peripheral arterial disease


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peripheral arterial disease

also

peripheral artery disease

n.
Atherosclerosis of the peripheral arteries, usually of the lower extremities, characterized by pain and cramping in the legs.

peripheral arterial disease (PAD)

a systemic form of atherosclerosis producing symptoms in the cardiac, cerebral, and renal vascular systems. It affects up to 2% of individuals between 37 and 69 years of age and about 10% of persons over 70 years of age. The incidence is highest among males with diabetes mellitus. Other risk factors include obesity and stress. Blood flow is restricted by an intraarterial accumulation of soft deposits of lipids and fibrin that harden over time, particularly at bends or bifurcations of the arterial walls. Patients generally are not aware of the changes until the diameter of the arterial lumen has been reduced by half. Early symptoms include intermittent claudication and ischemic rest pain. See also arterial insufficiency.

pe·riph·er·al ar·te·ri·al dis·ease

(PAD) (pĕr-if'ĕr-ăl ahr-tēr'ēr-ăl di-zēz')
Any disorder involving the arteries outside of, or peripheral to, the heart.

disease

pathogenic entity characterized by an identifiable aetiological agent, group of signs and symptoms and/or consistent anatomical alterations; see syndrome

peripheral vascular disease

generic term denoting reduced arterial supply to, and compromised venous/lymphatic return from, the lower limbs and feet; see disease, peripheral vascular
peripheral vascular disease; peripheral arterial disease; PAD generic term denoting lower-limb macrovascular disease (e.g. arteriosclerosis, atherosclerosis, arterial stensois or blockage) or the symptoms of macrovascular disease (e.g. intermittent claudication, rest pain, dry gangrene); patients with PAD are likely to have similar vascular effects in brain, heart and kidney arteries (see Table 1, Table 2and Table 3)
Table 1: Risk factors for the development of peripheral arterial disease (PAD)
Risk factorFeature of the risk factor
Modifiable factors
SmokingCigarette smoking is the most powerful risk factor for the development of PAD. It is dose-dependent and the risk declines within 6 months of quitting. A non-smoker is 10 times less likely to develop PAD than a smoker
Blood lipid disordersPlasma cholesterol levels of >5.2 mmol/L
Increased plasma concentrations of low-density lipoprotein (LDL) cholesterol, low plasma concentrations of high-density lipoproteins (HDLs), and higher concentrations of plasma triglycerides all correlate with increased incidence of PAD
Familial hypercholesterolaemia (affecting 1:500 in UK)
Familial combined hyperlipidaemia (affecting 1:250 in UK)
Diabetes mellitus (DM)Type 2 DM increases risk of PAD by 1.5-4.0, due to the associated hypertension, hyperlipidaemia and altered vascular reactivity
HypertensionRaised systolic blood pressure (BP) increases the risk of PAD and atherosclerosis by 4 due to endothelial injury caused by increased intra-arterial shear stresses at the blood-endothelium interface (raised systolic pressures are more predictive than raised diastolic pressures)
ObesityCentral obesity is an independent risk for PAD, but also predisposes to other risk factors for PAD, such as type 2 DM, hypertension
HomocysteineHomocysteine is an amino acid that in high levels is associated with thromboembolism
Haemostatic variablesIncreased levels of clotting factors VII, VIIIC and fibrinogen are associated with increased risk of atherosclerosis
Sedentary lifestyleLow levels of regular activity are associated with increased risk of PAD (higher levels of activity are associated with higher levels of plasma HDL-cholesterol and reduced blood pressures and facilitate the development of the collateral circulation)
Dietary deficienciesLow levels of antioxidant vitamins (vitamins C and E) and polyunsaturated fatty acids facilitate the formation of oxidized LDLs and thus predispose to the risk of PAD
Type A behaviours (TABs)People who tend to aggression, ambitiousness, restlessness, time urgency and high anxiety tend to an increased incidence of PAD, possibly due to increased levels of circulating catecholamines
Non-modifiable or fixed factors
Age and sexAtherosclerosis is more common in males, and in postmenopausal women
Family historyAtherosclerosis shows familial patterns of incidence, possibly due to genetic factors and/or lifestyle choices and patterns
Early environmentFetal origins hypothesis: adverse conditions in utero or infancy predispose to the risk of cardiovascular disease in later life (e.g. statistically, small-birth-weight babies have a higher incidence in adult life of hypertension, type 2 DM, altered plasma lipids, altered bone densities, altered stress responses, less elastic arteries, thicker-walled ventricles and 'age' quicker)
Table 2: Fontaine classification of peripheral arterial disease (PAD)
StageCharacteristic symptoms
1Clinically symptom-free vascular occlusion
2Exercise-induced ischaemia causing intermittent claudication
