It has become Endovascular therapy (balloon angioplasty) has become the first-line option in the treatment of diabetic foot as it allows the healing of ulcers and reduces the rate of amputation.
Diabetic foot ulceration (DFU) is recognized as one of the most serious complications of diabetes About 5% off all patients with type 2 diabetes will develop an arterial DFU problem. Up to 70% of all lower-leg amputations are performed in patients with diabetes, and up to 85% of all amputations are preceded by an ulcer. Ulcer prevention is therefore recognized to be the best way to prevent amputation. However, when an ulcer is present, the primary need is to achieve ulcer healing.(1)
Pathological basis of diabetic foot
Diabetic foot is a complex lesion caused by multiple factors. Tissue ischemia, peripheral neuropathy, and infection are the pathological basis of diabetic foot, and are usually combined. Peripheral neuropathy and tissue ischemia act as initiating factors in the pathogenesis, while infection is often secondary. (2)
Peripheral neuropathy in patients with diabetic foot
Diabetic peripheral neuropathy (DPN) is common in clinical practice and mostly coexists with vascular disease, involving motor, sensory, and autonomic nerves. In the initial stages, sensory neuropathy can lead to dysesthesia, increasing the susceptibility of the foot to pressure and mechanical and thermal injuries; thereafter, motor neuropathy alters foot biomechanics and leads to variations in anatomy, causing foot deformity, limited joint mobility, and changes in foot load. (2)
Ischemic or neuro-ischemic lesions in patients with diabetic foot
For every 1% increase in glycosylated hemoglobin (HbA1c), the risk of peripheral vascular disease (PAD) increases by 25%–28%. According to the results of a large cohort study in Europe, approximately half of the cases of diabetic foot originate from neuroischemic or ischemic lesions. Ischemia is the most important factor that prevents the healing of the lesions. Ischemia is therefore the root cause of diabetic foot that must be screened for first unless there is conclusive evidence. (2)
Neuroischemic lesions result from the synergistic effect of DPN and tissue ischemia, which reduces oxygen delivery to metabolic tissues. Macroangiopathy and microvascular dysfunction impair blood perfusion in diabetic foot. An important feature of diabetic macroangiopathy is that calcification of the arteries of the lower limb causes a significant decrease in vascular elasticity. From a clinical point of view, ischemic and neuroischemic lesions can be considered to be associated with the same pathogenic factor, which may require vascular recanalization treatment. (2)

Diabetic foot infections
Neuroischemic ulcers in diabetic foot are easily infected; however, infection is rarely the cause of the ulcers. Moreover, the occurrence of infection is closely related to the probability of amputation, especially in patients with PAD. Deep infection is characterized by osteomyelitis or soft tissue infection disseminated along the tendon, which is a direct factor related to the probability of amputation and fatality. Patient outcomes are associated with the extent of infection, comorbidities, and the presence or absence of PAD. (2)
Evaluation and grading of ulcers and infections
Ulcer area, depth of the involved tissue, co-infection, and tissue necrosis generally need to be considered in cases of diabetic foot ulcers. Although there is no uniform standard of evaluation, the Wagner classification is commonly used for the assessment of these factors at present. The diagnosis of diabetic foot infection can be made based on the symptoms and signs of local inflammation, including typical manifestations such as exudate; local redness; swelling and heat; pain; systemic symptoms of fever, leukocytosis, accelerated erythrocyte sedimentation rate; and elevated CRP. (2)
Infections occur mostly secondary to ulcers and may not be associated with them. The extent and degree of infection are important factors that affect the prognosis. A wide range of infections and significant systemic inflammatory response often predict the risk of amputation and death. (2)
Treatment options
There are four treatment options: conservative treatment, primary amputation, surgical bypass and endovascular revascularisation. The choice for any of these treatment options has to be made in a multidisciplinary team. The choice between surgical and endovascular treatments is made on the local anatomy, patient condition and the local expertise. (1)
Endovascular treatment
Endovascular treatment of (neuro) ischaemic DFU’s is mainly concentrated in the BTK arteries. Iliac and femoropopliteal lesions are also sometimes seen in diabetic patients but are a minority. To discuss endovascular treatment, we should focus on treating BTK lesions. Diabetic lesions are often long segmental lesions while atherosclerotic lesions are more often short. (1)
Treating long segmental diabetic lesions (Endovascular treatment) requires a dedicated centre with ample experience because these kinds of treatments need a personalized approach. Each procedure is tailored to the patient’s needs, possibilities and clinical situation. The endpoint of the treatment is ulcer healing and, in the same token, limb salvage. (1)
What are the indications of endovascular treatment of the diabetic foot?
