Ischemic neuropathy refers to injury of the peripheral nerves caused by either vessel occlusion or reduced oxygen delivery to the vasa nervorum [1]. This condition may occur after percutaneous coronary intervention (PCI) because medium-sized arteries may become occluded during or after the procedure. Although PCI is essential for the management of ST-elevation myocardial infarction (STEMI), vascular access carries a risk of procedure-related complications. However, mononeuropathy multiplex caused by thromboembolic events after PCI is exceedingly rare. In this report, we describe a case of distal ischemic mononeuropathies of the right lower limb that developed after PCI.

A 57-year-old man with a history of hypertension and long-term cigarette smoking presented to the emergency department of our hospital in May 2023 with dizziness. Electrocardiography confirmed STEMI. Laboratory evaluation revealed low high-density lipoprotein cholesterol levels. Immediate PCI was performed through the right femoral artery, and a temporary pacemaker was inserted through the right femoral vein. Following the procedure, the patient remained hemodynamically stable; however, beginning on the day of the procedure, he experienced mild pain in the right lower limb at rest, and erythematous discoloration over the dorsum of the foot was subsequently noted. The patient was transferred to another hospital for symptomatic management. Two days after transfer, he returned to the emergency department of our hospital with progressive motor weakness and marked discoloration of the right second to fourth toes. Contrast-enhanced computed tomography (CT) of the tibia, three-dimensional CT angiography and venography, and lumbar spine magnetic resonance imaging (MRI) were performed, and the patient was referred to our department for an electrodiagnostic examination. CT revealed complete occlusion of the right popliteal, proximal posterior tibial, anterior tibial, and peroneal arteries (Fig. 1). Lumbar spine MRI demonstrated mild central disc protrusion at the L2/L3 and L4/L5 levels (Fig. 2). The patient reported pain, swelling, and weakness in the right lower limb. Muscle strength was evaluated using the Medical Research Council (MRC) scale (0–5). Strength in the right lower limb was as follows: hip flexors and knee extensors, grade 5; ankle dorsiflexors, grade 3; first toe extensors, grade 2; and ankle plantar flexors, grade 3. Overall, the proximal muscles were intact, whereas the distal muscles exhibited marked weakness. Light-touch sensation was reduced over the posterior aspect of the right calf. Purplish discoloration and bullae were observed on the distal portions of the second to fourth toes and on the dorsum of the right foot.

Thrombectomy was performed on the day of the patient's return to the emergency department, 14 days after symptom onset, through open surgical access using right common femoral artery cutdown. Flow was restored in the right popliteal, anterior tibial, posterior tibial, and peroneal arteries; however, motor weakness in the right lower limb remained essentially unchanged after revascularization, and wound care was required for the right second to fourth toes, in which necrosis had already developed.

Initial electromyography (EMG) was performed 4 weeks after symptom onset and 2 weeks after revascularization. At the time of examination, motor strength remained similar to that observed during the 2 weeks after revascularization, whereas light-touch sensation over the posterior aspect of the right calf had partially improved but had not completely normalized. This sensory improvement is presumed to reflect restoration of intraneural blood flow following arterial recanalization. Despite ongoing wound care, toe discoloration did not improve, and progressive wound necrosis ultimately necessitated ray amputation of the second, third, and fourth toes approximately 1 month after the initial electrodiagnostic evaluation.

EMG was performed using surface electrodes and monopolar needle electrodes according to standard procedures. Motor and sensory nerve conduction study (NCS) findings are summarized in Table 1. The right peroneal motor response recorded from the extensor digitorum brevis muscle was unobtainable, and the right tibial motor response showed a lower amplitude than that on the left side. Likewise, the right sural, superficial peroneal, and saphenous sensory responses showed lower amplitudes than those on the left side. Needle EMG revealed fibrillation potentials and positive sharp waves in the right peroneus longus (PL) and tibialis posterior (TP) muscles, and positive sharp waves were also observed in the extensor hallucis longus (EHL) and gastrocnemius (GCM) muscles. In addition, single-unit recruitment was observed in the EHL, whereas reduced recruitment patterns were noted in the PL, TP, and GCM (Table 2).

The NCS findings were consistent with multiple mononeuropathies of the right lower limb confined to the distal segment below the knee. These lesions were presumed to be associated with ischemia caused by complete occlusion of the popliteal, anterior tibial, posterior tibial, and peroneal arteries due to a post-PCI embolic event, which was thought to have induced multiple neuropathies involving the distal nerves of the lower limb.

