Bohomolets Surgery 4th year Lecture #10

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Bohomolets Surgery 4th year Lecture #10

  1. 1. LECTURE 10 Chronic vascular diseases of the lower limb National O. Bogomolets Medical University Faculty Surgery Department N1 Kyiv 2008 Prof. Kucher M.
  2. 2. PATHOPHYSIOLOGY OF ARTERIAL DISEASE <ul><li>Most patients presenting to vascular surgeons have atherosclerosis. </li></ul><ul><li>This condition involves the following: </li></ul><ul><ul><li>endothelial cell injury; </li></ul></ul><ul><ul><li>subendothelial deposition of lipids </li></ul></ul><ul><ul><li>inflammatory cells; </li></ul></ul><ul><ul><li>smooth muscle cell migration and proliferation; </li></ul></ul><ul><ul><li>plaque haemorrhage, rupture and thrombosis </li></ul></ul>
  3. 3. Pathophysiology of atherosclerosis
  4. 4. CLINICAL FEATURES <ul><li>The clinical manifestations of arterial disease depend upon: </li></ul><ul><li>the site of the disease </li></ul><ul><li>whether the artery is an end-artery or well collateralized </li></ul><ul><li>the speed with which the disease develops </li></ul><ul><li>whether the underlying process is haemodynamic, thrombotic, atheroembolic or thromboembolic, or due to aneurysmal dilatation or dissection </li></ul><ul><li>the presence of other comorbidity and the general condition of the patient. </li></ul>
  5. 5. Anatomical site <ul><li>The patient's symptoms and signs will obviously depend upon the territory supplied by the affected artery: </li></ul><ul><li>coronary arteries: angina, myocardial infarction (MI) </li></ul><ul><li>cerebral circulation: stroke, transient ischaemic attack (TIA), amaurosis fugax, vertebrobasilar insufficiency (VBI) </li></ul><ul><li>renal arteries: hypertension, renal failure </li></ul><ul><li>mesenteric arteries: mesenteric angina, acute intestinal ischaemia </li></ul><ul><li>limbs: </li></ul><ul><ul><li>intermittent claudication (IC), </li></ul></ul><ul><ul><li>chronic critical limb ischaemia (CLI) </li></ul></ul><ul><ul><li>acute limb ischaemia. </li></ul></ul>
  6. 6. Collateral supply <ul><li>The clinical picture also depends upon whether the affected artery is essentially the only supply to the distal tissue (e.g. coronary artery and myocardium), or whether it is one of several arteries supplying the part (e.g. carotid artery and brain). This may vary between patients. </li></ul><ul><ul><li>For example, in a patient with a complete circle of Willis, the occlusion of one carotid artery may be asymptomatic. </li></ul></ul><ul><ul><li>In a patient where there is no such cross-circulation, occlusion is likely to cause a stroke </li></ul></ul>
  7. 7. Speed of onset <ul><li>Where atheroma develops slowly over months or years, a collateral supply to the distal part is likely to develop, such that when the main artery finally occludes, there may be little change in the patient's clinical status. The most common example is </li></ul><ul><ul><li>where the profunda (deep) femoral artery collateralizes around a diseased superficial femoral artery in patients with IC. </li></ul></ul><ul><ul><li>By contrast, the sudden occlusion of a previously normal artery is likely to cause severe distal ischaemia . </li></ul></ul>
  8. 8. Mechanism of injury <ul><li>A- critical stenosis of main artery compensated for by collateral vessels; only symptomatic on exercise. </li></ul><ul><li>B - acute thrombosis of a critical stenosis; little change in clinical status because of well-developed collaterals. </li></ul><ul><li>C - acute thrombosis of a non-critical stenosis; severe symptoms because collateral supply is poorly developed. </li></ul><ul><li>D - atheroembolism from ruptured, ulcerated plaque. </li></ul><ul><li>E - thromboembolism from the heart; severe ischaemia because of lack of collateral supply. </li></ul>
  9. 9. CHRONIC LOWER LIMB ARTERIAL DISEASE <ul><li>The lower limb arterial tree comprises </li></ul><ul><ul><li>the aorto-iliac segment above the inguinal ligament ('inflow') </li></ul></ul><ul><ul><li>the femoro-popliteal segment and the infra-popliteal segment ('outflow') </li></ul></ul>
  10. 10. <ul><li>Chronic lower limb ischaemia </li></ul><ul><li>presents as two distinct clinical entities: </li></ul><ul><li>intermittent claudication (IC) </li></ul><ul><li>critical limb ischaemia (CLI) </li></ul><ul><li>They have different epidemiologies, natural histories, treatments and prognoses </li></ul>
