Superficial femoral artery thrombosis after PFNA in an intertrochanteric fracture patient with sarcopenia and copd: a rare case report

Abstract

Background

Intertrochanteric fractures in elderly patients are prevalent in trauma orthopedics and constitute a significant cause of mortality among the elderly population. Proximal Femoral Nail Antirotation (PFNA) is recognized as the standard treatment modality for these fractures. While the prevention of lower limb venous thrombosis is a major clinical focus, postoperative femoral artery thrombosis remains exceedingly rare; however, it can lead to severe disability or even death if not managed promptly.

Methods

This case report discusses an 83-year-old male patient with sarcopenia and chronic obstructive pulmonary disease (COPD) who sustained an intertrochanteric fracture due to an accidental fall during hospitalization. The patient successfully underwent PFNA surgery. However, immediate postoperative findings indicated localized swelling in the left thigh, decreased skin temperature below the left knee, and non-palpable left popliteal, posterior tibial, and dorsalis pedis arteries, along with weakness in dorsiflexion of the left ankle and toes. Emergency bedside Doppler color ultrasound and lower limb CT angiography (CTA) revealed thrombosis of the superficial femoral artery with complete vascular occlusion. An interventional radiologist promptly performed percutaneous lower limb arterial thrombectomy and arterial balloon angioplasty. Postoperatively, the skin temperature of the affected limb returned to normal, and the popliteal, posterior tibial, and dorsalis pedis arteries became palpable. The mobility of the left ankle joint gradually returned to normal.

Results

Post-surgery, the patient’s hip pain significantly improved. Follow-up X-rays demonstrated satisfactory fracture reduction with effective internal fixation. No significant lower limb swelling, sensory deficits, or foot drop were observed.

Conclusion

Surgeons must maintain a heightened awareness of the potential complications associated with arterial thrombosis in the context of fractures. The formation of femoral artery thrombosis in this patient may be attributed to prolonged compression of the proximal femoral artery during intraoperative fracture reduction, compounded by the patient’s long-standing sarcopenia and COPD. These factors likely contributed to elevated levels of inflammatory markers and increased susceptibility to complications. Furthermore, pre-existing peripheral arterial disease, perioperative hypotension, hypercoagulable state, embolic disease, plaque instability, or trauma-associated vascular injury cannot be excluded as potential causative factors. It is imperative to conduct comprehensive preoperative screenings and to employ meticulous and gentle surgical techniques, particularly in elderly patients, to minimize the risk of complications. Furthermore, thorough and timely physical examinations before and after surgery are essential for the early detection of problems and improved patient outcomes. Lastly, clinical practice should enhance fall prevention strategies for elderly patients suffering from sarcopenia.

Introduction

Intertrochanteric femoral fractures represent one of the most prevalent types of hip fractures among elderly patients. The proximal femoral nail antirotation (PFNA) internal fixation has emerged as the predominant surgical method in clinical practice, providing numerous advantages including simplified operation, minimal trauma, excellent mechanical stability, and expedited recovery [1]. Common complications associated with PFNA include infection, deep vein thrombosis, fat embolism syndrome, acute compartment syndrome, and pudendal nerve palsy, all of which are significant concerns for clinicians [2]. Prior to the execution of PFNA internal fixation surgery, continuous traction of the lower limb is necessitated using a traction table, along with the placement of a blocking post at the medial proximal femur to facilitate reduction. During this procedure, prolonged compression of the muscle blood vessels may easily result in damage. If not promptly detected or improperly managed, this may lead to severe complications such as limb swelling, ischemia, numbness, restricted movement, and potentially limb necrosis, paralysis, or death.

Intertrochanteric femoral fractures complicated by lower extremity venous thrombosis represent a common clinical complication and a critical focus for clinical prevention. These fractures are typically managed with medications such as aspirin, rivaroxaban, or low-molecular-weight heparin, in conjunction with physical preventive measures [3, 4]. Additionally, delayed deep femoral artery injury accompanied by femoral vein thrombosis following hip fractures has been documented [5]. However, instances of intertrochanteric femoral fractures complicated by lower extremity arterial thrombosis remain rare in the literature. To our knowledge, only one case of femoral artery thrombosis following closed intramedullary nailing of the femur has been reported in 2013 [2]. In order to expand the relevant content, we reviewed several reports concerning pelvic fractures complicated by external iliac artery thrombosis. Pelvic fractures are prone to irritating or damaging the external iliac artery, and fractures of the pelvis (including the acetabulum) or surgeries involving related areas may lead to thrombosis of the external iliac artery [6, 7]. Similarly, due to its low incidence, external iliac artery occlusion is often clinically overlooked. Nevertheless, this condition can result in prolonged limb ischemia, potentially leading to amputation or hemipelvectomy, with a high risk of disability or mortality [8]. Furthermore, individual case reports have documented total hip arthroplasty complicated by external iliac artery thrombosis [9] and hemiarthroplasty complicated by common femoral artery thrombosis [10]. Postoperative findings included weak limb pulses and limb ischemia, which caused sciatic nerve palsy and foot drop in the operated limb, with computed tomography angiography confirming thrombosis in both the external iliac and femoral arteries.

