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Saphenous Nerve Entrapment Neuropathy After Closed Tibial Fracture

A Case Report

Haraguchi, Toshiaki MD, PhD1,2,a; Kume, Shinichiro MD, PhD1; Jimbo, Kotaro MD, PhD2; Gotoh, Masafumi MD, PhD1; Shiba, Naoto MD, PhD3; Okawa, Takahiro MD, PhD1

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doi: 10.2106/JBJS.CC.20.00670
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Painful neuropathies can be caused by nerve compression or neuromas. The causes of saphenous neuropathy include surgical and nonsurgical trauma1-4. Commonly, neuralgia and neuroma formation occurs after iatrogenic saphenous nerve injury, such as after orthopaedic surgeries or saphenectomy for vascular procedures1,2. After total knee arthroplasty, numbness owing to nerve damage has been reported in 55% to 100% of patients5-7. The incidence of saphenous nerve neuralgia and hyperesthesia after saphenectomy for vascular procedures is approximately 10% after 20 months1. The clinical importance of saphenous nerve damage has been amplified by recent studies showing that patient satisfaction correlates inversely with the presence of injury to the saphenous nerve8. To the best of our knowledge, postoperative neuropathic pain caused by saphenous nerve entrapment associated with orthopaedic injuries, such as closed tibial shaft fractures, has not yet been reported9.

Posttraumatic neuralgia is a complication with characteristics similar to those of peripheral neuropathy and complex regional pain syndrome (CRPS type II). The diagnosis can be challenging for clinicians unfamiliar with this condition or its clinical presentation. Herein, we report the case of a patient diagnosed with neuropathy caused by saphenous nerve entrapment after treatment of closed tibial shaft fracture.

The patient was informed that data concerning the case would be submitted for publication, and he provided consent.

Case Report

A 43-year-old male patient was brought by ambulance to our emergency department with complaints of severe left leg pain and swelling, after a motor vehicle accident (Fig. 1). There were no wounds or fracture blisters. The swelling was not severe. A detailed neurologic examination revealed no focal nerve deficits. His motor and sensory examinations were unremarkable, and his pain, although severe, was not located over any specific anatomic nerve distribution. The pain that increased while using or stretching the leg muscles was not clear. Closed fragmentary segmental fracture of the left tibia with proximal metadiaphyseal fibular fracture was diagnosed (Fig. 2). Five days after injury, surgical fixation with a standard intramedullary nail was performed. A postoperative neurological examination of the left lower limb revealed weakness of the extensor hallucis longus, extensor digitorum longus, and tibialis anterior muscles and numbness in the first web space; therefore, dysfunction of the left peroneal nerve was diagnosed. His recovery at 6 months postoperatively was good.

Fig. 1
Fig. 1:
Left lower extremity showing no evidence of open tibial fracture at the time of injury.
Fig. 2
Fig. 2:
Initial preoperative radiographs: (Fig. 2-A) anteroposterior view and (Fig. 2-B) lateral view. Fracture alignment is satisfactory with the intramedullary nail noted in situ.
Fig. 3
Fig. 3:
Anteroposterior and lateral radiographs 2 years postoperatively showing signs of healed fractures.

At the 2-year follow-up after his initial injury, full range of active and passive motion was observed and motor examination and reflexes of the lower extremity were unremarkable. However, the patient developed progressive and severe pain in the medial aspect of the left leg, especially after walking or standing for a few minutes. The pain was burning and tingling, with associated hyperesthesia of the affected area. The degree of pain was evaluated by the 100-mm visual analog scale, the resting pain was 20 mm, and the pain after walking for a few minutes was 80 mm. Nonunion was initially suspected. Radiographs of the tibia and fibula seemed to show healed fractures (Fig. 3). However, computed tomography (CT) demonstrated only partial bone union (Fig. 4). Further examination of the previously injured region revealed a positive Tinel sign along the course of the saphenous nerve. Leg pain was present along the distribution of the saphenous nerve distally. Magnetic resonance imaging (MRI) was difficult to interpret because of artifacts seen in the image because of the intramedullary rod. Ultrasonography revealed that the saphenous nerve was continuous without obvious swelling or stenosis and seemed nonadherent to the muscle tissue (Fig. 5). An injection of 2 cc of 1% lidocaine over the affected region resulted in temporary relief of the pain that radiated down to the medial ankle area.

Fig. 4
Fig. 4:
Computed tomography 2 years postoperatively demonstrating only partial bone healing at the site of fracture: Fig. 4-A coronal images, and Fig. 4-B sagittal images.
Fig. 5
Fig. 5:
Fig. 5-A Short-axis scan of ultrasonography showing the saphenous nerve (N) running posterior to the great saphenous vein (V). The saphenous nerve was continuous without obvious swelling or stenosis. Breaks in the fascia are not obvious. Fig. 5-B Long-axis scan of color Doppler ultrasonography showing the saphenous vein (V) in which flow is noted without stenosis or occlusion.
Fig. 6
Fig. 6:
Fig. 6-A Intraoperative photograph showing the saphenous nerve (N), with surrounding neuromatous scar (arrows), running posterior to the great saphenous vein (V). Fig. 6-B The nerve with adhesions to muscle tissue (arrows) through traumatic breaks in the fascia. Fig. 6-C After neurolysis, the nerve is in continuity.