  11. 11. On examination, the chronically ischaemic limb is usually characterized by: <ul><li>skin that is thin and dry </li></ul><ul><li>pallor, particularly on elevation. Upon dependency, the foot becomes bright red; this is known as dependent rubor or 'sunset foot', and is due to reactive hyperaemia (Buerger's test) </li></ul><ul><li>superficial veins that fill sluggishly in the horizontal position and empty upon minimal elevation (venous guttering) </li></ul><ul><li>nails that are brittle and crumbly </li></ul><ul><li>muscle wasting </li></ul><ul><li>reduced temperature </li></ul><ul><li>pulses that are weak or absent and sometimes associated with thrills on palpation and bruits on auscultation. </li></ul>
  12. 12. Pulse status <ul><li>All patients admitted to hospital must have their pulse status recorded. In IC and CLI, the popliteal and pedal pulses are usually absent. If there is aorto-iliac disease, then one or both femoral pulses will be weak or absent. The presence of a thrill and/or bruit denotes turbulent flow. </li></ul>
  13. 13. Ankle:brachial pressure index <ul><li>The severity of ischaemia can be estimated by determining the ratio between the ankle and brachial blood pressures. The latter is recorded in the normal way, the former using a cuff and a hand-held Doppler device. </li></ul><ul><ul><li>In health, the ankle:brachial pressure index (ABPI) should be at least 1; that is, the pressure at the ankle should be at least as high as that in the arm. </li></ul></ul><ul><ul><li>Patients with IC usually have an ABPI of 0.5-0.9, and </li></ul></ul><ul><ul><li>those with CLI usually have an ABPI of less than 0.5. </li></ul></ul>
  14. 14. <ul><li>IC usually leads to pain in the muscles of the calf because the disease most often affects the superficial femoral artery. </li></ul><ul><li>If the iliac arteries are affected as well, then the pain may also be felt in the thigh and even the buttock. </li></ul><ul><ul><li>The pain comes on after a reasonably constant 'claudication distance', and subsides rapidly and completely on cessation of walking. </li></ul></ul><ul><ul><li>Resumption of walking causes the pain to return. These and other features distinguish it from neurogenic and venous claudication </li></ul></ul>
  15. 15. <ul><li>IC usually leads to pain in the muscles of the calf because the disease most often affects the superficial femoral artery. </li></ul><ul><li>If the iliac arteries are affected as well, then the pain may also be felt in the thigh and even the buttock . </li></ul><ul><li>The pain comes on after a reasonably constant 'claudication distance', and subsides rapidly and completely on cessation of walking. Resumption of walking causes the pain to return. These and other features distinguish it from neurogenic and venous claudication </li></ul>I NTERMITTENT CLAUDICATION Clinical features
  16. 16. <ul><li>A - Typically, the earliest lesion is usually a stenosis in the superficial femoral artery (SFA) in the region of the adductor canal, which leads to IC after walking several hundred metres . Ankle pulses are palpable but diminished, and a bruit may be heard at or below the adductor canal. Ankle systolic pressures are often normal at rest but reduced following exercise. </li></ul><ul><li>Over the next few months or years, the collateral vessels of the profunda system enlarge to carry a higher proportion of the blood flow to the leg. In the majority of patients, symptoms gradually improve or even disappear </li></ul>
  17. 17. <ul><li>B - Thrombotic occlusion of the SFA leads to a sudden deterioration in walking distance. Ankle and popliteal pulses are now absent. </li></ul><ul><li>Further development of the collateral circulation leads to an improvement in symptoms. This phase of moderate claudication may remain apparently stable for several years. </li></ul>
  18. 18. <ul><li>C - the atherosclerosis may progress to involve other segments. Claudication is now severe , forcing the patient to stop every 50 metres or so, and the scope for spontaneous improvement is steadily diminishing </li></ul>
  19. 19. <ul><li>D -CLI develops as a result of multilevel disease. Such patients will often go on to develop night/rest pain and are at risk of tissue loss </li></ul>
  20. 20. <ul><li>INTERMITTENT CLAUDICATION (Summery) </li></ul><ul><li>Intermittent claudication is the most common manifestation of peripheral arterial disease, affecting 1 in 20 adults aged over 55 years </li></ul><ul><li>Limb loss is uncommon (1-2% per year), but myocardial infarction and stroke are three times more common than in a non-claudicant population (5-10% per year) </li></ul><ul><li>The mainstays of treatment are risk factor modification, statin, aspirin and exercise. This leads to an improvement in walking distance in the majority of patients; it also increases longevity </li></ul><ul><li>Patients should not normally be considered for surgical or endovascular intervention until they have been compliant with best medical therapy ( BMT )for at least 6 months </li></ul><ul><li>Intervention includes angioplasty, stenting and bypass surgery. Long-term results are much better in the aorto-iliac segment than below the inguinal ligament </li></ul>
