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REGIONAL ANESTHESIA

Guillain-Barré Syndrome in a Patient with Pancreatic Cancer After an Epidural-General Anesthetic

Department of Clinical Anesthesiology, Columbia University, College of Physicians and Surgeons, St. Luke's-Roosevelt Hospital Center, New York, New York

Address correspondence and reprint requests to Daniel M. Thys, MD, Professor of Anesthesiology, Columbia University, College of Physician and Surgeons, Chairman, Department of Anesthesiology, St. Luke's-Roosevelt Hospital Center, New York, NY 10019. Address e-mail to pdb9{at}columbia.edu or philb99{at}optonline.net

	Abstract

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Guillain-Barré syndrome is a rare occurrence in medicine and is probably rarer still as a postoperative complication. We report an uneventful operative course, during epidural-general anesthesia, in a patient undergoing pancreatectomy who presented with acute paralysis mimicking an acute cervical spinal cord syndrome or brachial plexus neuropathy. The signs and symptoms of right upper extremity paralysis occurred within 2 h postoperatively. Immediate work-up, which included magnetic resonance imaging, electromyography, and nerve conduction velocity studies, provided the diagnosis.

	Introduction

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Inexplicable diffuse peripheral neuropathy in the postoperative period is a diagnostic conundrum in which Guillain-Barré syndrome must be considered. Guillain-Barré syndrome is an unusual postoperative complication that usually has onset in the lower extremities. We report a case in a patient with pancreatic cancer who underwent pancreatectomy with epidural-general anesthesia and had onset in the upper extremities. The signs and symptoms initially mimicked an acute cervical spine or brachial plexus neuropathy. Neuroelectrodiagnostic evaluation led to the diagnosis of Guillain-Barré syndrome.

Postoperative peripheral neuropathy has a multifactorial etiology thought to include surgical trauma/traction, tourniquet pressure, worsening of preexisting neuropathy, and malpositioning of the patient with resultant pressure on a nerve (1–5). Male gender, obesity, preexisting asymptomatic nerve dysfunction, and prolonged hospitalization have been implicated as possible risk factors (5). Nerves can either be compressed directly by various instruments and operating room equipment such as retractors or the operating table and its attachments or indirectly through stretching over a bony prominence. We present a case in which no obvious nerve compression occurred but the patient experienced an acute postoperative peripheral polyneuropathy.

	Case Reports

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The patient was a 63-yr-old male admitted for exploratory laparoscopy, open partial pancreatectomy, and splenectomy for a pancreatic mass of the distal pancreas. His medical history was significant for recent type 2 diabetes mellitus, hypercholesterolemia, and hypertension. There was no history of diabetic or other polyneuropathy signs or symptoms. His medications were metformin, glipizide, atorvastatin, and candesartan. He smoked one pack of cigarettes per day and consumed a "few beers per day." His surgical history included a childhood tonsillectomy and adenoidectomy. Physical examination revealed a well developed, well-nourished male 188 cm tall weighing 87 kilograms. His physical examination, including a superficial neurological examination, and laboratory findings were within normal limits. The plan was for a combined epidural-general anesthetic. The epidural catheter was placed without difficulty in the sitting position at L3-4. The patient was placed supine with arms carefully abducted <90 degrees and padded. Anesthetic induction and tracheal intubation were accomplished with fentanyl 250 µg, propofol 200 mg, and succinylcholine 100 mg IV. The anesthetic was maintained with pancuronium 9 mg, additional fentanyl 500 µg, desflurane 2.89%–5.92%, nitrous oxide 60%, oxygen 40% and epidural bupivacaine 0.5% 40 mL over the entire operative time of 7 h and 11 min. The final intraoperative dose of bupivacaine 0.5% was given approximately 70 min before the end of the procedure. Lactated Ringer's solution 9,500 mL was given IV, the blood loss was estimated to be 1500 mL, and the urine output was 580 mL. No transfusions were given. The operative procedure consisted of a total pancreatectomy, splenectomy, duodenectomy, distal gastrectomy, cholecystectomy, and choledochojejunostomy. The operative procedure was extended as the surgeon attempted to get tissue margins free of cancer. Throughout the intraoperative course the patient had stable hemodynamics. The trachea was extubated without difficulty. On arrival in the postanesthesia care unit (PACU) the patient's vital signs were normal, he reported no pain (as a result of the functioning epidural), his epidural level of sensory anesthesia to temperature discrimination (alcohol swab test) was T-4 (fourth thoracic intercostal nerve level), and he had a full motor block of both lower extremities. An epidural patient-controlled analgesia (PCA) infusion of bupivacaine 0.125% and 4 µg/mL fentanyl at 10 mL/h was started immediately.

