Vascular etiologies of acute and chronic foot pain pose a significant burden on patient quality of life, ambulatory status, morbidity, mortality, and health care cost. The spectrum of the vascular pathologies is very wide and include osteonecrosis of the foot bones, acute limb ischemia (ALI), peripheral vascular disease (PVD), and diabetic foot ulcers (DFUs). Every one of the mentioned conditions have a typical clinical presentation and have different management strategies ranging from observation to significant surgery.

To understand and treat the vascular pathologies, it is paramount to understand the soft tissue, bony and vascular anatomy of the foot and ankle area. There are a lot of variations in the vascular anatomy also. Some vascular conditions are present at a certain age, some after surgical procedures, and others after trauma-like osteonecrosis of the talus navicular bone (Kohler disease), first metatarsal head avascular necrosis (AVN) after bunion surgery, second metatarsal necrosis (Freiberg disease), and AVN of the talus after talus fracture.

Critical limb ischemia (CLI) is the most severe form of vascular pathology that can be traumatic or atherosclerotic peripheral artery disease (PAD).¹ Patients with CLI are at high risk of nonhealing wounds, amputations, and mortality.²,³ Better understanding of the foot vasculature and perfusion should enable us to avoid these undesirable outcomes in patients with CLI.

Globally, the prevalence of diabetes mellitus has risen to 8.8% in 2015. Diabetes is a global epidemic and can lead to DFUs, which are estimated to affect up to 25% of all diabetic individuals during their lifetime due to neuropathy and coexisting vascular disease. Infected foot ulcers account for approximately 60% of lower extremity amputations, making infection perhaps the main cause of this tragic outcome.⁴,⁵,⁶ Diabetic foot wounds lead to approximately 71,000 diabetic limb amputations annually in the United States.⁷

In this chapter, we will review the vascular anatomy of the foot and ankle with relevant clinical applications. We will also briefly touch upon the various clinical conditions and their evidence-based treatment.

The arterial blood supply to the ankle and foot is provided by three arteries: posterior tibial, anterior tibial, and peroneal. There are occasional variations to this basic anatomy for instance absence of a posterior tibial artery or an absent or attenuated anterior tibial artery may occur in two percent of subjects.⁸ In these cases, the distal blood flow to the foot is accommodated by the branches of the peroneal artery and posterior tibial artery.

At the level of the ankle, the anterior tibial artery becomes the dorsalis pedis artery which continues distal and superficially just
lateral to the extensor hallucis longus tendon. At the level of the ankle joint, the dorsalis pedal artery gives rise to medial and lateral malleolar artery branches. It then gives rise to several lateral branches including artery to the sinus tarsi, lateral tarsal artery, arcuate artery, dorsal metatarsal arteries, and their terminal branches the dorsal digital arteries. The dorsalis pedis artery also gives off medial branches including first dorsal metatarsal artery which divides into medial and lateral branches at the level of the first metatarsophalangeal joint to become the dorsal digital artery supply of the great toe and medial second toe.

The peroneal artery typically divides into two segments in the distal aspect of the leg. An anterior or perforating branch pierces the intraosseous membrane between the tibia and fibula and courses anteriorly over the distal tibiofibular syndesmosis. This anterior perforating branch can contribute anastomoses to the dorsalis pedis artery, anterior lateral malleolar artery, artery of tarsal sinus, and the lateral tarsal artery. The posterior branch of the peroneal artery forms an anastomotic arcade with branches from the posterior tibial artery to supply the posterior heel and calcaneus.

The posterior tibial artery exists in the posteromedial corner of the ankle abutting the tendons of posterior tibialis, flexor digitorum longus, and flexor hallucis longus as well as the posterior tibial nerve. Its terminal branches give rise to a medial plantar artery passing above the interfascicular ligament and a lateral plantar artery passing under the interfascicular ligament, which will eventually anastomose with a posterior plexus that communicates with the dorsal metatarsal arteries. About 1 cm proximal to this division, the posterior tibialis artery gives rise to the artery of the tarsal canal, which eventually anastomoses with the artery of the sinus tarsi, providing the tenuous blood supply to the majority of the talar body and neck. Another important branch of the posterior tibial artery is the deltoid artery, which passes between the deep and superficial branches of the deltoid ligament and supplies the medial body of the talus. The deltoid branches are at risk of compromise during total ankle arthroplasty and medial talar resection and medial gutter preparation.⁹

Acute limb ischemia (ALI) is a surgical emergency with devastating consequences if left untreated including limb amputation and possibly death.¹⁰ Ischemia is suspected early with any extremity that is cold or painful or diagnosed later when the classic “six Ps” of ischemia are evident (pain, pallor, poikilothermia, pulselessness, paresthesia, and paralysis). Pain is typically the first sign of the ischemic limb and serves as a harbinger for impending critical arterial occlusion. Careful physical examination and prompt intervention of the acutely painful leg by the astute physician is paramount.

