Intermittent lumbar Claudication.
Explore the source record for details and available documents.
SEARCH · Search PubMed
Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.
Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.
Explore the source record for details and available documents.
The risk factors, epidemiology, diagnosis, and treatment of peripheral arterial disease are reviewed. Peripheral arterial disease is characterized by a gradual reduction in blood flow to one or more limbs secondary to atherosclerosis. Risk factors include smoking, diabetes mellitus, hyperlipidemia, and hypertension. The most common clinical manifestation is intermittent claudication. The prevalence of intermittent claudication in people over the age of 50 is 2-7% for men and 1-2% for women. The ankle:brachial pressure index (ABPI) is a useful measure of disease severity; an ABPI of 0.5-0.9 is common in intermittent claudication. The goals of therapy are to relieve or reduce ischemic symptoms, alleviate disability, improve in functional capacity, prevent progression that may result in gangrene and limb loss, and prevent cardiovascular and cerebrovascular events. Treatment includes risk-factor modification, drug therapy (primarily with antiplatelet agents), and revascularization procedures. Aspirin has been shown to be effective in reducing the associated risk of myocardial infarction and stroke. Ticlopidine appears to be a reasonable alternative for patients who are hypersensitive to aspirin. Clopidogrel has been shown to be more effective than aspirin in patients with recent myocardial infarction, recent stroke, or established peripheral arterial disease. There is controversy over the appropriate treatment for acute arterial occlusions. Risk-factor modification and antiplatelet drugs are the mainstays of therapy for patients with intermittent claudication, the most common manifestation of peripheral arterial disease.
INTRODUCTION: Intermittent arterial claudication is the master symptom in lower limbs arteriopathy. It is used as a reference in invasive or non-invasive arterial explorations. It allows to assess the evolutive degree of the disease and above all helps the therapeutic decision. The seat of claudication is traditionally acknowledged as being located immediately downstream of the significant arterial lesion. The purpose of our work was to verify such a notion and ascertain the relation between spontaneous and tread-mill induced claudication. PROTOCOL: 60 stage-2 arteritic patients were included in a prospective mode study. They were all taken in hospital for arteriographic check-up and vascular functional explorations: Doppler velocimetry, segment pressures, treadmill tests and pressure measurements after stress. The patients were classified according to age (table I), time of claudication record (table II) and lesions location (table III). All clinical and paraclinical data were recorded with a view to correlations interpretation. RESULTS AND DISCUSSION: The relation between spontaneous claudication and tread-mill induced claudication was studied with respect to lesion sites (table IV). Among 37 patients 46% of the claudications observed appeared at iliac stage in both cases (fig. 1). In 35 cases, femoral claudication was observed in 48% (fig. 2). As for distal claudication among 6 patients, 3 showed calf claudication in both cases, i had foot claudication and 2 showed discrepant claudication types. The relation between claudication and lesion site was not confirmed in all cases. Buttock claudication always appeared in relation with a lesion upstream or an internal iliac lesion.(ABSTRACT TRUNCATED AT 250 WORDS)
Explore the source record for details and available documents.
The authors report on a case of intermittent venous claudications in a 76-year-old man, who three months previously suffered a sudden acute attack of phlebitis in the right upper limb. The Doppler exam showed post-phlebitic failure of the humeral valve and diminished permeability of the axillobrachial axis of the vein, with sub-clavicular obstruction. The discussion provides an opportunity for reviewing the various anatomo-pathological definitions and explanations of the mechanism of intermittent venous claudications.
Intermittent claudication of neurogenic origin can be traced to three basic causes: --either a chronic circulatory deficiency in the arteries leading to the spinal cord, whether these arteries be the site of an atheroma of the ostia, an inflammation or a loco-regional compression. In such cases, the claudication is painless which differentiates it from the arteritis claudication of the lower limbs. --or to a compression of the roots of the cauda equina and to a lesser degree of the spinal cord, through a narrow rachidian canal that is hereditary or acquired, and relative or absolute. --or finally to a sheathing peripheral neuropathy of the lower limbs. The two latter causes are accompanied by pain, and make it necessary to widen the classical notion of the intermittent claudication (Dejerine's non painful intermittent claudication of the spinal cord).
