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14 Therapeutic Alternatives forVenous Ulcer
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podiatrists Carrizosa and Antonio from Mexico [42] described that in some patients an opera­tion to elongate the gastrocnemius medially alleviated the pain of venous ulcers.
We designed a study to corroborate these observations and to look for their causes and other variables. For this study, we selected patients with venous ulcers and a positive test for short gastrocnemius, as previously described, and a positive result on the Silfverskiold test [43, 44]; the patients underwent Doppler ultra­sound and measurements were made of the diameters and venous blood velocity in the great saphenous, popliteal, and femoral veins before and after gastrocnemius ultrasound morphology was determined. Short gastrocnemius syndrome was conrmed in all the patients and they were prepared for surgery, in which release of the medial tendon of the gastrocnemius was per­formed under local anesthesia, and a short cut was made in the popliteal fossa skin. This sur­gery releases the tendon of the gastrocnemius muscle, elongating it and recovering adequate function, with which we are able to get the calf muscle pump to work normally again, improv­ing gait biomechanics. With this procedure the musculoskeletal defect was corrected and sub­sequently the muscular pump worked again in better conditions [45]. We obtained the approval of the Ethics Committee and the patients’
informed consent for the procedure. The initial results are very encouraging; the venous ulcers closed within 1–4 weeks after the procedure, and gait improved considerably, as did the dor­siexion angles of the foot, making the test for short gastrocnemius negative. The diameter of the great saphenous vein decreased and the diameter of the gastrocnemius veins also decreased. The study has not yet been com­pleted. Some aspects of the study that deserve attention are that the patients need to re- learn to walk; we have seen that they are afraid to walk “normally” and they lean forward to move the foot. The gastrocnemius veins are usually tortu­ous or enlarged, and determination of this aspect could be a way of diagnosing pump failure; however, more details about the normal and pathologic features of gastrocnemius veins will be required [46]. The elongation of the internal tendon gives the gastrocnemius muscle better capacity to contract and consequently better capacity to pump the venous blood, and the venous hypertension is rapidly decreased sim­ply by walking. In the light of this study, we can ask ourselves some questions about venous ulcers: Is venous hypertension and valvular damage secondary to malfunction of the leg muscles? And do all the venous problems have their origin in alterations of the biomechanics of walking? (Figs.14.1, 14.2, and 14.3).
Fig. 14.1 Before and after release of the medial gastrocnemius tendon in a patient with venous ulcer
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Fig. 14.2 Left, abnormal gastrocnemius vein in Venous Chronic Insufciency (VCI); right contralateral gastrocnemius vein is normal (same patient)
F. VegaRasgado
Fig. 14.3 Left gastrocnemius vein postoperatively; right normal gastrocnemius vein in contralateral leg
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Conclusions
The treatments for venous ulcer are many and
varied; the main point in regard to treatment is
to obtain the correct diagnosis, as many ulcers
that are classied as venous do not meet the cri-
teria for this classication. In 354 leg ulcers,
Koerber found the prevalence of venous leg
ulcers to be 75.25%, of which 3.66% were arte-
rial leg ulcers, 14.66% were mixed ulcers
(venous and arterial), and 13.5% were vasculitic
ulcers [5]. There is a close relation of high rate
of arterial hypertension’s comorbidity (63.2%)
and leg ulcers and this with the prevalence of
ulcers with venous or mixed (arterial-venous)
etiology (about 80%). The cure rate varies from
41% for venous ulcers and decreases to 26% in
ulcers of mixed etiology [47]. For this reason,
drugs may be useful as general treatments in
ulcers of indeterminate etiology, but if only treat
ulcers from venous ethiology the treatment
needs to take into account other causes of
venous hypertension. With this in mind, the dis-
connection of reux points on the venous sys-
tem would be the most important treatment, but
as a venous ulcer is a delayed consequence of
chronic venous insufciency, compression also
plays an essential role in the treatment of dis-
ease, not only alone but as an adjunct with other
therapies. The three-layer system of bandaging
remains as the best method, while other thera-
pies such as drugs and exercise can be helpful.
The integral management of venous ulcers is
not a “magic procedure,” it is a logical matter
that requires common sense, a little science, and
a lot of patient care. To provide better treatment
for our patients, we also need to consider addi-
tional factors, such as gait biomechanics, mobil-
ity of the leg joints, muscle function, concomitant
diseases, and many other causes or complica-
tions of venous ulcers.
