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Journal of Postgraduate Medicine, Vol. 57, No. 2, April-June, 2011, pp. 126-128 Case Report Unilateral common peroneal nerve palsy following renal transplantation: A case report of tacrolimus neurotoxicity A Jain1, PJ Mathew1, M Modi2, K Mangal1 1 Department of Anaesthesia & Intensive Care, Post Graduate Institute of Medical Education and Research, Chandigarh, India Correspondence Address: A Jain, Department of Anaesthesia & Intensive Care, Post Graduate Institute of Medical Education and Research, Chandigarh, India, amitvasujain@gmail.com Date of Submission: 26-Sep-2010 Code Number: jp11033 PMID: 21654135 DOI: 10.4103/0022-3859.81871 Abstract Neurologic complications are not uncommon in renal transplant recipients. Acute femoral neuropathy, lumbosacral plexopathy, and sciatic neuropathy have been reported after kidney transplantation probably due to perioperative nerve compression and ischemia. To the best of our knowledge, common peroneal nerve (CPN) palsy has not been described in the early postoperative period following renal transplantation. Also, mononeuropathy due to tacrolimus (TAC) therapy has not been described so far. We report a case of isolated CPN palsy presenting as unilateral foot drop following renal transplantation and that improved only after replacing TAC with cyclosporine.Keywords: Common peroneal nerve palsy, peripheral neuropathies, renal transplantation, tacrolimus neurotoxicity Introduction Neurologic complications are not uncommon in renal transplant recipients. Postoperative peripheral neuropathies, including femoral, [1] lateral femoral cutaneous nerve, [1] ulnar, [2] and sciatic [3] nerves, have been reported in these patients. Factors, such as patient positioning and surgical handling, were implicated but none were associated with immunosuppressive therapy. Although common peroneal nerve (CPN) is one of the most common nerves involved in pressure-related neuropathy in postsurgical patients, CPN palsy as a complication of immunosuppressive therapy has not been reported after renal transplantation. We report a case of unilateral CPN palsy presenting as foot drop following renal transplantation and that improved only after tacrolimus (TAC) was completely discontinued and successfully replaced by cyclosporine. Case Report A 25-year-old man with end-stage renal disease was scheduled for allogenous kidney transplantation from a live related donor. The patient was on regular hemodialysis since 2 months and was asymptomatic since then. There was no evidence of peripheral or autonomic neuropathy in the preoperative period. He was premedicated with oral lorazepam 1 mg the night before and on the morning of surgery. Aspiration prophylaxis as oral omeprazole 40 mg and oral metoclopromide 10 mg was also given the night before and on the morning of the surgery. A 19-gauge epidural catheter was introduced at T11-T12 level before induction of anesthesia. Single attempt was successful and there was no blood tap. Anesthesia was induced with intravenous thiopentone 250 mg and fentanyl 100 μg and trachea was intubated with 8.5 mm I.D. endotracheal tube after adequate neuromuscular blockade with intravenous atracurium 25 mg. Isoflurane (0.8-1.0 %) in a mixture of oxygen and nitrous oxide (30:70) was used to maintain anesthesia. Intraoperative monitoring included noninvasive blood pressure, 5-lead electrocardiogram, pulse oximetry, nasopharyngeal temperature, end-tidal carbon dioxide, and central venous pressure. The patient was positioned supine for the surgery and measures were instituted to prevent hypothermia and pressure injuries. Intraoperatively 8 mL of 0.25% plain bupivacaine was administered for analgesia through epidural catheter. The total duration of surgery was 140 min. The trachea was extubated after return of consciousness and the patient was shifted to the intensive care unit with stable hemodynamics. The intraoperative urine output after transplantation was 250 mL. Postoperative analgesia was maintained with continuous epidural infusion of 6 mL (0.125%) bupivacaine for 24 h. Immunosuppressive therapy included oral TAC 0.2 mg/kg/d as two divided doses and oral prednisone 30 mg/d and was started 24 h before the surgery. The immediate postoperative period was uneventful. Foot drop of the left limb was observed on ambulation on the first postoperative day after recovery from epidural analgesia. Serum TAC level was 13 ng/mL (target concentration 10-15 ng/mL) during this period. A thorough neurologic examination revealed power of 0-1/5 in the dorsiflexor group of muscles. There was no associated sensory loss or any other neurologic deficit. Nerve conduction study revealed nonstimulable left peroneal nerve, suggestive of axonopathy with normal study of other peripheral nerves. Magnetic resonance imaging (MRI) of spine was normal. Pressure-induced CPN palsy was considered and conservative treatment was planned initially. There was no sign of improvement, and nerve conduction abnormality persisted after 