Propofol-Induced Bronchoconstriction: Two Case Reports

Abstract

We have anesthetized asthmatic or allergic patients with inhaled anesthetics expecting their bronchodilating effect. However, in a retrospective study (1), asthma attacks were more often observed during inhaled versus IV anesthesia. Propofol is considered to be safe for asthmatic patients because of its bronchodilating effect (2–4), although some reports describe patients having an allergic reaction to it (5,6). We describe two cases of bronchoconstriction by propofol in patients who had allergic diseases. Case Reports Case 1 A 42-yr-old woman (155 cm, 52 kg) was scheduled for tumor resection of the breast in September. She had had allergic rhinitis for 5 yr. She had taken antihistamine drugs only during spring. She had no other complications. Atropine 0.5 mg and midazolam 5 mg were IM administered 15 min before anesthetic induction. Anesthesia was induced with propofol (1% Diprivan™; AstraZeneca Japan, Osaka, Japan) 130 mg IV while breathing oxygen 6 L/min to insert a laryngeal mask airway. Suddenly, mask ventilation became impossible as a result of high resistance of the airway, and breathing sounds disappeared by auscultation. Endotracheal intubation was performed immediately. Epinephrine 0.5 mg and methylprednisolone 125 mg were administered IV. The lowest oxygen saturation (Spo2) was 80%. In 1 min, ventilation and Spo2 returned to normal. Thereafter, anesthesia was maintained with sevoflurane 1%–2% with nitrous oxide 4 L/min in oxygen 2 L/min. The trachea was extubated just after finishing surgery without any complications. Case 2 A 35-yr-old woman (160 cm, 58 kg) was scheduled for tumor resection of the breast in December. She had an atopic dermatitis in her childhood. She had taken an antihistamine drug for an allergic rhinitis in spring and early summer for 8 yr. She had no other complications. Atropine 0.5 mg and midazolam 5 mg were IM administered 15 min before anesthetic induction. Anesthesia was induced with propofol 150 mg IV followed by 4 mg · kg · −1h · −1 infusion and fentanyl 100 g IV while breathing nitrous oxide 3 L/min in oxygen 3 L/min. A laryngeal mask airway was inserted. However, just after the insertion, her face, neck, and chest were flushed, and wheezing was heard. Her blood pressure decreased and her heart rate increased. Anesthesia was changed to inhaled sevoflurane 1%–2% with nitrous oxide 4 L/min in oxygen 2 L/min. Aminophylline 250 mg was administered. In a few minutes, the flush decreased and wheezing disappeared. After completion of the surgery, the laryngeal mask airway was removed without event. Diprivan™, administered in both cases, includes soybean oil, glycerin, yolk lecithin, and sodium edetate. Discussion Bronchoconstriction occurred during induction of anesthesia by propofol in two patients with allergic diseases. During in vitro studies using isolated guinea pig trachea, propofol had an airway relaxant effect (7), which may have been a result of decreased vagal tone (3). Although the direct effects of propofol on airway smooth muscle occur with large doses, these are unlikely to be of primary clinical relevance (8). Large doses of propofol reduce histamine-induced contraction in human isolated airway smooth muscle either nonsensitized or immunologically passively sensitized with asthmatic serum (4). However, the relaxant potency of propofol on airway smooth muscle depends on the formulation of the drug used. Propofol showed a potency approximately three times higher when solubilized with hydroxypropyl-β-cyclodextrin compared with an oil-in-water emulsion of the drug (current formulation) (7). In healthy subjects, propofol did not induce any changes in immunoglobulin levels, complement C3, or plasma histamine concentration toward anaphylactoid reactions (9). However, some reports have suggested that propofol causes histamine release in healthy (9) and atopic patients (10), and may induce bronchospasm (6). The incidence of histamine release during anesthetic induction with propofol occurred in 15% of the patients with a history of allergy (11). The flush in Case 2 suggests histamine-induced allergic reaction. Respiratory resistance in clinical anesthesia was smaller in the induction with propofol than with thiopental (2,12). With thiopental, however, wheezing was heard in 40%–50% of the asthmatic patients (13). Mehr and Lindeman (14) reported that propofol had no benefit over thiopental in reducing peripheral airway responsiveness. Therefore, these comparative studies could not conclude that propofol can be safely used in allergic patients. In addition, the current commercially available formulation of propofol in Japan includes soybean oil and yolk lecithin, which are problematic for allergic patients. These additives might have induced allergic reaction in our two cases. Fourteen patients were reported to have life-threatening reactions within a few minutes after receiving propofol (6). One case was described with bronchospasm by propofol (5). Therefore, propofol should be used with caution in allergic patients. Light anesthesia also might induce bronchoconstriction. However, in our experience in nonallergic patients the same induction procedure has not induced bronchoconstriction during laryngeal mask airway insertion. Therefore, the depth of anesthesia induction used in these two patients might have been enough for laryngeal mask airway insertion. In conclusion, two cases with a history of allergic diseases were reported in which bronchoconstriction occurred during anesthetic induction with propofol.