Intermittent claudication is a common disabling condition that affects approximately 5% to 15% of patients with atherosclerotic disease. Recommended treatment involves lifestyle modification and physical conditioning through the adoption of a regular exercise program. These methods of treatment often have been unsuccessful in the past because of noncompliance, in large part related to the relatively minor degree of improvement experienced by the patient. However, some recent trials have resulted in greater relative improvements in both pain-free and maximal walking distances in some patients treated with medication. Surgical and endovascular options offer greater degrees of improvement but also greater morbidity and should be reserved as treatment for severe claudication. The efficacies, as well as common adverse reactions associated with current medications used to treat patients with intermittent claudication are reviewed.
CONTEXT: Many patients with intermittent claudication continue to be forwarded to the vascular surgeon for initial evaluation after arteriography has already been accomplished. OBJECTIVE: The main objective of this work was to analyze the usefulness and the need for this procedure. TYPE OF STUDY: Retrospective study. SETTING: The patients were divided into two groups: Group 1, with the arteriography already performed and Group 2 without the initial arteriography. PARTICIPANTS: One hundred patients with intermittent claudication were retrospectively studied. Other specialists had forwarded them for the first evaluation of intermittent claudication, without any previous treatment. MAIN MEASUREMENTS: All patients were treated clinically for at least a 6-month period. The total number of arteriographies performed in the two groups was compared and the need and usefulness of the initial arteriography (of Group 1) was also analyzed. RESULTS: The evolution was similar for both groups. The total number of arteriographies was significantly higher in Group 1 (Group 1 with 53 arteriographies vs. Group 2 with 7 arteriographies). For this group, it was found that arteriography was only useful in five cases (10%), because the surgeries were based on their findings. However, even in those cases, no need for arteriography was observed, as the procedure could have been performed at the time of surgical indication. CONCLUSION: There are no indications for arteriography in the early evaluation of patients with intermittent claudication, because it does not modify the initial therapy, independent of its result. In cases where surgical treatment is indicated, this procedure should only be performed prior to surgery.
BACKGROUND: Peripheral arterial occlusive disease (PAOD) is the most common peripheral vascular disorder in the elderly. A clear picture of the disease's course, especially in patients with non-critical limb ischaemia (Fontaine stages I and II), is essential for the general practitioner, who plays a key role in the diagnosis and management of PAOD. AIM: To evaluate the population-based evidence on the course and prognosis of PAOD. METHODS: An exhaustive literature search yielded 16 population-based studies on the prognosis of PAOD. The methodological qualities of the studies were assessed according to eight criteria. RESULTS: Thirteen studies of high methodological quality show that data on the course, cardiovascular morbidity, and mortality of asymptomatic PAOD are scarce. Only a small group of asymptomatic patients seem to develop intermittent claudication symptoms. However, asymptomatic patients appear to have the same increased risk for cardiovascular morbidity and mortality when compared with claudicants. No data were available on prognostic factors for intermittent claudication and cardiovascular morbidity in asymptomatic patients. The course, cardiovascular morbidity, and mortality of symptomatic PAOD are better documented. A small group of claudicants experience symptom progression. Smoking, hypertension, increasing age, and diabetes are the most relevant risk factors for intermittent claudication. Claudicants are at a higher risk for developing other cardiovascular diseases, resulting in a significantly increased mortality mainly owing to coronary heart disease. Intermittent claudication and a low ankle-brachial pressure index are significant predictors of mortality. Men had intermittent claudication and symptom progression more often than women. Cardiovascular (co-)morbidity was common in both male and female PAOD patients, but male PAOD patients had a higher mortality compared with female PAOD patients. CONCLUSION: Given the current knowledge on the prognosis of PAOD in the general population, an important task for (secondary) prevention is reserved for the general practitioner. Further research is required to document the course and prognosis of asymptomatic PAOD patients.
Explore the source record for details and available documents.
