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© 2001 International Anesthesia Research Society
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Introduction |
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Patients receiving oral or transdermal pharmacologic therapy with opioids and adjuvant therapy may experience adequate pain control in 80%–90% of the cases, provided that this therapy is administered by applying aggressive guidelines over time (1). Thus, in the other 10%–20% of the patients, some form of invasive therapy will be required (2). Neuraxial analgesia via an indwelling epidural or intrathecal catheter may provide analgesia to patients with cancer who do not achieve adequate pain control with aggressive systemic opioid or adjuvant therapy (1,2). Moreover, these techniques are indicated when severe pain cannot be controlled with noninvasive alternatives because of side effects, when there is a need for a local anesthetic to control a strong neuropathic component, or when patient preference supports their use.
Neuropathic pain associated with tumor invasion of neural structures is extremely difficult to control with systemic opioid or adjuvant therapy. We present a case of a patient with colon carcinoma with metastasis to the sacrum and sacral roots who developed paraplegia shortly after lumbar epidural analgesia was started. This rare problem adds to the list of the differential diagnosis of postepidural paraplegia.
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Case Report |
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TopIntroductionCase ReportDiscussionReferences |
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A 47-yr-old woman was referred to our pain service for intractable pain in her left pelvis, hip, and leg, but she had no complaint of any back pain problems. She had metastatic colon adenocarcinoma to the liver, lung, and left iliosacral region. Her symptoms did not improve with a course of radiotherapy to the sacral region. Despite titration of her medication (a transdermal fentanyl patch 175 µg/h q 72 h, hydromorphone 2–4 mg per os [PO] q 3 h as needed for breakthrough pain, rofecoxib 25 mg PO q 24 h, desipramine 150 mg PO at night [q HS], gabapentin 300 mg PO 3 times a day, and metoclopramide 20 mg PO before meals and q HS), she still had significant pain, and epidural analgesia was planned. There was no history of urinary retention or loss of sphincter function. Her physical examination was normal except for hepatomegaly 3 cm below the right costal margin. Her neurological evaluation showed sensory function to be normal, with the exception of an area of numbness in the left S1 distribution. Deep tendon reflexes were normal except for a decreased left ankle response. Flexion and extension of her hips, knees, and feet were normal. There was no back or leg pain on straight leg raise or abduction of the hips. Preprocedure prothrombin time was 15.3 s (upper limit of normal 15.3 s, international normalized ratio 1.4), partial thromboplastin time was 24 s, and platelet count was 435,000. During catheter insertion at the L4-5 interspace, the patient experienced persistent paresthesias in the posterior aspect of her left thigh, and the catheter was removed. A second attempt at the same interspace was successful, and the catheter was easily advanced 5 cm into the epidural space. After negative aspiration for cerebrospinal fluid or blood, and after a negative test dose of 3 mL 1.5% lidocaine with epinephrine 1:200,000, the catheter was secured. No blood was obtained during either of the catheter placements. An additional 5 mL bolus of 2% lidocaine was injected to confirm the presence of an adequate sensory block. The patient reported full pain control and was able to ambulate and sit on the toilet on her own for the first time in several months. She was discharged home 4 h after the insertion of the catheter with an infusion of hydromorphone 0.033 mg/mL, ropivacaine 2 mg/mL, and clonidine 4 µg/mL at 3 mL/h.
That evening, 12 h after therapy had been started, the patient came back to the hospital complaining of numbness and paralysis of both legs and inability to stand on her own. She had no sensory neurological abnormality above the waist. She was admitted to the hospital, the epidural infusion was discontinued, and her neurological condition improved over the next 4 h. However, she remained unable to flex both of her hips beyond 20 degrees. The rest of her neurological examination returned to baseline. Because she had persistent neurologic deficit, an emergency magnetic resonance imaging scan (MRI) of her lower thoracic and lumbar spine was performed. This study showed a new metastatic bone lesion on the T11 vertebra that was causing cord compression ( Fig. 1). Moreover, there was evidence for leptomeningeal disease. The patient received emergency radiotherapy and dexamethasone 8 mg IV q 6 h. Her neurological status continued to improve, and she was discharged ambulating independently 4 days later. She experienced improved analgesia with transdermal fentanyl, oral dexamethasone, and antineuropathic adjuvant medications, not needing breakthrough medication. She also reported a decrease in numbness over her left S1 dermatomal distribution. The patient died 1 mo later without recurrent neurologic deficit and with adequate pain control on the same regimen.