References
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clinical practice guidelines of the Society for Vascular Surgery and the American Venous Forum. J Vasc Surg. 2014:60 3S–59S.
2. Zimmet SE. Venous leg ulcers: modern evaluation. Dermatol Surg. 1999;25:236–41.
3. Suan SL, Lakhanpal S, Marquez J.Supercial vein ablation for the treatment of primary chronic venous ulcers. Phlebology. 2011;26:311–6.
4. Apollonio A, Antignani PL.Epidemiology and heal­ing of vascular ulcers in Italy. Preview of the SUV study results (AIUC September 2012): short report. Acta Phlebologica. 2012;13(2):101–3.
5. Koerber A, Schadendorf D.Genese des ulcus cruris. Hautarzt. 2009;60:488.
6. Nelzén O, Bergqvist D, Fransson I, Lindhagen A. Prevalence and aetiology of leg ulcers in a de ned population of industrial workers. Phlebology. 1996; 11:50–4.
7. Nelzén O, Bergqvist D, Lindhagen A.Leg ulcer etiol­ogy—a cross-sectional population study. J Vasc Surg. 1991;14:557–64.
8. Nelzén O, Bergqvist D, Lindhagen A.The prevalence of chronic lower-limb ulceration has been underesti­mated: results of a validated population questionnaire. Br J Surg. 1996;83:255–8.
9. Nelzenn O. Epidemiology of venous ulcers. In: En CK, Bergan JJ, editors. Venous ulcer. London: Elsevier; 2007. p.34–6.
10. Vega F.Fundamentos de Flebología. México: Instituto Mexicano de Flebología; 2013.
11. O’Meara S,CN. Compression for venous leg ulcer. Cochrane Database Syst Rev. 2012;11:CD000265.
12. Partsch H. Compression for the management of venous leg ulcers: which material do we have? Phlebology. 2014;29(1S):140–5.
13. Jünger M, Steins A, Hahn M, Häfner HM. Microcirculatory dysfunction in chronic venous insufciency (CVI). Microcirculation. 2000;7(S1): S3–S12.
14. Ogrin R, Darzins P, Khalil Z. Neurovascular changes after four-layer compression bandaging in people with chronic venous leg ulcers. Phlebology. 2007;22(2):49–55.
15. Mosti G.Compression in mixed ulcers: venous side. Phlebology. 2014;29(1S):13–7.
16. Mosti G, Cavezzi A.A prospective multicenter ran­domized controlled trial comparing the new 2-com­ponent bandage system Coban 2 with a zinc oxide bandage. Acta Vucanologica. 2010;8(3):119–27.
17. Vega Rasgado F, Rendón F-R.Treatment of veno­lymphatic ulcer with compression system of couma­rin-zinc-oxide. Spanish J Surg Res. 2007;X(3):161–5.
18. Schuler JJ, etal. Treatment of chronic venous ulcers using sequential gradient intermittent pneumatic com­pression. Phlebology. 1996;11:111–6.
19. van Gent WB, Catarinella FS, Nieman FHM, Toonder IM, van der Ham AC, Wittens CHA. Conservative versus surgical treatment of venous leg ulcers: 10-year follow up of a randomized, multicenter trial. Phlebology. 2015;30(1S):35–41.
20. Grover G, et al. Chronic venous leg ulcers: effects of foam sclerotherapy on healing and recurrence. Phlebology. 2016;31(1):34–41.
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21. Akesson H.Long-term clinical results following cor­rection of incompetent supercial and perforating veins in patients with deep venous incompetence and ulcers. Phlebology. 1993;8:128–31.
22. Sullivan PL, et al. Retrograde mechanico-chem­ical endovenous ablation of infrageniculate great saphenous vein for persistent venous stasis ulcers. Phlebology. 2014;29(10):654–7.
23. Owens PA. Ultrasound-guided foam sclerotherapy. Phlebology. 2007;22(1):24–9.
24. Williamsson C, etal. Catheter-directed foam sclero­therapy. Phlebology. 2014;29(10):688–93.
25. Vega RF, Ramirez C, et al. First Mexican sclero­therapy consensus. Primer Consenso Mexicano de Escleroterapia. Phlebologie. 2014;1:1–12.
26. Palfreyman SJ, Nelson EA. Dressings for healing venous leg ulcers. Cochrane Database Syst Rev. 2006;19(3):CD001103.
27. O’Meara S. Foam dressings for venous leg ulcers. Cochrane Database Syst Rev. 2013;31(5):009907.
28. O’Meara S, Martyn-St James M.Alginate dressings for venous leg ulcers. Cochrane Database Syst Rev. 2015;30(8):CD010182.
