Dorota Pyra-Łatkiewicz, Agnieszka Chruścicka, Jacek Krysa, Monika Olewińska-Okońska, Krzysztof Przesmycki
Malignant hyperthermia during anaesthesia for strabismus surgery
II Department of Anaesthesiology and Intensive Therapy,
Head: K. Przesmycki, M.D., Ph.D. Department of Anaesthesiology and Intensive Therapy, Children's Hospital,
Head: Z. Winiarczyk, M.D., Ph.D. Chair and I Department of Ophtalmology,
Head: prof. Z. Zagórski Medical Academy of Lublin, Poland
Summary
Malignant hyperthermia symptoms: hyperthermia (42.5°C), tachycardia (160 bpm) and muscle rigidity was observed 45 minutes after induction of anaesthesia in the 6-yr-old boy during strabismus surgery. Anaesthesia was induced with thiopental/fentanyl/suxametonium and maintained with N2O/O2, halothane and atracurium. Surgery was stopped, superficial cooling started, halothane and nitrous oxide disconnected and dandrolene sodium (2 x 30 mg) given (30 minutes after beginning of the episode). Immediately after dandrolene sodium all symptoms have eased and another 20 mg was given 10 hours after. The child recovered completely and was transferred to the low-dependence area 72 hrs after the episode.
Malignant hyperthermia (MH) is a life-threatening condition resulting from an abrupt increase in skeletal muscles tone. Suxamethonium and different anaesthetic agents may provoke this phenomenon. The incidence of MH is estimated at 1 per 250 000 cases of general anaesthesia. In patients anaesthetised with halogenated volatile anaesthetics or /and suxamethonium the rate is as high as 1 per 62 000 procedures [1].
MH is five times more frequent in paediatric patients, than in adults (from 1:10000 [2] to 1:15000 [3] anaesthesias). The typical age of development of MH is between 4 and 14 years [4]. Relatively more frequent development of MH in children undergoing strabismus surgery has been explained by the speculation, that strabismus may be an early sign of undiagnosed congenital myopathy [5]. In children with strabismus, after administration of halothane and suxamethonium, an isolated spasm of the masseter muscles is observed 4 times more frequently, than in other children (2.8% and 0.82%, respectively) [6]. The role of suxamethonium in provoking masseter spasm was emphasised by Schwartz et al. [7]. The authors did not observe a muscular spasm in children in whom pancuronium was used for tracheal intubation in strabismus surgery. Rosenberg and Fletcher [8] stated that in about 50% (40-60%) of patients in whom MH developed, masseter muscles stiffness was observed at induction of anaesthesia. These observations suggest that children operated on for strabismus are at greater risk of postoperative MH [3]. As compared with the adult population, one can estimate that this risk may be as high as 1 per 3000 anaesthesias (i.e. 20-fold greater).
The authors present the case report of a child in whom symptoms of MH developed during anaesthesia for strabismus surgery.
CASE REPORT
A 6-year-old boy (body weight: 22 kg) after preoperative examination (ASA goup I) was qualified for bilateral strabismus surgery under general anaesthesia. On the day of surgery he received as premedication midazolam 6 mg p.o., 30 minutes before transfer to the operating theatre. After preoxygenation, atropine 0.3 mg, fentanyl 0.1 mg thiopentone 125 mg and suxamethonium 40 mg were injected intravenously. Tracheal intubation was performed; no masseter spasm was observed. Artificial ventilation was performed manually (20/min) with a Kühn set. An O2/N2O mixture 1:2, at a flow of 6 L/min was used. Anaesthesia was maintained with halothane (1.5-0.5 v%) and atracurium (20 mg). Monitoring included ECG, non-invasive blood pressure and pulsoxymetry. The course of anaesthesia during the first 40 minutes of surgery was uneventful. At the end of strabismus correction on the right side (about 40-45 minutes of anaesthesia), a spasticity of the left arm occurred. Additional doses of atracurium (5 and 4 mg) had no effect; on the contrary, the spasticity increased, including masseter muscles. Hyperaemia of the skin, hyperthermia and tachycardia occurred. As malignant hyperthermia was being suspected of anaesthesia and surgery were immediately interrupted.
Artificial ventilation was continued manually at an increased rate (>30/min), with oxygen flow of 8 L/min, until the transfer of the child to the ITU. Tachycardia (160/min) and hyperthermia (superficial temperature: 42.5°C) were observed. External cooling was instituted. Dantrolene i.v. (20 mg t.i.d.) was started about 30 minutes after MH diagnosis (i.e. 75 min. from the start of anaesthesia). This resulted in the immediate muscle relaxation and heart rate decrease. Before transfer to the ITU, the boy received an additional dose of fentanyl 1 mg and midazolam 5 mg i.v. for sedation.
On admission to the ITU the body temperature was 35°C and bradycardia was observed. Dantrolene was continued at previous dose. The boy was ventilated with a Bird 8400 STi ventilator, SIMV mode (MV 6 L/min; RR 20/min; FI O2 0,25). After 6 hours, the endotracheal tube was removed. At hour 9 from admission an additional dose of 20 mg Dantrolene was administered i.v. because of the rise in body temperature to>37.7°C. The following 2 days in ITU were uneventful, and the boy was discharged to the ophtalmology department.
During the ITU stay, immediately after admission, creatinine phosphokinase (CPK) activity and WBC count were elevated 4430 IU/L (normal range: 22-269) and 16.3 T/L, respectively. Seven hours later, a slight decrease in arterial blood pH (7.33), pCO2 (33.7 mmHg; 4.5 kPa) and negative base excess (-7) persisted. On the 7th day of hospitalisation, CPK activity decreased to 3531 IU/L.
DISCUSSION
After the first 45 minutes of anaesthesia, to this point uneventful, the first warning sign was the increase of muscle tone of the upper extremity, persisting despite additional doses of atracurium. MH develops most frequently during the induction of anaesthesia, although it may manifest itself in the later period (recovery or postoperative) [9]. In the described case, an additional factor contributing to the late onset of MH, might be the influence of atracurium, administered at the beginning of anaesthesia at a relatively high dose. Hall et al. [10] stated that non-depolarising muscle relaxants may delay the onset of MH symptoms, both in experimental animals and in humans. Lack of muscle relaxation, after administration of a repeated dose of atracurium may additionally reflect the refractoriness of muscular spasm to non-depolarising relaxants, characteristic of MH [4].
Independently of the time of MH development, its course may be rapid. In the case presented in this report, the full clinical picture of MH developed within 5 minutes. It consisted of progressive spasm of all skeletal muscles (including masticators) leading to generalised extensor muscle stiffness, and unnatural skin hyperaemia accompanied by hyperthermia and tachycardia. According to Larach et al. [11] the main clinical features of MH are: skeletal muscles stiffness, tachycardia and fever. Two out of these 3 signs are relevant for the diagnosis of MH [11]. In the described case all 3 clinical signs were observed during anaesthesia. An early finding confirming the diagnosis of MH may be the abrupt rise in the end-tidal CO2 concentration. In this case, however, capnography was not a part of intraoperative monitoring, so the assessment of PECO2 and metabolic rate increase were not possible.
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Piśmiennictwo
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