Chronic Amphetamine Users Do Not Need More Drugs During General Anesthesia

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Studies of anesthesia in amphetamine users are scarce,1 and the retrospective study by Kram et al2 reporting that use of cocaine or amphetamines was not predictive of an increased need for analgesia and sedation in trauma patients is of particular interest.
A few years ago, when I was an anesthetist in Djibouti, I was warned that anesthesia in khat chewers required higher doses of narcotics and hypnotics. Khat (Catha edulis) leaves are legally chewed by the inhabitants of the African Horn and Arabia. They contain amphetamine alkaloids (cathine and cathinone) that cause adrenergic stimulation responsible for positive inotropic and vasoconstrictive effects. This chronic amphetamine abuse is a significant problem not only in these parts of the world where studies are infrequently performed but also in Western countries where similar drugs (ecstasy, methcathinone, or ephedrone)3 are consumed. Moreover, “Westerners” are more and more frequently taking care of immigrants from places where khat is legal but abused (like alcohol) and are unfamiliar with khat as a source of amphetamine.
There is a popular perception that patients who chronically ingest amphetamine or amphetamine-like drugs will require high doses of anesthetic drugs to achieve adequate analgesia, sedation, and anesthesia.4 In a work approved by the local ethnic committee of the French military hospital in Djibouti, I observed that the interaction between khat and general anesthesia was not what was commonly believed.
The preanesthetic consultation determined whether 32 consecutive patients undergoing general anesthesia were drug addicted (khat group, N = 14) or not (controls, N = 18). Induction consisted of alfentanil 0.02 mg/kg, propofol 2.5 mg/kg, and vecuronium. After endotracheal intubation, anesthesia was maintained with a mixture of oxygen (50%), nitrous oxide (50%), and isoflurane. Isoflurane end-tidal concentration was adjusted to maintain blood pressure (BP) at ±30% of its control value and alfentanil boluses to maintain heart rate at ±30% of the control value.
Biometric data, type of surgery, and induction doses were similar in both groups. During surgery, khat chewers consumed less alfentanil than controls: 1.5 ± 0.2 vs 2.1 ± 0.3 mg (P < .05). Although isoflurane consumption (mean end-tidal values) was not different (P = .09), BP was lower in the khat group (Figure; P < .02). Heart rate, ephedrine use, and time between extubation and first request for analgesics (145 ± 275 [khat] vs 65 ± 44 min [controls]) were not significantly different.
The lower BP in khat chewers, despite similar end-tidal concentrations of isoflurane and lower doses of alfentanil, may be related to a depletion of catecholamine receptor storage, a mechanism that has been suspected in chronic amphetamine abuse.1 Furthermore, Johnston et al5 demonstrated that amphetamine decreased the minimum alveolar concentration of halothane in dogs 21%.
In conclusion, acute and chronic amphetamine abuse must be distinguished. The chronic amphetamine users described here, who had not ingested their usual khat dose the day before surgery, did not need increased drug doses of either isoflurane or opioids. These findings are consistent with those of Kram et al.
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