Regurgitation can occur either during light (active regurgitation) or deep (passive regurgitation) anesthesia in ruminants and camelids in spite of preoperative fasting and withholding of water. Active regurgitation usually occurs during light anesthesia and is characterized by explosive discharge of large quantities of ruminal materials. Passive regurgitation occurs during deeper planes of anesthesia when the esophageal muscles and transluminal pressure gradients relax as a result of anesthetic‐induced muscle relaxation. If the airway is not protected, a large amount of ruminal materials can be aspirated into the trachea and reach the small airways. Aspiration of acidic stomach fluid causes immediate reflex airway closure and destruction of type II alveolar cells and pulmonary capillary lining cells. Consequently, pulmonary edema and hemorrhage, hypoxemia, and arterial hypotension develop due to loss of alveolar and capillary integrity leading to reflex airway closure, bronchospasm, dyspnea, hypoxemia, and cyanosis. Recovery from aspiration pneumonia depends on the pH and amount of ruminal materials aspirated [10]. Pigs tend to have very acidic stomach fluid with a pH as low as 1.5–2.5 [12], whereas the rumen pH remains within 5.5–6.5 in cattle, sheep, and goats [13] and 6.4–7.0 for C1 of camelids [14]. Thus, the greater impact of aspirating rumen contents lies in the amount of bacterial microflora and solid food materials aspirated. In pigs, the level of acidity of stomach fluid is the primary factor affecting the severity of damage to the pulmonary tissues upon aspiration. Severe consequences like reflex airway constriction, mechanical airway obstruction, and aspiration of bacteriologically active materials can still occur in the presence of a neutral pH in ruminants [10]. Animals may die before an endotracheal tube can be placed to protect the airway in extreme cases. Please refer to Chapter 7 for prevention and treatment of aspiration pneumonia. Preoperative withholding of feed and endotracheal intubation with an adequately inflated cuff immediately following induction of anesthesia are recommended in all anesthetized farm animals.
1.4 Salivation
Ruminants normally salivate profusely during anesthesia. Total amounts of saliva secretion in conscious adult cattle and sheep have been reported to be 50 l and 6–16 l per 24 hours, respectively [15, 16]. In the past, anticholinergics like atropine were used routinely as part of the anesthetic induction regimen in an effort to prevent salivation. However, atropine only reduces the water content of the saliva [17], thus causing the saliva to become more viscous and increasing the potential of airway obstruction, particularly in neonates. If the trachea is left unprotected during anesthesia, large amounts of saliva may be aspirated. Thus, tracheal intubation with appropriate inflation of the cuff immediately following induction should be instituted to protect the airway. For large ruminants, setting up the surgery table in a way that the head is lower and the throatlatch area is elevated relative to the mouth and thoracic inlet will help drainage and prevent pooling of the saliva and ruminal contents in the oral cavity (Figure 1.2). Placing a sandbag or rolled‐up towel under the neck of a small ruminant or camelid patient to elevate the throatlatch so that the mouth opening is lower than the occiput allows saliva to escape, avoiding the potential for aspiration (Figure 1.3). This technique also helps to minimize the flow of passive regurgitation during deep anesthesia [18].
Figure 1.2 Lateral recumbency of an adult bovid; note the elevation of the throatlatch.
Source: Illustration by Kim Crosslin.
Figure 1.3 Lateral recumbency of a small ruminant; note the elevation of the throatlatch.
1.5 Malignant Hyperthermia
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
