Most patients are asymptomatic; however, note that this usually reflects more sedentary lifestyle rather than lesser severity, and asymptomatic patients with PAD are at just as much risk of complication. (Note that coexisting diabetic neuropathy also increases the chances of the leg being asymptomatic.)
- Smoking probably causes about half of all cases.
- Diabetes carries a similar risk level to smoking.
- Increasing age increases prevalence.
- Tends to show up in men at younger ages, but difference in prevalence levels is similar between men and women.
- High cholesterol, hypertension, and CKD each increase risk by a factor of 1.5x.
- Remember to check for AF as a risk factor for acute ischaemia.
May be with claudication, acute limb-threatening ischaemia, or chronic limb-threatening ischaemia:
Aching or burning in leg muscles, reliably reproduced at a set distance on walking, relieved within minutes on rest, not exacerbated by position, not present at rest. Pain is usually in the calf, but can be in the thigh if the iliac artery is affected.
Acute limb-threatening ischaemia
ALTI is thromboembolic in nature. Embolic ALTI is typically in a normal artery (most usually a result of AF) and comes on very suddenly; this is the one that presents with one or more of the 6 Ps, as per medical school teaching, and needs treatment within hours, including embolectomy. Cases caused by thrombus typically form in an artery with existing arteriosclerosis; they tend to be more gradual onset and (due to pre-existing collateral arterial formation) less severe than the embolic ones. Cases due to thrombus can often be medically managed.
Chronic limb-threatening ischaemia
Caused by narrowing of multiple arteries to the point where the foot becomes severely ischaemic. Presents with rest pain and/or tissue loss. Although it’s less dramatic than ALTI, it’s a serious condition with a high risk of limb loss or death and requires same-day discussion with a vascular surgeon.
Rest pain: note that this is usually in the forefoot/toes rather than the leg muscles. Typically, this is continuous and worse when the foot is elevated – hence patients will get more severe pain at night, hang their foot over the side of the bed to relieve pain, and often sleep in a chair to relieve pain. The latter, unfortunately, tends to start up a vicious circle as sleeping with dependent feet leads to an increase in foot oedema which can reduce the arterial circulation further.
Tissue loss: May be ulceration (usually over pressure areas; hence the toes, the heel, or the metatarsal heads) or gangrene (usually of the toes).
CLTI often presents without prior symptoms of claudication. This is partly because patients may not walk far enough to get claudication, and partly because coexisting diabetic neuropathy is, for obvious reasons, common in CLTI patients.
CLTI usually requires a revascularisation procedure (or, in 15%, amputation) but can be managed conservatively in about 20% of patients. However, always discuss with a vascular surgeon.
Note that CLTI is easily missed. (In fact, the article I’m taking this information from is in the ‘Easily Missed’ section of the BMJ.) It often presents insidiously and is easily mistaken for cellulitis, gout, or plantar fasciitis. The patient may still have foot pulses (not common, but it happens, even in cases of embolisation in the early stages) or may feel as though they have foot pulses when they don’t (there is a substantial false positive as well as false negative rate for palpation of foot pulses – even when vascular surgeons do it, which is reassuring or worrying depending on your point of view). ABPIs can be misleading, partly due to collaterals and partly due to arterial wall calcification (see below). The foot may look lovely and pink if the patient is sitting in a chair and hence getting lots of downward blood flow. Moral of the story? Have a high index of suspicion, and do Buerger’s test (see below).
- Check peripheral pulses, obviously, going proximal to distal (I don’t know why or whether it matters which way you go, actually, but this is what the article says).
- Look for hidden tissue loss on the heel and between toes.
- Don’t bother too much with capillary refill, hair loss, or colour (I assume suspected acute ischaemia is an exception to the last) as they are of little diagnostic importance.
- If CLTI is suspected at all, then do Buerger’s test; the foot turns pale on elevation due to ischaemia and red on dependency due to reactive hyperaemia.
ABPI of 0.9 or less is diagnostic of PAD and 0.5 or less suggests critical limb ischaemia. However, beware arterial calcification; this can cause falsely elevated ABPI values due to arterial incompressibility. Tends to show up in people with diabetes and/or CKD.