We report a case involving an elderly patient who suffered an intertrochanteric femoral fracture complicated by sarcopenia and chronic obstructive pulmonary disease (COPD). This patient developed superficial femoral artery (SFA) thrombosis immediately following PFNA surgery. Prompt interventional thrombus aspiration was performed, enabling early and aggressive treatment. Patients with COPD often exhibit systemic inflammatory responses that can lead to coagulation disorders and thrombotic complications, making them a critical population for thrombosis prevention [11]. Sarcopenia, characterized by the loss of skeletal muscle mass and function, results in decreased physical function and mobility, thereby increasing the risks of falls, fractures, and mortality. In 2010, the European Working Group on Sarcopenia in Older People (EWGSOP) defined sarcopenia as an aging-related syndrome marked by reduced muscle mass, strength, and function. In 2018, the European Working Group on Sarcopenia in Older People 2 (EWGSOP2) revised this definition, describing sarcopenia as a syndrome characterized by a progressive and generalized loss of skeletal muscle mass, strength, and function [12]. Our research team has conducted long-term clinical studies on sarcopenia, revealing its significant impact on the recovery of patients with hip and spinal fractures [13–15]. This case report presents a rare instance of postoperative acute SFA thrombosis in a patient with an intertrochanteric fracture, sarcopenia, and COPD, which was promptly and effectively diagnosed and treated. This report aims to enhance awareness of arterial thrombotic complications in fracture patients with sarcopenia and COPD, while emphasizing the importance of fall prevention in the daily care of patients with sarcopenia.

Case report

This study was approved by the Ethics Committee of Jiangning Hospital, affiliated with Nanjing Medical University, and informed consent was obtained from both the patient and family members. This study was in accordance with the Declaration of Helsinki.

The patient was an 83-year-old male with COPD complicated by a pulmonary infection, who was hospitalized at a community hospital. During his hospitalization, he experienced an accidental fall while walking, resulting in left hip pain, limited hip joint mobility, significant local swelling, and an inability to stand or walk. He denied experiencing pain or movement disorders in other areas, including the head, neck, chest, or abdomen, and reported no symptoms such as headache, dizziness, nausea, vomiting, chest tightness, chest pain, palpitations, or heart palpitations. After undergoing left hip anteroposterior and lateral X-rays, as well as computed tomography (CT) scans at a local hospital, he was diagnosed with a left intertrochanteric femoral fracture, classified as Evans type ID and AO type A3 (Fig. 1A-B), along with COPD and a pulmonary infection (Fig. 2A-B). The patient was subsequently transferred to our hospital the day after the fracture for planned surgical treatment. The admission diagnoses included: (1) Left intertrochanteric femoral fracture; (2) COPD; (3) Community-acquired pneumonia; (4) Coronary atherosclerotic heart disease; (5) Multiple contusions. Following admission, hematological laboratory tests and color Doppler ultrasound examinations of the heart and lower limb vessels were conducted. The hematological tests revealed: hemoglobin level: 98 g/L (reference range 130–175), platelet count: 99 × 10^9/L (reference range 125–350), neutrophil percentage: 92.4% (reference range 40–75), D-dimer level: 2.4 (reference range 0-0.5), C-reactive protein (CRP): 169.56 mg/L (reference range < 10), prothrombin time (PT): 13.10 s (11–13), international normalized ratio (INR): 1.05 (0.8–1.2), activated partial thromboplastin time (APTT): 41.20 s (24–39), fibrinogen (FIB): 3.57 g/L (2.0–4.0), thrombin time (TT): 16.00 s (14–21), fibrinogen degradation products (FDP): 16.30 mg/L (0–5). These findings indicate anemia, thrombocytopenia, an infection status, and a hypercoagulable state in the patient. Color Doppler ultrasound of the lower extremity vessels revealed atherosclerotic plaques in the bilateral lower extremity arteries, along with segmental stenosis of the left anterior tibial artery. No significant abnormalities were observed in the bilateral lower extremity veins. Chest CT indicated the presence of chronic bronchitis and emphysema, as well as interstitial changes in both lungs characterized by scattered infections and mucus plugs in some bronchi of the left lower lobe. Additionally, small amounts of pleural effusion were noted on both sides and in the left interlobar fissure. A specialized physical examination demonstrated a complete external rotation deformity of the left lower limb, with left hip pain preventing further physical assessment. There was no significant swelling in either lower limb, skin temperature was normal, and the popliteal, posterior tibial, and dorsalis pedis arteries were palpable. The dorsalis pedis artery pulsation was symmetric bilaterally. Treatment consisted of infection control using bacteria-sensitive antibiotics, standardized administration of low molecular weight heparin for anticoagulation, and the use of compression stockings to prevent deep vein thrombosis (low molecular weight heparin was discontinued 24 h prior to surgery). The diagnosis of sarcopenia was established based on the skeletal muscle index (SMI, 35.6 cm²/m²), calculated from the patient’s grip strength (three measurements, average 21.6 kg) and total muscle area at the T12 pedicle level on chest CT scan (Fig. 3) [14].