In regard to the lower extremities, a careful physical examination should be performed. This includes palpation of dorsalis pedis and posterior tibial pulses of the affected limb with comparison to the unaffected limb. If pulses are absent or diminished, one should assess the pulses with doppler signal and compare to the contralateral unaffected limb as well as the upper extremities. Signs of ischemia are most pronounced one joint distal to the level of occlusion. Occlusion at the level of the popliteal or tibial trifurcation classically result in a well-perfused calf but ischemic foot. Whereas, occlusion more proximally at the femoral bifurcation will result in an ischemic lower leg and foot.

There are two causes of acute arterial ischemia: arterial embolism and arterial thrombosis.¹¹ Arterial embolism occurs when an obstructing mass, typically a blood clot, travels through the blood stream and lodges itself in a blood vessel, thereby obstructing distal flow resulting in distal ischemia. Most commonly, this mass is cardiac in origin.¹² Cardioembolic sources of blood clots include mural thrombi, which occur in states of altered cardiac contractility (ie, atrial fibrillation, myocardial infarction, and post-MI ventricular aneurysm). Other sources of cardiac emboli include damaged heart valves, mechanical heart valves,
endocarditis, cardiac tumors, and paradoxical emboli from a patent foramen ovale.

Arterial embolism may also originate from the vascular system itself. A traumatic arterial injury from a penetrating trauma or a high-energy fracture of the distal femur or proximal tibia (ie, knee fracture dislocation)¹³,¹⁴ may cause acute arterial thrombosis with the potential of that thrombus to dislodge and embolize more distally, or more importantly, the site of arterial thrombus formation may be the cause of CLI. Proximal arterial aneurysm either at the level of the abdominal aorta, femoral, or popliteal artery may also present with thromboembolic phenomena more distally.¹⁵

Thrombotic occlusion typically differs from acute arterial embolism; in that, the disease course is typically slower and there are warning signs prior to CLI. Associated conditions include atherosclerotic arterial disease and low-flow states (ie, congestive heart failure, hypotension, or hypovolemia). Intermittent claudication, recognized as pain of the legs associated with walking, is caused by arterial vessel narrowing that restricts blood flow to the lower extremity musculature and a mismatch between metabolic demand and end-tissue perfusion.¹⁶ The astute clinician, should however, be mindful that vascular claudication may mimic or be confused with neurogenic claudication, or the two entities may coexist. The differentiation may be challenging, but Nadeau et al concluded that neurogenic claudication, caused by lumbar spinal stenosis, typically presents with bilateral leg pain proximal to the knees that improves with sitting or leaning forward (ie, shopping cart sign), whereas vascular claudication, caused by peripheral arterial disease, typically presents with bilateral leg pain distal to the knees that improves with standing.¹⁷ Nonetheless, rupture of atherosclerotic plaque and acute arterial thrombosis can present with ALI and warrants urgent medical and/or surgical intervention.

The goals of therapy for ALI is reperfusion of the ischemic limb, which may be accomplished surgically or with endovascular thrombolysis.¹⁸ For the unstable patient or those without signs of limb-threatening ischemia, intravenous (IV) anticoagulation is also considered. Embolectomy, catheter-directed thrombolysis, endarterectomy, and vascular bypass are some of the tools necessary to assist with limb salvage.

Patients with diabetes have immunodeficiency, neuropathy, and arteriopathy leading to insensate extremities and susceptibility to infections.¹⁹ Sixty percent of the lower extremity amputations are because of the infected foot ulcer and underlying osteomyelitis.⁴,⁵,⁶ Managing infection requires proper diagnosis, classification of lesions, obtaining appropriate specimens for culture, empirical and then definitive antimicrobial therapy, and surgical intervention when indicated. Other factors that contribute to adverse outcomes are barefoot walking, illiteracy, poor socioeconomic status, ignorance about diabetic foot care by patient as well as primary care physicians, delayed presentation by patients, patient self-neglect, and belief in the substitute/alternative systems of medicine.

Almost all gears of the lower limb are involved; from skin, subcutaneous tissue, muscles, bones and joints, to nerves and blood vessels. Diabetic foot infection (DFI) is a consequence rather than the cause of DFUs. Infections usually start with a split in the cutaneous envelope, at the site of trauma, or ulceration. DFI is defined as infection in the soft tissue or bone anywhere below the malleoli in a diabetic person. Pathogenesis of DFI starts with neuropathy, and it is sensory, motor, and autonomic. Motor neuropathy leads to intrinsic foot muscle atrophy and wasting and imbalance. Such imbalance leads to the displacement of fat pads and associated foot deformities such as foot drop, clawed toes, hammer toes, and equinus deformity; therefore, creating areas susceptible to minimal trauma. Autonomic neuropathy leads to sensory dysfunction and compromised blood flow to sole of the foot. The function of sweat and sebaceous glands of foot is altered, skin becomes dry and keratinizes which cracks and fissures more easily, which is a portal of infection.²⁰,²¹ Atherosclerosis of small, medium, or large size arteries is common in diabetics and is a contributing factor to the development of infections. On top of all the above
factors, diabetics typically have a compromised immune system compared to nondiabetics leading to difficulty clearing infections. As well, high blood glucose is a good medium for growth of microbes, enhancing the virulence of these microorganisms.²²