Generalized Muscle Rigidity and Hypercarbia with Halothane and Isoflurane

The combination of halothane and succinylcholine is linked to masseter muscle spasm, generalized muscle rigidity, rhabdomyolysis with myoglobinuria, and malignant hyperthermia. However, reports of these symptoms are rare when succinylcholine is not used [1-4]. We present a case of generalized muscle rigidity in which succinylcholine was not used. Case Report A 2-yr-old girl with a history of asthma and developmental delay presented for bilateral anterior hip releases for flexion contractures. She had no surgical history or family history of anesthetic problems. She had been seen by a geneticist but had no genetic defect or syndrome associated with her physical problems or developmental delay. On physical examination, she had a short neck, lumbar lordosis, and a barrel chest. Her weight was 11 kg. She received oral premedication with midazolam and acetaminophen in the day surgery unit with good results. Routine monitors were used. General anesthesia was induced via a mask using oxygen, nitrous oxide, and halothane. When a satisfactory level of anesthesia had been established, tracheal intubation was attempted. Initial attempts were unsuccessful because of difficulty opening the mouth and extending the head. Intubation of the trachea was successful on the third attempt using a styletted 4.5-mm uncuffed endotracheal tube without direct visualization of the vocal cords. The tube was secured, and ventilation was spontaneous. The halothane (4%) was changed to isoflurane (2%), and peripheral IV access was attempted. During the attempt, the patient's arms were stiff; pronation and flexion at the elbow were impossible. A 24-gauge catheter was placed in the left wrist. The end-tidal carbon dioxide was 67 mm Hg. The isoflurane was discontinued, and the patient was hyperventilated with 50% oxygen/50% nitrous oxide. Thiopental (50 mg) and cisatracurium (1.5 mg) were given IV. An additional 20-gauge IV catheter and a 22-gauge right radial arterial catheter were placed. The muscle rigidity slowly improved over the next 10 min. The pHa value was 7.42, PaCO2 was 30 mm Hg, Pao2 was 286 mm Hg, bicarbonate was 19 mEq/L, and potassium was 4.3 mEq/L. The rectal temperature remained 36.5-36.8[degree sign]C. A caudal block was placed using 0.175% bupivacaine (10 mL). The case was continued using a propofol infusion. The urine output averaged 2 mL [center dot] kg-1 [center dot] h, and the urine remained clear. The operation lasted approximately 2.5 h. After surgery, the caudal block was repeated using 0.175% bupivacaine (6 mL) with preservative-free morphine (300 micro g). The patient awoke easily, and her trachea was extubated without incident. An intraoperative creatine kinase (CK) was 2,370 U/L, and a CK repeated 20 h after surgery was 18,046 U/L. Discussion Masseter muscle rigidity is classically described as tightness of the jaw muscles after the administration of succinylcholine. This tightness can usually be overcome by force and abates within two to three minutes. Differential diagnosis includes normal increase in tone in the muscles of mastication after succinylcholine, inadequate dose, myotonia, and temporomandibular joint abnormalities [1,2]. In 50% of patients experiencing masseter muscle rigidity, caffeine-halothane contracture testing indicates susceptibility to malignant hyperthermia (MH) [5]. Classic MH signs include tachycardia, tachypnea, hypercapnia, hyperkalemia, metabolic acidosis, hyperthermia, arrhythmias, and muscle rigidity [6]. MH may have a broad spectrum of presentation, depending on the triggering agent and the rapidity of onset. MH can be triggered by volatile anesthetics without succinylcholine; however, co-administration of succinylcholine often speeds the onset of signs. This case presented a clinical challenge to rule out MH, which was a possibility because of the rigidity (both masseter and generalized) and the increased end-tidal carbon dioxide. However, there was no change in heart rate or temperature, and blood gas analysis did not reveal any metabolic acidosis. The respiratory acidosis was relatively easy to correct by using controlled ventilation. Based on this and the fact that the rigidity improved rather quickly with the cessation of the volatile anesthetics, we believed that this was probably not a case of MH; however, we proceeded using nontriggering drugs and elected not to use dantrolene. Although we initially were hesitant to label the patient as MH-susceptible, her postoperative CK was so increased that we believe that an aborted episode of MH had occurred [7]. Generalized rigidity has been described in a patient with Smith-Lemli-Opitz syndrome after the use of halothane without succinylcholine [8]. This syndrome consists of microcephalus; elfin facies; motor, mental and growth delay; genital hypoplasia; and syndactyly of the toes. Patients with this syndrome have developed rigidity without other typical signs of MH; however, their CK values have not been increased to nearly the extent seen in our case. Rubiano et al. [9] have reported a case of rhabdomyolysis after halothane without succinylcholine in a patient later diagnosed with Duchenne's muscular dystrophy [9]. Our patient apparently does not have either of these syndromes. Perhaps generalized muscle rigidity can occur from volatile anesthetics without the concomitant use of succinylcholine. This rigidity can be associated with some symptoms, but not necessarily the classic symptoms, of MH. Although it is still unclear to us as to whether this would have developed into a fulminant episode of MH, it seems prudent to treat patients with generalized muscle rigidity as MH-susceptible.