Zivcić-Cosić Stela, Stalekar Hrvoje, Mamula Mihaela, Miletić Damir, Orlić Lidija, Racki Sanjin, Cicvarić Tedi
Department of Nephrology and Dialysis, Clinic for Internal Medicine, University Hospital Center Rijeka, School of Medicine, University of Rijeka, Rijeka, Croatia.
Acta Med Croatica. 2012 Oct;66 Suppl 2:76-80.
Avascular bone necrosis is a relatively rare but significant complication in renal transplant recipients because it causes progressive pain and invalidity. It can be the consequence of the action of numerous causative factors, but it is mostly connected to corticosteroid treatment.The underlying pathophysiologic mechanism is a diminished blood flow to the bone leading to necrosis and bone destruction. During the past 25-years period, 570 renal transplantations and five combined kidney and pancreas transplantations were performed in our centre. A part of the patients was lost to follow-up due to the separation of Croatia from the former Republic of Yugoslavia. After transplantation, we revealed aseptic necrosis of the femoral head in five female patients. All patients had a history of treatment with pulse doses of corticosteroids. At transplantation the average age of the patients was 52.2 yrs (range 46 to 62 yrs), and dialytic treatment before transplantation lasted in average 9.2 yrs (range 2.5 to 21.2 yrs). The period between renal transplantation and the development of clinical signs of avascular bone necrosis lasted in average 1.2 yrs (range 0.3 to 2.3 yrs). We will demonstrate our 62-year old female patient with terminal renal failure caused by post-streptococcal glomerulonephritis, who was treated with peritoneal dialysis 2.5 years before renal transplantation. Twenty months before renal transplantation the patient received pulse doses of corticosteroids, together with immunoglobulins and plasmapheresis, for the treatment of an acute polyradiculoneuritis Guillaine Barré. After transplantation a standard immunosuppressive protocol was applied which included tacrolimus, mycophenolate mofetil, corticosteroids and induction with basiliximab. Four months after transplantation the patient started to feel pain in the right hip after longer standing, in addition to the earlier long-lasting problems caused by bilateral coxarthrosis. The pelvic radiograph showed subchondral radiolucencies in the lateral part of the head circumference spreading into the proximal part of the neck of the right femur, which indicated the presence of aseptic necrosis, but these changes could have also been caused by coxarthrosis. Unexpectedly, magnetic resonance imaging (MRI) did not reveal changes characteristic for avascular bone necrosis. Due to the progressively worsening of pain and the radiographic finding, the patient was submitted to decompression surgery of the femoral head. The surgical procedure was performed under diascopic guidance (C-arm) which allowed the correct positioning of a Kuerschner wire. A cannulated drill (diameter 4.0 mm) was placed over the wire and we performed two drillings of the spongiosis of the femoral head through to the subchondral area. Postoperatively, the patient was soon verticalized and advised to walk with crooks during a period of six weeks. This time is necessary to allow the mineralisation and strengthening of the bone which is now better vascularised. The patient recovered well and had no more pain. In renal transplant recipients it is most important to raise suspicion and verify the presence of avascular bone necrosis early, because timely bone decompression surgery can eliminate pain and cure the patient or it can prevent or delay bone destruction. When clinical signs of avascular bone necrosis arise and radiographic or standard MRI findings are negative, additional investigations (i.e. SPECT or MRI with contrast) should be performed to confirm or exclude the diagnosis. In latter phases of the disease, surgical decompression of the femoral head cannot lead to permanent amelioration, and it is inevitable to perform more invasive surgical procedures like "resurfacing" or bone grafting in younger patients, or the implantation of total hip endoprotheses.
无血管性骨坏死在肾移植受者中是一种相对罕见但严重的并发症,因为它会导致进行性疼痛和残疾。它可能是多种致病因素作用的结果,但大多与皮质类固醇治疗有关。潜在的病理生理机制是骨血流减少,导致坏死和骨破坏。在过去25年期间,我们中心进行了570例肾移植和5例肾胰联合移植。由于克罗地亚从前南斯拉夫共和国独立出来,部分患者失去了随访。移植后,我们发现5名女性患者出现股骨头无菌性坏死。所有患者都有脉冲剂量皮质类固醇治疗史。移植时患者的平均年龄为52.2岁(范围46至62岁),移植前透析治疗平均持续9.2年(范围2.5至21.2年)。肾移植与无血管性骨坏死临床症状出现之间的时间平均为1.2年(范围0.3至2.3年)。我们将展示一名62岁的女性患者,她因链球菌感染后肾小球肾炎导致终末期肾衰竭,在肾移植前2.5年接受腹膜透析治疗。肾移植前20个月,患者接受脉冲剂量皮质类固醇,联合免疫球蛋白和血浆置换,用于治疗急性格林 - 巴利多发性神经根神经炎。移植后应用标准免疫抑制方案,包括他克莫司、霉酚酸酯、皮质类固醇和巴利昔单抗诱导治疗。移植后4个月,除了双侧髋关节病引起的早期长期问题外,患者长时间站立后开始感到右髋疼痛。骨盆X线片显示股骨头圆周外侧部分的软骨下透亮区扩展至右股骨颈近端,提示存在无菌性坏死,但这些改变也可能由髋关节病引起。出乎意料的是,磁共振成像(MRI)未显示无血管性骨坏死的特征性改变。由于疼痛逐渐加重和X线表现,患者接受了股骨头减压手术。手术在透视引导(C形臂)下进行,这允许正确定位克氏针。将空心钻(直径4.0毫米)置于针上,我们对股骨头的松质骨进行了两次钻孔直至软骨下区域。术后,患者很快就可以直立,并建议在六周内使用拐杖行走。这段时间对于使现在血管化更好的骨矿化和强化是必要的。患者恢复良好,不再疼痛。在肾移植受者中,最重要的是早期提高怀疑并核实无血管性骨坏死的存在,因为及时的骨减压手术可以消除疼痛并治愈患者,或者可以预防或延迟骨破坏。当出现无血管性骨坏死的临床症状且X线或标准MRI检查结果为阴性时,应进行额外检查(即SPECT或增强MRI)以确诊或排除诊断。在疾病的后期阶段,股骨头手术减压不能导致永久性改善,对于年轻患者不可避免地要进行更具侵入性的手术,如“表面置换术”或骨移植,或全髋关节假体植入。