Review UNDERSTANDING CHRONIC VENOUS HYPERTENSION Chronic venous hypertension accounts for about 70% of ulcers on the lower limb. It is important to understand the underlying pathophysiology of the condition in order to rationalise assessment and treatment approaches.

Irene Anderson is Senior Lecturer in Tissue Viability, University of Hertfordshire

Figure 1. A venous leg ulcer.

Venous disease is the underlying this article is to highlight key substances can pass through cause of venous ulceration (Figure areas in order to help healthcare them to nourish the tissues. 1). Although patients may cite professionals understand and trauma as the cause of their ulcer explain to patients the complex Veins are thinner than arteries it is in fact a wound complicated processes involved in venous and have three layers: the tunica by a disease process in the hypertension and leg ulcer lower leg (Rainey, 2002). It is development. Tunica adventitia important for the practitioner to Connective tissue understand the pathophysiology Veins in the lower leg of venous disease as this will Veins carry blood back to the enable them to make rational heart and the blood flows at a treatment decisions and explain relatively low pressure compared the importance of self care to arterial blood flow (which and compression therapy to carries the blood away from Tunica the patient. This article aims to the heart under high pressure) intima explain the pathophysiology of (Tortora and Grabowski, 2000). Endothelium chronic venous hypertension Internal elastic The arteries branch into smaller lamina and link this to clinical signs and smaller vessels, until the External elastic lamina and the symptoms experienced blood flows into capillaries. Smooth muscle cells by the patient. The mechanical The walls of capillaries are only Tunica media and cellular processes are very one cell thick (Tamir, 2002) so complex and the objective of that oxygen, glucose and other Figure 2. Structure of the vein.

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(previously called long and short veins [Waugh and Grant, 2001; Meissner et al, 2007]). Deep veins are held within the muscle fascia of the leg while superficial veins are less supported and are nearer the surface of the leg (Waugh and Grant, 2001). These are the veins which are visible, e.g. on the foot.

The perforator veins are named as such because they ‘perforate’ the fascia layer surrounding the muscles of the legs, linking the superficial and deep veins. Perforator veins allow venous blood to flow from the superficial veins into the deep veins with the highest number of these joining veins being near the calf muscle (Meissner et al, 2007).

All veins in the leg have valves to Figure 4. Chronic venous hypertension: ensure that venous blood travels backflow of venous blood increases the Figure 3. Venous blood flows up the back to the heart or from the blood volume in the leg veins forcing the leg and blackflow is prevented by one-way valves apart. one-way valves. superficial veins back to the deep veins via the perforators.These adventitia on the outside, tunica valves are particularly important in meets less resistance than media (middle layer) and the the lower leg as the blood needs when standing tunica intima, an inner layer of to flow upwards a considerable 8Breathing: On breathing in endothelial cells lining the vessel distance to the heart especially there is a negative pressure (Figure 2) (Waugh and Grant, if standing upright. If the valves created in the chest cavity. The 2001). The waste materials of do not work in the perforator abdominal pressure increases metabolism, such as carbon veins, blood is pushed out into as the diaphragm lowers and dioxide and lactic acid, filter in superficial veins, increasing the both mechanisms encourage the opposite direction into the pressure in these vessels. venous return capillaries which then join to form 8The calf-muscle pump: slightly larger vessels (venules, Venous flow in the lower leg this will now be discussed or tiny veins) which in turn join Venous blood returns to the heart in more detail. up to veins. mainly via the deep veins, which are bigger and stronger than the The calf-muscle pump The venous system is made superficial veins, and there are When blood is pumped into the up of a deep system and a three key mechanisms by which arteries by the heart, it is pushed superficial system, which are this blood flow is encouraged: forward under high pressure. joined by perforator (joining) veins 8Gravity: blood from the lower Only a little of this pressure is left ( Figure 3). The deep veins of the leg has to travel a long way once it has passed through the leg are the femoral, popliteal, against gravity to return to capillaries into the veins so the anterior and posterior tibial veins, the heart; therefore when the action of the muscles provides while the superficial veins are body is laying flat or when a pumping action that helps the great and small saphenous the legs are elevated the flow to push the blood up through