Fig. 1.

Imaging findings of intertrochanteric fracture of the left femur. Evans classification type ⅠD; AO classification type A3. A X-ray of the left hip joint. B CT of the left hip joint

Fig. 2.

Chest CT imaging. It reveals chronic bronchitis and emphysema; interstitial changes in both lungs with scattered infections, mucus plugs in some bronchi of the left lower lobe, and small amounts of pleural effusion bilaterally as well as in the left interlobar fissure. A Chest X-ray (PA view). B Axial lung window image

Fig. 3.

T12 pedicle level image on chest CT. The skeletal muscle index (SMI) was calculated as 35.6 cm²/m² by dividing the total muscle area of the erector spinae, latissimus dorsi, internal oblique, external oblique, rectus abdominis, external intercostal, and intercostal muscles by the square of the patient's height

After excluding surgical contraindications, the patient was scheduled for PFNA surgery (Fig. 4). The surgical procedure is briefly described as follows: The patient was placed under general anesthesia and positioned supine on the orthopedic traction table. Closed reduction of the left intertrochanteric fracture was performed under fluoroscopic guidance. The perineal traction post was placed at the root of the affected thigh and covered with sterile medical cotton pads to avoid soft‑tissue compression. Intraoperative skeletal traction and immobilization were performed using the traction table. Traction and positional adjustments were performed under fluoroscopic guidance. During traction‑assisted reduction, the affected lower limb was placed in 10°–15° internal rotation with mild adduction, achieving satisfactory fracture reduction. The total traction duration was 25 min, and the overall operative time was 30 min. No excessive reduction difficulty was encountered. Following successful reduction, the surgical area was disinfected with iodophor and draped with sterile sheets. A 5.0 cm incision was made approximately 5 cm above the greater trochanter on the lateral side of the left thigh, followed by dissection through the skin and subcutaneous tissues to reach the greater trochanter via blunt separation. Under fluoroscopy with the C-arm image intensifier, an entry point was created at the anteromedial one-third of the greater trochanter tip using an awl. A guide wire was inserted, and its correct positioning within the medullary cavity was confirmed again under fluoroscopy. After reaming the trochanteric region, an appropriately sized intramedullary nail was inserted. Under fluoroscopic guidance with a C-arm X-ray machine, a guide pin was placed in the lower middle position of the femoral neck on the anteroposterior view and at the midpoint on the lateral view. Following reaming, a spiral blade was inserted, and compression was applied to achieve close contact at the fracture site. Finally, distal locking screws were placed using a targeting device. Repeat fluoroscopy confirmed satisfactory fracture reduction and alignment with effective internal fixation. After achieving hemostasis, the surgical incision was irrigated and closed. No hemostatic agents, such as tranexamic acid, were used during the procedure.

Fig. 4.

Schematic diagram of PFNA surgery. Intraoperative traction and internal rotation of the left lower extremity are required, with the middle column obstructing and compressing the root of the left thigh (blue circle)

The patient was transferred to the Intensive Care Unit (ICU) for further treatment following surgery. Upon admission to the ICU, the patient exhibited localized swelling in the left thigh, a decrease in skin temperature below the left knee joint, and non-palpable left popliteal, posterior tibial, and dorsalis pedis arteries. Weakness was noted in the dorsiflexion of the left ankle and toes (Rutherford class IIb). An emergency bedside Doppler color ultrasound revealed arterial plaque formation in both lower limbs, thrombosis in the middle and lower segments of the left SFA, and no significant abnormalities in the veins of either lower limb. Emergency lower limb computed tomography angiography (CTA) demonstrated long-segment occlusion of the left SFA and occlusion of the upper segment of the right peroneal artery (Fig. 5).

Fig. 5.

CTA of bilateral lower extremity vessels. A Lower extremity vascular volume reconstruction image showing signs of luminal occlusion caused by embolism in the left superficial femoral artery. B Three-dimensional volume reconstruction image of lower extremity vessels demonstrating luminal occlusion due to embolism in the left superficial femoral artery. C Measurement of the length of arterial occlusion in the left lower extremity (blue line). D Fusion reconstruction image of lower extremity bones and vessels, with the starting segment of arterial occlusion located at the mid-to-upper femur

