CHAPTER 1 HOW COMPRESSION WORKS

Transcription

1 CHAPTER 1 HOW COMPRESSION WORKS The impact that compression has had on leg ulcer healing over the last two decades has been enormous. Although it is frequently reported that compression has been in use since the time of the Egyptians, the reality in clinical practice is that real improvements in outcome have only been seen in more recent years (Moffatt et al, 1992; Cullum et al, 2001). There are many reasons why this has occurred, but the most important are: the technological advances in compression therapy a greater understanding of the physiological mechanisms of compression (European Wound Management Association [EWMA], 2003) a concerted effort to introduce compression into clinical practice in many parts of the world. How does compression work? The physiological basis for compression therapy is now relatively well established for venous ulceration, although less so for lymphoedema and patients with complex conditions requiring compression (Lymphoedema Framework, 2006a, b). The highest level of compression is applied near the surface of the skin, with less applied to deeper structures such as veins and arteries. The amount of pressure applied depends on the degree of compression and the type of material used. Two recent position documents have summarised the way in which compression works on the venous, arterial and lymphatic circulation (EWMA, 2003; Lymphoedema Framework, 2006a). Much of the work presented in this chapter is drawn from these excellent resources. 1 Chap 1.indd 1 28/3/07 11:41:10

2 Compression Therapy in Practice Effects of compression on venous circulation The requirements for compression in venous disease vary according to whether the patient is bedridden or able to walk. This is because the pressure in the venous system is much higher when the patient is standing ( mmhg pressure), and is equal to the weight of the column of blood from the right atrium to the foot (Partsch, 2003) (Figure 1.1a). However, during walking (in a patient with normal venous circulation) when the calf and foot pumps are activated, the pressure rapidly drops to about mmhg (Figure 1.1b). When lying down, the pressure in the venous system is much lower and is further reduced if the legs are elevated. When venous disease occurs and the large veins become incompetent due to damage to the valves from deep vein thrombosis (DVT) or primary or secondary varicose veins, blood refluxes back towards the feet instead of passing smoothly up towards the heart. Blood oscillates between the damaged segments of valves. This leads to a gradual rise in pressure in the venous circulation, called ambulatory venous hypertension. Walking is no longer effective at reducing the pressure and changes occur in Figure 1.1a: Weight of the column of blood Pressure in leg veins (mmhg) without action of skeletal muscle pump Figure 1.1b: The effects of walking on reducing pressure in normal individuals, and those with degrees of venous disease compression Chap 1.indd 2 28/3/07 11:41:11

3 How compression works the microcirculation leading to oedema formation, tissue changes (lipodermatosclerosis) and, ultimately, ulceration in a small percentage of patients. The application of adequate compression has a number of haemodynamic effects that are discussed below. Haemodynamic effects Reduction in the diameter of the superficial and deep main veins. This leads to a reduction in the local blood volume (Figure 1.2). Accelerated flow. Narrowing of the vein diameter leads to increased flow velocity, providing the arterial circulation remains the same. Movement of blood into the central components of the body. The action of compression on the legs causes a shift in blood to the central components of the body (Figure 1.3). When bilateral compression is applied there can be a 5% increase in cardiac output and a potential overload to the heart in those with mild heart failure (Mostbeck et al, 1977). This is the reason why bilateral compression is not advised in these vulnerable patients, and low levels of pressure are introduced and monitored according to the patient s symptoms. Differences in level of compression according to the patient s position. Patients who are lying in bed require very low levels of pressure (> 10 mmhg) to control venous stasis. This is sufficient to prevent thrombus formation and is provided when using anti-embolic stockings. Pressures in excess of 30 mmhg do not have a beneficial effect if the patient remains lying down, as the venous pressure is reduced to the lowest possible level. When standing or walking, far higher levels of pressure are required to influence blood flow. The pressure during walking fluctuates between mmhg and, therefore, working pressures of mmhg are required to influence this (Partsch, 1991). Reduction of venous reflux Possibly one of the most important effects of compression is 3 Chap 1.indd 3 28/3/07 11:41:11

4 Compression Therapy in Practice its ability to reduce venous reflux (Partsch, 2003) (Figure 1.4). Inelastic and multi-layer bandage systems, such as Profore (Smith & Nephew), have been shown to be more effective at achieving this than single-layer, elastic bandages (Partsch et al, 1999). High compression reduces venous reflux in the deep and superficial venous systems in the standing position. Early theories suggested that this was a mechanical effect that brought the valves back into opposition, thus reducing venous reflux; however, this cannot be completely attributed to this, as venous reflux is also improved in those patients with a congenital abnormality causing an absence of valves (Partsch, 1991). How does compression work? Accelerating venous flow Reduction in vein diameter increases venous velocity Figure 1.2: Reduction in vein diameter with compression How does compression work? Redistributes blood to central sections of body Central haemodynamic effects Bilateral compression 20% increase in central blood volume and increased stroke volume Increased pre-load to heart Increased cardiac output Figure 1.3: Movement of blood into central components of the body 4 Chap 1.indd 4 28/3/07 11:41:12