- Pulse (you still remember that Finals question, right?)*
- FBC/E&C/glucose or HbA1c/lipids
- If patient under 50 yrs, thrombophilia screen
Indications for referral
Referral is not always necessary; asymptomatic patients and those with claudication only can be managed in primary care. (Document the ET at presentation in order to monitor whether progress is being made.) Note the following three situations:
1. Limb-threatening ischaemia, whether acute or chronic, requires urgent admission under the vascular team.
2. Diabetic foot ulcers in patients with PAD need urgent referral to the diabetic foot multidisciplinary team.
3. Patients with claudication symptoms that are affecting their quality of life and not improving after three months of supervised exercise therapy (see below) should be routinely referred to the vascular clinic for consideration of revascularisation.
- Stop smoking. Smoking cessation, for a PAD patient, not only reduces their risk of amputation, it also doubles their chance of surviving the next five years.
- Antiplatelet treatment. Clopidogrel is first choice (best risk of harms/benefits), aspirin is second choice. Don’t use both, though – the bleeding risk with dual therapy is too high. Warfarin is normally only used in cases of arterial emboli (or AF, I assume). NOACs weren’t mentioned; don’t know offhand whether or not any of them are licenced for arterial emboli in PAD.
- Exercise. There is apparently excellent evidence that supervised exercise programmes work significantly better than unsupervised exercise, but unfortunately the article didn’t clarify what ‘supervised’ was meant to mean here; I’m guessing I’m not actually meant to go out and watch all my patients with PAD walk several times a week. Anyway, the goal to aim for is walking for >30 minutes to near-maximal pain, at least three times a week for at least six months. Supervised exercise therapy actually works as well as angioplasty at improving both walking distance and quality of life. Interestingly, the improvement can occur even when ABPI remains the same.
- Naftidrofuryl oxalate can be effective and is a possible second-line treatment in patients who are no better with walking therapy but don’t want secondary care referral. It should be tried for 3 – 6 months but stopped if not making a difference at that time. Cilostazol is also an option, but naftidrofuryl is both the most efficacious (up to 60% improvement) and the most cost-effective.
- Advise weight loss if BMI >25, including giving ‘an optimal diet plan and a goal’. The article didn’t say what evidence there was for this.
Also, of course, PAD is a marker for other arteriopathy, so there are other things that aren’t particularly helpful for the PAD symptoms or risks but that are important to do anyway:
- Statins. Reduce both CVA and all-cause mortality (OR 0.77 in each case) but not clear whether they affect walking distance. It’s secondary prevention, not primary; use Atorvastatin 80 mg od as first choice and aim to reduce non-HDL concentration by 40%.
- Hypertension management. Ramipril is recommended as first-line therapy; the BMJ article says on page 202 that it doesn’t improve claudication symptoms (symptomatic review and meta-analysis) and on page 203 that ACE inhibitors improve walking distance in patients with claudication by an average of 86m. So, make what you will of that; maybe if I have time I’ll haul out the studies and try to figure it out. However, treatment of hypertension does of course improve overall cardiovascular risk, so worth going for anyway. Target is <140/90 in the under-80s and <150/90 in the over-80s.
- Work for good glycaemic control in diabetes; it doesn’t seem to reduce amputation risk, but it does reduce the risk of microvascular complications. Target is <48mmol/l.
At five years from diagnosis of PAD:
- Most patients with claudication will have stable or improved symptoms.
- Between 1 and 3.3% will have progressed to amputation.
- 20% will have died (I assume due to the association with other vasculopathies – MI, CVA, renovascular disease, vascular dementia, and mesenteric disease).
For patients with critical limb ischaemia the prognosis, not surprisingly, is a lot worse. By one year 30% will have had an amputation, and by five years 50% will be dead.
*In surgical finals, I was examining someone with possible PAD and started my presentation of examination findings by reeling off the pulse rate and rhythm. The examiner asked me why I mentioned that it was regular; turned out he was hoping I’d thought to exclude AF due to the increase in arterial thrombosis risk. Sadly, I wasn’t nearly that savvy and had simply been going through the standard list without thinking, so I missed a chance to impress him. It was a useful lesson, though (and I did pass, so I suppose that’s what matters).
Articles used in writing:
https://doi.org/10.1136/bmj.j5842 – PAD generally
https://doi.org/10.1136/bmj.j5460 – CLTI/ALTI