  21. 21. CRITICAL LIMB ISCHAEMIA <ul><li>Whereas IC is usually due to single-level disease, CLI is caused by multiple lesions affecting different arterial segments. </li></ul><ul><ul><li>These patients have tissue loss (ulceration or gangrene), with or without rest pain, </li></ul></ul><ul><ul><li>and, by definition, have an ankle blood pressure of less than 50 mmHg. </li></ul></ul><ul><ul><ul><li>Without revascularization, such patients will usually lose their limb-and often their life-in a matter of weeks or months. </li></ul></ul></ul>
  22. 22. Night and rest pain <ul><li>'Night pain' is due to the accumulation of metabolites, and occurs because the perfusion of the foot falls as a result of the loss of the beneficial effects of gravity, and because the patient's blood pressure and cardiac output also fall during sleep. </li></ul><ul><li>It is severe and wakes the patient from sleep, but may at first be relieved by hanging the limb out of bed. </li></ul><ul><li>As the disease progresses, the patient has to get up and walk about to obtain relief. The patient may volunteer a history of gaining relief from the pain by pressing the affected foot into a cold surface such as the kitchen floor. </li></ul>
  23. 23. The diabetic foot <ul><li>This refers to the combination of </li></ul><ul><ul><li>ischaemia, </li></ul></ul><ul><ul><li>neuropathy and </li></ul></ul><ul><ul><li>immunocompromise </li></ul></ul><ul><ul><li>that renders the feet of diabetic patients particularly susceptible to sepsis, ulceration and gangrene. Diabetic neuropathy affects the motor, sensory and autonomic nerves. </li></ul></ul>
  24. 24. Management of the diabetic foot <ul><li>If the blood supply is adequate, then dead tissue can be excised in the expectation that healing will occur, provided infection is controlled and the foot is protected from pressure (so-called off-loading) </li></ul><ul><li>If there is ischaemia as well, then the priority is to revascularize the foot, if possible </li></ul><ul><ul><li>Sadly, many diabetic patients present late, with extensive tissue loss and 'unreconstructable' disease, which accounts for the very high amputation rate. </li></ul></ul>
  25. 25. MANAGEMENT OF LOWER LIMB ISCHAEMIA <ul><li>Patients should be urged to comply with BMT , which comprises: </li></ul><ul><li>Immediate, absolute and permanent cessation from smoking </li></ul><ul><li>Control of hypertension </li></ul><ul><li>Control of hypercholesterolaemia. Thus, almost regardless of baseline cholesterol, patients with clinically apparent atherosclerosis and asymptomatic individuals at risk of developing symptomatic atherosclerosis (e.g. smokers, diabetics) require cholesterol-lowering therapy . While dietary advice is important, virtually all patients will require drug therapy, usually with statins , to obtain the necessary fall (around 30% from baseline) in total cholesterol. There is increasing evidence that statins, as well as having cholesterol-lowering properties, also stabilize atheromatous plaques and prevent the development and progression of aneurysmal disease through as yet incompletely understood anti-inflammatory mechanisms. </li></ul><ul><li>Prescription of an a ntiplatelet agent. This is normally aspirin (75 mg daily), but in the significant proportion of patients who state they are unable to tolerate this, clopidogrel (75 mg daily) is an equally effective alternative. There is no evidence that warfarin is of any benefit for most patients, although those who are in atrial fibrillation may benefit from anticoagulation. </li></ul><ul><li>Regular exercise (if possible). </li></ul><ul><li>Control of obesity . The identification and active treatment of patients with diabetes. This includes foot care . </li></ul>
  26. 26. MANAGEMENT OF LOWER LIMB ISCHAEMIA <ul><li>Active intervention, by either endovascular or open surgery, should not normally be considered until the patient has been compliant with BMT for at least 6 months. Obviously, revascularization is in addition to, not instead of, BMT , a point that often has to be emphasized to patients anxious to return to their previous lifestyle. </li></ul>
