Case 4 Chronic venous insufficiency
Description of chronic venous insufficiency
Definition
Chronic venous insufficiency (CVI) is a pathological condition of the venous system, characterised by impaired venous blood flow in the lower limbs. The disorder presents as pathological changes to the skin, subcutaneous tissue and vascular tissue, and is a precursor to varicose veins and venous leg ulceration.
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
Lifestyle history
Illicit drug use
| Diet and fluid intake | |
| Breakfast | Coffee, porridge with skim milk. |
| Morning tea | Coffee, apple. |
| Lunch | Vegetable hotpot, sandwich with white bread, lettuce, tomato and carrot, chicken salad with tomato, cucumber, mixed greens and mushrooms. |
| Afternoon tea | Cheese and water crackers, apple juice, coffee. |
| Dinner | Beef and onion stew, chicken curry with white rice, grilled haddock with steamed carrot, cauliflower and broccoli. |
| Fluid intake | 2–3 cups of percolated coffee a day, 2–3 cups of water a day, 1 cup of juice a day. |
| Food frequency | |
| Fruit | 1–2 serves daily |
| Vegetables | 3–4 serves daily |
| Dairy | 2 serves daily |
| Cereals | 3–4 serves daily |
| Red meat | 3 serves a week |
| Chicken | 4 serves a week |
| Fish | 1 serve a week |
| Takeaway/fast food | <1 time a week |
Physical examination
Palpation
Popliteal, posterior tibial and dorsalis pedis pulses are strong, regular and of equal amplitude bilaterally. No thrills are present over the neck, upper extremity, abdominal and lower extremity pulses or over the auscultatory areas of the heart. The point of maximum impulse (PMI) is located in the fifth intercostal space at the midclavicular line. The lower limbs and digits are warm. Mild pitting pedal oedema is present up to the ankle bilaterally, but is worse in the left foot. There is no palpable tenderness, numbness or fibrotic or sclerotic changes to the skin of the lower legs. Varicose veins over the bilateral popliteal fossae and calf are palpable.
