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Anesthesia & Analgesia:
doi: 10.1213/00000539-200008000-00049
Case Report

Vecuronium-Induced Neuromuscular Blockade in a Patient with Cerebral Palsy and Hemiplegia

Suzuki, Takahiro MD, PhD; Nakamura, Takashi MD, PhD; Saeki, Shigeru MD, PhD; Ogawa, Setsuro MD, PhD

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Author Information

Department of Anesthesiology, Surugadai Nihon University Hospital, Tokyo, Japan

April 21, 2000.

Address correspondence and reprint requests to Takahiro Suzuki, MD, Department of Anesthesiology, Surugadai Nihon University Hospital, 1-8-13, Kanda-Surugadai, Chiyoda-ku, Tokyo, Japan. Address e-mail to suzukit@cd5.so-net.ne.jp.

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Abstract

Implications: We evaluated vecuronium-induced neuromuscular block in both arms of a patient with cerebral palsy and hemiplegia. A remarkable resistance to vecuronium was observed in the hemiplegia side compared with cerebral palsy side. Complete recovery from neuromuscular block should be assessed in the cerebral palsy side that shows a delayed recovery.

We describe an anesthetic in a patient having symptoms of both cerebral palsy (CP) and hemiplegia (HP). This case report illustrates the comparative resistance to vecuronium between the CP and HP sides.

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Case Report

Our patient was a 44-yr-old man whose spastic CP had been diagnosed when he was a neonate. The range of motion of the patient’s limbs was severely limited because of spastic quadriplegia; however, he could walk by himself, although with difficulty. He was admitted to the hospital with a sudden immobilization of his left arm and leg and was found, by computed tomography, to have a cerebral tumor in the right cerebral hemisphere. The patient was scheduled for removal of the tumor during general anesthesia approximately 1 mo after the onset of HP. Laboratory examinations of blood and electrocardiogram were within normal range. Until the day before surgery, the patient took phenytoin 300 mg daily for prevention of seizure disorders.

The patient was premedicated with atropine 0.25 mg IM approximately 45 min before the induction of anesthesia. An IV cannula was inserted into the right saphenous vein, and an infusion of lactated Ringer’s solution was started. A blood pressure cuff was placed on the left lower limb to minimize interference with arm blood flow and neuromuscular monitoring. Anesthesia was induced with fentanyl 4 μg/kg and thiamylal 5 mg/kg IV, followed by controlled ventilation with 2.0% inspired sevoflurane in oxygen via a face mask. Immediately after the induction of anesthesia, bilateral ulnar nerves were stimulated simultaneously at the wrists with square-wave supramaximal stimuli of 0.2-ms duration, delivered in a twitch mode at 0.1 Hz, and the contraction of adductor pollicis muscles were measured by using accelerometrys. After evoked responses were stable, the patient was given vecuronium 0.1 mg/kg IV. Figure 1 shows that onset times were very slow in both the CP side (7.5 min) and the HP-combined side (8.3 min). The maximum blockade was 86% of control in the HP side, although complete block was achieved in the CP side. We administered additional vecuronium 0.05 mg/kg; however, a complete neuromuscular block was not obtained in the HP side (96% of control). Tracheal intubation was performed after maximal depression of twitch tension. Anesthesia was maintained by using 1.0%–2.0% sevoflurane, 50% nitrous oxide in oxygen, and supplemental IV fentanyl. Ventilation was adjusted to keep the end-tidal carbon dioxide within the range of 28–32 mm Hg. Esophageal temperature was maintained above 35°C with a heating mattress. Further incremental doses of vecuronium were not administered, and spontaneous recovery of neuromuscular function was allowed to occur.

Figure 1
Figure 1
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Clinical duration from the first injection of vecuronium to recovery of twitch to 25% of control (DUR25) and time to recovery from 25% to 75% of control were remarkably shorter in the HP side (33.3 min and 20.8 min) compared with the CP side (47.5 min and 32.2 min). Each surgical procedure and anesthesia were completed uneventfully.

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Discussion

In a previous study (1), we showed that complete neuromuscular blocks were obtained after IV vecuronium 0.1 mg/kg in all patients without neuromuscular disorders, and that mean onset time and DUR25 were 2.6 min and 44.2 min, respectively. In comparison with the results, resistance to vecuronium was demonstrated in both the HP and CP sides. However, the degree of resistance in the HP side was more pronounced, as evidenced by a less intense maximum neuromuscular block, slower onset, and a more rapid recovery of twitch responses.