HYPOTHESIS: Marked peripheral vasodilation and rubor characterize critically ischemic limbs on dependency. We believe that intermittent claudication is also associated with peripheral hemodynamic changes on postural alteration, which differ distinctly from normal. Evaluation of such differences and understanding of the underlying physiological derangements may be essential in the development of treatments for intermittent claudication. We comparatively assess the effect of posture on lower limb arterial hemodynamics in normal subjects and in patients with intermittent claudication (or Fontaine II) due to peripheral vascular disease, determined in the popliteal artery. DESIGN: A cohort study. SETTING: A university-associated tertiary care hospital. PATIENTS: Thirty-seven legs of 29 normal subjects (group A) and 50 legs of 36 patients with intermittent claudication (ankle-brachial index range, 0.39-0.76; median, 0.57) (group B). INTERVENTIONS: Popliteal artery volume flow (vFl), mean velocity, and luminal diameter were measured on (1) recumbency, (2) sitting, and (3) return to recumbency in groups A and B using color duplex imaging. MAIN OUTCOME MEASURES: The pulsatility index, peak systolic velocity, and end diastolic velocity (EDV) were measured on (1) recumbency, (2) sitting, and (3) return to recumbency. RESULTS: Popliteal artery vFl in normal subjects decreased from 110 +/- 43 mL/min on recumbency to 57 +/- 27 mL/min on sitting (P<.001) and returned to 111 +/- 46 mL/ min on resumption of recumbency (P<.001). Similarly, in patients with intermittent claudication, vFl decreased from 113 +/- 52 mL/min on recumbency to 76 +/- 41 mL/min on sitting (P<.001) and increased on resumption of recumbency to 114 +/- 53 mL/min (P<.001). There was no difference (P = .97) in the vFl between the study groups on recumbency, but sitting vFl in normal subjects was significantly lower than in patients with intermittent claudication (P = .04). The mean velocity, peak systolic velocity, and EDV displayed a similar pattern of change as vFl. The pulsatility index in both groups increased significantly on sitting (P<.001) and decreased on return to recumbency (P<.001). All data are given as mean +/- SD. CONCLUSIONS: Lower limb arterial vFl, mean velocity, peak systolic velocity, and EDV decrease significantly (P<.001) when posture is altered from recumbency to sitting, in normal subjects and in patients with intermittent claudication. A decrease in the EDV and an increase in the pulsatility index on sitting indicate enhancement of arterial resistance to flow secondary to peripheral vasoconstriction. Quantitative differences between the groups in vFl (P<.04), EDV (P<.01), and pulsatility index (P<.001) on dependency indicate that the orthostatic vasoactive response in patients with intermittent claudication is significantly subdued, reflecting a marked derangement in venoarteriolar response.
In order to develop transcutaneous oxygen tension (PtcO2) measurements into a practical method for assessing peripheral vascular disease, the relationships between extremity and chest wall PtcO2 were examined in subjects with and without systemic atherosclerotic disease. The ratio of extremity to chest PtcO2, or transcutaneous regional perfusion index (RPI) assessed limb oxygenation more reliably than did direct PtcO2 measurement by obviating the effects of changes in systemic oxygen delivery upon local PtcO2. The authors find that transcutaneous oximetry can be used during treadmill exercise testing and that the RPI is unchanged by exercise in all normal subjects. PtcO2 and RPI were then measured during rest, position change, and exercise testing in patients with intermittent claudication. Whereas normal subjects maintain a constant thigh and calf RPI during exercise, patients with intermittent claudication consistently manifested large decreases in RPI in these areas when they were exercised until symptomatic. The authors find no overlap between the responses of normal subjects and patients with claudication; positive findings are, therefore, highly specific for exercise-induced limb ischemia. Since transcutaneous RPI exercise testing is easily performed and highly reproducible, it is well suited to clinical use in the diagnosis and documentation of intermittent claudication. Furthermore, since limb ischemia can be quantified, this method lends itself both to grading the severity of disease and to evaluating clinical progression of disease. It is suggested that such a quantitative approach to evaluation of intermittent claudication may allow refinement and extension of the indications for operative intervention in patients with intermittent claudication.
