Nerve traction injuries are common clinical entities that can be confused with nerve palsies secondary to alternate etiologies.1–3 Common mechanisms of nerve injury include direct laceration, crush injury, compression injury, elevated compartment pressures, or traction injury. Traction injuries are commonly considered after high-energy trauma or aberrant patient positioning; however, this etiology of injury is less commonly encountered after external fixation for lower extremity injury.
Knowledge of the biomechanical properties of peripheral nerves and their mechanisms of injury in such clinical settings may be useful in the recognition of patients at risk for nerve traction injuries.1 This case involves a patient who underwent revision of external fixation for a Schatzker VI tibial plateau fracture with subsequent acute loss of common peroneal motor and sensory function, identified 1 hour postoperatively in the post-acute care unit and reversed on the immediate release of distraction from the external fixation construct.
A 42-year-old man who suffered an isolated, closed Schatzker VI tibial plateau fracture during a high-speed skiing accident was treated with immediate external fixation performed at another hospital (Figure 1). Seven days after the initial surgery, he presented to the authors' emergency department reporting fever, chills, and night sweats. Purulent drainage was noted from pin sites. He was neurovascularly intact, and there was no concern for compartment syndrome. Magnetic resonance imaging was performed, being concerning for a collection at the proximal pin site.
Anteroposterior (A) and lateral (B) radiographs taken in splint at initial presentation. Anteroposterior (C) and lateral (D) radiographs taken after initial external fixation performed at another institution.
The patient was indicated for irrigation, debridement, and revision of external fixation. The procedure was performed under general endotracheal anesthesia without intraoperative complication (Figure 2). No significant attempt was made to pull the fracture further out to length during revision external fixation.
Intraoperative anteroposterior (A) and lateral (B) radiographs of the knee during revision external fixation. Intraoperative radiographs showing revision of femoral pin sites (C) and tibial pin sites (D) during revision external fixation.
One hour postoperatively, the patient was found to be in severe pain in the post-anesthesia care unit. Vital signs were significant for hypertension and tachycardia. He was unable to dorsiflex the ankle or extend the toes. He exhibited diminished deep and superficial peroneal sensation. Compartments were compressible. There was no increase in pain with passive stretching of the toes.
With concern over development of compartment syndrome vs nerve traction injury, the tension on the external fixation device was immediately released in the post-anesthesia care unit. Within 3 minutes of tension release, ankle dorsiflexion and toe extension returned. The patient was observed during the course of the subsequent hour, showing continuous improvement in symptoms and on physical examination.
No notable events occurred in the 3-day interval prior to definitive fixation (Figure 3). Intraoperative cultures from revision external fixation were positive for methicillin-sensitive Staphylococcus aureus. The patient was treated with appropriate antibiotics in accordance with infectious disease consultant recommendations. He was discharged 8 days after definitive surgery. At the 3-month postoperative follow-up, the patient had maintained alignment, appropriate healing, and no residual neurologic deficits.
Anteroposterior (A) and lateral (B) radiographs of the knee after definitive open reduction and internal fixation.
The diagnosis of nerve traction injury can be challenging, particularly when the differential diagnosis includes nerve injury by an alternate mechanism. In the current case, the clinical suspicion for nerve injury secondary to traction was greater than that for compartment syndrome, given the immediacy of the time course (ie, on waking from anesthesia) and the lack of clinical increases in compartment swelling or pressure on physical examination. Additionally, revision of external fixation was performed 7 days after the initial injury, during which time the structural integrity of the limb becomes more rigid in the setting of primary callus formation.4 The change in mechanical properties during the subacute period places nerves at greater risk for stretch injury, as surrounding soft tissue may contract and subsequent lengthening of the limb causes greater stretch over a contracted nerve.
Given findings of motor and sensory deficits without concomitant increase in compartment pressures, the decision was made to immediately address traction injury with release of tension on the external fixation device. The almost immediate return of sensation and muscle strength suggests that nerve deficits were in fact secondary to a nerve traction injury, resulting in local ischemia rather than of a compartment syndrome etiology.5–7
Preventing tissue ischemia is essential to preventing nerve palsy.8–15 Understanding biomechanical properties of peripheral nerve structures in response to tensile forces is crucial in any procedure that lengthens the overall course of the nerve, such as extremity reconstructions in both trauma and elective settings.
Biomechanical studies of peripheral nerves suggest that even a relatively small elongation or strain may cause significant electrophysiological changes. Sunderland and Bradley7 performed pioneering work on nerve injury and determined that the elastic limit of nerve deformation was in the range of 14% to 17% elongation, with mechanical failure at 18% to 23% strain.
Notably, the work of Sunderland and Bradley7 was performed in vitro. Subsequent models further elucidated in vivo peripheral nerve response to strain. Lundborg and Rydevik6 studied the effect of stretch on intraneural nerve circulation in rabbit tibial nerves and found a decrease in venous blood flow at 8% strain. Such decreases in blood flow cause conduction changes. Brown et al16 studied rabbit tibial nerves in relation to electrophysiological changes and found that 15% strain produced a significant drop (99%) in compound muscle action potential amplitude. Similarly, Wall et al5 studied a model of in situ stretch injury in rabbit tibial nerves. They showed that at 6% strain, the muscle action potential decreased by 70%; at 12% conduction, it was completely blocked. Notably, the subjects in the 6% strain group exhibited almost full recovery, whereas the subjects in the 12% strain group exhibited little recovery.
Although these experimental models offer useful parameters on which clinical practice can be based, the individual patient and the nerve at risk must be considered. The elasticity and tensile strength of nerves as well as the capacity to resist traction deformation vary, being both nerve and host specific.17 This phenomenon may be magnified to a greater extent in the upper extremity, which is even more notable for the development of nerve palsies. In a rabbit animal model, Takai et al8 studied in situ stress and strain causing brachial plexus conduction block. They found that when the nerve strain reached 8%, the compound muscle action potential was not evoked.
Clinicians must keep the above-mentioned parameters in mind when performing procedures that may lengthen an extremity. They must employ a broad differential diagnosis when considering nerve injury and must use the signs, symptoms, and time course of presentation to narrow the diagnosis. Clinicians must be aware of the nerve traction sequelae during the postoperative period, when, as seen in the current case, this pathology may be acutely reversed.
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- Einhorn TA. The cell and molecular biology of fracture healing. Clin Orthop Relat Res. 1998; 355(suppl):S7–S21. doi:10.1097/00003086-199810001-00003 [CrossRef]
- Wall EJ, Massie JB, Kwan MK, Rydevik BL, Myers RR, Garfin SR. Experimental stretch neuropathy: changes in nerve conduction under tension. J Bone Joint Surg Br. 1992; 74(1):126–129.
- Lundborg G, Rydevik B. Effects of stretching the tibial nerve of the rabbit: a preliminary study of the intraneural circulation and the barrier function of the perineurium. J Bone Joint Surg Br. 1973; 55(2):390–401.
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