Denervation of lower motor neurons (2) and proliferation of acetylcholine receptors (AchR) (3–5) are recognized even after upper motor neuron injury. Upregulation of AchR results in resistance to nondepolarizing muscle relaxants (NDMRs) as early as three to seven days after motor neuron injury (3–5). Therefore, we reasoned that there had been sufficient time for AchR proliferation in this patient. Resistance to NDMRs in CP patients has also been reported (6). Moorthy et al. (6) concluded that CP patients showed resistance to vecuronium and rapid recovery from neuromuscular block, compared with non-CP patients. The resistance may be secondary to AchR proliferation. However, CP patients do not exhibit hyperkalemia to depolarizing blockade that often occurs in cases of upper or lower motor neuron diseases (7). Perhaps there is a difference in the degree or type of proliferation of AchR between CP and HP patients. There is a possibility that the difference contributes to the magnitude of resistance to vecuronium observed in the CP and HP sides.

Furthermore, we should consider possible interactions between vecuronium and anticonvulsant drugs. Chronically administered anticonvulsants, such as phenytoin (8–10), valproic acid (10) and carbamazepine (10–13), are relatively resistant to NDMRs, as seen by mechanisms that may include upregulation of AchR (8), increased α1-acid glycoprotein, which binds NDMRs in serum (8), increased metabolism of NDMRs via hepatic enzyme induction (14), increased clearance of NDMRs (13), and increased endplate anticholinesterase activity (10,11). Resistance to NDMRs after anticonvulsant therapy occurs after two weeks (8). Our patient had received long-term phenytoin therapy, which may have contributed to resistance to vecuronium. However, it was reported previously that mean DUR25 obtained after IV vecuronium 0.1 mg/kg was approximately 19 (9) to 28.1 (13) min in patients receiving chronic anticonvulsants therapy. In comparison with the results, a DUR25 of 47.5 min obtained in the CP side seemed to be long, even with 0.15 mg/kg. Additionally, it is impossible to explain the differences in recovery from neuromuscular block observed in the CP and HP sides by the mechanisms described above. From these points of view, chronic phenytoin therapy was unlikely to have influenced resistance to vecuronium in our patient.

In conclusion, the resistance to vecuronium observed in the HP side was more remarkable than in the CP side. The mechanism is not clear, but the difference is thought to relate to different degrees of AchR proliferation between the CP and HP sides. Clinically, our results suggest that complete recovery from neuromuscular block should be assessed adequately in the CP side that shows a delayed recovery, compared with the HP side.

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References

1. Suzuki T, Munakata K, Watanabe N, et al. Augmentation of vecuronium-induced neuromuscular block during sevoflurane anaesthesia: comparison with balanced anaesthesia using propofol or midazolam. Br J Anaesth 1999; 83:485–7.

2. Krueger KC, Waylonis GW. Hemiplegia: lower motor neuron electromyographic findings. Arch Phys Med Rehabil 1973; 54:360–4.

3. Martyn JAJ, White DA, Gronert GA, et al. Up-and-down regulation of skeletal muscle acetylcholine receptors: effects on neuromuscular blockers. Anesthesiology 1992; 76:822–43.

4. Carter JG, Sokoll MD, Gergis SD. Effect of spinal cord transection on neuromuscular function in the rat. Anesthesiology 1981; 55:542–6.

5. Yoshioka K, Miyata Y. Changes in distribution of the extrajunctional acetylcholine sensitivity along muscle fibers during development and following cordotomy in the rat. Neuroscience 1983; 9:437–43.

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7. Dierdorf SF, McNiece WL, Rao CC, et al. Effect of succinylcholine on plasma potassium in children with cerebral palsy. Anesthesiology 1985; 62:88–90.

8. Kim CS, Arnold FJ, Itani MS, et al. Decreased sensitivity to metocurine during long-term phenytoin therapy may be attributable to protein binding and acetylcholine receptor changes. Anesthesiology 1992; 77:500–6.

9. Ornstein E, Matteo RS, Schwartz AE, et al. The effect of phenytoin on the magnitude and duration of neuromuscular block following atracurium or vecuronium. Anesthesiology 1987; 67:191–6.

10. Tempelhoff R, Modica PA, Jellish WS, et al. Resistance to atracurium-induced neuromuscular blockade in patients with intractable seizure disorders treated with anticonvulsants. Anesth Analg 1990; 71:665–9.

11. Spacek A, Neiger FX, Klenn CG, et al. Rocuronium-induced neuromuscular block is affected by chronic carbamazepine therapy. Anesthesiology 1999; 90:109–12.

12. Norman J. Resistance to vecuronium. Anaesthesia 1993; 48:1068–9.

13. Alloul K, Whalley DG, Shutway F, et al. Pharmacokinetic origin of carbamazepine-induced resistance to vecuronium neuromuscular blockade in anesthetized patients. Anesthesiology 1996; 84:330–9.

14. Anderson GD. A mechanistic approach to antiepileptic drug interactions. Ann Pharmacother 1998; 32:554–63.

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