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the veins. This muscle pump is particularly important in the legs, Normal venous return because on standing, blood has to travel a long way, against The veins gravity, to return to the heart. Damage to valves • Trauma/surgery to lower leg As the calf muscle contracts, • Vein thrombosis the valves in the deep veins • Increased vein capacity are squeezed and they open • Occupation • Obesity to allow the blood to travel • Pregnancy upwards. As the calf muscle relaxes the valve closes and creates a negative pressure as the section between valves empties. This negative pressure Abnormal venous return draws blood from the superficial The signs veins, through the perforators to refill the chamber ready for • Incompetent valves • Inflammatory cells activated the next contraction of the calf • Backflow (reflux) • Tissue damage/destruction muscle (Meissner et al, 2007). • Capillary leakage • Reduced growth factor activity • Oedema • Impaired tissue repair • Haemosiderin staining In the lower limb the normal • Skin changes venous pressure may range from • Ankle flare about 100mmHg when standing • Varicose veins still, falling to about 22mmHg when walking (Meissner et al, 2007). These pressure changes also occur on ankle flexion and How it affects the patient during exercises where the heel is raised and the person stands The patient on tiptoe. These changes in • Pain pressure on activity illustrate • Discomfort the key role of exercise in • Feeling of heaviness in the legs the management of venous • Risk of trauma hypertension. Even moderate • Potential ulceration and ulcer recurrence exercise in patients with reduced mobility can still be undertaken.

Chronic venous hypertension The valves of the leg can become damaged by trauma, surgery to the lower leg that has involved Figure 5. Pathophysiology of chronic venous hypertension. cutting into veins, pregnancy, obesity, increased vein capacity on the vein wall and will affect increase. As the valves are unable and thrombosis. If the valves other parts of the venous system to prevent backflow of blood, are incompetent they will allow namely the perforators and the chronic venous hypertension backflow (reflux) of venous blood superficial system. As these results (Figures 4 and 5). Chronic in the deep vein and the volume veins stretch their valves here venous hypertension is the main of blood in the lower leg will will not close properly and the underlying cause of venous leg increase. This increased load volume of blood — and therefore ulceration (Morison and Moffatt, will cause a rise in the pressure the venous pressure — will 2004).

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Table 2

Signs of chronic venous hypertension

Signs Pathophysiology Common related signs and symptoms

Ankle flare Chronic venous hypertension causes the capillaries to swell. Visible capillaries through the skin, most often on the medial (inner) malleolus (ankle). The area may also become itchy.

Varicose veins Veins which are continually stretched lose elasticity and Prominent veins, varicosity may be palpable before becoming visible. Itch, pain the tunica media layer of the vein wall becomes fibrosed. especially after standing for long periods. Heavy bleeding if the vein is punctured. Increased volumes of blood cause the stretching and the valves can no longer close properly which increases the blood volume further because of backflow. the great and small saphenous and anterior tibial veins are most affected (Waugh and Grant, 2001).

Oedema Swollen capillaries allow fluid to leak into the tissue. Pain, discomfort, difficulty walking and finding suitable footwear, skin trauma, fluid Normally excess tissue fluid would be reabsorbed back into leakage through skin, blistering. Risk of infection such as cellulitis. the capillaries but this may not be possible as the capillary is already congested due to backflow of blood in the veins (Waugh and Grant, 2001)

Varicose eczema Inflammation, poor tissue nutrition and hydration. Link with Dry flaky skin, weeping skin, caused by sensitisers. Itch, skin trauma, skin venous hypertension is not fully understood. sensitivities. The skin initially is red and itchy, perhaps with scales and weeping blisters. As the condition becomes more chronic the skin can become much dryer and flaky, even with thick layers of dry scale known as hyperkeratosis (Cameron, 2007).

Lipodermatosclerosis Prolonged inflammation, tissue fibrosis. Dry, hard, woody skin. Changes in lower leg shape known as the ‘inverted champagne bottle’.