5 How compression works How does compression work? Compression increases forward flow Reduction in venous reflux Without compression applied Inelastic and four-layer bandage more effective than elastic material (Partsch et al, 1999) Improved valve function and reduced refl ux Figure 1.4: Reduction in venous reflex Improvement in venous pumping A vital component of a healthy venous circulation is an effective calf and foot pump to assist venous return (Figure 1.5). Many elderly patients with venous ulceration have poor mobility with factors such as osteoarthritis and rheumatoid arthritis reducing their ability to walk (Franks et al, 1995). Research has shown that reduced mobility and a fixed ankle joint significantly affect ulcer healing, with those who reach the stage of being chairbound being the most affected (Franks et al, 1995). How does compression work? O O F Improved venous pump function Compression assists calf muscle pump O F O Rest Systole Diastole Figure 1.5: Improved venous pump function 5 Chap 1.indd 5 28/3/07 11:41:13

6 Compression Therapy in Practice Reduction in ankle function Reduction in ankle function is common, although the exact mechanisms have not been clearly defined. Protracted periods of time wearing compression therapy may cause long-term damage to the ankle joint (arthrodesis) (Figure 1.6). Pain around the ankle may prevent the patient from exercising, with a gradual loss of ability to perform dorsiflexion, extension and circular movements. Sclerotic tissue changes may also contribute to the gradual loss of ankle function (Figure 1.7). Shortening of the Achilles tendon, as a result of ulceration in this area, or damage to the tendon are difficult clinical problems. Equinus deformity has been found in 10% of a chronic ulcer population in south-west London (Moffatt et al, 2004). This deformity causes reduction in venous return and delayed ulcer healing (Figure 1.8). The degree of venous incompetence influences the effectiveness of the venous pump function. Compression therapy, particularly inelastic systems and multi-layer bandage systems, have been shown to be more effective than elastic, single-layer bandages at improving venous pumping and reducing ambulatory venous hypertension (Partsch et al, 1981). Partsch suggests that this may be due to the bandages ability to narrow the veins during walking. Figure 1.6: Fixed ankle deformity Figure 1.7: Ankle deformity associated with venous ulceration Figure 1.8: Equinus deformity 6 Chap 1.indd 6 28/3/07 11:41:14

7 How compression influences oedema How compression works Oedema is the accumulation of fluid in the extravascular tissue. Oedema is associated with many different clinical conditions, and is a result of a number of complex mechanisms (EWMA, 2003). The causes of different types of oedema are depicted in Table 1.1. Table 1.1: Causes of oedema Physiology Possible cause Effect Increased capillary permeability Increased venous (capillary) pressure Increased oncotic tissue pressure Decreased oncotic capillary pressure Cellulitis, arthritis, hormonal cyclic oedema Heart failure, venous insufficiency, dependency syndrome Failure of lymph drainage Hypoalbuminaemia, nephrotic syndrome, hepatic failure Inflammatory oedema, idiopathic oedema Cardiac, venous oedema. Oedema due to sitting for a long time Lymphoedema Hypoproteinaemic oedema Source: Partsch H (2003) Understanding the pathophysiological effects of compression. In: European Wound Management Association (EWMA). Position Document: Understanding compression therapy London: MEP Ltd, 2003; 2 4 Increased permeability When inflammation occurs, due to any cause, a complex interaction takes place with the release of chemical mediators such as histamine that lead to oedema formation. The capillaries become more permeable allowing fluid to accumulate in the tissues as oedema. Increased venous pressure As already discussed, damage to the venous circulation causes reflux of venous blood and a rise in pressure in the venous system. This increase in capillary pressure causes enlargement of the pores within the wall of the vessel, and fluid and other macromolecules pass into 7 Chap 1.indd 7 28/3/07 11:41:17

8 Compression Therapy in Practice the interstitium. Other causes of oedema from increased venous pressure include: cardiac oedema where the heart can no longer pump blood effectively around the body (Figure 1.9) dependency oedema when the limb is kept hanging down and immobile (Figure 1.10). Increased oncotic pressure Oncotic pressure has been defined as, the osmotic pressure created by protein colloids in plasma. Figure 1.9: Oedema due to cardiac failure Figure 1.10: Dependency oedema 8 Chap 1.indd 8 28/3/07 11:41:17