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Discussion |
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TopIntroductionCase ReportDiscussionReferences |
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Paraplegia appearing shortly after a patient has had an epidural catheterization suggests a spinal hematoma, particularly if the patient had hemostatic abnormalities (3). The incidence is estimated at <1 in 150,000 epidurals (4), although with the concomitant use of enoxaparin, the incidence may be as frequent as 1 in 3100 continuous epidurals (5). Other possibilities include chemical toxicity (6), extradural air (7), extradural tumors (8), thoracic disk herniation (9), coincidental Guillain-Barré syndrome (10), and hysterical paraplegia (11). Our patient did not have hemostatic abnormalities, and her clinical picture began to improve shortly after the infusion ended. Thus, provided that the patient was receiving the intended concentration of ropivacaine and that it was delivered at the intended rate, the clinical picture suggested migration of the catheter into the intrathecal space with clinical improvement after the infusion was stopped. However, catheter aspiration was negative for cerebrospinal fluid, and the persisting residual neurological signs suggested another etiology. The patient’s inability to flex both hips was compatible with pathology at the lower thoracic level, and because the catheter had been inserted at the L4-5 interspace, an MRI of the lower thoracic and lumbar spine was performed.
Patients with a diagnosis of epidural metastasis experience back pain in 80%–95% of the cases at some point during the course of their disease (12). The intensity of pain and the degree of neurologic deficit is believed to be related to the size of the metastasis producing cord compression. Thus, conventional wisdom is that patients with small epidural lesions may not have pain and neurologic deficit (13). This was clearly not the case in our patient, as she never experienced back pain despite the significant size of her lesion (Fig. 1). We believe that the compliance of this patient’s epidural space was at the far end of the plateau portion of the compliance curve and that the administration of the local anesthetic progressively shifted her to the steep ascending portion of the curve. Thus, as volume increased in the epidural space, so did pressure, until the symptoms of cord compression were ultimately experienced.
This phenomenon has never been reported in a patient with epidural metastases. There have been reports of patients who developed limb paralysis after epidural anesthesia in the presence of spinal stenosis, but these patients did not experience reversible paraplegia (14,15). Although it could be argued that the appearance of symptoms was unrelated to epidural therapy, the return of her neurologic evaluation to baseline, except for her inability to fully flex her hips once the epidural infusion was stopped, argues against this possibility. It is interesting that an infusion of 3 mL/h in the epidural space produced symptoms of compression after 12 h of therapy. This might be explained by the presence of reactive fibrosis within the epidural space produced by the epidural metastasis, leptomeningeal disease, or both, either of which may have affected diffusion of drugs to the nerve roots, the spinal cord, and the epidural vessels (12,16). These three structures are reportedly responsible for the clearance of analgesic solutions administered in the epidural space (17). Thus, it is possible that the fluid administered into the epidural space was not cleared adequately from this area. Evaluation of the MRI by the neuroradiologist suggested the presence of leptomeningeal disease, but the sensitivity and specificity of MRI for the diagnosis of this condition is not good (18). Spinal fluid cytology or epidural fluid aspirate cytology, which were not performed in this patient, are the only ways to accurately diagnose this problem.