Two hours after admission to the PACU, the nurse noted that the patient was unable to move his right arm. Examination of the patient revealed weakness, flaccid paralysis, and loss of sensation and reflexes for most of the right upper extremity. Muscle strength was 0 (on a 0–5 Medical Research Council scale) for the deltoid, triceps, biceps, wrist extensors, and flexors and 2 for flexion of the fingers, but 1 for opposition and 4 for the trapezius. The left arm had normal strength. The lower extremities were affected by the epidural and could not be meaningfully examined. However, the patient no longer had a motor block and was able to move them equally and straight leg raise. A preliminary diagnosis of acute herniated cervical disk at level C5, C6, and/or C7 versus cervical spinal stenosis and acute spinal cord and/or nerve root compression was made. An emergency magnetic resonance image (MRI) (with contrast) of the head, neck, thoracic inlet, and brachial plexus revealed multilevel degenerative and discogenic disease with no spinal cord impingement; the brachial plexus and thoracic inlet were unremarkable, as was the brain. Methylprednisolone sodium 500 mg IV q 6 h was ordered and neurology and neurosurgery consults were called.

On postoperative day 1, 12 h later, the patient had regained some of his right arm strength and now complained of paresthesias in his left index, long finger, and thumb. The consulting neurologist requested discontinuation of the epidural PCA to facilitate further evaluation and the patient was placed on IV PCA. Neurological examination of the upper extremities revealed left triceps, biceps, wrist extension, wrist flexion to be 5/5, opponens pollicis 3/5, right triceps 4/5, biceps 4/5, wrist extension 4/5, wrist flexion 4/5, and opponens pollicis 1–2/5. Reflexes were absent in the right upper extremity and normal elsewhere in the body. There was circumferential loss of touch, pain, and vibration sense from the right thumb and index finger to the elbow. The left side had sensory loss in the thumb and index finger to the wrist. The rest of the examination including lower extremities and cranial nerves was within normal limits. The neurologist's initial clinical differential diagnosis of this right upper extremity monoparesis included brachial plexus injury or spinal cord lesion; however, the brain MRI and cervical spine MRI did not show any lesion. An MRI of the brachial plexuses with gadolinium enhancement and electromyography (EMG) nerve conduction studies were ordered. The neurosurgeon thought this clinically represented a seventh cervical nerve (C7) radiculopathy possibly caused by neuroforaminal or osteophyte compression or possibly a bilateral brachial plexopathy, although in his opinion this was less likely. Methylprednisolone sodium was tapered to 15 mg IV q 6 h. Regular insulin 4 q 4 h subcutaneously was begun in addition to sliding scale coverage.

On postoperative day 4, physical therapy was begun. The neurological examination remained stable with perhaps some return of sensation. Nerve conduction studies and a spinal tap were performed as further work-up. The cerebral spinal fluid (CSF) analysis showed protein 80 mg/dL (normal range, 12–60 mg/dL), glucose 87 mg/dL (normal range, 40–70 mg/dL), white blood cells 1, and red blood cells 1. Sensory nerve conduction studies of the right median and ulnar nerves revealed absent evoked responses. The right radial nerve revealed reduced amplitude and normal velocity. Right sural nerve conduction was normal. Motor nerve conduction studies of the right median nerve revealed reduced amplitude and slowing with an absent F wave. Right ulnar nerve conduction showed mild slowing and markedly prolonged F latency. Right peroneal nerve conduction revealed slow velocity and reduced amplitude with absent F waves. Right tibial nerve conduction was slowed and had a markedly prolonged F wave latency. Needle EMG of selected muscles revealed rare fibrillations, positive sharp waves, and reduced recruitment in the right first dorsal interosseus muscle (ulnar nerve). The right abductor pollicis brevis (median nerve) and the right biceps (musculocutaneous nerve) showed reduced and discrete recruitment, respectively. Motor unit potentials were normal. The neurophysiologist's interpretation was that this represented a demyelinating disease highly suggestive of Guillain-Barré syndrome in its postoperative occurrence. The consulting neurologist thought that this was either a brachial plexopathy or acute idiopathic demyelinating polyneuropathy (AIDP) (i.e., Guillain-Barré), which would be consistent with the normal CSF cell count and increased CSF protein. The patient was discharged home on postoperative day 11, after diabetic teaching, oncologic evaluation, and physical therapy evaluation and treatment had begun. Arrangements for outpatient physical therapy and outpatient follow-up with the oncologist, neurologist, and surgeon were also made. The patient made slow and steady progress and was deemed to have recovered from the paralysis in 6 months.