The vascular interventional specialist conducted a thorough consultation and evaluation, confirming that the patient had indications for emergency thrombectomy. The following emergency procedures were performed under local infiltration anesthesia: (1) Percutaneous lower extremity arterial thrombectomy; (2) Lower extremity arterial balloon angioplasty; (3) Left lower extremity arteriography. The procedures are briefly described as follows: The patient was positioned supine on the DSA examination table. After administering local anesthesia, a puncture of the right femoral artery was performed, followed by the insertion of a vascular sheath. With the assistance of a guidewire, the pigtail catheter tip was positioned at the left common iliac artery. Angiography revealed that the left internal iliac, external iliac, and common femoral arteries were visualized with patent lumens and smooth blood flow. However, the mid-to-distal segment of the left SFA and popliteal artery showed no significant opacification, with adjacent collateral vessels providing compensatory circulation. The peroneal artery, posterior tibial artery, and anterior tibial artery were visualized, exhibiting slow blood flow. A guidewire was introduced to facilitate the exchange for a 6 F long sheath, with the tip of the long sheath positioned in the left common femoral artery. A single-curve catheter was then introduced and advanced through the occluded segments of the SFA and popliteal artery, assisted by the guidewire and catheter. The catheter tip was placed in the distal popliteal artery, and contrast injection revealed extensive filling defects in the mid-to-distal popliteal artery and SFA. Subsequently, a Straub catheter was introduced to perform mechanical thrombectomy of the left SFA and popliteal artery. Post-procedural angiography demonstrated visualization of the main trunk of the SFA and popliteal artery, exhibiting a slender lumen and slightly reduced blood flow. The peroneal artery, posterior tibial artery, and anterior tibial artery were visualized with improved blood flow. Following this, Suruida balloon dilatation catheters (5*150 mm, 6*150 mm) were sequentially introduced to conduct segmental balloon angioplasty of the popliteal artery and SFA. Subsequent angiography revealed visualization of the left SFA and main trunk of the popliteal artery with smooth blood flow. The blood flow in the tibioperoneal trunk, anterior tibial artery, and posterior tibial artery improved, and the vascular network of the left foot appeared denser than before. Finally, the catheters and sheaths were removed, and the puncture site was closed using a vascular closure device, followed by pressure bandaging (Fig. 6).

Fig. 6.

Angiography and thrombus during mechanical thrombectomy procedure. A Angiography revealed no significant filling in the middle and distal segments of the superficial femoral artery and the popliteal artery, with normal filling observed in the left internal iliac, external iliac, and common femoral arteries. B, C The guidewire and catheter were used in combination to pass through the occluded segments of the superficial femoral artery and popliteal artery. D Thrombus aspiration was performed. E Balloon angioplasty was conducted on the superficial femoral artery and popliteal artery. F, G The main trunk of the left superficial femoral artery and popliteal artery showed filling. H Intraoperative photograph of the extracted thrombus

Immediately following interventional thrombectomy, the skin temperature of the left lower limb below the knee normalized. One hour post-procedure, the patient exhibited gradual improvement in active movement of the ankle and toes. By the second day after the intervention, the motor function of ankle and toe dorsiflexion was completely restored. No neurological deficits or limb movement disorders were observed during subsequent monitoring, and peripheral nerve function recovered fully.

The interventional thrombectomy procedure was successfully completed, and the patient was subsequently transferred back to the intensive care unit for ongoing treatment. Postoperatively, the swelling of the affected limb gradually diminished, and the skin temperature of the left lower limb returned to normal. The popliteal artery, posterior tibial artery, and dorsalis pedis artery were palpable. The motor function of the left ankle joint and foot showed gradual recovery. Postoperative bedside X-ray revealed favorable radiological outcomes of the fracture (Fig. 7A). The surgical incision healed appropriately without any signs of infection (Fig. 7B). The patient received daily subcutaneous low‑molecular‑weight heparin for postoperative anticoagulation. Postoperative lower‑extremity vascular ultrasonography revealed no arterial or venous thrombosis or other vascular abnormalities, indicating complete clearance of thrombus. Satisfactory perfusion of the affected limb was confirmed. After six days of intensive care unit (ICU) monitoring and management, the patient was transferred to the general orthopedic ward with stable vital signs. Unexpected loss of consciousness followed by cardiac arrest occurred on the second day after ward transfer; the patient’s family declined further resuscitation and requested hospital discharge against medical advice. The clinical timeline of the patient is presented in Table 1.

Fig. 7.

Postoperative follow-up examination. A Postoperative review of the left hip joint AP X-ray shows good fracture alignment with effective internal fixation in place. B The surgical incision has healed well

Table 1.

Perioperative Timeline of the Patient

Clinical Time Node	Time Value
Time from fracture to admission	1d
Time from admission to surgery	3 d
Duration of operation	30 min
Duration of traction	25 min
Time from surgery completion to detection of absent pulses	60 min
Time from surgery completion to Doppler	78 min
Time to thrombectomy procedure	75 min
Time to reperfusion achievement	80 min
ICU admission time	6 d
Time from transfer to general ward to discharge	1 d

Discussion

Intertrochanteric femoral fractures are prevalent among elderly patients [5]. Common complications after PFNA surgery include infection, pudendal nerve palsy, acute osteofascial compartment syndrome and fat embolism syndrome. Nevertheless, there are limited reports concerning lower extremity arterial thrombosis following PFNA surgery. While the prevention of venous thrombosis in lower extremity fractures is widely accepted among clinicians, arterial thrombosis has not been given adequate attention in clinical practice.