Haemosiderin staining Leakage of red cells from stretched capillaries stain the tissue Dark staining particularly in the area of the medial malleolus. a brown or rusty colour (Dealey, 2005).

It is not just valve incompetence as it becomes tangled in the veins prevents excess tissue that leads to venous fibrosis (Meissner et al, 2007). fluid being drawn back into the hypertension but also vein capillaries (Waugh and Grant, obstruction. After a venous Effects of chronic venous 2001). thrombosis the clot is broken hypertension down but may not completely The effects of chronic venous Normally there is a dynamic resolve and the residue may hypertension on the patient are balance between the fluid in become fibrous causing an outlined in Table 1 . An early sign the tissue and in the capillary; obstruction. If this also happens of chronic venous hypertension as tissue pressure rises fluid is to be in the area of a valve it may is oedema. It is caused when absorbed into the capillary and stop the valve working properly increased pressure in congested as capillary pressure rises, fluid is

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pushed out to the tissue. When common site of this is around the population. These symptoms there is venous congestion this medial malleolus. The skin will feel include night cramps, ‘restless mechanism is less likely to work, hard with no ‘give’ in the tissue legs’, leg heaviness and pain as the pressure in the capillary and may be extremely tender and (Nicolaides, 2005). does not fall sufficiently to allow is very vulnerable to trauma. As more fluid to be absorbed from this condition develops the skin Risk factors for venous the tissue. changes result in thickening that hypertension constricts the ankles and together Evidence for a link between When fluid leaks from the with the build up of oedema social class or income to venous capillary into the tissue, protein and tissue fibrosis results in a disease is weak but Lee et al is one of the molecules that change in the shape of the lower (1999) suggested in a review leaks out. These plasma proteins leg; referred to as an ‘inverted of studies from many countries then attract more fluid from the champagne bottle’ shape. that venous disease prevalence capillaries due to tissue osmotic Sometimes there is a condition may be lower in those educated pressure (Waugh and Grant, called atrophie blanche visible, to degree level than in those 2001), which means the tissue which are tiny white, scarred educated to secondary school oedema increases unless there is areas (Herrick et al, 2002) that level; this could be taken as some kind of intervention to help are very painful and vulnerable to a crude indication of likely prevent it such as compression trauma. Haemosiderin staining occupation. Occupations therapy or leg elevation is visible on the skin as a brown involving standing for long periods (Nicolaides, 2005). Compromised or rusty discoloration due to the especially if combined with heavy lymph drainage exacerbates leakage of red blood cells from lifting may be significant, as may the problem of oedema, as the stretched capillaries. being overweight, especially lymphatic system is impaired for women. in venous disease, with or Varicose veins without ulceration (Williams and Venous congestion will give rise There appears to be a link Mortimer, 2007). to varicose veins and a condition between pregnancy and varicose commonly referred to as ankle veins but it is unclear what the Skin changes flare (Table 1) where small direct effects are especially as Congestion means that nutrients capillaries and venules are visible varicose veins often appear in do not get to the tissues including under the skin mostly around the early pregnancy before there is the skin and this can result in inner malleolus. Varicose veins significant extra weight. Burnand dryness, eczema and so on may affect 10–20% of the adult (1999) adds that the most (Table 1). Skin changes are very population and 3% of those significant effect appears with common in venous disease. with varicose veins are thought the first pregnancy, although it Herrick et al (2002) state that up to experience leg ulceration is not clear why. Any studies on to 94% of people with venous (Morison and Moffatt, 1999), the relationship between the oral disease (including deep vein however, not everyone with a leg contraceptive pill, or menopause thrombosis) have skin changes. ulcer will also have overt signs and venous hypertension remain There does not, however, seem of varicose veins. Interestingly, a inconclusive. There may be a link to be a relationship between the long-term study of children found between venous hypertension degree of disease and these that 10% of 10–12 year olds had and smoking and this seems to changes, which suggests that early varicose vein development affect men more than women there is much that is not yet and this rose to 75% by the (Lee et al, 1999). A significant risk understood about the progression time they were 30 years old factor for venous disease and and causes of venous disease. (Nicolaides, 2005). Nicolaides varicose vein formation may be a points out that a range of studies diet deficient in fibre especially in Lipodermatosclerosis is hardening in various countries and age the presence of constipation. This of the skin with a ‘woody’ feel groups suggest symptoms of may cause increased abdominal and appearance, sometimes chronic venous disease may be pressure with consequent effects called induration. The most present in 25–84% of the adult on deep and superficial veins of

