Repeated failure of epidural analgesia: An association with epidural fat?

Repeated failure of epidural analgesia: An association with epidural fat?

Repeated Failure of Epidural Analgesia: An Association With Epidural Fat? Scott A. Lang, M.D., F.R.C.P.C., Peter Korzeniewski, M.D., F.R.C.P.C., Donal...

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Repeated Failure of Epidural Analgesia: An Association With Epidural Fat? Scott A. Lang, M.D., F.R.C.P.C., Peter Korzeniewski, M.D., F.R.C.P.C., Donald Buie, M.D., F.R.C.S.C., Stephan du Plessis, M.B., Ch.B., M.Med., Kimiko Paterson, M.D., and Gary Morris, M.D., F.R.C.P.C. Background and Objective: To report the case of a patient who experienced repeated failed epidural analgesia associated with an unusual amount of fat in the epidural space (epidural lipomatosis). Case Report: A 44-year-old female presented for an elective small bowel resection. An L1-2 epidural catheter was placed for postoperative analgesia. The patient gave no indication of having pain at the time of emergence from general anesthesia or in the first 2 hours in the recovery room. Assessment of the level of hypoesthesia to ice while the patient was comfortable in the recovery room suggested a functional epidural catheter (cephalad level of T10). Two hours after admission to the recovery room the patient began to complain of increasing pain. Another 6 mL 0.25% bupivacaine was administered via the catheter. The patient’s pain decreased, but remained substantial, and there was minimal evidence of sensory block above the T10 level. Subsequently, a T10 epidural catheter was placed. Testing confirmed proper placement of the catheter in the epidural space at the T10 level. A test dose of 5 mL 0.25% bupivacaine resulted in prompt and complete relief of the patient’s pain. However, the level of hypoesthesia to ice did not exceed the T10 level. Approximately 1 hour later the patient complained of increasing discomfort again. There was no evidence of any sensory block, and there was no response to a bolus of 8 mL 1% lidocaine. A thorough examination of the patient did not suggest any cause for the pain other than a malfunctioning epidural catheter. A third epidural catheter was placed at the T8-9 level. This catheter was again confirmed to be in the epidural space with a test dose of 10 mL 0.5% bupivacaine. The level of hypoesthesia to ice was restricted to a narrow bilateral band from T7-T9. Analgesia failed 2 hours later. The epidural catheter was removed and the patient’s pain was subsequently managed with intravenous patient-controlled analgesia (PCA) morphine. A magnetic resonance imaging (MRI) scan revealed extensive epidural fat dorsal to the spinal cord from C5-C7 and from T3-T9. An imaging diagnosis of asymptomatic epidural lipomatosis was established. Conclusion: We have described a case of repeated failure of epidural analgesia in a patient with epidural lipomatosis. Reg Anesth Pain Med 2002;27:494-500. Key Words:

Analgesia, Epidural, Laparotomy, Lipomatosis, Tachyphylaxis, Tsui test.

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nadequate epidural analgesia has been associated with undesirable catheter location in the epidural space1,2 (e.g., anterior or lateral epidural space), compartmentalization of administered drugs by tissue barriers3,4 (e.g., plica mediana dorsalis, mucopolysaccharide), catheter migration5,6 (e.g., in-

From the Departments of Anesthesia (S.A.L., P.K.), Surgery (D.B., S.d.P.), and Radiology (K.P.), Foothills Hospital, University of Calgary, Calgary, Alberta, Canada; and the Department of Anesthesia (G.M.), Royal University Hospital, University of Saskatchewan, Saskatoon, Canada. Accepted for publication March 26, 2002. Supported by Department of Anesthesia funds, Calgary. Reprint requests: Scott A. Lang, M.D., F.R.C.P.C., Department of Anesthesia, Foothills Hospital, 1403-19th St NW, Calgary, Alberta, Canada T2N 2T9. E-mail: [email protected]. © 2002 by the American Society of Regional Anesthesia and Pain Medicine. 1098-7339/02/2705-0010$35.00/0 doi:10.1053/rapm.2002.34323

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travascular, intramuscular), and erroneous catheter placement7,8 (e.g., paravertebral, interpleural). Equipment and technical factors may also influence the adequacy of epidural analgesia9,10 (e.g., catheter kinking, catheter occlusion, catheter-hub disconnect, catheter breakage). Even the mode of drug delivery has been implicated in restricted epidural spread and inadequate analgesia.11,12 We present a case of repeated failure of epidural analgesia in a patient with epidural lipomatosis. Three epidural catheters were placed for postoperative analgesia in succession. Analgesia was established initially with each catheter, but quickly faded. Analgesia could only be temporarily and briefly reestablished with large doses of local anesthetic. Despite large doses of local anesthetic, evidence of conduction block was restricted. The literature is briefly reviewed and a hypothesis presented for consideration.

