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 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Among the many factors that contribute to a nonhealing wound, circulatory compromise is a dominant variable. Regardless of whether the circulatory compromise is arterial or venous, the patient should be educated and supported in their efforts to quit smoking, minimize stress, achieve ideal body weight, limit fats in their diet, keep underlying disorders within check, and avoid a sedentary lifestyle. Patients with peripheral arterial disease (PAD) can maximize their tissue perfusion when nurses help them implement a few basic strategies into their lifestyles. Patients with chronic venous insufficiency (CVI) need to apply counterpressure and combat gravity to reduce venous hypertension, without which healing will not occur. When resources are limited, nurses can bridge the gap through coordination of care, patient teaching and support.
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PMID:Practical nursing measures for vascular compromise in the lower leg. 757 82

The aim of this study was to evaluate the effect of lacidipine and nifedipine on lower limb veins. Forty hypertensive patients, aged 30-50 years, with no deep venous thrombosis, venous insufficiency, or hypothyroidism underwent double-blind treatment with placebo (1 week), lacidipine 4 mg once daily (1 week), and slow-release nifedipine 20 mg twice daily (1 week) in randomized sequence. Echo-color Doppler examination of superficial, deep, communicating, and perforating veins of the legs was performed. The results showed venous insufficiency and hypertension after 1-week administration of lacidipine (5 and 15%, respectively) and nifedipine (10 and 25%, respectively) and only two cases (5%) of venous hypertension during placebo administration. Lower limb edema was observed in two patients (5%) during treatment with nifedipine slow-release (SR). The hemodynamic effects of lacidipine and nifedipine were reversible but may contribute to the mechanism of lower limb edema.
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PMID:Effects of lacidipine and nifedipine on lower limb veins in nonphlebopathic patients. 760 97

Several studies have suggested the presence of hemorheological abnormalities in venous insufficiency. The present prospective study was carried out to determine whether the increase in hemorheological disturbances parallels the evolution of the disease. Patients were recruited among ambulant outpatients and classified in 3 evolution stages of venous insufficiency according to the clinical and functional examination. Once a certain number of patients were included, the following successive inclusions were made in order to match for age and sex, in the other stages of venous insufficiency, the previously included patients. Since blood rheology is frequently altered in hypertension, diabetes and several other vascular pathologies, patients with those pathologies were not included. Sixty nine patients with venous insufficiency and 23 healthy subjects were tested, making up twenty three matching sets. Red blood cell (RBC) aggregation and disaggregation were assessed with the SEFAM erythroaggregameter on blood samples adjusted to 40% hematocrit. Statistical analysis showed a significant difference for the aggregation index (p = 0.0001), disaggregation shear rate (p = 0.0001) and fibrinogen (p = 0.006) between the 4 groups. Aggregability parameters increased gradually with the evolution of the disease, while the fibrinogen rise was significant only when varicose veins were present (stages 2 and 3). This progressive rise in RBC aggregability with the aggravation of venous insufficiency, by superimposing to the haemodynamic deficit, is likely to induce the formation of RBC aggregates in vivo, to perpetuate venous stasis and to contribute to the development of severe skin damages.
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PMID:Red cell aggregability increases with the severity of venous insufficiency. 765 8

CO2 baths are considered an integral feature of balneotherapy. Natural springs containing a concentration of CO2 probably sufficient to be clinically effective (> 1 g/l) as well as artificially enriched baths are applied. Phenomena like a marked erythema (at concentrations above 0.5 g/l) imply clinical efficacy beyond unspecific effects of baths (water immersion, thermal effects). Prolonged effects are postulated to exceed "direct" effects, thus forming the rationale for serial applications of CO2-baths. CO2 is believed to cause an acute induction of local vasodilation and a shift of the O2 binding curve, resulting in a facilitation of the delivery of O2 to the tissue. A positive impact of CO2-baths on the flow properties of blood has been reported. A wide variety of indications is mentioned in the literature, while clear evidence from controlled trials exists only for a minority of them, mainly for chronic circulatory disturbances based on atherosclerotic diseases such as peripheral arterial occlusive disease, trophic ulceration, microangiopathies of various origins, and mild hypertension. Some evidence supports the idea that CO2 baths might represent an efficient therapeutic means in the rehabilitation of coronary heart disease, myocardial infarction and stroke, and in the treatment of chronic venous insufficiency, certain inflammatory diseases, and functional disturbances.
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PMID:[Possibilities and limits of CO2 balneotherapy]. 801 66

The ulcus cruris is an ulcerative lesions caused by chronic venous stasis and chronic venous hypertension. Every pathologic obstacle to venous return can cause ulcus cruris. Ulcus could be brought back to 3 situations: postphlebitic syndrome, chronic venous insufficiency and primitive varicosities. The common denominator is always the increase in venous pressure, the appearance of reflux and venous stasis. Venous ulcers are possibly characterized by tissue degeneration and by bacterial superinfection. A particular bacterial flora is found in these injuries, it is qualitatively different from that of healthy skin. The therapy of ulcus cruris cannot leave out by its etiopathogenesis: the first treatment always consists in the stasis suppression to arrive quickly to a complete cicatricial would repair. In it three moments are recognizable: ulcus abstersion, disinfection and cicatrization. The venous ulcer is not cured when it is closed, but when it has no recurrency: the cicatrization is obtainable treating the principal causes, eliminating the venous stasis and anticipating the relapses.
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PMID:[The trophic venous ulcer. The physiopathological, microbiological and pharmacological aspects]. 802 44

