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Original Research |
1 Clinics of Radiodiagnostics, Department of Radiology I, Innsbruck Medical
University, Anichstrasse 35, Innsbruck, Tirol 6020, Austria.
2 Clinics of Plastic Surgery, Innsbruck Medical University, Innsbruck, Tirol
6020, Austria.
Received July 2, 2004;
revised December 6, 2004;
Address correspondence to H. Gruber
(hannes.gruber{at}uibk.ac.at).
Abstract
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SUBJECTS AND METHODS. In this prospective study, both peroneal nerves in nine patients with one-sided peroneal nerve palsy after closed knee luxation and the peroneal nerves of 11 healthy volunteers were investigated with sonography. Using statistical analysis, we tried to define the comparability and significance of the findings.
RESULTS. The mean cross-sectional area of healthy peroneal nerves in the genicular region was 0.18 cm2 (SD, 0.07 cm2). Impaired nerves were significantly discerned because of their increased cross-sectional area at the level of the injury (mean cross-sectional area, 0.7 cm2; SD, 0.46 cm2; p < 0.05). Identification of caliber changes and depiction of at least one nerve stump were found to be the most specific criteria for the definition of a major neural lesion. The ability of sonography to provide additional information about surrounding soft-tissue impairment (scar tissue and hematoma formation) proved helpful.
CONCLUSION. Sonography allows radiologists to visualize neural and extraneural pathology and to define the exact level and extent of lesions. Thus, it may be a valuable adjunct in the decision of whether surgical intervention is necessary.
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Clinically, a patient with traumatic peroneal nerve palsy presents mainly with a drop foot accompanied by pain and a sensory deficit on the anterolateral skin of the leg. If this is apparent on initial presentation, the nerve is usually inspected during reconstructive knee surgery [4].
Traumatic lesions of peripheral nerves in general may be summarized into two broad categories: Major injuries, such as complete and incomplete nerve ruptures, are defined by partial or complete axonal interruption, whereas incomplete ruptures usually spare the outer nerve sheath. Minor injuries are usually followed by moderate regional neural edema of the impaired nerve section without interruption of any neural elements [5, 6].
Each nerve injury needs its dedicated therapy and should therefore be diagnosed as clearly and as early as possible [7, 8]. In up to 80% of knee luxations with associated peroneal nerve palsy, nerve function recovers spontaneously and completely under conservative management. The progress of recovery is routinely monitored by electroneurographic testing—that is, by electroneurography and electromyography [1, 3, 5, 6]. If spontaneous nerve regeneration does not occur within 6 months, it is common practice to surgically inspect the nerve at the site of possible trauma to search for complete or incomplete nerve interruption and extraneural impairment [9]. If a frank rupture of the nerve is detected, nerve repair or grafting is performed, with a reported satisfactory outcome in between 35% and 90% of the cases. The outcome depends strongly on the degree of neural damage and the surgical technique used [1, 2, 10–13].
Electrophysiologic testing is an important tool for the initial diagnosis of a nerve lesion in general and for follow-up of a nerve lesion. However, electromyography and electroneurography do not allow clear differentiation between neural and extraneural causes of nerve palsy or between a damaged but continuous nerve and a completely dissected nerve [1, 9].
Precise knowledge about the length and exact localization of a damaged nerve segment is essential for surgical intervention. On one hand, certain preoperative information about the overall state of an injured nerve (state of the neural and perineural tissue) is important because exploratory inspection of a nerve itself may lead to additional inadvertent damage. If, on the other hand, the surgeon, during genicular ligament reconstruction, inspects a nerve at the site of most probable injury only (limited neurolysis), he or she may sometimes by chance expose an unaffected section of a nerve. Because of the mechanism of nerve injury during traction, however, a more proximal or distal segment of the nerve may be severely damaged. A limited nerve inspection without preoperative knowledge about the site of nerve injury may thus give the false impression of an unimpaired nerve and wrongly lead to conservative treatment of the nerve lesion [14, 15].
In our study, we investigated the peroneal nerves (impaired and healthy sides) of nine patients with peroneal nerve palsy after knee dislocation by means of sonography. We thereby aimed at a clear definition of the damaged section and extent of the lesion and whether a major or minor injury with or without extraneural obstruction, according to the definitions of Sunderland [7], exists. In a pretrial study, we investigated 11 healthy volunteers to define the average normal dimensions, typical course, and sonographic appearance of the unimpaired peroneal nerve.