Regional Anesthesia and Pain Medicine, Vol 27, No 5 (September–October), 2002: pp 494 –500

Failed Epidural Analgesia and Epidural Lipomatosis

Case Report A 44-year-old Caucasian female (weight, 50.9 kg; height, 175 cm; body mass index [BMI], 16.4) presented for an elective small bowel resection. She had a probable diagnosis of Crohn’s disease and had been suffering from postprandial crampy abdominal pain, nausea, occasional vomiting, abdominal distention, and borborygmi. She had lost 4.4 kg in the 5 months prior to her scheduled surgery. By history she also had Ehlers-Danlos syndrome and Ankylosing Spondylitis. She underwent a right hemicolectomy in 1996 for a cecal bezoar. At the time of admission, she was taking acetaminophen/ oxycodone, fluoxetine, Pentasa (5-aminosalicylic acid), lansoprazole, trimebutine, Buscopan (hyoscine butylbromide), metoclopramide, levothyroxine, cyclobenzaprine, zopiclone, and oral iron. She had been on prednisone intermittently for symptomatic flare-ups from 1987 to 1997. Enteroclysis demonstrated proximal small bowel dilatation with a decompressed terminal ileum suggestive of mechanical small bowel obstruction and she was scheduled for a laparotomy with possible small bowel resection. An L1-2 epidural catheter (Portex; Sims Portex, Keene, NH) was placed for postoperative analgesia via a 17-gauge Tuohy needle. The catheter was placed using a loss of resistance (LOR) with saline technique via a midline approach. The catheter was easily inserted 6 cm. There was no indication of blood or cerebrospinal fluid via either the needle or the catheter. Cefazolin, 1 gm, and metronidazole, 500 mg, were administered intravenously. General anesthesia was induced with a combination of intravenous fentanyl (250 ␮g) and propofol (100 mg). Endotracheal intubation was facilitated with rocuronium (3 mg) followed by succinylcholine (70 mg). Anesthesia was maintained with desflurane, supplemental intravenous fentanyl (150 ␮g), and a bolus of 6 mL 0.5% bupivacaine via the epidural catheter. Muscle relaxation was maintained with rocuronium (total of 30 mg). An upper abdominal incision (approximately T6-T11 dermatomes) was used. Multiple small bowel strictures were found and treated with resection and stricturoplasty and surgery was completed uneventfully. As the anesthetic lasted over 2 hours, the neuromuscular paralysis from the rocuronium was allowed to dissipate spontaneously. The trachea was extubated after resumption of spontaneous respirations, and the patient was transferred to the recovery room. The patient gave no indication of having pain at the time of emergence from general anesthesia or in the first 2 hours in the recovery room (Verbal Pain



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Score 3-4/10; 0 ⫽ no pain, 10 ⫽ worst pain). Assessment of the level of hypoesthesia to ice while the patient was comfortable in the recovery room suggested a functional epidural catheter (cephalad level of T10). The epidural catheter was promptly connected to an Abbott Pain Manager II patientcontrolled analgesia pump (Abbott Laboratories, North Chicago, IL) containing 0.1% bupivacaine and 5 ␮g/mL fentanyl (continuous infusion 7 mL/h, bolus 4 mL, lockout interval 12 minutes). Two hours after admission to the recovery room the patient began to complain of increasing pain. Another 6 mL 0.25% bupivacaine was administered via the catheter. The patient’s pain decreased, but remained substantial (Verbal Pain Rating decreased from 8 to 6), and there was little evidence of sensory block above the T10 level (ice and pin prick assessments). Subsequently, a T10 epidural catheter (Arrow FlexTip Plus Catheter, Product #JH-05500; Arrow International, Reading, PA) was placed with the patient in the left lateral decubitus position via a left paramedian approach with a 17-gauge Tuohy needle and a LOR to air technique. A confirmatory (Tsui) test13 again suggested proper placement of the catheter in the epidural space at the T10 level (bilateral motor response at approximately the T10 level at 5.0 mamp with a Digistim II nerve stimulator (Neurotechnology, Houston, TX, pulse width 200 ␮sec, 1 Hz). A test dose of 5 mL 0.25% bupivacaine resulted in prompt and complete relief of the patient’s pain. However, the level of hypoesthesia to ice did not extend cephalad to the T10 level. The new catheter was attached to the patient-controlled epidural analgesia (PCEA) device. Approximately 1 hour later the patient complained of increasing discomfort again. An acute pain service (APS) physician was called to assess the situation. Again, there was no evidence of any sensory block, and there was no response to a bolus of 8 mL 1% lidocaine. A thorough examination of the patient did not suggest any cause for pain other that a malfunctioning epidural catheter. The patient was told that this was very unusual, but it was likely that both epidural catheters had somehow migrated out of the epidural space. Alternative analgesia was discussed (i.e., intravenous patient-controlled analgesia [IVPCA]), but the patient elected to have another epidural catheter placed. A third epidural catheter (Portex; Sims Portex) was placed in the left lateral decubitus position via a midline approach with a 17-gauge Tuohy needle and a LOR to air technique at the T8-9 level. This catheter was tested with 10 mL 0.5% bupivacaine. Analgesia was re-established. However, the level of

