• F Christ, C Keser, and J Groh.
• Institut für Anästhesiologie, Ludwig-Maximilians-Universität München.
• Anaesthesist. 1996 Dec 1; 45 (12): 1192-5.

AbstractThis case report describes paralysis of the plantar flexors and extensors after a total hip replacement in a 33-year-old woman performed under epidural anaesthesia (PDA). Six years previously, the patient had undergone a bone marrow transplantation for chronic myeloid leukaemia. She had developed a deep vein thrombosis, a pulmonary embolus, and a severe graft-versus-host reaction of the skin, leading to markedly reduced mouth opening. The hip operation was performed using PDA following antithrombotic prophylaxis with low-molecular-weight heparin. Blood could initially be aspirated after advancing the PDA catheter, and a second puncture of the epidural space 1 segment higher enabled correct placement of the catheter. The patient received 500 ml Dextran 60 perioperatively and the operation was completed without any further problems. The PDA catheter was removed 2 h after the operation following the return of movement of both thighs. Fourteen hours after the completion of surgery it was noticed that the dressing over the epidural puncture site was bloodstained, the patient was incontinent, and complete loss of movement of the operated leg was present. An epidural haematoma was the suspected cause, but could not be definitely confirmed by a CT scan. Nevertheless, a laminectomy was undertaken to evacuate the suspected haematoma. As expected, tracheal intubation was only possible bronchoscopically. Intraoperatively, some low-grade epidural oozing at the level of the initial puncture site was observed, and a hemilaminectomy of 5 was performed. For the first time postoperatively, the bleeding time was measured and was markedly prolonged to 20 min (as described by Mielke, normal value up to 8 min). A coagulopathy was suggested, with the differential diagnosis of impaired platelet function. The paralysis of the plantar flexors and extensors and some sensory loss were still present 6 months after the operation. It remains uncertain whether the PDA in a patient receiving low-molecular-weight heparin resulting in a the suspected epidural haematoma was the cause of the neurological sequelae and in agreement with the consultant neurologist, we believe that a direct traumatic lesion of the L5/S1 segment or damage to the sciatic nerve are also likely causes of the symptoms. Undoubtedly, the lack of adequate postoperative neurological monitoring and the intraoperative administration of dextran despite the known epidural vascular lesion deserve criticism. This case report demonstrates the often complex development of neurological complications after nerve blocks, where a definite cause can frequently not be determined.

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