STUDY DESIGN: This study was done to assess the pathophysiology of neurogenic intermittent claudication by measuring the epidural pressure at walking. OBJECTIVES: Changes in epidural pressure during walking in patients with neurogenic intermittent claudication and in normal individuals were analyzed. SUMMARY OF BACKGROUND DATA: Neurogenic intermittent claudication may be caused by compression of the nerve roots or may be a result of nerve root ischemia. The exact pathogenesis of neurogenic intermittent claudication is uncertain. METHODS: Local epidural pressure changes at the stenotic level during walking were analyzed in 12 patients with lumber spinal stenosis and seven normal individuals. a flexible pressure transducer was inserted into the epidural space and placed at the L4-L5 level. The epidural pressure was monitored continuously during walking. The pattern of the pressure change was assessed by gait analysis using a foot switch. RESULTS: The pressure was changed during walking. The pressure had a wave pattern of increase and decrease, and this pattern was repeated during walking. Intermittent pressure increase was seen about 90 times per minute while walking at a velocity of 2 km/h. An increase in epidural pressure occurred at the double-supporting phase in each gait cycle. CONCLUSIONS: The pressure was high in spinal stenosis and low in normal individuals. The increase of epidural pressure at simple walking was higher than walking with lumbar flexion. Intermittent compression to the nerve roots during walking may be a cause of neurogenic intermittent claudication.
Chronic ischemia of the lower extremities with atherosclerosis background is being manifested by intermittent claudication. For treating the intermittent claudication many drugs are used, which may give rise to therapeutical side effects. In 50 patients with diagnosed arteriosclerosis affecting the lower extremities in II stage according to Fontain, a vegetable preparation PADMA-28 was applied for 16 weeks. A marked, statistically significant elongation of the claudication distance was achieved. That was measured, under standardized condition, on an ergometer-treadmill. Moreover, there was also a decrease in the index of blood platelets aggregation, a drop in the level of cholesterol, triglycerides, total lipids, beta lipoproteins, and an increase in ++alpha lipoproteins. Also 50 patients were receiving placebo for 16 weeks, but no positive results were observed in comparison with preparation PADMA-28. The studies were carried out by the method of double blind test, the latter was accomplished by randomized method. Observation, the performed biochemical examinations did not reveal any undesirable effect. Drug tolerance was excellent. The positive influence of the drug may result from summed action of components contained in the preparation namely: bioflavonoides, salicylates, valepotriates, tannins, phenol acids, ethereal oils and esters of acids. PADMA-28 may be a useful adjuvant to therapeutic methods with regard to chronic ischemia of the lower extremities in II stage, according to Fontain.
The purpose of this study was to evaluate the effect of intravenous prostaglandin E1 (PGE1) on the flow velocity of the ophthalmic artery and the central retinal artery in patients with peripheral vascular disease manifested by intermittent claudication. The flow velocity of these vessels is frequently decreased in vascular patients. Since these patients were already being treated with PGE1 for their intermittent claudication, the authors wanted to evaluate the effect on the flow velocity of the ocular vessels as well. A randomized 21-week study of two groups of vascular patients was performed. The first group had intermittent claudication. The second group had intermittent claudication and were also diabetics. Both groups were treated with intravenous PGE1 for their intermittent claudication. Using the color Doppler, the flow velocities of the ophthalmic artery and central retinal artery were measured before and after the intravenous treatment. Before treatment, the flow velocity of the ophthalmic artery and the central retinal artery was decreased when compared to that in the normals. After treatment, there was a significant increase in the systolic and diastolic phases of the flow velocity in both arteries. The systolic flow velocity increased by as much as 40%, and the diastolic flow velocity increased by as much as 80%. The flow velocities of the ophthalmic artery and the central retinal artery are frequently decreased in certain ocular diseases, and this decreased flow may contribute to the ocular pathology. If intravenous PGE1 is able to increase the flow velocity of these vessels in patients with peripheral vascular disease, it is possible that it is also able to increase the flow velocity of these vessels in patients with ocular disease as well. Intravenous PGE1 may prove to be a useful adjunct therapy in eyes when ischemia is part of the pathology.