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Fig 1. MRI and illustration of the thoracic spine and epidural space. (Inset) a, Abnormal amount of epidural fat; b, spinal cord; c, subcutaneous fat; d, Cerebrospinal fluid; e, normal epidural space and fat; f, dura; g, lamina of vertebra; h, Ligamentum flavum. (A) T1W1 (400/8/3) (repetition time/echo time/number of excitations). Sagittal T1-weighted imaging of a normal thoracic spine. (B) T1W1 (400/8/3). Sagittal T1-weighted imaging of the thoracic spine of the patient. An excessive amount of epidural fat is noted posteriorly in the central canal extending from T3 to T9. This epidural fat does not compress the thecal sac or spinal cord and has a high intensity signal (white) similar to the subcutaneous fat. The adjacent cerebrospinal fluid (CSF) has a low intensity signal (black), while the spinal cord has an intermediate intensity signal (dark grey).

hypoesthesia to ice was restricted to a narrow bilateral band from T7-T9. Analgesia failed 2 hours later. The epidural catheter was removed and the patient’s pain was subsequently managed with intravenous patient-controlled morphine (bolus dose 1.5 mg, lockout 6 minutes, no maximum) (Lifecare 4100 PCA Plus Infusor; Abbott Laboratories). A more detailed history acquired the next day revealed that several months ago she had been treated with oral prednisone for a presumptive diagnosis of Crohn’s disease. The patient agreed to a magnetic resonance imaging (MRI) scan of her spine. A neurosurgical consultation was acquired to facilitate the acquisition and interpretation of the MRI scan and to provide advice if any abnormality was found. The MRI scan

revealed extensive epidural fat dorsal to the spinal cord from C5-C7 and from T3-T9 (Fig 1A through D). A diagnosis of epidural lipomatosis was established. There was no evidence of spinal cord compression. As the patient was currently asymptomatic, she was discharged home with instructions to see her family physician regularly for reassessment regarding the diagnosis of epidural lipomatosis. A pathologic examination of the tissue removed at the time of surgery revealed diaphragm-like strictures in the resected specimen of small bowel. These were interpreted as likely secondary to nonsteroidal antiinflammatory drug treatment. There was no evidence of Crohn’s disease. The patient was discharged home with instructions to see her surgeon in 3 weeks time.

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Fig 1. (Cont’d) (C) T2W1 (3000/98.7/4). On sagittal T2-weighted imaging of the same region of thoracic spine, the excessive amount of epidural fat continues to have a high intensity signal (white) similar to the subcutaneous fat. The CSF has a high intensity signal (light grey), and the spinal cord has a low intensity signal (dark grey). (D) T1W1 (256/160/3). On axial T1-weighted imaging at the level of T6, the excessive amount of epidural fat occupies the posterior half of the central canal without spinal cord or thecal sac compression.

Discussion Inadequate epidural analgesia is a problem faced regularly on any acute pain service. The differential diagnosis can be lengthy, and troubleshooting can be labor-intensive (Table 1). Despite this, we believe that all 3 epidural catheters in our patient were placed properly. The Tsui test uses an electric current to stimulate motor nerve rootlets in the epidural space.13,14 The sensitivity and specificity of the Tsui test for identification of the epidural space are 100% and 91.6%, respectively.13 The first 2 catheters produced evidence of extensive bilateral segmental conduction block to ice below T10 that was associated, temporarily, with good to excellent

pain relief (e.g., total, but temporary, pain relief after 5 mL 0.25% bupivacaine injected via the second catheter). The third catheter (T8-9) produced a very restricted segmental area (T7-9) of hypoesthesia to ice after 10 mL 0.5% bupivacaine that only temporarily relieved the patient’s pain (⬍2 hours). Subsequent injections of local anesthetic via all 3 catheters failed to reproduce analgesia. Large volumes of local anesthetic (6 to 10 mL) failed to extend evidence of conduction block higher than T10 with the first 2 catheters and failed to extend evidence of conduction block outside a narrow T7-9 segmental band with the third catheter. These observations led us to perform a MRI scan to look for a space-occupying lesion.

