hanft J, Norwood P, et al. The ecacy and safety of dermagraft in
improving the healing of chronic diabetic foot ulcers: results of a prospective random‐
ized trial. Diabetes Care 2003;26:1701–5. doi:10.2337/diacare.26.6.1701
[107] Hart CE, Loewen‐Rodriguez A, Lessem J. Dermagraft: use in the treatment of chronic
wounds. Adv Wound Care 2011;1:138–41. doi:10.1089/wound.2011.0282
[108] Lazic T, Falanga V. Bioengineered skin constructs and their use in wound healing. Plast
Reconstr Surg 2011;127:75–90. doi:10.1097/PRS.0b013e3182009d9f
[109] Carter MJ, Waycaster C, Schaum K, et al. Cost‐eectiveness of three adjunct cellular/
tissue‐derived products used in the management of chronic venous leg ulcers. Value
Health 2014;17:801–13. doi:10.1016/j.jval.2014.08.001
[110] Hankin CS, Knispel J, Lopes M, et al. Clinical and cost ecacy of advanced wound care
matrices for venous ulcers. J Manag Care Pharm 2012;18:375–84.
[111] Da Costa RM, Ribeiro Jesus FM, Aniceto C, et al. Randomized, double‐blind, placebo‐
controlled, dose‐ranging study of granulocyte‐macrophage colony stimulating factor
in patients with chronic venous leg ulcers. Wound Repair Regen 1999;7:17–25.
[112] Demling RH, Niezgoda JA, Haraway GD, et al. Small intestinal submucosa wound
matrix and full‐thickness venous ulcers: preliminary results. Wounds 2004;16:18–22.
[113] Hill OR. Ultrasound biophysics: a perspective. Br J Cancer 1982;82:46–51.
[114] Moa C, Martin R, Smithdale R. Leg ulcer management. Oxford: Blackwell Publishing
Ltd.; 2007.
[115] Cameron MH. Thermal agents: cold and heat, ultrasound, and electrical currents. In:
Cameron MH, editor. Physical agents in rehabilitation: from research to practice. St.
Louis: WB Saunders; 2003, 2nd ed., p. 133–259.
[116] Busse JW, Bhandari M, Kulkarni AV, et al. The eect of low‐intensity pulsed ultrasound
therapy on time to fracture healing: a meta‐analysis. CMAJ 2002;166:437–41.
[117] Ernst E. Ultrasound for cutaneous wound healing. Phlebology 1995;10:2–4.
[118] Unger PG. Low‐frequency, noncontact, nonthermal ultrasound therapy: a review of the
literature. Ostomy Wound Manage 2008;54:57–60.
[119] Beheshti A, Shagh Y, Parsa H, et al. Comparison of high‐frequency and MIST ultra‐
sound therapy for the healing of venous leg ulcers. Adv Clin Exp Med 2014;23:969–75.
doi:10.17219/acem/37353
http://dx.doi.org/10.5772/63962
Venous Leg Ulceration
311
[120] Douglas WS, Simpson NB. Guidelines for the management of chronic venous leg
ulceration: report of a multidisciplinary workshop. Br J Dermatol 1995;132:446–52. doi:
10.1111/j.1365‐2133.1995.tb08681.x
[121] Chong C. Subfascial endoscopic perforating vein surgery (SEPS) for the treatment of
venous ulcers. Ostomy Wound Manage 2005;51:26–31.
[122] Weinzwieg N, Schuler J. Free tissue transfer in treatment of the recalcitrant chronic
venous ulcer. Ann Plast Surg 1997;38:611–9.
[123] Skouge JW. Techniques for split‐thickness skin grafting. J Dermatol Surg Oncol
1987;13:841–9.
[124] Padberg FT, Johnston MV, Sisto SA. Structured exercise improves calf muscle pump
function in chronic venous insuciency: a randomized trial. J Vasc Surg 2004;39:79–87.