  27. 27. MANAGEMENT OF LOWER LIMB ISCHAEMIA <ul><li>Endovascular management </li></ul><ul><li>Percutaneous transluminal (balloon) angioplasty (PTA) has been used successfully in the </li></ul><ul><ul><li>iliac </li></ul></ul><ul><ul><li>Femoral </li></ul></ul><ul><ul><li>popliteal and crural arteries </li></ul></ul><ul><ul><ul><li>PTA is performed under local anaesthesia. The lesion is identified on duplex ultrasound or arteriography and crossed with a wire. </li></ul></ul></ul>
  28. 28. MANAGEMENT OF LOWER LIMB ISCHAEMIA <ul><li>Endovascular management </li></ul><ul><li>A balloon catheter is introduced over the wire and the balloon inflated. This ruptures the atheromatous plaque, thereby enlarging the lumen. In supra-inguinal (aorto-iliac) occlusions and complex disease, metal stents may be deployed across the lesion to improve patency and reduce distal embolic complications </li></ul><ul><ul><li>Endoluminal repair of the aorto-iliac segment is routine practice in most vascular units because of its high patency rates and low morbidity, compared to open surgery. </li></ul></ul><ul><ul><li>Infra-inguinal PTA is also widely used in the management of IC and CLI. </li></ul></ul>
  29. 29. MANAGEMENT OF LOWER LIMB ISCHAEMIA <ul><li>Indications for arterial reconstruction </li></ul><ul><li>Intermittent claudication </li></ul><ul><li>Most surgeons are reluctant to perform infra-inguinal bypass surgery for IC because: </li></ul><ul><ul><li>The risk of limb loss is very low with BMT. </li></ul></ul><ul><ul><li>Those patients who fail to comply with BMT are those most likely to press for surgery because of on-going symptoms. However, they are also those at greatest operative risk and those least likely to gain durable benefit from their bypass. </li></ul></ul><ul><ul><li>Surgery is associated with a significant risk of mortality and major morbidity, the size of that risk depending on the procedure but probably exceeding 5% for infra-inguinal bypass and 10% for aorto-bifemoral bypass. </li></ul></ul><ul><ul><li>As most patients have bilateral disease, even if they have unilateral symptoms, successful surgery on one side often reveals limiting symptoms on the other, requiring a second operation. (This is also a problem with unilateral PTA/stenting.) </li></ul></ul><ul><li>Grafts have a finite patency, especially in those who fail to comply with BMT and, in particular, continue to smoke. </li></ul><ul><li>As soon as a bypass graft is inserted, collaterals circumventing the original lesion involute. For this reason, when the graft occludes, usually suddenly, the patient is normally returned to a worse level of ischaemia than before the operation. A patient who was previously a claudicant may now have acute limb-threatening ischaemia, which then forces the surgeon or radiologist to intervene again. </li></ul><ul><li>Secondary interventions, such as thrombolysis or re-operation, are technically more difficult, are associated with higher risk and enjoy a lower patency rate. </li></ul>
  30. 30. Principles of arterial reconstruction <ul><li>In the lower limb, common femoral endarterectomy, with or without a profundaplasty , is probably the most common example </li></ul>
  31. 31. Principles of arterial reconstruction <ul><li>Bypass grafting </li></ul><ul><li>For a surgical bypass operation to be successful in the long term, three conditions must be fulfilled: </li></ul><ul><ul><li>There must be high-flow, high-pressure blood entering the graft (inflow). </li></ul></ul><ul><ul><li>The conduit must be suitable. </li></ul></ul><ul><ul><li>The blood must have somewhere to go when it leaves the graft (outflow) </li></ul></ul><ul><li>Two main types of conduit are available: </li></ul><ul><ul><li>autogenous material, most commonly the ipsilateral long saphenous vein </li></ul></ul><ul><ul><li>prosthetic material, most commonly expanded polytetrafluoroethylene (ePTFE) or Dacron. </li></ul></ul>
  32. 32. Principles of arterial reconstruction Anatomic and Extra-anatomic Bypass
  33. 33. AMPUTATION <ul><li>INDICATIONS : </li></ul><ul><li>Amputation should only be considered where arterial reconstruction is considered by a vascular surgeon to be inappropriate or impossible. </li></ul><ul><li>In some cases, patients are admitted profoundly unwell and septic from spreading gangrene, and immediate amputation may be the only means of saving the patient's life. </li></ul>
  34. 34. AMPUTATION <ul><li>LEVEL OF AMPUTATION </li></ul>
  35. 35. PATHOPHYSIOLOGY OF VENOUS DISEASE <ul><li>ANATOMY </li></ul>