It is crucial to emphasize that arterial and venous thrombi differ fundamentally in their formation mechanisms and composition. Arterial thrombosis is primarily driven by vascular endothelial injury and platelet activation. Due to the high flow velocity and shear stress present in arteries, thrombosis seldom occurs solely due to blood stasis. The principal triggering factor is endothelial damage, which may result from atherosclerotic plaque rupture, vascular interventional procedures, or trauma, leading to the exposure of subendothelial collagen fibers. The damaged endothelium activates platelets, prompting their adherence and aggregation into platelet thrombi, while simultaneously initiating the extrinsic coagulation pathway, ultimately culminating in thrombus formation. Common predisposing factors include atherosclerosis, which can be exacerbated by hypertension, hyperlipidemia, diabetes, and smoking [16].

Venous thrombosis is primarily driven by slow blood flow combined with a hypercoagulable state. The sluggish blood flow velocity and low shear stress in veins render blood stasis the most critical predisposing factor, particularly in cases of prolonged bed rest, sedentary behavior, postoperative immobilization, and pregnancy. While vascular endothelial injury is typically mild and not a core factor, hypercoagulability—resulting from conditions such as tumors, pregnancy, oral contraceptive use, and coagulation factor abnormalities—further promotes thrombus formation. The slow blood flow facilitates the aggregation of coagulation factors and platelets, thereby activating the intrinsic coagulation pathway, with fibrin trapping a substantial number of red blood cells to form a thrombus. Common predisposing factors include prolonged immobilization, postoperative status, malignant tumors, and inherited coagulation disorders. Arterial thrombi are primarily composed of platelets and small amounts of fibrin, typically manifesting as white thrombi that adhere tightly to sites of vascular wall injury. In contrast, venous thrombi are mainly composed of red blood cells, abundant fibrin, and a limited number of platelets, predominantly appearing as red thrombi. They may exhibit a mixed structure, characterized by a white thrombus at the head and red thrombi in the body and tail portions, and are prone to detachment, resulting in emboli. When arterial thrombi occlude blood vessels, they induce acute tissue ischemia and hypoxia, potentially leading to limb necrosis in severe cases. Conversely, venous thrombosis obstructs venous return, resulting in limb swelling and pain. Furthermore, venous thrombi are more likely to detach, causing life-threatening complications such as pulmonary embolism [16, 17].

Studies have shown that thrombosis in the external iliac artery significantly increases the incidence of lower limb amputation by fivefold, triples the occurrence of compartment syndrome, and doubles the mortality rate compared to patients with other vascular injuries [18]. When a major artery is occluded, the affected limb typically presents with symptoms such as tingling, numbness, decreased skin temperature, cyanosis, weakened or absent arterial pulses, and diminished motor and sensory functions [19]. Upon manifestation of these symptoms, vascular Doppler ultrasound and CTA examinations should be conducted. Following diagnosis, prompt emergency intervention is crucial to prevent ischemic necrosis of the lower limb, which may ultimately lead to amputation or death. Carillo et al. [20] reported a case of amputation resulting from undiagnosed external iliac thrombosis, while Smejkal et al. [21] detailed a patient who underwent hip disarticulation due to external iliac artery occlusion.

Anatomical studies indicate that the femoral artery serves as the principal arterial blood supply to the lower extremity. As the continuation of the external iliac artery, it descends below the midpoint of the inguinal ligament, entering the femoral triangle of the thigh and giving rise to the deep femoral artery approximately 3–5 cm distal to the ligament. The deep femoral artery courses posteromedially to supply the posterior and medial muscle groups of the thigh. The remaining main trunk, referred to as the SFA, continues through the femoral triangle, traverses the adductor canal, and passes through the adductor hiatus to enter the popliteal fossa, where it ultimately becomes the popliteal artery [22, 23]. Postoperative thrombosis of the SFA can lead to a complete or critical interruption of arterial blood flow to the lower limb. Acute limb ischemia presents with symptoms characterized by Pain, Pallor, Pulselessness, Paresthesia, and Paralysis—collectively known as the 5P signs. In severe cases, complications such as rhabdomyolysis, acute kidney injury, systemic inflammatory response syndrome (SIRS), and sepsis may occur, with a risk of amputation. If the thrombus is partially recanalized or treatment is incomplete, chronic post-ischemic sequelae may develop, including intermittent claudication, rest pain, skin trophic disturbances, ulcers, or lower limb dysfunction [24, 25].