9 How compression works Increased oncotic pressure occurs in patients with lymphoedema, where there is a failure of the lymphatic system to transport the lymphatic load (EWMA, 2005). Lymphoedema is caused either by morphological or functional damage to the lymphatic system (Figure 1.11). Oedema containing protein, water, cell debris and hyaluronan accumulate in the interstitium and hypertension develops in those lymphatic vessels that remain functioning. Swelling generally involves the Figure 1.11: Lymphoedema limbs, but may also include the trunk, genitalia, fingers and toes. The accumulation and impaired transport of immune cells leads to chronic inflammatory changes. Chronic, recurrent episodes of cellulitis frequently occur (Figure 1.12), promoting further fibrotic tissue changes and the laying down of adipose tissue. These combined effects lead to a progressive worsening of the overall condition of the patient. Figure 1.12: Chronic, recurrent bouts of cellulitis 9 Chap 1.indd 9 28/3/07 11:41:18

10 Compression Therapy in Practice Practical point As soon as compression is removed rapid accumulation of oedema will occur. Therefore, compression must not be left off for any length of time, except when the patient goes to bed at night. Decreased oncotic capillary pressure Reduced oncotic capillary pressure occurs in conditions where there is a loss of protein from the body. The commonest causes are nephrotic syndrome and liver failure. Patients who are extremely malnourished and have a very low albumin level may also develop severe oedema. In this situation, the imbalance between the tissue oncotic pressure (higher pressure) and the capillary oncotic pressure (lower pressure), causes fluid to be drawn into the tissues and accumulate as oedema. Compression works by encouraging reabsorption of oedema into the lymphatic and venous circulation, and by preventing filtration from the capillary (Figure 1.13). This mechanism is defined as Starling s equation (Box 1.1). Research has shown that compression removes more water than other molecules such as proteins (Partsch et al, 1981). This means that the oncotic pressure in the tissues increases when the fluid component has been removed. This causes rapid accumulation of oedema and reinforces the need for the continuous use of compression. How does compression work? Improved lymphatic function and oedema reduction Reduced fi ltration and enhanced reabsorption Compression Filtration Reabsorption Filtration Reabsorption Compression Figure 1.13: Reduced filtration and increased absorption influences oedema 10 Increased fi ltration leading to oedema formation Chap 1.indd 10 28/3/07 11:41:19

11 How compression works Effects of compression on arterial circulation One of the most important priorities of assessment prior to using compression therapy is to ensure that the patient is not suffering from significant peripheral arterial occlusive disease (Figure 1.14). These issues are discussed further in Chapter 2. The recommendations for patients with reduced ankle to brachial pressure index (ABPI) are considered in Chapter 6 (International Leg Ulcer Algorithm, p. 63). There is general agreement that the level of compression should not impede arterial inflow, although the exact level has not been defined through research. International consensus recommends that high compression (> 35 mmhg) should not be applied if the patient has an ABPI below 0.8. The absolute ankle systolic pressure is also a useful guide, with a pressure below mmhg indicating that high compression should not be used (EWMA, 2003). It is important to remember that poor application of compression may apply very high pressures and every care should be taken to ensure correct bandage application to all patients with evidence of established peripheral arterial occlusive disease. A sudden increase in pain with compression often indicates that the disease has worsened, and compression should be discontinued and the patient reassessed. Figure 1.14: Ulceration associated with peripheral vascular disease (PVD) 11 Chap 1.indd 11 28/3/07 11:41:20

12 Compression Therapy in Practice Removal of oedema by the use of intermittent pneumatic compression (IPC) devices, that exert rapid cycles of pressure (30 80 mmhg), can effectively remove oedema, which has been shown to improve arterial flow (Mayrovitz and Larsen, 1997). Effects of compression on lymphatic circulation Compression shows an impressive reduction in oedema although the reasons remain poorly understood (Lymphoedema Framework, 2006a, b). A number of mechanisms have been proposed in a recent international focus document on lymphoedema bandaging, these are: reduction in capillary filtration shift of fluid into non-compressed parts of the body increase in lymphatic reabsorption and stimulation of lymphatic transport improvement in the venous pump in patients with venolymphatic dysfunction breakdown of fibrosclerotic tissue. (EWMA, 2005: 2) In addition to the mechanisms of compression described for venous disease, a number of other factors are important in the patient with lymphoedema. Compression shifts fluid from damaged areas receiving compression to healthy areas with functioning lymphatics. Compression, when performed as part of an intensive treatment (Chapters 12, 13 and 14), reduces microlymphatic hypertension in patients with lower limb lymphoedema. A normalisation of microlymphatic pressure can be seen after two weeks of intensive treatment with compression bandaging and manual lymphatic drainage (MLD) (Lymphoedema Framework, 2006a). A continuous pressure of mmhg appears to sustain this improvement over time. Studies using lymphoscintigraphy showed that after several weeks of 12 Box 1.1: Starling s equation F = c(pc-pt) - (πc-πt) F c Pc Pt πc πt net filtration force (which is the origin of lymph) filtration coefficient capillary blood pressure tissue pressure capillary oncotic pressure tissue oncotic pressure Chap 1.indd 12 28/3/07 11:41:21