3 weeks. TAC dose was then reduced to 0.15 mg/kg/d (25% reduction) but was of no benefit. Subsequently, TAC was switched to cyclosporine. Over the next few days he showed rapid and progressive improvement. He recovered fully and was discharged home after 2 months. Discussion We report left acute CPN palsy postoperatively in a renal transplant recipient that improved only after TAC was completely discontinued. CPN palsy after surgery with lithotomy position has been widely reported. Although extremely uncommon and an unexpected complication after surgery with supine position, CPN palsy has been reported following surgeries, such as robotic-assisted laparoscopic hemicolectomy, [4] liver surgery, [5] anterior cervical operation, [6] and cardiothoracic surgery. [7] Compression of the nerve with or without long duration of surgery and intraoperative hypotension were the factors involved. However, TAC as a cause for CPN pasly in the early postoperative period following renal transplantation has not been described in the literature. Neurotoxicity can be a serious complication due to the immunosuppressive regimen after renal transplantation. About 10%-28% of patients who are treated with calcineurin inhibitors (CNIs) develop some form of neurotoxicity. [8] This includes tremors, paraesthesias, and acute polyneuropathy that are more common with TAC than cyclosporine. Masri et al. described a case of pediatric renal transplant recipient who developed right brachial neuritis considered to be a neurotoxic manifestation of TAC. [8] Furthermore, cyclosporine has been associated with unilateral foot drop in a renal transplant patient. [9] The precise mechanism of peripheral neurotoxicity of CNIs, such as TAC, still remains unknown. The pathogenesis may be similar to that of central white matter lesions, where injury to both the major and minor vasculature may cause hypoperfusion or ischemia and local secondary toxicity in the white matter. [8] As in this case and reports from various other investigators, failure to respond to dose reduction raises the possibility of idiosyncrasy, particularly when the levels of TAC are within the desired therapeutic range. [8],[10] In such patients, prolonged exposure to even a lower dose of TAC not only may fail to reverse neurotoxicity but may result in irreversible neurologic damage. [11] Typically, improvement and eventually full recovery only occurred after TAC was completely discontinued and successfully replaced by cyclosporine. [10] The Naranjo Probability score [12] of 3 also suggests TAC as a possible cause of unilateral foot drop in our patient. Electrolyte and metabolic disturbances, such as hyper- or hyponatremia, hypomagnesemia, hypoglycemia, and hypercholesterolemia, have been implicated for CNS neurotoxicity, [10],[13] but none was present in our case; similarly, onset has often been associated with high blood pressure and fluid overload, [10] which were also not features of this case. It has been suggested that high levels of TAC may contribute to an early onset of neurotoxicity, but can occur with normal levels. [9],[10] The toxic effect due to abnormal metabolism of TAC by hepatic enzyme remains another possibility. The proton pump inhibitors, such as omeprazole, potentially inhibit metabolism of TAC and cyclosporine on CYP3A4 and increase their blood concentration in patients with CYP2C19 gene mutations. [14] Although we did not analyze our patient for CYP2C19 gene mutation, concentration-dose ratio of TAC was within normal limits, and thus ruled out this possibility. Severe neurotoxicity in renal patients is usually multifactorial. Subclinical uremic neuropathy contributing to the manifestation of TAC-mediated toxic neuropathy cannot be ruled out. The epidural catheter placement can also be implicated to cause postoperative nerve palsy. However, the catheter placement was atraumatic, postoperative MRI spine was normal, and the patient improved only after discontinuation of TAC favoring the diagnosis of TAC-induced CPN palsy. We were fortunate that our patient improved after TAC was replaced by cyclosporine. However, switching to CIN-free immunosuppression, for example, sirolimus and mycophenolate mofetil, might have been equally or more effective alternative to manage TAC-induced neurotoxicity. [15] In patients for whom a reduction or withdrawal of CINs would result in an increased risk of rejection, successful treatment of other causes of endothelial injury may also produce recovery. [16] In conclusion, we have discussed TAC as a rare but possible cause of unilateral common peroneal axonopathy in early postoperative period following renal transplantation. Anesthesiologists involved must be aware of the potential complication. Furthermore, quick recognition of TAC as a neurotoxic drug is important as recovery is very likely to be dependent on complete discontinuation of the drug. Replacing TAC with cyclosporine in this situation is a justified and a reasonable approach. References
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