  36. 36. PHYSIOLOGY <ul><li>the venous pressure at the ankle is approximately 100 mmHg: that is, the hydrostatic pressure exerted by the column of venous blood stretching from the ankle to the right atrium. </li></ul><ul><li>However, upon walking, the mechanisms described above reduce the ankle pressure to less than 25 mmHg (ambulatory venous pressure, AVP). </li></ul><ul><li>The symptoms and signs of lower limb venous disease are largely due to failure of these protective mechanisms and the presence of a high AVP. </li></ul>
  37. 37. VARICOSE VEINS CLASSIFICATION <ul><li>Trunk varices </li></ul><ul><li>These involve the main stem and/or major tributaries of the LSV and SSV, are usually > 4 mm in diameter (and may be much larger) (Fig. 25.35), lie subcutaneously, are palpable, do not usually discolour the overlying skin, and are present in about a third of the adult population. Although 2-3 times more women than men present for treatment, the prevalence is roughly equal between the sexes. There appears to be a familial tendency, and obesity, pregnancy, constipation and prolonged standing may be aggravating factors. </li></ul>
  38. 38. VARICOSE VEINS CLASSIFICATION <ul><li>Reticular varices </li></ul><ul><li>These lie deep in the dermis, are < 4 mm in diameter, are impalpable, and render the overlying skin dark blue. They are present in about 80% of the adult population, and may or may not be associated with trunk varices. </li></ul>
  39. 39. VARICOSE VEINS CLASSIFICATION <ul><li>Telangiectasia </li></ul><ul><li>These are also called spider and hyphen web veins. They lie superficially in the dermis, are usually 1 mm or less in diameter, are impalpable, and render the overlying skin purple or bright red. Again, they may be associated with trunk and reticular varices, and are present in 90% of adults. Like reticular veins, they appear to be more common in women, probably because of poorly understood hormonal reasons. </li></ul>
  40. 40. EPIDEMIOLOGY <ul><li>Varicose veins (VV) are so prevalent that they could almost be considered a variant of normal for a creature that spends its life on two as opposed to four legs. Their prevalence increases markedly with age and they are an almost universal finding in individuals over the age of 60. </li></ul>
  41. 41. CLINICAL FEATURES <ul><li>The great majority of individuals with VV are asymptomatic, or at least they do not seek treatment. Those that do attend the surgical clinic do so because they are unhappy about the appearance of their leg(s), and/or they associate lower limb symptoms with their VV, and/or they are concerned about developing complications. </li></ul>
  42. 42. Complications <ul><li>Only a small proportion of patients with VV go on to develop the complications of chronic venous insufficiency (CVI ): </li></ul><ul><ul><li>leg ulcers </li></ul></ul><ul><ul><li>Haemorrhage </li></ul></ul><ul><ul><li>thrombophlebitis. </li></ul></ul><ul><li>There is on-going controversy as to whether VV are a risk factor for DVT. </li></ul><ul><ul><li>In young, otherwise healthy individuals, they are probably not. </li></ul></ul><ul><ul><li>However, in the elderly, in whom VV are more likely to be associated with skin changes of chronic venous insufficiency and in whom they may be a marker for coexistent deep venous disease, they probably are. </li></ul></ul><ul><ul><li>At present, it is difficult to predict which patients will develop these complications and to know whether early VV surgery would prevent them, because the necessary longitudinal studies have never been done. </li></ul></ul>
  43. 43. Indications for treatment <ul><li>In correctly selected patients, it is clear that VV surgery is associated with a marked improvement in quality of life and symptom relief . </li></ul><ul><li>In patients with uncomplicated VV, surgeons must use their own judgement and experience to determine whether the patient truly does have symptoms, whether those symptoms are of venous aetiology, and, if so, whether they are likely to be relieved by surgery. </li></ul>
  44. 44. AETIOLOGY <ul><li>The aetiology of VV is unclear. The favoured hypothesis is: </li></ul><ul><ul><li>that there is a structural defect in the vein wall , which may, at least in part, be inherited and which causes progressive dilatation in response to increased venous pressure consequent upon our bipedal posture and other factors. </li></ul></ul><ul><ul><li>This leads to secondary incompetence of the valves , which in turn leads to more stress on the wall and more dilatation. </li></ul></ul><ul><li>Unlike the deep system, incompetence of superficial valves is only rarely due to post-thrombotic damage. </li></ul>