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The knees were slightly flexed (20°) with the ankle positioned on a cushion to allow the sonography transducer access to the popliteal region and to the lateral region of the shank. The common peroneal nerve was identified at the level of the sciatic nerve division. From there, it was followed distally to the peroneal nerve division and farther down to the penetration of the profound peroneal nerve between the fibular muscles. The shape, echotexture, integrity, and number of peroneal nerves in this region were recorded, and these data were stored electronically.
On transverse sonograms, the mediolateral and anteroposterior diameters and cross-sectional areas of the nerves were measured by standard measurement tools available on the HDI 5000 sonography scanner (i.e., caliper measurements). Measurements were performed at the level of the knee joint space and proximal fibular neck for the noninjured extremities of patients and volunteers and at the level of the maximum cross-sectional area in the genicular region of the injured ones. On longitudinal scans, the impaired nerves and their embedding tissue were assessed on the basis of the definitions of Sunderland [7], and the lesions were graded as minor damage (no rupture) or major damage (incompletely or completely ruptured).
For statistical analysis, the one-sided paired Student's t test was performed to compare the mean diameter and area measurements of the extremities of the volunteers with the noninjured nerves of the patients to check the comparability of the investigated subjects. Thereafter, data obtained from the impaired nerves were compared with the measurements taken in all healthy extremities (patients and volunteers) and evaluated statistically to show significant size alterations. A p value of less than 0.05 was considered to indicate a statistically significant difference in each evaluation.
Patients
In a prospective study from October 2001 to November 2003, nine consecutive
patients (seven male and two female patients; mean age, 36.2 years; age range,
15–75 years) presenting with peroneal motor palsy, sensory palsy, or
both after varus trauma with closed knee luxation after car (n = 4),
skiing (n = 3), motorbike (n = 1), and fitness center
(n = 1) accidents were examined with sonography. Knee luxation was
diagnosed with radiographs and CT scans, including coronal and sagittal
reformations.
All patients had undergone genicular reconstruction from a limited lateral popliteal access within an average delay of 2 days after the injury (range, 1–4 days). During the initial surgery, the peroneal nerves were inspected macroscopically and a limited neurolysis was performed in all patients. During this initial inspection, no changes of the peroneal nerves were documented by the surgeon.
Because peroneal palsy persisted after the initial reconstructive surgery, all patients underwent a thorough neurologic examination including electrophysiologic testing (electroneurography and electromyography). Sonography examinations of the impaired leg and unimpaired contralateral leg were performed following the algorithm described earlier. Clinical, electrophysiologic, and sonographic follow-ups were performed in all patients for at least 6 months after initial presentation.
During the sonography examinations of the impaired peroneal nerves, we looked for extraneural causes for nerve dysfunction such as hematoma, scarring, or soft-tissue derangement, and we recorded changes in the nerves themselves. Perifocal edema was defined as diffuse alteration in texture of hyperechoic soft tissue, poorly bordered and almost completely masking the texture of the perineural tissue on sonography. Scarring was defined as hyperechoic, streaky alteration of soft-tissue planes. Integrity of a peroneal nerve was basically defined according to the known morphologic criteria of healthy peripheral nerves on sonography—that is, by an intact outer nerve sheath and sustained continuity of all fascicular elements without caliber alterations exceeding the average norm defined in the pretrial investigation [9, 16–21].
Injured nerves were assessed as minor (no rupture) or major (incompletely or completely ruptured) damage. Complete nerve interruption was diagnosed if at least one nerve stump was clearly identified including a clear intraneural gap either with or without continuity of the hyperechogenic outer nerve sheath. Incomplete nerve disruption was defined by visualization of at least one clearly disrupted hypoechogenic fascicle group bordered by continuous fascicular elements including a local nerve waist and edematous neural fascicles (lost sharp lining at augmented caliber). A minor damaged nerve without interrupted fascicular elements was defined as sectional nerve-thickening with reduced or lost fascicular pattern, more intense hypoechogenic texture including loss of a sharp outer lining, thus indicating segmental neural edema.
The noninjured side of the patients was evaluated according to the algorithm used for the assessments of the volunteers.
At the time of the sonography examinations of the patients, the investigating radiologists were blinded to the results of electrodiagnostic tests (electroneurography and electromyography) and clinical examinations. Diagnoses were made in mutual consent.
Four patients underwent surgical reinspection with an altered and more extended approach due to the sonography findings.
Volunteers
Eleven healthy volunteers (seven men and four women; mean age, 38.4 years;
age range, 25–60 years) without any history of impairment in the knee
region were examined by means of sonography in a pretrial following the
standardized protocol described earlier. The shape, echotexture, topography,
and number of peroneal nerves were recorded, and the cross-sectional areas of
the peroneal nerves were measured at two levels each, as described
earlier.
