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|Year : 2011 | Volume
| Issue : 4 | Page : 476--477
Propofol-induced violent coughing in a patient with Becker's muscular dystrophy
Department of Anesthesia and Intensive Care, Alchemist Hospitals Ltd., Panchkula, Haryana, India
Department of Anesthesia and Intensive Care, Alchemist Hospitals Ltd., Panchkula, Haryana
Propofol anesthesia is often associated with decreased incidence of gagging, coughing or laryngospasm, and provides intense suppression on airway reflex during tracheal intubation and laryngeal mask airway insertion. Propofol pretreatment is also effective in reducing the occurrence of opioid-induced coughing. These benefits are often attributed to bronchodilator and sedative effects of propofol. However, severe coughing following sedative doses of 1% propofol has not been reported so far. We report a rare case of violent coughing following low-dose propofol infusion in a patient with Becker«SQ»s muscular dystrophy.
|How to cite this article:|
Jain A. Propofol-induced violent coughing in a patient with Becker's muscular dystrophy.Indian J Pharmacol 2011;43:476-477
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Jain A. Propofol-induced violent coughing in a patient with Becker's muscular dystrophy. Indian J Pharmacol [serial online] 2011 [cited 2020 May 28 ];43:476-477
Available from: http://www.ijp-online.com/text.asp?2011/43/4/476/83134
Propofol anesthesia is often associated with decreased incidence of gagging, coughing or laryngospasm and provides intense suppression of airway reflex during tracheal intubation and insertion of laryngeal mask airway.  Propofol pretreatment is also effective in reducing opioid-induced coughing.  These benefits have been attributed to bronchodilator and sedative effects of propofol. Reports of vigorous cough reaction to induction doses of propofol have been reported. However, severe coughing following sedative doses of 1% propofol has not been reported so far. , We report a rare case of violent coughing following low-dose propofol infusion in a patient with Becker's muscular dystrophy.
A 34-year-old male with perianal abscess and fistula-in-ano was scheduled for incision drainage and fistulectomy under saddle block. He was a known case of Becker's muscular dystrophy. His symptoms started at 18 years of age as slowly progressive weakness of bilateral lower limbs. The patient was unable to climb stairs; though, could walk with support. There was no difficulty in breathing and swallowing. He was able to cough forcefully on command. He was a non-smoker and had no history of allergy or asthma. As his baseline electrocardiogram was normal and he had no history suggestive of congestive heart failure. Surgical management was planned. Patient was given 1.8 ml of 0.5% bupivacaine intrathecally at L3-L4 interspace in the sitting position and he was made supine after 10 min. Subsequently, surgery was started in the lithotomy position. As the patient was very apprehensive, midazolam was given in 0.5 mg increments to a total dose of 1.5 mg in 20 min. As the patient was still anxious and was about to cry, a bolus of 30 mg propofol (1%) was administered followed by propofol infusion at the rate of 50 mg/hr. Patient became sedated and calm, but was arousable on verbal commands. His heart rate decreased from 110/min to 80/min and blood pressure was normal. However, after 2 min, patient started coughing violently and became extremely restless. There were no oropharyngeal secretions on suctioning and his chest was clear on auscultation. There were no episodes of desaturation. Propofol sedation was stopped immediately. Intravenous lignocaine 80 mg was given after 5 min of intermittent, though recurrent coughing. But, only a transient reduction in the severity of cough occurred. Subsequently, patient was nebulized with salbutamol. The intensity and severity of cough decreased progressively and subsided completely in the next 15 min. Further, intraoperative period was uneventful
The violent coughing induced following propofol sedation in our patient with Becker's dystrophy could be explained on the basis of variable effect of propofol on the cough and swallowing reflex. The sensitivity of cough reflex did not appear to be modified by estimated propofol concentrations as low as 1.2 μg ml -1 .  This, in combination with the suppression of swallowing reflex and laryngeal closure reflexes at sedative doses of propofol in our patient with possible preexisting subclinical swallowing abnormalities, might have resulted in a violent coughing response to minimal, yet undetected pooled oropharyngeal secretions.
Our hypothesis is further supported by the findings of Kohjitani et al.,  who investigated relationships between frequency of coughing episodes and intraoral use of water, water remaining in the oropharyngeal space, and mean infusion rate of propofol during dental treatments. They suggested that the sole impairment of laryngeal closure reflex induced by propofol could not explain susceptibility to coughing. However, water remaining in the oropharyngeal space, which was influenced by the swallowing response, could be one of the factors for induction of coughing.
Propofol-induced violent coughing has been reported previously, at induction doses. Borgeat et al., suggested that coughing was produced by sudden high propofol brain concentrations when high doses of 2% propofol (5 mg/kg) were used.  However, it is unlikely that these concentrations could be reached by low dose propofol treatment. Mitra et al., hypothesized an alternative explanation of violent coughing when lower doses of propofol (2 mg/kg of 1% propofol) are used.  They speculate that the propofol-induced apnea might induce airway smooth muscle contraction (because of raised P a CO 2 and acidemia), which in turn stimulates the irritant receptors, thus inducing coughing. Though apnea never developed in our patient, this could be an alternate mechanism in the described case.
This case highlights coughing as an under-recognized complication of propofol sedation. It remains a point of speculation whether propofol should be used in patients at risk such as Becker's muscular dystrophy.
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