Postoperative Course and Outcome
Upon transport to the postsurgical care unit and emergence from sedation, the patient experienced immediate resolution of her neuralgic symptoms. Pathology of the operative specimen showed a benign, disorganized arrangement of axons, Schwann cells, and perineural fibroblasts amidst a fibrous stroma, consistent with traumatic neuroma. At 1-month and 6-month follow-up visits, the patient remained symptom-free, aside from some continued anterior left knee pain near the site of intramedullary nail entry. Her positive Tinel sign had completely resolved, as did her neuralgic symptoms down the medial aspect of her leg. This proved consistent with a diagnosis of neuroma as the cause of the majority of her symptoms. Subjectively, she reported excellent overall pain relief and satisfaction with her treatment and postoperative course.
Discussion
Postoperative pain after intramedullary fixation of tibial shaft fractures is common and can be caused by several clinical entities.5,10 Anterior knee pain is a well-known complication present in up to 73% of patients treated with tibial nailing.10 Osteoarthritis of the knee or ankle as well as nonarthritic ipsilateral ankle pain are also common complaints, often resulting from tibial malunion or malrotation, leading to altered joint kinematics.11 Additionally, superficial peroneal nerve and tibial neurovascular bundle injuries have been reported as potential complications of distal interlocking screw placement, and should be considered in such patients.12
Another consideration for the development of postoperative pain is CRPS, which is thought to be caused by postinjury sympathetic activation that produces pain out of proportion to clinical examination findings.13 Although no postoperative incidence of CRPS in the setting of tibial nailing has been reported, it is a known contributor to poor functional outcomes after fractures or crush injuries to the lower extremity.9 When attempting to diagnose and treat chronic postoperative pain after tibial nailing, the clinician must keep these common etiologies in mind as well as an understanding of the adjacent anatomy.
The saphenous nerve originates from the third and fourth lumbar nerve roots, coursing beneath the inguinal ligament as part of the femoral nerve. As the terminal branch of the femoral nerve, the saphenous nerve runs in the Hunter canal beneath the fascia of the sartorius muscle. It is bordered laterally by the vastus medialis muscle, and posteriorly and laterally by the adductor longus and magnus muscles. The saphenous nerve then crosses the femoral artery superficially from medial to lateral as it courses distally in the canal. As it emerges from the adductor hiatus, the saphenous nerve runs superficial to the gracilis muscle around the posterior border of the sartorius muscle with the descending genicular artery, and becomes a subcutaneous structure at the level of the knee joint. The infrapatellar branch of the saphenous nerve provides sensation to the medial knee, and continues in a subcutaneous course just medial to the posterior aspect of the tibial shaft with the great saphenous vein. The nerve distally supplies sensory input from the medial foot and ankle.1,3,14
There are several causes of saphenous neuralgia related to surgical and nonsurgical trauma.2,3,15,16 The most common cause of nerve injury is iatrogenic traction or transection causing neuralgic sequelae from subsequent neuroma formation. The anatomy of the saphenous nerve puts it at particular risk when performing saphenectomy for vascular procedures, and its infrapatellar branch is at particular risk when performing a medial parapatellar approach for total knee arthroplasty.2,3 In the case of the surgically naïve patient, saphenous nerve entrapment syndromes have also been described, and occur most frequently at the level of the adductor hiatus or as the saphenous nerve courses between the sartorius and gracilis muscles proximal to the knee joint.16
As is illustrated in the present case, orthopedic trauma may be an additional cause of saphenous neuroma formation, leading to symptomatic neuralgia. This case suggests that symptomatic neuroma should be included in the differential diagnosis of posttraumatic pain in the orthopedic trauma patient. It is important to note that, although this case occurred after a severe injury, the intimate association of the saphenous nerve with the tibia places it in a vulnerable position, and traumatic transection is possible after closed injuries to the tibial metadiaphyseal junction or tibial shaft.
Neuroma formation occurs in response to damage to the endoneurium and axon. For an axon to repair properly, the damaged proximal segment must join with, and reenter, the distal stump. As axons attempt to regenerate, occasionally the proximal stump can escape into the surrounding tissue and form a painful neuroma consisting of a disorganized mass of Schwann cells, fibroblasts, blood vessels, and axons with various degrees of myelination. The subsequent neuralgia associated with neuroma formation is caused by chemical or mechanical stimulation of the damaged axons or by spontaneously evoked potentials in the damaged axons. These signals can manifest as a variety of symptoms, including paresthesia and allodynia.17,18