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Malignant hyperthermia, also referred to as porcine stress syndrome, is a genetic disorder that occurs due to mutation of the ryanodine receptors (ryr‐1 locus) of the calcium channels in the skeletal muscles [19–21]. The presence of abnormal ryanodine receptors allows a massive amount of calcium to be released from the cells into the sarcoplasmic reticulum, resulting in generalized extensive skeletal muscle contraction. Though malignant hyperthermia has been reported in other animal species, pigs and humans seem to be the most susceptible. Certain breeds of pigs, like Pietrain, Poland China, or Landrace, are very susceptible to this syndrome, while Large White, Yorkshire, and Hampshire, on the other hand, are much less so [22, 23]. The clinical signs of malignant hyperthermia syndrome in susceptible pigs are manifested in a sudden and dramatic rise in body temperature and end‐tidal CO₂ followed by muscle fasciculation, muscle rigidity, tachypnea, tachycardia, arrhythmias, myoglobinuria, metabolic acidosis, renal failure, and often death. The prognosis is usually poor once the episode is initiated. The triggering agents of malignant hyperthermia include stress (e.g. excitement, transportation, or preanesthetic handling), halogenated inhalation anesthetics (e.g. halothane, isoflurane, sevoflurane, and desflurane), and depolarizing neuromuscular blocking drugs (e.g. succinylcholine). Stress associated with transportation or preslaughter conditions can trigger malignant hyperthermia/porcine stress syndrome. Pigs affected by this mutation tend to develop pale, soft, and exudative meat, which can lead to significant economic loss for the procedures [24]. Lidocaine and ketamine have been indicated as triggering agents, but there is no evidence to support this theory [25].

Halogenated inhalation anesthetics are known triggers for malignant hyperthermia, and halothane has been indicated to be the most potent trigger [26]. However, a report in humans demonstrated that in a total of 75 malignant hyperthermia cases, 42 were isoflurane related, 12 were sevoflurane related, 11 were halothane related, eight were enflurane related, and only two were desflurane related [27]. Further study showed that the augmentation of caffeine‐induced contractures of frog sartorius muscle by isoflurane is three times and by enflurane is four times, whereas by halothane is 11 times [28]. Similarly, halothane appears to be the most potent and most frequently reported trigger of malignant hyperthermia in pigs. Isoflurane has been reported to trigger malignant hyperthermia in susceptible pigs like Pietrain or Pietrain‐mixed pigs [29]. Only one incidence of isoflurane‐induced malignant hyperthermia has been reported in a potbellied pig [30]. Sevoflurane‐induced malignant hyperthermia also has been reported in purebred Poland China pigs [31]. Episodes of malignant hyperthermia induced by desflurane have been reported in Large White, Pietrain, and Pietrain‐mixed pigs [29, 32].

A case of malignant hyperthermia in cattle was reported in an isoflurane‐anesthetized Angus bull [33]. At 75 minutes after induction, progressive increase of heart rate from 55 to 70 beats/minute and end‐tidal CO₂ from 38 to 60 mmHg occurred and the result of arterial blood gas taken at this time showed a respiratory acidosis (pHa 7.268) with moderate increase of PaCO₂ (from 29.7 to 66.4 mmHg) and a decrease in PaO₂ (from 449 to 267 mmHg). Isoflurane was discontinued at this time, but heart rate (from 70 to 155 beats/minute) and end‐tidal CO₂ (from 60 to 218 mmHg) continue to increase at 140 minutes post‐induction. Body temperatures recorded from nasopharyngeal probe increased from 39.5 °C (103.1 °F) at 75 minutes and 43.5 °C (110.3 °F) at 140 minutes. Unlike malignant hyperthermia in pigs [34, 35], muscle rigidity, one of the typical clinical signs of malignant hyperthermia, was not observed in this bull. In addition, clinical signs of malignant hyperthermia in pigs developed within minutes of exposure to triggering agent, whereas progression of the clinical signs in this case did not occur until 75 minutes after initiation of isoflurane. The delay onset of clinical signs has also been observed in horses [36], dogs [37], and cats [38]. Unfortunately, the bull developed ventricular fibrillation which progressed to asystole and cardiopulmonary resuscitation was unsuccessful [33].

In 1981, McGrath et al. [39] reported that intramuscular (IM) acepromazine at 1.1 and 1.65 mg/kg reduced the incidence of malignant hyperthermia by 40% and 73%, respectively. A lower dose of 0.55 mg/kg IM was only able to delay but not prevent the onset of the episode [39]. Because of limited availability of effective drugs for treatment, minimizing the stress prior to anesthesia and avoiding using anesthetics that are known triggers are imperative in susceptible animals to prevent a malignant hyperthermia episode. In recent years, the development of a DNA test for malignant hyperthermia has enabled the accurate identification of the malignant hyperthermia mutation genotypes from carriers to noncarriers, resulting in the elimination of the malignant hyperthermia mutation from breeding stock, which is a significant economic gain for the pork industry [40–42].