Bronchospasm Induced by Propofol in a Patient with Sick House Syndrome

Sick house syndrome (or sick building syndrome) is characterized by nonspecific complaints of mucosal irritation, headaches, nausea, and chest symptoms. It is believed that indoor environmental pollution causes these symptoms (1). Propofol is often used in patients with asthma because of its relaxant effects on airway smooth muscle (2–4). Yet, bronchospasm can be induced by propofol (5–7). These cases of bronchospasm are associated with anaphylactoid reactions. We report here a patient with sick house syndrome who suffered broncho-spasm without an anaphylactoid reaction. Case Report A 45-yr-old woman was admitted to a local hospital with a diagnosis of breast cancer and had been scheduled for a simple mastectomy. Her medical history included sick house syndrome, and her main symptom was a wheezing that had persisted for 6 yr. She had been treated with theophylline and fluticasone propionate inhalation. Her operation was stopped because bronchospasm occurred after the induction of anesthesia with propofol 80 mg and vecuronium 6 mg IV. She was transferred to our hospital with a presumed diagnosis of asthma. Preoperative examination was unremarkable except for a marked increase in eosinocytes (17.2%) and slight decrease in forced expiratory volume in 1 s (78%). Methylprednisolone 80 mg and aminophylline 125 mg were administered before the operation, and midazolam 2.5 mg and atropine 0.5 mg were administered 30 min before the operation. Preoperative baseline values of blood pressure, heart rate, and pulse oximetry (Spo2) were 126/82 mm Hg, 89 bpm, and 98%, respectively. Anesthesia was induced by propofol 100 mg without a significant change in arterial blood pressure. A minute after the injection of propofol, expiratory wheezes appeared. Spo2 decreased to 88%–92%. There were no signs of anaphylactoid reaction such as hypotension or skin erythema. Methylprednisolone 125 mg and aminophylline 250 mg were administered IV. One hour later, expiratory wheezes had disappeared gradually, and Spo2 had increased to 98%. Anesthesia was maintained with 0.5%–1.0% sevoflurane. During this time, surgery was terminated. Surgery was rescheduled 2 wk later. Anesthesia was induced with midazolam 4 mg and sevoflurane 2%–4%. A laryngeal mask was inserted without difficulty. Anesthesia was maintained with 2 L/min of nitrous oxide, 1 L/min of oxygen, and 1.5%–2.5% sevoflurane. There were no signs of bronchospasm during the surgery, although she had sudden intermittent attacks of severe headaches after surgery, and a magnetic resonance imaging angiograph revealed two unruptured brain aneurysms. Four weeks after the operation, the patient underwent interdermal skin tests. The dermal skin tests showed negative reactions for propofol, vecuronium, and other drugs. Drug lymphocyte stimulation tests (DLSTs) showed a positive reaction for propofol (Diprivan®) but a negative reaction for Intralipid® and other drugs (Table 1).Table 1: Result of Skin Testing and Drug Lymphocyte Stimulation Test (DLST)At 8 wk after the operation, she was scheduled for a craniotomy. Anesthesia was induced with midazolam, vecuronium, and sevoflurane and maintained with 4 L/min of nitrous oxide, 2 L/min of oxygen, 1.5%–2.5% sevoflurane, and 700 μg of fentanyl. There were no signs of bronchospasm, and she was discharged on postoperative Day 20. Discussion Propofol causes anaphylactoid reactions such as skin erythema, hypotension, and bronchospasm (5–7). There are few reports of bronchospasm induced by propofol without other presenting signs of anaphylaxis. Although no single test for determining the drug or drugs causing an anaphylactoid reaction has been established, skin testing is a simple and safe method for determining to which drug or drugs a patient is sensitive (8). It should be performed four to six weeks after the anaphylactoid reaction (8). Our patient underwent intradermal skin tests against a variety of anesthetics using the protocol described by Fisher (9) four weeks after suffering the second bronchospasm. However, there were no positive reactions to anesthetics in the intradermal skin tests. DLST is used to detect the sensitization drug in Type 1 or Type 4 allergy (10). Sensitivity and specificity of this drug in the patients with drug allergies were reported 62%–78% and 82%–93% of the time, respectively (11,12). In this patient, the DLST showed a positive reaction against propofol, suggesting that propofol might be responsible for the bronchospasm during the induction of anesthesia. Laxenaire et al. (5) reported propofol anaphylaxis in four patients with no previous history of exposure to the anesthetic. Our patient had no history of exposure to propofol and had been diagnosed with sick house syndrome. Her wheezing began to develop just after she had moved into a new house and occurred when she was in the new house. It was thought that her airway hypersensitivity had been caused by volatile organic compounds, such as formaldehyde, toluene, and xylene, used in the construction of the house (13,14). Although she was treated with methylprednisolone, her high eosinocyte level (17.2%) indicated that she still had bronchial hypersensitivity. This case indicates that propofol is not always a safe anesthetic for patients with asthma, especially drug-induced asthma. The increasing use of propofol for patients with asthma may result in more cases such as the one described here.