Neuropathy in Diabetic Patients After TKA

Diabetic neuropathy is one of the most recognized common complications of diabetes mellitus. It is estimated that diabetes mellitus is prevalent in nearly 6% of the US population.¹ Of which 7.5% are estimated to have evidence of neuropathy at time of diagnosis.¹

Peripheral neuropathies following arthroplasty are well known entities. An incidence of neuropathy has been reported between 0.1% and 5.9% after primary total hip arthroplasty (THA).^2,3 In revision THA the incidence of neurologic complications increases to 2.0% to 7.6%.² Neuropathies often involve the sciatic and femoral nerve distributions. Postoperative neuropathy also is a well-known complication after total knee arthroplasty (TKA). Neuropathy commonly involves the distribution of the peroneal nerve and is rarely seen in the tibial nerve. Several studies have reported an incidence of peroneal palsy from 1% to 10%.^4-6 The likelihood of nerve palsy has been associated with flexion contracture, valgus deformity, postoperative epidural anesthesia, external leg compression, tourniquet time, and postoperative hematoma.^4-7

Few reports exist in the literature that investigate neurologic complications of patients with diabetic neuropathy after TKA. This article presents two cases of polyneuropathy in patients with diabetes following TKA.

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Case Reports

Patient 1

A 54-year-old obese non-insulin dependent diabetic man with severe tricompartmental osteoarthritis of the knees (Figure 1) underwent cemented bilateral primary TKA with the Smith & Nephew Genesis II total knee system (Memphis, Tennessee) (Figure 2). Preoperatively the patient was without flexion contractures, valgus deformity, or evidence of diabetic neuropathy.

On postoperative day 2 he reported numbness over the plantar aspect of his left foot, as well as numbness of the right toes. On examination he was noted to have 4/5 quadriceps and hamstring strength bilaterally. Range of motion was 0° to 75° bilaterally. He was noted to have 2/5 dorsiflexion of the right ankle. He was also noted to have decreased sensation to pin prick plantarly of the left foot and absence of sensation over dorsum of the right foot.

On postoperative day 3, the patient had a continued foot drop and diminished sensation with slight improvement of symptoms on removal of compressive dressings. On postoperative day 4 the patient was ambulating with a front-wheeled walker and an ankle foot orthosis.

At discharge the etiology of his neuropathy was unknown. The patient’s neurological deficits persisted over the next 12 weeks. He subsequently underwent electrodiagnostic studies 3 months postoperatively. The patient was diagnosed with disturbances of the tibial, deep, and superficial peroneal, and sural nerves of the right foot, as well as a sural nerve deficit of the left foot. The patient continued in an outpatient therapy program, working on higher-level mobility skills and resuming activities of daily living.

Patient 2

A 56-year-old obese non-insulin dependent diabetic woman underwent revision right TKA secondary to recurrent arthrofibrosis 11 months after primary TKA (Figure 3). Preoperatively, she was noted to have range of motion from 30° to 70° without clinical evidence of neuropathic deficits and well fixed and well positioned components on plain radiographs. She underwent synovectomy and revision cemented TKA with the Smith & Nephew Genesis II system (Figure 4). She was noted to have intraoperative ROM 0° to 90°.

Immediately postoperatively she was noted to have 5/5 motor strength on testing of dorsiflexion and plantarflexion and sensate to touch over the tibial, peroneal, sural, and saphenous nerve distributions. On postoperative day 1 after redosing of epidural, she continued to have 5/5 motor strength, however she reported decreased sensation over the peroneal and tibial distributions.

On postoperative day 2 she was noted to have complete absence of motor and sensory function to the tibial, peroneal, saphenous, and sural nerves below the knee. She subsequently underwent hematoma decompression and evacuation. Intraoperatively, no large hematoma or notable neurovascular damage was noted.

At 3-week follow-up, she was not noted to have improvement of her motor and sensory deficits in the right lower extremity. Electrodiagnostic testing of the extremity revealed right sural and superficial peroneal sensory neuropathies as well as peroneal and tibial motor neuropathies. She was prescribed Gabapentin 300 mg 3 times daily and encouraged to continue her rehabilitation program.

Discussion

Neural ischemia due to compression has been proposed as a possible cause of neuropathy. The association between the use of pneumatic compression devices and the development of neuropathy has been well documented. The mechanism of injury appears to be direct mechanical pressure on local tissue and nerve, and resultant ischemia due to the tourniquet effect.

Numerous studies have shown that pressures >300 mm Hg for >120 minutes may be enough to produce transient neuropathies.⁸ Horlocker et al⁸ retrospectively reviewed 361 TKAs performed on 292 patients, 30 of whom had diabetes. They revealed a correlation between prolonged tourniquet time and peroneal but not tibial nerve palsy. Several factors may render the peroneal nerve more sensitive to tourniquet ischemia than the tibial nerve, including smaller size, less protective epineurium, and inferior vascular supply.