[125] Kelechi TJ, Johnson JJ. Chronic venous disease and venous leg ulcers: an evidence‐based
update. J Vasc Nurs 2015;33:36–46. doi:10.1016/j.jvn.2015.01.003
Wound Healing: New insights into Ancient Challenges312
Topical Wound Oxygen Versus Conventional
Provisional chapter
Topical Wound Oxygen Versus Conventional
Compression Dressings in the Management of
Refractory Venous Ulcers
Sherif Sultan, Wael Tawck, Edel P Kavanagh and
Niamh Hynes
Additional information is available at the end of the chapter
Abstract
Topical wound oxygen (TWO2) proposes an innovative therapy option in the manage‐
ment of refractory non‐healing venous ulcers (RVU) that aims to accelerate wound
healing. TWO2 accelerates epithelialisation. This leads to the development of a higher
tensile strength collagen, which lessens scarring and the risk of recurrence. Sixty‐seven
limbs with 67 ulcers were managed using TWO2 therapy, and 65 limbs with 65 ulcers
were managed using conventional compression dressings (CCD). The proportion of
ulcers completely healed by 12 weeks was 76% in patients managed with TWO2,
compared to 46% in patients managed with CCD (p < 0.0001). The mean reduction in
ulcer surface area at 12 weeks was 96% in the TWO2 therapy group, compared to 61%
in patients managed with CCD. The median time to full ulcer healing was 57 days in
the TWO2 group, in contrast to 107 days in patients managed with CCD (p < 0.0001).
TWO2 patients had a signicantly improved Quality‐Adjusted Time Spent Without
Symptoms of disease and Toxicity of treatment (Q‐TWiST) compared to CCD patients,
denoting an improved outcome (p < 0.0001). TWO2 reduces the time needed for RVU
healing and is successful in pain alleviation and MRSA elimination. TWO2 therapy
radically degrades recurrence rates. Utilising diused oxygen raises the capillary partial
pressure of oxygen (Po2) levels at the wound site, stimulating epithelialisation, and
granulation of new healthy tissue. Taking the social and individual aspects of chronic
venous ulceration into account, the use of TWO2 can provide an overwhelmingly
improved quality of life for long‐time suerers of this debilitating disease.
Keywords: topical wound oxygen, conventional compression dressings, refractory ve‐
nous ulcers, MRSA, epithelialisation
Compression Dressings in the Management of
Chapter 13
Refractory Venous Ulcers
Sherif Sultan, Wael Tawfick, Edel P Kavanagh and
Niamh Hynes
Additional information is available at the end of the chapter
http://dx.doi.org/10.5772/63566
1. Introduction
Chronic venous ulceration is a common disease. Its prevalence is 1% of the total population,
with 20% of venous ulcers presented in octogenarians [1–5]. Refractory venous leg ulceration
is a common basis of morbidity [6, 7] and leads to a reduced quality of life [8], especially in
the elderly population [4, 5]. It causes a considerable amount of work incapacity, social
exclusion and lack of self‐esteem [4]. There is a probable underestimation of the true extent
of venous leg ulceration in the general population due to its underreporting [7]. Venous ulcers
are characterised by a recurring paern of healing and subsequent 70% recurrence rate at
one year [9–14]. Venous ulceration places a huge monetary burden on the healthcare system
[15]. The cost of managing venous ulcers accrues to £400 million sterling per year in the UK
[16].
Ambulatory venous hypertension is one of the leading causes of chronic reperfusion
injury. This in turn provokes venous ulceration with its habitual history of chronicity
and recurrence [1]. Over the past 40 years, compression bandaging has been the gold
standard form of therapy for treatment of venous ulceration. We have learned that
compression will both improve perfusion and enhance healing [2, 17, 18]. Nevertheless,
active healthy tissue granulation can take upwards to 3 weeks to cultivate [19]. There‐
fore, the following question is posed: How can we speed up epithelial coverage in a
granulating wound?
1.1. Topical wound oxygen
Topical wound oxygen (TWO2) proposes an innovative therapy option in the management of
refractory non‐healing venous ulcers (RVU) that aims to accelerate wound healing. The
application of positive pressure oxygen to manage open wounds has been studied extensively
and has demonstrated promising clinical results [20–28]. The systemic complications associ‐
ated with the use of a full‐body hyperbaric chamber have been overcome by the application
of topical wound pure oxygen at an appropriate cycled pressure to only the specic wound
site. This maximizes the benecial wound healing eects and minimizes the negative systemic
side eects [29].
Delivered through a targeted delivery system, a Hyper‐Box, TWO2 accelerates epithelial‐
isation and eliminates MRSA within 72 h. This leads to the development of a higher
tensile strength collagen, which lessens scarring and the risk of recurrence [29–32].
Hyperbaric oxygen promotes angiogenesis and increases the expression of angiogenesis‐
related growth factors [33, 34]. It promotes leukocyte function with enhanced bactericidal
activity [35–40]. The intermient cycled pressure, under which TWO2 is delivered, stimulates
circulation, reduces oedema and provides a sealed humidied environment essential for
healing [41].
Wound Healing: New insights into Ancient Challenges314
Соседние файлы в папке Библиотека им академика М.И. Перельмана