UNDERSTANDING CHRONIC VENOUS HYPERTENSION Chronic Venous Hypertension Accounts for About 70% of Ulcers on the Lower Limb
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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. 20 Wound Essentials • Volume 3 • 2008 p20-32CVT.indd 2 17/6/08 16:07:25 Review (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 22 Wound Essentials • Volume 3 • 2008 p20-32CVT.indd 4 17/6/08 16:07:26 Review 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). 24 Wound Essentials • Volume 3 • 2008 p20-32CVT.indd 6 17/6/08 16:07:27 Review Review 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).