In this case, we observed that during the surgical procedure, the traction post of the traction table continuously compressed the left groin area (Fig. 4). Prolonged traction collectively led to intimal injury and plaque rupture in the SFA, potentially resulting in arterial thrombosis [26]. A similar pathological mechanism has been reported in acetabular surgery, where atherosclerotic plaque rupture caused iliac artery thrombosis [7, 27]. Furthermore, in total hip arthroplasty, direct pressure from the Hohmann retractor used for hip joint exposure can induce intimal tears and atherosclerotic plaque rupture, ultimately leading to arterial thrombosis [28]. This condition is particularly prevalent in elderly patients with a long history of hypertension and heavy smoking, significantly increasing the incidence of atherosclerosis. The patient in this case has a long-standing history of coronary atherosclerotic heart disease. Doppler ultrasound of the lower extremity vessels revealed multiple plaque formations, which increase the risk of lower extremity arterial thrombosis. Therefore, caution must be exercised when formulating the treatment plan. During the PFNA procedure, thick soft cotton padding should be placed at the root of the affected thigh, and the surgical duration should be minimized as much as possible. The pathogenesis of postoperative arterial thrombosis in the present case appears to be multifactorial, predominantly influenced by endothelial injury, atherosclerosis, platelet hyperactivation, a sustained inflammatory state, tissue hypoxia, and perioperative stress. Perioperative surgical trauma induces endothelial dysfunction and damage, which exposes subendothelial collagen, thereby triggering platelet adhesion and aggregation. In addition to surgical compression during fracture reduction, atherosclerotic plaque rupture and embolic events associated with perioperative hypercoagulability may also contribute to the underlying mechanisms. Pre-existing atherosclerotic lesions further narrow the arterial lumen, exacerbating local hemodynamic disturbances. Concurrently, perioperative stress activates systemic inflammatory cascades, leading to the upregulation of pro-thrombotic mediators and the promotion of a hypercoagulable state. Tissue hypoxia, resulting from impaired perfusion, reciprocally amplifies inflammatory responses and platelet activation, ultimately facilitating arterial thrombus formation and acute limb ischemia.

In cases of lower limb thrombosis, earlier intervention leads to improved clinical outcomes. The clinically recognized golden time window for intervention in acute lower limb arterial ischemia is within six hours [29]. During this period, ischemic damage to limb tissues is predominantly reversible. Timely restoration of blood supply through thrombectomy or thrombolysis can maximize limb function preservation, reduce the risk of amputation, and significantly decrease the incidence of postoperative complications, such as rhabdomyolysis and acute renal failure. If the duration of ischemia exceeds twelve hours, irreversible necrosis of muscle tissue may occur. Even if successful thrombectomy restores blood flow at this stage, the breakdown of muscle cells can release large amounts of myoglobin, potassium ions, and other substances, potentially leading to life-threatening complications, including rhabdomyolysis, hyperkalemia, and acute renal failure. When ischemia persists beyond twenty-four hours, the probability of limb necrosis increases significantly, often necessitating amputation to save the patient’s life. However, clinically determining the exact time of thrombus formation is typically challenging, particularly when it occurs during late-night hours, as elderly patients often cannot effectively communicate their discomfort symptoms. In this case, the patient exhibited no apparent lower limb symptoms prior to surgery. Fortunately, thrombosis in the SFA of the lower limb was promptly detected and diagnosed postoperatively, leading to immediate thrombectomy and early restoration of limb perfusion. However, not all patients are as fortunate. Magu et al. [7] reported a case involving a patient treated via the ilioinguinal approach for an anterior column acetabular fracture, who subsequently developed ischemic neuropathy of the sciatic nerve due to compromised blood supply. It was not until the sixth postoperative day, when ischemic changes became evident in the foot, that signs of vascular injury were recognized. Although the patient later underwent vascular reconstruction surgery, the muscle strength of the extensor hallucis longus and extensor digitorum longus remained at grade 4 without further recovery during the two-year follow-up period. Therefore, we underscore the critical importance of employing gentle surgical techniques, effectively protecting vital areas, conducting thorough postoperative physical examinations, and maintaining close monitoring.

Based on a comprehensive clinical assessment, we speculate that acute ischemia resulting from superficial femoral artery thrombosis may be the predominant cause of weakness in ankle and toe dorsiflexion in this case. The peroneal nerve and the distal limb muscles responsible for ankle dorsiflexion are highly dependent on an adequate arterial blood supply. When acute occlusion of the superficial femoral artery occurs following PFNA surgery, severe hypoperfusion develops in the distal lower extremity. Skeletal muscle and peripheral nerve tissues are sensitive to oxygen and nutrient deprivation; transient ischemia can rapidly lead to metabolic dysfunction and reversible motor weakness. Unlike persistent nerve palsy caused by surgical traction or direct nerve damage, ischemia-induced motor impairment is typically reversible once blood flow is restored. In this patient, limb perfusion was promptly re-established via endovascular intervention. Distal skin temperature recovered immediately after the procedure, and ankle and toe motor function gradually improved within one hour, achieving full neurological recovery by postoperative day 2. This time course of recovery provides strong circumstantial evidence suggesting that the dorsiflexion weakness was likely secondary to acute limb ischemia rather than structural nerve injury.