The patient’s leg pain may be attributed to saphenous nerve entrapment or neuroma. The patient had a strong desire to remove all hardware in the future. Hence, neurolysis and autologous bone grafting were performed 2 years after initial surgery. Intraoperatively, the saphenous nerve was inspected and found to be in continuity without obvious contusions, although locally, severe adhesion of the nerve at the fracture level was noted macroscopically (Fig. 6). The saphenous nerve had adhesions to the muscle through traumatic breaks in the fascial layer along the posterior aspect of the tibial shaft.

On the first postoperative day, the pain had improved significantly. At the 3-month follow-up, complete resolution of severe radiating leg pain was noted. At the 2-year clinical follow-up, he remained asymptomatic.


This case report provides 2 important clinical suggestions: (1) closed fracture of the tibial shaft can present as saphenous nerve entrapment, even in the absence of an open fracture, and (2) injection of lidocaine over the region of the potential injury site may be useful in the diagnosis of nerve entrapment. To our knowledge, this is the first report of a saphenous nerve entrapment after closed tibial shaft fracture because the saphenous nerve was pressed and pulled by the muscle tissue through traumatic breaks in the fascia.

Postoperative lower extremity pain after intramedullary fixation of tibial shaft fractures is common and can have several causes10. Chronic pain after lower extremity fracture can be caused by nonunion, infection, malalignment, painful hardware, and peroneal nerve damage11-13. Neuralgic dysfunction after intramedullary nailing of a tibial fracture is uncommon; if it occurs, the most common is peroneal nerve dysfunction. In a prospective series of 208 patients with tibial shaft fracture treated with an intramedullary nail, 1.9% continued to have a nerve deficit 1 year postoperatively14.

Postoperative pain may also be because of CRPS type II, caused by posttraumatic sympathetic or afferent activation or vasomotor instability that produces severe pain out of proportion to the examination findings15. Several etiologies should be considered while evaluating a patient with chronic pain after limb trauma. The clinician should also understand the relevant anatomy. The saphenous nerve originates from the third and fourth lumbar nerve roots. Being the largest cutaneous branch of the femoral nerve, it runs beneath the inguinal ligament as part of the femoral nerve and then through Hunter's canal beneath the sartorius muscle. The nerve divides into the sartorial and infrapatellar nerve branches at the level of the medial femoral condyle. The sartorial branch then progresses superficially as it penetrates the fascia between the gracilis and sartorius tendons and continues in a subcutaneous course just medial to the posterior aspect of the tibial shaft with the great saphenous vein to provide sensory innervation to the medial aspect of the leg and ankle15-17.

Saphenous nerve neuralgia related to surgical and nonsurgical trauma has several etiologies; however, posttraumatic neuralgia comprises <1% of adult patients presenting with lower extremity pain18. Moreover, the most common cause of nerve injury is iatrogenic traction or transection after orthopaedic procedures, causing neuralgia. The close association of the saphenous nerve with the tibia places it in a vulnerable position, and traumatic transection may occur after closed injuries of the tibial metadiaphyseal junction or tibial shaft. A review of the literature reveals only one report of a patient with saphenous nerve neuropathy after open tibial shaft fracture9.

Closed fracture of the tibial shaft may be a cause. Such reports may be rare because most patients accept mild pain or sensory deficits without pain. In this case, the patient had unbearable leg pain, especially while walking, because of severe adhesions of the nerve to the scar and muscle tissue through breaks in the fascia along its course. In general, muscle extrusion is caused by heightened compartment pressures on exertion with contracted muscle, causing fascial hernias. The saphenous nerve could be entrapped and pulled by muscle tissue, causing our patient’s symptoms.

Injection of 1% lidocaine to the affected area is useful for the definitive diagnosis of saphenous nerve neuropathy after intramedullary fixation of tibial shaft fractures9,19. The saphenous nerve is strictly sensory and has no motor function and may be difficult to examine clinically. Hence, lidocaine injection is an important diagnostic test, especially when attempting to differentiate painful neuropathy from other causes of posttraumatic lower extremity pain (e.g., CRPS type II)19. Other methods of the diagnostic evaluation of a patient with chronic pain include MRI and ultrasonography. However, tibial shaft fractures are often treated with intramedullary nailing, and MRI scans provide little diagnostic value, because of the extensive artifacts that limit visualization of the saphenous nerve and the soft tissue surrounding hernial defects. As ultrasonography has become increasingly available, it may be useful for diagnosis. However, it is operator-dependent, and therefore, findings may be missed if one does not consider the possibility of the diagnosis. Hence, lidocaine injections should ideally be performed for the diagnosis and treatment of symptomatic nerve entrapment. In conclusion, closed fractures of the tibial shaft can present with symptoms of saphenous nerve entrapment. Clinicians should consider a variety of etiologies in the diagnostic evaluation of a patient with chronic pain after limb trauma. The diagnosis may be elusive, especially in patients with less obvious clinical features. If a patient complains of lower extremity pain after intramedullary fixation of closed fractures of the tibial shaft, clinicians should consider the possibility of saphenous nerve entrapment neuropathy.

Note: The authors thank Dr. Hidehiro Nakamura for helpful discussions and comments on the manuscript.


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