Non-healing ulcers with or without infection and gangrene are the indications for percutaneous revascularisation. The inclusion is that the limb is still viable and that the treatment will contribute to the quality of life. A bedridden patient with dementia is therefore not a primary candidate for percutaneous revascularisation. (1)
Also, the choice between endovascular treatment and open surgery is often the outcome of a team discussion. Local expertise plays an important role in these discussions. High risk for surgery, non-availability of good venous material for a conduit, no segments for surgical anastomoses or poor outflow are often additional reasons to choose for an endovascular solution. But in many institutions, the endovascular approach is currently the first choice treatment option. The understanding that in diabetic patients ‘time is tissue’ has the consequence that treatment of an infected ulcer in diabetic patients should be handled as an emergency procedure, to be dealt with preferable within 24 h. (1)
Endovascular technique
Endovascular technique such as crural revascularisation is a specialized technique that should only performed after ample training and extensive experience. Procedures are performed by antegrade puncture; over the bifurcation approach should never be performed. (1)
In the BTK vessels, simple balloon angioplasty most often works fine; only in rare cases where prolonged low-pressure inflation does not produce good flow to the foot, a stent option might be considered. Because we are not aiming for long-term patency, primary stenting should not be performed. Also, stenting might block a repeat intervention, if necessary. In DFU lesions, stenting is even less desirable because the lesions are often long and not focal, compared with atherosclerosis. (1)
The current trend is to perform atherectomy followed by drug-coated balloon angioplasty, and to insert a stent only if there is significant dissection or residual stenosis. Atherectomy can be performed with laser, directional atherectomy device, or rotational atherectomy device. All these devices remove a certain amount of plaque and modify the plaque, allowing easier balloon angioplasty of the lesion. (3)
Most atherectomy procedures have a potential risk of embolization, especially in long lesions. Placement of a filter is advisable when treating long lesions even with devices that aspirate simultaneously. (3)
Calcified lesions may impede the crossing of a balloon catheter, thus hindering the angioplasty procedure. A low profile short and small 2×40-mm balloon can be used to predilate difficult-to-cross lesions, and follow by angioplasty with a larger-diameter balloon sized to the artery. (3)
The balloon should be pushed forward with a slight jabbing motion, as static friction is a greater stopping force than kinetic friction. Strong support is required for the balloon to cross a difficult-to-cross lesion. This can be achieved with a 4F sheath that is longer than the outer 6/7F sheath placed coaxially. The balloon placed inside the 4F sheath will have strong support for crossing the lesion. (3)
Two wires can be placed side by side across the lesion, and “seesaw balloon dilatation” with the leading edge of the balloon can help the balloon in crossing the calcified lesion. Other methods that can be used to modify a calcified lesion in order to allow balloon crossing includes gradual dilation with a tapered low-profile crossing microcatheter, rotational atherectomy, laser atherectomy device, and lithoplasty device. (3)
Pickling is a technique that uses the back end of the wire to jack hammer the calcified lesion in order to modify the lesion. Similarly, external piercing of a calcified plaque with an 18G or 21G needle can modify the plaque to allow balloon crossing and, thereby, balloon angioplasty. (3)
Some lesions can still be resistant to angioplasty despite the availability of lesion-modifying equipment and techniques. In these lesions, the plaque/vessel can be intentionally ruptured with a balloon expandable covered stent and relined with the SUPERA stent (Abbott) once an adequate diameter has been achieved. (3)
When to stop & fight another day?
Lower-limb arterial interventions can be complex procedures requiring many hours of surgery. Termination of the procedure should be considered if the patient is uncomfortable under local anesthesia. An uncomfortable patient is likely to move and cause problems with imaging, thus making the procedure extraordinarily difficult. (3)
The procedure may have already required the use of large volumes of contrast, which has the risk of causing acute kidney injury. Pedal arch intervention is best staged, as there are many anatomical variations that will need to be carefully studied before the procedure. Planning an intervention not only involves understanding the anatomy and the lesion, but may also require ensuring the availability of the appropriate equipment for the procedure. The patients’ medical comorbidities and how these influence the outcome should be factored into the decision-making process, and appropriate treatment goals need to be clearly established before starting the intervention. (3)

Outcome endovascular treatment
The outcome of both open surgery and endovascular treatment is broadly spoken the same for the endpoints ulcer healing and limb salvage and is between 78% and 85%. The patency of a bypass surgery is, however, reported to be better than that of an endovascular treatment. This is not a major issue for consideration because ulcer healing with subsequent limb salvage almost always takes place in a period within 6–9 months. (1)
Any patency beyond ulcer healing is often not needed because these diabetic patients mostly do not suffer from rest pain. An endovascular intervention normally has a patency that is enough to obtain the final goal of ulcer healing. That is why limb salvage after an endovascular treatment is always reported to be 20% higher than actual patency. This is why an endovascular revascularisation in a critical ischaemic foot is referred to as ‘temporary’ bypass. (1)
References
- JA Reekers and J. Lammer. Diabetic foot and PAD: the endovascular approach. Diabetes Metab Res Rev 2012; 28: 36-39.
- Li M. Guidelines and standards for comprehensive clinical diagnosis and interventional treatment for diabetic foot in China. Journal of Interventional Medicine 2021; 4: 117-129.
- Wong TY Endovascular treatment of diabetic foot ischemic ulcer - Technical review. Journal of Interventional Medicine 2020; 3: 17-26.