Our case involves an elderly male patient with comorbid sarcopenia and COPD, who sustained an intertrochanteric femoral fracture following a fall during hospitalization for pulmonary disease at a community hospital. Sarcopenia is a recognized risk factor for functional decline and disability in older adults, closely associated with impaired mobility, reduced gait speed, and diminished physical activity, serving as a well-established risk factor for falls and fractures [30]. Cohort data from the United Kingdom involving 387,025 middle-aged individuals demonstrated that pre-sarcopenia or sarcopenia status correlates with an increased risk of fractures and osteoporotic fractures [31]. Osteosarcopenia is a newly proposed syndrome that describes the coexistence of osteoporosis and sarcopenia, which is associated with elevated risks of fractures and mortality [32]. A cohort study of 2,000 community-dwelling elderly men in China demonstrated that sarcopenia could independently predict fracture risk even after adjusting for osteoporosis factors [33]. This situation creates a vicious cycle, as fracture incidents necessitate prolonged bed rest and immobilization, leading to accelerated loss of body nutrients that further exacerbates sarcopenia symptoms. Furthermore, another study indicated that muscle size and density were associated with mortality rates following hip fractures [34]. Therefore, for patients already diagnosed with sarcopenia, in addition to emphasizing nutritional support and physical exercise, fall prevention remains a crucial intervention.

Currently, there is no globally unified consensus on the diagnosis of sarcopenia. The existing diagnostic criteria include the EWGSOP2 consensus [35], the Asian Working Group for Sarcopenia consensus [36], and the standards published by the Sarcopenia Definition and Outcomes Consortium (SDOC) [37]. The variability in sarcopenia assessment and diagnostic results can be attributed to differences in the definition of sarcopenia and the diagnostic tools employed in research. The EWGSOP2 consensus remains the most widely recognized diagnostic standard for sarcopenia, encompassing core parameters such as (1) low muscle strength, (2) low muscle quantity or quality, and (3) low physical performance. If criterion 1 is met, sarcopenia should be suspected, while meeting criterion 2 confirms the diagnosis. Severe sarcopenia is diagnosed when all three criteria are satisfied. Muscle strength is typically measured using a hand dynamometer to assess grip strength of the dominant hand, while muscle mass is commonly evaluated through dual-energy X-ray absorptiometry (DEXA), bioelectrical impedance analysis, and L3 psoas SMI (calculated from CT or MRI as the total bilateral psoas area divided by the square of height). According to the EWGSOP2 consensus, probable sarcopenia is defined as isolated low handgrip strength (< 27 kg for men, < 16 kg for women); sarcopenia is confirmed when low muscle strength is accompanied by reduced appendicular skeletal muscle index (ASMI, appendicular skeletal muscle mass divided by height squared) measured via dual-energy X-ray absorptiometry (DXA, males <7.0 kg/m² and females <5.5 kg/m²), and severe sarcopenia is diagnosed if impaired physical performance including usual gait speed ≤ 0.8 m/s, Short Physical Performance Battery (SPPB) ≤ 8 points, five-time chair stand test ≥ 15 s or Timed Up and Go (TUG) test ≥ 20 s is present additionally [38]. However, we adopted the method proposed by Ursula N. from Harvard University, which utilizes the total muscle area (including erector spinae, latissimus dorsi, internal oblique, external oblique, rectus abdominis, external intercostal, and intercostal muscles) at the T12 pedicle level on chest CT scans, divided by the square of the patient’s height to calculate SMI for diagnosing sarcopenia. The cutoff values were defined as SMI < 42.6 cm²/m² for males and SMI < 30.6 cm²/m² for females [39]. Since hip surgery patients do not routinely undergo lumbar CT or MRI scans to avoid additional costs or radiation exposure, and as these COPD patients required thoracic CT scans, we adopted this criterion for diagnosing sarcopenia.

Current evidence indicates a significant association between sarcopenia and thrombosis in orthopedic surgeries. Patients diagnosed with sarcopenia demonstrate a higher incidence of deep vein thrombosis (DVT) following total knee arthroplasty (TKA) [40]. Additionally, during the perioperative period of complex thoracolumbar revision surgeries, sarcopenic patients exhibit an increased occurrence of DVT [41]. We hypothesize that this correlation may arise from the reduced muscle mass and strength characteristic of sarcopenic patients, which can impair muscle pump function and compromise blood circulation. Furthermore, sarcopenia is often associated with chronic inflammation and malnutrition. Chronic inflammation may enhance the synthesis of coagulation factors, while malnutrition can disrupt anticoagulant mechanisms, collectively exacerbating hypercoagulability and the formation of venous thrombosis. However, it is important to note that current research primarily focuses on venous thrombosis, leaving arterial thrombosis largely understudied.

Studies have shown that COPD is frequently associated with systemic inflammatory responses, which can result in coagulation disorders and thrombotic complications [11]. Pulmonary ventilation/perfusion dysfunction activates the sympathetic-adrenal medullary system, leading to vasoconstriction and further exacerbation of blood stasis. Microstructural analyses of thrombi indicate a heightened thrombotic tendency during acute exacerbations of COPD compared to patients in stable phases [42]. Meta-analyses have demonstrated that factors such as atelectasis, prolonged immobilization, invasive mechanical ventilation, tumors, and chest pain significantly increase the risk of venous thromboembolism (VTE) in COPD patients [43]. Similar to sarcopenia, the relationship between COPD and the formation of arterial thrombosis has not been adequately reported. In this study, prolonged bed rest due to fracture immobilization and the use of mechanical ventilation during surgery may have contributed to the formation of SFA thrombosis to some extent. Additionally, arterial embolism resulting from pre-existing peripheral artery disease, perioperative hypotension, a hypercoagulable state, embolic disease, plaque instability, or trauma-related vascular injury cannot be discounted.