No pain at rest
3Ischaemia at rest, causing rest pain
4Ulceration and ischaemic gangrene
Table 3: Clinical tests used in the diagnosis of peripheral arterial disease (PAD)
Test modalityDiagnostic indicators
Medical history• Evidence of atherosclerosis, such as ischaemic heart disease, cerebrovascular disease
• Risk of atherosclerosis, such as cigarette smoking, diabetes mellitus
Pulses in the lower limbPopliteal, posterior tibial, dorsalis pedis and peroneal pulses
• Pulse quality (bounding, full, normal, weak, absent)
• Rate (beats/minute)
• Regularity (regular, irregular, regularly irregular, irregularly irregular)
Presenting symptoms• Cold, numb feet
• Intermittent claudication
• Rest pain
• Painful ulceration
Ankle-brachial index (ABI)• 0.9-1.1 = normal
• 0.7-0.9 = PAD, some compromise of tissue viability
• 0.5-0.7 = severe PAD, compromised tissue viability
• <0.5 = threat of ischaemic gangrene/very poor tissue viability
• >1.2 = calcification of tunica media of leg/foot artery, compromised tissue viability
Segmental systolic pressureSerial measurement of systolic blood pressure along length of limb:
• A sudden decrease indicates the location of the vascular obstruction
Venous filling time
Note : this test is not valid if the patient has venous incompetence
The time it takes for veins to refill in a limb that has been drained of venous blood (with the patient supine, the leg is elevated to 45° for 1 minute, then the leg placed in a dependent position and the time taken for the dorsal foot veins to refill)
• <15 seconds = normal
• 20-30 seconds = moderate ischaemia
• >40 seconds = severe ischaemia
Buerger's testThe observation of the change in skin colour in response to limb elevation and dependency (with the patient supine, the leg is elevated to 45° for 1 minute, then the leg is placed in a dependent position and the time taken for normal skin colour to return is noted)
• <10 seconds = normal response
• Patchy persistent rubor indicates limb ischaemia
• Persistent pallor (>10 seconds) indicates limb ischaemia
• Persistent cyanosis indicates limb ischaemia
Buerger's angleThe colour response of the sole of the foot to limb elevation (with the patient supine, the leg is elevated and the angle of limb elevation is noted when the skin of medial longitudinal arch shows pallor)
• 60-70° = normal arterial supply to foot
• < 45° = compromised arterial supply to foot
• < 30° = severe compromised arterial supply to foot
Capillary refill time
Note: this test is not valid if the patient has signs of current Raynaud's disease
The time taken for normal skin tone of a horizontal limb to return after the nail bed or digital pulp has been compressed by thumb pressure
• <5 seconds = normal response
• >5 seconds = some ischaemia
• >15 seconds = marked ischaemia
Doppler sounds• Triphasic = normal
• Biphasic = normal/some loss of arterial elasticity
• Monophasic = loss of arterial elasticity/arterial stenosis
• Loud = high rate of blood flow
• Quiet = slow rate of blood flow
• No sound = no blood flow (proximal arterial occlusion)
Skin temperature
Note: this test is not valid if the patient has signs of current Raynaud's disease
• ~ 31°C = normal foot skin temperature
• <29°C = possible poor skin perfusion
References in periodicals archive ?
Gene Therapy for Critical Limb Ischemia and Peripheral Arterial Disease - Drug Profile 76
Relation of interleukin-6 and vascular cellular adhesion molecule-1 levels to functional decline in patients with lower extremity peripheral arterial disease.
In their study, forty three patients with 774 segments in patients with intermittent claudication and leg pain diagnosed as mild peripheral arterial disease had undergone Doppler USG followed by MDCT angiography of lower limbs.
Europen Manual of medicine-Lipids and Peripheral arterial disease.
LOT 3: Supply of angiography equipment monoplane with ceiling-mounting apparatus used for the pathology of coronary, cerebrovascular and peripheral arterial diseases, with maximum software including space planning, installation, commissioning and personnel training: 2 pcs.
Identify and understand important and diverse types of therapeutics under development for Peripheral Arterial Disease (PAD)/ Peripheral Vascular Disease (PVD).
Among non-diabetic subjects, the age-standardized prevalence of peripheral arterial disease was 3.
Treatment goals for peripheral arterial disease (PAD) always include reducing your risk of heart attack and stroke by immediately controlling your risk factors and through the use of medications.
3% of patients with peripheral arterial disease, various levels of coronary stenosis (P=0.
Peripheral Arterial Disease (PAD) is a highly prevalent atherosclerotic syndrome that affects approximately 8-12 million individual in the USA and is associated with significant morbidity and mor tality.
The significance of lower extremity peripheral arterial disease.
Effect of diagnostic criteria on the prevalence of peripheral arterial disease.

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