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the legs through straining (Lee et hypothesis is that growth factors correcting valve closure where al, 1999). may become trapped in the possible, reducing reflux of dermis, which renders them venous blood. Compression Theories of leg ulcer unable to repair damaged tissue therapy speeds up the blood formation (Agren and Gottrup, 2007). flow, which reduces the pressure The link between chronic venous Clearly there is great complexity in the capillaries allowing them hypertension and ulceration is in the role of, and interaction to drain fluid from the tissues to not fully understood (Coleridge between, cells. reduce oedema. The improved Smith, 2006) and this makes for circulation has an effect on the a real clinical challenge. There Recurrence rate of venous skin due to the improved delivery are theories about the effect ulcers and control of venous of nutrients and may soften of venous hypertension on hypertension lipodermatosclerotic skin (Oduncu capillaries, tissue and skin and The recurrence rate of venous et al, 2004) and reduce dryness. how these effects contribute to ulcers is significant because Haemosiderin staining will remain the development of a leg ulcer. chronic venous hypertension and the skin will still be at risk of There is some discussion and remains as a disease process. sensitivity but the overall condition debate about these theories but It has to be managed for should improve. Exercise will help the general consensus is that all the patient’s lifetime unless to reduce backflow by maximising may contribute to ulcer formation something can be done to the effect of the calf muscle. Leg and delayed healing although it correct the problems with the elevation will help venous return is not clear how (Coleridge valves. Obermayer et al (2006) by utilising the effects of gravity Smith, 2006). looked at outcomes in 173 for drainage. Vein surgery to patients with 239 ulcerated legs control reflux in superficial and The fibrin cuff theory suggests over seven years. The patients perforating veins aims to reduce that as cells leak out of stretched had compression therapy and venous hypertension (Obermayer capillaries fibrinogen (a substance surgery to superficial veins and et al, 2006). Jull (2007) reviewed involved in blood clotting) collects perforators. The major outcome systemic pharmaceutical agents on the outside of the capillaries was that the recurrence rate was for the management of venous as a cuff and over time forms 1.7% at six months and 4.6% disease concluding that much a fibrotic structure with other at five years. This compares cells such as collagen. These very favourably with reported cuffs form a barrier, which may recurrence rates of 28% with prevent nutrients from reaching compression therapy alone Key Points tissues and skin (Agren and (Moffatt and Dorman, 1995). Gottrup, 2007). Another theory Interestingly the Obermayer et al 8 Chronic venous hypertension involves white cell trapping. study included people with mixed accounts for about 70% of ulcers When venous pressure is high, aetiology (a degree of arterial in the lower limb. white cells such as leucocytes disease present alongside the and neutrophils increase in venous disease) and this group 8 It occurs as a result of damage to the valves of the leg which allows number and accumulate in the showed the same rate of healing backflow of venous blood and an capillary becoming ‘trapped’ and and recurrence as the others, increase to the volume of blood in causing a prolonged inflammatory indicating that correcting the the lower leg. response. This inflammatory venous hypertension is key to response includes the release of managing ulceration. 8 The effects of chronic venous hypertension include oedema, oxygen free radicals (destructive skin changes, pain discomfort and cells) and proteinases (cells that Management of chronic venous potential ulceration. break down tissue proteins), hypertension which lead to tissue destruction The main treatment for chronic 8 Treatment centres on compression, and the formation of skin changes venous hypertension with and exercise, skin care and elevation. such as lipodermatosclerosis without ulceration is compression (Coleridge Smith, 2006). Another therapy, which assists in