Horlocker et al⁸ also identified a preexisting neuropathy as a contributing factor to the development of clinically significant nerve palsy after TKA. Upton and McComas⁹ hypothesized that nerve fibers that have been compressed proximally are more vulnerable to injury at another site. In this scenario, known as the double crush phenomenon, a proximal nerve lesion causes a reduction in axonal flow and neural transmission resulting in clinically significant neurologic outcomes.⁹

The use of epidural anesthesia also has been associated with an increased risk of neuropathy after TKA. Several studies have proposed that injury to the lumbrosacral plexus may occur during catheter placement.^8,10 Injury to the plexus typically produces a diffuse neurologic deficit because the L4-S2 roots from which the peroneal and tibial nerves also innervates other peripheral nerves of the lower extremity.

Idusuyi and Morrey⁶ reported the use of epidural anesthesia was significantly associated with the presence of peroneal nerve palsy. Fifteen of 18 patients who had received epidural anesthesia were noted to have a palsy after discontinuation of the epidural.⁶ They also noted the relative risk of palsy was 2.8 times greater for patients who had received epidural anesthesia for TKA than for those who received general or spinal anesthesia.⁶ It is believed that epidural anesthesia decreases proprioception and sensory stimuli. Thereby, allowing the limb to rest in an unprotected state making susceptible to neurologic ischemia from local compression. In addition, intraoperative neurological damage may not have been readily apparent in the immediate postoperative period due to ongoing effects of epidural anesthesia.^6,8

Previous studies have identified the association of preoperative valgus or flexion deformities and nerve palsies. The presence of valgus deformities of >10° and flexion contracture of >20° may lead to increased risk of nerve damage after correction.^5-7

The etiology of neuropathy after TKA is multi-factorial. Neuropathy can be a major cause of morbidity, especially in patients with diabetes. Most diabetic patients are assymptomatic despite impaired conduction velocity, loss of stretch reflexes, and vibratory sensations.¹ As such, the operating surgeon should be mindful of potential deleterious outcomes in diabetic patients after TKA. Morbidity can be minimized by limiting tourniquet use, limiting epidural anesthesia, avoiding restrictive dressings, and avoiding aggressive correction of valgus deformities and flextion contractures.

References

1. Horowitz SH. Diabetic neuropathy. Clin Orthop Relat Res. 1993: 296:78-85.
2. Nercessian OA, Macaulay W, Stinchfield FE. Peripheral neuropathies following total hip arthroplasty. J Arthroplasty. 1994; 9:1048-1054.
3. Moeckel B, Huo MH, Salvati EA, Pellicci PM. Total hip arthroplasty in patients with diabetes mellitus. J Arthroplasty. 1993; 8:279-284.
4. Asp JP, Rand JA. Peroneal palsy after total knee arthroplasty. Clin Orthop Relat Res. 1990; 261:233-237.
5. Schinsky MF, Macaulay W, Parks ML, Kiernan H, Nercessian OA. Nerve injury after primary total knee arthroplasty. J Arthroplasty. 2001; 16:1048-1053.
6. Idusuyi OB, Morrey BF. Peroneal nerve palsy after total knee arthroplasty. Assessment of predisposing and prognostic factors. J Bone and Joint Surg Am. 1996; 78:177-184.
7. Rose HA, Hood RW, Otis JC, Ranawat CS, Insall JN. Peroneal nerve palsy following total knee arthroplasty. A review of The Hospital for Special Surgery experience. J Bone and Joint Surg Am. 1982; 64:347-350.
8. Horlocker TT, Cabanela ME, Wedel DJ. Does postoperative epidural analgesia increase the risk of peroneal nerve palsy after total knee arthroplasty? Anesth Analg. 1994; 79:495-500.
9. Upton ARM, McComas AJ. The double crush in nerve entrapment syndromes. Lancet. August 1973; 2:359-361.
10. Cohen DE, Van Duker B, Siegel S, Keon TP. Common peroneal nerve palsy associated with epidural analgesia. Anesth Analg. 1993; 76:429-431.

Authors

Drs Holland is from William Beaumont Army Medical Center, El Paso, Texas, and Dr Sands is from Harbin Clinic Orthopaedics and Sports Medicine, Rome, Georgia.

Dr Holland has no relevant financial relationships to disclose. Dr Sands is a paid consultant for Smith and Nephew.

Correspondence should be addressed to: Courtney A. Holland, MD, US Army Medical Corps, William Beaumont Army Medical Center, Dept of Orthopedics, 5005 N Piedras St, El Paso, TX 79912.