29. Dumville JC, Land L, Evans D, Peinemann F.Negative pressure wound therapy for treating leg ulcers. Cochrane Database Syst Rev. 2015;14(7):CD011354.
30. Mosti G.Wound care in venous ulcers. Phlebology. 2013;28(Suppl 1):79–85.
31. Smith M, etal. Biolm dressing for venous leg ulcers. Phlebology. 1992;7:108–13.
32. Simka M. Chronobiology of venous ulcers. Phlebology. 2010;25:29–34.
33. Barwell R, etal. Ankle motility is a risk factor for healing of chronic venous leg ulcers. Phlebology. 2001;16:38–40.
34. Bogachev VY, Lobanov VN.Electrical muscle stimu­lation with Veinoplus® device in the treatment of venous ulcers. Int Angiol. 2015;34(3):257–62.
35. Villa V, Froio A.Application of autologous platelet­rich gel to non healing vascular ulcers. Ital J Vasc Endovasc Surg. 2011;18(1):31–8.
36. Christenson JT. Postthrombotic or non-postthrom­botic severe venous insufciency. J Vasc Surg. 2007;46(2):316–21.
37. Christenson JT.Subcutaneous fasciotomy and eradi­cation of supercial venous reux. Phlebology. 2011;26:197–202.
38. Jull AB.Pentoxifylline for treating venous leg ulcers. Cochrane Database Syst Rev. 2012;1(12):CD001733.
39. Marinel-lo-Roura J, et al. Pharmacoeconomic analy­sis of pentoxifylline in venous leg ulcers treatment. Angiologia. 2007;59(1):45–54.
40. Scondotto G. Treatment of venous leg ulcers with sulodexide. Angiology. 1999;50(11):883–9.
41. Wu B, etal. Sulodexide for treating venous leg ulcers. Cochrane Database Syst Rev. 2016;6:CD10694.
42. Carrizosa Q, Antonio H. Relación del Sistema Aquíleo-Calcáneo-Plantar en las Úlceras venosas, valoración y tratamiento. Tesina de Diplomado. México: Instituto Mexicano de Flebología, Escuela Superior de Medicina I.P.N.Ciudad de México; 2015.
43. Barouk LS, Barouk P.Gastrocnemios cortos. Revista del pie y tobillo. 2012;XXVI(2):7–13.
44. Barouk LS, Barouk P. Gastrocnemios cortos- de la anatomía al tratamiento. Paris: Sauramps Medical; 2012.
45. De los Santos Real R, Morales MP, Payo RJ, Escalera AJ.Liberación proximal del gemelo medial por mínima incisión. Revista del pie y tobillo. 2011;XXV(1):42–6.
46. Uhl J-F, Gillot C.Anatomy of the veno-muscular pumps of the lower limb. Phlebology. 2015;30(3):180–93.
47. Apollonio A, etal. Epidemiology and healing of vas­cular ulcers in Italy. Acta Phlebologica. 2012;13(2): 101–3.
Compression Therapy forVenous
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Ulcer
GiovanniMosti
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15.1 Introduction
Leg ulcers have a venous pathophysiology in the vast majority of cases [1–4]. Supercial or deep venous insufciency and deep vein obstruction produce ambulatory venous hypertension due to venous reux and venous pumping function impairment. The impaired venous hemodynamics is the key pathophysiologic mechanism leading to skin damage through several intermediate steps.
Fibrin cuff formation around the microvessels leading to impaired gas (O2, CO2) exchange [5], white cell entrapment [6] causing skin necrosis, and growth factor inhibition [7] producing a stag­nation of the healing process have been consid­ered involved in ulcer onset and maintenance.
The treatment of venous leg ulcers (VLU) must be based on the correction of the hemodynamic impairment which can be achieved conservatively by means of compression therapy, walking, and leg elevation or by means of inva­sive procedures (open surgery, endovascular procedures as endovenous laser ablation, radio­frequency, foam sclerotherapy, conservative hemodynamic treatment).
G. Mosti Angiology Department, MD Barbantini Clinic, Lucca, Italy
Compression therapy is frequently considered the rst treatment option, and it is the only thera­peutical procedure which achieved the grade 1A in most recent guidelines [8, 9]. The crucial point is choosing the most effective compression modality, which is still a matter of debate.