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Regional Anesthesia and Pain Medicine Vol. 27 No. 5 September–October 2002 Table 1. Epidural Analgesia: Trouble-shooting Failed Analgesia Cause

Management Options

Catheter is not in the epidural space Subcutaneous5 Paraspinal muscle/fat5 Paravertebral7,22 Interpleural8 Intravascular23,24 Catheter is in the epidural space, but is not providing adequate analgesia Catheter in anterior epidural space1,27 Catheter in lateral epidural space2 Catheter or solution migrates out intervertebral foramen2,14,28-31 Catheter not placed at appropriate level (i.e., inadequate analgesia and/or excessive side effects precluding continued use)14,31 Other distribution problem (e.g., extensive dermatomal demand [e.g., thoracoabdominal T4-L1 incision], space occupying lesion [tumor,32 mucopolysaccharide,4 fat2], plica mediana dorsalis,3,33,34 fibrous adhesions,35 epidural air,36,37 diffusion barrier4,38 Pharmacokinetic55-57 problem (e.g., enhanced drug absorption/metabolism) Pharmacodynamic39,55-57 problem (e.g., receptor-mediated tolerance, drug interaction) Neural processing problem36,40,54,57 (e.g., conduction block insufficient to “handle” “intensity” of neural traffic) Central neurogenic pain41 Other source of pain remote from surgical site Technical problem with equipment (obstructed catheter9 [kink,10 connector obstruction or disconnection,9 blood clot, inflammation,38 manufacturing defect42]; pump failure43 [electronic, air-in-the-line, mechanical]) Human error44 (programming error, drug error) Leaking epidural site45,46

Prevent migration from epidural space by ensuring catheter is inserted an optimal distance (4-6 cm)25 and is well secured26 Tsui test13 and epidural local anesthetic test dose to confirm placement and to try to reestablish analgesia Replace catheter or choose alternative analgesic regimen

Tsui test13/local anesthetic test dose may help identify where catheter is Reposition* catheter by pulling it back24,47,48 Change programming parameters (e.g., increase bolus11 dose and/or infusion rate58) Change selection of drug/s (e.g., select opioid only [i.e., less dependence of catheter position49,50]) Replace catheter Identify and address other source/s of pain Identify and address technical problems and human error Apply pressure dressing over epidural exit site (personal observation) or consider crazy glue seal45 Consider dual epidural catheter for extensive dermatome requirements51,52 Consider multimodal53 or hybrid† analgesic regimen Consider epidurogram or MRI Consider consultation for management of chronic pain of central origin

*Controversial issue (pro and con). †Hybrid technique ⬅ A combination of two or more major analgesic interventions (e.g., intercostal nerve block and epidural catheter).

Epidural lipomatosis is a rare disorder.15 However, the experience of some investigators suggests that it may be underdiagnosed.16 It is characterized by an excessive amount of nonencapsulated fat in the epidural space. Excess epidural fat generally occurs in the posterior epidural space and can act as a space-occupying lesion resulting in variable compression of the spinal cord, dural sac, or nerve roots.15 Alternatively, asymmetric deposition of excess epidural fat can cause spinal cord pathology via rotational distortion.17 Patients typically present with back pain or variable symptoms of spinal cord or nerve root compression.15 Men are affected more often than women.15 The pathogenesis of the disorder is unknown.15 It has been reported to occur spontaneously18 or in association with steroid use,

endocrinopathies, or obesity,15,16,18 but may occur in patients without these risk factors.19 MRI is the diagnostic technique of choice.15 Treatment depends on presentation.15 Medical management15 may include strategies to induce weight loss, the elimination of medications thought to have a causal relationship with the development of epidural lipomatosis (e.g., steroids, ritonavir20), and the management of associated endocrinopathies (e.g., Cushing’s syndrome). Surgical management may involve multiple level laminectomies and decompression16,18 or endoscopic suction decompression via small bilateral laminotomies.21 We hypothesize in our patient that the extensive accumulation of epidural fat adversely affected the distribution of the drugs we administered in the

Failed Epidural Analgesia and Epidural Lipomatosis

epidural space (bupivacaine and fentanyl). The fat may have prevented symmetrical distribution of the drugs in the thoracic epidural space. Alternatively, the fat may have acted as a “depot” for the lipid soluble bupivacaine and fentanyl, effectively sequestering the analgesic agents. This could explain the very limited segmental conduction blocks obtained with concentrated solutions of bupivacaine and lidocaine. We hope that this case report stimulates other clinicians to consider such an association and encourages investigators with the appropriate tools to establish an animal model to elucidate the mechanisms by which excess epidural fat may impair epidural analgesia. In conclusion, repeated failure of epidural analgesia together with restricted segmental conduction block after the administration of large volumes of local anesthetic should prompt consideration of epidural lipomatosis. After more common causes of failed epidural analgesia have been ruled out, MRI should be considered.

Acknowledgment We thank Helen Schroeder for her assistance in preparation of this manuscript.

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