In conclusion, epidural metastasis may lead to fibrosis of the leptomeninges, nerve roots, spinal cord, and epidural vessels. The compliance curve of the epidural space may be greatly affected by the presence of this pathology, resulting in high epidural pressures once a continuous infusion is administered through an epidural catheter. We suggest that if a patient develops neurologic deficit shortly after an epidural infusion is started, that the epidural infusion be stopped and, if the neurologic deficit does not improve within hours, that an MRI be performed to accurately diagnose the cause of this deficit. If spinal cord compression is found, then radiation therapy and IV dexamethasone should be started as soon as possible.
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References |
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TopIntroductionCase ReportDiscussionReferences |
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- Jacox A, Carr DB, Payne R, et al. Management of cancer pain: clinical practice guidelines, no. 9, AHCPR publication no. 94–0592. Rockville, MD: US Department of Health and Human Services, Public Health Service, Agency for Health Care Policy and Research, 1994.
- Portenoy R. Managing pain in patients with advanced cancer: the role of neuraxial infusion. Oncology 1999; 13: 7–8.[Medline]
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Vandermeulen EP, Van Aken H, Vermylen J. Anticoagulants and spinal-epidural anesthesia. Anesth Analg 1994; 79: 1165–77.
[Free Full Text] - Tryba M. Epidural regional anesthesia and low molecular heparin: pro [in German]. Anästhesiol Intensivmed Notfallmed Schmerzther 1993; 28: 179–81.[Medline]
- Schroeder DR. Statistics: detecting a rare adverse drug reaction using spontaneous reports. Reg Anesth Pain Med 1998; 23: 183–9.[Web of Science][Medline]
- Drasner K, Rigler MA, Sessler DI, et al. Cauda equina syndrome following intended epidural anesthesia. Anesthesiology 1992; 77: 582–5.[Web of Science][Medline]
- Nay PG, Milazkiewicz R, Jothilingam S. Extradural air as a cause of paraplegia following lumbar analgesia. Anaesthesia 1993; 48: 402–4.[Web of Science][Medline]
- Hirlekar G. Paraplegia after epidural analgesia associated with an extradural spinal tumor. Anaesthesia 1980; 35: 363–4.[Web of Science][Medline]
- Matsuura JA, Makhoul RG, Posner MP, et al. Intradural herniation of a thoracic disc causing paraplegia coincident with epidural anesthesia. Anesth Analg 1997; 84: 922–3.[Web of Science][Medline]
- Collier C. Postoperative paraplegia: an unusual case. Anaesth Intensive Care 1994; 22: 293–5.[Web of Science][Medline]
- Laraki M, Orliaguet GA, Flandin C, et al. Hysterical paraplegia as a cause of transient paraplegia after epidural anesthesia. Anesth Analg 1996; 83: 876–7.[Web of Science][Medline]
- Lewis DW, Packer RJ, Raney B, et al. Incidence, presentation and outcome of spinal cord disease in children with systemic cancer. Pediatrics 1986; 178: 438–43.
- Livingston K, Parrin R. The neurosurgical management of spinal metastases causing cord and cauda equina compression. J Neurosurg 1978; 49: 839–43.[Medline]
- Skoven JS, Wainapel SF, Willock MM. Paraplegia following epidural anesthesia. Acta Neurol Scand 1985; 72: 437–43.[Web of Science][Medline]
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Yuen EC, Layzer RB, Weitz SR, Olney RK. Neurologic complications of lumbar epidural anesthesia and analgesia. Neurology 1995; 45: 1795–801.
[Abstract/Free Full Text] - Appelgren L, Nordborg C, Sjoberg M, et al. Spinal epidural metastasis: implications for spinal analgesia to treat refractory cancer pain. J Pain Symptom Manage 1997; 13: 25–42.[Web of Science][Medline]
- Bernards CM, Hill HF. The spinal nerve root sleeve is not a preferred route of redistribution of drugs from the epidural space to the spinal cord. Anesthesiology 1991; 75: 827–32.[Web of Science][Medline]
- Portenoy RK, Galer BS, Salomon O. Identification of epidural neoplasm: radiography and scintigraphy in the symptomatic and asymptomatic spine. Cancer 1989; 64: 2207–13.[Medline]
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