Surgical advances mean new interventional procedures to treat peripheral arterial disease are available, but with early diagnosis, many patients can be managed without going under the knife, says vascular and endovascular surgeon Dr Andrew Lennox, head of the Vascular and Renal Transplant Surgery department at Prince of Wales Hospital.

Claudication can indicate more serious cardiovascular pathology

While claudication itself is benign and the long-term limb loss rate is less than 10%, it is a marker of more serious disease that suggests further assessment is warranted, Dr Lennox says.

The mortality rate in new claudication patients is up to 30% at 10 years. Only a small percentage of these deaths are from leg-related regression. “The rest is strokes and heart attacks and renal failure and whatever. It’s a marker of disease, so if someone has it, that’s the time to get a stress test, a coronary angiogram, look at the renal function, check the carotids because that’s what will kill them, not the legs,” Dr Lennox explains.

“I’ve had claudicants who are lined up for an angioplasty who get a carotid scan and they’ve got a tight stenosis that needs treatment. They get some heart tests and they’ve got triple vessel disease, so they get their heart done. And the leg is the lowest rung of importance.”

Managing risk factors is important—antiplatelet therapy, smoking cessation, lipid-lowering therapy, blood glucose and blood pressure control and dietary modification can reduce the risk of cardiovascular disease progression and complications.

Mimics and misdiagnosis

Claudication is sometimes missed because other conditions mimic it, Dr Lennox says.

“The commonest would be spinal and arthritic referred pain. Myalgias are a small group.”

The symptom pattern helps distinguish PAD, with pain typically consistent, repetitive, and reproducible over the same distance, Dr Lennox says.

Pain is most common in the calf, but can also occur in the foot, thigh and buttock.

“A lot of buttock and thigh pain can get misdiagnosed as spinal or hip related,” he says, noting the absence of femoral pulses is sometimes missed on assessment.

“Someone could have hip and buttock pain and a weak or absent femoral pulse and have had spinal surgery because of a little bit of spinal stenosis. So the pulses are very important to pick up in terms of which ones are there and which ones aren’t there.”

Statin-related pain can also mimic claudication, but tends to be present when sitting.

“Patients who have the same pain when they’re sitting, it’s not claudication. It’s got to be an exercise-related thing,” Dr Lennox says.

Claudication is a sign of reversible ischaemia that is not yet limb-threatening.

“If they’re getting ischaemic pain at rest, that’s a critical limb ischaemia. And someone can’t have rest pain related to arterial disease if they have a palpable pulse, no matter how weak it is,” he adds.

“If they’ve got a pulse and they’ve got pain at night lying in bed, it’s from something else.”

Clinical tip
A patient with claudication can still have a palpable resting pulse in the foot, Dr Lennox says. In that situation, get the patient to do some heel raises or to step up and down a small step.

“If the pulse is still pretty well preserved then the pain is unlikely to be ischaemic in nature. But if it drops off after the exercise test that may well be a femoral stenosis.”

Investigation and referral

Along with assessing pulses, Dr Lennox says a Doppler can be useful for screening, especially in patients with a history of spinal problems or arthritis.

“If it looks completely normal then maybe look somewhere else for another source,” he says.

If pulses are reduced and the pain is clinically convincing for claudication, it is still reasonable to refer to the vascular surgeon even with a normal Doppler, says Dr Lennox.

The surgeon may consider a second or more extensive Doppler, or a CT angiogram.

“Those two scans are certainly complementary. We get information about treatment approaches,” he says.

“The exercise tests are also generally pretty good,” Dr Lennox says. Comparing resting and post-exercise ankle-brachial index “not only excludes all the atherosclerotic causes of claudication but also the rare popliteal entrapment syndrome, popliteal adventitial cystic disease—these very rare things would also have to have a hemodynamic abnormality for that to be consistent with the cause of the pain.”

If you’re still unsure, consider referral to a vascular specialist.

Non-interventional management is first line

Medication and exercise therapy are the mainstays of treatment in most cases, Dr Lennox says.

“There’s good evidence that an exercise program will get them walking further, particularly out to about 12 months from the onset of symptoms. If they’ve had it for three or four years, it’s not going to make a difference.”

Exercise encourages collateralisation, with research showing supervised programs lead to significantly greater improvements in maximal walking distance or time compared to home-based exercise or walking advice. (An unsupervised exercise program can be considered if patients are not able to take part in a supervised one.)

Exercise therapy should be sufficiently high intensity to elicit claudication symptoms, and should be performed for at least 30 to 45 minutes, three times per week, for a minimum of 12 weeks before re-assessment.

In patients with lifestyle-limiting symptoms that do not improve with exercise therapy and risk factor modification, you can trial cilostazol.

When is interventional therapy warranted?

The decision is nuanced, based on risk and the potential to achieve clinical or functional benefits, Dr Lennox says.

For example, someone who claudicates at 150 metres could get a stent done and “they’ll get a nice-looking ultrasound,” Dr Lennox says, but it may have little functional benefit if severe lung disease limits their walking to 200 metres anyway.

But intervention may benefit people who need or want to walk for practical or health reasons, such as to play golf, get to the shops, or take part in a cardiac rehab program, for example.

Dr Lennox says with the shift from bypass to percutaneous reopening of blocked vessels, more patients are suitable for intervention. “Recovery is so much better.”

These procedures are adapted from cardiology and mostly involve a day or overnight stay. While they still pose a risk of complications from punctures, “we have lots of things that would minimise that,” he says, noting techniques to cross and reopen complex blockages have improved significantly over the past few decades.

“We’ve basically gone from plain balloons to plain stents, stents with drugs on them to stents that dissolve to balloons with drugs on them. The view of trying to leave nothing behind is pretty much what we aim for.”

Advances in vessel preparation can also help to improve results from a balloon or stent. Atherectomy procedures can debulk plaque and devices have evolved substantially from the lasers used in the 90s.

“The most recent thing we’ve got in our bag of tricks is lithotripsy balloons that have high frequency ultrasound and basically smash the calcium in a plaque.” These can be used to prepare for stenting or as a standalone procedure, he explains.

Key messages

• Chronic PAD is not life-threatening but is a sign to check heart and carotids/stroke risk.
• Claudication is often misdiagnosed but has a distinct symptom pattern. Good history and examination are key, especially checking the pulses.
• If caught early, exercise (ideally a supervised program) can promote collateralisation to prevent/delay more procedural treatment.
• Selecting patients for treatment is nuanced and depends on severity of symptoms, clinical needs and plaque characteristics.
• New cardiology technologies are filtering into interventionalist procedures, with most aiming to leave as little foreign body in the patient as possible.