Epidural bleed and quadriplegia due to acquired platelet dysfunction unrelated to multiple spinal and epidural puncture (2003)

EDITOR: We present a patient who developed an epidural haematoma at the cervical and upper thoracic level that resulted in tetraplegia. However, this was not due to multiple spinal and epidural punctures at the lumbar and lower thoracic level for several orthopaedic procedures over several weeks of care. A 58-yr-old male, with no previous history of bleeding disorders, presented to the orthopaedic department with a tumour of the right femur. The diagnosis of a high-grade fibrosarcoma was confirmed by an open biopsy under spinal anaesthesia. A total resection of the femur and a reconstruction with a total femur megaprothesis was then performed under combined epidural and general anaesthesia; insertion of the epidural catheter at T11-T12 was uneventful. Patient-controlled epidural analgesia (PCEA) was initiated for relief of pain after operation. Three weeks later, a metastasis resection of the left femur with cemented osteosynthesis was performed, with epidural anaesthesia at L3-L4. Insertion of the epidural catheter was reported to have been technically difficult, but without complications. After 4 weeks, a revision due to haematoma formation in the right leg became necessary, which was performed under uneventful spinal anaesthesia at L3-L4. Another revision, again to stop haemorrhage, was performed 3 weeks later under epidural anaesthesia at L3-L4, and again PCEA was used. Investigations by haematologists 10 days after this revision did not reveal any specific disorders of coagulation. Primary haemostatic capacity was investigated by the PFA-100® Analyser (AD-TECH Communications, Hollywood, CA, USA), which measures primary haemostasis in vitro by uniquely simulating the in vivo hemodynamic conditions of platelet adhesion, activation and aggregation; and was on two occasions with 103 and 69 s (reference value 71-118 s) for closing time by a collagen/adenosine diphosphate (ADP) probe cell and closing times of 97 and 74 s (reference value 85-165 s) for closing time by a collagen/ epinephrine probe cell. This was interpreted as a normal primary haemostatic capacity without a clinically relevant decrease of platelet function. For further revision and explantation of the tumour prosthesis, regional anaesthesia was administered via the epidural catheter that had been inserted 16 days previously. Three days later, computed tomography (CT)-guided drainage of a lesion - highly suspicious for abscess and osteomyelitis in the pelvis - was undertaken. The epidural catheter was removed 26 days after insertion. Because of further haematoma formation in the right thigh and an abscess in the iliosacral joint, another revision was scheduled 2 weeks later. The right paramedian approach to the epidural space at L3-L4 using an 18-G Tuohy needle led to a loss of resistance at 6 cm, with bright red blood being withdrawn. A second puncture at L3-L4, using a lateral approach, led to a comparable incident - bright red blood was very easily withdrawn through the Tuohy needle. The quantity of blood was quite different from that seen with an 'ordinary' bloody tap. In the view of the patient's condition and his clearly stated preferences, a further epidural puncture was performed at the L2-L3 level using a left lateral approach. This was uneventful, with the catheter being inserted 5 cm into the epidural space with the needle in the cranial direction. However, approximately 7 min after placement, the catheter started to drain blood. The anaesthetic was changed to general anaesthesia. For postoperative pain control, intravenous PCA was used. Owing to the bloody punctures and abnormal coagulation parameters postoperatively, the epidural catheter was left in situ, and the patient was closely monitored by the acute pain service. Two days later, motor weakness in the left leg was noted. No sensory or motor pathologies in the right leg or upper extremities were detected. The epidural catheter was removed after verification that the plasma coagulation variables and platelet count were within normal ranges. On the evening of the same day, a paresis of the left arm was documented for the first time. Acute intracranial haemorrhage was excluded by cranial CT, which revealed signs of a previous ischaemic insult in the right hemisphere. However, since a recent ischaemic insult could not be excluded, therapeutic anticoagulation with heparin was initiated with a partial thrombin time between 70 and 80 s. Two days later, the patient developed a massive retroperitoneal haematoma, which necessitated immediate surgical intervention under general anaesthesia. The patient did not recover consciousness, but immediate CT did not reveal any new pathology. Although consciousness gradually returned after 24 h, the patient was tetraplegic. Immediate magnetic resonance imaging (MRI) showed evidence of an epidural haematoma extending from C2 to T3-T4 (Figs 1 and 2). MRI of the lower spine was unremarkable. There was no evidence of bleeding at the site where the multiple neuraxial blocks had been performed. Somatosensory and motor-evoked potentials did not elicit a cortical response. Motor and sensory