Treatment of lower-extremity chronic wounds doesn’t only entail preventing infections and mitigating any patient pain or discomfort, it also requires management of the underlying pathophysiology that caused them. That is often easier said than done since many patients may have several comorbid conditions, which can either be the cause of chronic wounds, hinder their treatment, or both. An example of the latter is Peripheral Artery Disease (PAD).
In 2015 there were 236.62 million individuals with PAD (or LEAD, Lower Extremity Artery Disease, as it is increasingly also referred to as today), up from 202 million in 2010 [1, 2]. This growing trend is likely to continue due to the general ageing of the population (particularly in economically developed countries) and an increase in several important risk factors .
One of the most important risk factors for PAD is diabetes mellitus (type 1 and type 2), which is also rapidly increasing in prevalence. It is estimated that there were 285 million adults with diabetes in 2010, 415 million in 2015, 451 million in 2017 and it is projected that number will increase to 693 million by 2045 [3, 4, 5].
Diabetes has numerous deleterious effects on the development, morbidity, severity of complications and the (un)timely diagnosis of PAD. It is estimated that at least 20 % of diabetic patients have PAD, but that number, although obtained by the Framingham Heart Study, represents only those with the symptomatic form of the disease (diagnosis of intermittent claudication) .
Ulcers and chronic wounds are also, not coincidentally, the topic of this blog post, or more specifically the contribution of PAD to their development, a reduction of healing rates and an increase in the incidence and severity of complications and the differentiation between wound types on the basis of their etiology. Naturally, any appropriate treatment regime is predicated on accurate and timely diagnosis of PAD and a comprehensive assessment of its severity.
This can usually be achieved only through the use of modern diagnostic devices, which can measure either the ABI, the Toe-Brachial Index (TBI) or both. However such tools might not be available in every wound care/compression therapy facility, despite their obvious usefulness, requiring instead the use of methods for identifying and stratifying at-risk patients. A comprehensive questionnaire is one such method.
The majority (72 %) of all lower-extremity ulcers are caused by Chronic Venous Insufficiency (CVI), while PAD is responsible for 10 % to 30 % of all cases with diabetes, i.e. neuropathic ulcers are a distant third with prevalence in the ballpark of 15 % to 25 % . Ulcers might also have a less common etiology, such as lymphatic or infectious, which represent only a very small number of cases, where the former (lymphatic ulcers) were found in only 2.5 % of patients enrolled in a comprehensive study of treatment of lower-extremity ulceration . It should be noted that patients might have ulcers of mixed etiology.
Successful treatment is predicated on the timely diagnosis of PAD and the management of risk factors (primarily modifiable ones such as smoking) with possible surgery/endovascular intervention – lest it is too late – and those arterial ischemic wounds that progress into gangrene and Critical Limb Ischemia (CLI). Diagnosis of CLI is unfortunately associated with high amputation rates (ranging from 10 % to 40 % for a 6-month period after diagnosis) and significant mortality (from 20 % in the 6-month period to 50 % in 5 years after diagnosis) [25-29].
Venous ulcers are usually (conservatively) managed using compression therapy, but its utility is limited in patients with only arterial insufficiency ulcers or those with both types of ulcers (due to the possible use of lower compression levels) and may be even be entirely inappropriate for those with severe PAD [35, 36]. The only exception is intermittent pneumatic compression (IPC) systems, which are suitable for improving healing rates in patients with venous, arterial and neuropathic ulcers [37-39].
The questionnaire for assessing the relative risk of PAD in wound care patients/patients with chronic wounds takes into account well-known risk factors for the disease with an additional emphasis on information pertinent to wound care/compression therapy providers.
Older patients (generally over 50 years of age) are at an increased risk of PAD, which might be asymptomatic .
There are statistically significant discrepancies in PAD prevalence and morbidity in individuals of different ethnic groups. Studies have shown that blacks (specifically African Americans) are at higher risk of developing PAD than whites .
Some studies have indicated greater prevalence of PAD (particularly more severe forms) in women than in men .
Current smokers have a far greater risk of developing PAD . Association between tobacco smoking and PAD is especially strong in female smokers who are at an up to 20-times greater risk for the disease than females who have never smoked . Information about past smoking (former smokers) is also important: the health benefits of smoking cessation don’t translate well to PAD as even former smokers are at an increased risk with up to 2.6-times greater prevalence of PAD (in comparison with non-smokers) .
Diabetes-induced hyperglycaemia greatly increases the incidence and prevalence of PAD .
Already present (diagnosed) CAD is indicative of possible atherosclerosis in other vascular beds – prevalence rates of PAD in CAD patients range from 22 % to 42 % [46-48].
History of MI and cerebrovascular events is associated with higher prevalence rates of PAD, often in its asymptomatic form (diagnosis on basis of the ABI score) [49-51].
Individuals with renal insufficiency are 9-times more likely to have an abnormal ABI score (defined as ABI <0.9, which is an indication of PAD) .
Patients with rheumatoid arthritis are more likely to have incompressible arteries, precluding the use of some diagnostic methods for PAD .
Incompressible arteries are quite likely in those who have answered the 5th, 8th and 9th question with YES – a warning sign for the examiner that diagnostic methods other than ABI (i.e. TBI) will have to be used.
Patients with COPD are at double the risk of developing PAD .
Abnormal levels of blood lipids and lipoproteins is associated with mild risk for development of large-vessel PAD .
Hypertension is a known risk factor for PAD (and other CVDs) .
Weight is a risk factor for PAD (and many other medical conditions) as studies have shown that older individuals with greater BMI (body mass index) have a higher incidence of PAD .
Accurately diagnosing intermittent claudication on the basis of physical sensations the patient feels during physical exertion and when still/resting is best done using the Edinburgh Claudication Questionnaire .
Reduced blood flow leads to disruption of normal thermoregulation.
Occlusion in the arteries of lower extremities reduces flow of nutrients to skin and toenails, leading to stunted growth and deformations. Pallor in the affected leg is possible when it is in an elevated position .
This is another tell-tale sign of PAD, but one that is typical for the advanced form of the disease.
This is not directly connected to diagnosing PAD as it is possible that a patient with venous ulcers was a recipient of compression therapy without prior PAD assessment, but it is a cue for an evaluation of the suitability of such treatment for the patient in question.
Diagnosis of erectile dysfunction carries a two-fold increase in the likelihood of PAD .
Patients with a family history of PAD are at twice the risk of the disease than those without such a familial medical history .
Comprehensive chronic wound assessment and treatment should include an ABI or TBI assessment to confirm or dismiss the presence of PAD. Where modern diagnostic tools are lacking, a comprehensive questionnaire may be used to identify at-risk patients who might benefit from further examination, but not in lieu of them.