13 How compression works compression therapy, improvement was not uniform and did not occur in those with severe, indurated lymphoedema (Lymphoedema Framework, 2006a). Phlebolymphoedema Patients with postphlebitic syndrome have reduced subfascial lymph transport and are at risk of developing clinical signs of lymphoedema (Haid et al, 1968) (Figure 1.15). Compression therapy with inelastic bandages has been shown to improve this situation. Compression stimulates the breakdown of fibrotic tissue. In patients with venous ulceration and lipodermatosclerosis, compression increases blood flow to areas of poor perfusion due to high tissue pressure. This leads to a gradual softening of the sclerotic tissue over time with long-term use of compression therapy (Falanga and Bucalo, 1993). Effects of compression on microcirculation There is increasing evidence that compression therapy influences cellular changes within the microcirculation. These are complex and poorly understood. Blood flow in the microcirculation accelerates, helping to prevent white cell adhesion and activation which leads to the release of inflammatory cytokines (Abu- Own et al, 1994). The role of proteases and degradation of the extracellular matrix is also being investigated. Reduction of pain with compression therapy may be a consequence of reducing the level of inflammatory cytokines, as healing progresses and oedema is controlled (Murphy et al, 2002). This is a rapidly Figure 1.15: Phlebolymphoedema 13 Chap 1.indd 13 28/3/07 11:41:21

14 Compression Therapy in Practice developing field and a full description of these issues lies outside the remit of this book. Conclusion It is important that practitioners understand the physiological mechanisms of compression therapy to be able to make informed decisions about the different types of compression material that may be most beneficial in different clinical situations. References Abu-Own A, Shami SK, Chittenden SJ, et al (1994) Microangiopathy of the skin and the effect of leg compression in patients with chronic venous insufficiency. J Acta Vasc Surg 19: Cullum NA, Nelson EA, Fletcher AW, Sheldon TA (2001) Compression for venous leg ulcers (Cochrane review). In: The Cochrane Library, Update software, Oxford European Wound Management Association (2003) Position Document. Understanding compression therapy. MEP Ltd, London European Wound Management Association (2005) Focus Document: Lymphoedema bandaging in practice. MEP Ltd, London Falanga V, Bucalo B (1993) Use of a durometer to assess skin hardness. J Am Acad Dermatol 29(1): Franks PJ, Moffatt CJ, Connolly M, Bosanquet N, Oldroyd MI, Greenhalgh RM, McCollum CN (1995) Factors associated with healing leg ulceration with high compression. Age Ageing 24: Haid H, Lofferer O, Mostbeck A, Partsch H (1968) Die Lymphkinetik beim postthrombotischen syndrom unter kompressionsverbanden. Med Klin 63(10): Lymphoedema Framework (2006a) Template for Practice: Compression hosiery in lymphoedema. MEP Ltd, London Lymphoedema Framework (2006b) Best Practice for the Management of Lymphoedema. International consensus. MEP Ltd, London Mayrovitz HN, Larsen PB (1997) Effects of compression bandaging on leg pulsatile blood flow. Clin Physiol 17: Moffatt CJ, Franks PJ, Doherty DC, Martin R, Blewett R, Ross F (2004). Prevalence of leg ulceration in a London population. Q J Med 97(7): Chap 1.indd 14 28/3/07 11:41:21

15 How compression works Moffatt CJ, Franks PJ, Oldroyd M, Bosanquet N, Brown P, Greenhalgh RM, McCollum CN (1992) Community clinics for leg ulcers and impact on healing. Br Med J 305: Mostbeck A, Partsch H, Peschi L (1977) Alteration of blood volume distribution throughout the body resulting from physical and pharmacological interventions. Vasa 6(2): Murphy MA, Joyce WP, Condron C, Bouchier-Hate D (2002) A reduction in serum cytokine levels parallels healing of venous ulcers in patients undergoing compression therapy. Eur J Endovasc Surg 23: Partsch H (2003) Understanding the pathophysiological effects of compression. In: European Wound Management Association (2003) Position Document: Understanding compression therapy. MEP Ltd, London Partsch H (1991) Compression therapy of the legs. A review. Dermatol Surg Oncol 17: Partsch H, Menzinger G, Mostbeck A (1999) Inelastic leg compression is more effective to reduce deep venous refluxes than elastic bandages. Dermatol Surg 25: Partsch H, Mostbeck A, Leitner G (1981) Experimental studies on the efficacy of pressure wave massage (Lymphapress) in lymphoedema. Z Lymphol 5(1): Chap 1.indd 15 28/3/07 11:41:22