All patients and volunteers had given informed consent for the procedures before the investigation was performed. All investigations were performed conformant to the Helsinki Declaration [22].
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The mean cross-sectional areas were 0.16 mm2 (SD, 0.05 cm2) at the level of the knee joint and 0.19 mm2 (SD, 0.06 cm2) at the level of the fibular neck. No statistically significant difference could be found for comparison of the measurements taken in the volunteers and in the nonimpaired legs of the patients (mean cross-sectional area: at the knee joint level, 0.16 cm2 [SD, 0.02 cm2], p = 0.24; and at the level of the fibular neck, 0.2 cm2 [SD, 0.06 cm2], p = 0.27).
Patients with Impaired Peroneal Nerves
In all nine patients, the peroneal nerve could clearly be identified and
visualized by means of sonography. Electrophysiologic data, sonography
findings and measurements, and summarized reports of secondary surgical
explorations are found in Table
1.
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Our sonography findings were confirmed directly by surgical reinspection in four patients: In one patient after a skiing accident (patient 1), the nerve appeared swollen but continuous and embedded in hyperechogenic edematous scar tissue, which hampered sonographic visualization proximal to the level of the knee joint space. In the accessible section, the nerve was thickened, with reduced fascicular pattern and lost sharp outer lining for approximately 10 cm, indicating intraneural edema caused by extraneural obstruction (minor lesion). The findings were confirmed at subsequent surgical nerve inspection because the surgeon who cared for the patient did not trust sonography findings and therefore limited neurolysis was performed.
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Another subject (patient 5) presented with persisting peroneal palsy after a skiing accident without evidence of functional recovery after primary surgical knee repair. On sonography, we were able to detect segmental swelling of the peroneal nerve with extraneural impairment and partially interrupted fascicle groups within the preserved outer nerve sheath (major lesion) (Fig. 2A). This situation was also confirmed at subsequent nerve inspection (Fig. 2B), where the nerve sheath was, in addition, found to be injected by fine inflammatory vessels. Loosening of the embedding perineural tissue, which impacted the injured nerve cross section, was performed by the surgeon in addition to peripheral fascicle sewing (personal report of the surgeon).
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The remaining five patients were treated conservatively with immobilization and transcutaneous electrical nerve stimulation. In these cases, sonography examinations could exclude major neural injuries and extraneural impairment, although one patient (patient 9) presented potential of denervation at electrophysiologic testing. In all these cases, only the neural echotexture was changed at different degrees, with lost or reduced hypoechogenic fascicular pattern and sharp outer hyperechogenic lining; however, the continuity of the fascicular elements was completely maintained (Fig. 3A, 3B, 3C).
The nine injured peroneal nerves presented with a significant augmentation of the measured maximum cross-sectional area (mean, 0.7 cm2; SD, 0.46 cm2) compared with the cross-sectional area of the nerves from the noninjured leg of the patients together with the nerves of the volunteer group (mean, 0.18 cm2; SD, 0.07 cm2) (p = 0.0046).
The sonography follow-up examinations of the conservatively treated patients showed restitution of normal peroneal nerve morphology on sonography (normalization of size and echotexture) after 6 months. In two patients, subtle persistent sensory deficits were still evident at neurologic testing.
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Luxation due to varus knee trauma results in instability and needs immediate surgical repair to restore satisfactory mechanical function of the articulation system [23, 24]. A concomitant injury of the peroneal nerve is reported to exist in approximately 15–25% of the cases. Here, the fibular neck works as a deflexion pulley, provoking different degrees of stretch lesions [3, 25–27].
The state-of-the-art workup of a potential nerve lesion includes a thorough clinical examination and electrodiagnostic studies. The latter are invaluable in helping to define the location of the lesion, grade the severity of the lesion, and predict recovery. Based on careful evaluation, one should be able to answer the following questions: Is a lesion present? If so, is the nerve likely to be in continuity (neurapraxia or axonotmesis), or is it transected or separated (neurotmesis)? Are any other associated conditions present? Where is the lesion? Is it a complete or an incomplete lesion? On the basis of the diagnostic results, one can estimate the most probable development and prognosis of a lesion and give a recommendation for further treatment.
Early surgery is generally indicated for injuries in which complete transection of a nerve is presumed or if the patient experiences an increasing neurologic deficit, which is often associated with a progressive pain syndrome. This can, for example, result from blunt trauma at a site of potential entrapment. The majority of nerve injuries from blunt trauma result in lack of continuity of lesion. When such a lesion is found, there is no way that its potential for recovery or the need for resection and repair can be determined on the basis of clinical and electrodiagnostic findings. Early operation is not indicated then; for 2–5 months, patients should be followed for clinical or electrophysiologic signs of regeneration on serial examinations.