OBJECTIVE: To measure the prevalence and incidence of intermittent claudication, to describe the mortality associated wtih the condition, and to assess the relevance of risk factors for vascular disease. DESIGN: A standard questionnaire on calf pain when walking was given in the prospective Speedwell study, and a range of risk factors were measured. The men were re-examined at intervals of three years, and deaths over 11 years were identified. SETTING: The general population. PARTICIPANTS: All men aged 45 to 59 registered with 16 general practitioners. RESULTS: The prevalence of intermittent claudication increased from almost nil at ages 45-49 to 2.9% at ages 60-64. The annual incidence increased from 0.3% in the youngest men to 0.5% in those in their early 60s. Intermittent claudication was related to the existence of ischaemic heart disease, particularly angina, at the first examination. The relative odds of men with angina developing intermittent claudication was 6.7 (95% confidence interval (95% CI) 3.6 to 12.4). The risk of death in men with intermittent claudication was substantially raised. After standardisation for age and smoking the relative odds of death was 3.8 (95% CI 2.2 to 6.5). The excess was entirely from circulatory causes. Systolic blood pressure, fasting plasma glucose, triglycerides, and white cell count were all independently associated with the development of intermittent claudication, but the most striking association was with smoking. CONCLUSIONS: Intermittent claudication is an indicator for a very high risk of death. This is only partly explained by its strong association with ischaemic heart disease.
We surveyed the recent condition of lower limbs with failed vascular reconstruction in patients with Buerger's disease. Forty-three patients (mean age: 41.2+/-8.7 years) received infrapopliteal vascular reconstruction at Nagoya University Hospital. Symptoms at the time of surgery were intermittent claudication in 11 patients, rest pain in 13 and ulcer/gangrene in 19. Inquiry about the condition of the lower limbs was made during March 1998. Eight patients were lost to follow-up and three patients had died. In the remaining 32 patients, mean follow-up period was 140.5+/-42.0 months. Graft was occluded within a week after surgery in six patients with ischemic ulcer/gangrene, three of whom underwent a major amputation while the trophic lesion healed in the remaining three patients. Two grafts were occluded among the 11 patients with intermittent claudication. One of these patients had mild rest pain and the other reported intermittent claudication. Two of the patients with intermittent claudication were lost to follow-up. Among the 13 patients with rest pain, one had died and six were lost-to-follow-up. Although the remaining six patients complained of intermittent claudication, half had an occluded graft. Of the 19 patients with ulcer/gangrene, two had died and all nine of those with occluded graft complained of intermittent claudication. Fate of limbs with failed vascular reconstruction was satisfactory.
BACKGROUND: Peripheral arterial disease (PAD) is associated with adaptive changes in the vascular and muscle extracellular matrix (ECM) in response to reduced blood flow. Matrix metalloproteinases (MMPs) and their inhibitors (TIMPs), are key modulators of ECM turnover. We hypothesized that patients with intermittent claudication (with low ankle-brachial blood pressure index, <0.8), and critical ischaemia would have raised circulating levels of MMP-9, TIMP-1 and TIMP-2 compared with healthy controls, reflecting an increase in proteolytic activity which may be related to ECM turnover in PAD. METHODS: We studied 36 patients (23 males; 65 +/- 9 years) with intermittent claudication and 43 (25 males; 68 +/- 12) patients with critical ischaemia. All patients had angiographic evidence confirming significant PAD. RESULTS: Circulating levels of MMP-9 and TIMP-1 were higher (both P < 0.0001) in the PAD patient groups compared with the controls. Patients with critical ischaemia had MMP-9 and TIMP-1 levels that were significantly higher than those with intermittent claudication. There were no differences in circulating TIMP-2 levels between patients and controls. There was a modest positive correlation between the white cell count (WCC) and MMP-9, both patients with intermittent claudication (Spearman, r = 0.398, P = 0.016) and critical ischaemia (r = 0.378, P = 0.014). CONCLUSION: We demonstrate higher levels of circulating MMP-9 and TIMP-1 in patients with intermittent claudication and critical ischaemia. Circulating concentrations of both markers can be related to disease severity, being higher in critical ischaemia compared with levels in intermittent claudication.