Meperidine-Induced Muscular Rigidity During Spinal Anesthesia?

Abstract

To the Editor: Opioid-induced muscular rigidity has become a well-known phenomenon since it was first described in 1953 (1). It has not been reported during spinal anesthesia. We report a case in which severe muscular rigidity apparently induced by IV meperidine occurred in a patient during spinal anesthesia. A 17-yr-old man (167 cm, 52 kg), whose medical history was not elicited, underwent an emergency appendectomy under spinal anesthesia. Before anesthesia, we administered 0.1 mg of fentanyl and 10 mg metoclopramide for sedation and prophylaxis of emesis, respectively. We then administered 4 mL of 0.5% isobaric bupivacaine intrathecally at the L3-4 interspace using a 27-gauge Whitacre spinal needle. Sensory block up to the level of Th2 was obtained, with complete abdominal wall relaxation and lower limb paralysis but without respiratory discomfort. We administered additional 0.2 mg fentanyl intermittently. Approximately 20 min into the operation, the patient shivered slightly, with the shivering gradually becoming more prominent over the next 10 min. We administered diazepam (5 mg) and meperidine (50 mg) IV, which caused the shivering to immediately disappear. However, after a few more minutes, the patient developed rigidity of the neck, masseter, upper extremities, thoracoabdominal region, and thighs. In particular, the abdominal wall’s rigidity markedly increased his intraabdominal pressure, causing much of the small intestine to extrude from the surgical incision. We discontinued the surgery. Because marked muscle rigidity remained, we induced general anesthesia, propofol, and succinylcholine, and successfully tracheally intubated the patient. Muscular rigidity immediately disappeared, and we resumed the operation. Subsequently, we used both spinal and general anesthesia for this patient, maintaining general anesthesia with 1%–1.5% sevoflurane in 2 L/min of oxygen and 2 L/min of air. The patient’s body temperature and end-tidal carbon dioxide tension remained between 38.0°C–38.2°C and 35–45 mm Hg, respectively, throughout anesthesia. Surgery, which lasted 1.5 h, was completed uneventfully without further administration of muscle relaxants being required. The patient was immediately tracheally extubated. Satisfactory analgesia remained from the spinal anesthesia; a pinprick test revealed analgesia up to the level of Th4, with continuing abdominal wall and lower limb paralysis. Meperidine is usually administered at 0.33–0.85 mg/kg or 25–50 mg for the treatment of shivering (2–5); hence the dose used in our case seemed to be appropriate. The muscular rigidity observed in this patient appears to have been induced by meperidine because the rigidity occurred within a few minutes of giving this drug. The differential diagnosis of such rigidity includes malignant hyperthermia and pain-induced agitation resulting from insufficient spinal anesthesia (6). However, such scenarios are unlikely in the presence of normal end-tidal carbon dioxide tension, pyrexia that only reached 38.2°C, and spinal anesthesia that produced an adequate block up to the level of Th2. In the present case, we gave metoclopramide and fentanyl before administering meperidine. Because both drugs are associated with muscular rigidity, they cannot be excluded as a possible cause of the rigidity observed in this case. However, for approximately 30 min after we administered metoclopramide and fentanyl, until we gave meperidine, the patient’s response to verbal stimuli was almost normal and complete muscular relaxation was obtained in the abdomen and lower extremities. Although we cannot exclude the possibility that metoclopramide and/or small dose fentanyl enhanced the rigidity, they do not appear to have directly caused it. To the best of our knowledge, opioid-induced muscular rigidity has not been reported during spinal anesthesia. Opioids have been proposed to cause rigidity as a result of their action on the central nervous system at the spinal or supraspinal level. Interestingly, although spinal anesthesia provided a complete nerve conduction blockade up to the level of Th2 in the present case, muscular rigidity obviously extended beyond the neck and upper extremities to the lower abdominal wall. Accordingly, opioid-mediated disinhibition of the central nervous system at a spinal or supraspinal level would not appear to be the sole mechanism of opioid-induced muscular rigidity as is conventionally described (6). In the present case, the establishment of complete muscular relaxation (abdominal wall, thighs) and anesthesia below Th2 until the administration of meperidine suggests that an unknown opioid action on the peripheral nervous system might have been involved in the mechanism of opioid-induced muscular rigidity. Norihito Kitagawa, MD Department of Anesthesiology Tsuruta Clinic for Orthopedic Surgery Ushizu, Saga, Japan [email protected] Mayuko Oda, MD Department of Anesthesiology Saga Memorial Hospital Takagise, Saga, Japan Tadahide Totoki, MD Saga Medical School Hospital Saga Medical School Nabeshima, Saga, Japan