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more evidence is required for Fowkes FGR, Bradbury AW (eds) a community leg ulcer service. J all agents. In addition, Jull Venous Disease: Epidemiology, Wound Care 4(2): 57–61 stated that aspirin or cinnarizine Management and Delivery of Morison M, Moffatt C (1999) Leg (a histamine antagonist) may Care. Springer, London 42–50 ulcers. In: Morison M, Moffatt play a role in conjunction with Cameron J (2007) C, Bridel-Nixon J, Bale S. compression therapy in ulcer Dermatological changes Nursing Management of Chronic healing, although this is by no associated with venous ulcers. Wounds. Mosby, London: means conclusive. Pentoxifylline Wound Essentials :2 60–6 177–220 may play a role in reducing the effects of leucocyte adhesion and Coleridge Smith P (2006) The Nicolaides AN (2005) Chronic zinc sulphate may positively affect causes of skin damage and leg venous disease and the ulcer healing but only where a ulceration in chronic venous leukocyte-endothelium zinc deficiency exists, which is disease. Lower Extrem Wounds interaction: from symptoms to difficult to establish. 5(3): 160–8 ulceration. Angiology 56: S11–S19 Dealey C (2005) The Care of Conclusion Wounds (3rd edn). Blackwell Obermayer A, Gostl K, Walli G, It is clear that there is still much Publishing, Oxford Benesch T (2006) Chronic venous to be understood about venous leg ulcers benefit from surgery: hypertension and management Herrick SE, Treharne LJ, long term results from 173 legs. will centre on compression, deGiorgio-Miller (2002) Dermal J Vasc Surg 44: 572–9 exercise, skin care and elevation changes in the lower leg for some time to come. The role of skin of patients with venous Oduncu H, Clark M, Williams RJ surgery is important but is perhaps hypertension. Lower Extrem (2004) Effect of compression on not as available to patients in the Wounds 1(2): 80–6 blood flow in lower limb wounds. Int Wound J 1(2): 107–113 UK as it could be — whether this Jull A (2007) An overview of is due to a lack of resources or pharmacological treatment Rainey J (2002) Wound Care: complexity of patient conditions is options for venous leg ulcers. In: A Handbook for Community unclear. If practitioners understand Morison MJ, Moffatt CJ, Franks Nurses. Whurr Publishers, risk factors, the underlying P (2007) Leg Ulcers: A Problem- London disease process and the effects of Based Learning Approach. Tamir E (2002) The Human Body intervention, they are much more Mosby Elsevier, London: 223–41 Made Simple (2nd edn). Churchill likely to communicate effectively Livingstone, London with patients and secure their Lee AJ, Evans CJ, Ruckley engagement in management of CV, Fowkes GR (1999) Does Tortora GJ, Grabowski SR the disease.WE lifestyle really affect venous (2000) Principles of Anatomy disease? In: Ruckley CV, Fowkes and Physiology. John Wiley, FGR, Bradbury AW (eds) Chichester Agren MS, Gottrup F (2007) Venous Disease: Epidemiology, Waugh A, Grant A (2001) Ross Causation of venous leg ulcers. Management and Delivery of and Wilson: Anatomy and In: Morison MJ, Moffatt CJ and Care. Springer, London: 32–41 Physiology in Health and Illness Franks PJ (2007) Leg Ulcers: Meissner MH, Moneta G, (9th edn). Churchill Livingstone, A Problem-Based Learning Burnand K, Gloviczki P, Lohr JM, London Approach. Edinburgh Mosby, Lurie F, Mattos MA, McLafferty Williams AF, Mortimer P (2007) Edinburgh: 141–54 RB, Mozes G, Rutherford RB, Lymphoedema of the lower Anderson I (2006) Aetiology, Padberg F, Sumner DS (2007) limb: causation, assessment assessment and management of The haemodynamics and and management. In: Morison leg ulcers. Wound Essentials 1: diagnosis of venous disease. J MJ, Moffatt CJ, Franks P (2007) 20–37 Vasc Surgery 46: 4s–24s Leg Ulcers: A Problem-Based Burnand K (1999) What makes Moffatt CJ, Dorman MC (1995) Learning Approach. Mosby veins varicose? In: Ruckley CV, Recurrence of leg ulcers within Elsevier, London: 243–60

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