function did not recover any further, and the patient was required to be artificially ventilated because of diaphragmatic paralysis. Since haemorrhage from the various surgical sites continued, requiring further blood transfusions, surgical decompression of the spinal cord was rejected. An analysis of platelet functional capacity conducted by a platelet research laboratory revealed an acquired severe thrombocytopathy with reduced fibrinogen binding and decreased CD62 and CD63 expression induced by thrombin or collagen. The expression of CD62 and CD63 reflects the secretion of platelet α-granules and dense bodies, respectively. This secretion is important for strengthening the thrombus. The team of orthopaedic surgeons and neurosurgeons decided that a decompressive laminectomy for a haematoma over five segments in a patient with thrombopathy was unlikely to be successful. The patient was ultimately transferred to a centre specializing in rehabilitation after spinal cord injury, but died 5 months after the initial diagnosis of a femoral fibrosarcoma.Figure 1: Magnetic resonance image of the cervical spine. The sagittal T2 image (TSE 3800/91) reveals a large posterior epidural collection that is mainly hypointense to cerebrospinal fluid and markedly compresses the dural sac from C2 to T3. Additionally, the spinal cord shows a long segment of abnormal increased intramedullary signal due to compression. Note small areas of increased signal within the epidural haematoma that suggest subacute blood collection (methaemoglobin) within an acute haematoma.Figure 2: Axial T2 image (GRE 550/18/20) showing dorsolateral extension of the haematoma in the posterior epidural space markedly deforming the thecal sac. There is an anterior rim of diminished signal that is felt to represent a combination of displaced dura and haemorrhagic components at the periphery of the haematoma in a different stage of evolution.In this patient, there was no obvious relationship between the blocks performed and the development of an epidural bleed. It demonstrates that spinal and epidural puncture in patients with coagulopathy will not necessarily produce an epidural haematoma, and how the blame for an epidural haematoma can be erroneously assigned to needle puncture. The incidence rate of paresthesiae and neurological injuries has been reported as ranging between 0.01 and 0.001% [1,2]. The most devastating complication is paraplegia caused by an epidural haematoma. Three instances of paraplegia, induced by spinal haematomas, out of 18 000 epidural blocks, have been reported in patients with compromised haemostasis. Other investigators experienced no complications in 100 000 patients receiving central neuraxial anaesthesia or analgesia [3], or in 4185 patients undergoing thoracic epidural anaesthesia [4]. To avoid epidural haematoma, it is essential to observe published guidelines and recommendations [5]. In addition to evaluating the coagulation profile thoroughly, it is extremely important to take a detailed history of the patient's preoperative medication, not forgetting enquiry about new inhibitors of thrombocyte aggregation (e.g. clopidogrel or ticlopidine), and any history of bleeding. The recurrent bleeding disorders in this patient were apparently due to a complex acquired platelet dysfunction that could not be detected using routine general coagulation tests or with the factor analysis conducted after consultation with haematologists. Only sophisticated experimental assays, not available in clinical practice, allowed the diagnosis of the acquired thrombopathy in our patient. Heparinization to improve the possible cortical infarct might also have further impaired haemostatic capacity, leading to the epidural haematoma. After a central neuraxial block, patients must be observed or monitored until the level of regional anaesthesia has declined by at least two segments. Special attention should be given to detecting persistent sensory or motor blocks, radicular back pain and urinary retention. If there are any clinical signs of an epidural haematoma, diagnostic and therapeutic procedures should be initiated immediately. The procedure of choice is MRI, which allows the extent of the haemorrhage to be determined. If MRI is unavailable, CT or myelography should be performed immediately. If the results are positive, an immediate laminectomy can improve the patient's prognosis. Even though there was no direct causal relationship between the neuraxis blocks and epidural bleeding in our patient, spinal and epidural punctures should only be performed after thorough evaluation when active bleeding occurs, despite a normal coagulation profile. T. P. Weber H. Van Aken B. E. Kehrel A. Meißner Department of Anaesthesiology and Intensive Care Medicine; University Hospital of Münster; Munster, Germany T. Brüssel Department of Anaesthesia and Pain Management; The Canberra Hospital; University of Sydney; Sydney, Australia V. Bullmann W. Winkelmann Department of Orthopaedics; University Hospital of Münster; Munster, Germany W. Heindel Department of Radiology; University Hospital of Münster; Munster, Germany N. Rolf Department of Anaesthesiology and Intensive Care Medicine; Marienkrankenhaus GmbH; Hamburg, Germany