On one side there are clear evidences that inelastic is more effective than elastic material in counteracting the venous hemodynamic impairment [10–14]. This should “ensure” a superior effectiveness in promoting a higher healing rate of VLU, which are due to venous hemodynamic impairment. In addition we have some evidences that the higher the compression pressure, the higher the healing rate [9, 15, 16], and this is clearly in favor of inelastic bandages which exert a much higher pressure than elastic materials.
On the other side, we have many papers claim­ing a greater effectiveness of elastic stockings or elastic bandages compared with inelastic mate­rial [17–30].
Nevertheless studies comparing elastic and inelastic devices have so many aws that their conclusions are hard to trust [31].
In this chapter we will try to provide updated information about compression therapy effects on venous hemodynamic and the most effective compression modality to achieve the best out­come in VLU treatment.
© Springer Nature Singapore Pte Ltd. 2018 A. K. Khanna, R. Jindal (eds.), Venous Disorders, https://doi.org/10.1007/978-981-13-1108-6_15
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15.2 Impaired Venous Hemodynamics
The venous pressure in the legs depends on body position: it is very low in supine position, it increases in the sitting position, and it is maximal in standing position. Actually in the sitting and standing position, the hydrostatic venous pres­sure results from the unbroken column of uid that extends from the right heart to the foot which can be easily measured by calculating the dis­tance from the right heart and the ankle in these different positions.
In the standing position, the venous pressure is about 70–80 mmHg both in normal individuals and in patients with venous disease. In the normal subjects, this pressure decreases signicantly during active movements (e.g., walking) down to 20–30 mmHg due to venous pumping function and valvular function that fragment the blood column and reduce the hydrostatic venous pres­sure [32]. In patients with venous insufciency, valves’ failure causes the column of standing blood in the vein to remain unbroken even during ambulation, and a minimal hydrostatic pressure decrease occurs. In some clinical situations (e.g., venous obstruction), the hydrostatic pressure can even increase during and immediately after ambulation: this is what we call ambulatory venous hypertension (AVH) which causes venous congestion.
15.3 Eectiveness
ofCompression Therapy inCounteracting Ambulatory Venous Hypertension (AVH)
Compression therapy increases the transmural pressure increasing the extravenous pressure so narrowing or occluding the leg veins. This is the prerequisite for the hemodynamic effectiveness of compression therapy, but venous narrowing/ occlusion can be possible only by applying an external pressure of the same magnitude or higher than intravenous pressure. Actually, it has been shown that due to different venous pressures in
different body positions, a low external pressure in the range of 20 mmHg is able to narrow or occlude the veins in the supine position, but the compression pressure must rise to 50mmHg in the sitting position and to close to 70–80mmHg in the standing position [33] to exert the same effect. These data were conrmed by studies with magnetic resonance imaging (MRI) showing that in the standing position, a pressure of 40mmHg is not able to occlude the veins that are com­pletely occluded with a pressure of 80 mmHg [34] which was dened as very strong in a recent consensus paper [35].
Such high external pressure approaching or overcoming the intravenous pressure may produce a vein occlusion at every step during physical activity, so restoring a kind of valve mechanism. In this way compression reduces the AVH [14] by reducing the venous reux [10, 11] and increasing the calf pumping function [12, 13].
15.4 Which Compression Material
Is Able toCounteract AVH
All compression devices are basically made up with elastic or inelastic material. When wrapped on the leg, they exert a compression pressure which, according to the Laplace law, depends on the stretch applied to the bandage, the number of turns, and the radius of the leg segment [36].
The two materials have completely different physical characteristics.
The elastic or long-stretch material (repre­sented by elastic stockings or elastic bandages with an extensibility higher than 100%) gives way to the muscle expansion, which occurs dur­ing standing and physical activity, resulting in a very low pressure difference between the resting and standing or walking conditions. The static stiffness index (SSI) which is the difference between the standing and the supine pressure is lower than 10mmHg that characterizes the elas­tic range [37, 38]. Also the difference between diastolic and systolic pressure during muscular activity, responsible of these called “massaging effect” [39] of compression devices over the calf muscle, is very low. These characteristics are
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consistently maintained independently on applied pressure and material (if elastic stockings or elas­tic bandages). In conclusion elastic material exerts a quite sustained pressure. In addition it tends to regain its initial length when stretched, and this “return force” is directly related to the stretch applied to the bandage. The “squeezing effect” of a too stretched elastic material can be painful and not tolerated by the patients after a short time from application. As a consequence, when properly stretched, an elastic bandage will exert a supine pressure of 30–40 mmHg. This pressure will rise by 4–8 mmHg in a standing position and will never approach the intravenous pressure resulting unable to narrow or occlude the veins and to exert a hemodynamic effect (Figs.15.1, 15.2, and 15.3). When we want to use elastic material to exert a very strong pressure in standing position, necessary to occlude the leg veins, elastic bandages must be applied with strong stretch, or several elastic stockings must
be superimposed: in both these circumstances, the “squeezing effect” of these materials will be painful and poorly tolerated, as reported (Fig.15.4).