Surgical thrombectomy and thrombolysis are two established treatment methods for arterial thrombosis. Surgical thrombectomy encompasses both interventional thrombus removal and open thrombectomy [44]. SFA thrombosis represents an acute lower limb ischemia emergency, with the primary management principle being the prompt restoration of arterial blood supply to preserve limb function and prevent systemic complications. Minimally invasive thrombectomy is considered the preferred treatment option due to its ability to directly remove the thrombus while minimizing trauma and facilitating rapid recovery, making it suitable for most patients. Pharmacological thrombolytic therapy, which includes agents such as urokinase and recombinant tissue plasminogen activator (rtPA), is indicated for patients with ischemia lasting less than 6 h and who do not exhibit limb necrosis. This therapy can be administered via peripheral intravenous or local catheter delivery. However, it is imperative to strictly adhere to exclusion criteria, including active bleeding, recent cerebral hemorrhage, and thrombocytopenia. In this case, we initially observed changes in skin temperature and the absence of major arterial pulses in the patient’s lower limbs, which strongly suggested acute arterial embolism. A bedside rapid vascular Doppler ultrasound was performed for preliminary diagnosis, followed by CT angiography (CTA), which confirmed thrombosis in the left SFA. Upon confirmation, percutaneous mechanical thrombectomy and balloon angioplasty of the lower limb artery were conducted to restore blood flow. This minimally invasive surgical approach facilitates faster recovery in elderly patients. Since distal pulses returned immediately after the procedure, open surgical intervention was deemed unnecessary. Postoperatively, standardized anticoagulation therapy with low-molecular-weight heparin was continued. Due to our early and timely detection and treatment, the patient gradually regained blood perfusion in the lower limbs postoperatively, without complications such as loss of sensory or motor functions.

Several limitations exist within the present case report. Firstly, this study is limited to a single case, lacking comparative data from more clinical cases. Potential selection bias exists, and individual physical conditions and postoperative recovery differences cannot be excluded. Secondly, we utilized the diagnostic criteria for sarcopenia established by Harvard University, which is derived from data predominantly involving Caucasian populations, potentially introducing bias. The diagnostic methodology employing chest CT necessitates additional research for validation. Given the presence of fracture, assessment of gait speed and physical function was unfeasible. Additionally, owing to the unanticipated risk of acute arterial embolism and negative preoperative screening for deep venous thrombosis, we did not conduct lower limb blood pressure measurement, comprehensive vascular ultrasound evaluation or vascular surgery consultation. Finally, due to limited long‑term follow‑up and relatively small sample size, the generalizability of this case report requires further validation. In conclusion, lower extremity arterial thrombosis following PFNA surgery for intertrochanteric femoral fractures is a rare complication that may result in disability or even mortality. It is vital for surgeons to be cognizant of this potential complication. Comprehensive preoperative screening, meticulous management, and careful surgical techniques are essential.

Conclusion

Although lower extremity arterial thrombosis following PFNA surgery for intertrochanteric femoral fractures is rare, its progression is rapid, and the outcomes can be severe once it occurs. Early detection, accurate diagnosis, and timely intervention are crucial. Patients with high-risk factors necessitate enhanced management and preventive measures. Lastly, for elderly patients with sarcopenia, daily care should be intensified to prevent falls, along with improved nutritional support and physical therapy.

Authors' contributions

Zhaoyang Yin contributed to data collection and the writing of the manuscript. Ge Gong was tasked with the analysis of sarcopenia and the writing of the manuscript. Peng Peng oversaw the development and implementation of interventional surgical plans. Qin Hu managed perioperative patient care and provided rehabilitation guidance. Hailong Zhang executed orthopedic surgeries. Jian Yin was involved in performing orthopedic surgeries, data collection, manuscript revision, and submission.

Funding

declaration.

This work was supported by grants from Jiangsu Province Elderly Health Scientific Research Project (LKM2024021), Kangda College of Nanjing Medical University Educational Research Project (KD2025JYYJYB040), Scientific Research Project of Jiangsu Provincial Health Commission (2022 − 208), Scientific Research Project of Jiangsu Provincial Health Commission (Z2022086), General Project of Lianyungang Municipal Health Commission (202212), and Clinical Research Project (2024LCYYQH034) at Jinling Hospital, Affiliated Hospital of Medical School, Nanjing University.

Data availability

The data that support the findings of this study are available from the corresponding author upon reasonable request.

Declarations

Ethics approval and consent to participate

This study was approved by the Ethics Committee of Jiangning Hospital, affiliated with Nanjing Medical University, and informed consent was obtained from both the patient and family members. This study was in accordance with the Declaration of Helsinki.

Consent for publication

The patient has provided written informed consent, allowing for the publication of their personal and clinical data, as well as any identifiable images included in this study.

Competing interests

The authors declare no competing interests.