Follow-up NCS and EMG were performed in the outpatient clinic in September 2025. The patient did not report sensory loss or paresthesia. Motor strength in the right lower limb had improved to grade 5 in the hip flexors and knee extensors, grade 4 in the ankle dorsiflexors, grade 3 in the first toe extensor, and grade 5 in the ankle plantar flexors on the MRC scale. The follow-up study showed improvement across multiple nerves, with increased amplitudes in the right sural, superficial peroneal, and saphenous nerves compared with the initial examination (Table 3). On needle EMG, previously observed abnormal spontaneous activities were no longer present. Polyphasic, large-amplitude motor unit action potentials were observed in the right PL, TP, EHL, and GCM, with reduced recruitment and a reduced interference pattern in the PL, TP, and EHL (Table 4).

PCI is the established standard of care for acute myocardial infarction, and contemporary guidelines recommend prompt reperfusion to reduce mortality and complications [2]. Although PCI outcomes have improved compared with those in earlier eras, complications, although rare, remain serious. Acute limb ischemia (ALI), defined as an abrupt decrease in limb perfusion that threatens limb viability, is a vascular emergency associated with a high risk of limb loss and death [3]. Previous studies have shown that delayed diagnosis and revascularization in patients with ALI are associated with significantly increased risks of limb loss and mortality [4]. When ALI occurs as a rare complication of PCI, early clinical suspicion, rapid recognition, and prompt revascularization are therefore essential to prevent irreversible tissue injury and improve clinical outcomes [3]. Previous studies have identified arterial access-site closure devices as a recognized cause of ALI after PCI, with reported incidence rates ranging from 0.1% to 0.7% [5]. In addition, a meta-analysis demonstrated that these devices are associated with a 2.1-fold increased risk of limb ischemia compared with manual compression [6]. Conversely, in cases unrelated to closure devices, post-PCI ALI may result from extensive aortic dissection [5] or atheroembolism related to manipulation of wires, catheters, and other devices during the procedure. In this case, hemostasis at the right femoral artery puncture site was achieved using a bioabsorbable vascular closure device. The patient had mild peripheral arterial disease (ankle-brachial index, 0.90), hypertension, a 30-pack-year smoking history, and low high-density lipoprotein cholesterol (35 mg/dL, below the reference threshold of 40 mg/dL for adult men), which may have increased his susceptibility to ALI [7].

Neuropathy caused by acute arterial occlusion is uncommon, and this case, involving unilateral complete occlusion of the popliteal artery with concomitant occlusion of the anterior tibial, posterior tibial, and peroneal arteries leading to mononeuropathy multiplex, is even rarer. The abnormal electrodiagnostic findings indicate involvement of the common peroneal, tibial, sural, and saphenous nerves, which are primarily supplied by vessels distal to the popliteal segment. Adams demonstrated in an animal model that ischemic histological changes required ligation of the inferior gluteal artery and all its nutrient branches [8]. Richards [9] further reported that nerves may remain oxygenated through diffusion despite partial occlusion of the vasa nervorum. In the present case, however, both the main arterial trunks and collateral channels were compromised, producing a critical reduction in endoneurial perfusion that most plausibly accounts for the neuropathy. With respect to the saphenous nerve, although it is supplied by the saphenous branch of the descending genicular artery arising from the femoral artery, extensive occlusion of the lower-extremity arteries may render it vulnerable to ischemia because collateral blood flow may be insufficient under severe ischemic conditions [10].

When a patient presents with unilateral lower-limb weakness, lumbosacral radiculopathy is among the primary diagnostic considerations. In this case, lumbar spine MRI showed disc bulging without definite evidence of radiculopathy. Vasculitic neuropathies, including vasculitic mononeuritis multiplex, should also be considered in patients who present with asymmetric motor weakness.

Although vasculitic neuropathy was considered, perinuclear and cytoplasmic antineutrophil cytoplasmic antibody testing was not performed; therefore, vasculitic mononeuritis multiplex could not be completely excluded.

In this patient, complete arterial occlusion likely persisted for several days before thrombectomy. Despite successful reperfusion, motor weakness persisted, and progressive necrosis of the right second to fourth toes necessitated ray amputation.

Peripheral nerves may be injured not only by ischemia itself but also by reperfusion, which animal studies have shown to exacerbate axonal and myelin degeneration compared with ischemia alone through oxidative and inflammatory mechanisms [11]. Although reperfusion ultimately facilitates long-term nerve regeneration, it may acutely worsen neural function. In this case, prolonged arterial occlusion likely caused substantial neural injury before thrombectomy, with additional aggravation from secondary reperfusion injury.

In conclusion, ischemic neuropathy caused by acute arterial occlusion after PCI is a rare complication. Early recognition of post-PCI arterial thrombosis is crucial for initiating immediate revascularization therapy. Prompt recognition and timely management are key to preventing motor deficits and optimizing functional recovery.

The ethical boards approved and waived informed consent for this case report (IRB HC25ZASI0095).