An advantage of elastic materials is that they are easy to apply, usually as a single component.
The inelastic material (short stretch or inex­tensible bandages, Velcro devices, hybrid pumps) exerts its effect by resisting the increase of mus­cle volume during muscular contraction in stand­ing position and during physical activity (the leg will give way) so producing higher peak pres­sures when standing or walking compared with elastic, long-stretch devices. Inelastic material doesn’t have any elastic ber and doesn’t have any return force: it doesn’t “squeeze” and can be applied with full stretch.
The modern composite, multilayer and mul­ticomponent, inelastic bandages, including a padding layer with the inelastic material as a last component, exert a relatively low and
Fig. 15.1 Compression pressure tracings of an elastic stocking of the second class according to the RAL regula­tory (mm 23–32 mmHg). Compression pressure increase by dorsiexions, standing up, and walking is very small: sustained pressure. DSI (dynamic stiffness index) is the dif-
ference between diastolic and systolic pressure performing foot dorsiexions in supine position; SSI (static stiffness index) is difference between standing and supine position. WPA (walking pressure amplitude) is the difference between systolic and diastolic pressure while walking
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Fig. 15.2 Compression pressure tracings of an elastic kit made up of two superimposed elastic stockings exerting about 40mmHg in supine position. Compression pressure
increase by dorsiexions, standing up, and walking is very small: sustained pressure despite of the resting pressure increase
Fig. 15.3 Compression pressure tracings of an elastic bandage exerting about 40 mmHg in supine position. The dynamic characteristic is the same as with elastic stockings or kits
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Fig. 15.4 Pressure curve of an elastic bandage applied with high stretch to exert a very strong standing pressure. It can be noticed that also the supine pressure must be
well- tolerated pressure at rest but a much higher pressure often higher than 70 mmHg during standing. The SSI is always >10 that character­izes the inelastic range. The intermittently strong or very strong pressure peaks during muscular exercise will overcome the intrave­nous pressure intermittently occluding the vein and so restoring a kind of valvular mechanism [14] (Figs.15.5 and 15.6).
In a few words, the inelastic material is able to adapt to the body position by exerting a rela­tively low pressure in the resting position (com­fortable) and a strong or very strong pressure in the standing position and during muscle activity (effective) coming close to an ideal compression device [40].
Unfortunately the multilayer, multicomponent inelastic bandages are difcult to apply and require expert and well-educated personnel. In a series of papers, it was demonstrated that only from 10 to 60% (depending on the paper) of health personnel treating venous ulcers were able to apply the target pressure with different inelas­tic bandages [41–45].
very strong as the pressure increase by standing is very small with elastic material. This strong and sustained pressure can be painful
15.5 Hemodynamic Eects ofCompression Materials
The different physical properties of elastic and inelastic materials result in completely different effects on venous hemodynamics.
Inelastic is signicantly more effective than
elastic material in:
• Reducing venous reux both in patient with
deep venous [10] and supercial venous incompetence [11]
• Improving the venous pumping function
severely reduced in venous insufciency [12, 13]
• Reducing AVH [14]
Inelastic material is able to reduce venous reux and increase venous pumping function even at a low/mild pressure range of 20–40mmHg [46] which has an important implication when inelastic compression necessary to improve venous hemodynamics must be applied with
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Fig. 15.5 Pressure curve of an inelastic bandage exerting a supine pressure of 60 mmHg. Compression pressure increase by dorsiexions, standing up, and walking is very
high: intermittent compression with high pressure peaks that overcome the intravenous pressure (represented by the red line) restoring a kind of valvular function
Fig. 15.6 Pressure curve exerted by a Velcro device designed for ulcer treatment. Also with this device, com­pression pressure increase by dorsiexions, standing up,
and walking is high overcoming the intravenous pressure and restoring a kind of valvular function