4: Chronic venous insufficiency

Case 4 Chronic venous insufficiency



Description of chronic venous insufficiency




Epidemiology


CVI affects between 0.1 per cent and seventeen per cent of men, and from 0.2 per cent to twenty per cent of women.1 While evidence that links CVI occurrence to gender is inconsistent, being female is associated with an increased risk of CVI manifestations, including varicose veins1 and venous leg ulceration.2 CVI prevalence is also associated with increasing age, a relationship that may be attributed to the decline in blood vessel wall integrity and calf muscle strength over time.1



Aetiology and pathophysiology


A number of risk factors are connected with the development of CVI. Family history and increasing age, for instance, are both associated with an increased risk.1 In terms of modifiable risk factors, several studies have observed a higher prevalence and severity of CVI and varicose veins among people in occupations that typically require prolonged periods of standing, such as nurses, flight attendants and factory workers.1 The reduced calf-muscle pump activity associated with prolonged standing may contribute to the pathogenesis of CVI because of excessive lower limb venous congestion and pressure.


Another modifiable risk factor of CVI is macrovascular insult, the cause of which may be credited to lower limb trauma, surgery, deep vein thrombosis (DVT) and/or pregnancy. The injury to the venous system triggers a cascade of events that contribute to CVI, including valvular incompetence, venous reflux (or retrograde blood flow), ambulatory venous hypertension, venous wall dilatation and elevated capillary filtration. Over time, these pathological changes lead to the formation of interstitial oedema, localised hypoxia, malnutrition and tissue destruction. Two mechanisms are believed to be responsible for the progression from a state of elevated capillary filtration pressure to changes in tissue perfusion and local architecture, including the extravasation or leakage of fibrinogen into the subcutaneous tisues and the subsequent formation of pericapillary cuffs, the intraluminal trapping of leucocytes and subsequent release of toxic metabolites, proteolytic enzymes and tissue necrosis factor-alpha. The extravasation of fibrinogen and leucocyte products into pericapillary tissue may also mediate inflammation, which suggests that CVI may be a disease of chronic inflammation.3



Clinical manifestations


The early stages of CVI typically manifest as lower leg fatigue, heaviness, discomfort and pruritus. As the disease progresses, visible changes to the skin and subcutaneous tissue begin to emerge, such as lower leg oedema, ochre pigmentation, stasis dermatitis and lipodermatosclerosis. In the more advanced stages of CVI, a person may also present with superficial and deep varicose veins, as well as venous leg ulceration. The functional and cosmetic implications of these manifestations can significantly affect a person’s quality of life.4




Clinical case


44-year-old woman with mild chronic venous insufficiency



Rapport


Adopt the practitioner strategies and behaviours highlighted in Table 2.1 (chapter 2) to improve client trust, communication and rapport, as well as the accuracy and comprehensiveness of the clinical assessment.





Medical history






Physical examination







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Jul 22, 2016 | Posted by in MANUAL THERAPIST | Comments Off on 4: Chronic venous insufficiency

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