Chronic venous insufficiency of the lower limbs is a frequent disorder that has costly repercussions for society as a whole. It is important to distinguish between abnormality of venous function and its most frequent causes, which are sequelae of deep venous thrombosis and varices of the lower limbs. Chronic venous insufficiency manifests by functional symptoms, based on the heavy leg syndrome, which is very frequent but not specific, and on objective distal signs that are highly specific. Both prognosis and cost of the disorder are based on such objective signs, cutaneous and subcutaneous complications of stasis and of venous hypertension, ranging from simple ochre dermatitis to recurring ulcers and ankylosis of the ankle. Dermo- and hypodermatitis and ulcers complicate less than 10% of chronic venous insufficiency but are responsible for most of the cost involved, two-thirds of which is linked to invalidity. Clinical grades of chronic venous insufficiency have been established, which should facilitate standardisation and comparison of epidemiological, pathophysiological and therapeutic data. Diagnosis of chronic venous insufficiency is by clinical examination, while etiological investigation should most often be done by technical investigation.
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PMID:[Mechanisms, epidemiology and clinical evaluation of venous insufficiency of the lower limbs]. 805 8

Several aspects comprise the medical treatment of chronic venous insufficiency: adoption of daily routines favouring mechanisms for return of venous blood; wearing of elastic stocking to reduce superficial venous hypertension, the basis of medical treatment; use of venotonic agents as adjuvant therapy; association of crenotherapy; and finally the possibility of sclerotherapy when such treatment can correct the dysfunction of the superficial venous network. Various therapeutic strategies should be considered to manage not only the functional and/or clinical signs of chronic venous insufficiency, but also the complications which may occur (varicose thrombosis and haemorrhage, or deep venous thrombosis). Lastly, prevention is based not only on respect of daily hygienic measures but above all on early treatment that is adapted to any deep venous thrombosis.
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PMID:[Medical treatment of chronic venous insufficiency]. 805 14

Ulceration of the skin is the most severe complication of chronic venous insufficiency of the lower limbs. The ulcer reflects a profound impairment of the venous anatomy and function, often the late sequel to a deep venous thrombosis. The available surgical techniques are rarely apt to repair these lesions completely. Medical treatment is palliative, based upon the strict control of superficial venous hypertension (leg drainage and compression) and the rational use of local therapies (ulcer cleanliness, debridement and dressing). The physician must obtain the co-operation of the patient and the help of a competent nurse. Failures and recurrences are frequent. Rather than to hopeless resignation or even to abandon, such drawbacks should lead to a critical reassessment of each step in the treatment to identify imperfections, and to correct them.
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PMID:[Treatment of skin ulcers of venous origin]. 805 15

Severe chronic venous insufficiency (CVI) demonstrates as chronic, hard-to-heal wounds of the lower extremity. The wound is the result of poor skin perfusion due to a complex series of pathologic events, often initiated by a deep vein thrombosis (DVT). As years pass, the DVT causes venous valvular damage and incompetence. The calf muscle pump fails to augment venous return, and venous blood pressure is chronically elevated upon standing. Mechanisms that normally prevent the transmission of venous hypertension back upstream to the dermal microcirculation are lost. Early dermal microvascular responses include increased fluid filtration and edema. An inflammatory response induces white cell activation and adhesion. It is thought that activated white cells are trapped in dermal capillaries and increase microvascular permeability. Plasma proteins leak into the tissue space, increasing the edema. Ischemic damage to the epidermis leads to epithelial cell necrosis and ulceration. The ulcer is often slow to heal, due to inadequate perfusion and delivery of substrates required for proper wound healing. Current treatments aim to improve calf pump function, reduce edema, improve perfusion, and enhance wound healing.
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PMID:The microvascular pathophysiology of chronic venous insufficiency. 825 61

Congestive heart failure is a frequent complication of massive obesity and a major cause of death. Prior to the cardiac decompensation stage, infraclinical haemodynamic disturbances can be observed in obese subjects with normal blood pressure: the cardiac output and cardiac index increase, due to a rise in systolic ejection volume, the total peripheral resistance falls and the intravascular volume augments. Cardiac adjustment takes place in the form of excentric left ventricular hypertrophy. Ventricular extrasystoles, often associated with this hypertrophy, might be the cause of sudden death in some obese patients. Arterial hypertension is about 3 times more frequent in obese subjects than in subjects of normal weight, and even more frequent in those with massive obesity. To the high preload due to obesity hypertension adds an increased after-load. This results in augmentation of the mass and work of the left ventricle with progressive alteration of its function. The incidence of coronary disease is increased in obese subjects, notably those with abnormal adiposity. Finally, the return circulation is very often perturbed, notably in gynecoid obesity: there is venous insufficiency with a higher risk for thromboembolism, and lymphatic insufficiency or capillary permeability disorders. A low-calorie diet and a physical rehabilitation of sedentary obese subjects facilitate weight reduction and at the same time tend to correct the associated metabolic disturbances; they reduce blood pressure and also seem to reduce the left ventricular hypertrophy.
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PMID:[Hemodynamics of massive obesity]. 831 Feb 45


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