However, care must be taken in interpreting subtle clinical or electrophysiologic hints of neural recovery because they do not guarantee recovery of effective function. In these cases, waiting longer for more definite clinical and electrical signs of reinnervation to occur may jeopardize end-organ integrity [28] and miss the most appropriate moment for effective and necessary surgical intervention.
With the given limitations of clinical examinations and electrodiagnosis, an imaging method that is able to provide clear information about an injured peroneal nerve would be helpful for the decision of whether conservative or surgical treatment is appropriate. Electroneurography and electromyography are problematic in this regard because they can identify neurotmesis (i.e., complete disruption of the axons and the outer nerve sheath), but cannot reliably distinguish between incomplete lesions (neurapraxia and axonotmesis). No information concerning potential extraneural impairments can be provided either (e.g., obstructing hematomas, encasing scar tissue). Nevertheless, minor nerve lesions caused by external obstruction are clearly an indication for surgery because recovery with conservative management is not to be expected [9].
Even in our small patient group, one false-positive result and one false-negative result were produced by electroneurography and electromyography concerning the indication for surgical reintervention. Both patients (one with signs of functional restitution at electrodiagnostic testing but nerve entrapment in extensive scar tissue and one with electrodiagnostic signs of denervation but only minor signs of nerve injury on sonography) would have undergone improper and potentially harmful therapy. Sonography, with its excellent soft-tissue resolution, generally proved valuable in this regard, reliably showing the state of the peroneal nerve and the condition of the surrounding soft tissues in all of our patients. The intraoperative situation of the impaired nerves of the four patients precisely correlated with our sonography findings.
In five patients, sonography was able to rule out major neural damage (in contrast to electrophysiologic tests) and extraneural impairment, which consequently led to a trial of conservative treatment, with achievement of recovery of nerve function at follow-up examinations (clinical, electrophysiologic, and sonography).
Sonography shows the recovery of a peroneal nerve by restitution of a normal fascicular pattern of a peripheral nerve, the standard caliber, and sharp outer lining.
As mentioned in several studies before this one, sonography of peripheral nerves requires experienced operators with profound knowledge of soft-tissue texture and topography and neural sonography. In addition, advanced technology sonography equipment with high-frequency linear-array transducers is indispensable [9]. Spatial resolution and contrast, and thus image quality, should be increased by pre- and postprocessing tools, such as compound imaging and multidirectional scanning, that reduce artifacts and improve presentation of small anatomic structures and pathologic processes. Nevertheless, soft-tissue alterations such as perineural edema or scar formation may hamper sonography assessments profoundly and may impede evaluations of an injured nerve at different degrees.
MRI, the only alternative imaging method we know of, has several problems concerning the assessment of peripheral nerves: the "irregular" and often not sufficiently predictable course, especially if the peroneal nerve makes planning an adequate scanning plane along the course of the nerve almost impossible. Imaging in high resolution is feasible with dedicated surface coils but only for limited nerve sections. These nerve sections of interest must be known beforehand, which is rarely possible and leads to disproportionately complex and time-consuming investigations. Without special surface coils, the inplane resolution of MRI is much lower than that of sonography and therefore does not permit assessment of subtle neural alterations in blunt peripheral nerve trauma. In our opinion, the present role of MRI can therefore be seen only in the assessment of perineural soft-tissue lesions that secondarily obstruct peripheral nerves. However, this impression is based on our limited experience with MRI of peripheral nerves, and there are no conclusive reports in the literature, to our knowledge, comparing sonography and MRI in the investigation of traumatic peripheral nerve lesions.
One limitation of our study is the small number of patients, which is due to the restrictive inclusion criteria, and thus a comparison of sonography findings with the gold standard (intraoperative presentation of the lesion) was possible in selected cases only. Validation of our results in a larger group of subjects is therefore certainly needed to reach a definite judgment of the potential of sonography for the diagnosis of traumatic peroneal nerve lesions.
In conclusion, our results show that sonography is a helpful tool in the assessment of distraction injuries of the peroneal nerve caused during knee luxation. Sonography allows major or minor injuries to be detected and the level and extent of the nerve lesion, if present, to be localized. This information is important for planning the most appropriate therapy (be it surgical or conservative) and helps to set the path for an optimum future prognosis for these lesions, which may otherwise result in longlasting medical and socioeconomic problems in a usually young and active group of patients.
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