  45. 45. EXAMINATION <ul><li>Percussion over a varix while palpating with the other hand at a higher or lower level will help trace the pattern. The level at which deep-to-superficial reflux is occurring can be checked by the Trendelenburg test </li></ul><ul><ul><li>The leg is elevated and a rubber tourniquet applied just below the saphenofemoral junction. The patient is then asked to stand. Veins fill slowly from arterial inflow but quickly from venous reflux. If venous distension below the tourniquet is controlled, the site of reflux must be above it. </li></ul></ul><ul><ul><li>By moving the tourniquet to different levels in the limb, the pattern of incompetence can be mapped out. </li></ul></ul>
  46. 46. EXAMINATION <ul><li>A more effective way to demonstrate reflux is to insonate over the site of incompetence and reflux with a portable continuous-wave Doppler ultrasound probe </li></ul>
  47. 47. MANAGEMENT <ul><li>Conservative treatment </li></ul><ul><li>Elderly patients or those with mild disease can be treated conservatively. </li></ul><ul><li>Elastic support hose </li></ul><ul><li>weight reduction </li></ul><ul><li>regular exercise </li></ul><ul><li>avoidance of prolonged standing </li></ul>
  48. 48. MANAGEMENT <ul><li>Sclerotherapy </li></ul><ul><ul><li>Standard injection treatment using liquid sclerosants is commonly used for </li></ul></ul><ul><ul><ul><li>small varices below the knee that are due to incompetence of local perforators </li></ul></ul></ul><ul><ul><ul><li>for small recurrent varices after surgery </li></ul></ul></ul><ul><ul><ul><li>for reticular and spider veins. </li></ul></ul></ul><ul><ul><li>Such sclerotherapy is not satisfactory for trunk varices associated with saphenofemoral or saphenopopliteal incompetence, as recurrence is inevitable. </li></ul></ul><ul><ul><li>However, ultrasound-guided foam sclerotherapy (UGFS) appears to be an equally effective alternative to surgery in a proportion of patients. </li></ul></ul><ul><ul><ul><li>In this procedure, the sclerosant is prepared and used as a foam, and introduced into the LSV or SSV under direct vision using duplex ultrasound control. </li></ul></ul></ul>
  49. 49. <ul><li>Surgery </li></ul><ul><li>Varicose vein surgery aims to remove varices and intercept incompetent connections between deep and superficial veins so that further varices do not form. </li></ul><ul><li>In patients with LSV disease, the SFJ is ligated flush with the femoral vein). </li></ul><ul><li>Recurrence is very much less likely if the long saphenous vein is stripped out from knee to groin. </li></ul>
  50. 50. Other new treatments <ul><li>As well as UGFS, several other novel treatments for VV have been introduced as an alternative to surgery. </li></ul><ul><li>radiofrequency </li></ul><ul><li>laser light energy to obliterate the LSV or SSV </li></ul><ul><li>Their potential advantage is that they can be performed as an outpatient or day-case procedure without general anaesthetic. However, the technology is expensive, not all patients are suitable </li></ul>
  51. 51. CHRONIC VENOUS INSUFFICIENCY <ul><li>PATHOPHYSIOLOGY </li></ul><ul><li>Chronic venous insufficiency (CVI) may be defined as the presence of irreversible skin damage in the lower leg as a result of sustained ambulatory venous hypertension. This hypertension is due to failure of the mechanisms that normally lower venous pressure upon ambulation </li></ul><ul><li>Venous reflux due to valvular incompetence (90%). This may affect the superficial veins, the deep veins or both, and may be due to primary valvular insufficiency (as in VV) or to post-thrombotic damage. </li></ul><ul><li>Venous obstruction (10%). This is usually post-thrombotic in nature . </li></ul>
  52. 52. MANAGEMENT <ul><li>Medical therapy </li></ul><ul><li>Dressings </li></ul><ul><li>Compression therapy </li></ul><ul><li>Surgical therapy </li></ul>
  53. 53. VENOUS THROMBOEMBOLISM (VTE) <ul><li>DVT is a common condition in medical and surgical patients and pulmonary embolism (PE) is consistently cited as the most common cause of potentially preventable death in the surgical patient. DVT also renders the leg prone to CVI and ulceration (the so-called post-phlebitic limb or syndrome). </li></ul><ul><li>PATHOPHYSIOLOGY </li></ul><ul><li>DVT probably begins in the calf in most cases (Fig. 25.40). Clot may extend into the popliteal, femoral or iliac veins, and even the inferior vena cava. In some cases, DVT originates in the pelvic veins. </li></ul>

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