	Discussion

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Ulnar neuropathy has been estimated to occur in approximately 0.2%–1% of noncardiac surgical patients (5). One prospective randomized study found that patients having surgery are commonly without symptoms of ulnar neuropathy for 2–7 days after surgery (5). This suggests that there are other causes of postoperative ulnar neuropathy besides positioning or that ulnar neuropathy exists preoperatively in a subclinical state that then becomes manifest after the stresses of surgery and/or anesthesia. This may also explain why the incidence has not decreased despite physician awareness and efforts to position and pad extremities to avoid this complication (2–5). The fact that this patient had abnormalities affecting the ulnar, median, radial, musculocutaneous nerves, and the nerve supply to the deltoid muscle suggests that the cause was more proximal in location along the brachial plexus. Alternatively, a metabolic (diabetes mellitus) or physiological (Guillain-Barré–AIDP) cause may have been at work damaging the nerves but not yet manifesting clinically. After 24 hours of large dose methylprednisolone sodium, there was partial recovery of strength in some muscles of the affected arm and new onset of mild paralysis symptoms (paresthesias, weakness) in the contralateral hand. The recent, insidious onset of diabetes as a consequence of destruction of the pancreas by carcinoma did not seem long-lived enough to cause diabetic sensorimotor peripheral neuropathy of this severity and acuteness. Also, other studies of diabetic neuropathy show a high degree of bilateral symmetry in nerve conduction studies (6)—something not present in this patient. In another study, Novella et al. (7) indicated that there may be an association between idiopathic neuropathy and undiagnosed type 2 diabetes or impaired glucose tolerance. Postoperative Guillain-Barré syndrome was considered in these patients; however, the CSF was not examined. CSF protein levels do not increase in traumatic compression injury to the brachial plexus but do increase (in greater proportion to cell count) in diabetic polyneuropathy and Guillain-Barré syndrome (8). Our patient had increased CSF protein without an increase in red or white blood cells.

The nerve conduction studies in our patient suggested that a chronic process could be excluded. After nerve injury EMG demonstrates decreased recruitment and absent F waves immediately. Normal conduction may be seen acutely, distal to the injury until axonal death occurs in 7–28 days (9–13). Subsequently, decreased amplitude and abnormal EMG findings with fibrillation occur. The decreased recruitment of the right hand first dorsal interossei muscle (ulnar nerve), abductor pollices brevis (median nerve), and biceps (musculocutaneous nerve) also suggests an immediate cause of peripheral nerve injury. The postoperative findings, which at first led us to suspect a herniated cervical disk or another type of spinal cord compression, are not common in diabetic polyneuropathy or suggest another process superimposed upon diabetic neuropathy (7). Gross et al. (14) reported four cases of peripheral neuropathy after pancreatitis and major pancreatic surgery. However, these patients were all critically ill, septic, were on multiple drug therapy, including metronidazole, and were on parenteral nutrition in which insufficient vitamin therapy was given. None of these conditions existed in our patient. At 6-month follow-up, our patient had 95%–100% return of muscle strength and function.

In conclusion, this reported Guillain-Barré Syndrome that presented as sudden postoperative paralysis mimicking an acute spinal cord or nerve root compression syndrome in its initial appearance. Understanding neuropathophysiology as reflected in nerve conduction studies and EMG was crucial in backdating the onset of the neuropathy and arriving at the diagnosis.

	Footnotes

 
Accepted for publication August 27, 2004.

	References

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This Article Abstract Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a colleague Similar articles in this journal Similar articles in Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via Web of Science (5) Citing Articles via Google Scholar Google Scholar Articles by Bamberger, P. D. Articles by Thys, D. M. Search for Related Content PubMed PubMed Citation Articles by Bamberger, P. D. Articles by Thys, D. M. Related Collections Complications Regional Anesthesia